We are IntechOpen, the world's leading publisher of Open Access books Built by scientists, for scientists

4,200+

Open access books available

116,000+

International authors and editors

125M+

Downloads

151 Countries delivered to Our authors are among the

Top 1%

most cited scientists

12.2% Contributors from top 500 universities

Selection of our books indexed in the Book Citation Index in Web of Science™ Core Collection (BKCI)

## Interested in publishing with us? Contact book.department@intechopen.com

Numbers displayed above are based on latest data collected. For more information visit www.intechopen.com

## **Meet the editor**

Dr. Yannis Dionyssiotis is specialized in Physical Medicine and Rehabilitation. He worked in the Laboratory for Research of the Musculoskeletal System at the University of Athens, in the Rehabilitation Department of KAT Hospital in Athens, Head of Physical Medicine and Rehabilitation Department in Rhodes General Hospital and Medical Director of Rehabilitation Center Amyntaio

of Florina General Hospital in Greece and as Stationsarzt in the Klinik für neurochirourg.-neurologische Frührehabilitation, Westpfalz-Klinikum, Germany. Currently, he is the Medical Director of Physical Medicine and Rehabilitation Department of European Interbalkan Medical Center in Thessaloniki and is also working as Research Fellow in the 1st Department of Orthopaedics in General University Hospital ATTIKON. Dr. Dionyssiotis has clinical experience as physiatrist including experience in a variety of clinical settings as clinician, researcher, clinical instructor and consultant. He also holds a Thesis in Osteoporosis and Metabolic Bone Diseases from National and Kapodistrian University of Athens. Dr. Dionyssiotis has an extensive list of professional presentations and publications in the areas of rehabilitation, spinal cord injury, multiple sclerosis and osteoporosis. He has served as reviewer for several international journals and has written books and papers for osteoporosis in spinal cord injury, exercise, spinal orthoses, jumping mechanography, falls, and botulinum toxin.

Contents

**Preface VII**

**Paraplegia 1**

George Sapkas

**Section 2 Management of Paraplegia 71**

**Spinal Cord Lesions 73**

Aris Papachristos

**Paraplegia 127**

Chapter 6 **Malnutrition in Paraplegia 129** Yannis Dionyssiotis

Ayoub Dakson and Sean D. Christie

Chapter 5 **Functional Electrical Stimulation in Paraplegia 109**

**Section 3 Complications and Special Musculoskeletal Issues in**

**and Management 3**

**Section 1 Introduction-Epidemiology - Classification - Prognosis of**

Chapter 1 **Paraplegia Caused by Infectious Agents; Etiology, Diagnosis**

Farhad Abbasi and Soolmaz Korooni Fardkhani

**Thoracoabdominal Aortic Interventions 25** Anisha H. Perera and Richard G.J. Gibbs

Chapter 4 **Role of Decompressive Surgery in Disorders Associated with**

Stamatios A. Papadakis, Spyridon Galanakos, Kleio Apostolaki, Konstantinos Kateros, Olga Antoniadou, George Macheras and

Chapter 3 **Spinal Cord Injuries Following Suicide Attempts 53**

Chapter 2 **Paraplegia as a Complication of Thoracic and**

### Contents

#### **Preface XI**



**X** Contents



Preface

Dear colleagues!

Warm regards

ing scientific knowledge.

It was my great pleasure to be the Editor of this project published by InTech. All authors were enthusiastic to present their work which resulted in a high quality scientific project. It was impossible to cover all aspects of paraplegia, but this attempt brought together scien‐ tists and experts from various disciplines related to the field. This project could be a start for the development of a network in the field of spinal cord injuries in general and for exchang‐

I would like to thank all authors who participated in this book project and the company

**Yannis Dionyssiotis, MD, PhD, FEBPRM** Rehabilitation Center "Aghios Loukas o Iatros",

Trikala Thessaly, Greece

1st Department of Orthopaedics, General University Hospital Attikon,

University of Athens,

Athens, Greece

InTech which produces continually high education free access publications.

### Preface

Chapter 7 **Body Composition in Paraplegia 155**

Chapter 8 **Paraplegia Related Osteoporosis 175**

Chapter 9 **Estimating Renal Function in Paraplegia 193**

Chapter 10 **Animal Models in Traumatic Spinal Cord Injury 209**

Chapter 11 **Mesenchymal Stem Cells in Spinal Cord Injury 229** N.K. Venkataramanaa and Rakhi Pal

Mahdi Sharif-Alhoseini and Vafa Rahimi-Movaghar

Chapter 12 **35 Years in Research on Spinal Cord Lesions and Repair 277**

Yannis Dionyssiotis

**VI** Contents

Yannis Dionyssiotis

Jennifer Pai Lee

**Section 4 Research in Paraplegia 207**

Giorgio Brunelli

Dear colleagues!

It was my great pleasure to be the Editor of this project published by InTech. All authors were enthusiastic to present their work which resulted in a high quality scientific project. It was impossible to cover all aspects of paraplegia, but this attempt brought together scien‐ tists and experts from various disciplines related to the field. This project could be a start for the development of a network in the field of spinal cord injuries in general and for exchang‐ ing scientific knowledge.

I would like to thank all authors who participated in this book project and the company InTech which produces continually high education free access publications.

Warm regards

**Yannis Dionyssiotis, MD, PhD, FEBPRM**

Rehabilitation Center "Aghios Loukas o Iatros", Trikala Thessaly, Greece

> University of Athens, 1st Department of Orthopaedics, General University Hospital Attikon, Athens, Greece

**Section 1**

**Introduction-Epidemiology - Classification -**

**Prognosis of Paraplegia**

**Introduction-Epidemiology - Classification - Prognosis of Paraplegia**

**Chapter 1**

**Paraplegia Caused by Infectious Agents; Etiology,**

Paraplegia or paralysis of lower extremities is caused mainly by disorders of the spinal cord and the cauda equina. They are classified as traumatic and non traumatic. Traumatic paraple‐ gia occurs mostly as a result of traffic accidents and falls caused by lateral bending, dislocation, rotation, axial loading, and hyperflexion or hyperextension of the cord. Non-traumatic paraplegia has multiple causes such as cancer, infection, intervertebral disc disease, vertebral injury and spinal cord vascular disease [1, 2]. Although the incidence of spinal cord injury is low, the consequences of this disabling condition are extremely significant for the individual, family and community [3]. A spinal cord injury not only causes paralysis, but also has longterm impact on physical, psychosocial, sexual and mental health. The consequences of spinal cord injury require that health care professionals begin thinking about primary prevention. Efforts are often focused on care and cure, but evidence-based prevention should have a greater role. Primary prevention efforts can offer significant cost benefits, and efforts to change behavior and improve safety can and should be emphasized. Primary prevention can be applied to various etiologies of injury, including motor vehicle crashes, sports injuries, and prevention of sequelae of infectious diseases and prompt and correct diagnosis and treatment of infections involving spinal cord and vertebrae [4]. Infections are important causes of

paraplegia. Several infections with different mechanisms can lead to paraplegia.

Several infections may cause paraplegia. They are classified into two categories: those that involve the spinal cord directly and those that involve vertebral column and cause pressure

> © 2014 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

**2. Infectious diseases and paraplegia**

**Diagnosis and Management**

Farhad Abbasi and Soolmaz Korooni Fardkhani

Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/56989

**1. Introduction**

### **Paraplegia Caused by Infectious Agents; Etiology, Diagnosis and Management**

Farhad Abbasi and Soolmaz Korooni Fardkhani

Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/56989

#### **1. Introduction**

Paraplegia or paralysis of lower extremities is caused mainly by disorders of the spinal cord and the cauda equina. They are classified as traumatic and non traumatic. Traumatic paraple‐ gia occurs mostly as a result of traffic accidents and falls caused by lateral bending, dislocation, rotation, axial loading, and hyperflexion or hyperextension of the cord. Non-traumatic paraplegia has multiple causes such as cancer, infection, intervertebral disc disease, vertebral injury and spinal cord vascular disease [1, 2]. Although the incidence of spinal cord injury is low, the consequences of this disabling condition are extremely significant for the individual, family and community [3]. A spinal cord injury not only causes paralysis, but also has longterm impact on physical, psychosocial, sexual and mental health. The consequences of spinal cord injury require that health care professionals begin thinking about primary prevention. Efforts are often focused on care and cure, but evidence-based prevention should have a greater role. Primary prevention efforts can offer significant cost benefits, and efforts to change behavior and improve safety can and should be emphasized. Primary prevention can be applied to various etiologies of injury, including motor vehicle crashes, sports injuries, and prevention of sequelae of infectious diseases and prompt and correct diagnosis and treatment of infections involving spinal cord and vertebrae [4]. Infections are important causes of paraplegia. Several infections with different mechanisms can lead to paraplegia.

#### **2. Infectious diseases and paraplegia**

Several infections may cause paraplegia. They are classified into two categories: those that involve the spinal cord directly and those that involve vertebral column and cause pressure

© 2014 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

effect on the spinal cord that eventually leads to paraplegia. In fact paraplegia can arise from a lesion either within or outside the spinal cord or cauda equina. These are classified as compressive and non compressive. Compression is caused either by bone or other masses. The main compressive causes are Pott's disease (tuberculosis of spine). The main non-compressive causes are transverse myelitis secondary to viral infections, HIV, TB and very occasionally syphilis [1]. Several bacterial, viral, mycobacterial, fungal and parasitic infections can cause paraplegia. Infectious myelitis is usually caused by neurotropic viruses or mycoplasma in conjunction with concomitant meningitis or encephalitis; these in turn either induces trans‐ verse myelitis accompanied by severe sensorimotor deficits or chiefly affect the gray matter [5].

**Etiology/ disease Diagnosis Medical treatment Surgical intervention Comment**

Penicillin, Doxycicline,

Doxycycline, amoxicillin, cefuroxime, ceftriaxone, cefotaxime

Doxycycline, rifampin, trimethoprimsulfamethoxazole, streptomycin, gentamicin, ciprofloxacin, ceftriaxone

Zidovudine and lamivudine may be used

Ganciclovir, foscarnet,

Amphotericin B, voriconazole, itraconazole

Amphotericin B, fluconazole, echinocandins

Amphotericin B, posaconazole, caspofungin

Schistosomiasis Stool exam, IFA, ELISA Praziquantel May be needed Steroid is usually used

Herpes zoster Serology, PCR, IHC Aciclovir Usually not necessary -

amoxicillin, ceftriaxone May be needed -

Paraplegia Caused by Infectious Agents; Etiology, Diagnosis and Management

Yes

ART Usually not necessary

Usually not necessary -

Usually not necessary -

Yes -

cidofovir Usually not necessary Combination therapy

Yes

Yes

Combination antibiotic therapy is necessary

5

http://dx.doi.org/10.5772/56989

Combination antibiotic therapy is necessary

> Four drugs combination is necessary

Combination antibiotic therapy is necessary (usually 3 antibiotics)

ART is used if HIV treatment is indicated

may be considered

Voriconazole is treatment of choice

Posaconazole is treatment of choice

for treatment

Subdural empyema MRI, CT Scan Antibiotic Yes

Epidural abscess MRI, CT Scan Antibiotic Yes

Tuberculosis MRI, CT-guided biopsy Anti TB drugs Yes

Syphilis MRI, CSF analysis,

Lyme ELISA, PCR, CSF analysis

Brucellosis MRI, Wright, 2ME, IFA,

CMV PP65 antigen, PCR

Candida Histopathology, culture

Zygomycosis Histopathology, culture

HIV

HTLV-I

Aspergillus

VDRL, FTA-ABS

ELISA

ELISA, Western blot, P24 antigen, IFA, RIPA

> Serology, antigen detection, PCR

Histopathology, serology, antigen detection and PCR, culture

**Table 1.** Summary of ethologic agents, diagnosis and treatment of paraplegia

#### **2.1. Bacterial infection**

One of the most important causes of paraplegia among infectious causes is bacterial infection. These organisms can produce subdural empyema, epidural abscesses, radiculomyelitis or cause spondylitis with bony destruction or pressure effect.

#### *2.1.1. Subdural empyema*

Subdural empyema refers to a collection of pus in the space between the dura and arachnoid [6]. Spinal subdural empyema is a rare condition [7] that usually occurs secondary to metastatic infection from a distant site. The clinical presentation of spinal subdural empyema is usually radicular pain and symptoms of spinal cord compression, which may occur at multiple levels. The clinical presentation is difficult to distinguish from that of spinal epidural abscess [6]. Spinal subdural space remains the least common area of localized infection in the central nervous system (CNS). Infectious processes of the subdural spinal space include subdural spinal empyema, subdural spinal abscess, infected spinal subdural cyst, and infectious spinal subdural cyst [8]. Etiologies of spinal subdural empyema include hematogenous spread from skin lesions, sepsis, direct spread from spinal osteomyelitis, complications of discography and rarely iatrogenic after spinal anesthesia, spinal epidural insertion or acupuncture [9-11]. The most affected region is the thoraco-lumbar spine [12] and the most frequent microbial isolate is Staphylococcus aureus, followed by streptococci and coagulase-negative staphylococci. Gram-negative bacilli are less frequently isolated cause [6]. Mycoplasma hominis has been isolated from subdural empyema although it is very rare [13].

#### *2.1.2. Epidural abscess*

Epidural abscess refers to a localized collection of pus between the dura mater and vertebral column. Epidural abscess of the spinal column is a rare condition that can be fatal if left untreated. It promptly progresses and can cause neurologic paralysis, urinary retention or cauda equina syndrome [14]. It usually occurs secondary to hematogenous dissemination from foci elsewhere in the body to the epidural space or by local extension from vertebral osteo‐ myelitis. Compromised immune system that occurs in patients with diabetes mellitus, AIDS, chronic renal failure, alcoholism, or cancer is a predisposing factor [6, 15]. Paraplegia and paralysis in spinal epidural abscess may be the result of spinal cord compression, spinal cord arterial or venous ischemia and thrombophlebitis or a combination of these. The most common Paraplegia Caused by Infectious Agents; Etiology, Diagnosis and Management http://dx.doi.org/10.5772/56989 5


**Table 1.** Summary of ethologic agents, diagnosis and treatment of paraplegia

effect on the spinal cord that eventually leads to paraplegia. In fact paraplegia can arise from a lesion either within or outside the spinal cord or cauda equina. These are classified as compressive and non compressive. Compression is caused either by bone or other masses. The main compressive causes are Pott's disease (tuberculosis of spine). The main non-compressive causes are transverse myelitis secondary to viral infections, HIV, TB and very occasionally syphilis [1]. Several bacterial, viral, mycobacterial, fungal and parasitic infections can cause paraplegia. Infectious myelitis is usually caused by neurotropic viruses or mycoplasma in conjunction with concomitant meningitis or encephalitis; these in turn either induces trans‐ verse myelitis accompanied by severe sensorimotor deficits or chiefly affect the gray matter [5].

One of the most important causes of paraplegia among infectious causes is bacterial infection. These organisms can produce subdural empyema, epidural abscesses, radiculomyelitis or

Subdural empyema refers to a collection of pus in the space between the dura and arachnoid [6]. Spinal subdural empyema is a rare condition [7] that usually occurs secondary to metastatic infection from a distant site. The clinical presentation of spinal subdural empyema is usually radicular pain and symptoms of spinal cord compression, which may occur at multiple levels. The clinical presentation is difficult to distinguish from that of spinal epidural abscess [6]. Spinal subdural space remains the least common area of localized infection in the central nervous system (CNS). Infectious processes of the subdural spinal space include subdural spinal empyema, subdural spinal abscess, infected spinal subdural cyst, and infectious spinal subdural cyst [8]. Etiologies of spinal subdural empyema include hematogenous spread from skin lesions, sepsis, direct spread from spinal osteomyelitis, complications of discography and rarely iatrogenic after spinal anesthesia, spinal epidural insertion or acupuncture [9-11]. The most affected region is the thoraco-lumbar spine [12] and the most frequent microbial isolate is Staphylococcus aureus, followed by streptococci and coagulase-negative staphylococci. Gram-negative bacilli are less frequently isolated cause [6]. Mycoplasma hominis has been

Epidural abscess refers to a localized collection of pus between the dura mater and vertebral column. Epidural abscess of the spinal column is a rare condition that can be fatal if left untreated. It promptly progresses and can cause neurologic paralysis, urinary retention or cauda equina syndrome [14]. It usually occurs secondary to hematogenous dissemination from foci elsewhere in the body to the epidural space or by local extension from vertebral osteo‐ myelitis. Compromised immune system that occurs in patients with diabetes mellitus, AIDS, chronic renal failure, alcoholism, or cancer is a predisposing factor [6, 15]. Paraplegia and paralysis in spinal epidural abscess may be the result of spinal cord compression, spinal cord arterial or venous ischemia and thrombophlebitis or a combination of these. The most common

cause spondylitis with bony destruction or pressure effect.

isolated from subdural empyema although it is very rare [13].

**2.1. Bacterial infection**

4 Topics in Paraplegia

*2.1.1. Subdural empyema*

*2.1.2. Epidural abscess*

organisms are Staphylococcus aureus, aerobic and anaerobic Streptococcus, Escherichia coli and Pseudomonas aeruginosa. Other organisms like Klebsiella pneumonia, Bacteroides fragilis, Enterococcus faecalis, Salmonella, Nocardia, etc. can cause spinal epidural abscess [6]. Paralysis in spinal epidural abscess may be the result of spinal cord compression, spinal cord arterial or venous ischemia and thrombophlebitis or a combination of these [16].

*2.1.4. Syphilis*

*2.1.5. Lyme*

*2.1.6. Brucellosis*

Syphilis is a sexually transmitted disease caused by the spirochete Treponema pallidum. The involvement of the CNS by Treponema pallidum has increased in the past 20 years, particularly as a result of HIV pandemic. However, tertiary forms, and especially syphilit‐ ic gumma, are rare as a result of the widespread use of penicillin. Spinal cord compres‐ sion due to syphilitic gumma is an exceptional event that may cause paraplegia [28]. Syphilitic myelitis is a very rare manifestation of neurosyphilis that may lead to paraple‐ gia [29]. There are several reports in literature about syphilitic aortic aneurysm with

Paraplegia Caused by Infectious Agents; Etiology, Diagnosis and Management

http://dx.doi.org/10.5772/56989

7

Lyme disease is a tick-borne infection caused by Borrelia burgdorferi [32]. It is one of the most important arthropod-borne zoonosis-pathogen [33] and is transmitted from infected Ixodes ticks to a mammalian host following a tick bite [34]. Lyme borreliosis causes a multisystemic disease which may result in dermatologic, musculoskeletal, cardiovascular, and neurologic manifestations [35]. Lyme borreliosis is a multisystem disease and when involve neurologic system is named neuroborrelosis. Each part of neurologic system may be involved. A broad range of neurologic disorders have been described in Lyme disease, of which peripheral facial nerve palsy and aseptic meningitis are more prevalent [36]. The most common clinical picture of neuroborreliosis is meningitis with cranial or peripheral neuropathies connected with radiculalgia. Encephalitis, myelitis, neuropathies, polyneuropathies, encephalopathies and cerebellar involvement are less common presentation [36, 37]. Acute transverse myelitis is a rare Borellia burgdorferi-related neurologic complication [36]. Encephalomyelitis is the most serious form of neuroborreliosis. Encephalopathy is due to neuroimmunomodulators, like lymphokines and by toxico-metabolic effect could be connected with each form of systemic borreliosis [37]. Neuroborreliosis can cause paraplegia. In Salonen's study paraplegia caused

Brucellosis is a systemic infectious disease caused by Brucella and a is common zoonosis that still remains a major health problem in certain parts of the world such as the Mediterranean region, the Middle East, and Latin America. It may involve multiple organs and tissues. Osteoarticular involvement is the most frequent complication of brucellosis, in which the diagnosis of brucella spondylitis is often difficult since the clinical presentation may be obscured by many other conditions [39]. Brucellosis can cause multisystemic involvement [40]. One of the most common complications is bone and joint involvement, particularly sacroilitis and spondylitis [41]. Brucella spondylitis may be complicated with paravertebral or epidural abscess, radiculitis and psoas abscess [42]. Rarely CNS involvement causes serious manifes‐ tations. Neurobrucellosis occurs less than 5% of patients and presents with meningitis, encephalitis, myelitis, myelopathy, stroke, paraplegia, radiculoneuritis, intracerebral abscess, epidural abscess, demyelination and cranial nerve involvement or any combination of these manifestations [40, 43]. Spinal epidural abscess may be caused due to brucellosis [44]. It is a

destructive spinal erosion that cause paraplegia [30, 31].

by lyme was complete, flaccid and upper motor neurone type [38].

#### *2.1.3. Tuberculosis*

Tuberculosis is one of the most common infections worldwide [17]. Extrapulmonary sites most commonly involved by tuberculosis are lymph nodes, pleura, genitourinary tract, bones and joints, meninges, peritoneum and pericardium. However all organ systems may be involved [18]. There are reports about disseminated tuberculosis involving CNS and spine [19]. Tuberculosis may involve any part of CNS. Meningitis, CNS tuberculoma [20] and spinal cord involvement are neurologic presentation of tuberculosis. In some cases one, several or all presentation may be present [21]. In developing countries, a recognized etiology of paraplegia can be tuberculous radiculomyelitis or tuberculomas, especially in patients with evidence of either active or latent tuberculosis. Spinal deformity arises from tuberculosis is the leading cause of paraplegia [22]. It arises from hematogenous spread of the tubercle bacillus from pulmonary infection. The paraplegia occurs either at the time of the primary infection or more commonly 3-5 years later by reactivation [1]. Spinal tuberculosis can present with wide spectrum of symptoms, with back pain being the most common symptom. It is the leading cause of non-traumatic paraplegia in developing countries [23]. Spine is affected in 50% of skeletal tuberculosis patients. Tuberculous infection of the spine causes a bony destruction and collapse of the vertebra, with a gibbus deformity, skip lesion, intervertebral disc involvement, epidural abscess, paravertebral abscess and edema in the soft tissue planes [17]. Characteris‐ tically, there is destruction of the intervertebral disk space and the adjacent vertebral bodies, collapse of the spinal elements, and anterior wedging leading to kyphosis and gibbus forma‐ tion. The thoracic region of vertebral column is most frequently affected. Formation of a 'cold' abscess around the lesion is another characteristic feature. The incidence of multi-level noncontiguous vertebral tuberculosis occurs more frequently than previously recognized. Common clinical manifestations include constitutional symptoms, back pain, spinal tender‐ ness, paraplegia and spinal deformities [24]. In Abbasi's study on tuberculosis spondylitis in Iran, back pain was detected in 100%, anorexia in 100%, fever in 90%, cough in 50% and limb paralysis in 2.5% of patients [25]. These entities should also be considered in high-risk patients or in patients who have emigrated from regions with a high prevalence of tuberculosis [22]. Neurological complications in spinal tuberculosis occur in active stage of disease by mechan‐ ical compression, instability and inflammation changes, while in healed disease, these occur due to intrinsic changes in spinal cord secondary to internal salient in long standing kyphotic deformity [26]. Tuberculomas are rare tumorlike growth of tuberculous tissue in the central nervous system, characterized by symptoms of expanding these lesions. They result from enlargement of a caseated tubercle. Intramedullary tuberculomas can cause paraplegia although it is a rare event [27].

#### *2.1.4. Syphilis*

organisms are Staphylococcus aureus, aerobic and anaerobic Streptococcus, Escherichia coli and Pseudomonas aeruginosa. Other organisms like Klebsiella pneumonia, Bacteroides fragilis, Enterococcus faecalis, Salmonella, Nocardia, etc. can cause spinal epidural abscess [6]. Paralysis in spinal epidural abscess may be the result of spinal cord compression, spinal cord

Tuberculosis is one of the most common infections worldwide [17]. Extrapulmonary sites most commonly involved by tuberculosis are lymph nodes, pleura, genitourinary tract, bones and joints, meninges, peritoneum and pericardium. However all organ systems may be involved [18]. There are reports about disseminated tuberculosis involving CNS and spine [19]. Tuberculosis may involve any part of CNS. Meningitis, CNS tuberculoma [20] and spinal cord involvement are neurologic presentation of tuberculosis. In some cases one, several or all presentation may be present [21]. In developing countries, a recognized etiology of paraplegia can be tuberculous radiculomyelitis or tuberculomas, especially in patients with evidence of either active or latent tuberculosis. Spinal deformity arises from tuberculosis is the leading cause of paraplegia [22]. It arises from hematogenous spread of the tubercle bacillus from pulmonary infection. The paraplegia occurs either at the time of the primary infection or more commonly 3-5 years later by reactivation [1]. Spinal tuberculosis can present with wide spectrum of symptoms, with back pain being the most common symptom. It is the leading cause of non-traumatic paraplegia in developing countries [23]. Spine is affected in 50% of skeletal tuberculosis patients. Tuberculous infection of the spine causes a bony destruction and collapse of the vertebra, with a gibbus deformity, skip lesion, intervertebral disc involvement, epidural abscess, paravertebral abscess and edema in the soft tissue planes [17]. Characteris‐ tically, there is destruction of the intervertebral disk space and the adjacent vertebral bodies, collapse of the spinal elements, and anterior wedging leading to kyphosis and gibbus forma‐ tion. The thoracic region of vertebral column is most frequently affected. Formation of a 'cold' abscess around the lesion is another characteristic feature. The incidence of multi-level noncontiguous vertebral tuberculosis occurs more frequently than previously recognized. Common clinical manifestations include constitutional symptoms, back pain, spinal tender‐ ness, paraplegia and spinal deformities [24]. In Abbasi's study on tuberculosis spondylitis in Iran, back pain was detected in 100%, anorexia in 100%, fever in 90%, cough in 50% and limb paralysis in 2.5% of patients [25]. These entities should also be considered in high-risk patients or in patients who have emigrated from regions with a high prevalence of tuberculosis [22]. Neurological complications in spinal tuberculosis occur in active stage of disease by mechan‐ ical compression, instability and inflammation changes, while in healed disease, these occur due to intrinsic changes in spinal cord secondary to internal salient in long standing kyphotic deformity [26]. Tuberculomas are rare tumorlike growth of tuberculous tissue in the central nervous system, characterized by symptoms of expanding these lesions. They result from enlargement of a caseated tubercle. Intramedullary tuberculomas can cause paraplegia

arterial or venous ischemia and thrombophlebitis or a combination of these [16].

*2.1.3. Tuberculosis*

6 Topics in Paraplegia

although it is a rare event [27].

Syphilis is a sexually transmitted disease caused by the spirochete Treponema pallidum. The involvement of the CNS by Treponema pallidum has increased in the past 20 years, particularly as a result of HIV pandemic. However, tertiary forms, and especially syphilit‐ ic gumma, are rare as a result of the widespread use of penicillin. Spinal cord compres‐ sion due to syphilitic gumma is an exceptional event that may cause paraplegia [28]. Syphilitic myelitis is a very rare manifestation of neurosyphilis that may lead to paraple‐ gia [29]. There are several reports in literature about syphilitic aortic aneurysm with destructive spinal erosion that cause paraplegia [30, 31].

#### *2.1.5. Lyme*

Lyme disease is a tick-borne infection caused by Borrelia burgdorferi [32]. It is one of the most important arthropod-borne zoonosis-pathogen [33] and is transmitted from infected Ixodes ticks to a mammalian host following a tick bite [34]. Lyme borreliosis causes a multisystemic disease which may result in dermatologic, musculoskeletal, cardiovascular, and neurologic manifestations [35]. Lyme borreliosis is a multisystem disease and when involve neurologic system is named neuroborrelosis. Each part of neurologic system may be involved. A broad range of neurologic disorders have been described in Lyme disease, of which peripheral facial nerve palsy and aseptic meningitis are more prevalent [36]. The most common clinical picture of neuroborreliosis is meningitis with cranial or peripheral neuropathies connected with radiculalgia. Encephalitis, myelitis, neuropathies, polyneuropathies, encephalopathies and cerebellar involvement are less common presentation [36, 37]. Acute transverse myelitis is a rare Borellia burgdorferi-related neurologic complication [36]. Encephalomyelitis is the most serious form of neuroborreliosis. Encephalopathy is due to neuroimmunomodulators, like lymphokines and by toxico-metabolic effect could be connected with each form of systemic borreliosis [37]. Neuroborreliosis can cause paraplegia. In Salonen's study paraplegia caused by lyme was complete, flaccid and upper motor neurone type [38].

#### *2.1.6. Brucellosis*

Brucellosis is a systemic infectious disease caused by Brucella and a is common zoonosis that still remains a major health problem in certain parts of the world such as the Mediterranean region, the Middle East, and Latin America. It may involve multiple organs and tissues. Osteoarticular involvement is the most frequent complication of brucellosis, in which the diagnosis of brucella spondylitis is often difficult since the clinical presentation may be obscured by many other conditions [39]. Brucellosis can cause multisystemic involvement [40]. One of the most common complications is bone and joint involvement, particularly sacroilitis and spondylitis [41]. Brucella spondylitis may be complicated with paravertebral or epidural abscess, radiculitis and psoas abscess [42]. Rarely CNS involvement causes serious manifes‐ tations. Neurobrucellosis occurs less than 5% of patients and presents with meningitis, encephalitis, myelitis, myelopathy, stroke, paraplegia, radiculoneuritis, intracerebral abscess, epidural abscess, demyelination and cranial nerve involvement or any combination of these manifestations [40, 43]. Spinal epidural abscess may be caused due to brucellosis [44]. It is a very rare disease which is usually a consequence of spondylodiscitis. The spinal column can be affected at any joint; however, the lumbar spine is the most common region, especially at the level of the L4-5 and L5-S1. Spinal involvement may be seen at the lumbar, thoracic and cervical spine [45]. There are several reports about paraplegia caused by brucellosis [46, 47].

Aspergillus may lead to epidural abscesses [58, 59], kyphosis, discharging sinus in the back, vertebral destruction and paraplegia [60]. Spondylodiscitis has been reported due to candida [61]. Zygomycosis may be the cause of epidural abscess and paraplegia usually in immuno‐ compromised patients [62]. Spinal cord histoplasmomosis with flaccid paralaysis has been

Paraplegia Caused by Infectious Agents; Etiology, Diagnosis and Management

http://dx.doi.org/10.5772/56989

9

Schistosomiasis is a parasitic disease caused by blood flukes of the genus Schistosoma. Currently more than 200 million people worldwide are affected. Neuroschistosomiasis constitutes a severe presentation of the disease. Neurological symptoms result from the inflammatory response of the host to egg deposition in the brain and spinal cord. Neurological complications of cerebral schistosomiasis include delirium, loss of consciousness, seizures, dysphasia, visual field impairment, focal motor deficits and ataxia [64]. Transverse myelitis and myeloradiculopathy affecting the conus medullaris and cauda equina are the most common spinal cord syndromes. Transverse myelitis can present as flaccid areflexic paraplegia with sensory level and sphincter dysfunction [65]. Schistosomal myelopathy tends to occur early after infection and is more likely to be symptomatic than cerebral schistosomiasis [64]. Involvement of the spinal cord is considered to be uncommon, although 1-5% of all cases of non traumatic paraplegia in endemic parts of Africa are reported to be caused by schistoso‐ miasis. Paraplegia occurs mostly with S. mansoni and occasionally with S. haematobium [1].

Rarely some other organisms like non-tuberculosis mycobacteria [66, 67], Nocardia [68], pasturella [69], etc may involve spinal column, cause spondylitis, epidural or subdural abscess

Spinal subdural empyema is an unpredictable disease, with an unfavorable outcome if left untreated. If there is suspicion of a spinal subdural abscess, urgent radiological examination followed by immediate surgical drainage and appropriate antibiotic therapy is warranted [70]. Morbidity and mortality in intracranial and spinal subdural empyema directly relate to the delay in diagnosis and therapy [71]. The diagnostic procedure of choice for spinal subdural empyema is magnetic resonance imaging (MRI) with gadolinium enhancement. Occasionally spinal subdural empyemas may be detected by computed tomography (CT) myelography where MRI is negative [72]. The timing of performing MRI is very important in these patients. Early diagnosis and emergent treatment is necessary to prevent neurologic deficits [12].

reported [63].

**2.4. Schistosomiasis**

**2.5. Other microorganism**

that may lead to paraplegia.

**3.1. Subdural empyema**

**3. Diagnosis**

#### **2.2. Viral infection**

Several viral infections can cause paraplegia. Paraplegia is a major neurological disorder in HIV infection. It can occur during the asymptomatic stage of HIV infection when CD4 counts are >200/cm3 and more commonly during the symptomatic stage when CD4 counts are low (<100/cm3). The main causes are opportunistic processes and direct HIV involvement of the spinal cord. Opportunistic infections include tuberculosis, herpes zoster, herpes simplex, cytomegalovirus (CMV), syphilis and co-infection with human T-lymphotropic virus-1 (HTLV-I) in endemic areas [1]. In developed countries, the most prominent reported spinal cord disease in HIV/AIDS patients is vacuolar myelopathy. Other causes of myelopathy in HIV/AIDS patients include opportunistic infections, neoplasms, vascular lesions and meta‐ bolic disease. In developing regions, opportunistic infections are more common [48]. In patients with HIV infection, chronic inflammation can lead to a lesion that compresses the spinal cord and should be considered in differential diagnosis [49]. HTLV-I is a retrovirus which is endemic in some areas of western, southern and central Africa with just a few clusters reported in eastern Africa. It is endemic in areas of Japan, the Caribbean and South America. It is transmitted perinatally, sexually and by blood transfusion. Chronic infection for up to 20-30 years can result in a slow progressive form of tropical spastic paraplegia known as HTLV-I associated myelopathy [1]. This diagnosis should be considered in every patient with progressive spastic paraplegia [50]. Herpes zoster myelitis may cause paraplegia especially in HIV positive patients. Subacute onset paraplegia with a sensory level, which developed 10 days after herpes zoster dermatomal rash, is typical presentation of disease [51]. Extensive necrotic and hemorrhagic changes with marked necrotizing vasculitis involved the entire spinal cord and spinal roots, may be seen [52]. Neurological syndromes attributed to CMV include encephalitis, myelitis, and peripheral neuropathy [53]. Acute lumbosacral polyradi‐ culopathy caused by the CMV infection is a rare neurological complication usually is seen in immunocompromised patients especially in AIDS. Progressive flaccid paraplegia with sensory disturbance, radicular pain, or bladder dysfunction are characteristic symptoms [54]. CMV may cause a severe motor polyradiculopathy by selective destruction of the motor neurons of ventral spinal roots and motor cranial nerves [55]. Several other viruses like Poliovirus, Entroviruse 71, Echovirus, Cocksackie B, Cocksackie A, etc can cause myelitis and paralysis.

#### **2.3. Fungal infection**

Aspergillosis of the spine has been reported infrequently. It has usually been attributed to hematogenous infection or spread from an adjacent pulmonary infection. Acute paraplegia may develop after aspergillus infection. Direct extension of aspergillus infection can cause spondylitis, vertebral destruction, spinal cord compression and paraplegia [56, 57]. Vertebral osteomyelitis caused by Aspergillus is rare and usually affects immunocompromised patients. Aspergillus may lead to epidural abscesses [58, 59], kyphosis, discharging sinus in the back, vertebral destruction and paraplegia [60]. Spondylodiscitis has been reported due to candida [61]. Zygomycosis may be the cause of epidural abscess and paraplegia usually in immuno‐ compromised patients [62]. Spinal cord histoplasmomosis with flaccid paralaysis has been reported [63].

#### **2.4. Schistosomiasis**

very rare disease which is usually a consequence of spondylodiscitis. The spinal column can be affected at any joint; however, the lumbar spine is the most common region, especially at the level of the L4-5 and L5-S1. Spinal involvement may be seen at the lumbar, thoracic and cervical spine [45]. There are several reports about paraplegia caused by brucellosis [46, 47].

Several viral infections can cause paraplegia. Paraplegia is a major neurological disorder in HIV infection. It can occur during the asymptomatic stage of HIV infection when CD4 counts

(<100/cm3). The main causes are opportunistic processes and direct HIV involvement of the spinal cord. Opportunistic infections include tuberculosis, herpes zoster, herpes simplex, cytomegalovirus (CMV), syphilis and co-infection with human T-lymphotropic virus-1 (HTLV-I) in endemic areas [1]. In developed countries, the most prominent reported spinal cord disease in HIV/AIDS patients is vacuolar myelopathy. Other causes of myelopathy in HIV/AIDS patients include opportunistic infections, neoplasms, vascular lesions and meta‐ bolic disease. In developing regions, opportunistic infections are more common [48]. In patients with HIV infection, chronic inflammation can lead to a lesion that compresses the spinal cord and should be considered in differential diagnosis [49]. HTLV-I is a retrovirus which is endemic in some areas of western, southern and central Africa with just a few clusters reported in eastern Africa. It is endemic in areas of Japan, the Caribbean and South America. It is transmitted perinatally, sexually and by blood transfusion. Chronic infection for up to 20-30 years can result in a slow progressive form of tropical spastic paraplegia known as HTLV-I associated myelopathy [1]. This diagnosis should be considered in every patient with progressive spastic paraplegia [50]. Herpes zoster myelitis may cause paraplegia especially in HIV positive patients. Subacute onset paraplegia with a sensory level, which developed 10 days after herpes zoster dermatomal rash, is typical presentation of disease [51]. Extensive necrotic and hemorrhagic changes with marked necrotizing vasculitis involved the entire spinal cord and spinal roots, may be seen [52]. Neurological syndromes attributed to CMV include encephalitis, myelitis, and peripheral neuropathy [53]. Acute lumbosacral polyradi‐ culopathy caused by the CMV infection is a rare neurological complication usually is seen in immunocompromised patients especially in AIDS. Progressive flaccid paraplegia with sensory disturbance, radicular pain, or bladder dysfunction are characteristic symptoms [54]. CMV may cause a severe motor polyradiculopathy by selective destruction of the motor neurons of ventral spinal roots and motor cranial nerves [55]. Several other viruses like Poliovirus, Entroviruse 71, Echovirus, Cocksackie B, Cocksackie A, etc can cause myelitis and paralysis.

Aspergillosis of the spine has been reported infrequently. It has usually been attributed to hematogenous infection or spread from an adjacent pulmonary infection. Acute paraplegia may develop after aspergillus infection. Direct extension of aspergillus infection can cause spondylitis, vertebral destruction, spinal cord compression and paraplegia [56, 57]. Vertebral osteomyelitis caused by Aspergillus is rare and usually affects immunocompromised patients.

and more commonly during the symptomatic stage when CD4 counts are low

**2.2. Viral infection**

**2.3. Fungal infection**

are >200/cm3

8 Topics in Paraplegia

Schistosomiasis is a parasitic disease caused by blood flukes of the genus Schistosoma. Currently more than 200 million people worldwide are affected. Neuroschistosomiasis constitutes a severe presentation of the disease. Neurological symptoms result from the inflammatory response of the host to egg deposition in the brain and spinal cord. Neurological complications of cerebral schistosomiasis include delirium, loss of consciousness, seizures, dysphasia, visual field impairment, focal motor deficits and ataxia [64]. Transverse myelitis and myeloradiculopathy affecting the conus medullaris and cauda equina are the most common spinal cord syndromes. Transverse myelitis can present as flaccid areflexic paraplegia with sensory level and sphincter dysfunction [65]. Schistosomal myelopathy tends to occur early after infection and is more likely to be symptomatic than cerebral schistosomiasis [64]. Involvement of the spinal cord is considered to be uncommon, although 1-5% of all cases of non traumatic paraplegia in endemic parts of Africa are reported to be caused by schistoso‐ miasis. Paraplegia occurs mostly with S. mansoni and occasionally with S. haematobium [1].

#### **2.5. Other microorganism**

Rarely some other organisms like non-tuberculosis mycobacteria [66, 67], Nocardia [68], pasturella [69], etc may involve spinal column, cause spondylitis, epidural or subdural abscess that may lead to paraplegia.

#### **3. Diagnosis**

#### **3.1. Subdural empyema**

Spinal subdural empyema is an unpredictable disease, with an unfavorable outcome if left untreated. If there is suspicion of a spinal subdural abscess, urgent radiological examination followed by immediate surgical drainage and appropriate antibiotic therapy is warranted [70]. Morbidity and mortality in intracranial and spinal subdural empyema directly relate to the delay in diagnosis and therapy [71]. The diagnostic procedure of choice for spinal subdural empyema is magnetic resonance imaging (MRI) with gadolinium enhancement. Occasionally spinal subdural empyemas may be detected by computed tomography (CT) myelography where MRI is negative [72]. The timing of performing MRI is very important in these patients. Early diagnosis and emergent treatment is necessary to prevent neurologic deficits [12].

#### **3.2. Epidural abscess**

A high level of clinical suspicion is necessary for rapid diagnosis and treatment initiation [73]. MRI with gadolinium enhancement is the diagnostic procedure of choice for diagnosis. MRI is recommended over CT scan because it can better visualize the spinal cord and epidural space in both sagittal and transverse sections and can also identify accompanying osteomyelitis, intramedullary spinal cord lesions, and discitis [6].

**3.5. Lyme**

detection in CSF [37].

**3.6. Brucellosis**

**3.7. Viral infection**

Serological tests, including enzyme linked immunosorbent assay (ELISA) and Western blot analysis can be used for diagnosis. B. burgdorferi polymerase chain reaction (PCR) may be used to confirm the diagnosis. Different techniques have been developed to aid in laboratory diagnosis of Lyme disease. Detection of serum antibodies is currently the most practical means of confirming B. burgdorferi infections. Although most assays may not detect low amounts of IgM antibody during the initial weeks of infection, application of a capture ELISA method has been reported to improve test sensitivity [80]. Detection of large amounts of IgM and IgG borrelia antibodies in the acute phase and complete disappearance of IgM antibody during the review period confirms the diagnosis [38]. Diagnosis of neuroborreliosis is based on culturing of B. burgdorferi from CSF, detection of specific antispirochaetal antibodies produced in subarachnoid space, detection of activated lymphocytes and antigens or borrelial DNA

Paraplegia Caused by Infectious Agents; Etiology, Diagnosis and Management

http://dx.doi.org/10.5772/56989

11

In endemic regions brucella spondylitis should always be considered in the differential diagnosis especially in older patients with back pain and constitutional symptoms. An early diagnosis will help to prevent the development of more severe complications such as spinal cord compression [47]. Rose Bengal, standard agglutination, indirect immunofluorescent assay (IFA) and ELISA tests usually used for diagnosis [41, 46]. Serologic tests provide valuable information but always point to a generic and not a specific diagnosis [81]. ESR and CRP are usually highly positive [82]. Imaging studies, including radiography, computed tomography, magnetic resonance imaging and bone scintigraphy have been used for diagnosis. Radiogra‐ phy is limited to evaluating the focal form of spinal brucellosis. CT and bone scintigraphy have limited value because of their inadequate soft tissue resolution. MRI is the method of choice to assess the extent of disease and follow up the treatment response. However, MRI has a low specificity to predict the exact cause spondylodiscitis, the index of suspicion should be high in regions where the disease is endemic [83].Serological test for Brucella is usually positive and MRI may reveal epidural abscess or spondylodiscitis [44]. Early diagnosis and specific

HIV is diagnosed by serological tests, including ELISA and Western blot. Several other tests such as P24 antigen, IFA, radioimmunoprecipitation assay (RIPA) and PCR may be used. Serologic assays, antigen detection and viral Isolation are used to diagnosis of HTLV infection. Serologic tests, PCR and Immunocytochemistry method are used for diagnosis of Varicella zoster virus (VZV) [52]. CMV infection should be included in the differential diagnosis of transcers myelitis of uncertain etiology [84]. CMV-DNA amplification in PCR method or immunohistochemical approach from CSF is a useful procedure for diagnosis of CMV infection [54]. If viremia exists PP65 antigen detection enables early and rapid diagnosis of CMV [85].

treatment are important to prevent later complications [41].

#### **3.3. Tuberculosis**

The diagnosis of Pott's disease is usually made by clinical suspicion, in combination with an elevated ESR and typical radiologic findings. Biopsy may be necessary for confirmation [1]. The awareness and suspicion of an atypical presentation of spinal tuberculosis should be high in order to obtain a good outcome [74]. MRI is the most valuable investigation in the patients with spinal tuberculosis. It is highly sensitive in detection of various pathological processes of Pott's disease [17]. For the diagnosis of spinal tuberculosis MRI is more sensitive imaging technique than x-ray and more specific than CT scan [24]. MRI allows the diagnosis of a tuberculous lesion, with a sensitivity of about 100% and specificity of 88%, well before deformity develops [74]. MRI frequently demonstrates involvement of the vertebral bodies on either side of the disk, disk destruction, cold abscess, vertebral collapse and presence of vertebral column deformities [24]. Marrow edema, preservation of disc space, subligamentous extension of abscess, paravertebral abscess, epidural extension, endplate erosions and discitis were consistently observed in 83% cases of spine tuberclusis on MRI [75]. If pus exists, the diagnosis may be confirmed by histopathological demonstration of Mycobacterium tubercu‐ losis in drained pus [76]. CT-guided needle biopsy from the affected site in the center of the vertebral body is the gold standard technique for early histopathological diagnosis [24].

#### **3.4. Syphilis**

The diagnosis of neurosyphilis depends on the serological detection of antibodies in both blood and cerebrospinal fluid (CSF). The Venereal Disease Research Laboratory (VDRL) is the screening test most commonly used. More sensitive and specific diagnostic antibody tests include the fluorescent treponemal antibody absorption (FTA) and the treponemal antibody immobilization test (TPI) [1]. CSF study confirms the diagnosis of neurosyphilis [77]. CSF pleocytosis with positive CSF VDRL often is obvious [78]. MRI appearance of syphilitic myelitis is not well documented and only a few cases have been reported. MRI of the spine shows diffuse high signal intensity in the whole spinal cord on T2-weighted images. Focal enhancement may be observed in the dorsal aspect cord on T1-weighted gadolinium-enhanced images [29]. MRI imaging provides documentation of spinal cord involvement and is useful in monitoring recovery [77]. Marked sclerosis and osteophytes restricted to lumbo-dorsal spine, absence of ligamentous calcification and lack of long standing spinal symptoms may be seen in patients with syphilitic paraplegia [79].

#### **3.5. Lyme**

**3.2. Epidural abscess**

10 Topics in Paraplegia

**3.3. Tuberculosis**

**3.4. Syphilis**

intramedullary spinal cord lesions, and discitis [6].

seen in patients with syphilitic paraplegia [79].

A high level of clinical suspicion is necessary for rapid diagnosis and treatment initiation [73]. MRI with gadolinium enhancement is the diagnostic procedure of choice for diagnosis. MRI is recommended over CT scan because it can better visualize the spinal cord and epidural space in both sagittal and transverse sections and can also identify accompanying osteomyelitis,

The diagnosis of Pott's disease is usually made by clinical suspicion, in combination with an elevated ESR and typical radiologic findings. Biopsy may be necessary for confirmation [1]. The awareness and suspicion of an atypical presentation of spinal tuberculosis should be high in order to obtain a good outcome [74]. MRI is the most valuable investigation in the patients with spinal tuberculosis. It is highly sensitive in detection of various pathological processes of Pott's disease [17]. For the diagnosis of spinal tuberculosis MRI is more sensitive imaging technique than x-ray and more specific than CT scan [24]. MRI allows the diagnosis of a tuberculous lesion, with a sensitivity of about 100% and specificity of 88%, well before deformity develops [74]. MRI frequently demonstrates involvement of the vertebral bodies on either side of the disk, disk destruction, cold abscess, vertebral collapse and presence of vertebral column deformities [24]. Marrow edema, preservation of disc space, subligamentous extension of abscess, paravertebral abscess, epidural extension, endplate erosions and discitis were consistently observed in 83% cases of spine tuberclusis on MRI [75]. If pus exists, the diagnosis may be confirmed by histopathological demonstration of Mycobacterium tubercu‐ losis in drained pus [76]. CT-guided needle biopsy from the affected site in the center of the vertebral body is the gold standard technique for early histopathological diagnosis [24].

The diagnosis of neurosyphilis depends on the serological detection of antibodies in both blood and cerebrospinal fluid (CSF). The Venereal Disease Research Laboratory (VDRL) is the screening test most commonly used. More sensitive and specific diagnostic antibody tests include the fluorescent treponemal antibody absorption (FTA) and the treponemal antibody immobilization test (TPI) [1]. CSF study confirms the diagnosis of neurosyphilis [77]. CSF pleocytosis with positive CSF VDRL often is obvious [78]. MRI appearance of syphilitic myelitis is not well documented and only a few cases have been reported. MRI of the spine shows diffuse high signal intensity in the whole spinal cord on T2-weighted images. Focal enhancement may be observed in the dorsal aspect cord on T1-weighted gadolinium-enhanced images [29]. MRI imaging provides documentation of spinal cord involvement and is useful in monitoring recovery [77]. Marked sclerosis and osteophytes restricted to lumbo-dorsal spine, absence of ligamentous calcification and lack of long standing spinal symptoms may be Serological tests, including enzyme linked immunosorbent assay (ELISA) and Western blot analysis can be used for diagnosis. B. burgdorferi polymerase chain reaction (PCR) may be used to confirm the diagnosis. Different techniques have been developed to aid in laboratory diagnosis of Lyme disease. Detection of serum antibodies is currently the most practical means of confirming B. burgdorferi infections. Although most assays may not detect low amounts of IgM antibody during the initial weeks of infection, application of a capture ELISA method has been reported to improve test sensitivity [80]. Detection of large amounts of IgM and IgG borrelia antibodies in the acute phase and complete disappearance of IgM antibody during the review period confirms the diagnosis [38]. Diagnosis of neuroborreliosis is based on culturing of B. burgdorferi from CSF, detection of specific antispirochaetal antibodies produced in subarachnoid space, detection of activated lymphocytes and antigens or borrelial DNA detection in CSF [37].

#### **3.6. Brucellosis**

In endemic regions brucella spondylitis should always be considered in the differential diagnosis especially in older patients with back pain and constitutional symptoms. An early diagnosis will help to prevent the development of more severe complications such as spinal cord compression [47]. Rose Bengal, standard agglutination, indirect immunofluorescent assay (IFA) and ELISA tests usually used for diagnosis [41, 46]. Serologic tests provide valuable information but always point to a generic and not a specific diagnosis [81]. ESR and CRP are usually highly positive [82]. Imaging studies, including radiography, computed tomography, magnetic resonance imaging and bone scintigraphy have been used for diagnosis. Radiogra‐ phy is limited to evaluating the focal form of spinal brucellosis. CT and bone scintigraphy have limited value because of their inadequate soft tissue resolution. MRI is the method of choice to assess the extent of disease and follow up the treatment response. However, MRI has a low specificity to predict the exact cause spondylodiscitis, the index of suspicion should be high in regions where the disease is endemic [83].Serological test for Brucella is usually positive and MRI may reveal epidural abscess or spondylodiscitis [44]. Early diagnosis and specific treatment are important to prevent later complications [41].

#### **3.7. Viral infection**

HIV is diagnosed by serological tests, including ELISA and Western blot. Several other tests such as P24 antigen, IFA, radioimmunoprecipitation assay (RIPA) and PCR may be used. Serologic assays, antigen detection and viral Isolation are used to diagnosis of HTLV infection. Serologic tests, PCR and Immunocytochemistry method are used for diagnosis of Varicella zoster virus (VZV) [52]. CMV infection should be included in the differential diagnosis of transcers myelitis of uncertain etiology [84]. CMV-DNA amplification in PCR method or immunohistochemical approach from CSF is a useful procedure for diagnosis of CMV infection [54]. If viremia exists PP65 antigen detection enables early and rapid diagnosis of CMV [85].

#### **3.8. Fungal infection**

In the era of transplantation and increase in use of immunosuppressive medications, spinal fungal infection should be considered in differential diagnosis of spinal infectious involvement [60]. The best method for diagnosis of fungal infection is biopsy and visualization of hyphae. Histopathologic findings confirm the diagnosis. Several serologic tests, antigen detection and PCR method for different fungal infection exist. Aspergillus can be identified by fungal culture and PCR [58]. Rhizopus may be identified by smear or culture from tissue biopsy [86].

**4.3. Tuberculosis**

treatment [24].

**4.4. Syphilis**

**4.5. Lyme**

ceftriaxone are alternative treatments [92].

respond to oral regimens [93].

Four anti tuberculosis drugs plus surgical intervention when indicated are cornerstones of treatment. In patients with multi drug resistant tuberculosis antibiogram and more prolong course of treatment is necessary. Anti tuberculosis therapy should be considered for at least 12 months [17]. A combination of conservative therapy and operative decompression when needed should form a comprehensive integrated course of treatment for spinal tuberculosis with neurological complications. The patients showing relatively preserved cord with evidence of edema or myelitis with predominantly fluid collection in extradural space on MRI may be managed by non-operative treatment, while the patients with extradural compression of mixed or granulomatous nature showing entrapment of spinal cord should be candidate for early surgical decompression. The disease focus should be debrided with removal of pus and sequestra. The viable bone should only be removed to decompress the spinal cord and resultant gap should be bridged by bone graft. The preserved volume of spinal cord with edema or myelitis and wet lesion on MRI usually would show good neural recovery. The spinal cord showing myelomalacia with reduced cord volume and dry lesion likely to show a poor neural recovery. The internal kyphectomy is indicated for paraplegia with healed disease. The best form of treatment of late onset paraplegia is the prevention of development of severe kyphosis in initial active stage of disease [26]. Surgery may be required in selected cases, e.g. large abscess formation, severe kyphosis, neurological deficit or lack of response to medical

Paraplegia Caused by Infectious Agents; Etiology, Diagnosis and Management

http://dx.doi.org/10.5772/56989

13

Recognition of unusual complication of neurosyphilis is important, because it is a treatable cause of parapalegia with good recovery [77]. Greater alertness to diagnosis may result in earlier therapy and thus possibly lead to improved prognosis [78]. Aqueous crystalline penicillin G 3-4 million units intravenous every 4 hours for 10-14 days is treatment of choice. For patients with penicillin allergy other regimens may be used. Docycicline, amoxicillin and

The tick-borne spirochete responsible for Lyme disease is highly antibiotic-sensitive. Treat‐ ment is highly effective in the vast majority of patients, including those with nervous system disease. Nervous system infection, most typically meningitis, cranial neuritis, radiculoneuritis, and other forms of mononeuropathy multiplex, is highly antibiotic responsive. In patients with infection not involving the CNS, oral treatment with amoxicillin, cefuroxime axetil, or doxycycline for 2-4 weeks is almost always curative. Despite historic preferences for parenteral treatment with ceftriaxone, cefotaxime, or meningeal dose penicillin, patients with the forms of nervous system involvement listed above are highly responsive to oral doxycycline. Parenteral regimens can be reserved for those very rare patients with parenchymal CNS involvement, other severe forms of infection or the approximately 5% of patients who fail to

#### **3.9. Schistosomiasis**

The diagnosis is difficult because the paraplegia mainly occurs during the early invasive phase of the adult worms, when there is little clinical or laboratory evidence of underlying schisto‐ some infection. Stool examination for eggs and rectal snips are used for diagnosis [1]. Ali‐ though laboratory investigations, including serological tests are of limited diagnostic value [87] Immunofluorescence assay and ELISA has been used for diagnosis [88].

#### **4. Treatment**

#### **4.1. Subdural empyema**

Treatment in virtually all cases of spinal subdural empyema requires prompt surgical drainage and antibiotic therapy [72] although a more expectant approach consisting of antibiotics and observation has also been proposed [8]. Provisional antibiotic therapy of spinal subdural empyemas should be directed against S. aureus and streptococci, and should include nafcillin, oxacillin, or vancomycin [72]. In some cases treatment with intravenous antibiotics and drainage is not enough and complete surgical excision of the lesion may be necessary [89].

#### **4.2. Epidural abscess**

The principles of therapy for spinal epidural abscess are prompt surgical decompression, drainage of the abscess, and long-term antimicrobial therapy. Empirical antimicrobial therapy for spinal epidural abscess must include antistaphylococcal agent plus coverage for aerobic gram-negative bacilli [6]. Recent reports have advocated for conservative, non-operative management of this devastating disorder with appropriate risk stratification. Crucial to a successful management strategy are definitive diagnosis, prompt intervention, and consistent follow-up care [90]. Although there are some case reports that present spinal epidural abscess treated with antibiotics alone [91] result of several studies strongly support immediate surgical decompression combined with appropriately tailored antibiotic therapy for the treatment of symptomatic spinal epidural abscess presenting with focal neurological deficit [90]. Recent evidence indicates the following areas of investigation and management can improve outcome in spinal epidural abscess: minimally invasive surgery early versus medical management when there are no significant neurological deficits, neuroradiologic arterial evaluation with therapies directed at vascular ischemia and thrombosis and aggressive rehabilitation [16].

#### **4.3. Tuberculosis**

**3.8. Fungal infection**

12 Topics in Paraplegia

**3.9. Schistosomiasis**

**4. Treatment**

**4.1. Subdural empyema**

**4.2. Epidural abscess**

In the era of transplantation and increase in use of immunosuppressive medications, spinal fungal infection should be considered in differential diagnosis of spinal infectious involvement [60]. The best method for diagnosis of fungal infection is biopsy and visualization of hyphae. Histopathologic findings confirm the diagnosis. Several serologic tests, antigen detection and PCR method for different fungal infection exist. Aspergillus can be identified by fungal culture and PCR [58]. Rhizopus may be identified by smear or culture from tissue biopsy [86].

The diagnosis is difficult because the paraplegia mainly occurs during the early invasive phase of the adult worms, when there is little clinical or laboratory evidence of underlying schisto‐ some infection. Stool examination for eggs and rectal snips are used for diagnosis [1]. Ali‐ though laboratory investigations, including serological tests are of limited diagnostic value

Treatment in virtually all cases of spinal subdural empyema requires prompt surgical drainage and antibiotic therapy [72] although a more expectant approach consisting of antibiotics and observation has also been proposed [8]. Provisional antibiotic therapy of spinal subdural empyemas should be directed against S. aureus and streptococci, and should include nafcillin, oxacillin, or vancomycin [72]. In some cases treatment with intravenous antibiotics and drainage is not enough and complete surgical excision of the lesion may be necessary [89].

The principles of therapy for spinal epidural abscess are prompt surgical decompression, drainage of the abscess, and long-term antimicrobial therapy. Empirical antimicrobial therapy for spinal epidural abscess must include antistaphylococcal agent plus coverage for aerobic gram-negative bacilli [6]. Recent reports have advocated for conservative, non-operative management of this devastating disorder with appropriate risk stratification. Crucial to a successful management strategy are definitive diagnosis, prompt intervention, and consistent follow-up care [90]. Although there are some case reports that present spinal epidural abscess treated with antibiotics alone [91] result of several studies strongly support immediate surgical decompression combined with appropriately tailored antibiotic therapy for the treatment of symptomatic spinal epidural abscess presenting with focal neurological deficit [90]. Recent evidence indicates the following areas of investigation and management can improve outcome in spinal epidural abscess: minimally invasive surgery early versus medical management when there are no significant neurological deficits, neuroradiologic arterial evaluation with therapies directed at vascular ischemia and thrombosis and aggressive rehabilitation [16].

[87] Immunofluorescence assay and ELISA has been used for diagnosis [88].

Four anti tuberculosis drugs plus surgical intervention when indicated are cornerstones of treatment. In patients with multi drug resistant tuberculosis antibiogram and more prolong course of treatment is necessary. Anti tuberculosis therapy should be considered for at least 12 months [17]. A combination of conservative therapy and operative decompression when needed should form a comprehensive integrated course of treatment for spinal tuberculosis with neurological complications. The patients showing relatively preserved cord with evidence of edema or myelitis with predominantly fluid collection in extradural space on MRI may be managed by non-operative treatment, while the patients with extradural compression of mixed or granulomatous nature showing entrapment of spinal cord should be candidate for early surgical decompression. The disease focus should be debrided with removal of pus and sequestra. The viable bone should only be removed to decompress the spinal cord and resultant gap should be bridged by bone graft. The preserved volume of spinal cord with edema or myelitis and wet lesion on MRI usually would show good neural recovery. The spinal cord showing myelomalacia with reduced cord volume and dry lesion likely to show a poor neural recovery. The internal kyphectomy is indicated for paraplegia with healed disease. The best form of treatment of late onset paraplegia is the prevention of development of severe kyphosis in initial active stage of disease [26]. Surgery may be required in selected cases, e.g. large abscess formation, severe kyphosis, neurological deficit or lack of response to medical treatment [24].

#### **4.4. Syphilis**

Recognition of unusual complication of neurosyphilis is important, because it is a treatable cause of parapalegia with good recovery [77]. Greater alertness to diagnosis may result in earlier therapy and thus possibly lead to improved prognosis [78]. Aqueous crystalline penicillin G 3-4 million units intravenous every 4 hours for 10-14 days is treatment of choice. For patients with penicillin allergy other regimens may be used. Docycicline, amoxicillin and ceftriaxone are alternative treatments [92].

#### **4.5. Lyme**

The tick-borne spirochete responsible for Lyme disease is highly antibiotic-sensitive. Treat‐ ment is highly effective in the vast majority of patients, including those with nervous system disease. Nervous system infection, most typically meningitis, cranial neuritis, radiculoneuritis, and other forms of mononeuropathy multiplex, is highly antibiotic responsive. In patients with infection not involving the CNS, oral treatment with amoxicillin, cefuroxime axetil, or doxycycline for 2-4 weeks is almost always curative. Despite historic preferences for parenteral treatment with ceftriaxone, cefotaxime, or meningeal dose penicillin, patients with the forms of nervous system involvement listed above are highly responsive to oral doxycycline. Parenteral regimens can be reserved for those very rare patients with parenchymal CNS involvement, other severe forms of infection or the approximately 5% of patients who fail to respond to oral regimens [93].

#### **4.6. Brucellosis**

Neurobrucellosis, if not treated early, can result in severe neurological morbidity and sequelae, which may be irreversible. Hence it is important to consider the possibility of neurobrucellosis in endemic region and treat aggressively (94). Treatment with streptomycin, rifampicin and doxycyclin significantly improve the symptoms [44]. Doxycycline, rifampin, trimethoprimsulfamethoxazole, streptomycin, gentamicin, ciprofloxacin and ceftriaxone are used for treatment of neurobrucellosis [95]. The mean duration of antimicrobial therapy is 18 weeks with range of 12-56 weeks. Prolonged duration of treatment especially in complicated cases in order to avoid possible sequelae is necessary [42]. In Gul's study duration of antibiotic therapy was ranged from 2 to 15 months (median 5 months) [96]. Neurobrucellosis and brucella spondylitis usually are treated with 3 drugs combination [46, 97]. The standard treatment of brucella spondylitis with a combination of two antibiotics for 6-12 weeks is associated with high rates of treatment failure and relapse. Prolonged administration of a triple combination of suitable antibiotics appears to be an effective treatment for brucella spondylitis [98]. The most commonly-used antibiotics are combinations of rifampin, doxycycline and trimetho‐ prim-sulfamethoxazole [99].

**4.9. Schistosomiasis**

**5. Conclusion**

**Acknowledgements**

**Author details**

Farhad Abbasi1

**References**

Praziquantel and corticoids have been successfully used to treat neuroschistosomiasis [65].

Paraplegia Caused by Infectious Agents; Etiology, Diagnosis and Management

http://dx.doi.org/10.5772/56989

15

Infectious diseases are important causes of non-traumatic paraplegia. High index of suspicion, precise history taking, exact physical examination and proper use of laboratory tests and radiologic studies are necessary for making accurate diagnosis. Sometimes the diagnosis is dependent to invasive procedure such as CT guided biopsy and subsequent histopathologic study, without them appropriate diagnosis may be impossible. Sometimes for accurate diagnosis using several laboratory and radiologic modalities, simultaneously, may be needed. Paying attention to specific treatment and its duration is very important. Sometimes combi‐ nation antibiotic therapy is needed. If treatment or its duration is not appropriate, relapse may occur. Although paraplegia due to infectious diseases can be with high mortality rate, early

[1] Howlwtt W.P. Paraplegia non traumatic. In: Howlwtt W. Neurology in Africa. Ber‐

[2] Chen Y, Tang Y, Vogel LC, Devivo MJ. Causes of spinal cord injury. Top Spinal Cord

Surgery has been tried for acute cases of failed medical treatment [1].

diagnosed and successful treatment can prevent neurological sequelae.

With special thanks to Dr Katayoun Vahdat and Dr Mohammad Javadi

and Soolmaz Korooni Fardkhani2

1 Bushehr University of Medical Sciences, Iran

2 Shiraz University of Medical Sciences, Iran

gen, Norway: Bodoni; 2012.p.231.

Inj Rehabil. 2013;19(1):1-8.

#### **4.7. Viral infection**

For treatment of HIV usually 2 nucleoside analogue plus one protease inhibitor or one nonnucleoside reverse transcriptase inhibitor are used. Although nucleoside analogues, such as zidovudine and lamivudine, have long been recognized to have activity against HTLV reverse transcription in vitro, there is little clinical evidence of their efficacy in vivo, so treatment of asymptomatic HTLV carriers is not indicated. A combination of zidovudine and lamivudine has been used for treatment, but no clinical improvement was seen, and there was no effect on HTLV-I proviral load or immunologic markers [100]. The most commonly antiviral agents used for treatment of CMV are: ganciclovir, foscarnet, cidofovir, valganciclovir and valaciclo‐ vir [101]. Ganciclovir has been used in patients with CMV polyradiculopathy successfully [53].

#### **4.8. Fungal infection**

Depending on fungal infection, antifungal regimen such as amphotericin B, posaconazol, voriconazol, etc may be used with surgical intervention. Voriconazole has been used to treat aspergillosis [58]. The gold standard of systemic antifungal treatment is voriconazole, which has been proved to be significantly superior to conventional amphotericin B. Liposomal amphotericin B appears to be a suitable alternative for primary treatment, while caspofungin, amphotericin B lipid complex or posaconazole have shown partial or complete response in patients who had been refractory to or intolerant of primary antifungal therapy [101]. Itraco‐ nazole is more frequently used in immunosuppressed patients who are able to take oral therapy and for use as sequential oral therapy [102]. Options for initial therapy for invasive Candida infections include fluconazole, echinocandin compounds or liposomal amphotericin B. Voriconazole is the secondary alternative treatment [101]. Amphotericin B, caspofungin or posaconazole are used for treatment of Zygomycosis [103, 104].

#### **4.9. Schistosomiasis**

**4.6. Brucellosis**

14 Topics in Paraplegia

prim-sulfamethoxazole [99].

**4.7. Viral infection**

**4.8. Fungal infection**

Neurobrucellosis, if not treated early, can result in severe neurological morbidity and sequelae, which may be irreversible. Hence it is important to consider the possibility of neurobrucellosis in endemic region and treat aggressively (94). Treatment with streptomycin, rifampicin and doxycyclin significantly improve the symptoms [44]. Doxycycline, rifampin, trimethoprimsulfamethoxazole, streptomycin, gentamicin, ciprofloxacin and ceftriaxone are used for treatment of neurobrucellosis [95]. The mean duration of antimicrobial therapy is 18 weeks with range of 12-56 weeks. Prolonged duration of treatment especially in complicated cases in order to avoid possible sequelae is necessary [42]. In Gul's study duration of antibiotic therapy was ranged from 2 to 15 months (median 5 months) [96]. Neurobrucellosis and brucella spondylitis usually are treated with 3 drugs combination [46, 97]. The standard treatment of brucella spondylitis with a combination of two antibiotics for 6-12 weeks is associated with high rates of treatment failure and relapse. Prolonged administration of a triple combination of suitable antibiotics appears to be an effective treatment for brucella spondylitis [98]. The most commonly-used antibiotics are combinations of rifampin, doxycycline and trimetho‐

For treatment of HIV usually 2 nucleoside analogue plus one protease inhibitor or one nonnucleoside reverse transcriptase inhibitor are used. Although nucleoside analogues, such as zidovudine and lamivudine, have long been recognized to have activity against HTLV reverse transcription in vitro, there is little clinical evidence of their efficacy in vivo, so treatment of asymptomatic HTLV carriers is not indicated. A combination of zidovudine and lamivudine has been used for treatment, but no clinical improvement was seen, and there was no effect on HTLV-I proviral load or immunologic markers [100]. The most commonly antiviral agents used for treatment of CMV are: ganciclovir, foscarnet, cidofovir, valganciclovir and valaciclo‐ vir [101]. Ganciclovir has been used in patients with CMV polyradiculopathy successfully [53].

Depending on fungal infection, antifungal regimen such as amphotericin B, posaconazol, voriconazol, etc may be used with surgical intervention. Voriconazole has been used to treat aspergillosis [58]. The gold standard of systemic antifungal treatment is voriconazole, which has been proved to be significantly superior to conventional amphotericin B. Liposomal amphotericin B appears to be a suitable alternative for primary treatment, while caspofungin, amphotericin B lipid complex or posaconazole have shown partial or complete response in patients who had been refractory to or intolerant of primary antifungal therapy [101]. Itraco‐ nazole is more frequently used in immunosuppressed patients who are able to take oral therapy and for use as sequential oral therapy [102]. Options for initial therapy for invasive Candida infections include fluconazole, echinocandin compounds or liposomal amphotericin B. Voriconazole is the secondary alternative treatment [101]. Amphotericin B, caspofungin or

posaconazole are used for treatment of Zygomycosis [103, 104].

Praziquantel and corticoids have been successfully used to treat neuroschistosomiasis [65]. Surgery has been tried for acute cases of failed medical treatment [1].

#### **5. Conclusion**

Infectious diseases are important causes of non-traumatic paraplegia. High index of suspicion, precise history taking, exact physical examination and proper use of laboratory tests and radiologic studies are necessary for making accurate diagnosis. Sometimes the diagnosis is dependent to invasive procedure such as CT guided biopsy and subsequent histopathologic study, without them appropriate diagnosis may be impossible. Sometimes for accurate diagnosis using several laboratory and radiologic modalities, simultaneously, may be needed. Paying attention to specific treatment and its duration is very important. Sometimes combi‐ nation antibiotic therapy is needed. If treatment or its duration is not appropriate, relapse may occur. Although paraplegia due to infectious diseases can be with high mortality rate, early diagnosed and successful treatment can prevent neurological sequelae.

#### **Acknowledgements**

With special thanks to Dr Katayoun Vahdat and Dr Mohammad Javadi

#### **Author details**

Farhad Abbasi1 and Soolmaz Korooni Fardkhani2

1 Bushehr University of Medical Sciences, Iran

2 Shiraz University of Medical Sciences, Iran

#### **References**


[3] Sandin KJ, Klaas SJ. Assessment and evaluation of primary prevention in spinal cord injury. Top Spinal Cord Inj Rehabil. 2013;19(1):9-14.

[16] Shah NH, Roos KL. Spinal epidural abscess and paralytic mechanisms. Curr Opin

Paraplegia Caused by Infectious Agents; Etiology, Diagnosis and Management

http://dx.doi.org/10.5772/56989

17

[17] Gehlot PS, Chaturvedi S, Kashyap R, Singh V. Pott's Spine: Retrospective Analysis of

[18] Yadegarynia D, Abbasi F, Keshtkar-Jahromi M, Gholamin S. Gastrointestinal Tuber‐ culosis with Cecum Involvement in a 33-Year-Old Woman. Iran J Med Sci. 2009;34(3):

[19] Goasdoué P, Dubayle P, Boyer B, Debord T, Le Clainche P, Pharaboz C. Disseminat‐

[20] Beshart M, Abbasi F, Behzad H.R. Tuberculosis meningitis, mutiple brain tuberculo‐ ma and ocular involvement in a 20 year old man. Journal of medical council of I.R.I.

[21] Beshart M, Abbasi F, Behzad H.R. A young Afghan man with prolonged fever and

[22] Hristea A, Constantinescu RV, Exergian F, Arama V, Besleaga M, Tanasescu R. Para‐ plegia due to non-osseous spinal tuberculosis: report of three cases and review of the

[23] Abbas A, Rizvi SR, Mahesri M, Salahuddin HR. Conservative management of spinal

[24] Garg RK, Somvanshi DS. Spinal tuberculosis: a review. J Spinal Cord Med.

[25] Abbasi F, Besharat M. Tuberculosis Spondylitis (Pott's Disease) in Iran, Evaluation of

[26] Jain AK, Kumar J. Tuberculosis of spine: neurological deficit. Eur Spine J. 2013 Jun;22

[27] Muthukumar N, Venkatesh G, Senthilbabu S, Rajbaskar R. Surgery for intramedul‐ lary tuberculoma of the spinal cord: report of 2 cases. Surg Neurol. 2006;66(1):69-7.

[28] Molina-Olier O, Tuñón-Pitalúa M, Alcalá-Cerra G, Niño-Hernández L, Moscote-Sala‐ zar L. Spinal cord compression due to intraspinal syphilitic gumma in one patient.

[29] Tsui EY, Ng SH, Chow L, Lai KF, Fong D, Chan JH. Syphilitic myelitis with diffuse

[30] Miura M, Kuraoka S, Kanazawa H, Oguma F, Irisawa H, Kasuya S, Sakashita I. Syph‐ ilitic thoracic aortic aneurysm with destruction of vertebral body, producing numb‐

spinal cord abnormality on MR imaging. Eur Radiol. 2002;12(12):2973-6.

ness of lower extremities and paraplegia. Kyobu Geka. 1995;48(11):953-6.

tuberculosis: initial series from pakistan. Asian Spine J. 2013;7(2):73-80.

MRI Scans of 70 Cases. J Clin Diagn Res. 2012;6(9):1534-8.

ed tuberculosis of unusual locations. J Radiol. 1997;78(9):659-61.

headache. Iran J Clin infect Dis. 2009;4(1):45-6.

literature. Int J Infect Dis. 2008;12(4):425-9.

40 Cases. Iran J Clin infect Dis. 2011;6 suppl:30-32

Clinical case. Acta Ortop Mex. 2012;26(3):197-201.

Neurol. 2013;26(3):314-7.

213-16

2008; 26(3);409-412.

2011;34(5):440-54.

Suppl 4:624-33.


[16] Shah NH, Roos KL. Spinal epidural abscess and paralytic mechanisms. Curr Opin Neurol. 2013;26(3):314-7.

[3] Sandin KJ, Klaas SJ. Assessment and evaluation of primary prevention in spinal cord

[4] Bellon K, Kolakowsky-Hayner SA, Chen D, McDowell S, Bitterman B, Klaas SJ. Evi‐ dence-based practice in primary prevention of spinal cord injury. Top Spinal Cord

[5] Hess ChW. Non-traumatic acute transverse spinal cord syndromes. Praxis.

[6] Tunkel A.R. Subdural empyema, epidural abscess and suppurative intracrainial thrombophelebitis. In: Mandell G.L, Benett J.E, Dolin R. Principle and practice of in‐

[7] Coumans JV, Walcott BP. Rapidly progressive lumbar subdural empyema following

[8] Sandler AL, Thompson D, Goodrich JT, van Aalst J, Kolatch E, El Khashab M, Nejat F, Cornips E, Mohindra S, Gupta R, Yassari R, Daniels LB, Biswas A, Abbott R. Infec‐ tions of the spinal subdural space in children: a series of 11 contemporary cases and review of all published reports. A multinational collaborative effort. Childs Nerv

[9] Chen MH, Chen MH, Huang JS. Cervical subdural empyema following acupuncture.

[10] Kalaycý M, Cadavi F, Altunkaya H, Gül S, Ackgöz B. Subdural empyema due to spi‐

[11] Volk T, Hebecker R, Ruecker G, Perka C, Haas N, Spies C. Subdural empyema com‐ bined with paraspinal abscess after epidural catheter insertion. Anesth Analg.

[12] Vural M, Arslantaş A, Adapinar B, Kiremitçi A, Usluer G, Cuong B, Atasoy MA. Spi‐ nal subdural Staphylococcus aureus abscess: case report and review of the literature.

[13] Delgado Tapia JA, Galera López J, Santiago Martín J, Galdo Abadín JR, Quirante Pi‐ zarro A, Cánovas Fernández E, García Villalba F. Subdural empyema due to Myco‐ plasma hominis after a cesarean section under spinal anesthesia. Rev Esp Anestesiol

[14] Sales JG, Tabrizi A, Elmi A, Soleimanpour J, Gavidel E. Adolescence spinal epidural abscess with neurological symptoms: case report, a lesson to be re-learnt. Med J Is‐

[15] Ohyagi M, Ohkubo T, Taniyama T, Tomizawa S, Okawa A, Yokota T, Mizusawa H. Spinal epidural abscess caused by bacteroides fragilis group after dilation and curet‐

tage for incomplete abortion. J Glob Infect Dis. 2012;4(2):132-4.

fectious diseases. 7th edition. Philadelphia, USA: Elsevier; 2010.p.1279-82.

acromial bursal injection. J Clin Neurosci. 2011;18(11):1562-3.

nal anesthesia. Acta Anaesthesiol Scand. 2005;49(3):426.

injury. Top Spinal Cord Inj Rehabil. 2013;19(1):9-14.

Inj Rehabil. 2013;19(1):25-30.

2005;94(30-31):1151-9.

16 Topics in Paraplegia

Syst. 2013;29(1):105-17.

2005;100(4):1222-3.

J Clin Neurosci. 2004;11(8):909-11.

Acta Neurol Scand. 2005;112(5):343-6.

Reanim. 2005;52(4):239-42.

lam Repub Iran. 2013;27(1):38-41.


[31] Leung JS, Mok CK, Leong JC, Chan WC. Syphilitic aortic aneurysm with spinal ero‐ sion. Treatment by aneurysm replacement and anterior spinal fusion. J Bone Joint Surg Br. 1977;59(1):89-92.

[45] Ekici MA, Ozbek Z, Gökoğlu A, Menkü A. Surgical management of cervical spinal epidural abscess caused by Brucella melitensis : report of two cases and review of the

Paraplegia Caused by Infectious Agents; Etiology, Diagnosis and Management

http://dx.doi.org/10.5772/56989

19

[46] Mousa AR, Koshy TS, Araj GF, Marafie AA, Muhtaseb SA, Al-Mudallal DS, Bushare‐ tulla MS. Brucella meningitis: presentation, diagnosis and treatment--a prospective

[47] Tur BS, Suldur N, Ataman S, Ozturk EA, Bingol A, Atay MB. Brucellar spondylitis: a

[48] Modi G, Ranchhod J, Hari K, Mochan A, Modi M. Non-traumatic myelopathy at the Chris Hani Baragwanath Hospital, South Africa--the influence of HIV. QJM.

[49] Grasso G, Meli F, Graziano F, Stagno V, Imbrucè P, Florena AM, Maugeri R, Iacopino DG. Chronic inflammation causing spinal cord compression in human immunodefi‐

[50] Gonzalez LA, Villa AM, Kohler G, Garcea O, Kremenchutzky M, Caceres F, Sanz OP, Sica RE. Further studies on HTLV-I associated myelopathy in Argentina. Medicina (B

[51] Amayo EO, Kwasa TO, Otieno CF. Herpes zoster myelitis: report of two cases. East

[52] Chrétien F, Gray F, Lescs MC, Geny C, Dubreuil-Lemaire ML, Ricolfi F, Baudrimont M, Levy Y, Sobel A, Vinters HV. Acute varicella-zoster virus ventriculitis and menin‐ go-myelo-radiculitis in acquired immunodeficiency syndrome. Acta Neuropathol.

[53] Kim YS, Hollander H. Polyradiculopathy due to cytomegalovirus: report of two cas‐ es in which improvement occurred after prolonged therapy and review of the litera‐

[54] Matsumoto R, Nakagawa S, Nakayama J, Hashimoto T, Shindo M. A case of acquired immune deficiency syndrome presenting acute lumbosacral polyradiculopathy due to opportunistic infection of cytomegalovirus. Rinsho Shinkeigaku. 1998;38(7):653-7.

[55] Behar R, Wiley C, McCutchan JA. Cytomegalovirus polyradiculoneuropathy in ac‐

[56] López-Cortés LE, Garcia-Vidal C, Ayats J, Gudiol C, Bodro M, Sánchez-Ortega I, Pe‐ ña C, Carratalá J. Invasive aspergillosis with extrapulmonary involvement: patho‐ genesis, clinical characteristics and prognosis. Rev Iberoam Micol. 2012;29(3):139-43.

[57] Kim CH, Kim MO, Yoon JS. Paraplegia Caused by Infection Extending to Spine Due to Aspergillosis: A Case Report. J Korean Acad Rehabil Med. 2001;25(3):519-522.

quired immune deficiency syndrome. Neurology. 1987;37(4):557-61.

rare cause of spinal cord compression. Spinal Cord. 2004;42(5):321-4.

ciency virus infection. Med Sci Monit. 2008;14(11):CS134-7.

literature. J Korean Neurosurg Soc. 2012;51(6):383-7

study of ten cases. Q J Med. 1986;60(233):873-85.

2011;104(8):697-703

Aires). 1998;58(4):411-4.

1993;86(6):659-65.

Afr Med J. 2002;79(5):279-80.

ture. Clin Infect Dis. 1993;17(1):32-7.


[45] Ekici MA, Ozbek Z, Gökoğlu A, Menkü A. Surgical management of cervical spinal epidural abscess caused by Brucella melitensis : report of two cases and review of the literature. J Korean Neurosurg Soc. 2012;51(6):383-7

[31] Leung JS, Mok CK, Leong JC, Chan WC. Syphilitic aortic aneurysm with spinal ero‐ sion. Treatment by aneurysm replacement and anterior spinal fusion. J Bone Joint

[32] Brangulis K, Tars K, Petrovskis I, Kazaks A, Ranka R, Baumanis V. Structure of an outer surface lipoprotein BBA64 from the Lyme disease agent Borrelia burgdorferi which is critical to ensure infection after a tick bite. Acta Crystallogr D Biol Crystal‐

[33] Büker, Picozzi, Kolb, Hatt. First detection of Borrelia burgdorferi-antibodies in freeliving birds of prey from Eastern Westphalia, Germany. Schweiz Arch Tierheilkd.

[34] Brangulis K, Petrovskis I, Kazaks A, Baumanis V, Tars K. Structural characterization of the Borrelia burgdorferi outer surface protein BBA73 implicates dimerization as a

[35] Potok OV, Brassard A. Lyme borreliosis: an update for Canadian dermatologists. J

[36] Erol I, Kılıçarslan B, Saygi S, Demir S, Alehan F. Acute transverse myelitis in a child with lyme disease and a review of literature. Pediatr Neurol. 2013;48(4):325-8.

[37] Zajkowska JM, Hermanowska-Szpakowicz T, Kondrusik M, Pancewicz SA. Neuro‐

[38] Salonen R, Rinne JO, Halonen P, Puusa A, Marttila R, Viljanen MK. Lyme borreliosis

[39] Lim KB, Kwak YG, Kim DY, Kim YS, Kim JA. Back pain secondary to Brucella spon‐

[40] Baykal T, Baygutalp F, Senel K, Levent A, Erdal A, Ugur M, Ozgocmen S. Spastic paraparesis and sensorineural hearing loss in a patient with neurobrucellosis. J Back

[41] Köse Ş, Senger SS, Çavdar G, Yavaş S. Case report on the development of a brucello‐

[42] Ulu-Kilic A, Sayar MS, Tütüncü E, Sezen F, Sencan I. Complicated brucellar spondy‐ lodiscitis: experience from an endemic area. Rheumatol Int. 2012; DOI: 10.1007/

[43] Tappe D, Melzer F, Schmoock G, Elschner M, Lâm TT, Abele-Horn M, Stetter C. Iso‐ lation of Brucella melitensis biotype 3 from epidural empyema in a Bosnian immi‐

[44] Lampropoulos C, Kamposos P, Papaioannou I, Niarou V. Cervical epidural abscess caused by brucellosis. BMJ Case Rep. 2012 Nov 27;2012. pii: bcr2012007070. doi:

logic syndromes in Lyme disease. Pol Merkur Lekarski. 2000;9(50):584-8.

associated with complete flaccid paraplegia. J Infect. 1994;28(2):181-4.

dylitis in the lumbar region. Ann Rehabil Med. 2012;36(2):282-6

sis-related epidural abscess. J Infect Dev Ctries. 2011;5(5):403-5.

grant in Germany. J Med Microbiol. 2012;61(Pt 9):1335-7.

functional mechanism. Biochem Biophys Res Commun. 2013;434(4):848-53.

Surg Br. 1977;59(1):89-92.

18 Topics in Paraplegia

logr. 2013;69(Pt 6):1099-107.

Cutan Med Surg. 2013;17(1):13-21.

Musculoskelet Rehabil. 2012;25(3):157-9

s00296-012-2555-5

10.1136/bcr-2012-007070.

2013;155(7):411-6.


[58] Jiang Z, Wang Y, Jiang Y, Xu Y, Meng B. Vertebral osteomyelitis and epidural abscess due to Aspergillus nidulans resulting in spinal cord compression: Case report and lit‐ erature review. J Int Med Res. 2013;41(2):502-10.

[73] Araújo F, Ribeiro C, Silva I, Nero P, Branco JC. Klebsiella pneumoniae Spinal Epidur‐ al Abscess treated conservatively: case report and review. Acta Reumatol Port.

Paraplegia Caused by Infectious Agents; Etiology, Diagnosis and Management

http://dx.doi.org/10.5772/56989

21

[74] Jain AK. Tuberculosis of the spine: a fresh look at an old disease. J Bone Joint Surg Br.

[75] Jain AK, Sreenivasan R, Saini NS, Kumar S, Jain S, Dhammi IK. Magnetic resonance

[76] Arora S, Kumar R. Tubercular spinal epidural abscess involving the dorsal-lumbarsacral region without osseous involvement. J Infect Dev Ctries. 2011 Jul 27;5(7):544-9.

[77] Jacquemin GL, Proulx P, Gilbert DA, Albert G, Morcos R. Functional recovery from paraplegia caused by syphilitic meningomyelitis. J Spinal Cord Med. 2002;25(2):

[79] Barón M, Heredero J, Prieto I, Lousa M, Masjuán J, Gobernado JM. Dorsal subdural

[80] Magnarelli LA. Laboratory diagnosis of Lyme disease. Rheum Dis Clin North Am.

[81] Bodmer K. Brucella spondylodiskitis. Schweiz Med Wochenschr. 1985;115(34):1160-5.

[82] Besharat M, Abbasi F, Korooni Fardkhani S. Epidemiological features, hematologic characteristics and clinical manifestations in adult patients with brucellosis. Iran J

[83] Arkun R, Mete BD. Musculoskeletal brucellosis. Semin Musculoskelet Radiol.

[84] Karacostas D, Christodoulou C, Drevelengas A, Paschalidou M, Ioannides P, Con‐ stantinou A, Milonas I. Cytomegalovirus-associated transverse myelitis in a non-im‐

[85] Yadegarynia D, Abbasi F, Haghighi M, Korooni Fardkhani S, Yadegarynia S. Pneu‐ monitis due to cytomegalovirus in an immunocompromised patient. Iran J Clin infect

[86] Mardani M, Abbasi F, Aghahasani M, Aghazade Sarhangipour K,Hoseinishokouh S.J, Talebzade A. Report of four cases of Rhinocerebral mucormycosis in Loghman

[87] Scrimgeour EM, Gajdusek DC. Involvement of the central nervous system in Schisto‐ soma mansoni and S. haematobium infection. A review. Brain. 1985;108 ( Pt 4):

hospital. Journal of army university of medical sciences. 2009; 7(2): 143-6.

munocompromised patient. Spinal Cord. 2002;40(3):145-9.

evaluation of tubercular lesion in spine. Int Orthop. 2012;36(2):261-9.

[78] Silber MH. Syphilitic myelopathy. Genitourin Med. 1989;65(5):338-41.

spinal abscess after epidural anesthesia. Neurologia. 1997;12(6):262-4.

2012;37(3):260-3.

2010;92(7):905-13.

1989;15(4):735-45.

2011;15(5):470-9.

Dis. 2009;4(4):238-240.

1023-38.

Clin infect Dis.2010;5(3):189-190.

133-7.


[73] Araújo F, Ribeiro C, Silva I, Nero P, Branco JC. Klebsiella pneumoniae Spinal Epidur‐ al Abscess treated conservatively: case report and review. Acta Reumatol Port. 2012;37(3):260-3.

[58] Jiang Z, Wang Y, Jiang Y, Xu Y, Meng B. Vertebral osteomyelitis and epidural abscess due to Aspergillus nidulans resulting in spinal cord compression: Case report and lit‐

[59] Chang HM, Yu HH, Yang YH, Lee WI, Lee JH, Wang LC, Lin YT, Chiang BL. Suc‐ cessful treatment of Aspergillus flavus spondylodiscitis with epidural abscess in a patient with chronic granulomatous disease. Pediatr Infect Dis J. 2012;31(1):100-1.

[60] Karthik K, Shetty AP, Rajasekaran S. Spontaneous cord transection due to invasive aspergillus spondylitis in an immunocompetent child. Eur Spine J. 2011;20 Suppl

[61] Werner BC, Hogan MV, Shen FH. Candida lusitaniae discitis after discogram in an

[62] Tuyumu K, Nakaya A, Miyauchi J, Okamoto S. Epidural abscess in the spine extend‐ ed from pulmonary zygomycosis during consolidation chemotherapy for acute lym‐

[63] Rivierez M, Heyman D, Brebion A, Landau-Ossondo M, Desbois N, Vally P. Spinal

[64] Carod-Artal FJ. Neurological complications of Schistosoma infection. Trans R Soc

[65] Carod-Artal FJ. Neuroschistosomiasis. Expert Rev Anti Infect Ther. 2010;8(11):

[66] II. Kim SH, Son DW, Lee SW, Song GS. An unusual case of post-operative spondylitis caused by mycobacterium intracellulare in an immunosuppressed patient. J Korean

[67] Edwards C, Diveronica M, Abel E. Epidural abscess caused by Mycobacterium ab‐

[68] West KR, Mason RC, Sun M. Nocardia spinal epidural abscess: 14-year follow-up.

[69] Fernández-Fernández FJ, Puerta-Louro R, Rodríguez-Conde I, de la Fuente-Aguado J. Epidural abscess caused by Pasteurella pneumotropica. Enferm Infecc Microbiol

[70] Bartels RH, de Jong TR, Grotenhuis JA. Spinal subdural abscess. Case report. J Neu‐

[71] De Bonis P, Anile C, Pompucci A, Labonia M, Lucantoni C, Mangiola A. Cranial and

[72] Greenlee JE. Subdural Empyema. Curr Treat Options Neurol. 2003;5(1):13-22.

spinal subdural empyema. Br J Neurosurg. 2009;23(3):335-40.

cord histoplasmoma. A case report. Neurochirurgie. 2002;48(1):44-8.

erature review. J Int Med Res. 2013;41(2):502-10.

immunocompetent patient. Spine J. 2011;11(10):e1-6.

phoblastic leukemia. Rinsho Ketsueki. 2011;52(8):718-21.

Trop Med Hyg. 2008;102(2):107-16.

Neurosurg Soc. 2011;50(5):460-3.

Orthopedics. 2012;35(1):e128-31.

Clin. 2011;29(8):637-8.

rosurg. 1992;76(2):307-11.

scessus. Am J Case Rep. 2012;13:180-2.

2:S188-92.

20 Topics in Paraplegia

1307-18.


[88] Peregrino AJ, Puglia PM, Nobrega JP, Livramento JA, Marques-Dias MJ, Scaff M. Schistosomiasis of the spinal cord: analysis of 80 cases. Arq Neuropsiquiatr. 2002;60(3-A):603-8.

[102] Yadegarynia D, Haghighi M, Abbasi F, Gholamin S, Yadegarynia S. Invasive asper‐ gillosis of pituitary gland in an immunocompetent patient. Iran J Clin infect Dis.

Paraplegia Caused by Infectious Agents; Etiology, Diagnosis and Management

http://dx.doi.org/10.5772/56989

23

[103] De Pasqual A, Deprez M, Ghaye B, Frère P, Kaschten B, Hayette MP, Radermecker M, Martin D, Canivet JL. Invasive pulmonary mucormycosis with invasion of the thoracic spine in a patient with myelodysplastic syndrome. Rev Med Liege. 2008 Dec;

[104] Gurevich M, Levi I, Steinberg R, Shonfeld T, Shapiro R, Israeli M, Sprecher H, Shalit I, Mor E. Mucormycosis in a liver allograft: salvage re-transplantation and targeted

immunosuppressive management. Transpl Infect Dis. 2012;14(5):E97-101.

2008;3(3):163-165

63(12):702-6.


[102] Yadegarynia D, Haghighi M, Abbasi F, Gholamin S, Yadegarynia S. Invasive asper‐ gillosis of pituitary gland in an immunocompetent patient. Iran J Clin infect Dis. 2008;3(3):163-165

[88] Peregrino AJ, Puglia PM, Nobrega JP, Livramento JA, Marques-Dias MJ, Scaff M. Schistosomiasis of the spinal cord: analysis of 80 cases. Arq Neuropsiquiatr.

[89] Barón M, Heredero J, Prieto I, Lousa M, Masjuán J, Gobernado JM. Dorsal subdural

[90] Connor DE Jr, Chittiboina P, Caldito G, Nanda A. Comparison of operative and non‐ operative management of spinal epidural abscess: a retrospective review of clinical and laboratory predictors of neurological outcome. J Neurosurg Spine. 2013;19(1):

[91] Pathak A, Singh P, Gehlot P, Dhaneria M. Spinal epidural abscess treated with antibi‐ otics alone. BMJ Case Rep. 2013 Apr 30;2013. pii: bcr2013009285. doi: 10.1136/

[92] Tramont E.C. Treponoma pallidum (Syphilis). In: Mandell G.L, Benett J.E, Dolin R. Principle and practice of infectious diseases. 7th edition. Philadelphia, USA: Elsevier;

[93] Halperin JJ. Nervous System Lyme Disease: Diagnosis and Treatment. Curr Treat

[94] Vajramani GV, Nagmoti MB, Patil CS. Neurobrucellosis presenting as an intra-me‐ dullary spinal cord abscess. Ann Clin Microbiol Antimicrob. 2005 16;4:14.

[95] Asadipooya K, Dehghanian1 AR, Ranjbar Omrani1 GH, Abbasi F. Short-course treat‐ ment in neurobrucellosis: A study in Iran. Neurology India. 2011;59 (1):101-3

[96] Gul HC, Erdem H, Bek S. Overview of neurobrucellosis: a pooled analysis of 187 cas‐

[97] Bucher A, Gaustad P, Pape E. Chronic neurobrucellosis due to Brucella melitensis.

[98] Ioannou S, Karadima D, Pneumaticos S, Athanasiou H, Pontikis J, Zormpala A, Sip‐ sas NV. Efficacy of prolonged antimicrobial chemotherapy for brucellar spondylodis‐

[99] Haji-Abdolbagi M, Rasooli-Nejad M, Jafari S, Hasibi M, Soudbakhsh A. Clinical and laboratory findings in neurobrucellosis: review of 31 cases. Arch Iran Med.

[100] Murphy E.L, Biswas H.H. Human T-Cell Lymphotropic Virus Types I and II. In: In: Mandell G.L, Benett J.E, Dolin R. Principle and practice of infectious diseases. 7th edi‐

[101] Abbasi F. Infectious diseases and clinical complications during treatment in CLL. In: Oppezzo P. Chronic lymphocytic leukemia. 1st edition. Rijeka, Croatia: InTech; 2012.

spinal abscess after epidural anesthesia. Neurologia. 1997;12(6):262-4.

2002;60(3-A):603-8.

119-27.

22 Topics in Paraplegia

bcr-2013-009285.

2010.p.3035-53

2008;11(1):21-5.

p 367-382.

Options Neurol. 2013 May 12.

es. Int J Infect Dis. 2009;13(6):e339-43.

Scand J Infect Dis. 1990;22(2):223-6.

citis. Clin Microbiol Infect. 2011;17(5):756-62.

tion. Philadelphia, USA: Elsevier; 2010.p. 2303-32


**Chapter 2**

**Paraplegia as a Complication of Thoracic and**

**Thoracoabdominal Aortic Interventions**

Anisha H. Perera and Richard G.J. Gibbs

http://dx.doi.org/10.5772/57528

**1. Introduction**

Additional information is available at the end of the chapter

**1.1. The thoracic aorta, its conditions and their management**

luminal blood within the layers of the aortic wall (Figure 3).

**The thoracic aorta** The thoracic aorta comprises the ascending aorta, transverse aortic arch and descending thoracic aorta (Figure 1). The aortic arch is the segment from where the carotid and subclavian vessels arise. The descending thoracic aorta begins immediately distal to the left subclavian artery and extends up to the diaphragm. A thoracic aortic aneurysm (TAA) is defined as dilatation of the thoracic aorta to a diameter at least 1.5 times greater than is normal at a given aortic level (Figure 2). Thoracoabdominal aortic aneurysms (TAAA) involve the thoracic aorta and extend into the abdominal aorta. They are classified according to the Crawford classification as types I to IV. Due to their extent and frequent involvement of the visceral vessels, management is invariably complex. TAAs often result from cystic medial degeneration weakening of the aortic wall, though the majority are associated with athero‐ sclerosis and risk factors such as hypertension, hypercholesterolemia and smoking. These aneurysms occur most frequently in the 6th and 7th decade of life. In younger patients TAA is commonly associated with connective tissue disorders such as Marfan, Ehlers-Danlos and Loeys-Dietz syndromes. Acute aortic syndrome comprises a spectrum of emergency condi‐ tions caused by disruption of the medial layer of the aortic wall, which includes aortic dissection, intramural haematoma and penetrating atherosclerotic ulcers. Thoracic aortic dissection (TAD) is defined as separation of the aortic media, with the presence of extra-

Asymptomatic and small TAAs are initially managed medically, whilst symptomatic (usually pain or compression symptoms) or rapidly expanding aneurysms as well as those greater than 6cm in diameter necessitate surgical intervention to prevent rupture. TADs many also be

> © 2014 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

### **Paraplegia as a Complication of Thoracic and Thoracoabdominal Aortic Interventions**

Anisha H. Perera and Richard G.J. Gibbs

Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/57528

#### **1. Introduction**

#### **1.1. The thoracic aorta, its conditions and their management**

**The thoracic aorta** The thoracic aorta comprises the ascending aorta, transverse aortic arch and descending thoracic aorta (Figure 1). The aortic arch is the segment from where the carotid and subclavian vessels arise. The descending thoracic aorta begins immediately distal to the left subclavian artery and extends up to the diaphragm. A thoracic aortic aneurysm (TAA) is defined as dilatation of the thoracic aorta to a diameter at least 1.5 times greater than is normal at a given aortic level (Figure 2). Thoracoabdominal aortic aneurysms (TAAA) involve the thoracic aorta and extend into the abdominal aorta. They are classified according to the Crawford classification as types I to IV. Due to their extent and frequent involvement of the visceral vessels, management is invariably complex. TAAs often result from cystic medial degeneration weakening of the aortic wall, though the majority are associated with athero‐ sclerosis and risk factors such as hypertension, hypercholesterolemia and smoking. These aneurysms occur most frequently in the 6th and 7th decade of life. In younger patients TAA is commonly associated with connective tissue disorders such as Marfan, Ehlers-Danlos and Loeys-Dietz syndromes. Acute aortic syndrome comprises a spectrum of emergency condi‐ tions caused by disruption of the medial layer of the aortic wall, which includes aortic dissection, intramural haematoma and penetrating atherosclerotic ulcers. Thoracic aortic dissection (TAD) is defined as separation of the aortic media, with the presence of extraluminal blood within the layers of the aortic wall (Figure 3).

Asymptomatic and small TAAs are initially managed medically, whilst symptomatic (usually pain or compression symptoms) or rapidly expanding aneurysms as well as those greater than 6cm in diameter necessitate surgical intervention to prevent rupture. TADs many also be

© 2014 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

**Figure 1. The aorta** (*Image by Miss S. M. Perera*)

initially managed medically with the focus on blood pressure control, although immediate surgical intervention is required in patients with visceral, renal or limb malperfusion or for complications such as secondary dilatation and aneurysm formation. Historically, open surgical repair was the treatment for both TAA and TAD. In recent years, the advent of the endovascular stent-graft has resulted in minimally invasive treatment options. Thoracic endovascular aortic repair (TEVAR) is the placement of an endovascular stent to treat path‐ ology of the thoracic aorta (Figure 4), and there has been a dramatic increase in the number of thoracic endografts placed in the recent years. TEVAR has now been adopted as the surgical approach of choice (particularly in the developed world), and in many countries it exceeds the number of open procedures performed for thoracic aortic pathologies.

use of distal aortic perfusion usually provided with an atrio-femoral bypass circuit, although total cardiopulmonary bypass with deep hypothermic circulatory arrest can also be utilized [1]. The aneurysmal aorta is replaced with a Dacron graft using a hand-sewn anastomosis, and vessels (visceral or head and neck) involved in the aneurysm are revascularized. Complica‐ tions include mortality, cardiovascular and respiratory compromise, bleeding, acute renal failure, stroke and paraplegia. For thoracic and thoracoabdominal aneurysm repair, operative mortality is significant and varies from 2.7 to 8.8% and 7.6 to 14 respectively [2-5]. Paraplegia/ paraparesis occurs in 2.7 to 12% in thoracic and 3.6 to 16% in thoracoabdominal open surgical

**Figure 2. Thoracic aortic aneurysm** CT angiogram of 7cm thoracic aortic aneurysm (arrow) in A) sagittal B) axial and

Paraplegia as a Complication of Thoracic and Thoracoabdominal Aortic Interventions

http://dx.doi.org/10.5772/57528

27

**Thoracic endovascular aortic repair** TEVAR allows aneurysm exclusion without the need for thoracotomy and aortic cross-clamping. A pre-sized covered stent-graft is inserted through the common femoral artery via a surgical groin incision and deployed under fluoroscopic guidance (Figure 4). Additional percutaneous access via the contralateral femoral or left brachial artery is obtained for placement of an imaging catheter. Similar to open techniques, any vessels involved in the aneurysm or dissection, both visceral and head and neck, are

procedures [2, 3, 5, 6].

C) coronal planes

**Open surgical repair** (Figure 5) Open surgery of TAA involves a left thoracotomy or thora‐ coabdominal incision, and the choice of specific surgical technique is dependent on aneurysm morphology, aortic anatomy and surgeon preference. The aorta is cross-clamped and mini‐ mizing ischemia time is vital to ensure adequate perfusion of the bowel, kidneys and lower limbs. The two most commonly applied approaches include a clamp-and-sew technique or the Paraplegia as a Complication of Thoracic and Thoracoabdominal Aortic Interventions http://dx.doi.org/10.5772/57528 27

**Figure 2. Thoracic aortic aneurysm** CT angiogram of 7cm thoracic aortic aneurysm (arrow) in A) sagittal B) axial and C) coronal planes

initially managed medically with the focus on blood pressure control, although immediate surgical intervention is required in patients with visceral, renal or limb malperfusion or for complications such as secondary dilatation and aneurysm formation. Historically, open surgical repair was the treatment for both TAA and TAD. In recent years, the advent of the endovascular stent-graft has resulted in minimally invasive treatment options. Thoracic endovascular aortic repair (TEVAR) is the placement of an endovascular stent to treat path‐ ology of the thoracic aorta (Figure 4), and there has been a dramatic increase in the number of thoracic endografts placed in the recent years. TEVAR has now been adopted as the surgical approach of choice (particularly in the developed world), and in many countries it exceeds the

**Open surgical repair** (Figure 5) Open surgery of TAA involves a left thoracotomy or thora‐ coabdominal incision, and the choice of specific surgical technique is dependent on aneurysm morphology, aortic anatomy and surgeon preference. The aorta is cross-clamped and mini‐ mizing ischemia time is vital to ensure adequate perfusion of the bowel, kidneys and lower limbs. The two most commonly applied approaches include a clamp-and-sew technique or the

number of open procedures performed for thoracic aortic pathologies.

**Figure 1. The aorta** (*Image by Miss S. M. Perera*)

26 Topics in Paraplegia

use of distal aortic perfusion usually provided with an atrio-femoral bypass circuit, although total cardiopulmonary bypass with deep hypothermic circulatory arrest can also be utilized [1]. The aneurysmal aorta is replaced with a Dacron graft using a hand-sewn anastomosis, and vessels (visceral or head and neck) involved in the aneurysm are revascularized. Complica‐ tions include mortality, cardiovascular and respiratory compromise, bleeding, acute renal failure, stroke and paraplegia. For thoracic and thoracoabdominal aneurysm repair, operative mortality is significant and varies from 2.7 to 8.8% and 7.6 to 14 respectively [2-5]. Paraplegia/ paraparesis occurs in 2.7 to 12% in thoracic and 3.6 to 16% in thoracoabdominal open surgical procedures [2, 3, 5, 6].

**Thoracic endovascular aortic repair** TEVAR allows aneurysm exclusion without the need for thoracotomy and aortic cross-clamping. A pre-sized covered stent-graft is inserted through the common femoral artery via a surgical groin incision and deployed under fluoroscopic guidance (Figure 4). Additional percutaneous access via the contralateral femoral or left brachial artery is obtained for placement of an imaging catheter. Similar to open techniques, any vessels involved in the aneurysm or dissection, both visceral and head and neck, are

**Figure 3. Aortic dissection** CT angiogram of type B aortic dissection in A) coronal and B) axial planes. Arrow indicates dissection flap caused by separation of the layers of the aortic wall, with blood within the layers forming a true and false lumen

**Epidemiology** Between 1999 and 2010, hospital admissions for total (ascending and descend‐ ing) thoracic aortic disease in the UK rose steadily from 7.2 to 8.8 per 100,000 of population (*p*=0.0001) for TAD, and from 4.4 to 9.0 (*p*<0.0001) for TAA [9]. Since separate coding for open repair and TEVAR was initiated in 2006, the rate of repairs for descending TAAs have more than doubled from 0.7 in 2005 to 1.9 per 100,000 population in 2010. The rates for open repair have been steady, and the observed increase is entirely attributable to the increased rate of TEVAR. The changes for type B aortic dissection are even more remarkable, where overall repair rates have increased from 0.1 per 100,000 in 2000 to 0.5 per 100,000 population (*p*=0.0001) in 2010. Data is from Hospital Episodes Statistics (HES) (England) and Health Solutions Wales PEDW Statistics (Wales). The changing trends indicate a likely increase in thoracic vascular workload in the future. Therefore recognizing, managing and reducing the incidence of spinal cord ischemia (SCI) as a complication of thoracic and thoracoabdominal aortic intervention is

**Figure 4. Thoracic endovascular aortic repair (TEVAR)** Angiogram images outlining procedural steps A) Guidewire and catheter in aortic arch (star). Stent-graft ensheathed within delivery device advanced up descending thoracic aor‐ ta (arrow head). Placed under fluoroscopic guidance and contrast angiogram performed. Arrow indicates thoracic aortic aneurysm B) Stent-graft deployed (arrow head). Contrast angiogram performed to confirm exclusion of aneur‐

Paraplegia as a Complication of Thoracic and Thoracoabdominal Aortic Interventions

http://dx.doi.org/10.5772/57528

29

**Anatomy** The blood supply to the thoracic spinal cord comes from a single anterior spinal artery (formed by the union of two branches from the vertebral arteries) and two paired posterior spinal arteries (also derived from the vertebral arteries), which run the length of the spinal cord [10]. The vascular anatomy is variable however, and these arteries may not be continuous along their course. Both the anterior and posterior spinal arteries are supplemented by segmental radicular arteries, which are small branches of the cervical, thoracic and lumbar vessels. The largest of the radicular arteries is the artery of Adamkiewicz, often given off at the level of T10 but it can vary in position from T7 to L4 [11]. This artery supplies the conus, but has a poor connection with the superior portion of the spinal cord. It is given off by the left

essential.

**1.2. The spinal cord**

ysm, correct position of stent and patency of all arch vessels

revascularized prior to stent-graft deployment. In instances of extensive arch or visceral open revascularization prior to stenting, the procedure is termed a hybrid procedure, denoting the combined open and endovascular approach. Recent advances in stent-graft technology have now allowed options for scalloped, fenestrated and branched grafts, mitigating the need for open surgical revascularization in suitable cases. Several challenges remain with TEVAR however, including narrow iliac diameter, vessel tortuosity, aortic arch angulation and the need for adequate sealing zones to ensure stable stent fixation. Complications include stroke, paraplegia, endoleak (persistent blood flow outside the lumen of the stent-graft and within the aneurysm sac due to incomplete sealing or exclusion of aneurysm sac, usually requiring further intervention), the need for re-intervention and less frequently mortality and conversion to open procedure. The global incidence for paraplegia post thoracic stenting varies from 0 to 9.8%, with a permanent paraplegia risk of 5.5%. The paraplegia risk for isolated descending thoracic stents is 0.9%, with poorer outcomes for more complex procedures involving fenes‐ trated and branched stents (7.1%) and visceral hybrid procedures (11.3%) [7]. Both immediate and delayed onset paraplegia have been observed following TEVAR, with cases of delayed neurological deficit occurring from twelve hours up to one month postoperatively [8].

**Figure 4. Thoracic endovascular aortic repair (TEVAR)** Angiogram images outlining procedural steps A) Guidewire and catheter in aortic arch (star). Stent-graft ensheathed within delivery device advanced up descending thoracic aor‐ ta (arrow head). Placed under fluoroscopic guidance and contrast angiogram performed. Arrow indicates thoracic aortic aneurysm B) Stent-graft deployed (arrow head). Contrast angiogram performed to confirm exclusion of aneur‐ ysm, correct position of stent and patency of all arch vessels

**Epidemiology** Between 1999 and 2010, hospital admissions for total (ascending and descend‐ ing) thoracic aortic disease in the UK rose steadily from 7.2 to 8.8 per 100,000 of population (*p*=0.0001) for TAD, and from 4.4 to 9.0 (*p*<0.0001) for TAA [9]. Since separate coding for open repair and TEVAR was initiated in 2006, the rate of repairs for descending TAAs have more than doubled from 0.7 in 2005 to 1.9 per 100,000 population in 2010. The rates for open repair have been steady, and the observed increase is entirely attributable to the increased rate of TEVAR. The changes for type B aortic dissection are even more remarkable, where overall repair rates have increased from 0.1 per 100,000 in 2000 to 0.5 per 100,000 population (*p*=0.0001) in 2010. Data is from Hospital Episodes Statistics (HES) (England) and Health Solutions Wales PEDW Statistics (Wales). The changing trends indicate a likely increase in thoracic vascular workload in the future. Therefore recognizing, managing and reducing the incidence of spinal cord ischemia (SCI) as a complication of thoracic and thoracoabdominal aortic intervention is essential.

#### **1.2. The spinal cord**

revascularized prior to stent-graft deployment. In instances of extensive arch or visceral open revascularization prior to stenting, the procedure is termed a hybrid procedure, denoting the combined open and endovascular approach. Recent advances in stent-graft technology have now allowed options for scalloped, fenestrated and branched grafts, mitigating the need for open surgical revascularization in suitable cases. Several challenges remain with TEVAR however, including narrow iliac diameter, vessel tortuosity, aortic arch angulation and the need for adequate sealing zones to ensure stable stent fixation. Complications include stroke, paraplegia, endoleak (persistent blood flow outside the lumen of the stent-graft and within the aneurysm sac due to incomplete sealing or exclusion of aneurysm sac, usually requiring further intervention), the need for re-intervention and less frequently mortality and conversion to open procedure. The global incidence for paraplegia post thoracic stenting varies from 0 to 9.8%, with a permanent paraplegia risk of 5.5%. The paraplegia risk for isolated descending thoracic stents is 0.9%, with poorer outcomes for more complex procedures involving fenes‐ trated and branched stents (7.1%) and visceral hybrid procedures (11.3%) [7]. Both immediate and delayed onset paraplegia have been observed following TEVAR, with cases of delayed neurological deficit occurring from twelve hours up to one month postoperatively [8].

**Figure 3. Aortic dissection** CT angiogram of type B aortic dissection in A) coronal and B) axial planes. Arrow indicates dissection flap caused by separation of the layers of the aortic wall, with blood within the layers forming a true and

false lumen

28 Topics in Paraplegia

**Anatomy** The blood supply to the thoracic spinal cord comes from a single anterior spinal artery (formed by the union of two branches from the vertebral arteries) and two paired posterior spinal arteries (also derived from the vertebral arteries), which run the length of the spinal cord [10]. The vascular anatomy is variable however, and these arteries may not be continuous along their course. Both the anterior and posterior spinal arteries are supplemented by segmental radicular arteries, which are small branches of the cervical, thoracic and lumbar vessels. The largest of the radicular arteries is the artery of Adamkiewicz, often given off at the level of T10 but it can vary in position from T7 to L4 [11]. This artery supplies the conus, but has a poor connection with the superior portion of the spinal cord. It is given off by the left

collection of interconnecting vessels supplying the paraspinous muscles including the iliopsoas anteriorly and erector spinae posteriorly (Figure 6). The configuration of the arterial network includes inputs not only from the intercostal and lumbar segmental vessels, but also from the subclavian and hypogastric arteries. The presence of this extensive network implies a considerable reserve to ensure spinal cord perfusion when some inputs are compromised. It also highlights the threat of steal phenomenon, as a significant finding of the study was how dramatically the muscular arterial component dominates the anatomy of the network when compared with the small arteries that feed the spinal cord directly. The studies reinforce the idea that the spinal cord circulation is a longitudinally continuous and flexible system, so that input from any single segmental artery along its length is unlikely to be critical. Various studies have already demonstrated that the total loss of segmental arteries sacrificed during TAAA repair is a more powerful predictor of the risk of paraplegia than loss of any individual

Paraplegia as a Complication of Thoracic and Thoracoabdominal Aortic Interventions

http://dx.doi.org/10.5772/57528

31

**Physiology** Cerebrospinal fluid (CSF) is secreted by the central nervous system and fills the ventricles and subarachnoid space of the brain and the spinal column. It protects the brain from physical impact, circulates nutrients and has a role in waste management. Spinal cord perfusion pressure is a balance between the inflow and outflow pressures within the closed confines of the spinal canal, calculated as mean arterial pressure (MAP) minus CSF pressure. The inflow depends principally on arterial pressure, which is largely determined by cardiac output, blood volume, and the competing demands of viscera and muscle tissue connected to the same collateral network. Theoretically therefore, decreasing the CSF pressure or increasing the blood pressure/MAP will improve spinal cord perfusion pressure. CSF pressure can be decreased by insertion of a lumbar CSF drain and allowing free drainage by gravity (Figure 7). The drain is transduced to obtain pressure measurements and the rate of CSF drainage is altered by adjusting the height of the drip chamber from the ground until the desired drainage rate and pressure is achieved. MAP is increased and maintained with the use of vasopressors, which induce vasoconstriction and thereby increase the MAP. The MAP is monitored with an

**Blood supply** Given that spinal cord blood supply is often segmental and dependent upon contribution from collateral arteries, the need for more extensive aortic replacement requires interruption of an increasing number of intercostal arteries providing spinal cord perfusion, thereby posing a higher risk of SCI [13]. Type II TAAAs have been reported to have a greater negative neurological outcome compared to less extensive type IV TAAAs. The increased risk of paraplegia with type I and type II TAAAs may also be due to interruption of intercostal arteries in the area of T9–L2 where the anterior spinal artery may be discontinuous and the spinal cord may be more dependent on collateral supply. Dissection and acute presentation

**Perfusion pressure** With open repair the placement of a proximal aortic clamp interferes with the autoregulatory response controlling cerebral perfusion with resulting fluctuations in cerebral blood flow [13]. Control of proximal hypertension following placement of an aortic

arterial line to provide invasive blood pressure readings.

have also been identified as variables associated with paralysis risk [14].

**1.3. Risk factors for spinal cord ischemia**

segmental artery.

**Figure 5. Open repair** Retraction of the diaphragm (star) with open repair of thoracoabdominal aortic aneurysm with Dacron graft (arrow head) and reimplantation of an intercostal artery (arrow) (*Image courtesy of Mr J. H. Wolfe)*

intercostal or lumbar artery in over 75% of patients and is recognized by its characteristic hairpin bend. Another important radicular artery is the mid-thoracic radicular branch, which arises from the T7 posterior intercostal artery and supplements the blood supply of the fourth to eighth segments of the thoracic spinal cord.

Previous consensus has been that identification and reimplantation of the artery of Adamkie‐ wicz during TAAA repair is the best strategy for preserving spinal cord blood supply and thereby preventing paraplegia. SCI remains a problem however and re-anastomosis of arteries, a difficult enough undertaking in the context of an open repair, is not possible with current endovascular techniques. Anatomic studies have been undertaken to establish the presence of an extensive collateral network that supports spinal cord perfusion and explains preservation of spinal cord perfusion when segmental vessels are interrupted [12]. It is reported that the thoracic and lumbar segmental arteries give rise to three major vessel groups which anasto‐ mose with one another and with the nutrient arteries of the spinal cord: 1) the intrathecal vessels; the anterior spinal artery and the longitudinal chain of epidural arcades lying between the spinal cord and the vertebral bodies, 2) the interconnecting vessels lying outside the spinal canal along the dorsal processes of the vertebral bodies and paravertebral tissues, 3) a large collection of interconnecting vessels supplying the paraspinous muscles including the iliopsoas anteriorly and erector spinae posteriorly (Figure 6). The configuration of the arterial network includes inputs not only from the intercostal and lumbar segmental vessels, but also from the subclavian and hypogastric arteries. The presence of this extensive network implies a considerable reserve to ensure spinal cord perfusion when some inputs are compromised. It also highlights the threat of steal phenomenon, as a significant finding of the study was how dramatically the muscular arterial component dominates the anatomy of the network when compared with the small arteries that feed the spinal cord directly. The studies reinforce the idea that the spinal cord circulation is a longitudinally continuous and flexible system, so that input from any single segmental artery along its length is unlikely to be critical. Various studies have already demonstrated that the total loss of segmental arteries sacrificed during TAAA repair is a more powerful predictor of the risk of paraplegia than loss of any individual segmental artery.

**Physiology** Cerebrospinal fluid (CSF) is secreted by the central nervous system and fills the ventricles and subarachnoid space of the brain and the spinal column. It protects the brain from physical impact, circulates nutrients and has a role in waste management. Spinal cord perfusion pressure is a balance between the inflow and outflow pressures within the closed confines of the spinal canal, calculated as mean arterial pressure (MAP) minus CSF pressure. The inflow depends principally on arterial pressure, which is largely determined by cardiac output, blood volume, and the competing demands of viscera and muscle tissue connected to the same collateral network. Theoretically therefore, decreasing the CSF pressure or increasing the blood pressure/MAP will improve spinal cord perfusion pressure. CSF pressure can be decreased by insertion of a lumbar CSF drain and allowing free drainage by gravity (Figure 7). The drain is transduced to obtain pressure measurements and the rate of CSF drainage is altered by adjusting the height of the drip chamber from the ground until the desired drainage rate and pressure is achieved. MAP is increased and maintained with the use of vasopressors, which induce vasoconstriction and thereby increase the MAP. The MAP is monitored with an arterial line to provide invasive blood pressure readings.

#### **1.3. Risk factors for spinal cord ischemia**

intercostal or lumbar artery in over 75% of patients and is recognized by its characteristic hairpin bend. Another important radicular artery is the mid-thoracic radicular branch, which arises from the T7 posterior intercostal artery and supplements the blood supply of the fourth

**Figure 5. Open repair** Retraction of the diaphragm (star) with open repair of thoracoabdominal aortic aneurysm with Dacron graft (arrow head) and reimplantation of an intercostal artery (arrow) (*Image courtesy of Mr J. H. Wolfe)*

Previous consensus has been that identification and reimplantation of the artery of Adamkie‐ wicz during TAAA repair is the best strategy for preserving spinal cord blood supply and thereby preventing paraplegia. SCI remains a problem however and re-anastomosis of arteries, a difficult enough undertaking in the context of an open repair, is not possible with current endovascular techniques. Anatomic studies have been undertaken to establish the presence of an extensive collateral network that supports spinal cord perfusion and explains preservation of spinal cord perfusion when segmental vessels are interrupted [12]. It is reported that the thoracic and lumbar segmental arteries give rise to three major vessel groups which anasto‐ mose with one another and with the nutrient arteries of the spinal cord: 1) the intrathecal vessels; the anterior spinal artery and the longitudinal chain of epidural arcades lying between the spinal cord and the vertebral bodies, 2) the interconnecting vessels lying outside the spinal canal along the dorsal processes of the vertebral bodies and paravertebral tissues, 3) a large

to eighth segments of the thoracic spinal cord.

30 Topics in Paraplegia

**Blood supply** Given that spinal cord blood supply is often segmental and dependent upon contribution from collateral arteries, the need for more extensive aortic replacement requires interruption of an increasing number of intercostal arteries providing spinal cord perfusion, thereby posing a higher risk of SCI [13]. Type II TAAAs have been reported to have a greater negative neurological outcome compared to less extensive type IV TAAAs. The increased risk of paraplegia with type I and type II TAAAs may also be due to interruption of intercostal arteries in the area of T9–L2 where the anterior spinal artery may be discontinuous and the spinal cord may be more dependent on collateral supply. Dissection and acute presentation have also been identified as variables associated with paralysis risk [14].

**Perfusion pressure** With open repair the placement of a proximal aortic clamp interferes with the autoregulatory response controlling cerebral perfusion with resulting fluctuations in cerebral blood flow [13]. Control of proximal hypertension following placement of an aortic

flow to an already ischemic spinal cord introduces oxygen, which is rapidly metabolized to form oxygen radicals [13]. Through lipid peroxidation with cell membrane destruction, there is release of excitatory amino acids known to have a role in spinal cord ischemia. Reperfusion also introduces inflammatory cells including leukocytes, which adhere to the microvasculature and release cytotoxic mediators. The cellular damage induced by this reperfusion process functions as debris in further occluding the microvasculature and propagating the ischemic insult. Inflammatory cytokines derived from visceral ischemia, when introduced to the spinal

**Figure 7. Insertion of lumbar cerebrospinal fluid (CSF) drain** A) Performed by anesthetist under aseptic conditions. Spinal needle inserted at or below L3/4 intervertebral space. Position confirmed by free drainage of CSF. Flexible cath‐ eter inserted through needle, needle withdrawn and catheter connected to drip chamber, sterile drainage bag and pressure transducer. B) CSF drained passively by gravity by adjusting height of drip chamber (arrow) off the ground

Paraplegia as a Complication of Thoracic and Thoracoabdominal Aortic Interventions

http://dx.doi.org/10.5772/57528

33

**Critical intercostal artery coverage** In contrast to open repair, cross-clamping of the aorta is not undertaken in endovascular repair, leaving blood pressure as a major determinant of spinal cord perfusion. With TEVAR, it is thought that stent-graft coverage of the critical thoracic intercostal arteries results in reduced perfusion of the thoracic spinal cord and watershed infarction. The mid-thoracic branch may also be more critical given that the artery of Adam‐ kiewitz can originate below the area involved in graft coverage. Loss of the artery of Adam‐ kiewitz in prior abdominal aortic repairs may explain why patients with prior repair are at higher risk of SCI during subsequent TAA repair. With the loss of thoracic radicular arteries due to occlusion, increased pressure is required through the anterior and posterior spinal arteries along with other collaterals to maintain adequate perfusion pressure of the spinal cord [10]. Given patients undergoing TEVAR are less susceptible to bleeding complications in comparison with open repair, they are able to tolerate higher intraoperative and postoperative

**Collateral circulation** SCI following stent-graft deployment can also be dependent upon the extent of existing collateral circulation. Other collaterals to the spinal cord include the hypo‐

cord following reperfusion, may compound this effect.

systemic pressures.

**Figure 6. Blood supply to the spinal cord** Schematic diagram demonstrating the relationships, relative sizes and in‐ terconnections among the segmental arteries (SA), the anterior radiculomedullary arteries (ARMA), the epidural ar‐ cades and the anterior spinal artery (ASA). Longitudinal anastomoses along the dorsal processes of the spine as well as dorsal communications (interstitial connections) between right and left branches of the segmental arteries are also shown. (*From Etz CD, Kari FA, Mueller CS, Silovitz D, Brenner RM, Lin HM, Griepp RB. The collateral network concept: a reassessment of the anatomy of spinal cord perfusion. J Thorac Cardiovasc Surg. 2011 Apr;141(4):1020-8. Reproduced with permission from Elsevier)*

cross-clamp maintains autoregulation in the coronary and cerebral circulation, often at the expense of adequate distal cord perfusion. Lowering proximal pressure decreases distal mean arterial pressure, which in the presence of an unchanged or possibly increased CSF pressure, results in decreased perfusion pressure of the distal cord. Thus, CSF drainage through insertion of a spinal drain (usually controlled to maintain a CSF pressure of less than 10-12mmHg) can reduce CSF pressure, thereby improving spinal cord perfusion.

**Reperfusion injury** Ischemia and reperfusion initiate neurochemical cellular responses that can exacerbate ischemia, which may in turn progress to infarction [14]. Restoration of blood

**Figure 7. Insertion of lumbar cerebrospinal fluid (CSF) drain** A) Performed by anesthetist under aseptic conditions. Spinal needle inserted at or below L3/4 intervertebral space. Position confirmed by free drainage of CSF. Flexible cath‐ eter inserted through needle, needle withdrawn and catheter connected to drip chamber, sterile drainage bag and pressure transducer. B) CSF drained passively by gravity by adjusting height of drip chamber (arrow) off the ground

flow to an already ischemic spinal cord introduces oxygen, which is rapidly metabolized to form oxygen radicals [13]. Through lipid peroxidation with cell membrane destruction, there is release of excitatory amino acids known to have a role in spinal cord ischemia. Reperfusion also introduces inflammatory cells including leukocytes, which adhere to the microvasculature and release cytotoxic mediators. The cellular damage induced by this reperfusion process functions as debris in further occluding the microvasculature and propagating the ischemic insult. Inflammatory cytokines derived from visceral ischemia, when introduced to the spinal cord following reperfusion, may compound this effect.

**Critical intercostal artery coverage** In contrast to open repair, cross-clamping of the aorta is not undertaken in endovascular repair, leaving blood pressure as a major determinant of spinal cord perfusion. With TEVAR, it is thought that stent-graft coverage of the critical thoracic intercostal arteries results in reduced perfusion of the thoracic spinal cord and watershed infarction. The mid-thoracic branch may also be more critical given that the artery of Adam‐ kiewitz can originate below the area involved in graft coverage. Loss of the artery of Adam‐ kiewitz in prior abdominal aortic repairs may explain why patients with prior repair are at higher risk of SCI during subsequent TAA repair. With the loss of thoracic radicular arteries due to occlusion, increased pressure is required through the anterior and posterior spinal arteries along with other collaterals to maintain adequate perfusion pressure of the spinal cord [10]. Given patients undergoing TEVAR are less susceptible to bleeding complications in comparison with open repair, they are able to tolerate higher intraoperative and postoperative systemic pressures.

cross-clamp maintains autoregulation in the coronary and cerebral circulation, often at the expense of adequate distal cord perfusion. Lowering proximal pressure decreases distal mean arterial pressure, which in the presence of an unchanged or possibly increased CSF pressure, results in decreased perfusion pressure of the distal cord. Thus, CSF drainage through insertion of a spinal drain (usually controlled to maintain a CSF pressure of less than 10-12mmHg) can

**Figure 6. Blood supply to the spinal cord** Schematic diagram demonstrating the relationships, relative sizes and in‐ terconnections among the segmental arteries (SA), the anterior radiculomedullary arteries (ARMA), the epidural ar‐ cades and the anterior spinal artery (ASA). Longitudinal anastomoses along the dorsal processes of the spine as well as dorsal communications (interstitial connections) between right and left branches of the segmental arteries are also shown. (*From Etz CD, Kari FA, Mueller CS, Silovitz D, Brenner RM, Lin HM, Griepp RB. The collateral network concept: a reassessment of the anatomy of spinal cord perfusion. J Thorac Cardiovasc Surg. 2011 Apr;141(4):1020-8. Reproduced*

**Reperfusion injury** Ischemia and reperfusion initiate neurochemical cellular responses that can exacerbate ischemia, which may in turn progress to infarction [14]. Restoration of blood

reduce CSF pressure, thereby improving spinal cord perfusion.

*with permission from Elsevier)*

32 Topics in Paraplegia

**Collateral circulation** SCI following stent-graft deployment can also be dependent upon the extent of existing collateral circulation. Other collaterals to the spinal cord include the hypo‐ gastric artery, internal iliac arteries, internal thoracic artery and branches of the subclavian artery. Therefore where possible these should be revascularized or preserved, particularly in high-risk individuals. Where there is adequate collateral preservation following stent deploy‐ ment, one would not expect to see clinical evidence of ischemia [13]. If collaterals are absent and critical intercostal arteries are covered, an ischemic event is more likely to occur. If the existing intercostal or lumbar artery collateral supply is marginal, tenuous cord perfusion results, which is more vulnerable to any postoperative hemodynamic insult. Incomplete or intermediate cord ischemia may exist in the regional distribution of the excluded intercostal arteries secondary to marginal collateralization. This may present as a delayed onset neuro‐ logical deficit as the vulnerable cord is more sensitive to decreases in spinal artery perfusion pressure. These decreases may be the result of postoperative hemodynamic compromise or delayed thrombosis of previously patent yet now covered intercostal arteries.

results revealed 235 patients underwent thoracic aortic stent-grafting; 111 (47%) thoracic aortic stent-grafts alone, with an additional 14 (6%) branched or fenestrated thoracic grafts, 30 (13%) arch hybrids and 80 (34%) visceral hybrids. The global incidence of SCI for all procedures was 23/235 (9.8%), which included emergency indications (ruptured TAAA and complex acute dissections). The incidence varied considerably between types of procedures. Of the twentythree cases of SCI, death occurred in four patients, recovery of function was seen in six and permanent paraplegia occurred in 13/235 patients (5.5%). Of the nine pre-specified factors investigated for association with SCI (age, sex, indication, urgency, type of procedure, duration of procedure, percentage of aorta covered, spinal drain usage and left subclavian artery coverage), only percentage of aortic coverage was significantly associated with the incidence of SCI on logistic regression; adjusted odds ratio per 10% increase in aorta covered=1.78[95% CI 1.18-2.71], *p*=0.007. In patients who developed SCI the operative time was increased (463.5 versus 307.2 minutes) and more stents were utilized (4 versus 2). Therefore the study concluded that SCI following thoracic and thoracoabdominal aortic endovascular intervention is signif‐ icantly associated with the proportion of aorta covered. The degree of risk varies between different types of procedures, and visceral hybrids appeared to carry the highest risk of SCI. The study however included a heterogeneous group of conditions (atherosclerotic degenera‐ tive aneurysms, chronic type B dissections and acute aortic syndromes) with differences in the complexity of procedures performed (endovascular, arch and visceral hybrid solutions). No patient developed SCI with less than 54% coverage of the aorta. This work demonstrated a significant rise in the risk of SCI with increasing magnitude of procedure type; TEVAR (stentgraft confined to the thoracic aorta) was associated with the least risk at 1.8% SCI and 0.9% permanent paraplegia, arch hybrid 10% and 6.7%, fenestrated or branched graft 14.3% and

Paraplegia as a Complication of Thoracic and Thoracoabdominal Aortic Interventions

http://dx.doi.org/10.5772/57528

35

**Chronic renal insufficiency** Ullery et al [16] also reported similar findings with an SCI rate of 2.8% with TEVAR (12 of 424), 14% with arch hybrid (6 of 43) and 17% with visceral hybrid (1 of 6), and a global incidence of 4% (9 of 473). The twelve patients experiencing SCI within the TEVAR cohort all underwent stent coverage from the origin of the left subclavian artery to the diaphragm (*p*<0.001), and multivariate regression analysis demonstrated chronic renal insufficiency to be independently associated with SCI (*p*=0.029). At SCI onset, therapeutic interventions increased blood pressure from mean MAP 77mmHg to 99mmHg, and decreased mean lumbar CSF pressure from 10mmHg to 7mmHg, both at time of neurological recovery. There was one mortality within 30 days (1/12, 8%), and 9 of 11 patients experienced complete

**Simultaneous closure of two vascular territories** A risk model was developed using a prospective 63-patient single-centre cohort [17]. This was then applied to data extracted from the multi-centre European Registry on Endovascular Aortic Repair Complications (EuREC), where 38 of 2235 patients (1.7%) developed SCI (data from 19 centres). In the single-centre cohort direct correlation was seen between the occurrence of symptomatic SCI and both prolonged intraoperative hypotension (*p*=0.04) and simultaneous closure of at least two independent spinal cord vascular territories (*p*=0.005), whilst previous closure of a single vascular territory was not associated with an increased risk of symptomatic spinal cord

7.1% and visceral hybrid 20% and 11.3%.

neurological recovery as a result of the interventions.

**Hypotension** It has been demonstrated that hypotension that precipitates spinal cord injury within the first 48 hours after open surgical intervention is quite subtle and depends on interpreting postoperative blood pressure with preoperative values in mind [15]. The findings of this study support a policy of maintaining blood pressures at high levels not only intrao‐ peratively, which has become practice with endovascular repair, but for at least 48 hours postoperatively. This should especially be emphasized in patients with antecedent hyperten‐ sion, and this finding is likely to be valid following both open and endovascular repair. Following TEVAR, MAP should be maintained at greater than 80mmHg with the use of vasopressors when required. As a rule, at our unit following TEVAR, patients are monitored on a high dependency unit (HDU) environment for 24-48 hours, and maintained on a nora‐ drenaline infusion of 0.01mcg/kg/minute. If the MAP drops below 80mmHg the infusion rate is increased and titrated in order to maintain an adequate MAP. Instigating timely manage‐ ment is crucial, and having a very low background infusion rate prevents common delays associated with initiating new treatment, particularly out of hours.

**Delayed onset spinal cord ischemia** The extent of neurological deficits attributed to SCI after TEVAR can range from mild paraparesis to flaccid paralysis [16]. At the most severe end of this clinico-pathologic spectrum, patients with complete paralysis are those who have suffered irreversible SCI due to spinal cord infarction. Patients at the opposite end of the spectrum represent a mild form of cord ischemia with the potential for reversibility and full neurological recovery. Delayed-onset SCI, which can occur up to several weeks after TEVAR, is also typically due to ischemia as opposed to infarction of the spinal cord, with the potential for recovery. Whereas a deficit noted immediately upon emergence from anesthesia would be attributed to an intraoperative cause, a delayed neurological deficit observed after a period of normal neurological function is secondary to a postoperative event. Indeed several postoper‐ ative events have been linked to the development of delayed-onset SCI, including hypotension, thrombosis, hematoma, embolization and elevated CSF pressures.

**Length of aortic coverage** The authors conducted a study to determine the incidence and risk factors for SCI following thoracic and thoracoabdominal aortic intervention using a prospec‐ tive database of all interventions between 2001 and 2009, including both elective and emer‐ gency cases [7]. Logistic regression was used to investigate the factors associated with SCI. The results revealed 235 patients underwent thoracic aortic stent-grafting; 111 (47%) thoracic aortic stent-grafts alone, with an additional 14 (6%) branched or fenestrated thoracic grafts, 30 (13%) arch hybrids and 80 (34%) visceral hybrids. The global incidence of SCI for all procedures was 23/235 (9.8%), which included emergency indications (ruptured TAAA and complex acute dissections). The incidence varied considerably between types of procedures. Of the twentythree cases of SCI, death occurred in four patients, recovery of function was seen in six and permanent paraplegia occurred in 13/235 patients (5.5%). Of the nine pre-specified factors investigated for association with SCI (age, sex, indication, urgency, type of procedure, duration of procedure, percentage of aorta covered, spinal drain usage and left subclavian artery coverage), only percentage of aortic coverage was significantly associated with the incidence of SCI on logistic regression; adjusted odds ratio per 10% increase in aorta covered=1.78[95% CI 1.18-2.71], *p*=0.007. In patients who developed SCI the operative time was increased (463.5 versus 307.2 minutes) and more stents were utilized (4 versus 2). Therefore the study concluded that SCI following thoracic and thoracoabdominal aortic endovascular intervention is signif‐ icantly associated with the proportion of aorta covered. The degree of risk varies between different types of procedures, and visceral hybrids appeared to carry the highest risk of SCI. The study however included a heterogeneous group of conditions (atherosclerotic degenera‐ tive aneurysms, chronic type B dissections and acute aortic syndromes) with differences in the complexity of procedures performed (endovascular, arch and visceral hybrid solutions). No patient developed SCI with less than 54% coverage of the aorta. This work demonstrated a significant rise in the risk of SCI with increasing magnitude of procedure type; TEVAR (stentgraft confined to the thoracic aorta) was associated with the least risk at 1.8% SCI and 0.9% permanent paraplegia, arch hybrid 10% and 6.7%, fenestrated or branched graft 14.3% and 7.1% and visceral hybrid 20% and 11.3%.

gastric artery, internal iliac arteries, internal thoracic artery and branches of the subclavian artery. Therefore where possible these should be revascularized or preserved, particularly in high-risk individuals. Where there is adequate collateral preservation following stent deploy‐ ment, one would not expect to see clinical evidence of ischemia [13]. If collaterals are absent and critical intercostal arteries are covered, an ischemic event is more likely to occur. If the existing intercostal or lumbar artery collateral supply is marginal, tenuous cord perfusion results, which is more vulnerable to any postoperative hemodynamic insult. Incomplete or intermediate cord ischemia may exist in the regional distribution of the excluded intercostal arteries secondary to marginal collateralization. This may present as a delayed onset neuro‐ logical deficit as the vulnerable cord is more sensitive to decreases in spinal artery perfusion pressure. These decreases may be the result of postoperative hemodynamic compromise or

**Hypotension** It has been demonstrated that hypotension that precipitates spinal cord injury within the first 48 hours after open surgical intervention is quite subtle and depends on interpreting postoperative blood pressure with preoperative values in mind [15]. The findings of this study support a policy of maintaining blood pressures at high levels not only intrao‐ peratively, which has become practice with endovascular repair, but for at least 48 hours postoperatively. This should especially be emphasized in patients with antecedent hyperten‐ sion, and this finding is likely to be valid following both open and endovascular repair. Following TEVAR, MAP should be maintained at greater than 80mmHg with the use of vasopressors when required. As a rule, at our unit following TEVAR, patients are monitored on a high dependency unit (HDU) environment for 24-48 hours, and maintained on a nora‐ drenaline infusion of 0.01mcg/kg/minute. If the MAP drops below 80mmHg the infusion rate is increased and titrated in order to maintain an adequate MAP. Instigating timely manage‐ ment is crucial, and having a very low background infusion rate prevents common delays

**Delayed onset spinal cord ischemia** The extent of neurological deficits attributed to SCI after TEVAR can range from mild paraparesis to flaccid paralysis [16]. At the most severe end of this clinico-pathologic spectrum, patients with complete paralysis are those who have suffered irreversible SCI due to spinal cord infarction. Patients at the opposite end of the spectrum represent a mild form of cord ischemia with the potential for reversibility and full neurological recovery. Delayed-onset SCI, which can occur up to several weeks after TEVAR, is also typically due to ischemia as opposed to infarction of the spinal cord, with the potential for recovery. Whereas a deficit noted immediately upon emergence from anesthesia would be attributed to an intraoperative cause, a delayed neurological deficit observed after a period of normal neurological function is secondary to a postoperative event. Indeed several postoper‐ ative events have been linked to the development of delayed-onset SCI, including hypotension,

**Length of aortic coverage** The authors conducted a study to determine the incidence and risk factors for SCI following thoracic and thoracoabdominal aortic intervention using a prospec‐ tive database of all interventions between 2001 and 2009, including both elective and emer‐ gency cases [7]. Logistic regression was used to investigate the factors associated with SCI. The

delayed thrombosis of previously patent yet now covered intercostal arteries.

34 Topics in Paraplegia

associated with initiating new treatment, particularly out of hours.

thrombosis, hematoma, embolization and elevated CSF pressures.

**Chronic renal insufficiency** Ullery et al [16] also reported similar findings with an SCI rate of 2.8% with TEVAR (12 of 424), 14% with arch hybrid (6 of 43) and 17% with visceral hybrid (1 of 6), and a global incidence of 4% (9 of 473). The twelve patients experiencing SCI within the TEVAR cohort all underwent stent coverage from the origin of the left subclavian artery to the diaphragm (*p*<0.001), and multivariate regression analysis demonstrated chronic renal insufficiency to be independently associated with SCI (*p*=0.029). At SCI onset, therapeutic interventions increased blood pressure from mean MAP 77mmHg to 99mmHg, and decreased mean lumbar CSF pressure from 10mmHg to 7mmHg, both at time of neurological recovery. There was one mortality within 30 days (1/12, 8%), and 9 of 11 patients experienced complete neurological recovery as a result of the interventions.

**Simultaneous closure of two vascular territories** A risk model was developed using a prospective 63-patient single-centre cohort [17]. This was then applied to data extracted from the multi-centre European Registry on Endovascular Aortic Repair Complications (EuREC), where 38 of 2235 patients (1.7%) developed SCI (data from 19 centres). In the single-centre cohort direct correlation was seen between the occurrence of symptomatic SCI and both prolonged intraoperative hypotension (*p*=0.04) and simultaneous closure of at least two independent spinal cord vascular territories (*p*=0.005), whilst previous closure of a single vascular territory was not associated with an increased risk of symptomatic spinal cord ischemia (*p*=0.56). The combination of prolonged hypotension and simultaneous closure of at least two territories exhibited the strongest association (*p*<0.0001). Applying the model to the entire EuREC cohort demonstrated a good correlation between the predicted and observed risk factors (kappa 0.77, 95% CI 0.65-0.90). As a result the study concluded that simultaneous closure of at least two vascular territories supplying the spinal cord is highly relevant, especially in combination with prolonged intraoperative hypotension.

had already substantially reduced paralysis risk. These findings suggest that factors that affect collateral blood flow and metabolism account for approximately 80% of paraplegia risk and intercostal blood flow accounts for 20% of risk. These figures imply there is a limit in being able to reduce paraplegia risk in patients undergoing endograft treatment for TAAAs.

Paraplegia as a Complication of Thoracic and Thoracoabdominal Aortic Interventions

http://dx.doi.org/10.5772/57528

37

In the era of endovascular repair, where intercostal artery re-implantation is not possible, physiological factors that affect spinal cord perfusion (MAP, CSFD), metabolism and ischemic tolerance (steroids, naloxone, hypothermia) and oxygen delivery (haemoglobin, MAP, oxygen saturations, temperature, cardiac function) are key tools to prevent paraplegia [14]. There is a range of effectiveness of the applied strategies amongst treatment centres, which tells us that treatment protocols to optimize contributing factors must be established and followed

**Internal iliac revascularization** [11] In addition to revascularization of the intercostal vessels, one must also consider the superior and inferior supply to the spinal cord via the subclavian arteries and internal iliac network. Revascularization of the internal iliac arteries should not only be considered in the context of buttock ischemia, but also in an attempt to maintain adequate spinal perfusion. Internal iliac flow should be preserved on at least one side and careful consideration must be given in the context of common and internal iliac aneurysms as

**Left subclavian artery revascularization** The left subclavian artery (LSCA) has achieved prominence in discussions regarding case planning for stent-graft insertion. Up to one third of patients undergoing TEVAR require coverage of the LSCA in order to achieve an adequate landing zone and proximal seal [21]. In these situations the stent-graft is placed across the origin of the artery and endovascular embolization of the vessel with percutaneous access via the brachial artery is required to prevent development of a type 2 endoleak (persistent blood flow into the aneurysm sac from collateral vessels). In selected cases LSCA revascularization is undertaken prior to endovascular stent deployment. This can be performed as a single or staged procedure. At our unit this is routinely performed as a single-stage procedure in a hybrid operating suite (surgical operating theatre equipped with advanced medical imaging devices required for endovascular procedures). An open left common carotid to left subclavian artery bypass is performed, commonly with a Dacron graft, prior to endovascular stenting across the origin of the LSCA (Figure 8). The LSCA provides important circulation to the spinal cord, brain, and arm, and therefore coverage is not without clinical consequences. Stroke, SCI and coronary ischemia in the setting of a left internal mammary artery bypass, as well as arm ischemia, have all been described. The left vertebral artery serves as the dominant vessel to the hindbrain in 60% of individuals, and as a result LSCA coverage can lead to a posterior circulation stroke. LSCA coverage can also compromise spinal blood flow with resultant SCI. It contributes to spinal cord perfusion by providing branches to the cephalad portions of the anterior and posterior spinal arteries [22]. Management of patients in whom the LSCA is sacrificed remains a source of considerable debate and controversy. Proponents of routine revascularization cite the increased risk of arm ischemia, stroke and SCI associated with LSCA coverage. Several other studies have shown that intentional coverage of the LSCA without revascularization is not associated with increased morbidity and lend support to those who

consistently to achieve the best results [14].

well as when a uni-iliac stent-graft is placed.

**Previous or concomitant abdominal aortic repair** Although the putative mechanism of loss of lumbar collateral perfusion in those who had prior aortic repairs appears reasonable, occurrence of SCI in this subset of patients has not been consistent. The outcomes of twentyeight patients who underwent staged TEVAR following previous or concomitant abdominal aortic repair were reported, of whom twenty-seven had cerebrospinal fluid drainage during and following thoracic repair. SCI developed in four of twenty-eight patients (14.3%); symp‐ toms manifested twelve hours postoperatively in one patient, with delayed onset in the remaining three patients ranging from three days to seven weeks postoperatively [18]. Irreversible cord ischemia occurred in three patients, with full recovery in one patient. This was in comparison to only one of 97 patients (1.0%) who developed SCI following TEVAR only, with no intervention to the abdominal aorta. The study showed that SCI occurred at a markedly higher rate in patients with previous or concomitant abdominal aortic repair, and this risk continued beyond the immediate postoperative period. Another study analysed a case series of 406 patients undergoing thoracic stent-grafting for various aortic pathology [19]. Prophylactic cerebrospinal fluid drainage (CSFD) was used selectively in only four cases. The incidence of paraplegia was 2.7% (n=11), with six patients having major permanent deficit. When analysing conditions influencing SCI, statistical correlation was found for previous conventional or endovascular abdominal aortic aneurysm repair (odds ratio [OR], 4.8) in addition to coverage of the entire descending thoracic aorta (OR, 3.6) and implantation of thoracoabdominal branched and fenestrated stent-grafts (OR, 9.5). Individual analyses revealed other conditions that might have played a role, such as embolization into the segmental arteries, severe visceral ischemia, profound hemorrhagic shock and heparininduced thrombocytopenia. At our unit we routinely perform CSFD on patients undergoing TEVAR following previous or concomitant abdominal aortic intervention.

#### **1.4. Adjuncts for the prevention of paraplegia**

**Intercostal artery re-implantation** (Figure 5) Acher et al demonstrated an 80% reduction in paraplegia risk using hypothermia, naloxone, steroids, spinal fluid drainage, intercostal ligation and optimizing hemodynamic parameters. The group then demonstrated that intercostal revascularization (either reimplantation or preservation where possible) further reduced their paraplegia risk index by 75% when evaluated using a highly accurate (R2 > 0.88) paraplegia risk index [20]. Intercostal arteries were reimplanted based on magnetic resonance angiography identification of intercostal arteries that supplied radicular arteries feeding the anterior spinal artery, or by patency and location at surgery. The incidence of paralysis after TAAA repair decreased from 4.83% to 0.88% and the paralysis risk index decreased from 0.26 to 0.05 when intercostal artery reimplantation was added to neuroprotective strategies that had already substantially reduced paralysis risk. These findings suggest that factors that affect collateral blood flow and metabolism account for approximately 80% of paraplegia risk and intercostal blood flow accounts for 20% of risk. These figures imply there is a limit in being able to reduce paraplegia risk in patients undergoing endograft treatment for TAAAs.

ischemia (*p*=0.56). The combination of prolonged hypotension and simultaneous closure of at least two territories exhibited the strongest association (*p*<0.0001). Applying the model to the entire EuREC cohort demonstrated a good correlation between the predicted and observed risk factors (kappa 0.77, 95% CI 0.65-0.90). As a result the study concluded that simultaneous closure of at least two vascular territories supplying the spinal cord is highly relevant,

**Previous or concomitant abdominal aortic repair** Although the putative mechanism of loss of lumbar collateral perfusion in those who had prior aortic repairs appears reasonable, occurrence of SCI in this subset of patients has not been consistent. The outcomes of twentyeight patients who underwent staged TEVAR following previous or concomitant abdominal aortic repair were reported, of whom twenty-seven had cerebrospinal fluid drainage during and following thoracic repair. SCI developed in four of twenty-eight patients (14.3%); symp‐ toms manifested twelve hours postoperatively in one patient, with delayed onset in the remaining three patients ranging from three days to seven weeks postoperatively [18]. Irreversible cord ischemia occurred in three patients, with full recovery in one patient. This was in comparison to only one of 97 patients (1.0%) who developed SCI following TEVAR only, with no intervention to the abdominal aorta. The study showed that SCI occurred at a markedly higher rate in patients with previous or concomitant abdominal aortic repair, and this risk continued beyond the immediate postoperative period. Another study analysed a case series of 406 patients undergoing thoracic stent-grafting for various aortic pathology [19]. Prophylactic cerebrospinal fluid drainage (CSFD) was used selectively in only four cases. The incidence of paraplegia was 2.7% (n=11), with six patients having major permanent deficit. When analysing conditions influencing SCI, statistical correlation was found for previous conventional or endovascular abdominal aortic aneurysm repair (odds ratio [OR], 4.8) in addition to coverage of the entire descending thoracic aorta (OR, 3.6) and implantation of thoracoabdominal branched and fenestrated stent-grafts (OR, 9.5). Individual analyses revealed other conditions that might have played a role, such as embolization into the segmental arteries, severe visceral ischemia, profound hemorrhagic shock and heparininduced thrombocytopenia. At our unit we routinely perform CSFD on patients undergoing

especially in combination with prolonged intraoperative hypotension.

36 Topics in Paraplegia

TEVAR following previous or concomitant abdominal aortic intervention.

**Intercostal artery re-implantation** (Figure 5) Acher et al demonstrated an 80% reduction in paraplegia risk using hypothermia, naloxone, steroids, spinal fluid drainage, intercostal ligation and optimizing hemodynamic parameters. The group then demonstrated that intercostal revascularization (either reimplantation or preservation where possible) further reduced their paraplegia risk index by 75% when evaluated using a highly accurate (R2

paraplegia risk index [20]. Intercostal arteries were reimplanted based on magnetic resonance angiography identification of intercostal arteries that supplied radicular arteries feeding the anterior spinal artery, or by patency and location at surgery. The incidence of paralysis after TAAA repair decreased from 4.83% to 0.88% and the paralysis risk index decreased from 0.26 to 0.05 when intercostal artery reimplantation was added to neuroprotective strategies that

> 0.88)

**1.4. Adjuncts for the prevention of paraplegia**

In the era of endovascular repair, where intercostal artery re-implantation is not possible, physiological factors that affect spinal cord perfusion (MAP, CSFD), metabolism and ischemic tolerance (steroids, naloxone, hypothermia) and oxygen delivery (haemoglobin, MAP, oxygen saturations, temperature, cardiac function) are key tools to prevent paraplegia [14]. There is a range of effectiveness of the applied strategies amongst treatment centres, which tells us that treatment protocols to optimize contributing factors must be established and followed consistently to achieve the best results [14].

**Internal iliac revascularization** [11] In addition to revascularization of the intercostal vessels, one must also consider the superior and inferior supply to the spinal cord via the subclavian arteries and internal iliac network. Revascularization of the internal iliac arteries should not only be considered in the context of buttock ischemia, but also in an attempt to maintain adequate spinal perfusion. Internal iliac flow should be preserved on at least one side and careful consideration must be given in the context of common and internal iliac aneurysms as well as when a uni-iliac stent-graft is placed.

**Left subclavian artery revascularization** The left subclavian artery (LSCA) has achieved prominence in discussions regarding case planning for stent-graft insertion. Up to one third of patients undergoing TEVAR require coverage of the LSCA in order to achieve an adequate landing zone and proximal seal [21]. In these situations the stent-graft is placed across the origin of the artery and endovascular embolization of the vessel with percutaneous access via the brachial artery is required to prevent development of a type 2 endoleak (persistent blood flow into the aneurysm sac from collateral vessels). In selected cases LSCA revascularization is undertaken prior to endovascular stent deployment. This can be performed as a single or staged procedure. At our unit this is routinely performed as a single-stage procedure in a hybrid operating suite (surgical operating theatre equipped with advanced medical imaging devices required for endovascular procedures). An open left common carotid to left subclavian artery bypass is performed, commonly with a Dacron graft, prior to endovascular stenting across the origin of the LSCA (Figure 8). The LSCA provides important circulation to the spinal cord, brain, and arm, and therefore coverage is not without clinical consequences. Stroke, SCI and coronary ischemia in the setting of a left internal mammary artery bypass, as well as arm ischemia, have all been described. The left vertebral artery serves as the dominant vessel to the hindbrain in 60% of individuals, and as a result LSCA coverage can lead to a posterior circulation stroke. LSCA coverage can also compromise spinal blood flow with resultant SCI. It contributes to spinal cord perfusion by providing branches to the cephalad portions of the anterior and posterior spinal arteries [22]. Management of patients in whom the LSCA is sacrificed remains a source of considerable debate and controversy. Proponents of routine revascularization cite the increased risk of arm ischemia, stroke and SCI associated with LSCA coverage. Several other studies have shown that intentional coverage of the LSCA without revascularization is not associated with increased morbidity and lend support to those who

group 2.7% vs. 0.8% in the revascularized group, *p*=0.35 [23]. In an effort to establish clinical practice guidelines for management of the LSCA with TEVAR, the Society of Vascular Surgery (SVS) selected a committee of experts within the field and commissioned a systematic review and meta-analysis of the literature. They employed the GRADE method (grading of recom‐ mendations assessment, development and evaluation) to develop and present their recom‐ mendations. The second study, commissioned by the SVS, demonstrated that coverage of the LSCA is associated with a trend towards increase in paraplegia and anterior circulation stroke and a significant increase in risk of arm ischemia and vertebrobasilar stroke [24]. However there was no association with death, myocardial infarction or transient ischaemic attack. All recommendations listed were made based on level C (low-quality) data, but nonetheless, the proposed SVS guidelines suggest routine preoperative revascularization of the LSA for elective cases requiring coverage of the origin of the vessel [25]. Recommendations include: 1) In patients undergoing elective TEVAR where achievement of a proximal seal necessitates coverage of the LSA, they suggest routine preoperative revascularization (despite the lowquality evidence); 2) In selected patients who have an anatomy that compromises perfusion to critical organs, routine preoperative LSA revascularization is strongly recommended (despite the low-quality evidence); and 3) In patients who need urgent TEVAR for lifethreatening acute aortic syndromes where achievement of a proximal seal necessitates coverage of the LSA, they suggest that revascularization should be individualized and addressed expectantly on the basis of anatomy, urgency and availability of surgical expertise.

Paraplegia as a Complication of Thoracic and Thoracoabdominal Aortic Interventions

http://dx.doi.org/10.5772/57528

39

However, other large single-institution studies with protocols for selective revasculariza‐ tion saw no differences in the rates of SCI. A recent large retrospective multi-centre review was performed on 1189 patients undergoing TEVAR [65]. Subgroup analysis was per‐ formed for non-covered LSCA (group A), covered LSCA (group B) and covered and revascularized LSCA (group C) which showed no significant difference between groups B and C (SCI 6.3% vs. 6.1%) and LSCA revascularization was not protective for SCI (7.5% vs. 4.1%, *p*=0.3). The study concluded that LSCA coverage does not appear to result in an increased incidence of SCI or stroke when a strategy of selective revascularization is adopted, and selective LSCA revascularization results in similar outcomes among the three cohorts studied. Complications from revascularization, understated in most studies, are worth considering. The key to favourable outcomes likely involves careful patient selec‐

**Elective sac perfusion via temporary controlled endoleak** With endovascular repair, in contrast to open surgical repair, identification and/or direct revascularization of important segmental vessels is not currently possible. SCI therefore remains a major challenge with endovascular repair, and innovations to reduce the occurrence of this complication are necessary. Early experience with a technique for maintaining perfusion of segmental vessels (intercostal and lumbar arteries) in the early postoperative period after endovascular repair of a TAAA with "sac perfusion branches" added to custom-made stent-grafts has been described [27]. The branched stent-graft and bridging stents to the branches are inserted under general anesthesia. The perfusion branches are left open in order to perfuse segmental vessels. The risk of SCI is greatest in the first few days following repair, and so the perfusion branches are

tion when selective revascularization is employed.

**Figure 8. Left subclavian artery revascularization** Left common carotid (CC) to left subclavian artery (LSCA, arrow) bypass with Dacron graft (arrow head) performed prior to endovascular stenting across origin of LSCA (star) to create adequate landing zone for exclusion of thoracic aortic aneurysm while maintaining flow to LSCA. Patent LSCA seen (arrow).

advocate more selective revascularization. Despite contributing to critical vascular beds, LSCA coverage is well tolerated in most patients due to collateral blood flow primarily from the right vertebral artery, basilar artery and circle of Willis arcade [22]. In addition, they argue that LSCA bypass and/or transposition is not entirely without risk, and should therefore be stratified according to the individual. Complications include left recurrent laryngeal nerve palsy, left phrenic nerve palsy and neck haematoma necessitating re-exploration. Absolute indications for LSCA revascularization include patent left internal mammary artery coronary bypass graft, dominant left vertebral artery, diminutive or absent right vertebral artery, left arm arteriovenous fistula for dialysis access and patent left axillo-femoral bypass graft. Relative indica‐ tions include long aortic coverage, previous abdominal aortic surgery and occlusion of the internal iliac or hypogastric arteries.

Two meta-analyses on the subject both reported an increase in SCI when the LSCA is covered. One observed an SCI rate of 2.3 vs. 2.8, *p*=0.005 for LSCA not covered vs. covered. However there was no protective effect from preoperative revascularization; SCI for the uncovered group 2.7% vs. 0.8% in the revascularized group, *p*=0.35 [23]. In an effort to establish clinical practice guidelines for management of the LSCA with TEVAR, the Society of Vascular Surgery (SVS) selected a committee of experts within the field and commissioned a systematic review and meta-analysis of the literature. They employed the GRADE method (grading of recom‐ mendations assessment, development and evaluation) to develop and present their recom‐ mendations. The second study, commissioned by the SVS, demonstrated that coverage of the LSCA is associated with a trend towards increase in paraplegia and anterior circulation stroke and a significant increase in risk of arm ischemia and vertebrobasilar stroke [24]. However there was no association with death, myocardial infarction or transient ischaemic attack. All recommendations listed were made based on level C (low-quality) data, but nonetheless, the proposed SVS guidelines suggest routine preoperative revascularization of the LSA for elective cases requiring coverage of the origin of the vessel [25]. Recommendations include: 1) In patients undergoing elective TEVAR where achievement of a proximal seal necessitates coverage of the LSA, they suggest routine preoperative revascularization (despite the lowquality evidence); 2) In selected patients who have an anatomy that compromises perfusion to critical organs, routine preoperative LSA revascularization is strongly recommended (despite the low-quality evidence); and 3) In patients who need urgent TEVAR for lifethreatening acute aortic syndromes where achievement of a proximal seal necessitates coverage of the LSA, they suggest that revascularization should be individualized and addressed expectantly on the basis of anatomy, urgency and availability of surgical expertise.

However, other large single-institution studies with protocols for selective revasculariza‐ tion saw no differences in the rates of SCI. A recent large retrospective multi-centre review was performed on 1189 patients undergoing TEVAR [65]. Subgroup analysis was per‐ formed for non-covered LSCA (group A), covered LSCA (group B) and covered and revascularized LSCA (group C) which showed no significant difference between groups B and C (SCI 6.3% vs. 6.1%) and LSCA revascularization was not protective for SCI (7.5% vs. 4.1%, *p*=0.3). The study concluded that LSCA coverage does not appear to result in an increased incidence of SCI or stroke when a strategy of selective revascularization is adopted, and selective LSCA revascularization results in similar outcomes among the three cohorts studied. Complications from revascularization, understated in most studies, are worth considering. The key to favourable outcomes likely involves careful patient selec‐ tion when selective revascularization is employed.

advocate more selective revascularization. Despite contributing to critical vascular beds, LSCA coverage is well tolerated in most patients due to collateral blood flow primarily from the right vertebral artery, basilar artery and circle of Willis arcade [22]. In addition, they argue that LSCA bypass and/or transposition is not entirely without risk, and should therefore be stratified according to the individual. Complications include left recurrent laryngeal nerve palsy, left phrenic nerve palsy and neck haematoma necessitating re-exploration. Absolute indications for LSCA revascularization include patent left internal mammary artery coronary bypass graft, dominant left vertebral artery, diminutive or absent right vertebral artery, left arm arteriovenous fistula for dialysis access and patent left axillo-femoral bypass graft. Relative indica‐ tions include long aortic coverage, previous abdominal aortic surgery and occlusion of the

**Figure 8. Left subclavian artery revascularization** Left common carotid (CC) to left subclavian artery (LSCA, arrow) bypass with Dacron graft (arrow head) performed prior to endovascular stenting across origin of LSCA (star) to create adequate landing zone for exclusion of thoracic aortic aneurysm while maintaining flow to LSCA. Patent LSCA seen

Two meta-analyses on the subject both reported an increase in SCI when the LSCA is covered. One observed an SCI rate of 2.3 vs. 2.8, *p*=0.005 for LSCA not covered vs. covered. However there was no protective effect from preoperative revascularization; SCI for the uncovered

internal iliac or hypogastric arteries.

(arrow).

38 Topics in Paraplegia

**Elective sac perfusion via temporary controlled endoleak** With endovascular repair, in contrast to open surgical repair, identification and/or direct revascularization of important segmental vessels is not currently possible. SCI therefore remains a major challenge with endovascular repair, and innovations to reduce the occurrence of this complication are necessary. Early experience with a technique for maintaining perfusion of segmental vessels (intercostal and lumbar arteries) in the early postoperative period after endovascular repair of a TAAA with "sac perfusion branches" added to custom-made stent-grafts has been described [27]. The branched stent-graft and bridging stents to the branches are inserted under general anesthesia. The perfusion branches are left open in order to perfuse segmental vessels. The risk of SCI is greatest in the first few days following repair, and so the perfusion branches are left open during this time. Five to ten days postoperatively the branches are then closed with Amplatzer plugs to complete exclusion of the aneurysm. This is performed via a single percutaneous groin puncture under local anesthesia, which allows continuous monitoring of neurological function. Test balloon occlusions of the branches are performed and there is clinical evaluation of the patient's neurological symptoms for approximately 30 minutes. If no symptoms are experienced, the branch is then closed. The choice of five to ten days for closure of the perfusion branch is empiric, as most delayed SCI occurs in the first 72 hours postoper‐ atively. This technique was used in ten patients with type II (the most extensive) TAAAs. One developed monoparesis of the right leg during a period of hypotension secondary to a cardiac event and died within 30 days. Two patients developed lower limb weakness after closure of the perfusion branches, but subsequently recovered full recovery. The concept behind the technique described is that perfusion of the sac by a controlled endoleak may protect spinal cord perfusion in the immediate postoperative period when the risk of hemodynamic insta‐ bility is greatest. Extensive segmental artery sacrifice can be delayed until the patient has recovered from the first stage of the procedure and some remodeling of the collateral network may have occurred. Two patients in this series developed neurological symptoms after closure of the perfusion branches, thus supporting the hypothesis that perfusion of the sac in the postoperative period does have a protective effect. If any symptoms are experienced the procedure can be abandoned and attempted at a later date when further remodeling of the collateral network is likely to have occurred. This small case series indicates that controlled perfusion of segmental vessels with a temporary controlled endoleak is feasible, and may be a useful adjunct to prevent SCI, providing protection to spinal cord perfusion during the immediate postoperative period when risk of SCI is greatest.

had lower postoperative motor strength scores (*p*=0.0340). Multivariate analysis of risk factors for neurological injury included (*p*<0.05) longer cross-clamp time, failure to actively cool with bypass and postoperative hypotension, whereas CSFD+IP were found to be protective. Logistic regression showed that CSFD+IP and active cooling significantly reduced the risk of injury and that the two combined modalities had a cumulative protective effect. In the third trial, which is the largest and most recent, TAAA repair was performed on 145 participants; 76 with CSFD and 69 without [32]. CSFD was initiated during the operation and continued for 48 hours after surgery. Paraplegia or paraparesis occurred in 9/74 patients (12.2%) in the control group vs. 2/82 (2.7%) receiving CSFD (*p*=0.03). Overall, CSFD resulted in an 80% reduction in the relative risk of postoperative deficits. The Cochrane meta-analysis showed an odds ratio (OR) of 0.48 (95 % confidence interval (CI) 0.25 to 0.92). For CSFD-only trials, OR was 0.57 (95% CI 0.28 to 1.17) and for intention-to-treat analysis in CSFD-only studies, the OR remained unchanged. The review therefore concluded that there is limited evidence that perioperative CSFD appears to reduce the rate of paraplegia after repair of type I and type II TAAA. CSFD is recommended as a component of the multimodal approach for the prevention of neurolog‐ ical injury, and use of CSFD alone as protection was not established from the available

Paraplegia as a Complication of Thoracic and Thoracoabdominal Aortic Interventions

http://dx.doi.org/10.5772/57528

41

The role of prophylactic CSFD in endovascular procedures is more contentious, and level 1 evidence supporting its role is currently lacking. Wong et al undertook a systematic review to determine if preoperative CSFD reduces SCI with TEVAR [33]. Study quality was generally poor to moderate (median Downs and Black score, 9). The systematic review identified 46 eligible studies comprising 4936 patients; overall, SCI affected 3.89% (95% confidence interval, 2.95.05% to 4.95%). Series reporting routine prophylactic drain placement or no prophylactic drain placement reported pooled SCI rates of 3.2% and 3.47% respectively. The pooled SCI rate from 24 series stating that prophylactic drainage was used selectively was 5.6%. However, in all of these series prophylactic CSFDs were placed only in patients deemed at high risk of perioperative SCI. Thus, there is an inherent bias in the analysis in that the CSFD group was at increased risk of SCI. The study concluded that the role of prophylactic CSFD is difficult to establish from the available literature, and high-quality studies are required to determine the role of prophylactic CSF drainage in TEVAR. A single-institution experience of TEVAR using the same proactive spinal cord ischemia protection protocol used in open repair reported proactive spinal cord protective protocols appear to reduce the incidence of spinal ischemia after TEVAR compared with previous series [34]. The spinal cord ischemia protection included routine spinal drainage (spinal fluid pressure <10 mm Hg), endorphin receptor blockade (naloxone infusion), moderate intraoperative hypothermia (<35°C), hypotension avoidance (MAP >90 mmHg) and optimizing cardiac function. From 2005 to 2012, 94 consecutive TEVARs were studied, including 48 for TAA. Mean length of aortic coverage was 161mm, correlating to 59.4% aortic coverage. One patient had delayed paralysis (1.1%) and recovered enough to ambulate easily without assistance. This study recommends that active, as opposed to reactive approaches to spinal ischemia provide a better long-term outcome, and multimodal protection

is essential, especially in cases of long segment coverage.

evidence.

**Cerebrospinal fluid drainage** (Figure 7) Use of prophylactic cerebrospinal fluid drainage in open surgery has been the subject of two meta-analyses [28, 29]. Although based on a small number of cases, both concluded that prophylactic drainage significantly reduces the risk of perioperative paraplegia or paraparesis. A Cochrane review undertaken to determine the effect of CSFD during thoracic and TAAA surgery on the risk of developing spinal cord injury concluded CSFD may increase the perfusion pressure to the spinal cord and hence reduce the risk of ischemic spinal cord injury [29]. To date, three randomized controlled trials have examined the benefits of lumbar CSFD in open TAAA repairs, which were the three trials included in the Cochrane review with a total of 287 participants operated on for type I or II TAAA. In the first trial of 98 participants (46 patients with CSFD and 52 controls), neurological deficits in the lower extremities occurred in 14 (30%) of the CSFD group and 17 (33%) of the controls [30]. The deficit was observed within 24 hours of the operation in 21 (68%), and from three to 22 days in 10 (32%) participants. CSFD did not have a statistically significant benefit in preventing paraplegia (*p*=0.8), and the only significant predictor of delayed deficits was postoperative hypotension (*p*=0.006). The second trial of 33 participants used a combination of CSFD and intrathecal papaverine (IP, a vasodilator and smooth muscle relaxant); 17 patients randomised to CSFD+IP and 16 to control group [31]. They showed the combined treatment had statistically significant reduction in the rate of postoperative neurological deficit (2/17 developed neurological injury) compared to controls (7/16, *p*=0.0392). Control patients also had lower postoperative motor strength scores (*p*=0.0340). Multivariate analysis of risk factors for neurological injury included (*p*<0.05) longer cross-clamp time, failure to actively cool with bypass and postoperative hypotension, whereas CSFD+IP were found to be protective. Logistic regression showed that CSFD+IP and active cooling significantly reduced the risk of injury and that the two combined modalities had a cumulative protective effect. In the third trial, which is the largest and most recent, TAAA repair was performed on 145 participants; 76 with CSFD and 69 without [32]. CSFD was initiated during the operation and continued for 48 hours after surgery. Paraplegia or paraparesis occurred in 9/74 patients (12.2%) in the control group vs. 2/82 (2.7%) receiving CSFD (*p*=0.03). Overall, CSFD resulted in an 80% reduction in the relative risk of postoperative deficits. The Cochrane meta-analysis showed an odds ratio (OR) of 0.48 (95 % confidence interval (CI) 0.25 to 0.92). For CSFD-only trials, OR was 0.57 (95% CI 0.28 to 1.17) and for intention-to-treat analysis in CSFD-only studies, the OR remained unchanged. The review therefore concluded that there is limited evidence that perioperative CSFD appears to reduce the rate of paraplegia after repair of type I and type II TAAA. CSFD is recommended as a component of the multimodal approach for the prevention of neurolog‐ ical injury, and use of CSFD alone as protection was not established from the available evidence.

left open during this time. Five to ten days postoperatively the branches are then closed with Amplatzer plugs to complete exclusion of the aneurysm. This is performed via a single percutaneous groin puncture under local anesthesia, which allows continuous monitoring of neurological function. Test balloon occlusions of the branches are performed and there is clinical evaluation of the patient's neurological symptoms for approximately 30 minutes. If no symptoms are experienced, the branch is then closed. The choice of five to ten days for closure of the perfusion branch is empiric, as most delayed SCI occurs in the first 72 hours postoper‐ atively. This technique was used in ten patients with type II (the most extensive) TAAAs. One developed monoparesis of the right leg during a period of hypotension secondary to a cardiac event and died within 30 days. Two patients developed lower limb weakness after closure of the perfusion branches, but subsequently recovered full recovery. The concept behind the technique described is that perfusion of the sac by a controlled endoleak may protect spinal cord perfusion in the immediate postoperative period when the risk of hemodynamic insta‐ bility is greatest. Extensive segmental artery sacrifice can be delayed until the patient has recovered from the first stage of the procedure and some remodeling of the collateral network may have occurred. Two patients in this series developed neurological symptoms after closure of the perfusion branches, thus supporting the hypothesis that perfusion of the sac in the postoperative period does have a protective effect. If any symptoms are experienced the procedure can be abandoned and attempted at a later date when further remodeling of the collateral network is likely to have occurred. This small case series indicates that controlled perfusion of segmental vessels with a temporary controlled endoleak is feasible, and may be a useful adjunct to prevent SCI, providing protection to spinal cord perfusion during the

**Cerebrospinal fluid drainage** (Figure 7) Use of prophylactic cerebrospinal fluid drainage in open surgery has been the subject of two meta-analyses [28, 29]. Although based on a small number of cases, both concluded that prophylactic drainage significantly reduces the risk of perioperative paraplegia or paraparesis. A Cochrane review undertaken to determine the effect of CSFD during thoracic and TAAA surgery on the risk of developing spinal cord injury concluded CSFD may increase the perfusion pressure to the spinal cord and hence reduce the risk of ischemic spinal cord injury [29]. To date, three randomized controlled trials have examined the benefits of lumbar CSFD in open TAAA repairs, which were the three trials included in the Cochrane review with a total of 287 participants operated on for type I or II TAAA. In the first trial of 98 participants (46 patients with CSFD and 52 controls), neurological deficits in the lower extremities occurred in 14 (30%) of the CSFD group and 17 (33%) of the controls [30]. The deficit was observed within 24 hours of the operation in 21 (68%), and from three to 22 days in 10 (32%) participants. CSFD did not have a statistically significant benefit in preventing paraplegia (*p*=0.8), and the only significant predictor of delayed deficits was postoperative hypotension (*p*=0.006). The second trial of 33 participants used a combination of CSFD and intrathecal papaverine (IP, a vasodilator and smooth muscle relaxant); 17 patients randomised to CSFD+IP and 16 to control group [31]. They showed the combined treatment had statistically significant reduction in the rate of postoperative neurological deficit (2/17 developed neurological injury) compared to controls (7/16, *p*=0.0392). Control patients also

immediate postoperative period when risk of SCI is greatest.

40 Topics in Paraplegia

The role of prophylactic CSFD in endovascular procedures is more contentious, and level 1 evidence supporting its role is currently lacking. Wong et al undertook a systematic review to determine if preoperative CSFD reduces SCI with TEVAR [33]. Study quality was generally poor to moderate (median Downs and Black score, 9). The systematic review identified 46 eligible studies comprising 4936 patients; overall, SCI affected 3.89% (95% confidence interval, 2.95.05% to 4.95%). Series reporting routine prophylactic drain placement or no prophylactic drain placement reported pooled SCI rates of 3.2% and 3.47% respectively. The pooled SCI rate from 24 series stating that prophylactic drainage was used selectively was 5.6%. However, in all of these series prophylactic CSFDs were placed only in patients deemed at high risk of perioperative SCI. Thus, there is an inherent bias in the analysis in that the CSFD group was at increased risk of SCI. The study concluded that the role of prophylactic CSFD is difficult to establish from the available literature, and high-quality studies are required to determine the role of prophylactic CSF drainage in TEVAR. A single-institution experience of TEVAR using the same proactive spinal cord ischemia protection protocol used in open repair reported proactive spinal cord protective protocols appear to reduce the incidence of spinal ischemia after TEVAR compared with previous series [34]. The spinal cord ischemia protection included routine spinal drainage (spinal fluid pressure <10 mm Hg), endorphin receptor blockade (naloxone infusion), moderate intraoperative hypothermia (<35°C), hypotension avoidance (MAP >90 mmHg) and optimizing cardiac function. From 2005 to 2012, 94 consecutive TEVARs were studied, including 48 for TAA. Mean length of aortic coverage was 161mm, correlating to 59.4% aortic coverage. One patient had delayed paralysis (1.1%) and recovered enough to ambulate easily without assistance. This study recommends that active, as opposed to reactive approaches to spinal ischemia provide a better long-term outcome, and multimodal protection is essential, especially in cases of long segment coverage.

#### **1.5. Adjuncts for the detection of paraplegia**

**Spinal cord monitoring** The priority with thoracic and TAAA repair is the prevention of spinal cord ischemia, followed by the detection and treatment of its occurrence as early as possible to limit injury [35]. These repairs generally require the use of general anesthesia and this is routine practice at our unit. As a result neurological injury is impossible to detect intraopera‐ tively through clinical examination. Neurophysiologic monitoring can therefore be employed in this setting to detect intraoperative injury so that timely interventions can be instigated to improve spinal cord perfusion. In certain institutions TEVAR is performed under loco-regional anaesthesia and if this is the case, routine neuromonitoring or spinal cord protection with CSFD is not required as management such as CSFD can be implemented when clinically required based on examination of the conscious patient.

as to whether ischemic events are coincidental or isolated peripheral vascular events (clots and emboli causing distal damage) or secondary to a reduction in spinal cord perfusion. Lower extremity perfusion disturbances may occur for a variety of reasons during these procedures and the raw SSEP signals provide ambiguous quantitative correlation to intraoperative events [35]. The use of MEP requires specialized anesthetic protocols such as the use of short-acting paralytics during intubation only and eliminating the use of halogenated agents, which can make the procedure more challenging for the anesthetic team. However, the availability of intravenous anesthetics such as propofol and remifentanyl make MEP monitoring during TAAA repairs feasible when indicated. Patients undergoing these procedures are often sedated in the postoperative period making clinical assessment difficult, and they do not routinely undergo continued neurophysiologic monitoring during this time. The postopera‐ tive period is one of great hemodynamic instability and it is quite possible that a number of patients develop SCI at this time. For this reason it is suggested that patients continue to undergo monitoring until they arouse from anesthesia. MEPS cannot be monitored on extubated patients due to the pain involved in delivering the stimulus, but SSEP can be continued postoperatively. Another disadvantage of such neuromonitoring techniques is the need for neurophysiology expertise to interpret the complex waveforms, which is not always available or practical, particularly in the emergency setting. The authors are currently con‐ ducting a feasibility study for a technique of physician-interpreted (i.e. anesthetic and surgical

Paraplegia as a Complication of Thoracic and Thoracoabdominal Aortic Interventions

http://dx.doi.org/10.5772/57528

43

teams) MEP monitoring, without the requirement of neurophysiology input.

corroborate these findings.

Monitoring of spinal cord integrity remains challenging and difficult to interpret and further tests for the timely diagnosis of SCI are required. A recent study evaluated the feasibility of non-invasive monitoring of the paraspinal collateral network oxygenation using near-infrared spectroscopy (NIRS) prior to, during and after TAAA repair in a small clinical series [38]. NIRS optrodes were positioned bilaterally over the thoracic and lumbar paraspinous muscles (and thereby the paraspinous vasculature collateral network) to transcutaneously monitor muscle oxygenation in the collateral network to provide real-time non-invasive monitoring potentially indicating pending SCI in 20 patients undergoing repair of type I, II and III TAAAs. Lumbar oxygenation dropped significantly during open repair (n=15) after proximal aortic crossclamping, but fully recovered after restoration of pulsatile flow to 98.5% of baseline. During TEVAR (n=3), stent-graft deployment did not significantly affect lumbar oxygenation. Three patients developed SCI, and in these patients lumbar oxygenation reduction after aortic crossclamping was significantly lower compared to those with no neurological deficit (*p*=0.041). The study demonstrated this technique is feasible, and lumbar collateral network oxygenation levels directly respond to compromise of aortic circulation. Further studies are needed to

**Biomarkers** Although ischemia-related damage with thoracic aortic repair usually occurs intraoperatively, confirmation of neurological injury often does not occur until the postop‐ erative period when anesthetic effects have resolved and the patients can be evaluated clinically [39]. Often patients remain sedated for prolonged periods following their procedure and therefore methods to detect the onset of acute SCI during the intraopera‐ tive and immediate postoperative period would be extremely valuable. Biomarkers for the

The two types of intraoperative monitoring used regularly, either alone or in combination, are transcortical motor evoked potentials (MEP) and somatosensory evoked potentials (SSEP) [35]. MEPs are recorded from muscles in the extremities by delivering multi-pulse electrical stimulation to the scalp overlying the motor cortex. The evoked potentials elicited from this stimulation travel from the motor cortex through cortical spinal tracts, anterior horn cell, peripheral nerve, and finally to muscle. An interruption in this pathway will result in loss of the motor evoked potential [36]. Somatosensory evoked potential involves repetitive stimu‐ lation of peripheral nerves such as the posterior tibial nerve at the ankle or median nerve at the wrist, followed by the recording of the averaged electrical response in the peripheral nerve, spine, and the cerebral sensory cortex [35]. Most experts in the field believe that intraoperative neuromonitoring is critical in these procedures, although this is largely based on personal clinical experience. These decisions are not based on randomized controlled trials nor do they take into account potential complications and consequences that false positives can have on outcomes in these patients. For example a study examined 97 cases of open (40) and thoracic endovascular stent repairs (57), which were performed with MEP and SSEP monitoring [37]. They used a 50% reduction in amplitude of both cortical SSEPs and transcranial MEP com‐ pound motor action potentials as their criteria for potential signs of spinal ischemia. Results included; 63 event-free patients with normal potentials, fourteen patients with accurate correlation between elicited potentials and corresponding neurological outcomes (initial drop and subsequent regeneration in ten patients, six with normal neurological outcomes, four with transient neurological deficit postoperatively and four who suffered paraplegia with no intraoperative evoked potential), three false-positives, one false-negative and sixteen cases with associated with medication (halogenated anesthetic) interaction or technical issues. They observed a sensitivity of 93% and a specificity of 96% for the neurophysiological monitoring.

The choice of whether to use neuromonitoring remains unclear as there still remain difficulties in the successful use of MEPs from the standpoint of safety, technology and experience [35]. In these particular operations there is a significant downside in falsely identifying spinal cord ischemia with MEPs. The maneuvers utilized to treat spinal ischemia such as induced hypertension and arterial reimplantation have potential complications themselves including an increased risk of bleeding, increased length of surgery and even increased mortality [37]. SSEPs may fail to reliably predict all presentations of paralysis and cannot provide evidence as to whether ischemic events are coincidental or isolated peripheral vascular events (clots and emboli causing distal damage) or secondary to a reduction in spinal cord perfusion. Lower extremity perfusion disturbances may occur for a variety of reasons during these procedures and the raw SSEP signals provide ambiguous quantitative correlation to intraoperative events [35]. The use of MEP requires specialized anesthetic protocols such as the use of short-acting paralytics during intubation only and eliminating the use of halogenated agents, which can make the procedure more challenging for the anesthetic team. However, the availability of intravenous anesthetics such as propofol and remifentanyl make MEP monitoring during TAAA repairs feasible when indicated. Patients undergoing these procedures are often sedated in the postoperative period making clinical assessment difficult, and they do not routinely undergo continued neurophysiologic monitoring during this time. The postopera‐ tive period is one of great hemodynamic instability and it is quite possible that a number of patients develop SCI at this time. For this reason it is suggested that patients continue to undergo monitoring until they arouse from anesthesia. MEPS cannot be monitored on extubated patients due to the pain involved in delivering the stimulus, but SSEP can be continued postoperatively. Another disadvantage of such neuromonitoring techniques is the need for neurophysiology expertise to interpret the complex waveforms, which is not always available or practical, particularly in the emergency setting. The authors are currently con‐ ducting a feasibility study for a technique of physician-interpreted (i.e. anesthetic and surgical teams) MEP monitoring, without the requirement of neurophysiology input.

**1.5. Adjuncts for the detection of paraplegia**

42 Topics in Paraplegia

based on examination of the conscious patient.

**Spinal cord monitoring** The priority with thoracic and TAAA repair is the prevention of spinal cord ischemia, followed by the detection and treatment of its occurrence as early as possible to limit injury [35]. These repairs generally require the use of general anesthesia and this is routine practice at our unit. As a result neurological injury is impossible to detect intraopera‐ tively through clinical examination. Neurophysiologic monitoring can therefore be employed in this setting to detect intraoperative injury so that timely interventions can be instigated to improve spinal cord perfusion. In certain institutions TEVAR is performed under loco-regional anaesthesia and if this is the case, routine neuromonitoring or spinal cord protection with CSFD is not required as management such as CSFD can be implemented when clinically required

The two types of intraoperative monitoring used regularly, either alone or in combination, are transcortical motor evoked potentials (MEP) and somatosensory evoked potentials (SSEP) [35]. MEPs are recorded from muscles in the extremities by delivering multi-pulse electrical stimulation to the scalp overlying the motor cortex. The evoked potentials elicited from this stimulation travel from the motor cortex through cortical spinal tracts, anterior horn cell, peripheral nerve, and finally to muscle. An interruption in this pathway will result in loss of the motor evoked potential [36]. Somatosensory evoked potential involves repetitive stimu‐ lation of peripheral nerves such as the posterior tibial nerve at the ankle or median nerve at the wrist, followed by the recording of the averaged electrical response in the peripheral nerve, spine, and the cerebral sensory cortex [35]. Most experts in the field believe that intraoperative neuromonitoring is critical in these procedures, although this is largely based on personal clinical experience. These decisions are not based on randomized controlled trials nor do they take into account potential complications and consequences that false positives can have on outcomes in these patients. For example a study examined 97 cases of open (40) and thoracic endovascular stent repairs (57), which were performed with MEP and SSEP monitoring [37]. They used a 50% reduction in amplitude of both cortical SSEPs and transcranial MEP com‐ pound motor action potentials as their criteria for potential signs of spinal ischemia. Results included; 63 event-free patients with normal potentials, fourteen patients with accurate correlation between elicited potentials and corresponding neurological outcomes (initial drop and subsequent regeneration in ten patients, six with normal neurological outcomes, four with transient neurological deficit postoperatively and four who suffered paraplegia with no intraoperative evoked potential), three false-positives, one false-negative and sixteen cases with associated with medication (halogenated anesthetic) interaction or technical issues. They observed a sensitivity of 93% and a specificity of 96% for the neurophysiological monitoring.

The choice of whether to use neuromonitoring remains unclear as there still remain difficulties in the successful use of MEPs from the standpoint of safety, technology and experience [35]. In these particular operations there is a significant downside in falsely identifying spinal cord ischemia with MEPs. The maneuvers utilized to treat spinal ischemia such as induced hypertension and arterial reimplantation have potential complications themselves including an increased risk of bleeding, increased length of surgery and even increased mortality [37]. SSEPs may fail to reliably predict all presentations of paralysis and cannot provide evidence

Monitoring of spinal cord integrity remains challenging and difficult to interpret and further tests for the timely diagnosis of SCI are required. A recent study evaluated the feasibility of non-invasive monitoring of the paraspinal collateral network oxygenation using near-infrared spectroscopy (NIRS) prior to, during and after TAAA repair in a small clinical series [38]. NIRS optrodes were positioned bilaterally over the thoracic and lumbar paraspinous muscles (and thereby the paraspinous vasculature collateral network) to transcutaneously monitor muscle oxygenation in the collateral network to provide real-time non-invasive monitoring potentially indicating pending SCI in 20 patients undergoing repair of type I, II and III TAAAs. Lumbar oxygenation dropped significantly during open repair (n=15) after proximal aortic crossclamping, but fully recovered after restoration of pulsatile flow to 98.5% of baseline. During TEVAR (n=3), stent-graft deployment did not significantly affect lumbar oxygenation. Three patients developed SCI, and in these patients lumbar oxygenation reduction after aortic crossclamping was significantly lower compared to those with no neurological deficit (*p*=0.041). The study demonstrated this technique is feasible, and lumbar collateral network oxygenation levels directly respond to compromise of aortic circulation. Further studies are needed to corroborate these findings.

**Biomarkers** Although ischemia-related damage with thoracic aortic repair usually occurs intraoperatively, confirmation of neurological injury often does not occur until the postop‐ erative period when anesthetic effects have resolved and the patients can be evaluated clinically [39]. Often patients remain sedated for prolonged periods following their procedure and therefore methods to detect the onset of acute SCI during the intraopera‐ tive and immediate postoperative period would be extremely valuable. Biomarkers for the real-time detection of ongoing SCI or prediction of an increased risk for paralysis would potentially provide time to intervene and would be of great benefit in preventing SCI. Tissue ischemia caused by decreased spinal cord or brain perfusion is a potent and powerful stressor that triggers many metabolic and inflammatory pathways [36]. CSF is produced continuously and the total CSF compartment volume is replaced three times a day under normal conditions. The composition of CSF is dependent on metabolite production from the brain, and as CSF bathes the neural tissues of the brain and spinal cord, it should allow detection of the biochemical products of acute central nervous system ischemia more rapidly than in serum, particularly if the blood brain barrier is intact. Specific biochemical mark‐ ers that have been examined to date include lactate, pCO2, neuron-specific enolase (NSE), glucose, pH and S100β. Existing molecular markers for neurological injury such as S100β have low sensitivity and specificity making them unsuitable for routine clinical use. These markers also increase in serum at other times including during surgical procedures unrelated to acute brain injury, are often slow to increase and hence not useful for rapid 'on-table' detection. The biochemical signs of cerebrospinal injury have been shown to occur in patients without any clinically detectable neurological deficits and it is often difficult to establish a pattern of proportionality between the degree of ischemia and biomarker parameter increases. In addition, the markers can be confounded by conditions such as hemolysis, extra-cerebral sources and resuscitation, thereby not providing a sensitive prognostic tool [39]. As a result, none of the putative markers of injury in blood or CSF reliably detect early brain or spinal cord ischemia or validated surrogate endpoint meas‐ ures as yet.

have been applied to generate multivariate profiles of metabolites, mainly using nuclear magnetic resonance (NMR) spectroscopy and mass spectrometry (MS) methods that can measure a wide range of metabolites simultaneously. The data are then analyzed using multivariate statistics [43]. Rapid evaporative ionization mass spectrometry is an emerging technique that allows near real-time characterization of human tissue in vivo by analysis of aerosol smoke released during electrosurgical dissection, and this technique has shown that near real-time spectro-profiling in the clinical environment is a possibility [44]. CSF provides an ideal medium for analysis of biomarkers indicating neurological injury since metabolites of anaesthetic agents and other drugs are restricted by the blood-brain barrier. Patients undergoing TAA and TAAA at our unit routinely have a spinal drain inserted preoperatively if clinically indicated, and this spinal drain remains in situ for approximately 48 to 72 hours postoperatively. This provides a constant source of CSF available for study, and the authors are currently conducting a study to analyse CSF using a metabolic phenotyping approach to identify novel biomarkers for neurological ischemia, with a view to developing a platform for

Paraplegia as a Complication of Thoracic and Thoracoabdominal Aortic Interventions

http://dx.doi.org/10.5772/57528

45

In order to define the outcome of patients experiencing SCI after TEVAR and determine the differences in the evolution of long-term functional recovery and the effect on survival, 607 TEVARs performed between 2000 and 2011 were analysed [45]. Fifty-seven patients (9.4%) were noted to have postoperative SCI. SCI developed immediately in twelve patients, had delayed onset in forty and was indeterminate in five patients due to postoperative sedation. Three patients (25%) with immediate SCI had measurable functional improvement based on ambulatory status, whereas twenty-eight (70%) of the delayed-onset patients experienced some degree of neurological recovery (*p*=0.04). Of the thirty-four patients with complete data available, twenty-six (76%) reported quantifiable functional improvement, but only thirteen (38%) experienced return to their preoperative baseline. Estimated mean survival for patients with and without SCI was 37.2 and 71.6 months respectively (*p*<0.0006). Patients with func‐ tional improvement had a mean survival of 53.9 months compared with 9.6 months for those without improvement (*p*<0.0001). The study concluded that only a minority of patients experience complete return to baseline function after SCI with TEVAR, and outcomes in patients without early functional recovery are particularly poor. Patients experiencing delayed SCI are more likely to have functional improvement and following neurological recovery may

In addition to the personal consequences to the patient, family and carers, paraplegia is associated with a significant economic burden. Recurring annual costs of caring for patients with chronic spinal cord injury is a large economic burden on health care systems, but information on costs of spinal cord injury care beyond the acute and initial post-acute phase is minimal [46]. The annual direct medical costs associated with healthcare for a sample of 675 patients with chronic spinal cord injury greater than two years after injury were investigated. The total (inpatient and outpatient) annual direct medical cost was \$21,450 per patient. Average inpatient cost per patient for complete and incomplete thoracic spinal cord injury was

anticipate similar life expectancy compared to patients without SCI.

near real-time intraoperative diagnostics.

**1.6. Outcomes of paraplegia**

**Heat shock proteins** Heat shock proteins (HSPs) are members of highly conserved families of molecular chaperones that have multiple roles in vivo, and they are rapidly induced by severe stress. The inducible members of the HSP70 and HSP27 families are associated with cellular protection and recovery after a near lethal stress and have also been used as markers for tissues or organs that have been exposed to near-lethal stress [41]. The levels of HSPs in CSF from patients undergoing thoracic aneurysm repair have been analyzed. Blood and CSF samples were collected at regular intervals, and CSF was analyzed by enzyme-linked immunosorbent assay for HSP70 and HSP27. These results were correlated with intraoperative somatosensoryevoked potentials measurements and postoperative paralysis. They found the levels of these proteins in many of these patients are elevated and that the degree of elevation correlates with the risk of permanent paralysis. They hypothesized that sequential intraoperative measure‐ ments of heat shock proteins HSP70 and HSP27 levels in CSF could predict those patients who are at greatest risk for paralysis during thoracic aneurysm repair. Further work is in progress by the group to develop these markers to prevent or attenuate this severe complication.

**Metabonomics** An individual's phenome describes the biochemical expression of genomic and environmental disease risk and is based on the analysis of small molecules and metabo‐ lites. Metabonomics is the quantitative measurement of the dynamic multiparametric meta‐ bolic response of living systems to pathphysiological stimuli used in patient phenotyping [42]. Emerging techniques enable rapid measurement of large arrays of metabolites, which could greatly enhance the 'on table' decision-making process during surgery. Spectroscopic methods have been applied to generate multivariate profiles of metabolites, mainly using nuclear magnetic resonance (NMR) spectroscopy and mass spectrometry (MS) methods that can measure a wide range of metabolites simultaneously. The data are then analyzed using multivariate statistics [43]. Rapid evaporative ionization mass spectrometry is an emerging technique that allows near real-time characterization of human tissue in vivo by analysis of aerosol smoke released during electrosurgical dissection, and this technique has shown that near real-time spectro-profiling in the clinical environment is a possibility [44]. CSF provides an ideal medium for analysis of biomarkers indicating neurological injury since metabolites of anaesthetic agents and other drugs are restricted by the blood-brain barrier. Patients undergoing TAA and TAAA at our unit routinely have a spinal drain inserted preoperatively if clinically indicated, and this spinal drain remains in situ for approximately 48 to 72 hours postoperatively. This provides a constant source of CSF available for study, and the authors are currently conducting a study to analyse CSF using a metabolic phenotyping approach to identify novel biomarkers for neurological ischemia, with a view to developing a platform for near real-time intraoperative diagnostics.

#### **1.6. Outcomes of paraplegia**

real-time detection of ongoing SCI or prediction of an increased risk for paralysis would potentially provide time to intervene and would be of great benefit in preventing SCI. Tissue ischemia caused by decreased spinal cord or brain perfusion is a potent and powerful stressor that triggers many metabolic and inflammatory pathways [36]. CSF is produced continuously and the total CSF compartment volume is replaced three times a day under normal conditions. The composition of CSF is dependent on metabolite production from the brain, and as CSF bathes the neural tissues of the brain and spinal cord, it should allow detection of the biochemical products of acute central nervous system ischemia more rapidly than in serum, particularly if the blood brain barrier is intact. Specific biochemical mark‐ ers that have been examined to date include lactate, pCO2, neuron-specific enolase (NSE), glucose, pH and S100β. Existing molecular markers for neurological injury such as S100β have low sensitivity and specificity making them unsuitable for routine clinical use. These markers also increase in serum at other times including during surgical procedures unrelated to acute brain injury, are often slow to increase and hence not useful for rapid 'on-table' detection. The biochemical signs of cerebrospinal injury have been shown to occur in patients without any clinically detectable neurological deficits and it is often difficult to establish a pattern of proportionality between the degree of ischemia and biomarker parameter increases. In addition, the markers can be confounded by conditions such as hemolysis, extra-cerebral sources and resuscitation, thereby not providing a sensitive prognostic tool [39]. As a result, none of the putative markers of injury in blood or CSF reliably detect early brain or spinal cord ischemia or validated surrogate endpoint meas‐

**Heat shock proteins** Heat shock proteins (HSPs) are members of highly conserved families of molecular chaperones that have multiple roles in vivo, and they are rapidly induced by severe stress. The inducible members of the HSP70 and HSP27 families are associated with cellular protection and recovery after a near lethal stress and have also been used as markers for tissues or organs that have been exposed to near-lethal stress [41]. The levels of HSPs in CSF from patients undergoing thoracic aneurysm repair have been analyzed. Blood and CSF samples were collected at regular intervals, and CSF was analyzed by enzyme-linked immunosorbent assay for HSP70 and HSP27. These results were correlated with intraoperative somatosensoryevoked potentials measurements and postoperative paralysis. They found the levels of these proteins in many of these patients are elevated and that the degree of elevation correlates with the risk of permanent paralysis. They hypothesized that sequential intraoperative measure‐ ments of heat shock proteins HSP70 and HSP27 levels in CSF could predict those patients who are at greatest risk for paralysis during thoracic aneurysm repair. Further work is in progress by the group to develop these markers to prevent or attenuate this severe complication.

**Metabonomics** An individual's phenome describes the biochemical expression of genomic and environmental disease risk and is based on the analysis of small molecules and metabo‐ lites. Metabonomics is the quantitative measurement of the dynamic multiparametric meta‐ bolic response of living systems to pathphysiological stimuli used in patient phenotyping [42]. Emerging techniques enable rapid measurement of large arrays of metabolites, which could greatly enhance the 'on table' decision-making process during surgery. Spectroscopic methods

ures as yet.

44 Topics in Paraplegia

In order to define the outcome of patients experiencing SCI after TEVAR and determine the differences in the evolution of long-term functional recovery and the effect on survival, 607 TEVARs performed between 2000 and 2011 were analysed [45]. Fifty-seven patients (9.4%) were noted to have postoperative SCI. SCI developed immediately in twelve patients, had delayed onset in forty and was indeterminate in five patients due to postoperative sedation. Three patients (25%) with immediate SCI had measurable functional improvement based on ambulatory status, whereas twenty-eight (70%) of the delayed-onset patients experienced some degree of neurological recovery (*p*=0.04). Of the thirty-four patients with complete data available, twenty-six (76%) reported quantifiable functional improvement, but only thirteen (38%) experienced return to their preoperative baseline. Estimated mean survival for patients with and without SCI was 37.2 and 71.6 months respectively (*p*<0.0006). Patients with func‐ tional improvement had a mean survival of 53.9 months compared with 9.6 months for those without improvement (*p*<0.0001). The study concluded that only a minority of patients experience complete return to baseline function after SCI with TEVAR, and outcomes in patients without early functional recovery are particularly poor. Patients experiencing delayed SCI are more likely to have functional improvement and following neurological recovery may anticipate similar life expectancy compared to patients without SCI.

In addition to the personal consequences to the patient, family and carers, paraplegia is associated with a significant economic burden. Recurring annual costs of caring for patients with chronic spinal cord injury is a large economic burden on health care systems, but information on costs of spinal cord injury care beyond the acute and initial post-acute phase is minimal [46]. The annual direct medical costs associated with healthcare for a sample of 675 patients with chronic spinal cord injury greater than two years after injury were investigated. The total (inpatient and outpatient) annual direct medical cost was \$21,450 per patient. Average inpatient cost per patient for complete and incomplete thoracic spinal cord injury was \$30,612 and \$24,883 respectively, which included laboratory, nursing, pharmacy, radiology, surgery and inpatient stay costs. Average outpatient costs were \$9954 and \$8925 respectively. However, community care costs such as nursing home or respite stays, occupational therapy and home adaptations, as well as indirect costs such as carers and sickness benefits also need to be considered. To our knowledge there are no studies to date quantifying the economic burden of paraplegia as a complication of aortic intervention.

CSFD-Cerebrospinal fluid drainage

LSCA-Left subclavian artery

MEP-Motor evoked potentials

SSEP-Somatosensory evoked potentials

and Richard G.J. Gibbs

Department of Vascular Surgery, St Mary's Hospital, Imperial College Healthcare NHS

Paraplegia as a Complication of Thoracic and Thoracoabdominal Aortic Interventions

http://dx.doi.org/10.5772/57528

47

[1] Conrad MF, Cambria RP. Contemporary management of descending thoracic and thoracoabdominal aortic aneurysms: endovascular versus open. Circulation.

[2] Yamauchi T, Takano H, Nishimura M, Matsumiya G, Sawa Y. Paraplegia and para‐ paresis after descending thoracic aortic aneurysm repair: a risk factor analysis. Ann

[3] Estrera AL, Rubenstein FS, Miller CC 3rd, Huynh TT, Letsou GV, Safi HJ. Descend‐ ing thoracic aortic aneurysm: surgical approach and treatment using the adjuncts cerebrospinal fluid drainage and distal aortic perfusion. Ann Thorac Surg. 2001;72(2)

[4] Coselli JS, Lemaire SA, Koksoy C, Schmittling ZC, Curling PE. Cerebrospinal fluid drainage reduces paraplegia after thoracoabdominal aortic aneurysm repair: results

[5] Safi HJ, Miller CC 3rd, Huynh TT, Estrera AL, Porat EE, Winnerkvist AN, Allen BS, Hassoun HT, Moore FA. Distal aortic perfusion and cerebrospinal fluid drainage for thoracoabdominal and descending thoracic aortic repair: ten years of organ protec‐

[6] Svensson LG, Crawford ES, Hess KR, Coselli JS, Safi HJ. Experience with 1509 pa‐ tients undergoing thoracoabdominal aortic operations. J Vasc Surg. 1993;17(2) 357-70.

of a randomized clinical trial. J Vasc Surg. 2002;35(4) 631–9.

\*Address all correspondence to: r.gibbs@imperial.ac.uk

Thorac Cardiovasc Surg. 2006;12(3) 179-83.

tion. Ann Surg. 2003;238(3) 372-80.

OR-Odds ratio

**Author details**

Anisha H. Perera\*

Trust, London, UK

481-6.

2008;117(6) 841-52.

**References**

#### **1.7. Spinal cord imaging**

At our unit magnetic resonance (MR) imaging of the spine is performed if SCI is suspected to confirm the diagnosis and exclude any other cause of myelopathy such as extrinsic compres‐ sion. MRI is the most sensitive method for verifying cord ischemia or infarction, and current techniques of diffusion-weighted images can be particularly sensitive and diagnostic. Mawad et al conducted a study where magnetic resonance (MR) imaging was obtained on 25 patients developing symptoms of spinal cord ischemia following resection and graft replacement of thoracoabdominal aortic aneurysms [47]. MR studies were abnormal in 17 patients, which correlated well with the somatosensory evoked potential studies, which were abnormal in all 17 patients. All the MRI signal abnormalities were found in the low thoracic cord and conus medullaris, regardless of the severity of the clinical findings. Four patients with mid thoracic aneurysms experienced transient SCI with good clinical outcome where patients were ambulatory following recovery; MR abnormality was in the low thoracic region in one patient and low thoracic region and conus in three, with focal abnormal MR signals limited to grey matter. Twelve patients with mid thoracic and thoracoabdominal aneurysms experienced complete SCI where patients were not ambulatory with 0/5 motor function assessed on the muscle strength scale 0-5; MR abnormality was in the conus in five patients, mid to low thoracic region and conus in five patients, low thoracic region in one and low thoracic region and conus in one, with diffuse abnormal MR signals involving both grey and white matter. Significant advances in MRI modalities and techniques have taken place since the study was published in 1990, but identification of the most common sites for spinal cord ischemia following aneurysm repair remains an important finding.

#### **Abbreviations**

TAA-Thoracic aortic aneurysm TAAA-Thorocoabdominal aortic aneurysm TAD-Thoracic aortic dissection TEVAR-Thoracic Endovascular Aortic Repair MAP-Mean arterial pressure CSF-Cerebrospinal fluid SCI-Spinal cord ischemia

CSFD-Cerebrospinal fluid drainage LSCA-Left subclavian artery

OR-Odds ratio

\$30,612 and \$24,883 respectively, which included laboratory, nursing, pharmacy, radiology, surgery and inpatient stay costs. Average outpatient costs were \$9954 and \$8925 respectively. However, community care costs such as nursing home or respite stays, occupational therapy and home adaptations, as well as indirect costs such as carers and sickness benefits also need to be considered. To our knowledge there are no studies to date quantifying the economic

At our unit magnetic resonance (MR) imaging of the spine is performed if SCI is suspected to confirm the diagnosis and exclude any other cause of myelopathy such as extrinsic compres‐ sion. MRI is the most sensitive method for verifying cord ischemia or infarction, and current techniques of diffusion-weighted images can be particularly sensitive and diagnostic. Mawad et al conducted a study where magnetic resonance (MR) imaging was obtained on 25 patients developing symptoms of spinal cord ischemia following resection and graft replacement of thoracoabdominal aortic aneurysms [47]. MR studies were abnormal in 17 patients, which correlated well with the somatosensory evoked potential studies, which were abnormal in all 17 patients. All the MRI signal abnormalities were found in the low thoracic cord and conus medullaris, regardless of the severity of the clinical findings. Four patients with mid thoracic aneurysms experienced transient SCI with good clinical outcome where patients were ambulatory following recovery; MR abnormality was in the low thoracic region in one patient and low thoracic region and conus in three, with focal abnormal MR signals limited to grey matter. Twelve patients with mid thoracic and thoracoabdominal aneurysms experienced complete SCI where patients were not ambulatory with 0/5 motor function assessed on the muscle strength scale 0-5; MR abnormality was in the conus in five patients, mid to low thoracic region and conus in five patients, low thoracic region in one and low thoracic region and conus in one, with diffuse abnormal MR signals involving both grey and white matter. Significant advances in MRI modalities and techniques have taken place since the study was published in 1990, but identification of the most common sites for spinal cord ischemia following

burden of paraplegia as a complication of aortic intervention.

aneurysm repair remains an important finding.

TAAA-Thorocoabdominal aortic aneurysm

TEVAR-Thoracic Endovascular Aortic Repair

**Abbreviations**

TAA-Thoracic aortic aneurysm

TAD-Thoracic aortic dissection

MAP-Mean arterial pressure

CSF-Cerebrospinal fluid SCI-Spinal cord ischemia

**1.7. Spinal cord imaging**

46 Topics in Paraplegia

MEP-Motor evoked potentials

SSEP-Somatosensory evoked potentials

#### **Author details**

Anisha H. Perera\* and Richard G.J. Gibbs

\*Address all correspondence to: r.gibbs@imperial.ac.uk

Department of Vascular Surgery, St Mary's Hospital, Imperial College Healthcare NHS Trust, London, UK

#### **References**


[7] Drinkwater SL, Goebells A, Haydar A, Bourke P, Brown L, Hamady M, Gibbs RG; Regional Vascular Unit, St Mary's Hospital, Imperial College NHS Trust. The inci‐ dence of spinal cord ischaemia following thoracic and thoracoabdominal aortic endo‐ vascular intervention. Eur J Vasc Endovasc Surg. 2010;40(6) 729-35.

nal aortic repair: is the increased risk of spinal cord ischemia real? Ann Vasc Surg.

Paraplegia as a Complication of Thoracic and Thoracoabdominal Aortic Interventions

http://dx.doi.org/10.5772/57528

49

[19] Zipfel B, Buz S, Redlin M, Hullmeine D, Hammerschmidt R, Hetzer R. Spinal cord ischemia after thoracic stent-grafting: causes apart from intercostal artery coverage.

[20] Acher CW, Wynn MM, Mell MW, Tefera G, Hoch JR. A quantitative assessment of the impact of intercostal artery reimplantation on paralysis risk in thoracoabdominal

[21] Peterson BG, Eskandari MK, Gleason TG, Morasch MD. Utility of left subclavian ar‐ tery revascularization in association with endoluminal repair of acute and chronic

[22] Lee TC, Andersen ND, Williams JB, Bhattacharya SD, McCann RL, Hughes GC. Re‐ sults with a selective revascularization strategy for left subclavian artery coverage during thoracic endovascular aortic repair. Ann Thorac Surg. 2011;92(1) 97-103. [23] Cooper DG, Walsh SR, Sadat U, Noorani A, Hayes PD, Boyle JR. Neurological com‐ plications after left subclavian artery coverage during thoracic endovascular aortic repair: a systematic review and meta-analysis. J Vasc Surg. 2009;49(6) 1594-601. [24] Rizvi AZ, Murad MH, Fairman RM, Erwin PJ, Montori VM. The effect of left subcla‐ vian artery coverage on morbidity and mortality in patients undergoing endovascu‐ lar thoracic aortic interventions: a systematic review and meta-analysis. J Vasc Surg.

[25] Matsumura JS, Lee WA, Mitchell RS, Farber MA, Murad MH, Lumsden AB, Green‐ berg RK, Safi HJ, Fairman RM; Society for Vascular Surgery. The Society for Vascular Surgery Practice Guidelines: management of the left subclavian artery with thoracic

[26] Maldonado TS, Dexter D, Rockman CB, Veith FJ, Garg K, Arko F, Bertoni H, Ellozy S, Jordan W, Woo E. Left subclavian artery coverage during thoracic endovascular aort‐ ic aneurysm repair does not mandate revascularization. J Vasc Surg. 2013;57(1)

[27] Harrison SC, Agu O, Harris PL, Ivancev K. Elective sac perfusion to reduce the risk of neurologic events following endovascular repair of thoracoabdominal aneurysms.

[28] Cinà CS, Abouzahr L, Arena GO, Laganà A, Devereaux PJ, Farrokhyar F. Cerebrospi‐ nal fluid drainage to prevent paraplegia during thoracic and thoracoabdominal aort‐ ic aneurysm surgery: a systematic review and meta-analysis. J Vasc Surg. 2004;40

[29] Khan SN, Stansby G.Cerebrospinal fluid drainage for thoracic and thoracoabdominal aortic aneurysm surgery. Cochrane Database Syst Rev. 2012;(10) CD003635.

aortic aneurysm repair. Ann Surg. 2008 Oct;248(4):529-40.

thoracic aortic pathology. J Vasc Surg. 2006;43(3) 433-9.

endovascular aortic repair. J Vasc Surg. 2009;50(5) 1155-8.

2006;20(2) 188-94.

2009;50(5) 1159-69.

J Vasc Surg. 2012;55(4) 1202-5.

116-24.

36-44.

Ann Thorac Surg. 2013;96(1) 31-8.


nal aortic repair: is the increased risk of spinal cord ischemia real? Ann Vasc Surg. 2006;20(2) 188-94.

[19] Zipfel B, Buz S, Redlin M, Hullmeine D, Hammerschmidt R, Hetzer R. Spinal cord ischemia after thoracic stent-grafting: causes apart from intercostal artery coverage. Ann Thorac Surg. 2013;96(1) 31-8.

[7] Drinkwater SL, Goebells A, Haydar A, Bourke P, Brown L, Hamady M, Gibbs RG; Regional Vascular Unit, St Mary's Hospital, Imperial College NHS Trust. The inci‐ dence of spinal cord ischaemia following thoracic and thoracoabdominal aortic endo‐

[8] Gravereaux EC, Faries PL, Burks JA, Latessa V, Spielvogel D, Hollier LH, Marin ML. Risk of spinal cord ischemia after endograft repair of thoracic aortic aneurysms. J

[9] von Allmen RS, Anjum A, Powell JT. Incidence of descending aortic pathology and evaluation of the impact of thoracic endovascular aortic repair: a population-based study in England and Wales from 1999 to 2010. Eur J Vasc Endovasc Surg. 2013;45(2):

[10] McGarvey ML, Mullen MT, Woo EY, Bavaria JE, Augoustides YG, Messé SR, Cheung AT. The treatment of spinal cord ischemia following thoracic endovascular aortic re‐

[11] Bicknell CD, Riga CV, Wolfe JH. Prevention of paraplegia during thoracoabdominal

[12] Etz CD, Kari FA, Mueller CS, Silovitz D, Brenner RM, Lin HM, Griepp RB. The collat‐ eral network concept: a reassessment of the anatomy of spinal cord perfusion. J Thor‐

[13] Carroccio A, Marin ML, Ellozy S, Hollier LH. Pathophysiology of paraplegia follow‐ ing endovascular thoracic aortic aneurysm repair. J Card Surg. 2003;18(4) 359-66. [14] Acher C, Wynn M. Paraplegia after thoracoabdominal aortic surgery: not just assist‐ ed circulation, hypothermic arrest, clamp and sew, or TEVAR. Ann Cardiothorac

[15] Etz CD, Luehr M, Kari FA, Bodian CA, Smego D, Plestis KA, Griepp RB. Paraplegia after extensive thoracic and thoracoabdominal aortic aneurysm repair: does critical spinal cord ischemia occur postoperatively? J Thorac Cardiovasc Surg. 2008;135(2)

[16] Ullery BW, Cheung AT, Fairman RM, Jackson BM, Woo EY, Bavaria J, Pochettino A, Wang GJ. Risk factors, outcomes, and clinical manifestations of spinal cord ischemia

[17] Czerny M, Eggebrecht H, Sodeck G, Verzini F, Cao P, Maritati G, Riambau V, Beyers‐ dorf F, Rylski B, Funovics M, Loewe C, Schmidli J, Tozzi P, Weigang E,Kuratani T, Livi U, Esposito G, Trimarchi S, van den Berg JC, Fu W, Chiesa R, Melissano G, Ber‐ toglio L, Lonn L, Schuster I, Grimm M. Mechanisms of symptomatic spinal cord is‐ chemia after TEVAR: insights from the European Registry of Endovascular Aortic

[18] Baril DT, Carroccio A, Ellozy SH, Palchik E, Addis MD, Jacobs TS, Teodorescu V, Marin ML. Endovascular thoracic aortic repair and previous or concomitant abdomi‐

following thoracic endovascular aortic repair. J Vasc Surg. 2011;54(3) 677-84.

Repair Complications (EuREC). J Endovasc Ther. 2012;19(1) 37-43.

aortic aneurysm repair. Eur J Vasc Endovasc Surg. 2009 Jun;37(6) 654-60.

vascular intervention. Eur J Vasc Endovasc Surg. 2010;40(6) 729-35.

Vasc Surg. 2001;34(6) 997-1003.

pair. Neurocrit Care. 2007;6(1) 35-9.

ac Cardiovasc Surg. 2011;141(4) 1020-8.

Surg. 2012;1(3) 365-72.

324-30.

154-9.

48 Topics in Paraplegia


[30] Crawford ES, Svensson LG, Hess KR, Shenaq SS, Coselli JS, Safi HJ, Mohindra PK, Rivera V. A prospective randomized study of cerebrospinal fluid drainage to prevent paraplegia after high-risk surgery on the thoracoabdominal aorta. J Vasc Surg. 1991;13(1) 36-45.

undergoing thoracic aneurysm repair correlate with the probability of postoperative

Paraplegia as a Complication of Thoracic and Thoracoabdominal Aortic Interventions

http://dx.doi.org/10.5772/57528

51

[42] Nicholson JK, Lindon JC, Holmes E. 'Metabonomics': understanding the metabolic responses of living systems to pathophysiological stimuli via multivariate statistical analysis of biological NMR spectroscopic data. Xenobiotica. 1999;29(11) 1181-9. [43] Nicholson JK, Holmes E, Kinross JM, Darzi AW, Takats Z, Lindon JC. Metabolic phe‐ notyping in clinical and surgical environments. Nature. 2012;491(7424) 384-92. [44] Balog J, Sasi-Szabó L, Kinross J, Lewis MR, Muirhead LJ, Veselkov K, Mirnezami R, Dezső B, Damjanovich L, Darzi A, Nicholson JK, Takáts Z. Intraoperative tissue iden‐ tification using rapid evaporative ionization mass spectrometry. Sci Transl Med.

[45] Desart K, Scali ST, Feezor RJ, Hong M, Hess PJ Jr, Beaver TM, Huber TS, Beck AW. Fate of patients with spinal cord ischemia complicating thoracic endovascular aortic

[46] French DD, Campbell RR, Sabharwal S, Nelson AL, Palacios PA, Gavin-Dreschnack D. Health care costs for patients with chronic spinal cord injury in the Veterans

[47] Mawad ME, Rivera V, Crawford S, Ramirez A, Breitbach W. Spinal cord ischemia af‐ ter resection of thoracoabdominal aortic aneurysms: MR findings in 24 patients. AJR

Health Administration. J Spinal Cord Med. 2007;30(5) 477-81.

paralysis. Cell Stress Chaperones. 2008;13(4) 435-46.

2013;5(194) 194ra93.

repair. J Vasc Surg. 2013;58(3) 635-42.

Am J Roentgenol. 1990;155(6) 1303-7.


undergoing thoracic aneurysm repair correlate with the probability of postoperative paralysis. Cell Stress Chaperones. 2008;13(4) 435-46.

[42] Nicholson JK, Lindon JC, Holmes E. 'Metabonomics': understanding the metabolic responses of living systems to pathophysiological stimuli via multivariate statistical analysis of biological NMR spectroscopic data. Xenobiotica. 1999;29(11) 1181-9.

[30] Crawford ES, Svensson LG, Hess KR, Shenaq SS, Coselli JS, Safi HJ, Mohindra PK, Rivera V. A prospective randomized study of cerebrospinal fluid drainage to prevent paraplegia after high-risk surgery on the thoracoabdominal aorta. J Vasc Surg.

[31] Svensson LG, Hess KR, D'Agostino RS, Entrup MH, Hreib K, Kimmel WA, Nadolny E, Shahian DM. Reduction of neurologic injury after high-risk thoracoabdominal

[32] Coselli JS, Lemaire SA, Koksoy C, Schmittling ZC, Curling PE. Cerebrospinal fluid drainage reduces paraplegia after thoracoabdominal aortic aneurysm repair: results

[33] Wong CS, Healy D, Canning C, Coffey JC, Boyle JR, Walsh SR. A systematic review of spinal cord injury and cerebrospinal fluid drainage after thoracic aortic endograft‐

[34] Bobadilla JL, Wynn M, Tefera G, Acher CW. Low incidence of paraplegia after thora‐ cic endovascular aneurysm repair with proactive spinal cord protective protocols. J

[35] McGarvey ML. Effective tool or necessary evil: intraoperative monitoring during

[36] Hecker JG, McGarvey M. Heat shock proteins as biomarkers for the rapid detection of brain and spinal cord ischemia: a review and comparison to other methods of de‐

tection in thoracic aneurysm repair. Cell Stress Chaperones. 2011;16(2) 119-31.

[37] ter Wolbeek C, Hartert M, Conzelmann LO, Peivandi AA, Czerny M, Gottardi R, Be‐ yersdorf F, Weigang E. Value and pitfalls of neurophysiological monitoring in thora‐ cic and thoracoabdominal aortic replacement and endovascular repair. Thorac

[38] Coselli JS, Tsai PI. Motor evoked potentials in thoracoabdominal aortic surgery:

[39] Etz CD, von Aspern K, Gudehus S, Luehr M, Girrbach FF, Ender J, Borger M, Mohr FW. Near-infrared Spectroscopy Monitoring of the Collateral Network Prior to, Dur‐ ing, and After Thoracoabdominal Aortic Repair: A Pilot Study. Eur J Vasc Endovasc

[40] Anderson RE, Winnerkvist A, Hansson LO, Nilsson O, Rosengren L, Settergren G, Vaage J. Biochemical markers of cerebrospinal ischemia after repair of aneurysms of the descending and thoracoabdominal aorta. J Cardiothorac Vasc Anesth. 2003;17(5)

[41] Hecker JG, Sundram H, Zou S, Praestgaard A, Bavaria JE, Ramchandren S, McGar‐ vey M. Heat shock proteins HSP70 and HSP27 in the cerebral spinal fluid of patients

thoracic aneurysm repairs. J Clin Neurophysiol. 2012;29(2) 154-6.

aortic operation. Ann Thorac Surg. 1998;66(1) 132–8.

ing. J Vasc Surg. 2012;56(5) 1438-47.

Vasc Surg. 2013;57(6) 1537-42.

Cardiovasc Surg. 2010;58(5) 260-4.

CON. Cardiol Clin. 2010;28(2) 361-8.

Surg. 2013;46 (6) 651-6.

598-603.

of a randomized clinical trial. J Vasc Surg. 2002;35(4) 631–9.

1991;13(1) 36-45.

50 Topics in Paraplegia


**Chapter 3**

**Spinal Cord Injuries Following Suicide Attempts**

Suicide has become an increasing concern as there are an estimated one million completed suicides per year worldwide. Suicide rates have increased by 60% over the last 50 years, particularly in developing countries. Suicide attempts are up to 20 times more. In 1996 more than 150,000 people committed suicide in 38 countries of the World Health Organization European Region. Suicide is currently one of the most important causes of death in Europe among young and middle-aged people, especially men. In some European Countries, in the age group 15-34, suicide ranks second among the most common causes of death. Nine of the ten countries with the highest suicide rates in the world are in the European Region [1].

In the EUROSAVE (European Review of Suicide and Violence Epidemiology) study, Finland had the highest suicide rate, while Greece had the lowest for the latest available year (1997). Greece also had the lowest undetermined deaths in 1984 and 1997 [2]. According to the Rutz and Wasserman study, increases in male adolescent suicide rates from 1979-1996 that were observed in Sweden, Ireland and Greece can partly be attributed to improved suicide statistics [3]. Botsis [4] suggests that in Greece formal statistics by the National Statistics Office are not representative of reality when they refer to reported suicides. Families avoid reporting suicide

Completed suicide rates for Greece (1960-2009) suggest a fluctuation between 2.8 and 4.0 per 100,000 for the years 1975 and 1985, respectively [1,5]. According to the table of Basic Statistics from Health for All (HFA) for the year 2006 in Greece there is a rate of 3.5 in suicides and self-inflicted injuries at all ages per 100,000. This rate is relatively stable for

> © 2014 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

as the cause of death for religious reasons. Natural causes are reported instead.

Stamatios A. Papadakis, Spyridon Galanakos,

Additional information is available at the end of the chapter

Kleio Apostolaki, Konstantinos Kateros, Olga Antoniadou, George Macheras and

George Sapkas

**1. Introduction**

http://dx.doi.org/10.5772/57409

### **Spinal Cord Injuries Following Suicide Attempts**

Stamatios A. Papadakis, Spyridon Galanakos, Kleio Apostolaki, Konstantinos Kateros, Olga Antoniadou, George Macheras and George Sapkas

Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/57409

#### **1. Introduction**

Suicide has become an increasing concern as there are an estimated one million completed suicides per year worldwide. Suicide rates have increased by 60% over the last 50 years, particularly in developing countries. Suicide attempts are up to 20 times more. In 1996 more than 150,000 people committed suicide in 38 countries of the World Health Organization European Region. Suicide is currently one of the most important causes of death in Europe among young and middle-aged people, especially men. In some European Countries, in the age group 15-34, suicide ranks second among the most common causes of death. Nine of the ten countries with the highest suicide rates in the world are in the European Region [1].

In the EUROSAVE (European Review of Suicide and Violence Epidemiology) study, Finland had the highest suicide rate, while Greece had the lowest for the latest available year (1997). Greece also had the lowest undetermined deaths in 1984 and 1997 [2]. According to the Rutz and Wasserman study, increases in male adolescent suicide rates from 1979-1996 that were observed in Sweden, Ireland and Greece can partly be attributed to improved suicide statistics [3]. Botsis [4] suggests that in Greece formal statistics by the National Statistics Office are not representative of reality when they refer to reported suicides. Families avoid reporting suicide as the cause of death for religious reasons. Natural causes are reported instead.

Completed suicide rates for Greece (1960-2009) suggest a fluctuation between 2.8 and 4.0 per 100,000 for the years 1975 and 1985, respectively [1,5]. According to the table of Basic Statistics from Health for All (HFA) for the year 2006 in Greece there is a rate of 3.5 in suicides and self-inflicted injuries at all ages per 100,000. This rate is relatively stable for

<sup>© 2014</sup> The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

the years 2000-2009 (3.5-3.6) [1]. Recently, Greece began to experience the effects of the extreme financial crisis, and reports in the mass media and journals support a possible casual link between the economic crisis and suicide rates. However, scientific data concerning this matter is still controversial [5-7].

methods of suicide may vary from one country to another. In the United States for instance, jumping is among the least common methods of committing suicide (less than 2% of all reported suicides in the United States for 2005), while in Hong Kong, jumping is the most common method of committing suicide, accounting for 52.1% of all reported suicide cases in 2006 and similar rates for the years prior to that [27,28]. Community samples estimate that 8– 10% of all those who attempt suicide will eventually die as a result of self-harm, most of these

Spinal Cord Injuries Following Suicide Attempts

http://dx.doi.org/10.5772/57409

55

Patients who attempt suicide by jumping from a height usually suffer from multiple injuries. These may be of two types: deceleration type injuries and direct impact injuries [31]. The former, which are internal organ injuries, result from the tendency to displace the tissue in the direction of motion upon impact, while the movement of the body is arrested by the ground [30]. A number of studies show that most of the patients who attempt suicide by jumping suffer from serious psychiatric disorders. These patients suffer from a broad spectrum of psychiatric symptoms: schizophrenia, depression, drugs or alcohol abuse, personality disorder and manic

Spinal cord injury (SCI) literature estimates suicide as being responsible for approximately 5% of deaths, though this varies greatly between populations [24-37]. Risk tends to be higher in the years immediately post-injury, but there is an increased life-time risk if an individual has

Several studies have examined the post-injury predictions for patients who survived after a suicide attempt, and various findings arise. Haenel and Jehle [38], conducted a research in Switzerland, on patients who had become paraplegic after a suicide attempt, and who had to spend a certain time in the Basel and Nottwil (canton of Lucerne) centre for paraplegics. They evaluated the records and catamnestic date of 38 patients with a mean age of 38 years, between the years of 1982-1996 and a follow up study was conducted. Catamnestic investigations performed from one month to 14 years after the suicidal attempt were based on a structured dialogue with a standardized, computerized questionnaire. The results showed that the most frequently encountered suicidal method, leading to the paraplegic lesion, was a fall from a window of a building (89,6 %). In 55% of the cases, a psychiatric disorder had been diagnosed prior to the suicide attempt, with depression, alcohol and drug dependence appearing as the most common diagnoses. Thirty-seven per cent of patients had attempted suicide at least once before and 34 % had been hospitalized for psychiatric reasons prior to the incident. The paraplegic lesions of the patients were equally distributed between thoracic, cervical and lumbar lesions. The most disturbing problem reported by patients after the paralysis was sexual impairment. Despite the limited number of cases and the rather short interval between the suicide attempt and the follow-up investigation, results seem to indicate that such patients

are not likely to commit suicide on a later occasion, excluding one single case.

Anderson and Allan [24] conducted a survey in a Scottish spinal rehabilitation unit, on the demographics and patients outcome with vertebral fracture after suicide attempt. Forty-six (44 having detailed data available) patients were identified with 95% of injuries resulting from falls. Thirty-six people had pre-existing mental health problems (82%) with 15 (34%) having this diagnosis established shortly after admission. Seventy-five per cent received follow-up

within 5 years of the attempt depending on the diagnosis [29,30].

depression [32,33].

ever attempted suicide or self-harm [24].

In many European countries suicidal behavior constitutes a major public and mental health problem. It is also a considerable drain of resources in both primary and secondary health care settings [8]. Furthermore, adolescent suicide and attempted suicide have been recognized as a growing health problem in the rest of the world [9]. Young people of both sexes often make repeated suicide attempts [10-12]. Deliberate self-harm is also associated with increased risk of repetition and suicide [13,14].

Several possible theories have been proposed to explain the increased risk conferred by multiple attempts. One possibility is that multiple attempts reflect persistent risk factors (e.g., a chronic or recurring psychiatric disorder or adverse psychosocial conditions). Esposito et al. [15] studied 74 single attempters (SAs) and 47 multiple attempters (MAs; ages 12-18) seen in an emergency department after a suicide attempt and found higher rates of mood disorder diagnosis among MAs. Joiner [16], suggests that multiple suicide attempts increase the risk for subsequent attempts because practice allows MAs to acquire the ability to engage in more serious suicidal behavior.

In Greece, one study in 76 suicide attempters between the ages of 9-20 years, reported an 18 fold greater frequency of psychiatric disorder, 14-fold greater frequency of other problems (relational), 9.7-fold greater frequency of smoking and 4.7-fold greater frequency of psycho‐ social and environmental problems [17]. A six year retrospective study of self inflicted burns with ages ranging from 18-90 years concluded that of the 1435 admissions between April 1997- April 2003, 3.69% attempted suicide by self burn. Of these, females 57%, males 43%, with a high mortality rate of 75.4%. In 43.3% there was a preexisting psychiatric disorder [18].

A study in another internal medicine clinic from November 1999 to November 2000 of 146 drug intoxications, of which male 34.2% and female 65.8%, refers that 38.3% had a history of mental illness, 31.5% were in need of psychiatric help and 42.5% had a previous suicide attempt. Mental State Examination diagnoses included depression (20.96%), psychosis (15.32%), dysthymic disorder (16.2%), anxiety disorder (22.58%) and personality disorder (8.8%) [19]. Other studies refer to substance use increasing suicidal ideation or behavior [20], rising trends in male suicides, higher rates among widowed men [21,22], and an unusual peak in the summer [23], or spring and summer [21].

#### **2. Spinal cord injury data**

A substantial amount of research indicates that self-harm by falling is a rare phenomenon, accounting for 4–7% of suicidal deaths in the developed world [24,25]. The mostet common mode of attempted suicide is drug ingestion. Completed suicides and violent suicide attempts are less common and include hanging, falls/jumps, and firearms [26]. The incidence of different methods of suicide may vary from one country to another. In the United States for instance, jumping is among the least common methods of committing suicide (less than 2% of all reported suicides in the United States for 2005), while in Hong Kong, jumping is the most common method of committing suicide, accounting for 52.1% of all reported suicide cases in 2006 and similar rates for the years prior to that [27,28]. Community samples estimate that 8– 10% of all those who attempt suicide will eventually die as a result of self-harm, most of these within 5 years of the attempt depending on the diagnosis [29,30].

the years 2000-2009 (3.5-3.6) [1]. Recently, Greece began to experience the effects of the extreme financial crisis, and reports in the mass media and journals support a possible casual link between the economic crisis and suicide rates. However, scientific data

In many European countries suicidal behavior constitutes a major public and mental health problem. It is also a considerable drain of resources in both primary and secondary health care settings [8]. Furthermore, adolescent suicide and attempted suicide have been recognized as a growing health problem in the rest of the world [9]. Young people of both sexes often make repeated suicide attempts [10-12]. Deliberate self-harm is also associated with increased risk

Several possible theories have been proposed to explain the increased risk conferred by multiple attempts. One possibility is that multiple attempts reflect persistent risk factors (e.g., a chronic or recurring psychiatric disorder or adverse psychosocial conditions). Esposito et al. [15] studied 74 single attempters (SAs) and 47 multiple attempters (MAs; ages 12-18) seen in an emergency department after a suicide attempt and found higher rates of mood disorder diagnosis among MAs. Joiner [16], suggests that multiple suicide attempts increase the risk for subsequent attempts because practice allows MAs to acquire the ability to engage in more

In Greece, one study in 76 suicide attempters between the ages of 9-20 years, reported an 18 fold greater frequency of psychiatric disorder, 14-fold greater frequency of other problems (relational), 9.7-fold greater frequency of smoking and 4.7-fold greater frequency of psycho‐ social and environmental problems [17]. A six year retrospective study of self inflicted burns with ages ranging from 18-90 years concluded that of the 1435 admissions between April 1997- April 2003, 3.69% attempted suicide by self burn. Of these, females 57%, males 43%, with a high mortality rate of 75.4%. In 43.3% there was a preexisting psychiatric disorder [18].

A study in another internal medicine clinic from November 1999 to November 2000 of 146 drug intoxications, of which male 34.2% and female 65.8%, refers that 38.3% had a history of mental illness, 31.5% were in need of psychiatric help and 42.5% had a previous suicide attempt. Mental State Examination diagnoses included depression (20.96%), psychosis (15.32%), dysthymic disorder (16.2%), anxiety disorder (22.58%) and personality disorder (8.8%) [19]. Other studies refer to substance use increasing suicidal ideation or behavior [20], rising trends in male suicides, higher rates among widowed men [21,22], and an unusual peak

A substantial amount of research indicates that self-harm by falling is a rare phenomenon, accounting for 4–7% of suicidal deaths in the developed world [24,25]. The mostet common mode of attempted suicide is drug ingestion. Completed suicides and violent suicide attempts are less common and include hanging, falls/jumps, and firearms [26]. The incidence of different

concerning this matter is still controversial [5-7].

in the summer [23], or spring and summer [21].

**2. Spinal cord injury data**

of repetition and suicide [13,14].

54 Topics in Paraplegia

serious suicidal behavior.

Patients who attempt suicide by jumping from a height usually suffer from multiple injuries. These may be of two types: deceleration type injuries and direct impact injuries [31]. The former, which are internal organ injuries, result from the tendency to displace the tissue in the direction of motion upon impact, while the movement of the body is arrested by the ground [30]. A number of studies show that most of the patients who attempt suicide by jumping suffer from serious psychiatric disorders. These patients suffer from a broad spectrum of psychiatric symptoms: schizophrenia, depression, drugs or alcohol abuse, personality disorder and manic depression [32,33].

Spinal cord injury (SCI) literature estimates suicide as being responsible for approximately 5% of deaths, though this varies greatly between populations [24-37]. Risk tends to be higher in the years immediately post-injury, but there is an increased life-time risk if an individual has ever attempted suicide or self-harm [24].

Several studies have examined the post-injury predictions for patients who survived after a suicide attempt, and various findings arise. Haenel and Jehle [38], conducted a research in Switzerland, on patients who had become paraplegic after a suicide attempt, and who had to spend a certain time in the Basel and Nottwil (canton of Lucerne) centre for paraplegics. They evaluated the records and catamnestic date of 38 patients with a mean age of 38 years, between the years of 1982-1996 and a follow up study was conducted. Catamnestic investigations performed from one month to 14 years after the suicidal attempt were based on a structured dialogue with a standardized, computerized questionnaire. The results showed that the most frequently encountered suicidal method, leading to the paraplegic lesion, was a fall from a window of a building (89,6 %). In 55% of the cases, a psychiatric disorder had been diagnosed prior to the suicide attempt, with depression, alcohol and drug dependence appearing as the most common diagnoses. Thirty-seven per cent of patients had attempted suicide at least once before and 34 % had been hospitalized for psychiatric reasons prior to the incident. The paraplegic lesions of the patients were equally distributed between thoracic, cervical and lumbar lesions. The most disturbing problem reported by patients after the paralysis was sexual impairment. Despite the limited number of cases and the rather short interval between the suicide attempt and the follow-up investigation, results seem to indicate that such patients are not likely to commit suicide on a later occasion, excluding one single case.

Anderson and Allan [24] conducted a survey in a Scottish spinal rehabilitation unit, on the demographics and patients outcome with vertebral fracture after suicide attempt. Forty-six (44 having detailed data available) patients were identified with 95% of injuries resulting from falls. Thirty-six people had pre-existing mental health problems (82%) with 15 (34%) having this diagnosis established shortly after admission. Seventy-five per cent received follow-up from mental health services. Ninety-five per cent returned to their pre-injury (or similar) residence. Length of stay and functional independence measure for the deliberate self harm group were compared with a non-deliberate self harm group. High levels of mental health and substance abuse problems were detected necessitating formal mental health assessment and follow-up. Deliberate self harm as a mechanism for injury appears to have a significant impact on length of stay in the centre only if the patient has fracture without spinal cord injuries. Immediate rehabilitation outcomes are similar to that of non-deliberate self-harm group. The authors noted in the limitations of the study that the sample size was small and a retrospective methodology concerning an accurate history and outcome was difficult. However, the particular study demonstrates that the patients benefited by their time in rehabilitation and had comparable outcomes to a non-deliberate self harm group in the short term. Despite the fact that substance and mental health problems were significant in this group, these difficulties appear to impact little on immediate rehabilitation and discharge.

died, 3 from suicide. Of the 34 alive at follow up, 7 had attempted suicide, and 2 reported suicidal thoughts. A 44% had had a psychiatric admission since the SCI and 56% were taking

Spinal Cord Injuries Following Suicide Attempts

http://dx.doi.org/10.5772/57409

57

In another research conducted by Christiansen and Jensen [39] in 2007, the incidence of repetition of suicide attempt, suicide and all deaths was examined, and the influence of psychiatric illness and socio-demographic factors on these was analysed. The study was a Danish register-based survival analysis that retrieved personal data on socio-economic, psychiatric and mortality conditions from various registers. Suicide-attempters (2.614) and non-attempters (39.210) were analysed being matched by gender, age and place of residence. The average follow-up period for suicide-attempters was 3.88 years, during which 271 of them died. By comparison, death occurred four times more often among suicide-attempters than among non-attempters. Suicide was far more common among attempters (61, 2.33%) than among non-attempters (16, 0.04%). A proportion of the attempters (31.33%) repeated their attempt within the follow-up period. The most reliable predictors for suicide and death were repetition, suicide attempt method and treatment for mental illness, while the most reliable

It is clear that the results of the different studies vary, but most of them agree, as Christiansen and Jensen [39] state, that individuals with a history of suicide attempts form a well-defined high-risk group for suicide, and are in need of treatment immediately after the episode. Staff attending to the physical and psychiatric needs of these patients must work together and should inform of the risk of subsequent suicidal behavior, after a first episode of attempted suicide. Furthermore, departments which are in contact with suicidal individuals need action plans to ensure that all such individuals receive proper treatment immediately after the suicide attempt. The injuries and life changing conditions following the suicide attempt, add to the existing problems of the patients, especially those with a psychiatric disorder. Further research could take a closer look at the individual factors that lead to mortality in the spinal cord injuries of the deliberate self-harm patients and perhaps suggest mechanisms to reduce mortality. It may also be profitable to examine the risk to self that all individuals bring with them into rehabilitation by merit of their past deliberate self harm or mental health history, as a way of better focused support for all of those with spinal cord injuries after rehabilitation [24].

Thirty-two patients (8 males and 24 females) that were treated for SCIs in the Athens University Orthopaedic Department, as a result of deliberate self harm, are presented. Their ages varied from 18 to 65 years, and the average age was 35 years. There were 16 singles (50%), 14 married (44%) and 2 divorced (6%) patients. Thirteen patients were employed (41%), six housewives (19%), seven unemployed (22%), three students / pupils (9%) and three with various occupa‐ tions (9%). In terms of religion, 28 were Christian Orthodox (88%), one Roman Catholic (3%), one Jewish (3%), one Muslim (3%) and one (3%) with an unknown religious affiliation.

predictors for repetition were age, gender and mental illness.

psychiatric medication.

**3. Sample presentation**

**3.1. Patients and methods**

Kennedy et al. [34], conducted a retrospective review examining the admission records of 137 individuals, of mean age 32, with SCI as a result of a suicide attempt between the period 1951 to 1992. The research took place in the National Spinal Injuries Centre in Stoke Mandeville Hospital in Bucks, UK. They explored and identified the type of psychiatric condition evident around the time of injury and reviewed outcome information of this sample with specific focus on mortality, especially further evidence of deliberate self harm. The subsequent database comprised among others, cause, level and completeness of injury, height fallen, psychiatric history, psychiatric diagnosis, date of last contact, further suicide attempts, date and cause of death, date and place of discharge. Previous suicide attempts had been made by 23%. The cause of injury in 85% of cases was 'falls'. Thirty-three people are known to have died, of whom eight (24%) committed suicide. During the period between the first and last SCI examined within this study (1951-1992) 1.6% (n=137) of the total sample of patients treated at the rehabilitation centre sustained an SCI as a result of a suicide attempt. Recommendations for further research include an adaptation of the psychological autopsy approach which would provide additional information to that which is normally available in actual suicides.

Stanford et al. [25], conducted a research to State SCI services at New South Wales, Australia to determine the incidence of acute SCI due to suicide attempt from 1970 to 2000. They examined demographics, injuries, mental illness, functional outcomes and nature of subse‐ quent deaths of 2752 acute spinal cord injury admissions. Of these, 56 were attempted suicide (55 falls, one gun-shot wound). The median age was 30 years. Psychiatric diagnoses varied, the most common of which were personality disorder, schizophrenia, depression, chronic alcohol abuse, mood disorder and chronic substance abuse. Follow-up was available in 47 cases (84%) at an average of 8 years. Four subsequent deaths were by suicide. Community placement outcomes for survivors were good, however the subsequent death by suicide was high.

Biering et al. [35], during 1965 to 1987 examined 45 patients who were admitted to the Rehabilitation Hospital in Hornbaek, Denmark because of SCI due to suicide attempts. The median age at injury was 31 years. In 38 instances (84%), SCI was caused by jumps from buildings. 62% had previously been admitted to psychiatric hospitals, and 31% had previously attempted suicide. A follow up study was conducted in 1988-89. At follow up, 11 patients had died, 3 from suicide. Of the 34 alive at follow up, 7 had attempted suicide, and 2 reported suicidal thoughts. A 44% had had a psychiatric admission since the SCI and 56% were taking psychiatric medication.

In another research conducted by Christiansen and Jensen [39] in 2007, the incidence of repetition of suicide attempt, suicide and all deaths was examined, and the influence of psychiatric illness and socio-demographic factors on these was analysed. The study was a Danish register-based survival analysis that retrieved personal data on socio-economic, psychiatric and mortality conditions from various registers. Suicide-attempters (2.614) and non-attempters (39.210) were analysed being matched by gender, age and place of residence. The average follow-up period for suicide-attempters was 3.88 years, during which 271 of them died. By comparison, death occurred four times more often among suicide-attempters than among non-attempters. Suicide was far more common among attempters (61, 2.33%) than among non-attempters (16, 0.04%). A proportion of the attempters (31.33%) repeated their attempt within the follow-up period. The most reliable predictors for suicide and death were repetition, suicide attempt method and treatment for mental illness, while the most reliable predictors for repetition were age, gender and mental illness.

It is clear that the results of the different studies vary, but most of them agree, as Christiansen and Jensen [39] state, that individuals with a history of suicide attempts form a well-defined high-risk group for suicide, and are in need of treatment immediately after the episode. Staff attending to the physical and psychiatric needs of these patients must work together and should inform of the risk of subsequent suicidal behavior, after a first episode of attempted suicide. Furthermore, departments which are in contact with suicidal individuals need action plans to ensure that all such individuals receive proper treatment immediately after the suicide attempt. The injuries and life changing conditions following the suicide attempt, add to the existing problems of the patients, especially those with a psychiatric disorder. Further research could take a closer look at the individual factors that lead to mortality in the spinal cord injuries of the deliberate self-harm patients and perhaps suggest mechanisms to reduce mortality. It may also be profitable to examine the risk to self that all individuals bring with them into rehabilitation by merit of their past deliberate self harm or mental health history, as a way of better focused support for all of those with spinal cord injuries after rehabilitation [24].

#### **3. Sample presentation**

#### **3.1. Patients and methods**

from mental health services. Ninety-five per cent returned to their pre-injury (or similar) residence. Length of stay and functional independence measure for the deliberate self harm group were compared with a non-deliberate self harm group. High levels of mental health and substance abuse problems were detected necessitating formal mental health assessment and follow-up. Deliberate self harm as a mechanism for injury appears to have a significant impact on length of stay in the centre only if the patient has fracture without spinal cord injuries. Immediate rehabilitation outcomes are similar to that of non-deliberate self-harm group. The authors noted in the limitations of the study that the sample size was small and a retrospective methodology concerning an accurate history and outcome was difficult. However, the particular study demonstrates that the patients benefited by their time in rehabilitation and had comparable outcomes to a non-deliberate self harm group in the short term. Despite the fact that substance and mental health problems were significant in this group, these difficulties

Kennedy et al. [34], conducted a retrospective review examining the admission records of 137 individuals, of mean age 32, with SCI as a result of a suicide attempt between the period 1951 to 1992. The research took place in the National Spinal Injuries Centre in Stoke Mandeville Hospital in Bucks, UK. They explored and identified the type of psychiatric condition evident around the time of injury and reviewed outcome information of this sample with specific focus on mortality, especially further evidence of deliberate self harm. The subsequent database comprised among others, cause, level and completeness of injury, height fallen, psychiatric history, psychiatric diagnosis, date of last contact, further suicide attempts, date and cause of death, date and place of discharge. Previous suicide attempts had been made by 23%. The cause of injury in 85% of cases was 'falls'. Thirty-three people are known to have died, of whom eight (24%) committed suicide. During the period between the first and last SCI examined within this study (1951-1992) 1.6% (n=137) of the total sample of patients treated at the rehabilitation centre sustained an SCI as a result of a suicide attempt. Recommendations for further research include an adaptation of the psychological autopsy approach which would

provide additional information to that which is normally available in actual suicides.

Stanford et al. [25], conducted a research to State SCI services at New South Wales, Australia to determine the incidence of acute SCI due to suicide attempt from 1970 to 2000. They examined demographics, injuries, mental illness, functional outcomes and nature of subse‐ quent deaths of 2752 acute spinal cord injury admissions. Of these, 56 were attempted suicide (55 falls, one gun-shot wound). The median age was 30 years. Psychiatric diagnoses varied, the most common of which were personality disorder, schizophrenia, depression, chronic alcohol abuse, mood disorder and chronic substance abuse. Follow-up was available in 47 cases (84%) at an average of 8 years. Four subsequent deaths were by suicide. Community placement outcomes for survivors were good, however the subsequent death by suicide was high.

Biering et al. [35], during 1965 to 1987 examined 45 patients who were admitted to the Rehabilitation Hospital in Hornbaek, Denmark because of SCI due to suicide attempts. The median age at injury was 31 years. In 38 instances (84%), SCI was caused by jumps from buildings. 62% had previously been admitted to psychiatric hospitals, and 31% had previously attempted suicide. A follow up study was conducted in 1988-89. At follow up, 11 patients had

appear to impact little on immediate rehabilitation and discharge.

56 Topics in Paraplegia

Thirty-two patients (8 males and 24 females) that were treated for SCIs in the Athens University Orthopaedic Department, as a result of deliberate self harm, are presented. Their ages varied from 18 to 65 years, and the average age was 35 years. There were 16 singles (50%), 14 married (44%) and 2 divorced (6%) patients. Thirteen patients were employed (41%), six housewives (19%), seven unemployed (22%), three students / pupils (9%) and three with various occupa‐ tions (9%). In terms of religion, 28 were Christian Orthodox (88%), one Roman Catholic (3%), one Jewish (3%), one Muslim (3%) and one (3%) with an unknown religious affiliation.

The cause of injury was a fall from a building in 29 cases (91%), a fall from a window in one case (3%), a fall from a bridge in one case (3%) and a fall inside the house in one case (3%). Concerning the level of injury, in 16 cases (50%) it was at the lumbar level, in 9 cases (28 %) at the cervical, in 5 cases (16%) at thoracic and 2 cases (6%) regarded the sacral vertebrae (Figures 1 and 2). In 20 cases (62.5%) the injury was incomplete and in 12 cases (37.5%) complete. The psychiatric diagnosis was schizophrenia in 12 patients (38%), depression in 8 patients (25%), drugs or alcohol abuse in 3 cases (9%), personality disorder in one patient (3%), bipolar disorder in one patient (3%), other psychiatric reasons in one patient (3%) and in 6 cases (19%) there was no specific diagnosis (generally marital or work related). The height of the falls ranged from 2 to 12 m and all patients landed on solid ground. Operative treatment which included laminectomies, spine instrumentation and fusion was performed in all patients.

**Figure 2.** Anteroposterior radiograph of the same case.

Initial clinical data of the 32 patients included in this study are shown in Table 1. At admission, ATLS guidelines were used for all patients. Associated injuries of the abdomen were present in five patients (patients 1, 4, 10 and 22). In these patients, a laparotomy was necessary for intraperitoneal bleeding, spleen and kidney injury, and mesenteric tear prior to the surgical operation for the spine fracture. Head injuries were revealed with CT scan in six patients (patients 3, 7, 8, 14, 26 and 30). In these cases craniotomy and decompression were performed first, before stabilization of the spinal fractures. Thoracic injuries (ribs fractures or sternum fracture) were present in three patients (patients 3, 5 and 28). Conservative treatment with assisted ventilation was necessary in these cases. Long bone fractures (femoral, tibial, bimal‐ leolar, calcaneal, radial and humeral), including pelvic fractures, were treated by external fixation or closed reduction and immobilization in plaster or temporary splint. Subsequently, reduction and internal fixation, if required, were performed from 8 hours to 5 days later.

Spinal Cord Injuries Following Suicide Attempts

http://dx.doi.org/10.5772/57409

59

Regarding the treatment of the spinal fractures – dislocations, instrumentation devices including titanium rods, transpedicular screws, sacral bars and bone grafting were used on all patients. Patients were evaluated by a consulting psychiatrist as soon as their condition and cooperation permitted. Assessment included an interview and a complete mental status

The only complications encountered were two cases of aspiration pneumonia, one of which resulted in prolonged stay on the intensive therapy unit due to difficulty weaning the patient

**3.2. Results**

examination.

**Figure 1.** Lateral radiograph showing a fracture of the sacrum.

**Figure 2.** Anteroposterior radiograph of the same case.

#### **3.2. Results**

The cause of injury was a fall from a building in 29 cases (91%), a fall from a window in one case (3%), a fall from a bridge in one case (3%) and a fall inside the house in one case (3%). Concerning the level of injury, in 16 cases (50%) it was at the lumbar level, in 9 cases (28 %) at the cervical, in 5 cases (16%) at thoracic and 2 cases (6%) regarded the sacral vertebrae (Figures 1 and 2). In 20 cases (62.5%) the injury was incomplete and in 12 cases (37.5%) complete. The psychiatric diagnosis was schizophrenia in 12 patients (38%), depression in 8 patients (25%), drugs or alcohol abuse in 3 cases (9%), personality disorder in one patient (3%), bipolar disorder in one patient (3%), other psychiatric reasons in one patient (3%) and in 6 cases (19%) there was no specific diagnosis (generally marital or work related). The height of the falls ranged from 2 to 12 m and all patients landed on solid ground. Operative treatment which included laminectomies, spine instrumentation and fusion was performed in all patients.

58 Topics in Paraplegia

**Figure 1.** Lateral radiograph showing a fracture of the sacrum.

Initial clinical data of the 32 patients included in this study are shown in Table 1. At admission, ATLS guidelines were used for all patients. Associated injuries of the abdomen were present in five patients (patients 1, 4, 10 and 22). In these patients, a laparotomy was necessary for intraperitoneal bleeding, spleen and kidney injury, and mesenteric tear prior to the surgical operation for the spine fracture. Head injuries were revealed with CT scan in six patients (patients 3, 7, 8, 14, 26 and 30). In these cases craniotomy and decompression were performed first, before stabilization of the spinal fractures. Thoracic injuries (ribs fractures or sternum fracture) were present in three patients (patients 3, 5 and 28). Conservative treatment with assisted ventilation was necessary in these cases. Long bone fractures (femoral, tibial, bimal‐ leolar, calcaneal, radial and humeral), including pelvic fractures, were treated by external fixation or closed reduction and immobilization in plaster or temporary splint. Subsequently, reduction and internal fixation, if required, were performed from 8 hours to 5 days later.

Regarding the treatment of the spinal fractures – dislocations, instrumentation devices including titanium rods, transpedicular screws, sacral bars and bone grafting were used on all patients. Patients were evaluated by a consulting psychiatrist as soon as their condition and cooperation permitted. Assessment included an interview and a complete mental status examination.

The only complications encountered were two cases of aspiration pneumonia, one of which resulted in prolonged stay on the intensive therapy unit due to difficulty weaning the patient off the ventilator. All patients were discharged from hospital approximately 6–8 weeks after the operation with a custom-made thermoplastic thoracolumbar or lumbosacral orthosis for another 8 weeks and instructions for physical therapy and rehabilitation programs. After discharge 13 patients returned to their homes and 19 to another hospital or entered residential care.

8 56/M

9 41/F

10 27/F

11 31/F

12 39/M

13 46/F

14 51/F

15 36/M

16 19/F

17 39/M

18 41/F

19 47/F

Fall from building

Fall from building

Fall from building

Fall from building

Fall from building

Fall from building

Fall from building

Fall from building

Fall from building

Fall from building

Fall from bridge

Fall from building

Central cord syndrome

Incomplete paraplegia

Completeparaple gia

Bowel and bladderdysfunctio n;saddle anesthesia;compl ete L4– S1paraplegia

> Complete tetraplegia

> Complete tetraplegia

> Complete tetraplegia

Incomplete tetraplegia

Complete tetraplegia

Incomplete paraplegia

Complete tetraplegia

Incomplete paraplegia

C2 - C3 fracture, dislocation

L4 fracture

L1 fracture

L4 fracture

C2 - C3 fracture, dislocation

C2 - C3 fracture, dislocation

C2 - C3 fracture, dislocation

Sacral fracture, Dennis III

> C2 - C3 fracture, dislocation

> L4 fracture

Anterior plating 2 years

22

Spinal Cord Injuries Following Suicide Attempts

months Recovery

http://dx.doi.org/10.5772/57409

10 years None

9 years None

None

None

Death (renal failure)

None

30 months

25 months

14 months

34

Anterior plating 8 years None

months Recovery

3 years Recovery

Laminectomy; titanium rods and transpedicular screws

Laminectomy; titanium rods and transpedicular screws

Laminectomy; titanium rods and transpedicular screws

AnteriorC2 - C3 plating

Anterior plating

Anterior plating

Transiliac sacral bars

Laminectomy; titanium rods and transpedicular screws

C7 fracture Anterior plating 1 year Recovery

C2 - C3 fracture Anterior plating 3 years

Death (renal failure)

61



off the ventilator. All patients were discharged from hospital approximately 6–8 weeks after the operation with a custom-made thermoplastic thoracolumbar or lumbosacral orthosis for another 8 weeks and instructions for physical therapy and rehabilitation programs. After discharge 13 patients returned to their homes and 19 to another hospital or entered residential

> **Associated Lesion**

L4 fracture, humeral shaft fracture

L2 fracture

T9 fracture

L3 fracture

T5 - T6 fracture, dislocation

L4 fracture

C2 - C3 fracture, dislocation

**Surgical treatment**

Laminectomy; titanium rods and transpedicular screws, humeral external fixation

Laminectomy; titanium rods and transpedicular screws

Laminectomy; titanium rods and transpedicular screws

Laminectomy; titanium rods and transpedicular screws

Laminectomies; titanium rods and transpedicular screws

Laminectomy; titanium rods and transpedicular screws

Anterior plating

**Followup**

**Recovery and outcome**

6 years Recovery

8 years Recovery

2 years None

months Recovery

1 year None

5 years Recovery

Death, second suicide attempt at 2 years

17 months

18

care.

60 Topics in Paraplegia

**Patient Age/**

1 23/F

2 18/M

3 34/F

4 42/F

5 20/F

6 48/F

7 65/F

**gender**

**Mechanism of injury**

> Fall from building

> Fall from building

> Fall from building

> Fall from window

> Fall from building

> Fall from building

> Fall from building

**Neurological deficits at admission**

Bowel and bladderdysfunctio n;saddle anesthesia;incom plete L5-S1 paraplegia

> Incomplete paraplegia

Completeparaple gia

> Incomplete paraplegia

Completeparaple gia

> Incomplete paraplegia

Incompletetetrapl egia


transpedicular screws

Laminectomy; titanium rods and transpedicular screws

Laminectomies; titanium rods and transpedicular screws

Laminectomy; titanium rods and transpedicular screws, cast for the distal radius fracture

Laminectomy; titanium rods and transpedicular screws

31

Spinal Cord Injuries Following Suicide Attempts

13 months

months Recovery

http://dx.doi.org/10.5772/57409

63

4 years Recovery

8 years Recovery

Death (renal failure)

29 55/F

30 50/F

31 44/F

32 23/M

**3.3. Discussion**

1:3.4 to 1:0.6) [40].

**Table 1.** Clinical data of the patients

Fall from building

Fall from building

Fall from building

Fall from building

1). All survivors received psychiatric follow-up.

Incomplete paraplegia

Complete paraplegia

Incomplete paraplegia

Incomplete paraplegia

L4 fracture

T8 - T9 fracture, dislocation

> L3 fracture, distal radius fracture

L4 fracture

The mean follow-up was 6 years (range: 12 months – 10 years). At follow-up, only 27 of the patients were available for evaluation due to the death of 5 patients 1-3 years post injury. Of the five patients one had committed suicide (patient 7) and the other four had presented medical complications [renal failure in 3 patients (patients 8, 14 and 30) and pneumonia in one (patient 21)]. Of the remaining patients, two were involved in further unsuccessful suicide attempts due to psychiatric problems, 1 to 3 years post first injury (patients 10 and 24) (Table

Adolescent suicide and attempted suicide have been recognized as a growing health problem in both Europe and the rest of the world [9]. The highest average person-based ratio of male: female suicide attempt rate was found in the age group 15-24 years (1: 1.9), the next highest in the age group 45-54 years (1: 1.7). This ratio decreases in the age group up to 55 to 1: 1.4 (range:

In the two Greek studies referring to attempted suicide hospitalized in internal medicine wards due to drug intoxication and self poisoning there is a definite precedence of females with the


**Table 1.** Clinical data of the patients

The mean follow-up was 6 years (range: 12 months – 10 years). At follow-up, only 27 of the patients were available for evaluation due to the death of 5 patients 1-3 years post injury. Of the five patients one had committed suicide (patient 7) and the other four had presented medical complications [renal failure in 3 patients (patients 8, 14 and 30) and pneumonia in one (patient 21)]. Of the remaining patients, two were involved in further unsuccessful suicide attempts due to psychiatric problems, 1 to 3 years post first injury (patients 10 and 24) (Table 1). All survivors received psychiatric follow-up.

#### **3.3. Discussion**

20 34/F

62 Topics in Paraplegia

21 53/M

22 38/F

23 47/F

24 41/F

25 35/M

26 36/F

27 27/F

28 33/F

Fall from building

Fall from building

Fall from building

Fall from building

Fall from building

Fall inside the house

> Fall from building

> Fall from building

> Fall from building

Incomplete paraplegia

Complete paraplegia

Incomplete paraplegia

Brown - Sequard syndrome

> Incomplete paraplegia

> Incomplete paraplegia

> Incomplete tetraplegia

> Incomplete paraplegia

Complete paraplegia L4 fracture

Transverse fracture of the sacrum with anterior displacement

L1 - L2 fracture, distal radius fracture

T8 fracture

L4 fracture

L4 fracture

L5 fracture

T9 - T10 fracture, dislocation

C6 - C7 fracture Anterior plating

Laminectomy; titanium rods and transpedicular screws

laminectomies; titanium rods and transpedicular screws; bone grafting

Laminectomies; titanium rods and transpedicular screws, cast for the distal radius fracture

Laminectomy; titanium rods and transpedicular screws

Laminectomy; titanium rods and transpedicular screws

Laminectomy; titanium rods and transpedicular screws

Laminectomy; titanium rods and transpedicular screws

Laminectomies; titanium rods and

1 year Recovery

Death (pneumonia)

32 months

23

months Recovery

2 years Recovery

4 years Recovery

months Recovery

months Recovery

7 years Recovery

2 years None

15

19

Adolescent suicide and attempted suicide have been recognized as a growing health problem in both Europe and the rest of the world [9]. The highest average person-based ratio of male: female suicide attempt rate was found in the age group 15-24 years (1: 1.9), the next highest in the age group 45-54 years (1: 1.7). This ratio decreases in the age group up to 55 to 1: 1.4 (range: 1:3.4 to 1:0.6) [40].

In the two Greek studies referring to attempted suicide hospitalized in internal medicine wards due to drug intoxication and self poisoning there is a definite precedence of females with the first showing a percentage of male 34.2% and female 65.8% [22], and the second a ratio of male to female of 1:1.97 in an age group of 20-30 years [23]. Other studies also report parasuicide as more common in females and younger ages [41,42]. Contrarily, in the nationwide study of 1980-1995 of suicides a mean age-standardized rate of 5.86/100,000 males to 1.89/100,000 females was demonstrated. In addition, an increase in suicide rates was reported with age for males, with rising trends in the ages of 45-54yrs and decreasing rates for females in the 15-24yrs and 75-84yrs age group. Mostly violent methods are used among men [22]. This male to female trend is confirmed in the Epirus study where a mean age-standardized suicide rate per year 4/100,000 males was reported to 1.29 females/100,000. Once again a significant rising trend was shown for male suicides in the ages 35-44yrs and 65-74yrs, while low female rates were found in the under 35yrs age group [21].

well tolerated by these patients and interferes with their nursing care. Rigid internal fixation,

Spinal Cord Injuries Following Suicide Attempts

http://dx.doi.org/10.5772/57409

65

The results of our study and others show that most of the patients who attempt suicide by jumping suffer from serious psychiatric disorders [32,33]. These patients suffer from a broad spectrum of psychiatric symptoms: schizophrenia, depression, drugs or alcohol abuse, personality disorder and manic depression. The proportion of patients with schizophrenia is far higher than found in general suicide attempts where it is estimated to range from 5% to 10%. Sometimes they have active suicidal ideation or even a detailed suicidal plan. Thus, the treatment approach for such patients must take into account their psychiatric state. The psychiatric manifestations create subjective distress for the patient and may hinder or even

In this sample of patients the fact that most individuals appeared to have responded to treatment, indicated that all admissions following self-harm should have access to appropriate psychiatric treatment. The finding that three of the patients within this study, attempted suicide following SCI, suggests that a small number of the people who have attempted suicide will re-attempt. We believe that routine screening for suicide and risk assessments might highlight those who are most at risk of re-attempting suicide, thus allowing healthcare professionals to be aware of these individuals and adopt appropriate strategies to address

The prevalence of psychiatric and mental health problems illustrated in this series highlights the importance of educating staff in the care of patients with mental health problems. In view of the special needs of these individuals, services should ensure regular follow-up to prevent deterioration and monitor progress. Moreover, future clinical research should also evaluate

Until now it has been difficult to obtain comparable international data on suicide attempts, owing to disparities in definitions, survey designs and study methods. It has been our experience that psychiatric conditions, and especially suicide risk, should be evaluated and treated as early as possible during the orthopaedic or surgical hospitalization. Management requires both psychopharmacological therapy and psychotherapy. It has to be directed towards the achievement of symptomatic relief and, if possible, towards the remission of the primary psychiatric disorder. The management of these patients in the orthopaedic or surgical ward is difficult, because of restlessness, noncooperation of the patient and the problem of staff inexperienced in handling the psychiatric patient. When prolonged orthopaedic and rehabilitation management is necessary, it is suggested that the patient be transferred to the

the specific problems of people who have both SCI and a psychiatric diagnosis.

psychiatric hospital while continuing the necessary orthopaedic treatment.

whenever possible for unstable fractures, is recommended.

suicidal ideation and behavior.

**4. Conclusions**

prevent the medical and surgical care of the patient in some instances [50].

In the current study, the ratio between males to females was 1:3. Females were more likely to make a more dangerous jump that increased their mortality. Others suggest that young males tended to use more lethal methods in attempts and to repeat more often than females [29]. A previous suicide attempt is in itself the strongest predictor of future suicide and local rates of attempted suicide and regional and national suicide rates in young people, especially males, are strongly correlated [43]. There is an association between repeated suicide attempts and completed suicide, particularly in males and when a violent method has been used [44,45].

The underlying psychology of suicide is complex and unique to each individual. However, certain themes emerge from studying individuals who have attempted or completed suicides. In all age groups, depression, alcohol and drug dependence, as well as history of mental illness are known to be risk factors for suicide [46]. Twenty percent of people who attempt suicide will make another attempt within the year, and 10% ultimately succeed [26]. Injuries resulting from direct impact are mostly fractures [47]. The area over which the impact force is applied influences the severity of the fractures [48]. The smaller the area over which the patients land, the greater the load/ unit area. Patients who land on their legs tend to sustain more serious injuries than those who land on their sides.

There were two main combinations of fractures in this series. The patients with spinal fracture combined with pelvic and extremity fractures. Only three of them sustained upper extremity fractures (patients 1, 22 and 31). Twelve patients presented with pelvic or lower extremity fractures associated with upper extremity fractures. The difference between the two groups shows that fractures in the upper extremities usually exclude fractures of the spine. Upon impact, the falling body has a kinetic energy which is converted, in its major part, into fracture energy. In the first group most of the kinetic energy is dissipated to the lower extremities, pelvis and spine, causing fractures at these sites. In the second group, patients use their upper extremities in an attempt to protect themselves, possibly via more flexion at the hip level. This increased flexion converts the remaining energy into forward rotational energy of the trunk exposing the extended upper extremities to fractures. It is probable that this form of energy dissipation protects the spine from fracture.

The initial treatment should be limited to life-saving procedures and short spine and limb stabilization procedures [49]. Fractures should be treated by methods that will allow early mobilization and transfer to the psychiatric ward. Treatment by traction or spica cast is not well tolerated by these patients and interferes with their nursing care. Rigid internal fixation, whenever possible for unstable fractures, is recommended.

The results of our study and others show that most of the patients who attempt suicide by jumping suffer from serious psychiatric disorders [32,33]. These patients suffer from a broad spectrum of psychiatric symptoms: schizophrenia, depression, drugs or alcohol abuse, personality disorder and manic depression. The proportion of patients with schizophrenia is far higher than found in general suicide attempts where it is estimated to range from 5% to 10%. Sometimes they have active suicidal ideation or even a detailed suicidal plan. Thus, the treatment approach for such patients must take into account their psychiatric state. The psychiatric manifestations create subjective distress for the patient and may hinder or even prevent the medical and surgical care of the patient in some instances [50].

In this sample of patients the fact that most individuals appeared to have responded to treatment, indicated that all admissions following self-harm should have access to appropriate psychiatric treatment. The finding that three of the patients within this study, attempted suicide following SCI, suggests that a small number of the people who have attempted suicide will re-attempt. We believe that routine screening for suicide and risk assessments might highlight those who are most at risk of re-attempting suicide, thus allowing healthcare professionals to be aware of these individuals and adopt appropriate strategies to address suicidal ideation and behavior.

The prevalence of psychiatric and mental health problems illustrated in this series highlights the importance of educating staff in the care of patients with mental health problems. In view of the special needs of these individuals, services should ensure regular follow-up to prevent deterioration and monitor progress. Moreover, future clinical research should also evaluate the specific problems of people who have both SCI and a psychiatric diagnosis.

#### **4. Conclusions**

first showing a percentage of male 34.2% and female 65.8% [22], and the second a ratio of male to female of 1:1.97 in an age group of 20-30 years [23]. Other studies also report parasuicide as more common in females and younger ages [41,42]. Contrarily, in the nationwide study of 1980-1995 of suicides a mean age-standardized rate of 5.86/100,000 males to 1.89/100,000 females was demonstrated. In addition, an increase in suicide rates was reported with age for males, with rising trends in the ages of 45-54yrs and decreasing rates for females in the 15-24yrs and 75-84yrs age group. Mostly violent methods are used among men [22]. This male to female trend is confirmed in the Epirus study where a mean age-standardized suicide rate per year 4/100,000 males was reported to 1.29 females/100,000. Once again a significant rising trend was shown for male suicides in the ages 35-44yrs and 65-74yrs, while low female rates were found

In the current study, the ratio between males to females was 1:3. Females were more likely to make a more dangerous jump that increased their mortality. Others suggest that young males tended to use more lethal methods in attempts and to repeat more often than females [29]. A previous suicide attempt is in itself the strongest predictor of future suicide and local rates of attempted suicide and regional and national suicide rates in young people, especially males, are strongly correlated [43]. There is an association between repeated suicide attempts and completed suicide, particularly in males and when a violent method has been used [44,45]. The underlying psychology of suicide is complex and unique to each individual. However, certain themes emerge from studying individuals who have attempted or completed suicides. In all age groups, depression, alcohol and drug dependence, as well as history of mental illness are known to be risk factors for suicide [46]. Twenty percent of people who attempt suicide will make another attempt within the year, and 10% ultimately succeed [26]. Injuries resulting from direct impact are mostly fractures [47]. The area over which the impact force is applied influences the severity of the fractures [48]. The smaller the area over which the patients land, the greater the load/ unit area. Patients who land on their legs tend to sustain more serious

There were two main combinations of fractures in this series. The patients with spinal fracture combined with pelvic and extremity fractures. Only three of them sustained upper extremity fractures (patients 1, 22 and 31). Twelve patients presented with pelvic or lower extremity fractures associated with upper extremity fractures. The difference between the two groups shows that fractures in the upper extremities usually exclude fractures of the spine. Upon impact, the falling body has a kinetic energy which is converted, in its major part, into fracture energy. In the first group most of the kinetic energy is dissipated to the lower extremities, pelvis and spine, causing fractures at these sites. In the second group, patients use their upper extremities in an attempt to protect themselves, possibly via more flexion at the hip level. This increased flexion converts the remaining energy into forward rotational energy of the trunk exposing the extended upper extremities to fractures. It is probable that this form of energy

The initial treatment should be limited to life-saving procedures and short spine and limb stabilization procedures [49]. Fractures should be treated by methods that will allow early mobilization and transfer to the psychiatric ward. Treatment by traction or spica cast is not

in the under 35yrs age group [21].

64 Topics in Paraplegia

injuries than those who land on their sides.

dissipation protects the spine from fracture.

Until now it has been difficult to obtain comparable international data on suicide attempts, owing to disparities in definitions, survey designs and study methods. It has been our experience that psychiatric conditions, and especially suicide risk, should be evaluated and treated as early as possible during the orthopaedic or surgical hospitalization. Management requires both psychopharmacological therapy and psychotherapy. It has to be directed towards the achievement of symptomatic relief and, if possible, towards the remission of the primary psychiatric disorder. The management of these patients in the orthopaedic or surgical ward is difficult, because of restlessness, noncooperation of the patient and the problem of staff inexperienced in handling the psychiatric patient. When prolonged orthopaedic and rehabilitation management is necessary, it is suggested that the patient be transferred to the psychiatric hospital while continuing the necessary orthopaedic treatment.

#### **Author details**

Stamatios A. Papadakis1\*, Spyridon Galanakos1 , Kleio Apostolaki2 , Konstantinos Kateros3 , Olga Antoniadou4 , George Macheras1 and George Sapkas5

ic variables of European parasuicides. Paper presented at the WPA Satellite Symposi‐

Spinal Cord Injuries Following Suicide Attempts

http://dx.doi.org/10.5772/57409

67

[9] Hultιn A., Jiang G.-X., Wasserman D., Hawton K., Hjelmeland H, De Leo D, Ostamo A, Salander-Renberg E, Schmidtke A. Repetition of attempted suicide among teen‐ agers in Europe: frequency, timing and risk factors. European Child & Adolescent

[10] Brent DA, Kolko DJ,Wartella ME, Boylan M, Moritz G, Baugher M, Zlenak J. Adoles‐ cent psychiatric inpatients' risk of suicide attempt at 6-month follow-up. Journal of

[11] Pfeffer CR, Klerman GL, Hurt SW, Kaukuma T, Peskin JR, Siefker CA. Suicidal chil‐ dren grow up: rates and psychosocial risk factors for suicide attempts during followup. Journal of the American Academy of Child & Adolescent Psychiatry 1993;32:106–

[12] Larsson B,Melin L, Breitholtz E,Andersson M. Short-term stability of depressive symptoms and suicide attempts in Swedish adolescents. Acta Psychiatrica Scandi‐

[13] Haw C, Bergen H, Casey D, Hawton K. Repetition of deliberate self-harm: a study of characteristics and subsequent deaths in patients presenting to a general hospital ac‐ cording to extent of repetition. Suicide & Life Threatening Behaviour 2007;37(4):

[14] Zahl DL, Hawton K. Repetition of DSH and subsequent suicide risk: long-term fol‐ low-up study of 11,583 patients. The British Journal of Psychiatry 2004;185:70-75. [15] Esposito C, Spirito A, Boergers J, Donaldson D. Affective, behavioral, and cognitive functioning in adolescents with multiple suicide attempts. Suicide & Life Threaten‐

[16] Joiner TE. Why People Die by Suicide. Cambridge, MA: Harvard University Press;

[17] Menti E, Lekka NP, Assimakopoulos K, Varvarigou A, Beratis NG, Beratis S. Smok‐ ing, psychosocial factor, psychopathologic behaviour and other related conditions in hospitalized youth suicide attempters. Comprehensive Psychiatry 2007;48(6):522-528.

[18] Tsati E, Iconomou T, Tzivaridou D, Keramidas E, Papadopoulos S, Tsoutsos D. Selfinflicted burns in Athens Greece: a six year retrospective study. The Journal of Burn

[19] Tountas C, Sotiropoulos A, Skliros SA. Kotsini V, Peppas TA, Tamvakos E, Pappas S. Voluntary self-poisoning as a cause of admission to a tertiary hospital internal medi‐

cine clinic in Pireaus Greece within a year. BMC Psychiatry 2001;1:4

the American Academy of Child and Adolescent Psychiatry 1993;32:95-105.

um"Suicidal Behaviour". Budapest, 1996.

Psychiatry 2001;10:161–169.

navica 1991;83:385–390.

ing Behaviour 2003;33:389-399.

Care & Rehabilitation 2005;26(1):75-78.

2005;46Y93, 203-222.

113.

379-396.

\*Address all correspondence to: snapmd@gmail.com

1 D' Department of Orthopaedics, "KAT-EKA" General Hospital, Athens, Greece

2 Private Psychology and Psychotherapy Practice, Athens, Greece

3 A' Department of Orthopaedics, "G. Gennimatas" General Hospital, Athens, Greece

4 Private Psychiatry Practice , Athens, Greece

5 A' Department of Orthopaedics, University of Athens, "Attikon" University Hospital, Haidari, Greece

#### **References**


ic variables of European parasuicides. Paper presented at the WPA Satellite Symposi‐ um"Suicidal Behaviour". Budapest, 1996.

**Author details**

66 Topics in Paraplegia

Olga Antoniadou4

Haidari, Greece

**References**

ber 2013)

2008

2003;13(2): 108-114.

Stamatios A. Papadakis1\*, Spyridon Galanakos1

4 Private Psychiatry Practice , Athens, Greece

, George Macheras1

2 Private Psychology and Psychotherapy Practice, Athens, Greece

\*Address all correspondence to: snapmd@gmail.com

, Kleio Apostolaki2

and George Sapkas5

1 D' Department of Orthopaedics, "KAT-EKA" General Hospital, Athens, Greece

3 A' Department of Orthopaedics, "G. Gennimatas" General Hospital, Athens, Greece

5 A' Department of Orthopaedics, University of Athens, "Attikon" University Hospital,

[1] World Health Organisation. Suicide prevention (SUPRE). http://www.who.int/ mental\_health/prevention/suicide/suicideprevent/en/index.html (accessed 3 Novem‐

[2] Chishti P, Stone DH, Corcoran P, Williamson E, Petridou E; Eurosave Working Group Suicide mortality in the European Union. European Journal of Public Health

[3] Rutz EM, Wasserman D. Trends in adolescent suicide mortality in the WHO Europe‐

[4] Kazalotti E, Xinou A. Suicide. Article, Eleftherotipia, Daily Newspaper 19th January

[5] Fountoulakis KN, Grammatikopoulos IA, Koupidis SA, Siamouli M, Theodorakis PN. Health and the financial crisis in Greece. The Lancet, 2012;379(9820):1001-1002.

[6] Economou M, Madianos M, Peppou LE, Theleritis C, Stefanis CN. Suicidality and the

[7] Kentikelenis A, Karanikolos M, Papanicolas I, Basu S, Mckee M, Stuckler D. Health effects of financial crisis: omens of a Greek tragedy. The Lancet 2011;378:1457-1458

[8] Schmidtke A, Bille-Brahe U, Kerkhof A, DeLeo D, Bjerke T, Crepet P, Haring C, Mi‐ chel K, Salander-Renberg E, Wassermann D, Fricke S, Weinacker B. Results of the WHO/EURO Multicentre Study on Parasuicide: Rates, Trends and Sociodemograph‐

an Region. European Child & Adolescent Psychiatry 2004;13(5):321-331.

economic crisis in Greece. The Lancet 2012;380(9839):337.

, Konstantinos Kateros3

,


[20] Giotakos O. Suicidal ideation, substance use, and sense of coherence in Greek male conscripts. Military Medicine 2003;168(6):447-50

[34] Kennedy P, Rogers B, Speer S, Frankel H. Spinal cord injuries and attempted suicide:

Spinal Cord Injuries Following Suicide Attempts

http://dx.doi.org/10.5772/57409

69

[35] Biering-Sorensen F, Pederson W, Giortz Muller P. Spinal cord injury due to suicide

[36] Hartkopp A, Hansen H, Seidenschnur AM, Biering-Sorensen E. Suicide in a spinal cord injured population: its relation to functional status. Archives of Physical Medi‐

[37] Kewman DG, Tate DG. Suicide in SCI: a psychological autopsy. Rehabilitation Psy‐

[38] Haenel T, Jehle O. Paraplegia after suicidal attempt. Psychiatriche Praxis 2003;30(4):

[39] Christiansen E., Jensen BF. Risk of repetition of suicide attempt, suicide or all deaths after an episode of attempted suicide: a register-based survival analysis. The Austral‐

[40] Petronis KR. Samuels JF, Moscicki EK, Anthony JC. An epidemiologic investigation of potential risk factors for suicide attempts. Social Psqchiatry and Psychiatric Epi‐

[41] Poma SZ, Magno N, Belletti S, Toniolo E (2007) Parasuicide in Rovigo (North of Italy)

[42] Prosser JM, Perrone J, Pines JM (2007) The epidemiology of intentional non-fatal self-

[43] Hawton K, Arensman E, Wasserman D, Hultén A, Bille-Brahe U, Bjerke T, Crepet P, Deisenhammer E, Kerkhof A, De Leo D, Michel K, Ostamo A, Philippe A, Querejeta I, Salander-Renberg E, Schmidtke A, Temesváry B. Relation between attempted sui‐ cide and suicide rates among young people in Europe. Journal of Epidemiology and

[44] Granboulan V, Rabain D, Basquin M (1995). The outcome of adolescent suicide at‐

[45] Hawton K, Fagg J, Platt S, Hawkins M. (1993). Factors associated with suicide after parasuicide in young people. British Journal of Psychiatry 306: 1641–1644.

[46] Castle K, Duberstein PR, Meldrum S, Conner KR, Conwell Y. Risk factors for suicide in blacks and whites: an analysis of data from the 1993 National Mortality Follow‐

[47] Lewis WS, Lee AB, Grantham SA. ``Jumpers syndrome'': the trauma of high free fall

back Survey. American Journal of Psychiatry. 2004; 161:452-458.

as seen at Harlem Hospital. Journal of Trauma 1965;5(6):812-818.

harm poisoning in the United States: 2001-2004. J Med Toxicol 3 (1): 20-4

ian and New Zealand Journal of Psychiatry 2007;41(3):257-265.

during the period 2000-2005. J Prev Med Hyg 48(3): 79-82

a retrospective review. Spinal Cord 1999;37(12):847–852.

attempts. Paraplegia 1992;30(2):139-144.

chology 1998;43(2):143–151.

demiology. 1990;25:193-199.

Community Health 1998;52(3):191–194.

tempts.Acta Psychiatrica Scandinavica 91:265-270.

212-215.

cine and Rehabilitation 1998;79(11):1356–1361.


[34] Kennedy P, Rogers B, Speer S, Frankel H. Spinal cord injuries and attempted suicide: a retrospective review. Spinal Cord 1999;37(12):847–852.

[20] Giotakos O. Suicidal ideation, substance use, and sense of coherence in Greek male

[21] Vougiouklakis T, Boumba VA, Mitselou A, Peschos D, Gerontopoulos K. Trends in suicide mortality in the deprived region of Epirus (north-west Greece) during the pe‐

[22] Zacharakis CA, Madianos MG, Papadimitriou GN, Stefanis CN. Suicide in Greece 1980-1995:Patterns and Social Factors. Social Psychiatry and Psychiatry Epidemiolo‐

[23] Hatziolis AI, Sion ML, Eleftheriadis NP, Toulis E, Efstratiadis G, Vartzopoulos D, Ziakas AG.Parasuicidal poisoning treated in a Greek medical ward; epidemiology and clinical experience. Human and Experimental Toxicology 2001;20(12):611-617.

[24] Anderson J, Allan DB. Vertebral fracture secondary to suicide attempt: demographics and patient outcome in a Scottish spinal rehabilitation unit. The Journal of Spinal

[25] Stanford RE, Soden R, Bartrop R, Mikk M, Taylor TKF. Spinal cord and related inju‐ ries after attempted suicide: psychiatric diagnosis and long-term follow-up. Spinal

[26] Crandall M, Luchette F, Esposito TJ, West M, Shapiro M, Bulger E. Attempted sui‐ cide and the elderly trauma patient: Risk factors and outcomes. Journal of Trauma.

[27] Centre of Suicidal Research and prevention-University of Hong-Kong 2004. http://

[28] HKJC Centre for Suicide Research and Prevention, University of Hong Kong 2006. Retrieved 2009-09-10. "Method uses for completing suicide". http://

[29] Beautrais AL. Serious suicide attempts in young people: a case control study. Ameri‐

[30] Suominen K, Isometsä E, Suokas J, Haukka J, Achte K, Lönnqvist K. Completed sui‐ cide after a suicide attempt: a 37-year follow-up study. American Journal of Psychia‐

[31] Maubl KI, Whitley ER, Cardea JA.Vertical deceleration injuries. Surgery Gynecology

[32] Sims A., O'Brien K. An account of mentally ill people who jump from buildings.

[33] Prasad A., Lloyd GG.Attempted suicide by jumping. Acta Psychiatrica Scandinavica

conscripts. Military Medicine 2003;168(6):447-50

gy 1998;33(10):471-476.

68 Topics in Paraplegia

Cord Medicine 2011;34(4):380-387.

csrp.hku.hk/WEB/eng/statistics.asp#3.

csrp.hku.hk/WEB/eng/statistics.asp#3.

can Journal of Psychiatry 1996;153:1009–1014.

Cord 2007;45(6):437-443.

2007; 62(4):1021-1028.

try 2004;161(4):563–64.

1983;68:394.

& Obstetrics 1981;153(2):233-236.

Medicine Science and the Law 1979;19:195.

riod 1998-2002. Medicine Science and the Law 2005;45(1):39-46.


[48] Snyder RG. Human tolerance to extreme impacts in free-fall. Aeroscace Medicine 1963;34: 695-709.

**Section 2**

**Management of Paraplegia**


### **Management of Paraplegia**

[48] Snyder RG. Human tolerance to extreme impacts in free-fall. Aeroscace Medicine

[49] Burri C., Kreuzer U., Limmer J. Principles and practice of fracture treatment in the

[50] Katz K, Gonen N, Goldberg I, Mizrahit J Radwan M, Yosipovitch Z..Injuries in at‐

tempted suicide by jumping from a height. Injury 1988;19:371-374.

multiple injured patient. Injury 1982;14(1):44-50.

1963;34: 695-709.

70 Topics in Paraplegia

**Chapter 4**

**Role of Decompressive Surgery in Disorders Associated**

Paraplegia/tetraplegia represents a significant neurologic disability with loss of motor and sensory function in the lower extremities and/or impairment of sexual, urinary and intestinal functions. Involvement of the spinal cord explains most cases of paraplegia/tetraplegia with pathological lesions commonly resulting from trauma or a progressive neoplastic disease of the spine. In such cases, paraplegia/tetraplegia occurs either acutely or results from a chroni‐ cally progressive spinal pathology, warranting urgent surgical decompression. Surgical decision-making and the rationale for spinal decompression are based on the anticipated increased risk of paraplegia/tetraplegia in cases where there is evidence of progressive functional loss. This chapter aims to review the current state of spinal surgery and to provide an evidence-based approach to the management of common compressive spinal disorders associated with paraplegia/tetraplegia, including degenerative conditions, such as acute traumatic spinal cord injury, cervical spondylotic myelopathy and spinal metastatic dis‐

ease.The surgical management of each category is discussed separately below.

The anatomical structures maintaining spinal stability and various methods of assessment of spinal instability are discussed. The reminder of the chapter explores up-to-date evidence on the management of compressive myelopathies. In addition, we discuss the most recent evidence and clinical guidelines surrounding the acute management of traumatic cervical spinal cord injury and timing of surgical decompression. Furthermore, this chapter outlines the epidemiology and pathophysiology of cervical spondylotic myelopathy, which is ex‐ plained in order to provide a foundation to the understanding of prognosis and timing of surgical decompression. Different approaches including anterior and posterior decompression are discussed, explaining the rationale for each approach based on an appraisal of published clinical evidence. The advantages and disadvantages of laminectomy with arthrodesis are

> © 2014 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

**with Spinal Cord Lesions**

Ayoub Dakson and Sean D. Christie

http://dx.doi.org/10.5772/58408

**1. Introduction**

Additional information is available at the end of the chapter

### **Role of Decompressive Surgery in Disorders Associated with Spinal Cord Lesions**

Ayoub Dakson and Sean D. Christie

Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/58408

#### **1. Introduction**

Paraplegia/tetraplegia represents a significant neurologic disability with loss of motor and sensory function in the lower extremities and/or impairment of sexual, urinary and intestinal functions. Involvement of the spinal cord explains most cases of paraplegia/tetraplegia with pathological lesions commonly resulting from trauma or a progressive neoplastic disease of the spine. In such cases, paraplegia/tetraplegia occurs either acutely or results from a chroni‐ cally progressive spinal pathology, warranting urgent surgical decompression. Surgical decision-making and the rationale for spinal decompression are based on the anticipated increased risk of paraplegia/tetraplegia in cases where there is evidence of progressive functional loss. This chapter aims to review the current state of spinal surgery and to provide an evidence-based approach to the management of common compressive spinal disorders associated with paraplegia/tetraplegia, including degenerative conditions, such as acute traumatic spinal cord injury, cervical spondylotic myelopathy and spinal metastatic dis‐ ease.The surgical management of each category is discussed separately below.

The anatomical structures maintaining spinal stability and various methods of assessment of spinal instability are discussed. The reminder of the chapter explores up-to-date evidence on the management of compressive myelopathies. In addition, we discuss the most recent evidence and clinical guidelines surrounding the acute management of traumatic cervical spinal cord injury and timing of surgical decompression. Furthermore, this chapter outlines the epidemiology and pathophysiology of cervical spondylotic myelopathy, which is ex‐ plained in order to provide a foundation to the understanding of prognosis and timing of surgical decompression. Different approaches including anterior and posterior decompression are discussed, explaining the rationale for each approach based on an appraisal of published clinical evidence. The advantages and disadvantages of laminectomy with arthrodesis are

© 2014 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

reviewed and compared to laminectomy alone and other techniques such as laminoplasty. Finally, management of spinal metastasis as an important etiology for paraplegia is explained. The rationale to surgical decompression is explored on the basis of clinical trials with brief elaboration on the epidemiology and pathophysiology of spinal metastasis.

1985; Denis 1983). This is in contrast to failure of the anterior column only as seen in compres‐

Role of Decompressive Surgery in Disorders Associated with Spinal Cord Lesions

http://dx.doi.org/10.5772/58408

75

More importantly, spinal instability is better represented as a spectrum of instability ranging from stable to unstable spinal injury rather than an all-or-none phenomenon. Two types of spinal instability are described: acute and chronic instability. Acute instability occurs most commonly in the context of trauma, infectious and neoplastic diseases of the spine, whereas chronic instability usually results from a degenerative spinal process or as a consequence of acute instability. In acute spinal instability, two different types occur; overt and limited. The former is defined as loss of the ability of the spine to support the trunk during normal movement, which occurs in the context of loss of the ventral and dorsal integrities of the spinal column. For instance, compromise of the vertebral body integrity is seen in compression and burst fractures resulting in ventral column disruption, which can be assessed with plain radiographs or CT. Compromise of the dorsal integrity of the spinal column often results from disruption of the ligamentous structures or fractures of the dorsal elements. Assessment of ligamentous injury is aided by MRI imaging with the addition of fat suppression or short T1 inversion recovery (STIR) sequences for better visual distinction of the ligamentous structures. Isolated MRI signal change indicates increased water content within the ligamentous struc‐ tures and does not necessarily confirm complete disruption of the disco-ligamentous struc‐ tures unless accompanied by evidence of locked facets or facet dislocation, which is considered an absolute indication of posterior ligamentous disruption (Vaccaro 2007). The presence of

On the other hand, limited instability is represented by disruption of either the anterior or posterior integrity of the spine with preservation of the other. For instance, wedge or burst fractures of the vertebral body with no evidence of disruption of the posterior integrity resemble limited instability, which allows for non-operative management, and may include external orthoses such as a brace. Having said that, overt instability can be missed and misjudged as limited instability especially when in the context of overlooking disruption of

In current practice, few scoring systems exist to aid assessment of spinal instability in cervical and thoracolumbar spinal injury. As discussed above, the Spine Trauma Study Group published a classification system for subaxial cervical spine injuries, named the Subaxial Injury Classification (SLIC) and Severity Scale, describing the morphological, discoligamentous complex (DLC) and clinical neurological parameters associated with cervical spine injury (Anderson 2007; Vaccaro 2007). In terms of describing the morphology of the fracture, the greater instability associated with the spinal fracture, the higher the number of points given (Table 1). For instance, facet dislocation and fracture-dislocation injuries are considered highly unstable with failure of three columns (4 points), compared to simple compression fractures, which are associated with single column failure (1 point). In addition, the SLIC severity scoring system sheds further light on the importance of disruption of the posterior column, which requires evidence of perched or dislocated facet and facet diastasis > 2mm, as well as MRI signal change at the entire disc (2 points). The presence of T2-weighted STIR MRI signal change at the ligamentous structures or isolated widening of the interspinous space on plain radio‐

overt instability requires definite surgical stabilization.

the posterior ligamentous structures.

sion fractures.

#### **2. Requirement for spinal stability**

Spinal stability constitutes a crucial factor in the surgical management of most spine disorders, serving as a strong indication for surgical intervention in many diseases of the spine. Spinal instability may co-exist with traumatic disorders of the spine as well as non-traumatic disorders such as metastatic and degenerative disease.

Spinal stability has been defined conceptually by Panjabi et al. (1993) as the ability of the spine, under physiologic loads, to limit displacement and deformity in order to prevent neurologic deficits, due to injury to the neural elements (spinal cord and nerve roots), and pain as a result of structural changes. Loss of the ability of the spine to resist displacement is recognized as spinal instability, which increases the risk of neural injury or occurs in association with neural injury. Resistance against such deforming forces stems from passive, active and neural control spinal subsystems, which form the spinal stabilizing system. The skeletal system represents osseous and ligamentous structures including vertebrae, intervertebral discs, spinal ligaments, facet articulations and joint capsules, which all contribute to passive spinal resistance forces. The active subsystem is resembled by muscles and related tendons that surround the spinal column, possessing an active force against spinal deformity and neural injury. Finally, the neural and feedback subsystem is composed of a variety of sensory receptors in ligamentous and muscular structures forming part of the neural feedback system acting reflexively on active and thereby passive subsystems to prevent spinal deformity and neural injury.

The first structural description of spinal stability in the context of a two-column approach was published by Frank Holdsworth et al. (1970). He proposed that spinal instability is sufficiently accounted for by rupture of the posterior ligamentous complex (PLC). However, emerging biomechanical evidence is contradictory in that isolated disruption of the PLC is not necessarily a cause of spinal instability except in cases where evidence of disruption of the posterior longitudinal ligament and tearing of the annulus fibrosis also exists. Therefore, Denis et al. (1983) suggested a three-column approach in assessing the stability of the spine following acute spinal trauma. The anterior longitudinal ligament together with two thirds of the vertebral body form the anterior column, whereas the middle column encompasses the posterior longitudinal ligament, the posterior annulus fibrosis, and the posterior one-third the vertebral body. The posterior column resembles the posterior bony complex (posterior arch) and PLC (supraspinous ligament, interspinous ligament, capsule and ligamentum flavum). This approach will be helpful when describing fractures of the spine and their relation to clinical instability. For instance, one way to differentiate compression fractures from unstable burst fractures is failure of the anterior and middle columns, which is readily visualized on lateral radiographs and CT in burst fractures rendering the spine mechanically unstable (Louis 1985; Denis 1983). This is in contrast to failure of the anterior column only as seen in compres‐ sion fractures.

reviewed and compared to laminectomy alone and other techniques such as laminoplasty. Finally, management of spinal metastasis as an important etiology for paraplegia is explained. The rationale to surgical decompression is explored on the basis of clinical trials with brief

Spinal stability constitutes a crucial factor in the surgical management of most spine disorders, serving as a strong indication for surgical intervention in many diseases of the spine. Spinal instability may co-exist with traumatic disorders of the spine as well as non-traumatic

Spinal stability has been defined conceptually by Panjabi et al. (1993) as the ability of the spine, under physiologic loads, to limit displacement and deformity in order to prevent neurologic deficits, due to injury to the neural elements (spinal cord and nerve roots), and pain as a result of structural changes. Loss of the ability of the spine to resist displacement is recognized as spinal instability, which increases the risk of neural injury or occurs in association with neural injury. Resistance against such deforming forces stems from passive, active and neural control spinal subsystems, which form the spinal stabilizing system. The skeletal system represents osseous and ligamentous structures including vertebrae, intervertebral discs, spinal ligaments, facet articulations and joint capsules, which all contribute to passive spinal resistance forces. The active subsystem is resembled by muscles and related tendons that surround the spinal column, possessing an active force against spinal deformity and neural injury. Finally, the neural and feedback subsystem is composed of a variety of sensory receptors in ligamentous and muscular structures forming part of the neural feedback system acting reflexively on active

and thereby passive subsystems to prevent spinal deformity and neural injury.

The first structural description of spinal stability in the context of a two-column approach was published by Frank Holdsworth et al. (1970). He proposed that spinal instability is sufficiently accounted for by rupture of the posterior ligamentous complex (PLC). However, emerging biomechanical evidence is contradictory in that isolated disruption of the PLC is not necessarily a cause of spinal instability except in cases where evidence of disruption of the posterior longitudinal ligament and tearing of the annulus fibrosis also exists. Therefore, Denis et al. (1983) suggested a three-column approach in assessing the stability of the spine following acute spinal trauma. The anterior longitudinal ligament together with two thirds of the vertebral body form the anterior column, whereas the middle column encompasses the posterior longitudinal ligament, the posterior annulus fibrosis, and the posterior one-third the vertebral body. The posterior column resembles the posterior bony complex (posterior arch) and PLC (supraspinous ligament, interspinous ligament, capsule and ligamentum flavum). This approach will be helpful when describing fractures of the spine and their relation to clinical instability. For instance, one way to differentiate compression fractures from unstable burst fractures is failure of the anterior and middle columns, which is readily visualized on lateral radiographs and CT in burst fractures rendering the spine mechanically unstable (Louis

elaboration on the epidemiology and pathophysiology of spinal metastasis.

**2. Requirement for spinal stability**

74 Topics in Paraplegia

disorders such as metastatic and degenerative disease.

More importantly, spinal instability is better represented as a spectrum of instability ranging from stable to unstable spinal injury rather than an all-or-none phenomenon. Two types of spinal instability are described: acute and chronic instability. Acute instability occurs most commonly in the context of trauma, infectious and neoplastic diseases of the spine, whereas chronic instability usually results from a degenerative spinal process or as a consequence of acute instability. In acute spinal instability, two different types occur; overt and limited. The former is defined as loss of the ability of the spine to support the trunk during normal movement, which occurs in the context of loss of the ventral and dorsal integrities of the spinal column. For instance, compromise of the vertebral body integrity is seen in compression and burst fractures resulting in ventral column disruption, which can be assessed with plain radiographs or CT. Compromise of the dorsal integrity of the spinal column often results from disruption of the ligamentous structures or fractures of the dorsal elements. Assessment of ligamentous injury is aided by MRI imaging with the addition of fat suppression or short T1 inversion recovery (STIR) sequences for better visual distinction of the ligamentous structures. Isolated MRI signal change indicates increased water content within the ligamentous struc‐ tures and does not necessarily confirm complete disruption of the disco-ligamentous struc‐ tures unless accompanied by evidence of locked facets or facet dislocation, which is considered an absolute indication of posterior ligamentous disruption (Vaccaro 2007). The presence of overt instability requires definite surgical stabilization.

On the other hand, limited instability is represented by disruption of either the anterior or posterior integrity of the spine with preservation of the other. For instance, wedge or burst fractures of the vertebral body with no evidence of disruption of the posterior integrity resemble limited instability, which allows for non-operative management, and may include external orthoses such as a brace. Having said that, overt instability can be missed and misjudged as limited instability especially when in the context of overlooking disruption of the posterior ligamentous structures.

In current practice, few scoring systems exist to aid assessment of spinal instability in cervical and thoracolumbar spinal injury. As discussed above, the Spine Trauma Study Group published a classification system for subaxial cervical spine injuries, named the Subaxial Injury Classification (SLIC) and Severity Scale, describing the morphological, discoligamentous complex (DLC) and clinical neurological parameters associated with cervical spine injury (Anderson 2007; Vaccaro 2007). In terms of describing the morphology of the fracture, the greater instability associated with the spinal fracture, the higher the number of points given (Table 1). For instance, facet dislocation and fracture-dislocation injuries are considered highly unstable with failure of three columns (4 points), compared to simple compression fractures, which are associated with single column failure (1 point). In addition, the SLIC severity scoring system sheds further light on the importance of disruption of the posterior column, which requires evidence of perched or dislocated facet and facet diastasis > 2mm, as well as MRI signal change at the entire disc (2 points). The presence of T2-weighted STIR MRI signal change at the ligamentous structures or isolated widening of the interspinous space on plain radio‐ graphs is considered intermediate evidence of ligamentous disruption (1 point). SLIC score of ≥ 5 points is highly suggestive of spinal instability and requirement for surgical stabilization, with or without spinal cord or nerve root decompression (Arabi 2013).

neurorehabilitation program. Much research has been published in an effort to establish what factors alter the neurologic and functional outcomes after SCI in order to optimize targeted management of acute SCI. The management of acute SCI, particularly cervical SCI includes a multifaceted and stepwise approach starting with pre-hospital care, leading to emergency medical or physiological strategies as well as decompressive spinal surgery with large emphasis on timely diagnosis of acute SCI. The main role of surgical interventions is to restore

Role of Decompressive Surgery in Disorders Associated with Spinal Cord Lesions

http://dx.doi.org/10.5772/58408

77

The most commonly injured part of the spinal cord is the cervical cord, accounting for more than two-thirds of all SCI and commonly associated with tetraplegia more so than paraplegia. This is important since patients with cervical traumatic SCI are prone to developing hemody‐ namic instability and respiratory failure in the acute setting, which are thought to worsen their end outcome. In this chapter, the scope is limited to cervical spine injuries, and their manage‐

Young males are most commonly affected by spinal cord injury. Males are 3 to 20 times more likely to suffer SCI than females. Bimodal age preference is observed in SCI patients with the second peak occurring in elderly patients following a fall (Hall 1978; DeVivo 1980). The prevalence of SCI in the USA is estimated to reach up to 400,000, with estimated hospital occupancy of about 2000 beds annually. Although about a third of spinal fractures occur in the cervical region, only 10-20% of these are associated with spinal cord injuries (Hu 1996). SCI co-exists with traumatic brain injuries in up to 8% of cases and up to 10% of patients with SCI demonstrate other spinal fractures (Holly 2002). The most common cause of traumatic SCI is traffic collisions including motor vehicle collisions, or other traumas involving a motorcycle or a pedestrian. Elderly patients over the age of 65 are at risk of SCI following a fall, which often occurs at home. Pre-existing cervical canal stenosis or degenerative spondylosis in this age group are associated with certain clinical types of incomplete SCI, specifically central cord

Timely and careful pre-hospital and initial in-hospital acute management should optimize the role of surgery in helping patients with SCI. Understanding the pathophysiology of cervical SCI is a pre-requisite to explaining the rationale and research basis of acute prompt manage‐ mentof cervical SCI.Respiratorycompromise andhypoventilationare commonincervical cord injuries, resulting from paralysis of the intercostal muscles. Residual diaphragmatic function allows for independent breathing unless the injury is above the outflow of the phrenic nerves at the spinal nerve roots C3-C5. Furthermore, patients with cervical SCI can present frequent‐ ly with hypothermia due to disruption of the connections to the sympathetic chain, which has asubstantialoutflowwithinthethoracic spinal cordsegmentsT8-10.Hypotensioninthe context of cervical spine injury may result from loss of the sympathetic tone and reduced peripheral

vascular resistance. This is commonly associated with bradycardia and hypothermia.

spinal stability and prevent further neurologic deterioration.

ment, highlighting recent evidence and guidelines publications.

**3.2. Pathophysiology and types of cervical SCI**

**3.1. Epidemiology**

syndrome.


**Table 1.** Subaxial Injury Classification (SLIC) and severity scale

#### **3. Traumatic cervical spinal cord injury**

Trauma to the spinal cord is commonly associated with considerable disability and is mani‐ fested by loss of function, including tetra-/paraplegia as well as genitourinary and gastroin‐ testinal dysfunction, and chronic pain. Acute SCI affects about 250,000 individuals in North America, and has been estimated to account for a lifetime cost of \$500,000 to \$2 millions per case, with an overall annual cost of \$7 billion in the USA (DeVivo 1997; Sadowsky 1999). The annual incidence of traumatic SCI ranges from 28 and 55 cases per million people with about 10,000 cases reported annually in the USA (McDonald 2002). Patients sustain considerable deficits and disabilities that require multidisciplinary approach to treatment and an intensive neurorehabilitation program. Much research has been published in an effort to establish what factors alter the neurologic and functional outcomes after SCI in order to optimize targeted management of acute SCI. The management of acute SCI, particularly cervical SCI includes a multifaceted and stepwise approach starting with pre-hospital care, leading to emergency medical or physiological strategies as well as decompressive spinal surgery with large emphasis on timely diagnosis of acute SCI. The main role of surgical interventions is to restore spinal stability and prevent further neurologic deterioration.

The most commonly injured part of the spinal cord is the cervical cord, accounting for more than two-thirds of all SCI and commonly associated with tetraplegia more so than paraplegia. This is important since patients with cervical traumatic SCI are prone to developing hemody‐ namic instability and respiratory failure in the acute setting, which are thought to worsen their end outcome. In this chapter, the scope is limited to cervical spine injuries, and their manage‐ ment, highlighting recent evidence and guidelines publications.

#### **3.1. Epidemiology**

graphs is considered intermediate evidence of ligamentous disruption (1 point). SLIC score of ≥ 5 points is highly suggestive of spinal instability and requirement for surgical stabilization,

**Sub-Axial Injury Classfication Scale Points**

No abnormality 0 Compression 1 Burst 2 Distraction (facet perch, hyperextension) 3 Rotation/translation (facet dislocation, unstbale teardrop fracture) 4

Intact 0 Intermediate (isolated interspinous widening, MRI signal change only) 1 Disrupted (widening of disc space, facet perch or dislocation) 2

Intact 0 Root injury 1 Complete cord injury 2 Incomplete cord injury 3 Continous cord compression (in setting of neurological deficit) +1

Trauma to the spinal cord is commonly associated with considerable disability and is mani‐ fested by loss of function, including tetra-/paraplegia as well as genitourinary and gastroin‐ testinal dysfunction, and chronic pain. Acute SCI affects about 250,000 individuals in North America, and has been estimated to account for a lifetime cost of \$500,000 to \$2 millions per case, with an overall annual cost of \$7 billion in the USA (DeVivo 1997; Sadowsky 1999). The annual incidence of traumatic SCI ranges from 28 and 55 cases per million people with about 10,000 cases reported annually in the USA (McDonald 2002). Patients sustain considerable deficits and disabilities that require multidisciplinary approach to treatment and an intensive

with or without spinal cord or nerve root decompression (Arabi 2013).

*Morphology*

76 Topics in Paraplegia

*Disco-ligamentous Complex (DLC)*

**Table 1.** Subaxial Injury Classification (SLIC) and severity scale

**3. Traumatic cervical spinal cord injury**

*Neurological status*

Young males are most commonly affected by spinal cord injury. Males are 3 to 20 times more likely to suffer SCI than females. Bimodal age preference is observed in SCI patients with the second peak occurring in elderly patients following a fall (Hall 1978; DeVivo 1980). The prevalence of SCI in the USA is estimated to reach up to 400,000, with estimated hospital occupancy of about 2000 beds annually. Although about a third of spinal fractures occur in the cervical region, only 10-20% of these are associated with spinal cord injuries (Hu 1996). SCI co-exists with traumatic brain injuries in up to 8% of cases and up to 10% of patients with SCI demonstrate other spinal fractures (Holly 2002). The most common cause of traumatic SCI is traffic collisions including motor vehicle collisions, or other traumas involving a motorcycle or a pedestrian. Elderly patients over the age of 65 are at risk of SCI following a fall, which often occurs at home. Pre-existing cervical canal stenosis or degenerative spondylosis in this age group are associated with certain clinical types of incomplete SCI, specifically central cord syndrome.

#### **3.2. Pathophysiology and types of cervical SCI**

Timely and careful pre-hospital and initial in-hospital acute management should optimize the role of surgery in helping patients with SCI. Understanding the pathophysiology of cervical SCI is a pre-requisite to explaining the rationale and research basis of acute prompt manage‐ mentof cervical SCI.Respiratorycompromise andhypoventilationare commonincervical cord injuries, resulting from paralysis of the intercostal muscles. Residual diaphragmatic function allows for independent breathing unless the injury is above the outflow of the phrenic nerves at the spinal nerve roots C3-C5. Furthermore, patients with cervical SCI can present frequent‐ ly with hypothermia due to disruption of the connections to the sympathetic chain, which has asubstantialoutflowwithinthethoracic spinal cordsegmentsT8-10.Hypotensioninthe context of cervical spine injury may result from loss of the sympathetic tone and reduced peripheral vascular resistance. This is commonly associated with bradycardia and hypothermia.

Injury to the spinal cord occurs because of stretching, crushing, vascular compromise or compression. Incomplete cervical SCI encompasses three different subtypes with potentially different pathophysiological mechanisms. These include central cord syndrome, anterior cord syndrome and spinal cord hemisection or Brown-Sequard syndrome. Traumatic central cord syndrome (TCCS) is the most common incomplete cervical cord injury accounting for up to half of SCI clinical syndromes and about 9% of all SCIs in one series (McKinley 2007; Bosch 1971). It occurs more frequently in elderly patients with spinal canal stenosis associated with cervical spondylosis in the form of bony spurs anteriorly and thickened ligamentum flavum posteriorly (Schneider 1954). The pathophysiology of TCCS is poorly understood, however, the proposed mechanism of injury is thought to be secondary to a hyperextension injury during a fall resulting in inward buckling of the ligamentum flavum and compression of the cord dorsoventrally, occasionally with central cord hemorrhage and venous infarction (Quencer 1992). The spinal segments C3-4 and C4-5 are commonly affected in more than two thirds of TCCS cases (Aarabi 2011). In post-mortem reports of patients deceased following TCCS, spinal cord damage adopts tubular and central orientation, which may or may not extend several cervical segments rostrocaudally (Schneider 1954). Histological examination suggests a predominant white matter injury with axonal damage associated with myelin loss affecting the lateral columns (Quencer 1992). Clinically, patients with TCCS exhibit motor weakness in the upper extremities out of proportion to weakness in the lower extremities. One systematic review of the literature searching a common diagnostic criterion of TCCS found an average 11 ASIA motor points difference between upper and lower extremities motor scores, suggesting it can be utilized to aid diagnosis (Pouw 2010). Some sensory disturbance occurs variably and includes allodynia as well as sphincter dysfunction in the form of urinary retention. The prognosis in more than two thirds of cases is favorable with recovery of lower extremities motor function permitting independent ambulation and recovery of bladder function (Schneider 1958; Roth 1990; Dvorak 2005). However, some residual fine motor deficits in the hands frequently persist.

The Brown-Sequard syndrome is associated with a rare incidence of 3.6% and usually results from a penetrating injury, such as gunshot or knife wounds, although its development in the context of blunt injury and extra-dural cord compression was also described (McKinley 2007; Roth 1991). Patient manifest with ipsilateral motor and proprioceptive, touch and vibratory sense loss associated with contralateral pain sensation loss. The majority of patients with Brown-Sequard syndrome are able to ambulate independently and recover their bladder

Role of Decompressive Surgery in Disorders Associated with Spinal Cord Lesions

http://dx.doi.org/10.5772/58408

79

An initial rapid approach for assessment of the airway, circulation and breathing is employed in acute prompt management of cervical spine injuries. Pre-hospital safe immobilization of the cervical spine and maintenance of normal axial alignment of the body is required in order to avoid iatrogenic spinal cord injury or worsening of an existing injury. Cervical spinal cord injury is associated with respiratory failure manifesting as hypoventilation secondary to paralysis of chest wall musculature. Unilateral or bilateral paralysis of the diaphragm may result in injuries with tetraplegia when the C3-C5 spinal segmental outflow to the phrenic nerves is disrupted. The laryngeal mask airway has been used increasingly in the setting of acute trauma and respiratory insufficiency with satisfactory outcomes (Moller 2000). In addition to respiratory compromise, loss of sympathetic tone occurs in cervical SCI, resulting in decreased cardiac preload secondary to venous pooling and loss of compensatory sympa‐ thetic reflex tachycardia (Troll 1975), thereby causing hemodynamic instability and hypoten‐ sion. According to clinical guidelines, admission of cervical SCI to the intensive care unit is recommended on the basis of class III evidence in order to ensure cardiac monitoring of respiratory and cardiovascular parameters and prompt treatment of respiratory and cardio‐ vascular compromise (Hadley 2013; Casha and Christie 2011). Furthermore, data from retrospective investigations found significant association between mean arterial pressure of 85 – 90 mmHg post-operatively for 7 days and clinical recovery, necessitating adequate augmentation of blood pressure in an intermediate or intensive care unit (Casha and Christie

According to early retrospective studies, intravenous glucocorticoid administraiton in the early stage of traumatic SCI was thought to harbor some beneficial effect in halting secondary neuronal injury and improving neurologic outcome (Short 2000). However, prospective randomized studies provided class I, II and III evidence demonstrating increased risk of adverse effects such as wound infection, acute steroid myelopathy, respiratory failure, sepsis and death in SCI patients treated with steroids. A number of landmark studies have been published in the field including the National Acute Spinal Cord Injury Study (NASCIS) I, II and III trials. In NASCIS I, investigators conducted a multicenter, double-blinded randomized trial comparing low-dose methylprednisone (MP) to high-dose regimen in patients with acute SCI treated for 10 days (Bracken 1984 and 1985). The study failed to demonstrate a difference in outcome at 6 weeks, 6 months and 12 months follow-up periods. Although the study was limited due to lack of a control group and absent power analysis, the authors noted signifi‐

control (Roth 1991).

2011; Ryken 2013).

**3.3. Initial evaluation and acute management of SCI**

Patients with traumatic anterior cord syndrome present with immediate or delayed bilateral paralysis associated with dissociated sensory loss manifesting as loss of pain and temperature consistent with the level of the lesion and preservation of dorsal column function including discriminatory touch, proprioception and vibratory sense. The incidence is very rarely and found to be less than 1% in one series by McKinley et al. (2007). Pollock et al. (1953) first described these neurologic deficits in a series of 27 patients, with a proposition that anterior spinal artery occlusion is the mechanism for the injury following traumatic vertical and anterior compression. However, acute traumatic injury to the anterior portion of the cervical cord by structural disruption and dislocated bone fragments or herniated disc or actual direct destruction of the ventral aspect of the cord was also described in the central cord syndrome (Schneider 1954). These patients unfortunately have the poorest prognosis especially if no improvement is observed within the first 24 hours post-injury (Schneider 1954; Foo 1981; Stuaffer 1975).

The Brown-Sequard syndrome is associated with a rare incidence of 3.6% and usually results from a penetrating injury, such as gunshot or knife wounds, although its development in the context of blunt injury and extra-dural cord compression was also described (McKinley 2007; Roth 1991). Patient manifest with ipsilateral motor and proprioceptive, touch and vibratory sense loss associated with contralateral pain sensation loss. The majority of patients with Brown-Sequard syndrome are able to ambulate independently and recover their bladder control (Roth 1991).

#### **3.3. Initial evaluation and acute management of SCI**

Injury to the spinal cord occurs because of stretching, crushing, vascular compromise or compression. Incomplete cervical SCI encompasses three different subtypes with potentially different pathophysiological mechanisms. These include central cord syndrome, anterior cord syndrome and spinal cord hemisection or Brown-Sequard syndrome. Traumatic central cord syndrome (TCCS) is the most common incomplete cervical cord injury accounting for up to half of SCI clinical syndromes and about 9% of all SCIs in one series (McKinley 2007; Bosch 1971). It occurs more frequently in elderly patients with spinal canal stenosis associated with cervical spondylosis in the form of bony spurs anteriorly and thickened ligamentum flavum posteriorly (Schneider 1954). The pathophysiology of TCCS is poorly understood, however, the proposed mechanism of injury is thought to be secondary to a hyperextension injury during a fall resulting in inward buckling of the ligamentum flavum and compression of the cord dorsoventrally, occasionally with central cord hemorrhage and venous infarction (Quencer 1992). The spinal segments C3-4 and C4-5 are commonly affected in more than two thirds of TCCS cases (Aarabi 2011). In post-mortem reports of patients deceased following TCCS, spinal cord damage adopts tubular and central orientation, which may or may not extend several cervical segments rostrocaudally (Schneider 1954). Histological examination suggests a predominant white matter injury with axonal damage associated with myelin loss affecting the lateral columns (Quencer 1992). Clinically, patients with TCCS exhibit motor weakness in the upper extremities out of proportion to weakness in the lower extremities. One systematic review of the literature searching a common diagnostic criterion of TCCS found an average 11 ASIA motor points difference between upper and lower extremities motor scores, suggesting it can be utilized to aid diagnosis (Pouw 2010). Some sensory disturbance occurs variably and includes allodynia as well as sphincter dysfunction in the form of urinary retention. The prognosis in more than two thirds of cases is favorable with recovery of lower extremities motor function permitting independent ambulation and recovery of bladder function (Schneider 1958; Roth 1990; Dvorak 2005). However, some residual fine motor deficits in the

Patients with traumatic anterior cord syndrome present with immediate or delayed bilateral paralysis associated with dissociated sensory loss manifesting as loss of pain and temperature consistent with the level of the lesion and preservation of dorsal column function including discriminatory touch, proprioception and vibratory sense. The incidence is very rarely and found to be less than 1% in one series by McKinley et al. (2007). Pollock et al. (1953) first described these neurologic deficits in a series of 27 patients, with a proposition that anterior spinal artery occlusion is the mechanism for the injury following traumatic vertical and anterior compression. However, acute traumatic injury to the anterior portion of the cervical cord by structural disruption and dislocated bone fragments or herniated disc or actual direct destruction of the ventral aspect of the cord was also described in the central cord syndrome (Schneider 1954). These patients unfortunately have the poorest prognosis especially if no improvement is observed within the first 24 hours post-injury (Schneider 1954; Foo 1981;

hands frequently persist.

78 Topics in Paraplegia

Stuaffer 1975).

An initial rapid approach for assessment of the airway, circulation and breathing is employed in acute prompt management of cervical spine injuries. Pre-hospital safe immobilization of the cervical spine and maintenance of normal axial alignment of the body is required in order to avoid iatrogenic spinal cord injury or worsening of an existing injury. Cervical spinal cord injury is associated with respiratory failure manifesting as hypoventilation secondary to paralysis of chest wall musculature. Unilateral or bilateral paralysis of the diaphragm may result in injuries with tetraplegia when the C3-C5 spinal segmental outflow to the phrenic nerves is disrupted. The laryngeal mask airway has been used increasingly in the setting of acute trauma and respiratory insufficiency with satisfactory outcomes (Moller 2000). In addition to respiratory compromise, loss of sympathetic tone occurs in cervical SCI, resulting in decreased cardiac preload secondary to venous pooling and loss of compensatory sympa‐ thetic reflex tachycardia (Troll 1975), thereby causing hemodynamic instability and hypoten‐ sion. According to clinical guidelines, admission of cervical SCI to the intensive care unit is recommended on the basis of class III evidence in order to ensure cardiac monitoring of respiratory and cardiovascular parameters and prompt treatment of respiratory and cardio‐ vascular compromise (Hadley 2013; Casha and Christie 2011). Furthermore, data from retrospective investigations found significant association between mean arterial pressure of 85 – 90 mmHg post-operatively for 7 days and clinical recovery, necessitating adequate augmentation of blood pressure in an intermediate or intensive care unit (Casha and Christie 2011; Ryken 2013).

According to early retrospective studies, intravenous glucocorticoid administraiton in the early stage of traumatic SCI was thought to harbor some beneficial effect in halting secondary neuronal injury and improving neurologic outcome (Short 2000). However, prospective randomized studies provided class I, II and III evidence demonstrating increased risk of adverse effects such as wound infection, acute steroid myelopathy, respiratory failure, sepsis and death in SCI patients treated with steroids. A number of landmark studies have been published in the field including the National Acute Spinal Cord Injury Study (NASCIS) I, II and III trials. In NASCIS I, investigators conducted a multicenter, double-blinded randomized trial comparing low-dose methylprednisone (MP) to high-dose regimen in patients with acute SCI treated for 10 days (Bracken 1984 and 1985). The study failed to demonstrate a difference in outcome at 6 weeks, 6 months and 12 months follow-up periods. Although the study was limited due to lack of a control group and absent power analysis, the authors noted signifi‐

cantly higher rate of infections at the surgical site with mortality being three-folds higher in the high-dose MP treatment group. The second NASCIS trial was published in 1990 with 487 patients with acute SCI randomized into to MP, naloxone and placebo groups (Bracken 1990, 1991 and 1992). No difference in primary neurologic utcomes was observed. However, posthoc subanalysis demonstrated mean improvement of 5 points in the ASIA motor score and mean improvement of 4 points in the ASIA sensory score in the MP group compared to controls at 6 months. However, this treatment effect was only realized when treatment was adminis‐ tered within 8 hours of injury, excluding 291 patients who were treated outside this time window. Furthermore, complications such as gastrointestinal hemorrhage, wound infections and pulmonary embolism occured more frequently in patients treated with MP. NASCIS II has been downgraded by some to level III evidence indicating weak positive evidence supporting MP use. This is due to the inconsistency of claimed benefits, lack of functional outcome assessments, the arbitary nature of the eight-hour cut-off time and the high rate of patient exclusion in the subanalysis. NASCIS II provided class I evidence demonstrating harmful adverse effects of steroid use. In NASCIS III, 16 centers in the United States and Canada were enrolled in a prospective double-blinded study including 499 patients presenting with acute SCI within 8 hours randomized into treatment with MP IV infusion for 24 hours (n=166), MP IV infusion for 48 hours (n=166) and tirilazad treatment for 48 hours (n=167) which is a chemically engineered ''super-steroid'' (Bracken 1997 and 1998). Because of the reported positive effect of steroids in NASCIS II, all three groups patients received a loading dose of MP prior to randomization and no placebo-controlled group was included. The study failed to demonstrate a significant difference in neurologic outcome between the three treatment groups at one year (P=0.053), providing class I evidence lacking positive effect of steroid use in acute SCI even when initiated within 8 hours of injury. Of note, there was a transient 5 and 6 ASIA motor score improvements in the 48-hour MP treatment group compared to the 24 hour MP group at 6 weeks (P=0.04) and 6 months (p=0.01), respectively. Similar to NASCIS I and II, there was a trend towards serious complications associated with steroid use in NASCIS III reporting a consistent pattern of adverse effects. Furthermore, a French investigator group published the fourth prospective randomized trial investigating the use of steroids in acute SCI (Pointillart 2000). In this study, 106 patients were randomized into treatment with MP, nimodipine, MP+nimodipine and no pharmacological treatment. The authors demonstrated no significant difference in neurologic recovery between the treatment groups. Therefore, current clinical practice guidelines are not in favor of administering IV steroids even during the early stage of acute SCI due to the higher incidence of adverse effects and lack of clear clinical benefit (Hurlbert 2013). As a result a number of professional organizations in North America have relegated steroid use following spinal cord injury to a weak treatment option only.

is achieved via anterior, posterior or combined surgical approaches focused at decompression of the neural elements and surgical arthrodesis in patients with a mechanically unstable spine in order to provide immediate stabilization and early mobilization as well as preventing further spinal deformity and pain. Therefore, the presence of clinical evidence of cervical cord injury as well as spinal instability represents surgical indications for decompressive and stabilization surgery. In patients with complete cervical cord injury, the primary goal of surgery is to restore spinal stability due to the low likelihood of neurologic recovery given the severity of cord injury. On the other hand, patients with incomplete cervical cord injury and evidence of compromise of the spinal canal should undergo surgical decompression and stabilization in order to aid neurologic recovery. Class II evidence based on the Surgical Timing in Acute Spinal Cord Injury Study (STASCIS) suggests improvement of neurologic function particularly when early surgery (within 24 hours) was instituted. In this prospective, multi‐ centre cohort study of 313 patients with acute cervical SCI, the authors found that about 20% of patients treated early showed 2 or more AIS grade improvements, compared to 9% in the late surgery group at 6 months follow-up (OR=2.6, 95% CI:1.1-6.0). However, in the context of other subgroups of incomplete cervical SCI, such as traumatic central cord syndrome, there is only class III evidence based on retrospective studies suggesting superiority of surgical decompression over conservative management (Dahdaleh 2013). There is no class I or II evidence examining the efficacy or timing of surgical decompression in TCCS. Therefore, early clinical diagnosis of spinal cord injury and characterization of its severity is crucial when

Role of Decompressive Surgery in Disorders Associated with Spinal Cord Lesions

http://dx.doi.org/10.5772/58408

81

considering surgical management to optimize the potential for neurologic recovery.

halo orthoses.

Furthermore, classification of cervical spine fractures may assist in surgical-decision making. Cervical spinal fractures or dislocations may or may not be accompanied by spinal cord injury or neurologic deficits such as paraplegia. In either case, reduction of these injuries can be achieved by closed reduction techniques including tong and halo traction, followed by restoration of spinal stability (if compromised). The latter is accomplished via surgical stabilization or external orthosis, such as various cervical collars, cervicothoracic braces and

Cervical spine fractures are generally classified into fractures of the atlas, axis and fractures of the subaxial cervical vertebrae. Fractures of the atlas and axis rarely present with neurologic deficits (Sonntag 1988;Crockard 1993; Sonntag 1988), and therefore their discussion is out of the scope of this chapter. On the other hand, fractures of cervical spine below the level of the atlas and axis are relatively common and more frequently involved in decompressive spinal surgery; they affect C5 and C6 vertebrae accounting, respectively, for 40% and 36% of cervical spine fractures in one review (Benzel 1987). The morphology of these fractures is crucial in determining the course of management and likelihood of neurologic compromise, and includes compression, burst, teardrop fractures and facet dislocation injuries. The Subaxial Injury Classification (SLIC) and Severity Scale is recommended as a valid and useful tool to guide surgical management. It describes the morphological, ligamentous and clinical neuro‐ logical parameters associated with cervical spine injury (Table 1) (Anderson 2007; Vaccaro 2007). The overall inter-rater reliability has a correlation coefficient of 0.71. Clinical guidelines for acute cervical spine injuries published recommendations based on class I evidence to utilize

#### **3.4. Surgical indications**

The goals of surgery in the context of cervical spinal cord injury are to facilitate neurologic recovery and prevent further injury to the neural elements and to restore spinal stability. This is achieved via anterior, posterior or combined surgical approaches focused at decompression of the neural elements and surgical arthrodesis in patients with a mechanically unstable spine in order to provide immediate stabilization and early mobilization as well as preventing further spinal deformity and pain. Therefore, the presence of clinical evidence of cervical cord injury as well as spinal instability represents surgical indications for decompressive and stabilization surgery. In patients with complete cervical cord injury, the primary goal of surgery is to restore spinal stability due to the low likelihood of neurologic recovery given the severity of cord injury. On the other hand, patients with incomplete cervical cord injury and evidence of compromise of the spinal canal should undergo surgical decompression and stabilization in order to aid neurologic recovery. Class II evidence based on the Surgical Timing in Acute Spinal Cord Injury Study (STASCIS) suggests improvement of neurologic function particularly when early surgery (within 24 hours) was instituted. In this prospective, multi‐ centre cohort study of 313 patients with acute cervical SCI, the authors found that about 20% of patients treated early showed 2 or more AIS grade improvements, compared to 9% in the late surgery group at 6 months follow-up (OR=2.6, 95% CI:1.1-6.0). However, in the context of other subgroups of incomplete cervical SCI, such as traumatic central cord syndrome, there is only class III evidence based on retrospective studies suggesting superiority of surgical decompression over conservative management (Dahdaleh 2013). There is no class I or II evidence examining the efficacy or timing of surgical decompression in TCCS. Therefore, early clinical diagnosis of spinal cord injury and characterization of its severity is crucial when considering surgical management to optimize the potential for neurologic recovery.

cantly higher rate of infections at the surgical site with mortality being three-folds higher in the high-dose MP treatment group. The second NASCIS trial was published in 1990 with 487 patients with acute SCI randomized into to MP, naloxone and placebo groups (Bracken 1990, 1991 and 1992). No difference in primary neurologic utcomes was observed. However, posthoc subanalysis demonstrated mean improvement of 5 points in the ASIA motor score and mean improvement of 4 points in the ASIA sensory score in the MP group compared to controls at 6 months. However, this treatment effect was only realized when treatment was adminis‐ tered within 8 hours of injury, excluding 291 patients who were treated outside this time window. Furthermore, complications such as gastrointestinal hemorrhage, wound infections and pulmonary embolism occured more frequently in patients treated with MP. NASCIS II has been downgraded by some to level III evidence indicating weak positive evidence supporting MP use. This is due to the inconsistency of claimed benefits, lack of functional outcome assessments, the arbitary nature of the eight-hour cut-off time and the high rate of patient exclusion in the subanalysis. NASCIS II provided class I evidence demonstrating harmful adverse effects of steroid use. In NASCIS III, 16 centers in the United States and Canada were enrolled in a prospective double-blinded study including 499 patients presenting with acute SCI within 8 hours randomized into treatment with MP IV infusion for 24 hours (n=166), MP IV infusion for 48 hours (n=166) and tirilazad treatment for 48 hours (n=167) which is a chemically engineered ''super-steroid'' (Bracken 1997 and 1998). Because of the reported positive effect of steroids in NASCIS II, all three groups patients received a loading dose of MP prior to randomization and no placebo-controlled group was included. The study failed to demonstrate a significant difference in neurologic outcome between the three treatment groups at one year (P=0.053), providing class I evidence lacking positive effect of steroid use in acute SCI even when initiated within 8 hours of injury. Of note, there was a transient 5 and 6 ASIA motor score improvements in the 48-hour MP treatment group compared to the 24 hour MP group at 6 weeks (P=0.04) and 6 months (p=0.01), respectively. Similar to NASCIS I and II, there was a trend towards serious complications associated with steroid use in NASCIS III reporting a consistent pattern of adverse effects. Furthermore, a French investigator group published the fourth prospective randomized trial investigating the use of steroids in acute SCI (Pointillart 2000). In this study, 106 patients were randomized into treatment with MP, nimodipine, MP+nimodipine and no pharmacological treatment. The authors demonstrated no significant difference in neurologic recovery between the treatment groups. Therefore, current clinical practice guidelines are not in favor of administering IV steroids even during the early stage of acute SCI due to the higher incidence of adverse effects and lack of clear clinical benefit (Hurlbert 2013). As a result a number of professional organizations in North America have relegated steroid use following spinal cord injury to a weak treatment option

The goals of surgery in the context of cervical spinal cord injury are to facilitate neurologic recovery and prevent further injury to the neural elements and to restore spinal stability. This

only.

80 Topics in Paraplegia

**3.4. Surgical indications**

Furthermore, classification of cervical spine fractures may assist in surgical-decision making. Cervical spinal fractures or dislocations may or may not be accompanied by spinal cord injury or neurologic deficits such as paraplegia. In either case, reduction of these injuries can be achieved by closed reduction techniques including tong and halo traction, followed by restoration of spinal stability (if compromised). The latter is accomplished via surgical stabilization or external orthosis, such as various cervical collars, cervicothoracic braces and halo orthoses.

Cervical spine fractures are generally classified into fractures of the atlas, axis and fractures of the subaxial cervical vertebrae. Fractures of the atlas and axis rarely present with neurologic deficits (Sonntag 1988;Crockard 1993; Sonntag 1988), and therefore their discussion is out of the scope of this chapter. On the other hand, fractures of cervical spine below the level of the atlas and axis are relatively common and more frequently involved in decompressive spinal surgery; they affect C5 and C6 vertebrae accounting, respectively, for 40% and 36% of cervical spine fractures in one review (Benzel 1987). The morphology of these fractures is crucial in determining the course of management and likelihood of neurologic compromise, and includes compression, burst, teardrop fractures and facet dislocation injuries. The Subaxial Injury Classification (SLIC) and Severity Scale is recommended as a valid and useful tool to guide surgical management. It describes the morphological, ligamentous and clinical neuro‐ logical parameters associated with cervical spine injury (Table 1) (Anderson 2007; Vaccaro 2007). The overall inter-rater reliability has a correlation coefficient of 0.71. Clinical guidelines for acute cervical spine injuries published recommendations based on class I evidence to utilize SLIC as a clinical and radiographic tool to assess and communicate information regarding spinal cord injury (Arabi 2013). SLIC scores of 1 to 3 suggest non-operative management, whereas scores 5 and above are suggestive of surgical management. A SLIC score of 4 represents indeterminate management when clinical judgment of the surgeon plays an important rule in deciding between operative and non-operative managements.

dislocation associated with traumatic disc herniation. On the other hand, patients sustaining spinal cord injury in the context of unilateral or bilateral facet dislocation and no evidence of traumatic disc herniation, there is no evidence favoring one approach over another. However, an informed decision could be made based on patient's preferences in terms of the different risk profiles of both surgical approaches which include mainly dysphagia and hoarseness of voice and risk of injury to visceral organs such as the trachea and esophagus in anteriorly treated patients, versus local wound infection and post-operative pain with posterior ap‐ proaches. The advantage of a posterior approach is increased surgeon's familiarity (Dvorak 2007). Should a posterior approach be employed, open reduction with complete resection of ligamentum flavum and lateral mass fixation and fusion are achieved. Of note, some degrees of post-surgical kyphosis are identified in patients treated with posterior fixation, which is thought to result from intervertebral disc injury and progressive collapse. Although the longterm clinical effects of this finding is yet to be evaluated, pre-operative sagittal alignment of the spinal column in patients with facet injuries should be noted prior to undergoing anterior

Role of Decompressive Surgery in Disorders Associated with Spinal Cord Lesions

http://dx.doi.org/10.5772/58408

83

Anterior surgical decompression and stabilization can be utilized even in cases with posterior spinal instability as demonstrated above in the context of unilateral facet injury. Furthermore, burst fractures are associated with disruption of two columns and retropulsion of bone fragments into the cervical canal, rendering spinal cord injury common. The mechanism of injury is largely the result of axial compression forces. Post-traumatic syringomyelia may ensue in patients with persistent canal compression and impairment of CSF circulation. The presence of posterior column failure and neurologic deficits specific to neurologic injury at the level of the burst fracture necessitates surgical decompression and stabilization. An anterior surgical approach with corpectomy or cage fitting and plate fixation is suggested by one retrospective investigation favoring anterior rather than posterior approaches with better decompression and better neurologic recovery and mechanical reconstitution of the motion

Teardrop fractures represent about 5% of cervical spine fractures and result from flexion compression injury, which is commonly seen in injuries associated with diving into shallow waters (Gehweiler 1979; Torg 1991). They represent chip fractures commonly affecting the anterior-inferior aspect of the vertebral body. The severity of injury varies considerably with the most severe injuries seen in the context of a coronal split through the anterior aspect of the vertebral body with dislocation of the other part of the vertebral body posteriorly into the spinal canal (Schneider 1956). Surgical management is indicated in these fractures due to their high likelihood of spinal instability and neurologic injury. Other surgical indications include posterior column failure suggested by distraction and dislocation of the facet joint(s) with or without increased interlaminar distance (Allen 1982). Fisher and Leith et al. (2002) published retrospective data showing greater degrees of improved sagittal alignment with lower rate of treatment failures when patients are treated surgically via anterior cervical plating. However,

or posterior stabilization (Lifeso 2000; Elgafy 2006).

*3.4.3. Anterior surgical approaches*

segments (Toh 2006; Lanuzzi 2006).

#### *3.4.1. Surgical approaches*

The determination of the surgical approach (anterior, posterior or combined) is influenced by the type of spinal cord injury, the mechanism of injury and the location of spinal cord com‐ pression in the anterior-posterior dimension of the cervical canal.

#### *3.4.2. Posterior surgical approaches*

In patients with flexion-type injuries to the subaxial cervical spine, the preferred surgical approach is posterior decompression and fusion. The rationale behind this surgical plan is restoring spinal stability and decompressing the spinal cord at the direction of main tissue disruption. The indications for posterior approaches include the presence of posterior liga‐ mentous injury, facet dislocation and traumatic subluxation (Dvorak 2007). The integrity of the anterior column has to be preserved and there should be no evidence of anterior spinal cord compression, otherwise, a combined anterior-posterior approach should be considered.

Facet dislocation may occur unilaterally in association with flexion-rotation injury, or bilater‐ ally in the context of hyperflexion injury indicating increased instability due to the disruption of the posterior ligamentous complex. A quarter of patients with unilateral dislocated facet are neurologically intact, with more than one-third manifesting with nerve root injuries and onethird with either complete or incomplete injuries (Andreshak 1997). On the other hand, bilateral facet dislocation is associated with a high rate of spinal cord injury and, hence, surgical reduction and stabilization with or without decompression may be indicated. For instance, in a retrospective review of 68 patients with facet fracture-dislocation injuries 68% of patients with bilateral facet dislocation were found to have complete spinal cord injuries, with ≤ 10 patients being neurologically intact (Hadley 1992). Since more than two-third of patients with unilateral or bilateral facet dislocations demonstrate evidence of poor anatomic alignment, surgical stabilization is indicated (Sears 1990). Despite that facet injuries result from flexiontype trauma, up to at least 50% of patients with facet dislocation injuries demonstrate evidence of disco-ligamentous injury with traumatic disc herniation in pre-reduction MRI. Although class I prospective, randomized evidence has demonstrated that surgical stabilization with anterior discectomy and fusion compared to posterior fixation is equally viable treatment option for unilateral facet dislocation injuries (Kwon 2007), the presence of traumatic disc herniation influences the choice of surgical approach. An anterior approach is favored in this context because of direct decompression of the anterior aspect of spinal canal and subsequent restoration of spinal stability by closed reduction and anterior bone graft placement and plate fixation (Lanuzzi 2006; Razack 2000). The risk profile of this approach in this clinical situation includes incomplete reduction intra-operatively and possible posterior ligament in folding. Therefore, tight and full reduction must be ensured prior to anterior fixation in cases with facet dislocation associated with traumatic disc herniation. On the other hand, patients sustaining spinal cord injury in the context of unilateral or bilateral facet dislocation and no evidence of traumatic disc herniation, there is no evidence favoring one approach over another. However, an informed decision could be made based on patient's preferences in terms of the different risk profiles of both surgical approaches which include mainly dysphagia and hoarseness of voice and risk of injury to visceral organs such as the trachea and esophagus in anteriorly treated patients, versus local wound infection and post-operative pain with posterior ap‐ proaches. The advantage of a posterior approach is increased surgeon's familiarity (Dvorak 2007). Should a posterior approach be employed, open reduction with complete resection of ligamentum flavum and lateral mass fixation and fusion are achieved. Of note, some degrees of post-surgical kyphosis are identified in patients treated with posterior fixation, which is thought to result from intervertebral disc injury and progressive collapse. Although the longterm clinical effects of this finding is yet to be evaluated, pre-operative sagittal alignment of the spinal column in patients with facet injuries should be noted prior to undergoing anterior or posterior stabilization (Lifeso 2000; Elgafy 2006).

#### *3.4.3. Anterior surgical approaches*

SLIC as a clinical and radiographic tool to assess and communicate information regarding spinal cord injury (Arabi 2013). SLIC scores of 1 to 3 suggest non-operative management, whereas scores 5 and above are suggestive of surgical management. A SLIC score of 4 represents indeterminate management when clinical judgment of the surgeon plays an

The determination of the surgical approach (anterior, posterior or combined) is influenced by the type of spinal cord injury, the mechanism of injury and the location of spinal cord com‐

In patients with flexion-type injuries to the subaxial cervical spine, the preferred surgical approach is posterior decompression and fusion. The rationale behind this surgical plan is restoring spinal stability and decompressing the spinal cord at the direction of main tissue disruption. The indications for posterior approaches include the presence of posterior liga‐ mentous injury, facet dislocation and traumatic subluxation (Dvorak 2007). The integrity of the anterior column has to be preserved and there should be no evidence of anterior spinal cord compression, otherwise, a combined anterior-posterior approach should be considered.

Facet dislocation may occur unilaterally in association with flexion-rotation injury, or bilater‐ ally in the context of hyperflexion injury indicating increased instability due to the disruption of the posterior ligamentous complex. A quarter of patients with unilateral dislocated facet are neurologically intact, with more than one-third manifesting with nerve root injuries and onethird with either complete or incomplete injuries (Andreshak 1997). On the other hand, bilateral facet dislocation is associated with a high rate of spinal cord injury and, hence, surgical reduction and stabilization with or without decompression may be indicated. For instance, in a retrospective review of 68 patients with facet fracture-dislocation injuries 68% of patients with bilateral facet dislocation were found to have complete spinal cord injuries, with ≤ 10 patients being neurologically intact (Hadley 1992). Since more than two-third of patients with unilateral or bilateral facet dislocations demonstrate evidence of poor anatomic alignment, surgical stabilization is indicated (Sears 1990). Despite that facet injuries result from flexiontype trauma, up to at least 50% of patients with facet dislocation injuries demonstrate evidence of disco-ligamentous injury with traumatic disc herniation in pre-reduction MRI. Although class I prospective, randomized evidence has demonstrated that surgical stabilization with anterior discectomy and fusion compared to posterior fixation is equally viable treatment option for unilateral facet dislocation injuries (Kwon 2007), the presence of traumatic disc herniation influences the choice of surgical approach. An anterior approach is favored in this context because of direct decompression of the anterior aspect of spinal canal and subsequent restoration of spinal stability by closed reduction and anterior bone graft placement and plate fixation (Lanuzzi 2006; Razack 2000). The risk profile of this approach in this clinical situation includes incomplete reduction intra-operatively and possible posterior ligament in folding. Therefore, tight and full reduction must be ensured prior to anterior fixation in cases with facet

important rule in deciding between operative and non-operative managements.

pression in the anterior-posterior dimension of the cervical canal.

*3.4.1. Surgical approaches*

82 Topics in Paraplegia

*3.4.2. Posterior surgical approaches*

Anterior surgical decompression and stabilization can be utilized even in cases with posterior spinal instability as demonstrated above in the context of unilateral facet injury. Furthermore, burst fractures are associated with disruption of two columns and retropulsion of bone fragments into the cervical canal, rendering spinal cord injury common. The mechanism of injury is largely the result of axial compression forces. Post-traumatic syringomyelia may ensue in patients with persistent canal compression and impairment of CSF circulation. The presence of posterior column failure and neurologic deficits specific to neurologic injury at the level of the burst fracture necessitates surgical decompression and stabilization. An anterior surgical approach with corpectomy or cage fitting and plate fixation is suggested by one retrospective investigation favoring anterior rather than posterior approaches with better decompression and better neurologic recovery and mechanical reconstitution of the motion segments (Toh 2006; Lanuzzi 2006).

Teardrop fractures represent about 5% of cervical spine fractures and result from flexion compression injury, which is commonly seen in injuries associated with diving into shallow waters (Gehweiler 1979; Torg 1991). They represent chip fractures commonly affecting the anterior-inferior aspect of the vertebral body. The severity of injury varies considerably with the most severe injuries seen in the context of a coronal split through the anterior aspect of the vertebral body with dislocation of the other part of the vertebral body posteriorly into the spinal canal (Schneider 1956). Surgical management is indicated in these fractures due to their high likelihood of spinal instability and neurologic injury. Other surgical indications include posterior column failure suggested by distraction and dislocation of the facet joint(s) with or without increased interlaminar distance (Allen 1982). Fisher and Leith et al. (2002) published retrospective data showing greater degrees of improved sagittal alignment with lower rate of treatment failures when patients are treated surgically via anterior cervical plating. However, a combined anterior and posterior approach has been recommended in cases with severe bony and ligamentous injury (Toh 2006; Cybulski 1992).

usually occurs in a younger group of patients and results from acute cervical disc herniation in association with cytokine-mediated inflammatory demyelinating effect on the large-fiber axons leading to motor deficits in the first week (Yoshizawa 1995). In contrast, chronic radiculopathy is associated with osteophyte formation, annulus wear and tear, laxity and

Role of Decompressive Surgery in Disorders Associated with Spinal Cord Lesions

http://dx.doi.org/10.5772/58408

85

Spinal cord injury or myelopathy in the context of degenerative cervical disease occurs in relation to static, dynamic and ischemic factors (Dadashev 2011). Static factors include the spondylotic process through which narrowing of the cervical canal occurs, as described above. The normal diameter of the cervical canal is about 17-18 mm wide, with significant cervical canal stenosis considered to be less than 13 mm (Yue 2001). Dynamic factors result in episodic compression of the spinal cord with flexion being association with ventral cord compression against osteophytes and with extension causing dorsal cord compression secondary to ligamentous hypertrophy. Finally, an ischemic process ensues as being evidenced from pathological changes within both gray and white mater undergoing ischemic changes. It is postulated that spinal cord compression secondary to cervical stenosis restricts pial and intramedullary arterioles as well as causing venous engorgement leading to infarction. In

The natural history of CSM is variable and differs across cases, making prediction of the clinical course very challenging. On the other hand, selection of cases and the indication for surgery can be guided by the extent of clinical severity (Matz 2009). Kadanka and colleagues et al. (2000) conducted a prospective trial of 48 patients with mild CSM (mJOA scale score >12), randomized to surgery (n=21) or non-operative treatment (n=27). The modified Japanese Orthopedic Association (mJOA) scale score is a grading system used for myelopathy, with mJOA scale score > 12 used to define mild CSM. Both groups in that study improved equally on the mJOA scale score, 10-minute walk test and activity-dependent livings at 2 years followup. Similarly, the same authors randomized a larger sample of 64 patients to surgical or conservative treatment groups, demonstrating no significant difference in neurologic recovery at a longer follow-up period of 3 years (Kadanka 2005). At much longer follow-up of 10 years, the authors presented results on 25 patients treated conservatively, compared to 22 patients treated surgically with no difference in improvement (Kadanka 2011). However, this study is limited with a small sample size and its power analysis showed reduced statistical capacity to detect smaller differences between the two groups. Based on these findings (Class II evidence), clinical guidelines and a systematic review of the literature suggested that both operative and non-operative management options may be offered in the treatment of mild CSM (defined as mJAO scale score > 12) in the short term (3 years) (Mummaneni 2009). Non-operative strategies include prolonged immobilization in a stiff cervical collar, ''low-risk'' activity modification or bed rest, and anti-inflammatory analgesia. Furthermore, Bednarik et al. (1999) and Wada et al. (2001) prospectively followed patients with moderate to severe CSM (mJOA scale score < 12) postoperatively at 2 years and 5-15 years, respectively, demonstrating neurologic improve‐ ment. However, a non-operative comparison group was lacking, thereby conferring Class III

peeling of the ligamentous structures with facet hypertrophy.

severe and chronic cases, formation of a syringomyelia can also occur.

**4.2. Surgical management**

#### **4. Cervical spondylotic myelopathy**

Cervical spondylosis refers to a chronic degenerative process that affects the disco-ligamentous structures of the cervical spine leading to symptoms related to compression of the spinal cord (myelopathy) or nerve roots (radiculopathy). The progressive nature of the disease process warrants timely operative intervention in order to prevent motor paralysis and autonomic dysfunction related to severe myeloradiculopathy. Cervical spondylotic myelopathy (CSM) is the most common cause of myelopathy in elderly patients, and is associated with significant morbidity in its moderate and severe forms. Although some of the surgical approaches for the treatment of both is similar, the goal of surgery for cervical myelopathy differs in that it aims to provide decompression of the spinal cord to halt the progression of myelopathy, and to stabilize the spine and reinstate its alignment. In addition, the natural history of both disorders is different, with myelopathy being largely a progressive disease, interrupted by long periods of plateauing (Lees 1963; Nurick 1972). On the other hand, a certain degree of myelopathy and radiculopathy may co-exist warranting treatment of both.

#### **4.1. Pathophysiology**

Cervical spondylopathy results in loss of the intervertebral disc height secondary to noninflammatory disc degeneration associated with a "wear-and-tear" process and, in some cases, repetitive trauma. Other accompanying changes include hypertrophy of the facet/zygopo‐ physeal joint and hypertrophy of the posterior longitudinal ligament and ligamentum flavum causing ligamentous laxity and buckling into the cervical canal. Loss of the hydrophilic proteoglycan content of the intervertebral disc occurs as aging advances. This results in loss of the disc height and reduces its ability as a shock absorber, which in turn shifts axial loading force into the annulus fibrosis at the outer periphery of the disc. Eventually, the annulus undergoes wear and tear associated with thinning and weakening of the outer fibers of the annulus that provide anchoring to the bony matrix of the outer periphery of the vertebral body. This part of the annulus is named Sharpey's fibers. Their weakness is associated with formation of osteophytes due to reactive bony growth. Protrusion of the nucleus content of the disc through the strained and weakened annulus occurs, acutely. The process of disc herniation and osteophyte formation has a knock-on effect on the posterior longitudinal ligament causing ligamentous hypertrophy and ossification.

Mechanical pain symptoms have been postulated to originate from degenerative cervical disc and facet joints, based on the finding of rich innervations occurring in these structures (Ahn 2007; Dwyer 1990; Bogduk 2003). It is thought that a tear through the annulus fibrosis is sufficient to cause axial neck pain through afferent sensory fibers.

Pain related to acute or chronic radiculopathy is distinctively different from axial neck pain in that it follows the dermatomal distribution of the affected nerve root. Acute radiculopathy usually occurs in a younger group of patients and results from acute cervical disc herniation in association with cytokine-mediated inflammatory demyelinating effect on the large-fiber axons leading to motor deficits in the first week (Yoshizawa 1995). In contrast, chronic radiculopathy is associated with osteophyte formation, annulus wear and tear, laxity and peeling of the ligamentous structures with facet hypertrophy.

Spinal cord injury or myelopathy in the context of degenerative cervical disease occurs in relation to static, dynamic and ischemic factors (Dadashev 2011). Static factors include the spondylotic process through which narrowing of the cervical canal occurs, as described above. The normal diameter of the cervical canal is about 17-18 mm wide, with significant cervical canal stenosis considered to be less than 13 mm (Yue 2001). Dynamic factors result in episodic compression of the spinal cord with flexion being association with ventral cord compression against osteophytes and with extension causing dorsal cord compression secondary to ligamentous hypertrophy. Finally, an ischemic process ensues as being evidenced from pathological changes within both gray and white mater undergoing ischemic changes. It is postulated that spinal cord compression secondary to cervical stenosis restricts pial and intramedullary arterioles as well as causing venous engorgement leading to infarction. In severe and chronic cases, formation of a syringomyelia can also occur.

#### **4.2. Surgical management**

a combined anterior and posterior approach has been recommended in cases with severe bony

Cervical spondylosis refers to a chronic degenerative process that affects the disco-ligamentous structures of the cervical spine leading to symptoms related to compression of the spinal cord (myelopathy) or nerve roots (radiculopathy). The progressive nature of the disease process warrants timely operative intervention in order to prevent motor paralysis and autonomic dysfunction related to severe myeloradiculopathy. Cervical spondylotic myelopathy (CSM) is the most common cause of myelopathy in elderly patients, and is associated with significant morbidity in its moderate and severe forms. Although some of the surgical approaches for the treatment of both is similar, the goal of surgery for cervical myelopathy differs in that it aims to provide decompression of the spinal cord to halt the progression of myelopathy, and to stabilize the spine and reinstate its alignment. In addition, the natural history of both disorders is different, with myelopathy being largely a progressive disease, interrupted by long periods of plateauing (Lees 1963; Nurick 1972). On the other hand, a certain degree of myelopathy and

Cervical spondylopathy results in loss of the intervertebral disc height secondary to noninflammatory disc degeneration associated with a "wear-and-tear" process and, in some cases, repetitive trauma. Other accompanying changes include hypertrophy of the facet/zygopo‐ physeal joint and hypertrophy of the posterior longitudinal ligament and ligamentum flavum causing ligamentous laxity and buckling into the cervical canal. Loss of the hydrophilic proteoglycan content of the intervertebral disc occurs as aging advances. This results in loss of the disc height and reduces its ability as a shock absorber, which in turn shifts axial loading force into the annulus fibrosis at the outer periphery of the disc. Eventually, the annulus undergoes wear and tear associated with thinning and weakening of the outer fibers of the annulus that provide anchoring to the bony matrix of the outer periphery of the vertebral body. This part of the annulus is named Sharpey's fibers. Their weakness is associated with formation of osteophytes due to reactive bony growth. Protrusion of the nucleus content of the disc through the strained and weakened annulus occurs, acutely. The process of disc herniation and osteophyte formation has a knock-on effect on the posterior longitudinal ligament causing

Mechanical pain symptoms have been postulated to originate from degenerative cervical disc and facet joints, based on the finding of rich innervations occurring in these structures (Ahn 2007; Dwyer 1990; Bogduk 2003). It is thought that a tear through the annulus fibrosis is

Pain related to acute or chronic radiculopathy is distinctively different from axial neck pain in that it follows the dermatomal distribution of the affected nerve root. Acute radiculopathy

and ligamentous injury (Toh 2006; Cybulski 1992).

radiculopathy may co-exist warranting treatment of both.

ligamentous hypertrophy and ossification.

sufficient to cause axial neck pain through afferent sensory fibers.

**4.1. Pathophysiology**

84 Topics in Paraplegia

**4. Cervical spondylotic myelopathy**

The natural history of CSM is variable and differs across cases, making prediction of the clinical course very challenging. On the other hand, selection of cases and the indication for surgery can be guided by the extent of clinical severity (Matz 2009). Kadanka and colleagues et al. (2000) conducted a prospective trial of 48 patients with mild CSM (mJOA scale score >12), randomized to surgery (n=21) or non-operative treatment (n=27). The modified Japanese Orthopedic Association (mJOA) scale score is a grading system used for myelopathy, with mJOA scale score > 12 used to define mild CSM. Both groups in that study improved equally on the mJOA scale score, 10-minute walk test and activity-dependent livings at 2 years followup. Similarly, the same authors randomized a larger sample of 64 patients to surgical or conservative treatment groups, demonstrating no significant difference in neurologic recovery at a longer follow-up period of 3 years (Kadanka 2005). At much longer follow-up of 10 years, the authors presented results on 25 patients treated conservatively, compared to 22 patients treated surgically with no difference in improvement (Kadanka 2011). However, this study is limited with a small sample size and its power analysis showed reduced statistical capacity to detect smaller differences between the two groups. Based on these findings (Class II evidence), clinical guidelines and a systematic review of the literature suggested that both operative and non-operative management options may be offered in the treatment of mild CSM (defined as mJAO scale score > 12) in the short term (3 years) (Mummaneni 2009). Non-operative strategies include prolonged immobilization in a stiff cervical collar, ''low-risk'' activity modification or bed rest, and anti-inflammatory analgesia. Furthermore, Bednarik et al. (1999) and Wada et al. (2001) prospectively followed patients with moderate to severe CSM (mJOA scale score < 12) postoperatively at 2 years and 5-15 years, respectively, demonstrating neurologic improve‐ ment. However, a non-operative comparison group was lacking, thereby conferring Class III evidence for the operative management of moderate to severe CSM (Matz 2009). On the other hand, patients with severely progressive CSM were observed to demonstrate low likelihood of spontaneous partial remission or cessation of progression of CSM (Clarke and Robinson 1956).

al. (2001) revealed similar rates of neurologic improvement as represented by improved Nurick scores of 0.84 in the laminectomy group compared to 1.24 in the group treated with laminec‐ tomy and fusion, at 3.3 years follow-up. However, the authors also noted increased incidence of postoperative kyphotic deformity in the laminectomy alone group (24%), compared to 7% in the fusion group. This holds true in reviews of cases with CSM treated with laminectomy and fusion demonstrating very low or zero rate of swan neck deformity post-operatively (Kumar 1999;Houten 2003), whereas cases treated with laminectomy are predisposed to develop late deformity as well as destabilization which requires repeat surgery (Guigui 1998; Sim 1974; Mastunagna 1999). Therefore, laminectomy with fusion is recommended over laminectomy alone especially in young patients, or in cases associated with risk of spinal

Role of Decompressive Surgery in Disorders Associated with Spinal Cord Lesions

http://dx.doi.org/10.5772/58408

87

Laminoplasty has been used with comparable results to laminectomy with fusion in terms of improved neurologic recovery in the treatment of CSM (Class III; recommendation D) (Mummaneni 2009). In patients with CSM or ossification of the posterior longitudinal liga‐ ment, Heller et al. (2001) retrospectively compared laminectomy with fusion (13 patients) and laminoplasty (13 patients). The authors noted statistically non-significant greater improve‐ ment in Nurick scores in the laminoplasty group (from 2.2 to 1.1) compared to the laminectomy with fusion group (from 2.2 to 1.5). However, the range of cervical movement was retained in the laminoplasty group compared to laminectomy with fusion (P<0.002). In addition, a significantly greater complication rate was reported in the latter group with development of hardware failure in 2, neurologic deterioration in 2, pseudoarthrosis in 5 and deep infection in one case. No complications were noted in the laminoplasty group. The difference in complication rate is subject to criticism in relation to probable selection bias associated with selection of matched controls in whom fusion is more likely due to kyphosis, thereby rendering this study Class III evidence (Mummaneni 2009). In addition, two retrospective reviews of laminectomy with fusion found favorable neurologic recovery (improved neurologic outcome or no deterioration) and zero or low rate of complication associated with this approach (Houten 2003; Huang 2003). Therefore, no recommendation was made of laminoplasty over laminec‐ tomy with fusion in terms of improved neurologic recovery in evidence-based published

Anterior surgical approaches for decompression of the cervical spine in CSM include anterior cervical discectomy with fusion (ACDF) and anterior cervical corpectomy with fusion (ACCF). Based on class III evidence, patients with CSM have been shown to respond to multilevel anterior cervical spine decompression, however, with varying proportions of complications associated with each technique (Mummaneni 2009; Cunningham 2011). In a retrospective study by Nirala et al. (2004), 201 patients underwent multilevel anterior cervical spine decompression with fusion (autograft) and without anterior plate fixation. Patients were subdivided into ACDF (n=69) and ACCF (n=132), with the functional outcome was assessed using Odom's criteria, whereas dynamic plain films were used to assess radiographic out‐ comes. Patients wore a hard cervical collar for 3 months postoperatively. After 10 years, the fusion rate was higher in the ACCF group (94%) compared to the ACDF group (69.6%) (P< 0.001). There was no statistically significant difference in the functional outcome between the

instability (Class III; strength of recommendation D) (Mummaneni 2009).

guidelines.

In addition to the severity of CSM, surgical treatment < 1 year from the onset of CSM is associated with improved neurologic outcome, compared to patients treated within 1-2 years or > 3 years (Phillips 1973). Early treatment within one year was found to be a predictor of good prognosis in one systematic review (Tetreault 2013). Similarly, the severity of baseline myelopathic changes correlates with the prognosis postoperatively suggesting reduced likelihood of reversibility of myelopathy in its severe stage. It is not entirely clear whether the progression of severe disease could be significantly halted by surgical decompression.

#### **4.3. Surgical approaches**

The surgical approach for the treatment of CSM is broadly categorized into anterior and posterior approaches. The superiority of any one approach over another in terms of the rate of neurologic recovery has been the subject of debate for a few decades. Furthermore, all upto-date evidence demonstrated comparable neurologic recovery between the different anterior and posterior surgical approaches, although the risk profiles of these approaches are different as being shown by two systematic reviews of the literature (Mummaneni 2009; Cunningham 2010). Unfortunately, current studies suffer many methodological flaws associated with bias and the presence of confounding factors. Nonetheless, in order to select the optimal approach for the patient with CSM, knowledge of the advantages and disadvantages of each technique is pre-requisite for informed and rationale surgical decision-making (Table 2).


**Table 2.** Summary of the advantages and disadvantages of anterior and posterior approaches for CSM. Adapted from Dadashev et al. (2011)

Options for posterior surgical approaches for the treatment of CSM encompass laminectomy without fusion, laminectomy with lateral mass fusion and laminoplasty. In comparing laminectomy alone with laminectomy with fusion, the retrospective review by Perez-Lopez et al. (2001) revealed similar rates of neurologic improvement as represented by improved Nurick scores of 0.84 in the laminectomy group compared to 1.24 in the group treated with laminec‐ tomy and fusion, at 3.3 years follow-up. However, the authors also noted increased incidence of postoperative kyphotic deformity in the laminectomy alone group (24%), compared to 7% in the fusion group. This holds true in reviews of cases with CSM treated with laminectomy and fusion demonstrating very low or zero rate of swan neck deformity post-operatively (Kumar 1999;Houten 2003), whereas cases treated with laminectomy are predisposed to develop late deformity as well as destabilization which requires repeat surgery (Guigui 1998; Sim 1974; Mastunagna 1999). Therefore, laminectomy with fusion is recommended over laminectomy alone especially in young patients, or in cases associated with risk of spinal instability (Class III; strength of recommendation D) (Mummaneni 2009).

evidence for the operative management of moderate to severe CSM (Matz 2009). On the other hand, patients with severely progressive CSM were observed to demonstrate low likelihood of spontaneous partial remission or cessation of progression of CSM (Clarke and Robinson

In addition to the severity of CSM, surgical treatment < 1 year from the onset of CSM is associated with improved neurologic outcome, compared to patients treated within 1-2 years or > 3 years (Phillips 1973). Early treatment within one year was found to be a predictor of good prognosis in one systematic review (Tetreault 2013). Similarly, the severity of baseline myelopathic changes correlates with the prognosis postoperatively suggesting reduced likelihood of reversibility of myelopathy in its severe stage. It is not entirely clear whether the progression of severe disease could be significantly halted by surgical decompression.

The surgical approach for the treatment of CSM is broadly categorized into anterior and posterior approaches. The superiority of any one approach over another in terms of the rate of neurologic recovery has been the subject of debate for a few decades. Furthermore, all upto-date evidence demonstrated comparable neurologic recovery between the different anterior and posterior surgical approaches, although the risk profiles of these approaches are different as being shown by two systematic reviews of the literature (Mummaneni 2009; Cunningham 2010). Unfortunately, current studies suffer many methodological flaws associated with bias and the presence of confounding factors. Nonetheless, in order to select the optimal approach for the patient with CSM, knowledge of the advantages and disadvantages of each technique

*Advantages Disadvantages*

**Table 2.** Summary of the advantages and disadvantages of anterior and posterior approaches for CSM. Adapted from

Options for posterior surgical approaches for the treatment of CSM encompass laminectomy without fusion, laminectomy with lateral mass fusion and laminoplasty. In comparing laminectomy alone with laminectomy with fusion, the retrospective review by Perez-Lopez et

Technically challenging Graft complications Loss of motion

Adjacent segment disease

Inconsistent axial pain relief

Indirect decompression Postoperative kyphosis Instability limitations Late instability

is pre-requisite for informed and rationale surgical decision-making (Table 2).

Direct decompression Stabilization with arthrodesis Correction of deformity Good axial pain relief

Less loss of motion No graft complications Less technically demanding

1956).

86 Topics in Paraplegia

**4.3. Surgical approaches**

**Anterior approach**

**Posterior approach**

Dadashev et al. (2011)

Laminoplasty has been used with comparable results to laminectomy with fusion in terms of improved neurologic recovery in the treatment of CSM (Class III; recommendation D) (Mummaneni 2009). In patients with CSM or ossification of the posterior longitudinal liga‐ ment, Heller et al. (2001) retrospectively compared laminectomy with fusion (13 patients) and laminoplasty (13 patients). The authors noted statistically non-significant greater improve‐ ment in Nurick scores in the laminoplasty group (from 2.2 to 1.1) compared to the laminectomy with fusion group (from 2.2 to 1.5). However, the range of cervical movement was retained in the laminoplasty group compared to laminectomy with fusion (P<0.002). In addition, a significantly greater complication rate was reported in the latter group with development of hardware failure in 2, neurologic deterioration in 2, pseudoarthrosis in 5 and deep infection in one case. No complications were noted in the laminoplasty group. The difference in complication rate is subject to criticism in relation to probable selection bias associated with selection of matched controls in whom fusion is more likely due to kyphosis, thereby rendering this study Class III evidence (Mummaneni 2009). In addition, two retrospective reviews of laminectomy with fusion found favorable neurologic recovery (improved neurologic outcome or no deterioration) and zero or low rate of complication associated with this approach (Houten 2003; Huang 2003). Therefore, no recommendation was made of laminoplasty over laminec‐ tomy with fusion in terms of improved neurologic recovery in evidence-based published guidelines.

Anterior surgical approaches for decompression of the cervical spine in CSM include anterior cervical discectomy with fusion (ACDF) and anterior cervical corpectomy with fusion (ACCF). Based on class III evidence, patients with CSM have been shown to respond to multilevel anterior cervical spine decompression, however, with varying proportions of complications associated with each technique (Mummaneni 2009; Cunningham 2011). In a retrospective study by Nirala et al. (2004), 201 patients underwent multilevel anterior cervical spine decompression with fusion (autograft) and without anterior plate fixation. Patients were subdivided into ACDF (n=69) and ACCF (n=132), with the functional outcome was assessed using Odom's criteria, whereas dynamic plain films were used to assess radiographic out‐ comes. Patients wore a hard cervical collar for 3 months postoperatively. After 10 years, the fusion rate was higher in the ACCF group (94%) compared to the ACDF group (69.6%) (P< 0.001). There was no statistically significant difference in the functional outcome between the two groups. This study presents class III evidence favoring ACCF over ACDF when plate fixation is not used (Grade D recommendation). In contrast, anterior plate fixation in ACDF and ACCF is associated with equal fusion rates reported in one systematic review to reach greater than 90% (Fraser and Hartl 2007). However, in three-level disc disease, the fusion rate was significantly lower in the ACDF group (82.5%) compared to cases treated with ACCF (96%) (P=0.03). This systematic review represents class III evidence due to the lack of application of a standardized methodology for systematic reviews and to violating the inclusion and exclusion criteria. Therefore, a grade D recommendation underlies the utilization of either ACDF or ACCF with plate fixation in the treatment of multilevel anterior CSM.

and posterior compression of the cord resulting in significant progressive myelopathy, a combined anterior-posterior approach is recommended to ensure complete decompression.

Role of Decompressive Surgery in Disorders Associated with Spinal Cord Lesions

http://dx.doi.org/10.5772/58408

89

Cancer-related complications led to about half a million deaths in 2008, with annual newly detected cancer rate of about 1.4 million new cases (Sciubba 2010). Up to 70% of all cancer patients will develop metastasis, most commonly to the lungs and liver, followed by skeletal structures. The most common osseous site for metastasis is the spine, which occurs in 40% of all cancer patients (Aaron 1994;Black 1979; Zerick 1994). Of these patients with spinal meta‐ static disease, up to 20% will develop symptomatic epidural spinal cord compression, which accounts for 20,000 to 30,000 cases per year in the USA (Kwok 2006). Post-mortem studies showed that up to 90% of patients deceased with cancer were found to have evidence of spinal metastatic disease (Wong 1990; Cobb 1977). Up to half patients with spinal metastasis require treatment, with 5-10% being surgically treated (Bell 1997;Bilsky 2005; Walsh 1997; York 1999).

The incidence of metastatic spinal disease peaks at the age groups between 40-65 years (Perrin 1982). The most common primary tumors that metastasize to the spine are breast, lung, melanoma or prostate cancers, which correspond to the common occurrence of these primary malignancies (Constans 1983; Helweg-Larsen 1994). The rates of spinal metastases in prostate, breast, melanoma and lung cancers correspond to about 90%, 74%, 55% and 45%, respectively (Wong 1990). Of note, 10% of cases present clinically with spinal metastatic disease without previous history of known primary malignancy (Gerszten 2000), with 50% of these cases found

The most common region of the spine affected by metastatic disease is the thoracic spine, which corresponds to 70%, followed by the lumbar spine (20%) and cervical (10%) spine, (Gerszten 2000, Byme 1992; Gilbert 1978). Metastases occur extra-durally, with the intra-dural and intramedullary spaces being very rare metastatic targets representing up to about 8% of cases (Schijns 2000). The vertebral body is involved in more than 80% of cases with the posterior half being the initial site of invasive disease (Gerszten 2000). The reminder of cases often manifest

The routes of metastatic spread include hematogenous spread, which is the most common mechanism, manifest by metastases to the vertebral body occurring through hematogenous spread secondary to their rich blood supply (Arguello 1990), followed by direct invasion and spread through shedding of tumor cells in the CSF. Direct invasion to the sacral and lumbar spine were reported in the context of prostate cancer (Ross 2005). CSF seeding of tumor cells occurs following mobilization of intra-axial cranial malignancies, and may result in drop

**5. Metastatic spinal diseases**

to have primary lung malignancy (Stark 1982).

**5.2. Characteristics of spinal metastasis**

with paravertebral metastasis.

metastasis (Perrin 1982).

**5.1. Epidemiology**

Furthermore, the use of anterior plate fixation in ACDF and ACCF is associated with nonunion rates of 42% and 31%, respectively at about 3.3-year follow-up (Swank 1997). Of note, a major confounding factor is the increased use of dynamic plates in ACDF compared to constrained plates in ACCF with the latter being associated with higher fusion rates. Another study by Wang et al. (2001) failed to find a statistically significant difference in fusion rates between the two groups.

Early complications in ACDF include dysphagia (9.5%), neck hematoma (5.6%) with 2.4% of patients requiring surgery, recurrent laryngeal nerve palsy (3.1%), dural laceration (0.5%) and esophageal perforation (0.3%). The latter was associated with death in one patient (1 about 1000 patients). Less common complications include wound infection and Horner's syndrome. Late complications of ACDF include non-union and adjacent-segment disease. The presence for adjacent-segment disease was found to be associated with a plate-to-disc distance of < 5 mm. This complication is thought to occur at an annual rate up to 3% over 10 years. Further studies are required to elucidate the clinical nature of these changes. Furthermore, other factors that can affect the fusion rate include plate fixation and smoking (Bolesta 2000; Fraser and Hartl 2007).

To summarize, the location of spinal cord compression in relation to the anterior-posterior diameter of the cervical canal is a crucial factor influencing the direction of the surgical approach. In cases with predominantly anterior multilevel disease affecting more three levels, ACCF with plate fixation could be considered over ACDF due to a suggestion of lower rates of fusion in the latter group. However, patients with CSM resulting from less than three-level disease, ACDF and ACCF with plate fixation are equally indicated. On the other hand, patients with features of CSM resulting from multi-level disease affecting more than three levels may benefit from a posterior approach. Laminoplasty is associated with significantly increased incidence of neck pain, but fewer complications and possibly greater range of cervical motion range as well as comparable neurologic improvement rate when compared to laminectomy with fusion and even to anterior approaches including ACDF and multilevel ACCF. Therefore, laminoplasty maybe utilized in patients who are able to tolerate some post-operative neck pain with the benefit of retained cervical mobility. Furthermore, laminectomy without fusion is discouraged in patients with a kyphotic deformity or straight spine due to a significant risk of development of postoperative swan-neck deformity of the cervical spine (Rao 2006; Benzel 1991;Anderson 2009; Kaptain 2009). In younger and healthier patients with significant anterior and posterior compression of the cord resulting in significant progressive myelopathy, a combined anterior-posterior approach is recommended to ensure complete decompression.

#### **5. Metastatic spinal diseases**

#### **5.1. Epidemiology**

two groups. This study presents class III evidence favoring ACCF over ACDF when plate fixation is not used (Grade D recommendation). In contrast, anterior plate fixation in ACDF and ACCF is associated with equal fusion rates reported in one systematic review to reach greater than 90% (Fraser and Hartl 2007). However, in three-level disc disease, the fusion rate was significantly lower in the ACDF group (82.5%) compared to cases treated with ACCF (96%) (P=0.03). This systematic review represents class III evidence due to the lack of application of a standardized methodology for systematic reviews and to violating the inclusion and exclusion criteria. Therefore, a grade D recommendation underlies the utilization of either

Furthermore, the use of anterior plate fixation in ACDF and ACCF is associated with nonunion rates of 42% and 31%, respectively at about 3.3-year follow-up (Swank 1997). Of note, a major confounding factor is the increased use of dynamic plates in ACDF compared to constrained plates in ACCF with the latter being associated with higher fusion rates. Another study by Wang et al. (2001) failed to find a statistically significant difference in fusion rates

Early complications in ACDF include dysphagia (9.5%), neck hematoma (5.6%) with 2.4% of patients requiring surgery, recurrent laryngeal nerve palsy (3.1%), dural laceration (0.5%) and esophageal perforation (0.3%). The latter was associated with death in one patient (1 about 1000 patients). Less common complications include wound infection and Horner's syndrome. Late complications of ACDF include non-union and adjacent-segment disease. The presence for adjacent-segment disease was found to be associated with a plate-to-disc distance of < 5 mm. This complication is thought to occur at an annual rate up to 3% over 10 years. Further studies are required to elucidate the clinical nature of these changes. Furthermore, other factors that can affect the fusion rate include plate fixation and smoking (Bolesta 2000; Fraser and

To summarize, the location of spinal cord compression in relation to the anterior-posterior diameter of the cervical canal is a crucial factor influencing the direction of the surgical approach. In cases with predominantly anterior multilevel disease affecting more three levels, ACCF with plate fixation could be considered over ACDF due to a suggestion of lower rates of fusion in the latter group. However, patients with CSM resulting from less than three-level disease, ACDF and ACCF with plate fixation are equally indicated. On the other hand, patients with features of CSM resulting from multi-level disease affecting more than three levels may benefit from a posterior approach. Laminoplasty is associated with significantly increased incidence of neck pain, but fewer complications and possibly greater range of cervical motion range as well as comparable neurologic improvement rate when compared to laminectomy with fusion and even to anterior approaches including ACDF and multilevel ACCF. Therefore, laminoplasty maybe utilized in patients who are able to tolerate some post-operative neck pain with the benefit of retained cervical mobility. Furthermore, laminectomy without fusion is discouraged in patients with a kyphotic deformity or straight spine due to a significant risk of development of postoperative swan-neck deformity of the cervical spine (Rao 2006; Benzel 1991;Anderson 2009; Kaptain 2009). In younger and healthier patients with significant anterior

ACDF or ACCF with plate fixation in the treatment of multilevel anterior CSM.

between the two groups.

88 Topics in Paraplegia

Hartl 2007).

Cancer-related complications led to about half a million deaths in 2008, with annual newly detected cancer rate of about 1.4 million new cases (Sciubba 2010). Up to 70% of all cancer patients will develop metastasis, most commonly to the lungs and liver, followed by skeletal structures. The most common osseous site for metastasis is the spine, which occurs in 40% of all cancer patients (Aaron 1994;Black 1979; Zerick 1994). Of these patients with spinal meta‐ static disease, up to 20% will develop symptomatic epidural spinal cord compression, which accounts for 20,000 to 30,000 cases per year in the USA (Kwok 2006). Post-mortem studies showed that up to 90% of patients deceased with cancer were found to have evidence of spinal metastatic disease (Wong 1990; Cobb 1977). Up to half patients with spinal metastasis require treatment, with 5-10% being surgically treated (Bell 1997;Bilsky 2005; Walsh 1997; York 1999).

The incidence of metastatic spinal disease peaks at the age groups between 40-65 years (Perrin 1982). The most common primary tumors that metastasize to the spine are breast, lung, melanoma or prostate cancers, which correspond to the common occurrence of these primary malignancies (Constans 1983; Helweg-Larsen 1994). The rates of spinal metastases in prostate, breast, melanoma and lung cancers correspond to about 90%, 74%, 55% and 45%, respectively (Wong 1990). Of note, 10% of cases present clinically with spinal metastatic disease without previous history of known primary malignancy (Gerszten 2000), with 50% of these cases found to have primary lung malignancy (Stark 1982).

#### **5.2. Characteristics of spinal metastasis**

The most common region of the spine affected by metastatic disease is the thoracic spine, which corresponds to 70%, followed by the lumbar spine (20%) and cervical (10%) spine, (Gerszten 2000, Byme 1992; Gilbert 1978). Metastases occur extra-durally, with the intra-dural and intramedullary spaces being very rare metastatic targets representing up to about 8% of cases (Schijns 2000). The vertebral body is involved in more than 80% of cases with the posterior half being the initial site of invasive disease (Gerszten 2000). The reminder of cases often manifest with paravertebral metastasis.

The routes of metastatic spread include hematogenous spread, which is the most common mechanism, manifest by metastases to the vertebral body occurring through hematogenous spread secondary to their rich blood supply (Arguello 1990), followed by direct invasion and spread through shedding of tumor cells in the CSF. Direct invasion to the sacral and lumbar spine were reported in the context of prostate cancer (Ross 2005). CSF seeding of tumor cells occurs following mobilization of intra-axial cranial malignancies, and may result in drop metastasis (Perrin 1982).

#### **5.3. Clinical manifestation**

Patients with spinal metastatic disease may present with pain symptoms and/or neurologic deficits, associated with constitutional or systematic symptoms including weight loss and anorexia.

symptoms refractory to medical treatment, obtaining a tissue diagnosis and preserving

Role of Decompressive Surgery in Disorders Associated with Spinal Cord Lesions

http://dx.doi.org/10.5772/58408

91

Surgical intervention is considered in tumors relatively resistant to radiation treatment including sarcoma, lung and colon cancers, renal cell carcinoma, and breast cancer (Cole 2008). Other indications for surgery include evidence of spinal instability, compression of the cord or nerve roots, pain refractory to medical treatment and deterioration of neurologic function during radiation therapy indicating treatment failure. The three-column involvement, discussed above, has been used by Tomita et al. (Tomita 2001) as evidence of increased spinal instability and therefore an indication for surgical management. The authors discussed other features suggesting spinal instability including vertebral body collapse > 50%, transitional deformity and involvement of the same column in more than one level. Other investigators regarded bone fragments repulsion into the spinal canal as evidence of spinal instability (Cybulski 1989). Although spinal instability has been discussed as a strong indication for surgery in different conditions related to spinal injury, a clear unifying definition of spinal

On the other hand, patient's life expectancy represents a crucial factor in surgical decisionmaking, with an estimated life expectancy greater than 3 or 6 months considered favorable in the context of surgical management of spinal metastatic disease (Sciubba 2010). Different prognostic systems have been devised in order to help stratify patients into different groups

Tokuhashi and colleagues et al (Tokuhashi 2005; Tokuhashi 1990) established a scoring system based on the general medical condition as described by the Karnofsky performance status, number of extra-spinal metastases, number of vertebral metastases, the treatment status of major internal organ metastases, primary tumor type and the presence of neurologic dysfunc‐ tion (Table 4). Non-operative or radiation treatment is indicated in cases with scores ranging from 0 to 8, with an estimated life expectancy less than 6 months. Patients with scores ranging from 12 to 15 were found to have a life expectancy of one year or more, and were treated with circumferential excisional surgery with reconstruction and stabilization. Palliative decom‐ pression surgery utilizing a posterior approach with or without instrumentation is offered to patients with a score of 9 to 11. Stratification of cases according to the Tokuhashi scoring system

Furthermore, Tomita and colleagues et al. (2001) devised a scoring system based on the advances of surgical techniques taking into account the grade of malignancy (slow, moderate or rapid growth), visceral metastases and bone metastases. Patients with scores of up to 3 points, wide marginal excision is recommended for local long-term control, whereas scores of 4 or 5 indicate marginal or intralesional excision for intermediate-term control. Scores of 6 or 7 suggest short-term palliation with palliative surgery, and scores of 8 to 10 indicates nonoperative supportive care. These scoring systems represent useful tools to communicate a host of important prognostic factors rather than absolute conclusions for surgical decision-making, which relies on other factors such as spinal instability and patient's factors including co-

has been validated and used in other studies (Ulmar 2005; Enkaoua 1997).

ambulation and autonomic function by decompressing the neural elements.

instability is still debated.

morbidities.

according to prognosis to help guide surgical treatment.

Pain is the initial complaint in up to 95% of patients with spinal metastases, preceding any neurologic deficits by weeks to months (Bach 1990; Helweg-Larsen 1994; Weinstein 1987). In contrast, about 10% of patients with undiagnosed extra-spinal primary malignancy present with pain as their initial complaint (Livingston 1978). Patients with spinal metastases describe three different categories of pain; tumor-related, mechanical and radicular pain. Tumorrelated or local pain is often progressive and characterized as dull constant ache localized to the metastatic region of the spine, and responsive to nonsteroidal antiinflammatory drugs (Gokaslan 1996). It may worsen in the morning or nocturnally. It's postulated to result from dilatation and engorgement of spinal venous channels secondary to tumor growth leading to mass effect on pain-sensitive structures, such as the dura, periosteum and spinal cord. Pain radiating to the sacro-iliac region and to the interscapular area occur in association with lumbar and thoracic metastatic disease, respectively. On the other hand, mechanical pain results from vertebral body destruction and collapse, associated with some degree of spinal instability leading to increased physiological stress on spinal support structures including ligamentous and muscular structures. Mechanical pain manifests as pain provoked by movement and standing, as well as coughing, and relieved by resting. Radicular pain is caused by invasion of the intervertebral foramina leading to compression of nerve roots and pain radiating across the dermatome subserved by the affected nerve root.

Neurological symptoms result from either compression of the spinal cord or nerve roots, causing myelopathy or radiculopathy, respectively, or both. Myelopathy related to spinal metastasis usually presents with gait difficulty associated with spasticity and motor weakness, which is the most common presenting symptom second to pain in up to 85% of patients (Greenberg 1980; Posner 1995). Myelopathic motor weakness is often followed by bladder and bowel dysfunction (Schiff 1996). Urinary retention and increased frequency of urinary tract infection in males suggest a diagnosis of neurogenic bladder. Isolated autonomic or bladder dysfunction rarely occurs in isolation and is usually accompanied by other symptoms, except in cases with conus medullaris compression. Without treatment, patients with motor deficits progress to complete paraplegia (Botterell 1959). The initial neurological status of the patient correlates with prognosis, thereby necessitating a thorough neurologic examination. Certain scales can be used for neurological and functional assessments, including the American Spinal Injury Association (ASIA) Impairment Scale (AIS), the Frankel scale and the Eastern Cooper‐ ative Oncology Group (ECOG) Performance Score.

#### **5.4. Rationale for selection of cases for surgical management**

The management of spinal metastatic disease can be challenging and requires a multidiscipli‐ nary approach involving neurosurgical expertise as well as radiation and medical oncology and patient's input. Surgical interventions in most cases are palliative, aimed at relieving pain symptoms refractory to medical treatment, obtaining a tissue diagnosis and preserving ambulation and autonomic function by decompressing the neural elements.

**5.3. Clinical manifestation**

the dermatome subserved by the affected nerve root.

ative Oncology Group (ECOG) Performance Score.

**5.4. Rationale for selection of cases for surgical management**

anorexia.

90 Topics in Paraplegia

Patients with spinal metastatic disease may present with pain symptoms and/or neurologic deficits, associated with constitutional or systematic symptoms including weight loss and

Pain is the initial complaint in up to 95% of patients with spinal metastases, preceding any neurologic deficits by weeks to months (Bach 1990; Helweg-Larsen 1994; Weinstein 1987). In contrast, about 10% of patients with undiagnosed extra-spinal primary malignancy present with pain as their initial complaint (Livingston 1978). Patients with spinal metastases describe three different categories of pain; tumor-related, mechanical and radicular pain. Tumorrelated or local pain is often progressive and characterized as dull constant ache localized to the metastatic region of the spine, and responsive to nonsteroidal antiinflammatory drugs (Gokaslan 1996). It may worsen in the morning or nocturnally. It's postulated to result from dilatation and engorgement of spinal venous channels secondary to tumor growth leading to mass effect on pain-sensitive structures, such as the dura, periosteum and spinal cord. Pain radiating to the sacro-iliac region and to the interscapular area occur in association with lumbar and thoracic metastatic disease, respectively. On the other hand, mechanical pain results from vertebral body destruction and collapse, associated with some degree of spinal instability leading to increased physiological stress on spinal support structures including ligamentous and muscular structures. Mechanical pain manifests as pain provoked by movement and standing, as well as coughing, and relieved by resting. Radicular pain is caused by invasion of the intervertebral foramina leading to compression of nerve roots and pain radiating across

Neurological symptoms result from either compression of the spinal cord or nerve roots, causing myelopathy or radiculopathy, respectively, or both. Myelopathy related to spinal metastasis usually presents with gait difficulty associated with spasticity and motor weakness, which is the most common presenting symptom second to pain in up to 85% of patients (Greenberg 1980; Posner 1995). Myelopathic motor weakness is often followed by bladder and bowel dysfunction (Schiff 1996). Urinary retention and increased frequency of urinary tract infection in males suggest a diagnosis of neurogenic bladder. Isolated autonomic or bladder dysfunction rarely occurs in isolation and is usually accompanied by other symptoms, except in cases with conus medullaris compression. Without treatment, patients with motor deficits progress to complete paraplegia (Botterell 1959). The initial neurological status of the patient correlates with prognosis, thereby necessitating a thorough neurologic examination. Certain scales can be used for neurological and functional assessments, including the American Spinal Injury Association (ASIA) Impairment Scale (AIS), the Frankel scale and the Eastern Cooper‐

The management of spinal metastatic disease can be challenging and requires a multidiscipli‐ nary approach involving neurosurgical expertise as well as radiation and medical oncology and patient's input. Surgical interventions in most cases are palliative, aimed at relieving pain

Surgical intervention is considered in tumors relatively resistant to radiation treatment including sarcoma, lung and colon cancers, renal cell carcinoma, and breast cancer (Cole 2008). Other indications for surgery include evidence of spinal instability, compression of the cord or nerve roots, pain refractory to medical treatment and deterioration of neurologic function during radiation therapy indicating treatment failure. The three-column involvement, discussed above, has been used by Tomita et al. (Tomita 2001) as evidence of increased spinal instability and therefore an indication for surgical management. The authors discussed other features suggesting spinal instability including vertebral body collapse > 50%, transitional deformity and involvement of the same column in more than one level. Other investigators regarded bone fragments repulsion into the spinal canal as evidence of spinal instability (Cybulski 1989). Although spinal instability has been discussed as a strong indication for surgery in different conditions related to spinal injury, a clear unifying definition of spinal instability is still debated.

On the other hand, patient's life expectancy represents a crucial factor in surgical decisionmaking, with an estimated life expectancy greater than 3 or 6 months considered favorable in the context of surgical management of spinal metastatic disease (Sciubba 2010). Different prognostic systems have been devised in order to help stratify patients into different groups according to prognosis to help guide surgical treatment.

Tokuhashi and colleagues et al (Tokuhashi 2005; Tokuhashi 1990) established a scoring system based on the general medical condition as described by the Karnofsky performance status, number of extra-spinal metastases, number of vertebral metastases, the treatment status of major internal organ metastases, primary tumor type and the presence of neurologic dysfunc‐ tion (Table 4). Non-operative or radiation treatment is indicated in cases with scores ranging from 0 to 8, with an estimated life expectancy less than 6 months. Patients with scores ranging from 12 to 15 were found to have a life expectancy of one year or more, and were treated with circumferential excisional surgery with reconstruction and stabilization. Palliative decom‐ pression surgery utilizing a posterior approach with or without instrumentation is offered to patients with a score of 9 to 11. Stratification of cases according to the Tokuhashi scoring system has been validated and used in other studies (Ulmar 2005; Enkaoua 1997).

Furthermore, Tomita and colleagues et al. (2001) devised a scoring system based on the advances of surgical techniques taking into account the grade of malignancy (slow, moderate or rapid growth), visceral metastases and bone metastases. Patients with scores of up to 3 points, wide marginal excision is recommended for local long-term control, whereas scores of 4 or 5 indicate marginal or intralesional excision for intermediate-term control. Scores of 6 or 7 suggest short-term palliation with palliative surgery, and scores of 8 to 10 indicates nonoperative supportive care. These scoring systems represent useful tools to communicate a host of important prognostic factors rather than absolute conclusions for surgical decision-making, which relies on other factors such as spinal instability and patient's factors including comorbidities.

The Spinal Instability Neoplastic Score (SINS) is a useful tool for the assessment of spinal instability in patients with spinal metastatic disease. It utilises clinical and radiographic data in order to facilitate the classification and assessment of spinal instability (Table 3). SINS was formulated by the Spine Oncology Study Group (Fisher and colleagues et. al.,2010) on the basis of a systematic review and modified Delphi criteria evaluating factors crucial for the assess‐ ment of spinal stability. With a sensitivity and specificity of 95.7% and 79.5%, respectively, and confirmed near-perfect inter-and intra-rater reliability (Fourney 2011; Fisher 2010), SINS stratifies patients with spinal metastatic disease into three categories; those with stable spine (0-6 points), potentially unstable spine (7-12 points) and unstable spine (13-15points).

**General condition** Poor PS <40% 0

3 or more 0 1-2 1 0 2

Role of Decompressive Surgery in Disorders Associated with Spinal Cord Lesions

http://dx.doi.org/10.5772/58408

93

3 or more 0 1-2 1 0 2

Unremovable 0 Removable 1 No mets 2

Lung, osteosarcoma, stomach, bladder, pancreas, esophagus 0 Liver, gallbladder, unknown 1 Others 2 Kidney, uterus 3 Rectum 4 Thyroid, prostate, breast, carcinoid tumor 5

Complete (Frankel A, B) 0 Incomplete (Frankel C, D) 1 None (Frankel E) 2

Substantial development in the surgical techniques and approach for spinal stabilization over the past three decades have been associated with longer survival and improved neurologic outcomes in patients with spinal metastatic disease (Scuibba 2010). Historically, the mainstay of surgical intervention was based on simple laminectomy, representing the only surgical intervention at the time. The aim of the procedure was to obtain tissue diagnosis or relief of pain. However, a high rate of complications reaching up to 11% was associated with this approach, including spinal instability, wound infection and dehiscence (Findlay 1984). In addition, a retrospective study of 235 patients treated with posterior decompressive laminec‐ tomy with or without radiation demonstrated no difference in the rate of neurologic recovery between the two groups (Gilbert 1978). The association of simple laminectomy with morbidity such as increased risk of spinal instability and its susceptibility to failure rendered surgical management of spinal metastatic disease less efficacious with little value. In addition, simple

Moderate 50-70% 1 Good > 80% 2

**No. Of extraspinal bone metastases**

**No of metastases in the vertebral**

**Metastases to the major organs**

**foci**

**body**

**Primary cancer**

**Spinal cord palsy**

**5.5. Surgical management**

**Table 4.** Tokuhashi prognostic scoring system for spinal metastatic disease


**Table 3.** The Spinal Instability Neoplastic Score (SINS) system.


**Table 4.** Tokuhashi prognostic scoring system for spinal metastatic disease

#### **5.5. Surgical management**

The Spinal Instability Neoplastic Score (SINS) is a useful tool for the assessment of spinal instability in patients with spinal metastatic disease. It utilises clinical and radiographic data in order to facilitate the classification and assessment of spinal instability (Table 3). SINS was formulated by the Spine Oncology Study Group (Fisher and colleagues et. al.,2010) on the basis of a systematic review and modified Delphi criteria evaluating factors crucial for the assess‐ ment of spinal stability. With a sensitivity and specificity of 95.7% and 79.5%, respectively, and confirmed near-perfect inter-and intra-rater reliability (Fourney 2011; Fisher 2010), SINS stratifies patients with spinal metastatic disease into three categories; those with stable spine

(0-6 points), potentially unstable spine (7-12 points) and unstable spine (13-15points).

Pain-free lesion 0 Occasional pain but not mechanical 1 Yes – mechanical pain 3

Blastic 0 Mixed (lytic/blastic) 1 Lytic 2

Normal alignment 0 De novo deformity (kyphosis/scoliosis) 2 Sublaxation/translation present 4

None 0 No collapse with "/> 50% body involvement 1 < 50% 2 "/> 50% collapse 3

None 0 Unilateral 1 Bilateral 3

**Location** Rigid (S2-5) 0

3

Semi-rigid (T3-T10) 1 Mobile spine (C3-C6,L2-L4) 2

Junctional (Occiput-C2,C7-T2,T11-

**Radiographic spinal alignment**

**Vertebral body collapse**

**elements**

**Posterolateral involvement of spinal**

**Table 3.** The Spinal Instability Neoplastic Score (SINS) system.

L1,L5-S1)

92 Topics in Paraplegia

**Pain**

**Bone lesion**

Substantial development in the surgical techniques and approach for spinal stabilization over the past three decades have been associated with longer survival and improved neurologic outcomes in patients with spinal metastatic disease (Scuibba 2010). Historically, the mainstay of surgical intervention was based on simple laminectomy, representing the only surgical intervention at the time. The aim of the procedure was to obtain tissue diagnosis or relief of pain. However, a high rate of complications reaching up to 11% was associated with this approach, including spinal instability, wound infection and dehiscence (Findlay 1984). In addition, a retrospective study of 235 patients treated with posterior decompressive laminec‐ tomy with or without radiation demonstrated no difference in the rate of neurologic recovery between the two groups (Gilbert 1978). The association of simple laminectomy with morbidity such as increased risk of spinal instability and its susceptibility to failure rendered surgical management of spinal metastatic disease less efficacious with little value. In addition, simple laminectomy did not also address anterior compression of the spinal cord or thecal sac resulting from a metastatic lesion at the vertebral body.

**5.6. Surgical approach**

transpedicular approach.

Posterior approaches to surgical management of spinal metastatic disease have become more popular especially with the introduction of the transpedicular approach, which allows for circumferential decompression of the spinal cord and reconstruction of the vertebral body. This approach has been found effective in the lumbar and thoracolumbar spine according to a review of 140 patients in whom this approach was utilized leading to 75% rate of regain of the ability to walk post-operatively and more than 95% improvement of pain. Alternatively, single-stage posterolateral vertebrectomy (SPLV) with costotransversectomies provide wider exposure compared to direct posterior approaches in the surgical management of thoraco‐ lumbar spinal metastases. Street and colleagues et al. (2007) provide data on 42 patients treated with this approach demonstrating that all patients remained neurologically stable or improved after surgery. The complication rate was 26% (n=11) with nine patients requiring early reoperation including seven patients for wound failures. The approach involves performing laminectomy at the metastatic level with pedicle screw insertion prior to bilateral total facetectomies and complete pedicle resection to the base of the vertebral body. Circumferential decompression of the neural elements is achieved with resection of the posterior rib, rib head and costrotransverse joint to facilitate wide resection. Reconstruction of the vertebrectomy defect is achieved by introducing cement. Placing bilateral rods to ensure spinal stabilization completes the procedure. The authors favor this approach over the combined anteroposterior approach due to the increased risk of respiratory adverse effects and prolonged anesthetic time in the combined approach. In addition, the wide exposure and improved working angle offered by SPLV provide greater advantage compared to the conventional posterolateral

Role of Decompressive Surgery in Disorders Associated with Spinal Cord Lesions

http://dx.doi.org/10.5772/58408

95

The utilization of minimally invasive spine surgery has been extrapolated to thoracolumbar spinal metastatic disease (Deutsch 2008; Huang 2006; Singh 2006). Deutsch and colleagues et al. (2008) described the results of a minimally invasive transpedicular vertebrectomy in 8 patients with spinal thoracic metastatic disease in whom an anterior approach via thoracotomy was deemed unsuitable due to significant co-morbidities and limited life expectancy. For patients presenting with metastases affecting thoracic spinal levels T4 to T11, in whom minimally invasive surgery was performed, the authors described resection of the pedicles though a 22-mm diameter tubular retractor, followed by dorsal decompression of the neural elements with partial vertebrectomy and ventral decompression. A bilateral approach with transpedicular resection was used in order to ensure total decompression of the ventral canal. No instrumentation was used in this approach and all patients received postoperative radiation treatment. The average length of the procedure is 2.2 hours. The authors noted neurologic improvement in 5 out of 8 patients (62.5%) post-surgically with a similar rate of improvement in pain. In addition, two patients with paraparesis preoperatively were able to ambulate unassisted post-surgery. The one-year survival was 37.5% and no evidence of tumor recurrence and spinal instability at one-year follow-up in survivors. The authors recommend‐ ed this approach as a palliative measure in selected cases in order to provide pain relief and improved ambulation without significant tissue trauma and increased risk of adverse effects otherwise noted in open anterior approaches. A major disadvantage of this approach is limited

Therefore, radiation alone was the only effective treatment available until the evolution of spinal stabilization and instrumentation techniques. Some early reports of internal fixation in addition to laminectomy suggested improved surgical outcomes, which re-introduced surgical management as an effective and safe intervention in spinal metastatic disease. For instance, more than 90% of patients treated with internal fixation demonstrated increased ambulation and improved pain control postoperatively, compared to 57% treated with laminectomy alone (Sherman 1986). Results from the first prospective randomized controlled trial were presented in 2005 by Patchell et al. comparing the efficacy of radiation treatment alone and combined surgical circumferential decompression of the spinal cord with tumor resection and stabiliza‐ tion, followed by adjuvant radiation therapy. There was a statistically significant higher rate of post-treatment ambulation in the surgery group reaching 84% compared to 57% in the radiation treatment group (P=0.001) (Table 5). The median duration of ambulation in the surgery group was found to be 122 days, compared to 13 days in the radiation group (P=0.003). About 60% of patients regained the ability to walk post-surgically compared to 19% receiving radiation alone (P=0.012). Other secondary outcomes associated with surgery included improved continence rates, muscle strength (ASIA scores) and improved functional ability (Frankel scores).


**Table 5.** Outcomes following treatment with radiation alone versus surgery with radiation (Patchell 2005).

Furthermore, Witham et al. (2006) performed a systematic review assessing the literature on the treatment of spinal metastatic disease between 1964 and 2005. The author found a mean 64% improvement in motor function associated with mean 88% improvement of pain control when laminectomy with posterior stabilization is utilized, compared to a mean 42% improve‐ ment in motor function in laminectomy with or without radiation treatment. Importantly, patients with anterior decompression and stabilization demonstrated the highest rate of neurologic improvement with 75% of cases exhibiting improvement. The role of anterior decompression of the spinal cord has become more apparent since the majority of the tumour burden in metastatic disease is often found anterior or antero-lateral to the spinal cord. This finding was highlighted by Siegal and colleagues et al. (1982), illustrating 91% rate of regaining ambulation in patients with ventral metastatic compression of the cord following anterior decompression. Multiple studies demonstrated similar results, thereby underlining circum‐ ferential spinal cord decompression as one of the principles of surgical management of spinal metastatic diseases beside reconstruction and stabilization (Klimo 2011).

#### **5.6. Surgical approach**

laminectomy did not also address anterior compression of the spinal cord or thecal sac

Therefore, radiation alone was the only effective treatment available until the evolution of spinal stabilization and instrumentation techniques. Some early reports of internal fixation in addition to laminectomy suggested improved surgical outcomes, which re-introduced surgical management as an effective and safe intervention in spinal metastatic disease. For instance, more than 90% of patients treated with internal fixation demonstrated increased ambulation and improved pain control postoperatively, compared to 57% treated with laminectomy alone (Sherman 1986). Results from the first prospective randomized controlled trial were presented in 2005 by Patchell et al. comparing the efficacy of radiation treatment alone and combined surgical circumferential decompression of the spinal cord with tumor resection and stabiliza‐ tion, followed by adjuvant radiation therapy. There was a statistically significant higher rate of post-treatment ambulation in the surgery group reaching 84% compared to 57% in the radiation treatment group (P=0.001) (Table 5). The median duration of ambulation in the surgery group was found to be 122 days, compared to 13 days in the radiation group (P=0.003). About 60% of patients regained the ability to walk post-surgically compared to 19% receiving radiation alone (P=0.012). Other secondary outcomes associated with surgery included improved continence rates, muscle strength (ASIA scores) and improved functional ability

**Ambulation**

**Maintained**

**ambulation (%) Re-gained (%)**

**Mean survival (days)**

resulting from a metastatic lesion at the vertebral body.

**Posttreatment**

**ambulatory rate (%) Retained (days)**

**Surgery and XRT** 84 122 94 62 126 **XRT alone** 57 13 74 19 100

Furthermore, Witham et al. (2006) performed a systematic review assessing the literature on the treatment of spinal metastatic disease between 1964 and 2005. The author found a mean 64% improvement in motor function associated with mean 88% improvement of pain control when laminectomy with posterior stabilization is utilized, compared to a mean 42% improve‐ ment in motor function in laminectomy with or without radiation treatment. Importantly, patients with anterior decompression and stabilization demonstrated the highest rate of neurologic improvement with 75% of cases exhibiting improvement. The role of anterior decompression of the spinal cord has become more apparent since the majority of the tumour burden in metastatic disease is often found anterior or antero-lateral to the spinal cord. This finding was highlighted by Siegal and colleagues et al. (1982), illustrating 91% rate of regaining ambulation in patients with ventral metastatic compression of the cord following anterior decompression. Multiple studies demonstrated similar results, thereby underlining circum‐ ferential spinal cord decompression as one of the principles of surgical management of spinal

**Table 5.** Outcomes following treatment with radiation alone versus surgery with radiation (Patchell 2005).

metastatic diseases beside reconstruction and stabilization (Klimo 2011).

(Frankel scores).

94 Topics in Paraplegia

Posterior approaches to surgical management of spinal metastatic disease have become more popular especially with the introduction of the transpedicular approach, which allows for circumferential decompression of the spinal cord and reconstruction of the vertebral body. This approach has been found effective in the lumbar and thoracolumbar spine according to a review of 140 patients in whom this approach was utilized leading to 75% rate of regain of the ability to walk post-operatively and more than 95% improvement of pain. Alternatively, single-stage posterolateral vertebrectomy (SPLV) with costotransversectomies provide wider exposure compared to direct posterior approaches in the surgical management of thoraco‐ lumbar spinal metastases. Street and colleagues et al. (2007) provide data on 42 patients treated with this approach demonstrating that all patients remained neurologically stable or improved after surgery. The complication rate was 26% (n=11) with nine patients requiring early reoperation including seven patients for wound failures. The approach involves performing laminectomy at the metastatic level with pedicle screw insertion prior to bilateral total facetectomies and complete pedicle resection to the base of the vertebral body. Circumferential decompression of the neural elements is achieved with resection of the posterior rib, rib head and costrotransverse joint to facilitate wide resection. Reconstruction of the vertebrectomy defect is achieved by introducing cement. Placing bilateral rods to ensure spinal stabilization completes the procedure. The authors favor this approach over the combined anteroposterior approach due to the increased risk of respiratory adverse effects and prolonged anesthetic time in the combined approach. In addition, the wide exposure and improved working angle offered by SPLV provide greater advantage compared to the conventional posterolateral transpedicular approach.

The utilization of minimally invasive spine surgery has been extrapolated to thoracolumbar spinal metastatic disease (Deutsch 2008; Huang 2006; Singh 2006). Deutsch and colleagues et al. (2008) described the results of a minimally invasive transpedicular vertebrectomy in 8 patients with spinal thoracic metastatic disease in whom an anterior approach via thoracotomy was deemed unsuitable due to significant co-morbidities and limited life expectancy. For patients presenting with metastases affecting thoracic spinal levels T4 to T11, in whom minimally invasive surgery was performed, the authors described resection of the pedicles though a 22-mm diameter tubular retractor, followed by dorsal decompression of the neural elements with partial vertebrectomy and ventral decompression. A bilateral approach with transpedicular resection was used in order to ensure total decompression of the ventral canal. No instrumentation was used in this approach and all patients received postoperative radiation treatment. The average length of the procedure is 2.2 hours. The authors noted neurologic improvement in 5 out of 8 patients (62.5%) post-surgically with a similar rate of improvement in pain. In addition, two patients with paraparesis preoperatively were able to ambulate unassisted post-surgery. The one-year survival was 37.5% and no evidence of tumor recurrence and spinal instability at one-year follow-up in survivors. The authors recommend‐ ed this approach as a palliative measure in selected cases in order to provide pain relief and improved ambulation without significant tissue trauma and increased risk of adverse effects otherwise noted in open anterior approaches. A major disadvantage of this approach is limited visualization and risk of incomplete decompression. On the other hand, the role of minimally invasive technique is greatly employed in percutaneous vertebroplasty and kyphoplasty in the treatment of painful pathological fractures secondary to underlying metastases (Fourney 2003; Binning 2004). Vertebroplasty is performed by injecting cement percutaneously into the vertebral body. This technique is used in patients with a painful osteolytic metastatic lesion without evidence of disruption of the posterior aspect of the body cortex and without severe loss of the body height (Jensen 2002; Weill 1996). Vertebroplasty is particularly helpful in this group of patients since radiation treatment may not provide pain relief for up to two weeks post-treatment (Binning 2004). Kyphoplasty differs from vertebroplasty in that an expandable balloon is placed into the vertebral body to create space hosting the cement. This technique has been shown to reduce the risk of kyphotic deformity and provides effective and sustained pain relief (Pflugmacher 2007; Fourney 2003.

[7] Anderson, P. A. *et al.* Cervical spine injury severity score. Assessment of reliability. *The Journal of bone and joint surgery. American volume* 89, 1057-1065, doi:10.2106/JBJS.F.

Role of Decompressive Surgery in Disorders Associated with Spinal Cord Lesions

http://dx.doi.org/10.5772/58408

97

[8] Andreshak, J. L. & Dekutoski, M. B. Management of unilateral facet dislocations: a

[9] Arguello, F. *et al.* Pathogenesis of vertebral metastasis and epidural spinal cord com‐

[10] Bach, F. *et al.* Metastatic spinal cord compression. Occurrence, symptoms, clinical presentations and prognosis in 398 patients with spinal cord compression. *Acta neu‐*

[11] Baptiste, D. C. & Fehlings, M. G. Pathophysiology of cervical myelopathy. *The spine journal : official journal of the North American Spine Society* 6, 190S-197S, doi:10.1016/

[12] Bednarik, J. *et al.* The value of somatosensory- and motor-evoked potentials in pre‐ dicting and monitoring the effect of therapy in spondylotic cervical myelopathy. Pro‐

[13] Bell, G. R. Surgical treatment of spinal tumors. *Clinical orthopaedics and related research*,

[14] Benzel, E. C., Lancon, J., Kesterson, L. & Hadden, T. Cervical laminectomy and den‐ tate ligament section for cervical spondylotic myelopathy. *Journal of spinal disorders* 4,

[15] Benzel, E. C. & Larson, S. J. Functional recovery after decompressive spine operation

[16] Bilsky, M. H., Boakye, M., Collignon, F., Kraus, D. & Boland, P. Operative manage‐ ment of metastatic and malignant primary subaxial cervical tumors. *Journal of neuro‐*

[17] Binning, M. J., Gottfried, O. N., Klimo, P., Jr. & Schmidt, M. H. Minimally invasive treatments for metastatic tumors of the spine. *Neurosurgery clinics of North America* 15,

[18] Black, P. Spinal metastasis: current status and recommended guidelines for manage‐

[19] Bogduk, N. The anatomy and pathophysiology of neck pain. *Physical medicine and re‐*

[20] Bolesta, M. J., Rechtine, G. R., 2nd & Chrin, A. M. Three- and four-level anterior cer‐ vical discectomy and fusion with plate fixation: a prospective study. *Spine* 25,

review of the literature. *Orthopedics* 20, 917-926 (1997).

spective randomized study. *Spine* 24, 1593-1598 (1999).

for cervical spine fractures. *Neurosurgery* 20, 742-746 (1987).

*surgery. Spine* 2, 256-264, doi:10.3171/spi.2005.2.3.0256 (2005).

*habilitation clinics of North America* 14, 455-472, v (2003).

459-465, doi:10.1016/j.nec.2004.04.010 (2004).

ment. *Neurosurgery* 5, 726-746 (1979).

2040-2044; discussion 2045-2046 (2000).

pression. *Cancer* 65, 98-106 (1990).

*rochirurgica* 107, 37-43 (1990).

j.spinee.2006.04.024 (2006).

54-63 (1997).

286-295 (1991).

00684 (2007).

#### **Author details**

Ayoub Dakson and Sean D. Christie

Dalhousie University, Dept. Surgery (Neurosurgery), Dept. Medical Neurosciences, Halifax, Nova Scotia, Canada

#### **References**


[7] Anderson, P. A. *et al.* Cervical spine injury severity score. Assessment of reliability. *The Journal of bone and joint surgery. American volume* 89, 1057-1065, doi:10.2106/JBJS.F. 00684 (2007).

visualization and risk of incomplete decompression. On the other hand, the role of minimally invasive technique is greatly employed in percutaneous vertebroplasty and kyphoplasty in the treatment of painful pathological fractures secondary to underlying metastases (Fourney 2003; Binning 2004). Vertebroplasty is performed by injecting cement percutaneously into the vertebral body. This technique is used in patients with a painful osteolytic metastatic lesion without evidence of disruption of the posterior aspect of the body cortex and without severe loss of the body height (Jensen 2002; Weill 1996). Vertebroplasty is particularly helpful in this group of patients since radiation treatment may not provide pain relief for up to two weeks post-treatment (Binning 2004). Kyphoplasty differs from vertebroplasty in that an expandable balloon is placed into the vertebral body to create space hosting the cement. This technique has been shown to reduce the risk of kyphotic deformity and provides effective and sustained

Dalhousie University, Dept. Surgery (Neurosurgery), Dept. Medical Neurosciences, Halifax,

[1] Aarabi, B. *et al.* Predictors of outcome in acute traumatic central cord syndrome due to spinal stenosis. *Journal of neurosurgery. Spine* 14, 122-130, doi:

[2] Aarabi, B. *et al.* Subaxial cervical spine injury classification systems. *Neurosurgery* 72

[3] Aaron, A. D. The management of cancer metastatic to bone. *JAMA : the journal of the*

[4] Ahn, N. U., Ahn, U. M., Ipsen, B. & An, H. S. Mechanical neck pain and cervicogenic headache. *Neurosurgery* 60, S21-27, doi:10.1227/01.NEU.0000249258.94041.C6 (2007).

[5] Allen, B. L., Jr., Ferguson, R. L., Lehmann, T. R. & O'Brien, R. P. A mechanistic classi‐ fication of closed, indirect fractures and dislocations of the lower cervical spine. *Spine*

[6] Anderson, P. A. *et al.* Laminectomy and fusion for the treatment of cervical degenera‐ tive myelopathy. *Journal of neurosurgery. Spine* 11, 150-156, doi:

Suppl 2, 170-186, doi:10.1227/NEU.0b013e31828341c5 (2013).

*American Medical Association* 272, 1206-1209 (1994).

pain relief (Pflugmacher 2007; Fourney 2003.

10.3171/2010.9.SPINE09922 (2011).

10.3171/2009.2.SPINE08727 (2009).

Ayoub Dakson and Sean D. Christie

**Author details**

96 Topics in Paraplegia

Nova Scotia, Canada

7, 1-27 (1982).

**References**


[21] Bosch, A., Stauffer, E. S. & Nickel, V. L. Incomplete traumatic quadriplegia. A tenyear review. *JAMA : the journal of the American Medical Association* 216, 473-478 (1971).

[33] Cobb, C. A., 3rd, Leavens, M. E. & Eckles, N. Indications for nonoperative treatment of spinal cord compression due to breast cancer. *Journal of neurosurgery* 47, 653-658,

Role of Decompressive Surgery in Disorders Associated with Spinal Cord Lesions

http://dx.doi.org/10.5772/58408

99

[34] Cole, J. S. & Patchell, R. A. Metastatic epidural spinal cord compression. *Lancet neu‐*

[35] Constans, J. P. *et al.* Spinal metastases with neurological manifestations. Review of 600 cases. *Journal of neurosurgery* 59, 111-118, doi:10.3171/jns.1983.59.1.0111 (1983). [36] Crockard, H. A., Heilman, A. E. & Stevens, J. M. Progressive myelopathy secondary to odontoid fractures: clinical, radiological, and surgical features. *Journal of neurosur‐*

[37] Cunningham, M. R., Hershman, S. & Bendo, J. Systematic review of cohort studies comparing surgical treatments for cervical spondylotic myelopathy. *Spine* 35,

[38] Cybulski, G. R., Douglas, R. A., Meyer, P. R., Jr. & Rovin, R. A. Complications in three-column cervical spine injuries requiring anterior-posterior stabilization. *Spine*

[39] Dahdaleh, N. S. & Hitchon, P. W. Thoracolumbar spinal extradural arachnoid cysts.

[40] Denis, F. The three column spine and its significance in the classification of acute

[41] Deutsch, H., Boco, T. & Lobel, J. Minimally invasive transpedicular vertebrectomy for metastatic disease to the thoracic spine. *Journal of spinal disorders & techniques* 21,

[42] DeVivo, M. J. Causes and costs of spinal cord injury in the United States. *Spinal cord*

[43] Dvorak, M. F. *et al.* The surgical approach to subaxial cervical spine injuries: an evi‐ dence-based algorithm based on the SLIC classification system. *Spine* 32, 2620-2629,

[44] Dvorak, M. F. *et al.* Factors predicting motor recovery and functional outcome after traumatic central cord syndrome: a long-term follow-up. *Spine* 30, 2303-2311 (2005).

[45] Dwyer, A., Aprill, C. & Bogduk, N. Cervical zygapophyseal joint pain patterns. I: A

[46] Elgafy, H. *et al.* The radiographic failure of single segment posterior cervical instru‐ mentation in traumatic cervical flexion distraction injuries. *Topics in spinal cord injury*

*Neurosurgery* 72, E318-319, doi:10.1227/NEU.0b013e31827bc093 (2013).

*rology* 7, 459-466, doi:10.1016/S1474-4422(08)70089-9 (2008).

*gery* 78, 579-586, doi:10.3171/jns.1993.78.4.0579 (1993).

537-543, doi:10.1097/BRS.0b013e3181b204cc (2010).

thoracolumbar spinal injuries. *Spine* 8, 817-831 (1983).

101-105, doi:10.1097/BSD.0b013e31805fea01 (2008).

study in normal volunteers. *Spine* 15, 453-457 (1990).

doi:10.1097/BRS.0b013e318158ce16 (2007).

*rehabilitation* 12, 20-29 (2006).

17, 253-256 (1992).

35, 809-813 (1997).

doi:10.3171/jns.1977.47.5.0653 (1977).


[33] Cobb, C. A., 3rd, Leavens, M. E. & Eckles, N. Indications for nonoperative treatment of spinal cord compression due to breast cancer. *Journal of neurosurgery* 47, 653-658, doi:10.3171/jns.1977.47.5.0653 (1977).

[21] Bosch, A., Stauffer, E. S. & Nickel, V. L. Incomplete traumatic quadriplegia. A tenyear review. *JAMA : the journal of the American Medical Association* 216, 473-478 (1971).

[22] Botterell, E. H. & Fitzgerald, G. W. Spinal cord compression produced by extradural malignant tumours; early recognition, treatment and results. *Canadian Medical Associ‐*

[23] Bracken, M. B. Treatment of acute spinal cord injury with methylprednisolone: re‐ sults of a multicenter, randomized clinical trial. *Journal of neurotrauma* 8 Suppl 1,

[24] Bracken, M. B. *et al.* Efficacy of methylprednisolone in acute spinal cord injury. *JA‐*

[25] Bracken, M. B. *et al.* Methylprednisolone or naloxone treatment after acute spinal cord injury: 1-year follow-up data. Results of the second National Acute Spinal Cord Injury Study. *Journal of neurosurgery* 76, 23-31, doi:10.3171/jns.1992.76.1.0023 (1992).

[26] Bracken, M. B. *et al.* A randomized, controlled trial of methylprednisolone or nalox‐ one in the treatment of acute spinal-cord injury. Results of the Second National Acute Spinal Cord Injury Study. *The New England journal of medicine* 322, 1405-1411, doi:

[27] Bracken, M. B. *et al.* Methylprednisolone and neurological function 1 year after spinal cord injury. Results of the National Acute Spinal Cord Injury Study. *Journal of neuro‐*

[28] Bracken, M. B. *et al.* Administration of methylprednisolone for 24 or 48 hours or tiri‐ lazad mesylate for 48 hours in the treatment of acute spinal cord injury. Results of the Third National Acute Spinal Cord Injury Randomized Controlled Trial. National Acute Spinal Cord Injury Study. *JAMA : the journal of the American Medical Association*

[29] Bracken, M. B. *et al.* Methylprednisolone or tirilazad mesylate administration after acute spinal cord injury: 1-year follow up. Results of the third National Acute Spinal Cord Injury randomized controlled trial. *Journal of neurosurgery* 89, 699-706, doi:

[30] Byrne, T. N. Spinal cord compression from epidural metastases. *The New England journal of medicine* 327, 614-619, doi:10.1056/NEJM199208273270907 (1992).

[31] Casha, S. & Christie, S. A systematic review of intensive cardiopulmonary manage‐ ment after spinal cord injury. *Journal of neurotrauma* 28, 1479-1495, doi:10.1089/neu.

[32] Clarke, E. & Robinson, P. K. Cervical myelopathy: a complication of cervical spondy‐

*MA : the journal of the American Medical Association* 251, 45-52 (1984).

*ation journal* 80, 791-796 (1959).

98 Topics in Paraplegia

S47-50; discussion S51-42 (1991).

10.1056/NEJM199005173222001 (1990).

277, 1597-1604 (1997).

2009.1156 (2011).

10.3171/jns.1998.89.5.0699 (1998).

*surgery* 63, 704-713, doi:10.3171/jns.1985.63.5.0704 (1985).

losis. *Brain : a journal of neurology* 79, 483-510 (1956).


[47] Enkaoua, E. A. *et al.* Vertebral metastases: a critical appreciation of the preoperative prognostic tokuhashi score in a series of 71 cases. *Spine* 22, 2293-2298 (1997).

[61] Greenberg, H. S., Kim, J. H. & Posner, J. B. Epidural spinal cord compression from metastatic tumor: results with a new treatment protocol. *Annals of neurology* 8,

Role of Decompressive Surgery in Disorders Associated with Spinal Cord Lesions

http://dx.doi.org/10.5772/58408

101

[62] Guigui, P., Benoist, M. & Deburge, A. Spinal deformity and instability after multile‐ vel cervical laminectomy for spondylotic myelopathy. *Spine* 23, 440-447 (1998).

[63] Hadley, M. N., Fitzpatrick, B. C., Sonntag, V. K. & Browner, C. M. Facet fracture-dis‐

[64] Hadley, M. N. & Walters, B. C. Introduction to the Guidelines for the Management of Acute Cervical Spine and Spinal Cord Injuries. *Neurosurgery* 72 Suppl 2, 5-16, doi:

[65] Hall, F. M. Radiographs in cervical spine trauma. *AJR. American journal of roentgenolo‐*

[66] Helweg-Larsen, S. & Sorensen, P. S. Symptoms and signs in metastatic spinal cord compression: a study of progression from first symptom until diagnosis in 153 pa‐

[67] Holdsworth, F. Fractures, dislocations, and fracture-dislocations of the spine. *The*

[68] Holly, L. T. *et al.* Cervical spine trauma associated with moderate and severe head injury: incidence, risk factors, and injury characteristics. *Journal of neurosurgery* 96,

[69] Houten, J. K. & Cooper, P. R. Laminectomy and posterior cervical plating for multile‐ vel cervical spondylotic myelopathy and ossification of the posterior longitudinal lig‐ ament: effects on cervical alignment, spinal cord compression, and neurological

[70] Houten, J. K. & Cooper, P. R. Laminectomy and posterior cervical plating for multile‐ vel cervical spondylotic myelopathy and ossification of the posterior longitudinal lig‐ ament: effects on cervical alignment, spinal cord compression, and neurological

[71] Hu, R., Mustard, C. A. & Burns, C. Epidemiology of incident spinal fracture in a com‐

[72] Huang, P., Gupta, M. C., Sarigul-Klijn, N. & Hazelwood, S. Two in vivo surgical ap‐ proaches for lumbar corpectomy using allograft and a metallic implant: a controlled clinical and biomechanical study. *The spine journal : official journal of the North Ameri‐*

[73] Huang, R. C., Girardi, F. P., Poynton, A. R. & Cammisa Jr, F. P. Treatment of multile‐ vel cervical spondylotic myeloradiculopathy with posterior decompression and fu‐

*Journal of bone and joint surgery. American volume* 52, 1534-1551 (1970).

outcome. *Neurosurgery* 52, 1081-1087; discussion 1087-1088 (2003).

outcome. *Neurosurgery* 52, 1081-1087; discussion 1087-1088 (2003).

*can Spine Society* 6, 648-658, doi:10.1016/j.spinee.2006.04.028 (2006).

location injuries of the cervical spine. *Neurosurgery* 30, 661-666 (1992).

361-366, doi:10.1002/ana.410080404 (1980).

10.1227/NEU.0b013e3182773549 (2013).

tients. *Eur J Cancer* 30A, 396-398 (1994).

plete population. *Spine* 21, 492-499 (1996).

285-291 (2002).

*gy* 131, 555-556, doi:10.2214/ajr.131.3.555 (1978).


[61] Greenberg, H. S., Kim, J. H. & Posner, J. B. Epidural spinal cord compression from metastatic tumor: results with a new treatment protocol. *Annals of neurology* 8, 361-366, doi:10.1002/ana.410080404 (1980).

[47] Enkaoua, E. A. *et al.* Vertebral metastases: a critical appreciation of the preoperative prognostic tokuhashi score in a series of 71 cases. *Spine* 22, 2293-2298 (1997).

[48] Fehlings, M. G. & Wilson, J. R. Multicenter clinical research networks for traumatic spinal cord injury: a critical pathway to discovery. *Journal of neurosurgery. Spine* 17,

[49] Findlay, G. F. Adverse effects of the management of malignant spinal cord compres‐

[50] Fisher, C. G. *et al.* A novel classification system for spinal instability in neoplastic dis‐ ease: an evidence-based approach and expert consensus from the Spine Oncology

[51] Fisher, C. G. *et al.* A novel classification system for spinal instability in neoplastic dis‐ ease: an evidence-based approach and expert consensus from the Spine Oncology

[52] Fisher, C. G., Dvorak, M. F., Leith, J. & Wing, P. C. Comparison of outcomes for un‐ stable lower cervical flexion teardrop fractures managed with halo thoracic vest ver‐

[53] Foo, D., Subrahmanyan, T. S. & Rossier, A. B. Post-traumatic acute anterior spinal

[54] Fourney, D. R. *et al.* Spinal instability neoplastic score: an analysis of reliability and validity from the spine oncology study group. *Journal of clinical oncology : official jour‐ nal of the American Society of Clinical Oncology* 29, 3072-3077, doi:10.1200/JCO.

[55] Fourney, D. R. *et al.* Percutaneous vertebroplasty and kyphoplasty for painful verte‐ bral body fractures in cancer patients. *Journal of neurosurgery* 98, 21-30 (2003).

[56] Fraser, J. F. & Härtl, R. Anterior approaches to fusion of the cervical spine: a metaa‐

[57] Gehweiler, J. A., Jr., Clark, W. M., Schaaf, R. E., Powers, B. & Miller, M. D. Cervical spine trauma: the common combined conditions. *Radiology* 130, 77-86, doi:

[58] Gerszten, P. C. & Welch, W. C. Current surgical management of metastatic spinal

[59] Gilbert, R. W., Kim, J. H. & Posner, J. B. Epidural spinal cord compression from meta‐ static tumor: diagnosis and treatment. *Annals of neurology* 3, 40-51, doi:10.1002/ana.

[60] Gokaslan, Z. L. Spine surgery for cancer. *Current opinion in oncology* 8, 178-181 (1996).

nalysis of fusion rates. *Journal of Neurosurgery: Spine* 6, 298-303 (2007).

disease. *Oncology* 14, 1013-1024; discussion 1024, 1029-1030 (2000).

Study Group. *Spine* 35, E1221-1229, doi:10.1097/BRS.0b013e3181e16ae2 (2010).

Study Group. *Spine* 35, E1221-1229, doi:10.1097/BRS.0b013e3181e16ae2 (2010).

sion. *Journal of neurology, neurosurgery, and psychiatry* 47, 761-768 (1984).

4-5; discussion 5, doi:10.3171/2012.5.AOSPINE12416 (2012).

sus anterior corpectomy and plating. *Spine* 27, 160-166 (2002).

2010.34.3897 (2011).

100 Topics in Paraplegia

10.1148/130.1.77 (1979).

410030107 (1978).

cord syndrome. *Paraplegia* 19, 201-205, doi:10.1038/sc.1981.42 (1981).


sion with lateral mass plate fixation and local bone graft. *Journal of spinal disorders & techniques* 16, 123-129 (2003).

[85] Kwon, B. K. *et al.* A prospective randomized controlled trial of anterior compared with posterior stabilization for unilateral facet injuries of the cervical spine. *Journal of*

Role of Decompressive Surgery in Disorders Associated with Spinal Cord Lesions

http://dx.doi.org/10.5772/58408

103

[86] Lees, F. & Turner, J. W. Natural History and Prognosis of Cervical Spondylosis. *Brit‐*

[87] Lifeso, R. M. & Colucci, M. A. Anterior fusion for rotationally unstable cervical spine

[88] Livingston, K. E. & Perrin, R. G. The neurosurgical management of spinal metastases causing cord and cauda equina compression. *Journal of neurosurgery* 49, 839-843, doi:

[89] Louis, R. Spinal stability as defined by the three-column spine concept. *Anatomia*

[90] Matsunaga, S., Sakou, T. & Nakanisi, K. Analysis of the cervical spine alignment fol‐

[91] Matz, P. G. *et al.* The natural history of cervical spondylotic myelopathy. *Journal of*

[92] McDonald, J. W. & Sadowsky, C. Spinal-cord injury. *Lancet* 359, 417-425, doi:10.1016/

[93] McKinley, W., Santos, K., Meade, M. & Brooke, K. Incidence and outcomes of spinal cord injury clinical syndromes. *The journal of spinal cord medicine* 30, 215-224 (2007).

[94] Moller, F., Andres, A. H. & Langenstein, H. Intubating laryngeal mask airway (IL‐ MA) seems to be an ideal device for blind intubation in case of immobile spine. *Brit‐*

[95] Mummaneni, P. V. *et al.* Cervical surgical techniques for the treatment of cervical spondylotic myelopathy. *Journal of neurosurgery. Spine* 11, 130-141, doi:

[96] Nirala, A. P., Husain, M. & Vatsal, D. K. A retrospective study of multiple interbody grafting and long segment strut grafting following multilevel anterior cervical de‐

[97] Nurick, S. The natural history and the results of surgical treatment of the spinal cord disorder associated with cervical spondylosis. *Brain : a journal of neurology* 95, 101-108

[98] Panjabi, M. M. *et al.* Articular facets of the human spine. Quantitative three-dimen‐

compression. *British journal of neurosurgery* 18, 227-232 (2004).

lowing laminoplasty and laminectomy. *Spinal cord* 37, 20-24 (1999).

*neurosurgery. Spine* 11, 104-111, doi:10.3171/2009.1.SPINE08716 (2009).

*neurosurgery. Spine* 7, 1-12, doi:10.3171/SPI-07/07/001 (2007).

*ish medical journal* 2, 1607-1610 (1963).

fractures. *Spine* 25, 2028-2034 (2000).

10.3171/jns.1978.49.6.0839 (1978).

S0140-6736(02)07603-1 (2002).

*ish journal of anaesthesia* 85, 493-495 (2000).

sional anatomy. *Spine* 18, 1298-1310 (1993).

10.3171/2009.3.SPINE08728 (2009).

(1972).

*clinica* 7, 33-42 (1985).


[85] Kwon, B. K. *et al.* A prospective randomized controlled trial of anterior compared with posterior stabilization for unilateral facet injuries of the cervical spine. *Journal of neurosurgery. Spine* 7, 1-12, doi:10.3171/SPI-07/07/001 (2007).

sion with lateral mass plate fixation and local bone graft. *Journal of spinal disorders &*

[74] Hurlbert, R. J. *et al.* Pharmacological therapy for acute spinal cord injury. *Neurosur‐*

[75] Ianuzzi, A. *et al.* Biomechanical evaluation of surgical constructs for stabilization of cervical teardrop fractures. *The spine journal : official journal of the North American Spine*

[76] Jensen, M. E. & Kallmes, D. E. Percutaneous vertebroplasty in the treatment of malig‐

[77] Kadanka, Z., Bednarik, J., Novotny, O., Urbanek, I. & Dusek, L. Cervical spondylotic myelopathy: conservative versus surgical treatment after 10 years. *European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society* 20, 1533-1538, doi:

[78] Kadanka, Z. *et al.* Conservative treatment versus surgery in spondylotic cervical myelopathy: a prospective randomised study. *European spine journal : official publica‐ tion of the European Spine Society, the European Spinal Deformity Society, and the Europe‐*

[79] Kadanka, Z. *et al.* Predictive factors for spondylotic cervical myelopathy treated con‐ servatively or surgically. *European journal of neurology : the official journal of the Europe‐ an Federation of Neurological Societies* 12, 55-63, doi:10.1111/j.1468-1331.2004.00896.x

[80] Kaptain, G. J., Simmons, N. E., Replogle, R. E. & Pobereskin, L. Incidence and out‐ come of kyphotic deformity following laminectomy for cervical spondylotic myelop‐

[81] Klimo, P., Jr., Thompson, C. J., Kestle, J. R. & Schmidt, M. H. A meta-analysis of sur‐ gery versus conventional radiotherapy for the treatment of metastatic spinal epidural

[82] Kumar, V. G., Rea, G. L., Mervis, L. J. & McGregor, J. M. Cervical spondylotic myel‐ opathy: functional and radiographic long-term outcome after laminectomy and pos‐

[83] Kwok, Y., Tibbs, P. A. & Patchell, R. A. Clinical approach to metastatic epidural spi‐ nal cord compression. *Hematology/oncology clinics of North America* 20, 1297-1305, doi:

[84] Kwok, Y., Tibbs, P. A. & Patchell, R. A. Clinical approach to metastatic epidural spi‐ nal cord compression. *Hematology/oncology clinics of North America* 20, 1297-1305, doi:

disease. *Neuro-oncology* 7, 64-76, doi:10.1215/S1152851704000262 (2005).

terior fusion. *Neurosurgery* 44, 771-777; discussion 777-778 (1999).

*gery* 72 Suppl 2, 93-105, doi:10.1227/NEU.0b013e31827765c6 (2013).

*Society* 6, 514-523, doi:10.1016/j.spinee.2005.12.001 (2006).

*an Section of the Cervical Spine Research Society* 9, 538-544 (2000).

athy. *Journal of Neurosurgery: Spine* 93, 199-204 (2000).

nant spine disease. *Cancer journal* 8, 194-206 (2002).

*techniques* 16, 123-129 (2003).

102 Topics in Paraplegia

10.1007/s00586-011-1811-9 (2011).

10.1016/j.hoc.2006.09.008 (2006).

10.1016/j.hoc.2006.09.008 (2006).

(2005).


[99] Patchell, R. A. *et al.* Direct decompressive surgical resection in the treatment of spinal cord compression caused by metastatic cancer: a randomised trial. *Lancet* 366, 643-648, doi:10.1016/S0140-6736(05)66954-1 (2005).

[112] Schneider, R. C. The diagnosis and treatment of trauma to the central nervous sys‐

Role of Decompressive Surgery in Disorders Associated with Spinal Cord Lesions

http://dx.doi.org/10.5772/58408

105

[113] Schneider, R. C., Cherry, G. & Pantek, H. The syndrome of acute central cervical spi‐ nal cord injury; with special reference to the mechanisms involved in hyperextension injuries of cervical spine. *Journal of neurosurgery* 11, 546-577, doi:10.3171/jns.

[114] Schneider, R. C., Thompson, J. M. & Bebin, J. The syndrome of acute central cervical spinal cord injury. *Journal of neurology, neurosurgery, and psychiatry* 21, 216-227 (1958).

[115] Sciubba, D. M. & Gokaslan, Z. L. Are patients satisfied after surgery for metastatic spine disease? *The spine journal : official journal of the North American Spine Society* 10,

[116] Sciubba, D. M. *et al.* Diagnosis and management of metastatic spine disease. A re‐ view. *Journal of neurosurgery. Spine* 13, 94-108, doi:10.3171/2010.3.SPINE09202 (2010).

[117] Siegal, T., Siegal, T., Robin, G., Lubetzki-Korn, I. & Fuks, Z. Anterior decompression of the spine for metastatic epidural cord compression: a promising avenue of thera‐

[118] Sim, F. H., Svien, H. J., Bickel, W. H. & Janes, J. M. Swan-neck deformity following extensive cervical laminectomy. A review of twenty-one cases. *The Journal of bone and*

[119] Singh, K. *et al.* Current concepts in the management of metastatic spinal disease. The role of minimally-invasive approaches. *The Journal of bone and joint surgery. British vol‐*

[120] Sonntag, V. K., Hadley, M. N., Dickman, C. A. & Browner, C. M. Atlas fractures: treatment and long-term results. *Acta neurochirurgica. Supplementum* 43, 63-68 (1988).

[121] Stark, R. J., Henson, R. A. & Evans, S. J. Spinal metastases. A retrospective survey

[122] Stauffer, E. S. Diagnosis and prognosis of acute cervical spinal cord injury. *Clinical*

[123] Street, J. *et al.* Single-stage posterolateral vertebrectomy for the management of meta‐ static disease of the thoracic and lumbar spine: a prospective study of an evolving surgical technique. *Journal of spinal disorders & techniques* 20, 509-520, doi:10.1097/BSD.

[124] Swank, M. L., Lowery, G. L., Bhat, A. L. & McDonough, R. F. Anterior cervical allog‐ raft arthrodesis and instrumentation: multilevel interbody grafting or strut graft re‐ construction. *European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research*

from a general hospital. *Brain : a journal of neurology* 105, 189-213 (1982).

py? *Annals of neurology* 11, 28-34, doi:10.1002/ana.410110106 (1982).

tem. *The Medical clinics of North America* 40, 1369-1384 (1956).

63-65, doi:10.1016/j.spinee.2009.10.004 (2010).

*joint surgery. American volume* 56, 564-580 (1974).

*orthopaedics and related research*, 9-15 (1975).

0b013e3180335bf7 (2007).

*Society* 6, 138-143 (1997).

*ume* 88, 434-442, doi:10.1302/0301-620X.88B4.17282 (2006).

1954.11.6.0546 (1954).


[112] Schneider, R. C. The diagnosis and treatment of trauma to the central nervous sys‐ tem. *The Medical clinics of North America* 40, 1369-1384 (1956).

[99] Patchell, R. A. *et al.* Direct decompressive surgical resection in the treatment of spinal cord compression caused by metastatic cancer: a randomised trial. *Lancet* 366,

[100] Perez-Lopez, C. *et al.* [Efficacy of arthrodesis in the posterior approach of cervical myelopathy: comparative study of a series of 36 cases]. *Neurocirugia* 12, 316-323; dis‐

[101] Perrin, R. G., Livingston, K. E. & Aarabi, B. Intradural extramedullary spinal meta‐ stasis. A report of 10 cases. *Journal of neurosurgery* 56, 835-837, doi:10.3171/jns.

[102] Pflugmacher, R., Beth, P., Schroeder, R. J., Schaser, K. D. & Melcher, I. Balloon ky‐ phoplasty for the treatment of pathological fractures in the thoracic and lumbar spine caused by metastasis: one-year follow-up. *Acta radiologica* 48, 89-95, doi:

[103] Phillips, D. G. Surgical treatment of myelopathy with cervical spondylosis. *Journal of*

[104] Pollock, L. J. *et al.* Relation of recovery of sensation to intraspinal pathways in inju‐ ries of the spinal cord. *A.M.A. archives of neurology and psychiatry* 70, 137-150 (1953).

[105] Pouw, M. H. *et al.* Diagnostic criteria of traumatic central cord syndrome. Part 1: a systematic review of clinical descriptors and scores. *Spinal cord* 48, 652-656, doi:

[106] Quencer, R. M. *et al.* Acute traumatic central cord syndrome: MRI-pathological corre‐

[107] Rao, R. D., Gourab, K. & David, K. S. Operative treatment of cervical spondylotic myelopathy. *The Journal of bone and joint surgery. American volume* 88, 1619-1640, doi:

[108] Razack, N., Green, B. A. & Levi, A. D. The management of traumatic cervical bilateral facet fracture-dislocations with unicortical anterior plates. *Journal of spinal disorders*

[109] Roth, E. J., Lawler, M. H. & Yarkony, G. M. Traumatic central cord syndrome: clinical features and functional outcomes. *Archives of physical medicine and rehabilitation* 71,

[110] Ryken, T. C. *et al.* The acute cardiopulmonary management of patients with cervical spinal cord injuries. *Neurosurgery* 72 Suppl 2, 84-92, doi:10.1227/NEU.

[111] Schijns, O. E., Kurt, E., Wessels, P., Luijckx, G. J. & Beuls, E. A. Intramedullary spinal cord metastasis as a first manifestation of a renal cell carcinoma: report of a case and

review of the literature. *Clinical neurology and neurosurgery* 102, 249-254 (2000).

643-648, doi:10.1016/S0140-6736(05)66954-1 (2005).

*neurology, neurosurgery, and psychiatry* 36, 879-884 (1973).

cussion 323-314 (2001).

104 Topics in Paraplegia

1982.56.6.0835 (1982).

10.1080/02841850601026427 (2007).

10.1038/sc.2009.155 (2010).

10.2106/JBJS.F.00014 (2006).

0b013e318276ee16 (2013).

13, 374-381 (2000).

18-23 (1990).

lations. *Neuroradiology* 34, 85-94 (1992).


[125] Tetreault, L. A., Karpova, A. & Fehlings, M. G. Predictors of outcome in patients with degenerative cervical spondylotic myelopathy undergoing surgical treatment: results of a systematic review. *European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society*, doi:10.1007/s00586-013-2658-z (2013).

[137] Wang, J. C., McDonough, P. W., Kanim, L. E., Endow, K. K. & Delamarter, R. B. In‐ creased fusion rates with cervical plating for three-level anterior cervical discectomy

Role of Decompressive Surgery in Disorders Associated with Spinal Cord Lesions

http://dx.doi.org/10.5772/58408

107

[138] Weill, A. *et al.* Spinal metastases: indications for and results of percutaneous injection of acrylic surgical cement. *Radiology* 199, 241-247, doi:10.1148/radiology.199.1.8633152

[139] Weinstein, S. M. & Walton, O. Management of pain associated with spinal tumor. *Neurosurgery clinics of North America* 15, 511-527, doi:10.1016/j.nec.2004.04.017 (2004).

[140] Witham, T. F., Khavkin, Y. A., Gallia, G. L., Wolinsky, J. P. & Gokaslan, Z. L. Surgery insight: current management of epidural spinal cord compression from metastatic spine disease. *Nature clinical practice. Neurology* 2, 87-94; quiz 116, doi:10.1038/

[141] Wong, D. A., Fornasier, V. L. & MacNab, I. Spinal metastases: the obvious, the occult,

[142] York, J. E. *et al.* Combined chest wall resection with vertebrectomy and spinal recon‐ struction for the treatment of Pancoast tumors. *Journal of neurosurgery* 91, 74-80

[143] Yoshizawa, H., Kobayashi, S. & Morita, T. Chronic nerve root compression. Patho‐ physiologic mechanism of nerve root dysfunction. *Spine* 20, 397-407 (1995).

[144] Yue, W. M., Tan, S. B., Tan, M. H., Koh, D. C. & Tan, C. T. The Torg--Pavlov ratio in cervical spondylotic myelopathy: a comparative study between patients with cervical spondylotic myelopathy and a nonspondylotic, nonmyelopathic population. *Spine*

and fusion. *Spine* 26, 643-646; discussion 646-647 (2001).

(1996).

(1999).

[145]

ncpneuro0116 (2006).

26, 1760-1764 (2001).

and the impostors. *Spine* 15, 1-4 (1990).


[145]

[125] Tetreault, L. A., Karpova, A. & Fehlings, M. G. Predictors of outcome in patients with degenerative cervical spondylotic myelopathy undergoing surgical treatment: results of a systematic review. *European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical*

[126] Toh, E., Nomura, T., Watanabe, M. & Mochida, J. Surgical treatment for injuries of the middle and lower cervical spine. *International orthopaedics* 30, 54-58, doi:10.1007/

[127] Tokuhashi, Y., Matsuzaki, H., Oda, H., Oshima, M. & Ryu, J. A revised scoring sys‐ tem for preoperative evaluation of metastatic spine tumor prognosis. *Spine* 30,

[128] Tokuhashi, Y., Matsuzaki, H., Toriyama, S., Kawano, H. & Ohsaka, S. Scoring system for the preoperative evaluation of metastatic spine tumor prognosis. *Spine* 15,

[130] Torg, J. S., Pavlov, H., O'Neill, M. J., Nichols, C. E., Jr. & Sennett, B. The axial load teardrop fracture. A biomechanical, clinical and roentgenographic analysis. *The*

[131] Troll, G. F. & Dohrmann, G. J. Anaesthesia of the spinal cord-injured patient: cardio‐ vascular problems and their management. *Paraplegia* 13, 162-171, doi:10.1038/sc.

[132] Ulmar, B. *et al.* The Tokuhashi score: significant predictive value for the life expectan‐ cy of patients with breast cancer with spinal metastases. *Spine* 30, 2222-2226 (2005).

[133] Vaccaro, A. R. *et al.* The subaxial cervical spine injury classification system: a novel approach to recognize the importance of morphology, neurology, and integrity of the disco-ligamentous complex. *Spine* 32, 2365-2374, doi:10.1097/BRS.0b013e3181557b92

[134] Wada, E. *et al.* Subtotal corpectomy versus laminoplasty for multilevel cervical spon‐ dylotic myelopathy: a long-term follow-up study over 10 years. *Spine* 26, 1443-1447;

[135] Walsh, G. L. *et al.* Anterior approaches to the thoracic spine in patients with cancer: indications and results. *The Annals of thoracic surgery* 64, 1611-1618 (1997).

[136] Wang, J. C. *et al.* Single-stage posterolateral transpedicular approach for resection of epidural metastatic spine tumors involving the vertebral body with circumferential reconstruction: results in 140 patients. Invited submission from the Joint Section Meeting on Disorders of the Spine and Peripheral Nerves, March 2004. *Journal of neu‐*

*rosurgery. Spine* 1, 287-298, doi:10.3171/spi.2004.1.3.0287 (2004).

[129] Tomita, K. *et al.* Surgical strategy for spinal metastases. *Spine* 26, 298-306 (2001).

*American journal of sports medicine* 19, 355-364 (1991).

*Spine Research Society*, doi:10.1007/s00586-013-2658-z (2013).

s00264-005-0016-4 (2006).

2186-2191 (2005).

106 Topics in Paraplegia

1110-1113 (1990).

1975.27 (1975).

(2007).

discussion 1448 (2001).

**Chapter 5**

**Functional Electrical**

Aris Papachristos

**1. Introduction**

tion (FNS or FNMS).

http://dx.doi.org/10.5772/58625

**Stimulation in Paraplegia**

Additional information is available at the end of the chapter

user's shoe, would activate a stimulator worn by the user.

Functional Electrical Stimulation (FES) is a technique of eliciting controlled neural activation through the application of low levels of electrical current. FES was initially referred to as Functional Electrotherapy by Liberson [1] and it was not until 1967 that the term Functional Electrical Stimulation was established by Moe and Post [2]. In 1965 Offner patented a system used to treat foot drop with the title "Electrical stimulation of muscle deprived of nervous control with a view of providing muscular contraction and producing a functionally useful moment" [3]. Another term often used equally to FES is Functional Neuromusclular Stimula‐

The first commercially available FES devices treated foot drop in hemiplegic patients by stimulating the peroneal nerve during gait. In this case, a switch, located in the heel end of a

Structural discontinuity in the spinal cord after injury results in a disruption in the impulse conduction resulting in loss of various bodily functions depending upon the level of injury. The initial goal of FES technology was to provide greater mobility to the patients after SCI. However, with the advances in biomedical engineering within the last 2 decades, FES is no more limited to locomotion alone. Therefore, the definition of FES has changed considerably and is now considered to be the technique of applying safe levels of electric current to stimulate various organs of the body rendered disabled due to SCI. Electrical stimulation in the form of functional electrical stimulation (FES) can help facilitate and improve limb mobility along with

> © 2014 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

other body functions lost due to injury e.g. sexual, bladder or bowel functions.

**Chapter 5**

## **Functional Electrical Stimulation in Paraplegia**

#### Aris Papachristos

Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/58625

#### **1. Introduction**

Functional Electrical Stimulation (FES) is a technique of eliciting controlled neural activation through the application of low levels of electrical current. FES was initially referred to as Functional Electrotherapy by Liberson [1] and it was not until 1967 that the term Functional Electrical Stimulation was established by Moe and Post [2]. In 1965 Offner patented a system used to treat foot drop with the title "Electrical stimulation of muscle deprived of nervous control with a view of providing muscular contraction and producing a functionally useful moment" [3]. Another term often used equally to FES is Functional Neuromusclular Stimula‐ tion (FNS or FNMS).

The first commercially available FES devices treated foot drop in hemiplegic patients by stimulating the peroneal nerve during gait. In this case, a switch, located in the heel end of a user's shoe, would activate a stimulator worn by the user.

Structural discontinuity in the spinal cord after injury results in a disruption in the impulse conduction resulting in loss of various bodily functions depending upon the level of injury. The initial goal of FES technology was to provide greater mobility to the patients after SCI. However, with the advances in biomedical engineering within the last 2 decades, FES is no more limited to locomotion alone. Therefore, the definition of FES has changed considerably and is now considered to be the technique of applying safe levels of electric current to stimulate various organs of the body rendered disabled due to SCI. Electrical stimulation in the form of functional electrical stimulation (FES) can help facilitate and improve limb mobility along with other body functions lost due to injury e.g. sexual, bladder or bowel functions.

© 2014 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

#### **2. Mechanism of FES operation**

Both nerves and muscle fibres respond to electric current. However, for practical purposes FES is mostly used to directly stimulate nerve fibres, as a much lower amount of current is required to generate an action potential in a nerve than the one required for muscular depolarisation.

levels. The source should be flexible to generate complex electrical waveforms, such as

Functional Electrical Stimulation in Paraplegia

http://dx.doi.org/10.5772/58625

111

The numbers of channels, which can range from one to several, govern the sophistication required for complex outputs like FES assisted standing. The programmable microprocessor activates the various channels sequentially or in unison to synchronize the complex output of the stimulator. Electrodes provide the interface between the electrical stimulator and the nervous system. Various types of electrodes have been developed and are available ranging from non-invasive surface electrodes to invasive implantable ones. Implantable electrodes provide more specific and selective stimulation to the desired muscle group than the surface electrodes. The feedback control of the FES system can be either open-looped or closed-looped. Open-looped control is used for simple tasks such as for muscle strengthening alone, and requires a constant electrical output from the stimulator. In a closed-looped system, the parameters for electrical stimulation are constantly modified by a computer via feedback information on muscle force and joint position thus stimulating various muscle groups simultaneously leading to a combination of muscular contraction needed for a complex

The efforts to develop a suitable human functional stimulator which can achieve synergistic activity of various muscles accelerated in the late 1980s and early 1990s. In 1987, Davis proposed the development of a FES system based on multi-cochlear implant technology to restore function in paraplegic patients [9]. Kralj proposed the use of FES for restoring standing and walking in spinal cord injured (SCI) patients [4]. Other parallel studies at that time also concluded that FES assisted walking is feasible in patients with incomplete SCI even with severe motor loss [7, 10]. In all lower limb applications the general method for restoration of standing is the application of electrical stimulation to the quadriceps. The restoration and/or improvement of gait has typically involved the stimulation of two sites. These have been the quadriceps, during the stance phase of gait and the peroneal nerve, producing a patterned flexion response during the swing phase of the ipsilateral limb [6]. FES has greater potential for functional use in incomplete spinal cord injury (ISCI) patients due to the preservation of some motor and sensory function [7,8]. Paraplegic patients using FES for ambulation still require the use of walker or other orthotic devices for stabilising the ankle, knees and hips. Several gait programs for the ISCI subjects have been established. Applications of FES can be divided into two classes: (A) neuroprostheses for use as permanent assistive devices, and (B) FES to facilitate exercise and be used in temporary therapeutic interventions to improve voluntary function. This latter class of applications has been termed functional electrical therapy (FET). Therapeutic applications include cardiovascular conditioning and the preven‐ tion of muscular atrophy through exercise. Functional applications assist with vital body functions lost due to SCI. The FES devices were initially designed in an attempt to provide assistance with standing or walking, provided the paraplegic patient had adequate upper body

triangular or quasitrapezoidal waveforms [60].

sophisticated functional activity such as walking.

**3. Standing and walking**

motor control and strength [13,32].

The main component of a FES system is the microprocessor-based electronic stimulator which determines when and how the stimulation is provided, with channels for delivery of individual pulses through a set of electrodes connected to the neuromuscular system. The microprocessor contains programs for sitting, standing, walking etc. It serves to generate a train of impulses that grossly imitate the neural triggers that would have normally passed through the spinal cord to the appropriate peripheral nerves below spinal cord lesion for these different programs. These stimuli thus trigger action potentials in the peripheral nerves which in turn activate muscle contractions in the associated muscles fibers [11]. When properly applied, the energy transfer is both safe and efficient. Low levels of current can be safely injected to neural tissue with a minimal but biologically acceptable response. Furthermore, the energy amplification is substantial, since a small stimulus can generate a considerable action. For example, an electrical stimulus of a few milliwatts generates as much as a hundred newton-meters of torque in the lower limb.

It is proven nowadays that FES exersice is improving cardiovascular fitness, and decreasing the risk of diabetes, as well as reducing osteoporosis [12, 54-59]. FES exercise and weight bearing also reduce the risk of pressure sores by improving tissue oxygen levels, increasing muscle bulk, and altering seated pressure distribution [12]

Another use of electrical signals is to use afferent signals from intact structures whose communication links with other body systems have been destroyed or diminished by an injury or disease to provide feedback to guide motor activity.

It is conceptually possible, therefore, to obtain "artificial" control with electrical stimulation over virtually all structures which rely upon neural communication for their activation. This encompasses virtually all of the critical motor and sensory pathways involved in paralysis of the central nervous system.

The frequency, pulse width/duration, duty cycle, intensity/amplitude, ramp time, pulse pattern, program duration, program frequency, and muscle groups activated are parameters taken into account. Frequency refers to the pulses produced per second during stimulation and is stated in units of Hertz (Hz, e.g., 40 Hz=40 pulses per second). The frequencies of electrical stimulation used can vary widely depending on the goals of the task or intervention, but most clinical regimens use 20-50Hz patterns for optimal results [20]. In order to avoid fatigue or discomfort, constant low frequency stimulation is typically used, which produces a smooth contraction at low force levels. In a study comparing several different frequencies and stimulation patterns, frequencies under 16Hz were not sufficient to elicit a strong enough contraction to allow the quadriceps to extend to a target of 40º. Commercial stimulators provide many different waveforms and pulse settings capable of producing contractions at therapeutic levels. The source should be flexible to generate complex electrical waveforms, such as triangular or quasitrapezoidal waveforms [60].

The numbers of channels, which can range from one to several, govern the sophistication required for complex outputs like FES assisted standing. The programmable microprocessor activates the various channels sequentially or in unison to synchronize the complex output of the stimulator. Electrodes provide the interface between the electrical stimulator and the nervous system. Various types of electrodes have been developed and are available ranging from non-invasive surface electrodes to invasive implantable ones. Implantable electrodes provide more specific and selective stimulation to the desired muscle group than the surface electrodes. The feedback control of the FES system can be either open-looped or closed-looped. Open-looped control is used for simple tasks such as for muscle strengthening alone, and requires a constant electrical output from the stimulator. In a closed-looped system, the parameters for electrical stimulation are constantly modified by a computer via feedback information on muscle force and joint position thus stimulating various muscle groups simultaneously leading to a combination of muscular contraction needed for a complex sophisticated functional activity such as walking.

#### **3. Standing and walking**

**2. Mechanism of FES operation**

lower limb.

110 Topics in Paraplegia

the central nervous system.

Both nerves and muscle fibres respond to electric current. However, for practical purposes FES is mostly used to directly stimulate nerve fibres, as a much lower amount of current is required to generate an action potential in a nerve than the one required for muscular depolarisation.

The main component of a FES system is the microprocessor-based electronic stimulator which determines when and how the stimulation is provided, with channels for delivery of individual pulses through a set of electrodes connected to the neuromuscular system. The microprocessor contains programs for sitting, standing, walking etc. It serves to generate a train of impulses that grossly imitate the neural triggers that would have normally passed through the spinal cord to the appropriate peripheral nerves below spinal cord lesion for these different programs. These stimuli thus trigger action potentials in the peripheral nerves which in turn activate muscle contractions in the associated muscles fibers [11]. When properly applied, the energy transfer is both safe and efficient. Low levels of current can be safely injected to neural tissue with a minimal but biologically acceptable response. Furthermore, the energy amplification is substantial, since a small stimulus can generate a considerable action. For example, an electrical stimulus of a few milliwatts generates as much as a hundred newton-meters of torque in the

It is proven nowadays that FES exersice is improving cardiovascular fitness, and decreasing the risk of diabetes, as well as reducing osteoporosis [12, 54-59]. FES exercise and weight bearing also reduce the risk of pressure sores by improving tissue oxygen levels, increasing

Another use of electrical signals is to use afferent signals from intact structures whose communication links with other body systems have been destroyed or diminished by an injury

It is conceptually possible, therefore, to obtain "artificial" control with electrical stimulation over virtually all structures which rely upon neural communication for their activation. This encompasses virtually all of the critical motor and sensory pathways involved in paralysis of

The frequency, pulse width/duration, duty cycle, intensity/amplitude, ramp time, pulse pattern, program duration, program frequency, and muscle groups activated are parameters taken into account. Frequency refers to the pulses produced per second during stimulation and is stated in units of Hertz (Hz, e.g., 40 Hz=40 pulses per second). The frequencies of electrical stimulation used can vary widely depending on the goals of the task or intervention, but most clinical regimens use 20-50Hz patterns for optimal results [20]. In order to avoid fatigue or discomfort, constant low frequency stimulation is typically used, which produces a smooth contraction at low force levels. In a study comparing several different frequencies and stimulation patterns, frequencies under 16Hz were not sufficient to elicit a strong enough contraction to allow the quadriceps to extend to a target of 40º. Commercial stimulators provide many different waveforms and pulse settings capable of producing contractions at therapeutic

muscle bulk, and altering seated pressure distribution [12]

or disease to provide feedback to guide motor activity.

The efforts to develop a suitable human functional stimulator which can achieve synergistic activity of various muscles accelerated in the late 1980s and early 1990s. In 1987, Davis proposed the development of a FES system based on multi-cochlear implant technology to restore function in paraplegic patients [9]. Kralj proposed the use of FES for restoring standing and walking in spinal cord injured (SCI) patients [4]. Other parallel studies at that time also concluded that FES assisted walking is feasible in patients with incomplete SCI even with severe motor loss [7, 10]. In all lower limb applications the general method for restoration of standing is the application of electrical stimulation to the quadriceps. The restoration and/or improvement of gait has typically involved the stimulation of two sites. These have been the quadriceps, during the stance phase of gait and the peroneal nerve, producing a patterned flexion response during the swing phase of the ipsilateral limb [6]. FES has greater potential for functional use in incomplete spinal cord injury (ISCI) patients due to the preservation of some motor and sensory function [7,8]. Paraplegic patients using FES for ambulation still require the use of walker or other orthotic devices for stabilising the ankle, knees and hips. Several gait programs for the ISCI subjects have been established. Applications of FES can be divided into two classes: (A) neuroprostheses for use as permanent assistive devices, and (B) FES to facilitate exercise and be used in temporary therapeutic interventions to improve voluntary function. This latter class of applications has been termed functional electrical therapy (FET). Therapeutic applications include cardiovascular conditioning and the preven‐ tion of muscular atrophy through exercise. Functional applications assist with vital body functions lost due to SCI. The FES devices were initially designed in an attempt to provide assistance with standing or walking, provided the paraplegic patient had adequate upper body motor control and strength [13,32].

The use of these FES devices designed to permit or improve ambulation is not simple or without risks. Paraplegic patients require extensive training to build muscle strength in the upper body in order to achieve FES assisted ambulation. The amount of energy spent with FES walking is almost twice than that for normal walking, although the achievable speed is slower than that of normal walking [18,19]. The risk of injury with FES assisted ambulation is more likely to be higher due to fatigue of the stimulated muscle causing an increase incidence of fall and fractures. These factors limit the true functional utilisation of these systems. Another major practical problem associated with the current FES locomotive models is mainly related to feedback control. In spite of these associated limitations for everyday mobility in daily life, there are potential functional, medical and psychological benefits of FES assisted standing and walking. These devices can help increase their level of independence by providing some assistance with standing while transferring from the wheelchair to a car, climbing a few steps or reaching for a higher object.

The system provides stimulation output to 12 surface electrodes that are attached to the skin at appropriate placements. These stimulation pulses trigger action potentials in the intact peripheral nerves to generate muscle contraction. Another noninvasive, transcutaneous FES system is the six-channel stimulator from the Ljubljana University but it was not commercial‐ ized and not FDA approved. In opposite the Parastep system received FDA approval in 1994 is nowadays widely available. It has been evaluated for its ambulation performance and medical/psychological effects.[14,16,17]. Factors considered to be a candidate for ambulation with the Parastep system include the presence of neurologically stable and complete SCI, level of injury (preferably between T4 and T12), patient motivation, degree of spasticity, muscle contractile response to electrical stimulation, cardio-respiratory capacity, and musculoskeletal

Functional Electrical Stimulation in Paraplegia

http://dx.doi.org/10.5772/58625

113

Current technology using surface and percutaneous electrodes has distinct disadvantages. Systems using percutaneous electrodes are prone to infection if poorly maintained, and systems using surface electrodes make donning and doffing difficult. Moreover, as the number of channels increases, surface electrodes become impractical and inconvenient, making them generally best suited for short-term therapeutic applications. In addition, selectively activating individual muscles deep to the skin (such as the hip flexors) with surface stimulation or obtaining repeatable stimulated responses from day to day is difficult or impossible. Neural prostheses or Neuroprosthetics are implantable devices which use electrical current that can substitute a motor, sensory or cognitive modality that might have been damaged as a result of an injury or a disease. Familiar examples include cochlear implants and cardiac pacemakers. The Freehand system was the first motor-system neuroprosthesis to receive marketing approval. These devices have been safely and effectively installed worldwide in the upper limbs in patients with cervical SCI to provide active handgrasp after paralysis without major complications. External system components included a custom rechargeable wearable external control unit, command hand switch, transmitting coil, charger, and clinical programming

Fully implanted pacemaker-like systems offer numerous advantages over surface and percutaneous stimulation for long-term clinical use, including improved convenience, cosmesis, reliability, and repeatability. In these systems, muscle or nerve-based electrodes are installed surgically and connected to an implanted stimulation device, so no material crosses

FES systems using implanted intramuscular electrodes with percutaneous leads have provid‐ ed up to 48 channels of stimulation for improved stability and forward progression and finer control of movement during walking. Multichannel implanted FES systems for walking after motor complete paraplegia have provided a swing-through and reciprocal gait [29,30]. They reduced donning time and improved day-to-day repeatability compared with surface FES

systems and eliminated site care of percutaneous systems.

integrity.

station.

the skin.

**3.2. Implanted FES systems**

#### **3.1. Non-invasive FES systems**

Parastep I is a FDA approved FES system for short distance ambulation that uses a walker support for balance [14,15]. The Parastep is a non-invasive system and consists of the following components:


**Figure 1.** Advertisement of the Parastep System

The system provides stimulation output to 12 surface electrodes that are attached to the skin at appropriate placements. These stimulation pulses trigger action potentials in the intact peripheral nerves to generate muscle contraction. Another noninvasive, transcutaneous FES system is the six-channel stimulator from the Ljubljana University but it was not commercial‐ ized and not FDA approved. In opposite the Parastep system received FDA approval in 1994 is nowadays widely available. It has been evaluated for its ambulation performance and medical/psychological effects.[14,16,17]. Factors considered to be a candidate for ambulation with the Parastep system include the presence of neurologically stable and complete SCI, level of injury (preferably between T4 and T12), patient motivation, degree of spasticity, muscle contractile response to electrical stimulation, cardio-respiratory capacity, and musculoskeletal integrity.

#### **3.2. Implanted FES systems**

The use of these FES devices designed to permit or improve ambulation is not simple or without risks. Paraplegic patients require extensive training to build muscle strength in the upper body in order to achieve FES assisted ambulation. The amount of energy spent with FES walking is almost twice than that for normal walking, although the achievable speed is slower than that of normal walking [18,19]. The risk of injury with FES assisted ambulation is more likely to be higher due to fatigue of the stimulated muscle causing an increase incidence of fall and fractures. These factors limit the true functional utilisation of these systems. Another major practical problem associated with the current FES locomotive models is mainly related to feedback control. In spite of these associated limitations for everyday mobility in daily life, there are potential functional, medical and psychological benefits of FES assisted standing and walking. These devices can help increase their level of independence by providing some assistance with standing while transferring from the wheelchair to a car, climbing a few steps

Parastep I is a FDA approved FES system for short distance ambulation that uses a walker support for balance [14,15]. The Parastep is a non-invasive system and consists of the following

**•** a microcomputer controlled neuromuscular stimulation unit

**•** a unit for pre-testing main system operation and electrode cables

**•** a control and stability walker with finger activated control switches.

or reaching for a higher object.

**3.1. Non-invasive FES systems**

**•** surface applied skin electrodes

**Figure 1.** Advertisement of the Parastep System

**•** power and electrode cables

components:

112 Topics in Paraplegia

**•** a battery

Current technology using surface and percutaneous electrodes has distinct disadvantages. Systems using percutaneous electrodes are prone to infection if poorly maintained, and systems using surface electrodes make donning and doffing difficult. Moreover, as the number of channels increases, surface electrodes become impractical and inconvenient, making them generally best suited for short-term therapeutic applications. In addition, selectively activating individual muscles deep to the skin (such as the hip flexors) with surface stimulation or obtaining repeatable stimulated responses from day to day is difficult or impossible. Neural prostheses or Neuroprosthetics are implantable devices which use electrical current that can substitute a motor, sensory or cognitive modality that might have been damaged as a result of an injury or a disease. Familiar examples include cochlear implants and cardiac pacemakers. The Freehand system was the first motor-system neuroprosthesis to receive marketing approval. These devices have been safely and effectively installed worldwide in the upper limbs in patients with cervical SCI to provide active handgrasp after paralysis without major complications. External system components included a custom rechargeable wearable external control unit, command hand switch, transmitting coil, charger, and clinical programming station.

Fully implanted pacemaker-like systems offer numerous advantages over surface and percutaneous stimulation for long-term clinical use, including improved convenience, cosmesis, reliability, and repeatability. In these systems, muscle or nerve-based electrodes are installed surgically and connected to an implanted stimulation device, so no material crosses the skin.

FES systems using implanted intramuscular electrodes with percutaneous leads have provid‐ ed up to 48 channels of stimulation for improved stability and forward progression and finer control of movement during walking. Multichannel implanted FES systems for walking after motor complete paraplegia have provided a swing-through and reciprocal gait [29,30]. They reduced donning time and improved day-to-day repeatability compared with surface FES systems and eliminated site care of percutaneous systems.

standing up and for forward progression during walking. Clinical reviews also indicate that brace users are consistently unable to achieve significant functional ambulation without some sort of pelvic control and that adequate hip flexion is an essential component of walking with braces. In conclusion only few individuals with paraplegia choose to use their orthosis for

Functional Electrical Stimulation in Paraplegia

http://dx.doi.org/10.5772/58625

115

First in 1973, a hybrid actuator was described for orthotic systems in which the anatomical joint could be controlled internally by means of FES or externally by means of a hypothetical three-state joint actuator incorporated onto an exoskeletal brace [33]. This work initiated the field of hybrid orthotics and, specifically, defined the concept of a hybrid neuroprosthesis

Hybrid neuroprosthesis (HNP) potentially can combine the best features of mechanical bracing and FES into new systems for walking after SCI that offer more advantages than the individual components acting alone. The exoskeletal mechanical components of hybrid systems have been generally passive devices to minimize size, weight, and energy consumption, while the

Surface and intramuscular FES systems have been combined with a conventional trunk-hipknee-ankle-foot orthosis (THKAFO) for reciprocal gait in individuals with complete thoracic level SCI. The addition of FES to the glutei for example during stance when individuals used lower-limb bracing reduced crutch forces [51,52] and provided forward propulsion by driving the stance leg into extension. Users with paraplegia (complete T4-T12 SCI) required 70 percent of their maximum upper-limb aerobic capacity when walking with an RGO alone, while walking with an RGO combined with FES required 32 percent of the upper-limb and 25 percent of the lower-limb aerobic capacity, effectively shifting the metabolic burden from the muscles of the arms, shoulders and trunk to the large, otherwise paralyzed, muscles of the legs [53]. The RGO Generation II is a reciprocating gait orthosis combined with FES which was devel‐ oped by Louisiana State University Medical Center and Durr-Fillauer Medical, Inc. It employs concurrent electrostimulation of the rectus femoris and hamstrings to assist in rising and balancing and a ratchet-type latching device to improve safety and stability in standing. Alternating stimulation of the rectus femoris and contralateral hamstrings are used for

In summary, an HNP combining bracing and FES has been shown to significantly improve walking distance and reduce energy consumption. A reciprocal coupling of the hips provides good trunk stability, and flexion-to-extension coupling ratios favoring flexion improve step length and energy cost. Unlocking the orthotic knee joints during the swing phase of gait improves foot-to-floor clearance and reduces energy cost, while locking them during stance

To date only a few ambulatory external powered exoskeletons have been built. An ambulatory system named HAL that combines a powered exoskeleton with a customized walker was designed at the Sogang University [43-45]. A walker ensures complete balance and reduces

(HNP), in which FES is combined with external mechanical components*.*

FES component serves as an active mechanism for limb propulsion.

activities other than therapeutic exercise [34].

locomotion [42].

postpones muscle fatigue from stimulation.

**3.4. Hybrid FES – External Powered Orthosis Ambulation systems**

#### **3.3. Hybrid FES-Orthosis ambulation systems**

A variety of mechanical orthoses have been designed and tested for lower-limb function after SCI. The reciprocal gait orthosis (RGOs) stabilize ankles, knees, hips, and trunk to provide upright posture and couple hip flexion with contralateral hip extension to facilitate walking. The long leg braces only fix the ankle and knee joints to provide stability and prevent collapse. In some configurations, the addition of a pelvic band provides extra stability. Most orthoses provide good postural stability, especially when the hip joints are reciprocally coupled to prevent bilateral hip flexion. With all mechanical braces, upper-body strength is required for standing up and for forward progression during walking. Clinical reviews also indicate that brace users are consistently unable to achieve significant functional ambulation without some sort of pelvic control and that adequate hip flexion is an essential component of walking with braces. In conclusion only few individuals with paraplegia choose to use their orthosis for activities other than therapeutic exercise [34].

First in 1973, a hybrid actuator was described for orthotic systems in which the anatomical joint could be controlled internally by means of FES or externally by means of a hypothetical three-state joint actuator incorporated onto an exoskeletal brace [33]. This work initiated the field of hybrid orthotics and, specifically, defined the concept of a hybrid neuroprosthesis (HNP), in which FES is combined with external mechanical components*.*

Hybrid neuroprosthesis (HNP) potentially can combine the best features of mechanical bracing and FES into new systems for walking after SCI that offer more advantages than the individual components acting alone. The exoskeletal mechanical components of hybrid systems have been generally passive devices to minimize size, weight, and energy consumption, while the FES component serves as an active mechanism for limb propulsion.

Surface and intramuscular FES systems have been combined with a conventional trunk-hipknee-ankle-foot orthosis (THKAFO) for reciprocal gait in individuals with complete thoracic level SCI. The addition of FES to the glutei for example during stance when individuals used lower-limb bracing reduced crutch forces [51,52] and provided forward propulsion by driving the stance leg into extension. Users with paraplegia (complete T4-T12 SCI) required 70 percent of their maximum upper-limb aerobic capacity when walking with an RGO alone, while walking with an RGO combined with FES required 32 percent of the upper-limb and 25 percent of the lower-limb aerobic capacity, effectively shifting the metabolic burden from the muscles of the arms, shoulders and trunk to the large, otherwise paralyzed, muscles of the legs [53].

The RGO Generation II is a reciprocating gait orthosis combined with FES which was devel‐ oped by Louisiana State University Medical Center and Durr-Fillauer Medical, Inc. It employs concurrent electrostimulation of the rectus femoris and hamstrings to assist in rising and balancing and a ratchet-type latching device to improve safety and stability in standing. Alternating stimulation of the rectus femoris and contralateral hamstrings are used for locomotion [42].

In summary, an HNP combining bracing and FES has been shown to significantly improve walking distance and reduce energy consumption. A reciprocal coupling of the hips provides good trunk stability, and flexion-to-extension coupling ratios favoring flexion improve step length and energy cost. Unlocking the orthotic knee joints during the swing phase of gait improves foot-to-floor clearance and reduces energy cost, while locking them during stance postpones muscle fatigue from stimulation.

#### **3.4. Hybrid FES – External Powered Orthosis Ambulation systems**

**3.3. Hybrid FES-Orthosis ambulation systems**

**Figure 2.** Cleveland FES Standing/Transfer System.

114 Topics in Paraplegia

A variety of mechanical orthoses have been designed and tested for lower-limb function after SCI. The reciprocal gait orthosis (RGOs) stabilize ankles, knees, hips, and trunk to provide upright posture and couple hip flexion with contralateral hip extension to facilitate walking. The long leg braces only fix the ankle and knee joints to provide stability and prevent collapse. In some configurations, the addition of a pelvic band provides extra stability. Most orthoses provide good postural stability, especially when the hip joints are reciprocally coupled to prevent bilateral hip flexion. With all mechanical braces, upper-body strength is required for

To date only a few ambulatory external powered exoskeletons have been built. An ambulatory system named HAL that combines a powered exoskeleton with a customized walker was designed at the Sogang University [43-45]. A walker ensures complete balance and reduces the weight of the device by housing the battery, DC motors, and control unit, with cables transmitting power to the joints.

joint trajectories stay consistent in the presence of time-varying muscle behavior, providing consistent and repeatable gait. Compared to using a powered exoskeleton alone, the addition of FES reduces electrical power consumption while providing additional joint torques. Certain therapeutic effects of the use of FES have been studied. The medical advantages of short distance ambulation include increased blood flow to lower limbs, increase in lower limb muscle mass, reduced spasticity, lower heart rate at sub peak work intensities and beneficial effects on digestion, bowel and bladder. Psychological benefits achieved through FES assisted walking such as the associated increase in self esteem and reduction in depression are all well documented. Most of the studies conducted which have evaluated the role of FES assisted

Functional Electrical Stimulation in Paraplegia

http://dx.doi.org/10.5772/58625

117

Other functional applications of FES which help to restore useful functions and thus improve the quality of life include bladder and bowel voiding and electro-ejaculation. Voluntary control of bowel and bladder function is either lost or considerably impaired depending upon the level and severity of SCI and can lead to multiple complications. The Vocare bladder system (Finetech-Brindley bladder system) is a surgically implantable sacral anterior root stimulator

Secondary use of the device is to aid in bowel evacuation. It was approved by FDA in 1998. It consists of an external controller and transmitter and an implantable receiver-stimulator and electrodes. This system is operated by radio frequency signals transmitted to electrodes placed

that allows individuals with complete spinal cord injury to urinate on demand [60].

walking have a very small sample size and a short follow up time [48,51].

**4. Bladder, bowel and sexual function**

**Figure 4.** The Finetech-Brindley Bladder Control System

ReWalk developed by Argo Medical Technologies Ltd. enables paraplegics, with the aid of crutches for balance, to stand up, sit

down, walk about including slopes, and even climb stairs.[46]. ReWalk features servomotors located at the hip and knee joints, rechargeable batteries, and a wrist remote control that commands the type of desired motion. Since ambulatory exoskeletons are meant to be used by paraplegics and people with severely impaired locomotion capabilities, two crucial problems must be considered – ensuring full balance and determining the intention of the motion of the user. To overcome these problems, external balancing aids have been considered – crutches, canes, or walkers are used to ensured balance, whereas joysticks or keypads are used to command the desired motion.

In 2010 Berkeley Bionics unveiled eLEGS, which stands for "Exoskeleton Lower Extremity Gait System". eLEGS is another hydraulically powered exoskeleton system, and allows paraplegics to stand and walk with crutches or a walker. In 2011 eLEGS was renamed Ekso. Ekso weighs 20 kg, it has a maximum speed of 3.2 km/h and a battery life of 6 hour [47].

**Figure 3.** "eLegs" exoskeleton by Berkeley Bionics

A new promising exoskeleton named Indego is seeking for FDA approval in 2015 developed in Vanderbilt University [49,50].

All of these devices can be coupled with FES. Compared to using FES alone, the powered exoskeleton provides joint motions that are otherwise difficult to achieve consistently (e.g. hip flexion). Even for motions that can be achieved using FES, the exoskeleton ensures that the joint trajectories stay consistent in the presence of time-varying muscle behavior, providing consistent and repeatable gait. Compared to using a powered exoskeleton alone, the addition of FES reduces electrical power consumption while providing additional joint torques. Certain therapeutic effects of the use of FES have been studied. The medical advantages of short distance ambulation include increased blood flow to lower limbs, increase in lower limb muscle mass, reduced spasticity, lower heart rate at sub peak work intensities and beneficial effects on digestion, bowel and bladder. Psychological benefits achieved through FES assisted walking such as the associated increase in self esteem and reduction in depression are all well documented. Most of the studies conducted which have evaluated the role of FES assisted walking have a very small sample size and a short follow up time [48,51].

#### **4. Bladder, bowel and sexual function**

the weight of the device by housing the battery, DC motors, and control unit, with cables

ReWalk developed by Argo Medical Technologies Ltd. enables paraplegics, with the aid of

down, walk about including slopes, and even climb stairs.[46]. ReWalk features servomotors located at the hip and knee joints, rechargeable batteries, and a wrist remote control that commands the type of desired motion. Since ambulatory exoskeletons are meant to be used by paraplegics and people with severely impaired locomotion capabilities, two crucial problems must be considered – ensuring full balance and determining the intention of the motion of the user. To overcome these problems, external balancing aids have been considered – crutches, canes, or walkers are used to ensured balance, whereas joysticks or keypads are

In 2010 Berkeley Bionics unveiled eLEGS, which stands for "Exoskeleton Lower Extremity Gait System". eLEGS is another hydraulically powered exoskeleton system, and allows paraplegics to stand and walk with crutches or a walker. In 2011 eLEGS was renamed Ekso. Ekso weighs

A new promising exoskeleton named Indego is seeking for FDA approval in 2015 developed

All of these devices can be coupled with FES. Compared to using FES alone, the powered exoskeleton provides joint motions that are otherwise difficult to achieve consistently (e.g. hip flexion). Even for motions that can be achieved using FES, the exoskeleton ensures that the

20 kg, it has a maximum speed of 3.2 km/h and a battery life of 6 hour [47].

transmitting power to the joints.

116 Topics in Paraplegia

crutches for balance, to stand up, sit

used to command the desired motion.

**Figure 3.** "eLegs" exoskeleton by Berkeley Bionics

in Vanderbilt University [49,50].

Other functional applications of FES which help to restore useful functions and thus improve the quality of life include bladder and bowel voiding and electro-ejaculation. Voluntary control of bowel and bladder function is either lost or considerably impaired depending upon the level and severity of SCI and can lead to multiple complications. The Vocare bladder system (Finetech-Brindley bladder system) is a surgically implantable sacral anterior root stimulator that allows individuals with complete spinal cord injury to urinate on demand [60].

**Figure 4.** The Finetech-Brindley Bladder Control System

Secondary use of the device is to aid in bowel evacuation. It was approved by FDA in 1998. It consists of an external controller and transmitter and an implantable receiver-stimulator and electrodes. This system is operated by radio frequency signals transmitted to electrodes placed on the sacral spinal nerves (S2-S4) and leads to bladder/large bowel and urethral/ anal sphincter contraction. At the time of implantation, a posterior rhizotomy through laminectomy at sacral level is performed to abolish the uninhibited reflex bladder contractions. This eliminates the reflex incontinence caused by the activation of the sensory reflex pathway. However it also causes a loss of perineal sensations and reflex erection and ejaculation if present. Patient selection criteria for Vocare implantation include neurologically stable and clinically complete supra-sacral SCI and intact parasympathetic innervation to detrusor musculature. The major disadvantage of this system is the need for major surgery for implan‐ tation and posterior rhizotomy. However, this device offers an improved quality of life, social ease, as well as a reduction and prevention of urinary tract infections and their associated complication (61,62,65li) Another added benefit of this system is enhanced bowel evacuation with most patients reporting a reduction in the time required for bowel evacuation along with a reduction in constipation and faecal impaction. A slower stimulation time sequence is required for defeacation than for micturation. Approximately 60% of men can also produce penile erection using this device. Electroejaculation is one of the several techniques now available to harvest viable sperm for the purposes of artificial insemination or in vitro fertilization. An electric probe is inserted into the rectum near the prostate to stimulate the nerves and contract the pelvis muscles, causing ejaculation [63,64]. The ejaculate is collected from the urethra and prepared for use in artificial insemination. Caution need to be taken in men with SCI who have a history of autonomic dysreflexia as electroejaculation can cause a significant increase in blood pressure and heart rate.

In general, FES cycling ergometers can be divided into two major types, mobile and stationary types. The mobile type, a locomotion device, focuses on muscle training as well as giving some mobility to subjects whose muscles can still be excited. Several research groups have developed a mobile cycling system using standard or recumbent tricycles for SCI subjects. Usually, the mobile type of cycling ergometer is an open-loop system, which is not only a rehabilitation

Functional Electrical Stimulation in Paraplegia

http://dx.doi.org/10.5772/58625

119

The stationary type of cycling ergometer is usually used for aerobic exercise training in subjects with an SCI to condition their muscle strength and enhance cardiopulmonary function.

modality but also a recreational activity.

**Figure 5.** The"RehaBike"by Hasomed (outdoor bike)

**Figure 6.** "RehaMove" FES System coupled with Motomed stationary bike

#### **4.1. FES cycling and rowing**

A safe and economic alternative to FES-induced gait training is the employment of FES synchronized to the cycling movement, which entails a coordinated activation of the lower limb muscles, approximating the cyclic movements of locomotion. In contrast to FES standing and walking systems, an FES-cycling system uses stimulator cycling software to control sequential stimulation of the large leg-actuating muscles of paralyzed leg muscles to produce cyclical leg motion. Currently, FES cycling exercise (FESCE) is often used in rehabilitation therapy. There are a number of subsequent investigations reporting physiological adaptations after regular cycling exercise training, which demonstrated that cycling exercise increases muscle strength and endurance and bone density [66-71] suppresses spasticity [72,73], improves cardiopulmonary function, and provides many other physiological and psycholog‐ ical benefits for subjects with an SCI [74-78]. Typically, the quadriceps,hamstrings, and gluteus groups are activated in an appropriate sequence which is out of phase bilaterally to maintain a forward driving torque. The level of stimulation applied to the muscles (which, in turn, determines the amount of torque and cadence produced at the pedals) is controlled by the stimulation software. The advantage of FES-cycling over FES-walking and standing exercise is that individuals with paralysis can perform the exercise, and it can also enhance an indi‐ vidual's suitability for FES standing and walking. Presently, there are many commercial FES cycling ergometers available, such as the BerkelBike (BerkelBike BV, AV's-Hertogenbosch, the Netherlands), Ergys and Regys (Therapeutic Alliances, Fairborn, Ohio, USA), and Motomed (Reck, Betzenweiler, Germany).

In general, FES cycling ergometers can be divided into two major types, mobile and stationary types. The mobile type, a locomotion device, focuses on muscle training as well as giving some mobility to subjects whose muscles can still be excited. Several research groups have developed a mobile cycling system using standard or recumbent tricycles for SCI subjects. Usually, the mobile type of cycling ergometer is an open-loop system, which is not only a rehabilitation modality but also a recreational activity.

**Figure 5.** The"RehaBike"by Hasomed (outdoor bike)

on the sacral spinal nerves (S2-S4) and leads to bladder/large bowel and urethral/ anal sphincter contraction. At the time of implantation, a posterior rhizotomy through laminectomy at sacral level is performed to abolish the uninhibited reflex bladder contractions. This eliminates the reflex incontinence caused by the activation of the sensory reflex pathway. However it also causes a loss of perineal sensations and reflex erection and ejaculation if present. Patient selection criteria for Vocare implantation include neurologically stable and clinically complete supra-sacral SCI and intact parasympathetic innervation to detrusor musculature. The major disadvantage of this system is the need for major surgery for implan‐ tation and posterior rhizotomy. However, this device offers an improved quality of life, social ease, as well as a reduction and prevention of urinary tract infections and their associated complication (61,62,65li) Another added benefit of this system is enhanced bowel evacuation with most patients reporting a reduction in the time required for bowel evacuation along with a reduction in constipation and faecal impaction. A slower stimulation time sequence is required for defeacation than for micturation. Approximately 60% of men can also produce penile erection using this device. Electroejaculation is one of the several techniques now available to harvest viable sperm for the purposes of artificial insemination or in vitro fertilization. An electric probe is inserted into the rectum near the prostate to stimulate the nerves and contract the pelvis muscles, causing ejaculation [63,64]. The ejaculate is collected from the urethra and prepared for use in artificial insemination. Caution need to be taken in men with SCI who have a history of autonomic dysreflexia as electroejaculation can cause a

A safe and economic alternative to FES-induced gait training is the employment of FES synchronized to the cycling movement, which entails a coordinated activation of the lower limb muscles, approximating the cyclic movements of locomotion. In contrast to FES standing and walking systems, an FES-cycling system uses stimulator cycling software to control sequential stimulation of the large leg-actuating muscles of paralyzed leg muscles to produce cyclical leg motion. Currently, FES cycling exercise (FESCE) is often used in rehabilitation therapy. There are a number of subsequent investigations reporting physiological adaptations after regular cycling exercise training, which demonstrated that cycling exercise increases muscle strength and endurance and bone density [66-71] suppresses spasticity [72,73], improves cardiopulmonary function, and provides many other physiological and psycholog‐ ical benefits for subjects with an SCI [74-78]. Typically, the quadriceps,hamstrings, and gluteus groups are activated in an appropriate sequence which is out of phase bilaterally to maintain a forward driving torque. The level of stimulation applied to the muscles (which, in turn, determines the amount of torque and cadence produced at the pedals) is controlled by the stimulation software. The advantage of FES-cycling over FES-walking and standing exercise is that individuals with paralysis can perform the exercise, and it can also enhance an indi‐ vidual's suitability for FES standing and walking. Presently, there are many commercial FES cycling ergometers available, such as the BerkelBike (BerkelBike BV, AV's-Hertogenbosch, the Netherlands), Ergys and Regys (Therapeutic Alliances, Fairborn, Ohio, USA), and Motomed

significant increase in blood pressure and heart rate.

**4.1. FES cycling and rowing**

118 Topics in Paraplegia

(Reck, Betzenweiler, Germany).

The stationary type of cycling ergometer is usually used for aerobic exercise training in subjects with an SCI to condition their muscle strength and enhance cardiopulmonary function.

**Figure 6.** "RehaMove" FES System coupled with Motomed stationary bike

The time course and training frequency are major factors that determine the therapeutic effects of cycling exercise. It is commonly recommended that subjects with an SCI receive at least 2-3 times per week and 30 min per time in a cycling rehabilitation program. In addition, it was reported that detraining from cycling exercise can soon induce a quick reversal of physical fitness within 1 week. The selection of electrical stimulation parameters is also an important issue considered in FESCE studies. Commonly, the FES cycling stimulation current is delivered to the large paralyzed leg muscles via surface electrodes. The stimulation output can either be regulated current or regulated voltage, which depends on the control design of the FES cycling stimulator. Commonly, the stimulation frequency is selected in the range of 10~50 Hz. However, a relatively higher stimulation frequency (> 50 Hz) can produce higher forces and therefore higher power for pedaling the ergometer compared to lower stimulation frequencies (10~50 Hz). But higher stimulation frequencies may rapidly result in ATP depletion at neuromuscular junctions and cause muscle fatigue.

[6] Bajd T, Andrews BJ, Kralj A, Katakis J (1986) Restoration of walking in patients with incomplete spinal cord injuries by use of electrical stimulation-preliminary results.

Functional Electrical Stimulation in Paraplegia

http://dx.doi.org/10.5772/58625

121

[7] Bajd T, Kralj A, Turk R, Benko H, Sega J (1989) Use of functional electrical stimula‐ tion in the rehabilitation of patients with incomplete spinal cord injuries. J Biomed

[8] Kralj A, Bajd T (1989) Functional Electrical Stimulation: Standing and Walking After

[9] Davis R, Eckhouse J, Patrick J, et al. Computerised 22 channel stimulator for limb

[10] Graupe D, Kohn KH. Functional neuromuscular stimulator for short distance ambu‐ lation by certain thoracic level spinal cord injured paraplegics. Surg Neurol.

[11] Rattay F, Resatz S, Dimitrijevic MR, et al. Mechanisms of electrical stimulations with neural prosthesis. Neuromodulation.2003;6(1):42–56. doi: 10.1046/j.

[12] Samar Hamid and Ray Hayek. Role of electrical stimulation for rehabilitation and re‐ generation after spinal cord injury: an overview. Eur Spine J. 2008 Sep;17(9):1256-69.

[13] Gorman PH. An update on functional electrical stimulation after spinal cord in‐

[14] Graupe D. An overview of the state of the art of noninvasive FES for independent ambulation by thoracic level paraplegics.Neurol Res. 2002;24(5):431–442. doi:

[16] Brissot R, Gallien P, Le Bot MP, et al. Clinical experience wit functional electrical stimulation-assisted gait with parastep in spinal cord injured patients. Spine.

[17] Gallien P, Brissot R, Eyssette M, et al. Restoration of gait by functional electrical stim‐

[18] Jacobs PL, Johnson B, Mahoney ET. Physiologic responses to electrically assisted and frame-supported standing in persons with paraplegia. J Spinal Cord Med.2003;26(4):

[19] Spadone R, Merati G, Bertocchi E, Mevio E, Veicsteinas A, Pedotti A. et al. Energy consumption of locomotion with orthosis versus Parastep-assisted gait: a single case study. Spinal Cord. 2003;41(2):97–104 (x) Sadowsky CL. Electrical stimulation in spi‐

ulation for spinal cord injured patients. Paraplegia. 1995;33(11):660–664

movement. Appl Neurophysiol. 1987;50:444–448. doi: 10.1159/000100760

Clin Prosthet Orthot 10: 111-114.

1525-1403.2003.03006

doi: 10.1007/s00586-008-0729-3.

10.1179/016164102101200302

384–389.

[15] SIGMEDICS, INC. http://www.sigmedics.com

Eng 11: 96-102 doi: 10.1016/0141-5425(89)90115-5.

Spinal Cord Injury. CRC Press, Inc, Boca Raton, Florida, USA.

1998;50(3):202–207. doi: 10.1016/S0090-3019(98)00074-3

jury.Neurorehabil Neural Repair. 2000;14:251–263.

2000;25(4):501–508. doi: 10.1097/00007632-200002150-00018.

nal cord injury. Neurorehabilitation.2001;16:165–169

In conclusion FES cycling plays an important role for each individual. It enables – in addition to the described beneficial physiological effects – the implementation of a physical activity and thereby, in terms of an improved participation, leads to a better quality of live.

#### **Author details**

Aris Papachristos\*

Address all correspondence to: arispapa76@gmail.com

Rehabilitation Center "Kentavros", Volos, Greece

#### **References**


The time course and training frequency are major factors that determine the therapeutic effects of cycling exercise. It is commonly recommended that subjects with an SCI receive at least 2-3 times per week and 30 min per time in a cycling rehabilitation program. In addition, it was reported that detraining from cycling exercise can soon induce a quick reversal of physical fitness within 1 week. The selection of electrical stimulation parameters is also an important issue considered in FESCE studies. Commonly, the FES cycling stimulation current is delivered to the large paralyzed leg muscles via surface electrodes. The stimulation output can either be regulated current or regulated voltage, which depends on the control design of the FES cycling stimulator. Commonly, the stimulation frequency is selected in the range of 10~50 Hz. However, a relatively higher stimulation frequency (> 50 Hz) can produce higher forces and therefore higher power for pedaling the ergometer compared to lower stimulation frequencies (10~50 Hz). But higher stimulation frequencies may rapidly result in ATP depletion at

In conclusion FES cycling plays an important role for each individual. It enables – in addition to the described beneficial physiological effects – the implementation of a physical activity and

[1] Liberson, W. T.; Holmquest, H. J.; Scot, D.; Dow, M. (1961). "Functional electrothera‐ py: Stimulation of the peroneal nerve synchronized with the swing phase of the gait of hemiplegic patients". *Archives of physical medicine and rehabilitation* 42: 101–105.

[2] J. H. Moe and H. W. Post, "Functional electrical stimulation for ambulation in hemi‐

[4] Kralj A, Orobelnik S (1973) Functional electrical stimulation-A new hope for paraple‐

[5] Bajd T, Kralj A, Turk R, Benko H, Sega J (1983) The use of a four channel stimulator

as an ambulatory aid for paraplegic patients. Phys Ther 63: 1116-1120.

thereby, in terms of an improved participation, leads to a better quality of live.

neuromuscular junctions and cause muscle fatigue.

Address all correspondence to: arispapa76@gmail.com

plegia," The Lancet, vol. 82, pp. 285–288, July 1962

gic patients? Bull Prosthet Res 10(20): 75-102

Rehabilitation Center "Kentavros", Volos, Greece

[3] Offner et al. (1965), Patent 3,344,792

**Author details**

120 Topics in Paraplegia

Aris Papachristos\*

**References**


[20] Baker LL, Bowman BR, McNeal DR. Effects of waveform on comfort during neuro‐ muscular electrical stimulation. Clin Orthop.1988;233:75–85.

[33] Christopher and Dana Reeve Foundation's(32) Paralysis Resource Center http://

Functional Electrical Stimulation in Paraplegia

http://dx.doi.org/10.5772/58625

123

[34] Tomovic R, Vukobratovic M, Vodovnik L. Hybrid actuators for orthotic systems: Hy‐ brid assistive systems. In: Popovic D, editor. Advances in external control on human extremities. proceedings I-X of the Fourth International Symposium on External Con‐ trol of Human Extremities; 1972 Aug 28-Sep 2: Dubrovnik, Yugoslavia. Aalborg

[35] Moore P, Stallard JS. A clinical review of adult paraplegic patients with complete le‐

[36] Isakov E, Douglas R, Berns P. Ambulation using the reciprocating gait orthosis and

[37] Yang L, Granat MH, Paul JP, Condie DN, Rowley DI. Further development of hybrid functional electrical stimulation orthoses. Spinal Cord. 1996;34(10):611-14.

[38] Solomonow M, Aguilar E, Reisin E, Baratta RV, Best R, Coetzee T, D'Ambrosia R. Re‐ ciprocating gait orthosis powered with electrical muscle stimulation (RGO II). Part I: Performance evaluation of 70 paraplegic patients. Orthopedics. 1997;20(4):315-24 [39] Nene AV, Jennings SJ. Hybrid paraplegic locomotion with the ParaWalker using in‐ tramuscular stimulation: A single subject study. Paraplegia. 1989;27(2):125-32.

[40] Marsolais EB, Kobetic R, Polando G, Ferguson K, Tashman S, Gaudio R, Nandurkar S, Lehneis HR. The Case Western Reserve University hybrid gait orthosis. J Spinal

[41] Kobetic R, Marsolais EB, Triolo RJ, Davy DT, Gaudio R, Tashman S. Development of a hybrid gait orthosis: A case report. J Spinal Cord Med. 2003;26(3):254-58.

[42] Solomonow M, Baratta R, Hirokawa S, Rightor N, Walker W, Beaudette P, Shoji H, D'Ambrosia R. The RGO Generation II: muscle stimulation powered orthosis as a practical walking system for thoracic paraplegics.Orthopedics (1989, 12(10):

[43] Suzuki K, Mito G, Kawamoto H, Hasegawa Y, Sankai Y. Intention-based walking support for paraplegia patients with Robot Suit HAL. Advanced Robotics. 2007 Dec;

[44] Tsukahara A, Kawanishi R, Hasegawa Y, Sankai Y. Sit-to-Stand and Stand-to-Sit Transfer Support for Complete Paraplegic Patients with Robot Suit HAL. Advanced

[45] Neuhaus PD, Noorden JH, Craig TJ, Torres T, Kirschbaum J, Pratt JE. Design and evaluation of Mina: A robotic orthosis for paraplegics. Rehabilitation Robotics

[46] Baker, B., ''Walk of Life,'' The Engineer, Vol. 293, No. 7750, pp. 30–31, June 16, 2008.

(ICORR), 2011 IEEE International Conference; 2011. pp. 1–8

(Denmark): Center for Sensory-Motion Interaction; 1972.

sion using the ORLAU Parawalker. Paraplegia. 1991;29:191-96.

functional electrical stimulation. Paraplegia. 1992;30(4):239-45.

www.christopherreeve.org/

Cord Med. 2000;23(2):100-108.

Robotics. 2010;24:1615–1638.

1309-1315)

21:1441–1469.


[33] Christopher and Dana Reeve Foundation's(32) Paralysis Resource Center http:// www.christopherreeve.org/

[20] Baker LL, Bowman BR, McNeal DR. Effects of waveform on comfort during neuro‐

[21] Scheiner A, Polando G, Marsolais EB. Design and clinical application of a double he‐ lix electrode for functional electrical stimulation. IEEE Trans Biomed Eng. 1994;41(5):

[22] Marsolais EB, Kobetic R. Implantation techniques and experience with percutaneous intramuscular electrodes in the lower extremities. J Rehabil Res Dev. 1986;23(3):1-8.

[23] Nandurkar S, Marsolais EB, Kobetic R. Percutaneous implantation of iliopsoas for functional neuromuscular stimulation. Clin Orthop Relat Res. 2001 Aug;(389):

[24] Shimada Y, Sato K, Abe E, Kagaya H, Ebata K, Oba M, Sata M. Clinical experience of functional electrical stimulation in complete paraplegia. Spinal Cord. 1996;34(10):

[25] Kobetic R, Marsolais EB. Synthesis of paraplegic gait with multichannel functional neuromuscular stimulation. IEEE Trans Rehabil Eng. 1994;2(2):66-79. DOI:

[26] Kobetic R, Triolo RJ, Marsolais EB. Muscle selection and walking performance of multichannel FES systems for ambulation in paraplegia. IEEE Trans Rehabil Eng.

[27] Holle J, Frey M, Gruber H, Kern H, Stohr H, Thoma H. Functional electrostimulation of paraplegics: Experimental investigations and first clinical experience with an im‐

[28] Brindley GS, Polkey CE, Rushton DN. Electrical splinting of the knee in paraplegia.

[29] Kobetic R, Triolo RJ, Uhlir JP, Bieri C, Wibowo M, Polando G, Marsolais EB, Davis JA Jr, Ferguson KA. Implanted functional electrical stimulation system for mobility in paraplegia: A follow-up case report. IEEE Trans Rehabil Eng. 1999;7(4):390-98. DOI:

[30] Von Wild K, Rabischong P, Brunelli G, Benichou M, Krishnan K. Computer added locomotion by implanted electric stimulation in paraplegic patients (SUAW). Acta

[31] Guiraud D, Stieglitz T, Koch KP, Divoux JL, Rabischong P. An implantable neuro‐ prosthesis for standing and walking in paraplegia: 5-year patient follow-up. J Neural

[32] Kobetic R, To CS, Schnellenberger JR, Audu ML, Bulea TC, Gaudio R, Pinault G, Tashman S, Triolo RJ. Development of hybrid orthosis for standing, walking, and

stair climbing after spinal cord injury. J Rehabil Res Dev. 2009;46:447–62.

plantable stimulation device. Orthopedics. 1984;7(7):1145-60

Eng. 2006; 3(4):268-75. DOI:10.1088/1741-2560/3/4/003

muscular electrical stimulation. Clin Orthop.1988;233:75–85.

425-31.DOI:10.1109/10.293216

615-19

122 Topics in Paraplegia

10.1109/86.313148

210-17.DOI:10.1097/00003086-200108000-00030

1997; 5(1):23-29. DOI:10.1109/86.559346

Paraplegia. 1979;16(4):428-37

Neurochir Suppl. 2001;79:99-104.

10.1109/86.808942


[60] Brindley G. The first 500 patients with sacral anterior root stimulator implants:Gener‐

Functional Electrical Stimulation in Paraplegia

http://dx.doi.org/10.5772/58625

125

[61] Creasey GH, Grill JH, Hoi SU, et al. An Implantable neuroprosthesis for restoring bladder and bowel control to patients with spinal cord injuries: a multicenter trial.

[62] Heruti RJ, Katz H, Menashe Y, et al. Treatment of male infertility due to spinal cord injury using rectal probe electroejaculation: the Israeli experience. Spinal Cord.

[64] M Possover, J Baekelandt, A Kaufmann, V Chiantera. Spinal Cord (2008) Laparoscop‐ ic endopelvic sacral implantation of a Brindley controller for recovery of bladder

[65] J Vastenholt, G Snoek, H Buschman, H van der Aa, E Alleman, M Ijzerman.A 7 year follow-up of sacral anterior root stimulation for bladder control in patients with a spinal cord injury; quality of life and users experiences. Spinal Cord (2003) 41;

[66] Duffell LD et.al. (2008) Long-term intensive electrically stimulated cycling by spinal cord-injured people: effect on muscle properties and their relation to power output.

[67] Janssen TWJ et.al. (1998) Clinical efficacy of electrical stimulation exercise training: effects on health, fitness and function. Topics in Spinal Cord Injury Rehabilitation, 3,

[68] Mohr T et.al. (1997) Long term adaption to electrically induced cycle training in se‐

[69] Baldi JC, et.al. (1998) Muscle atrophy is prevented in patients with acute spinal cord

[70] Demchak TJ, et.al. (2005) Effects of functional electric stimulation cycle ergometry training on lower limb musculature in acute SCI individuals. J Sports Science Med, 4,

[71] Sloan KE, et.al. (1994) Musculoskeletal effects on an electrical stimulation induced cy‐

[72] Krause P, et.al. (2008) Changes in spastic muscle tone increase in patients with spinal cord injury using functional electrical stimulation and passive leg movements. Clini‐

[73] Van der Salm A, et.al. (2006) Comparison of electric stimulation methods for reduc‐ tion of triceps suraespasticity in spinal cord injury. Arch Phys Med Rehabil, 87(2):

injury using functional electrical stimulation. Spinal Cord, 36(7):463-9.

vere spinal cord injured individuals. Spinal Cord, 35(1):1-16.

cling programme in the spinal injured. Paraplegia, 32(6):407-15.

Arch Phys Med Rehabil. 2001;82:1512–1519. doi: 10.1053/apmr.2001.25911.

al description. Paraplegia.1994;32:795–805

2001;39(3):168–175. doi: 10.1038/sj.sc.3101120. [63] Finetech Medica, UK. http://finetech-medical.co.uk/

function in a paralyzed patient. 46; 70-73

Muscle Nerve, 38(4):1304-11.

397-402.

33-49

263-271.

222-8.

cal Rehali, 22(7), 627-34.


[47] Ekso Bionics, Berkeley, California. http://eksobionics.com/

bilitation Engineering, IEEE Transactions 2011;19:652–659

Spinal Cord Injury. *Journal of Applied Sciences, 10: 2785-2792.*

analysis of three patients. Paraplegia. 1987;25(1):32-38.

bot. 2011 Jun;2011:1–6.

124 Topics in Paraplegia

Orthot Int. 1995;19(2):108-14

72(11):890-96

2005;86(7):1502-4.

[48] Ragnarsson KT. Functional electrical stimulation after spinal cord injury: current use, therapeutic effects and future directions. Spinal Cord. 2008 Apr;46:255–74

[49] Quintero HA, Farris RJ, Goldfarb M. Control and implementation of a powered low‐ er limb orthosis to aid walking in paraplegic individuals. IEEE Int Conf Rehabil Ro‐

[50] Farris RJ, Quintero HA, Goldfarb M. Preliminary Evaluation of a Powered Lower Limb Orthosis to Aid Walking in Paraplegic Individuals. Neural Systems and Reha‐

[51] R. Jailani, M.O. Tokhi and S. Gharooni, 2010. Hybrid Orthosis: The Technology for

[52] McClelland M, Andrews BJ, Patrick JH, Freeman PA, El Masri WS. Augmentation of the Oswestry Parawalker orthosis by means of surface electrical stimulation: Gait

[53] Stallard J, Major RE. The influence of orthosis stiffness on paraplegic ambulation and its implications for functional electrical stimulation (FES) walking systems. Prosthet

[54] Petrofsky JS, Smith JB. Physiologic costs of computer-controller walking in persons with paraplegia using a reciprocating-gait orthosis. Arch Phys Med Rehabil. 1991;

[55] Edwards BG, Marsolais EB. Metabolic responses to arm ergometry and functional

[56] Mahoney ET, Bickel CS, Elder C, Black C, Slade JM, Apple D Jr, Dudley GA. Changes in skeletal muscle size and glucose tolerance with electrically stimulated resistance training in subjects with chronic spinal cord injury. Arch Phys Med Rehabil.

[57] Lew RD. The effects of FNS on disuse osteoporosis. Proceedings of the 10th Annual Conference of Rehabilitation Engineering Society of North America; 1987; San Jose,

[58] Y Dionyssiotis, G Trovas, A Galanos, P Raptou, N Papaioannou, P Papagelopoulos, K Petropoulou, G P Lyritis (2007) Bone loss and mechanical properties of tibia in spi‐

[59] Betz R, Boden B, Triolo R, Mesgarzadeh M, Gardner E, Fife R. Effects of functional electrical stimulation on the joints of adolescents with spinal cord injury. Paraplegia. 1996;34(3):127-36R. J. Weber, "Functional neuromuscular stimulation," in Rehabilita‐

nal cord injured men. *J Musculoskelet Neuronal Interact* 7: 1. 62-68 Jan/Mar

tion Medicine: Principles and Practice. Philadelphia, PA: Lippincott, 1993

neuromuscular stimulation. J Rehabil Res Dev. 1990;27(2):107-14

CA. Washington (DC): RESNA Press; 1987. p. 616-17.


[74] Griffin L, et.al. (2009). Functional electrical stimulation cycling improves body com‐ position, metabolic and neural factors in persons with spinal cord injury. J Electro‐ myogr Kinesiol. 19(4):614-22.

**Section 3**

**Complications and Special Musculoskeletal**

**Issues in Paraplegia**


**Complications and Special Musculoskeletal Issues in Paraplegia**

[74] Griffin L, et.al. (2009). Functional electrical stimulation cycling improves body com‐ position, metabolic and neural factors in persons with spinal cord injury. J Electro‐

[75] Berry HR, et.al. (2008) Cardio-respiratory and power adaptations to stimulated cycle training in paraplegia.Medicine & Science in Sports & Exercise, 40(0), 1573-1580. [76] Hettinga DM, Andrews BJ (2008). Oxygen consumption during functional electrical stimulation-assisted exercise in persons with spinal cord injury: implications for fit‐

[77] Gerrits HL, et.al. (2001) Peripheral vascular changes after electrically stimulated cycle training in people with spinal cord injury. Arch Phys Med Rehabil, 82(6):832-9. [78] Janssen TWJ et.al. (1998) Clinical efficacy of electrical stimulation exercise training: effects on health, fitness and function. Topics in Spinal Cord Injury Rehabilitation, 3,

myogr Kinesiol. 19(4):614-22.

33-49.

126 Topics in Paraplegia

ness and health. Sports Med, 38(10), 825-38.

**Chapter 6**

**Malnutrition in Paraplegia**

Additional information is available at the end of the chapter

newly introduced concept in nutritional deficiency [5, 6, 7].

Despite the advances in medical and nutritional science surveys show that 40-50% of patients admitted to hospitals are at risk of nutritional deficiency; one in three hospitalized patients are malnourished upon admission and up to 12% are severely malnourished [1, 2]. Malnutrition is a state in which a deficiency, excess or imbalance of energy, protein and other nutrients causes adverse effects on body form, function and clinical outcome [3, 4]. Studies report a variable prevalence of obesity from 40 to 66% in persons with SCI completing the spectrum of

After the lesion paralysis and loss of function that usually occur and well documented hypercatabolic responses may lead to deleterious effects such as loss of lean body mass, obesity, increased susceptibility to infections, and reduced wound healing [5, 8, 9]. Unwanted weight gain should be prevented because induces the risk for diseases such as diabetes, coronary heart disease and dyslipidaimias in this population [8]. Mortality and pathogenesis of critically ill patients are affected by nutritional status. Body fat has been identified as a significant predictor of mortality. Moreover, some disorders such as carbohydrate intolerance, insulin resistance, lipid abnormalities, and heart disease occur prematurely and at a higher prevalence in disabled populations may be related to immobi‐ lization and skeletal muscle denervation [10]. According to the above the term malnutri‐ tion should include not only undernourishment but also obesity [11]. Therefore, the objective should be either the maintenance of optimal nutritional status of the patient, either to supplement the deficiencies in nutrients. Nutrition support therapy should be tailored to each patient. An optimal nutritional assessment and management of the disabled subject can minimize the complications associated with acute traumatic injury and long-term

> © 2014 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Yannis Dionyssiotis

**1. Introduction**

rehabilitation [12].

http://dx.doi.org/10.5772/58382

#### **Chapter 6**

### **Malnutrition in Paraplegia**

Yannis Dionyssiotis

Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/58382

#### **1. Introduction**

Despite the advances in medical and nutritional science surveys show that 40-50% of patients admitted to hospitals are at risk of nutritional deficiency; one in three hospitalized patients are malnourished upon admission and up to 12% are severely malnourished [1, 2]. Malnutrition is a state in which a deficiency, excess or imbalance of energy, protein and other nutrients causes adverse effects on body form, function and clinical outcome [3, 4]. Studies report a variable prevalence of obesity from 40 to 66% in persons with SCI completing the spectrum of newly introduced concept in nutritional deficiency [5, 6, 7].

After the lesion paralysis and loss of function that usually occur and well documented hypercatabolic responses may lead to deleterious effects such as loss of lean body mass, obesity, increased susceptibility to infections, and reduced wound healing [5, 8, 9]. Unwanted weight gain should be prevented because induces the risk for diseases such as diabetes, coronary heart disease and dyslipidaimias in this population [8]. Mortality and pathogenesis of critically ill patients are affected by nutritional status. Body fat has been identified as a significant predictor of mortality. Moreover, some disorders such as carbohydrate intolerance, insulin resistance, lipid abnormalities, and heart disease occur prematurely and at a higher prevalence in disabled populations may be related to immobi‐ lization and skeletal muscle denervation [10]. According to the above the term malnutri‐ tion should include not only undernourishment but also obesity [11]. Therefore, the objective should be either the maintenance of optimal nutritional status of the patient, either to supplement the deficiencies in nutrients. Nutrition support therapy should be tailored to each patient. An optimal nutritional assessment and management of the disabled subject can minimize the complications associated with acute traumatic injury and long-term rehabilitation [12].

© 2014 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

This chapter reviews methods of nutritional assessment and describes the physiopathological mechanisms of malnutrition, reviews specific nutritional studies, and the supplemental support which can be used in paraplegic subjects.

Men: Resting Metabolic Rate (RMR) (kcal/d)=67+Body Weight x 13.75+Height x 5 – Age x 6.8

Malnutrition in Paraplegia http://dx.doi.org/10.5772/58382 131

Ideal body weight is calculated by the Hamwi rule of thumb while metabolically active weight (MAW) is calculated as 25% of excess weight (actual weight − ideal weight) added to the ideal body weight [26]. The Ireton-Jones equations include one specifically for obese patients and

Nonobese: RMR (kcal/d)=Wt x 5 – Age x 10+Gender x 281+Trauma x 292+1925 (for gender:

To determine accurately the early energy expenditure after spinal cord injury, studies com‐ pared measurements of real resting energy expenditure (REE) with the Harris-Benedict equation (basic energy expenditure, BEE) [18]. During the first two weeks after the injury, the exact measurements of REE are similar to the estimated calorie needs, when used with BEE stressor/injury factor of 1.6. To avoid overestimation of calorie needs, the deletion of factor activity of 1.2 (rest in bed) is proposed. Kearns et al. reported that in 10 patients, the mean REE after acute injury was only 67% of BEE predicted by Harris-Benedict formula. They hypothe‐ sized that non-specific changes in neurogenic stimuli and reduced oxygen consumption by relaxing muscles contributed to their findings. Also, an interesting feature observed is that the REE was raised by 5% with the return of muscle tone [29]. Jeejeboy and Cerra proposed an alternative approach that uses body weight (kg) alone as a determining factor, and omits the variables of age, sex and height as used in HB equation. This type of assessment has proven to be accurate and efficient over time [30, 31]. Ireton-Jones and Owen et al. have developed specific formulas for the obese patient, which is common in SCI subjects. The predefined types

may overestimate their needs due to increased fat mass in this population [21, 22, 32].

Patients admitted in the hospital should be examined for actual or potential occurrence of malnutrition because of an unintentional weight loss or gain. In the clinic this examina‐ tion includes measurements of body weight depicting a loss of more than 10% of normal body weight within 6 months or loss of more than 5% of usual body weight within 1 month or 20% more or less than ideal body weight (IBW), calculation of body mass index (BMI) <18, depletion of visceral protein (serum albumin <3.5 g/dl, serum transferrin <200 mg/dl, serum cholesterol <160 mg/dl, serum pre – albumin <15 mg/ml, creatinine height index (CHI) <75% (measured by 24-hour creatinine excretion, which is typically associated with muscle mass of the patient as an indicator of malnutrition, especially in young men), and the presence of diet modifications (patient receives total parenteral nutrition (TPN) or enteral nutrition (EN), inadequate food intake due instructions for stopping any food by mouth (NPO), liquid diet, disorders of absorption, reduced swallowing capacity, in‐ creased metabolic needs, gastrointestinal disturbances (nausea, vomiting, diarrhea, constipa‐

Women: RMR (kcal/d)=655+Body Weight x 9.6+Height x 1.85 – Age x 4.7 [25].

Obesity: RMR (kcal/d)=Wt x 9+Gender x 606 – Age x 12+1844 [27].

[18, 24].

one for general critical care populations:

**2.3. Assessment of subjects in the clinical setting**

male=1, female=0) [28].

#### **2. Nutritional assessment**

For an initial assessment of nutritional status serial measurements to assess trends over time and then monitor the response to a dietary intervention may be useful. The proposed assess‐ ments should be interpreted collectively including the examination of possible factors that contribute to the nutritional status, such as age, sex, over-or under-hydration, interactions between drugs-food, metabolic stress, infection, and the existence of other diseases[13].

#### **2.1. Diet history**

During hospitalization adequate intake of nutrients is intercepted by many factors, and may be caused by anorexia, early satiety, immobility, depression. Moreover, gastrointestinal function is compromised: gastric dilatation and paralytic ileus occurs often, although the intestinal activity usually returns within the first week after injury.

#### **2.2. Nutritional requirements**

The provision of energy and nutritional requirements is a very important factor for patient management. Malnutrition, in this case undernourishment or over nutrition-obesity, can lead to muscle loss, atrophy of the lining of the intestine, immunochemical reduction, poor wound healing and fluid overload, hyperglycemia, high levels of urea nitrogen in blood, high triglycerides, elevated liver enzymes, respiratory exhaustion due to increased production of CO2, and difficulty weaning from the oxygen, respectively. The assessment of nutritional requirements includes not only calculations but also the opinion of an expert clinician in order to assess the clinical and morphometric data before applying the equations that provide the energy and protein requirements [14].

There have been several methods for predicting energy expenditure (EE); the components and the methods for its determination and estimation, summarizing their main advantages and limitations have been recently reviewed [15]. However, because of various confusing factors such as infections and sepsis, hyper nutrition supportive nutritional diets, clinical procedures, postoperative medications, and changes in body weight such as sarcopenia, obesity, amputa‐ tions and significant weight loss, the prediction equations can be complex and invalid [16].

A group of equations among these are Mifflin–St Jeor equation [17], the Harris-Benedict equation [18], the American College of Chest Physicians (ACCP) recommendation based on kcal/kg body weight [19], the Faisy equation [20], the Ireton-Jones equations [21, 22] and the Penn State equations [23, 24]. Because the Mifflin equation was designed for healthy people is not analyzed here.

The Harris-Benedict is calculated by sex with the following formula:

Men: Resting Metabolic Rate (RMR) (kcal/d)=67+Body Weight x 13.75+Height x 5 – Age x 6.8 [18, 24].

Women: RMR (kcal/d)=655+Body Weight x 9.6+Height x 1.85 – Age x 4.7 [25].

Ideal body weight is calculated by the Hamwi rule of thumb while metabolically active weight (MAW) is calculated as 25% of excess weight (actual weight − ideal weight) added to the ideal body weight [26]. The Ireton-Jones equations include one specifically for obese patients and one for general critical care populations:

Obesity: RMR (kcal/d)=Wt x 9+Gender x 606 – Age x 12+1844 [27].

This chapter reviews methods of nutritional assessment and describes the physiopathological mechanisms of malnutrition, reviews specific nutritional studies, and the supplemental

For an initial assessment of nutritional status serial measurements to assess trends over time and then monitor the response to a dietary intervention may be useful. The proposed assess‐ ments should be interpreted collectively including the examination of possible factors that contribute to the nutritional status, such as age, sex, over-or under-hydration, interactions between drugs-food, metabolic stress, infection, and the existence of other diseases[13].

During hospitalization adequate intake of nutrients is intercepted by many factors, and may be caused by anorexia, early satiety, immobility, depression. Moreover, gastrointestinal function is compromised: gastric dilatation and paralytic ileus occurs often, although the

The provision of energy and nutritional requirements is a very important factor for patient management. Malnutrition, in this case undernourishment or over nutrition-obesity, can lead to muscle loss, atrophy of the lining of the intestine, immunochemical reduction, poor wound healing and fluid overload, hyperglycemia, high levels of urea nitrogen in blood, high triglycerides, elevated liver enzymes, respiratory exhaustion due to increased production of CO2, and difficulty weaning from the oxygen, respectively. The assessment of nutritional requirements includes not only calculations but also the opinion of an expert clinician in order to assess the clinical and morphometric data before applying the equations that provide the

There have been several methods for predicting energy expenditure (EE); the components and the methods for its determination and estimation, summarizing their main advantages and limitations have been recently reviewed [15]. However, because of various confusing factors such as infections and sepsis, hyper nutrition supportive nutritional diets, clinical procedures, postoperative medications, and changes in body weight such as sarcopenia, obesity, amputa‐ tions and significant weight loss, the prediction equations can be complex and invalid [16]. A group of equations among these are Mifflin–St Jeor equation [17], the Harris-Benedict equation [18], the American College of Chest Physicians (ACCP) recommendation based on kcal/kg body weight [19], the Faisy equation [20], the Ireton-Jones equations [21, 22] and the Penn State equations [23, 24]. Because the Mifflin equation was designed for healthy people is

intestinal activity usually returns within the first week after injury.

The Harris-Benedict is calculated by sex with the following formula:

support which can be used in paraplegic subjects.

**2. Nutritional assessment**

**2.2. Nutritional requirements**

energy and protein requirements [14].

not analyzed here.

**2.1. Diet history**

130 Topics in Paraplegia

Nonobese: RMR (kcal/d)=Wt x 5 – Age x 10+Gender x 281+Trauma x 292+1925 (for gender: male=1, female=0) [28].

To determine accurately the early energy expenditure after spinal cord injury, studies com‐ pared measurements of real resting energy expenditure (REE) with the Harris-Benedict equation (basic energy expenditure, BEE) [18]. During the first two weeks after the injury, the exact measurements of REE are similar to the estimated calorie needs, when used with BEE stressor/injury factor of 1.6. To avoid overestimation of calorie needs, the deletion of factor activity of 1.2 (rest in bed) is proposed. Kearns et al. reported that in 10 patients, the mean REE after acute injury was only 67% of BEE predicted by Harris-Benedict formula. They hypothe‐ sized that non-specific changes in neurogenic stimuli and reduced oxygen consumption by relaxing muscles contributed to their findings. Also, an interesting feature observed is that the REE was raised by 5% with the return of muscle tone [29]. Jeejeboy and Cerra proposed an alternative approach that uses body weight (kg) alone as a determining factor, and omits the variables of age, sex and height as used in HB equation. This type of assessment has proven to be accurate and efficient over time [30, 31]. Ireton-Jones and Owen et al. have developed specific formulas for the obese patient, which is common in SCI subjects. The predefined types may overestimate their needs due to increased fat mass in this population [21, 22, 32].

#### **2.3. Assessment of subjects in the clinical setting**

Patients admitted in the hospital should be examined for actual or potential occurrence of malnutrition because of an unintentional weight loss or gain. In the clinic this examina‐ tion includes measurements of body weight depicting a loss of more than 10% of normal body weight within 6 months or loss of more than 5% of usual body weight within 1 month or 20% more or less than ideal body weight (IBW), calculation of body mass index (BMI) <18, depletion of visceral protein (serum albumin <3.5 g/dl, serum transferrin <200 mg/dl, serum cholesterol <160 mg/dl, serum pre – albumin <15 mg/ml, creatinine height index (CHI) <75% (measured by 24-hour creatinine excretion, which is typically associated with muscle mass of the patient as an indicator of malnutrition, especially in young men), and the presence of diet modifications (patient receives total parenteral nutrition (TPN) or enteral nutrition (EN), inadequate food intake due instructions for stopping any food by mouth (NPO), liquid diet, disorders of absorption, reduced swallowing capacity, in‐ creased metabolic needs, gastrointestinal disturbances (nausea, vomiting, diarrhea, constipa‐ tion). Unintentional weight gain is an increase in body weight that occurs when a person takes in more calories than the body needs or uses [33, 34].

calculation is used, the IBW should be adjusted for body type (frame sizes: small-IBW 10% reduction, middle size-no changes required, large size-IBW increased by 10%) and spinal cord injury (paraplegia-decrease IBW by 10-15%, tetraplegia-by 15-20%, respectively). The weight in admission is probably the most reliable measure of weight in determining the actual body weight (ABW) of the patient because is unreliable postoperatively or during an acute illness due to administration of fluids or due to edematous condition. As a chronic index, one can assume that the weight gain or loss is associated with an increase or decrease in lean body mass. To determine the weight which should be used on the nutritional calculations, first % IBW should be calculated through the equation: % IBW=actual body weight (actual body weight, ABW / ideal body weight (IBW) x 100. If the actual body weight (ABW) is less than IBW, use ABW, to define the nutritional requirements, if is greater than IBW, but less than 120%, it is necessary to determine nutritional needs using the adjusted relationship of body weight in the calculation needs: IBW+(ABW-IBW x 0.25). The nutrition‐ al status of patients can be categorized according to their ABW as a percentage of IBW as follows: over 200% of IBW (pathologic obesity), over 150% of IBW (obese), more than 120% IBW (overweight), 100% of IBW+/-10% (normal), 80-90% of IBW (mildly malnourished), 70-80% of IBW (moderately malnourished), less than 70% of IBW (severe nutritional

Malnutrition in Paraplegia http://dx.doi.org/10.5772/58382 133

As with the visceral and somatic visceral proteins, non-dietary factors (i.e. blood loss, chronic infections, and fluid overload) should be considered as potential reasons for the reduction of serum concentrations [1]. Proteins are essential for tissue growth, mainte‐ nance and rebuilding their synthesis of hormones, enzymes, antibodies and cells trans‐ port molecules. In cases of protein excess protein is either metabolized for energy or stored as fat. The recommendations for protein intake in patients with spinal cord injury vary with respect to acute or chronic phase of the lesion and the presence of decubitus ulcers or not. Specific proteins (albumin, transferrin, and pre-albumin) are biochemical indicators used

The level of serum albumin is not a definitive measure of visceral protein status, but reflects the complex relationship between synthesis, degradation, and distribution. Given the long half-life of 21 days, serum albumin cannot be effectively used for monitoring the acute response to nutritional therapy. Therefore, albumin levels should be included in the initial profile for food control and monitoring purposes during hospitalization for measuring trends of visceral protein or as an indicator of chronic nutritional status. Beside this limitation there are many non-dietary factors that reduce the levels of albumin, regard‐ less of nutritional status (inadequate composition: acute stress, hypoxia, impaired diges‐ tion, as in malabsorption, modified status as edematous fluid status and fluid overload,

deficiency–malnutrition), respectively [1].

**3. Biochemical measurements**

for assessing nutritional status [44].

chronic loss of protein) (Table 2) [36].

For able bodied persons the World Health Organization (WHO) advocates use of BMI as a population-level indicator of obesity which is not a direct measure of body fat, but a more accurate indicator of overweight and obesity than relying on weight alone. BMI is calculated using the equation weight (Kg)/height (m2 ), which is a very practical and useful measure that allows the easy determination of categories of weight status. In able-bodied subjects over‐ weight is defined as a BMI of 25–29.9 kg/m2 and obesity as a BMI of ≥30.0 kg/m<sup>2</sup> and extreme obesity≥40 kg/m<sup>2</sup> (Table 1) [35, 36].


**Table 1.** Classifications based on the weight for BMI and obesity category (published with permission from Dionyssiotis Y. [36])

In a chronic SCI population with paraplegia values of body mass index (BMI, kg/m2 ) were not significant vs. controls, which is a finding in line with the literature [10, 37]. Neverthe‐ less, Gupta et al demonstrated the usefulness of BMI as an indicator of obesity [38]. Whether the criteria of BMI may assess obesity in people with spinal cord injury the latest studies show the opposite [39]. The applicability of conventional BMI cut off values is into question [40, 41]. Another critical issue is that the relationship between BMI and disease is typical‐ ly U-or J-shaped with those in the middle categories of BMI having the lowest risk compared to the lowest extreme and upper levels of BMI. It is under question if the cut-points for underweight, normal, overweight, and obese used in able-bodied populations can be applied to disabled subjects [42]. Not many studies investigated BMI in patients with MS. Nevertheless, BMI was found statistically less compared to age comparable controls [43].

Anthropometric standards such as the ideal body weight (IBW), the triceps skin fold thickness and the middle arm circumference which are common tools for assessment of nutrition may not be valid for disabled subjects due to water changes, atrophy of mus‐ cles because of immobility, increased body fat, and the inevitable weight loss beyond the normal. Patients' early weight loss is mainly due to loss of muscle rather than fat which bias the results of validity. In chronic paraplegics, the ideal weight has been estimated to be 4.5 to 6.5 kg below their respective controls finding which is in line with our recently published results [37]. Indeed, height and weight measurements are the key elements in nutritional assessment. The IBW is determined by the height. No matter which method of calculation is used, the IBW should be adjusted for body type (frame sizes: small-IBW 10% reduction, middle size-no changes required, large size-IBW increased by 10%) and spinal cord injury (paraplegia-decrease IBW by 10-15%, tetraplegia-by 15-20%, respectively). The weight in admission is probably the most reliable measure of weight in determining the actual body weight (ABW) of the patient because is unreliable postoperatively or during an acute illness due to administration of fluids or due to edematous condition. As a chronic index, one can assume that the weight gain or loss is associated with an increase or decrease in lean body mass. To determine the weight which should be used on the nutritional calculations, first % IBW should be calculated through the equation: % IBW=actual body weight (actual body weight, ABW / ideal body weight (IBW) x 100. If the actual body weight (ABW) is less than IBW, use ABW, to define the nutritional requirements, if is greater than IBW, but less than 120%, it is necessary to determine nutritional needs using the adjusted relationship of body weight in the calculation needs: IBW+(ABW-IBW x 0.25). The nutrition‐ al status of patients can be categorized according to their ABW as a percentage of IBW as follows: over 200% of IBW (pathologic obesity), over 150% of IBW (obese), more than 120% IBW (overweight), 100% of IBW+/-10% (normal), 80-90% of IBW (mildly malnourished), 70-80% of IBW (moderately malnourished), less than 70% of IBW (severe nutritional deficiency–malnutrition), respectively [1].

#### **3. Biochemical measurements**

tion). Unintentional weight gain is an increase in body weight that occurs when a person

For able bodied persons the World Health Organization (WHO) advocates use of BMI as a population-level indicator of obesity which is not a direct measure of body fat, but a more accurate indicator of overweight and obesity than relying on weight alone. BMI is calculated

allows the easy determination of categories of weight status. In able-bodied subjects over‐

**Classification BMI (kg/m2) Obesity Category**

**Table 1.** Classifications based on the weight for BMI and obesity category (published with permission from

In a chronic SCI population with paraplegia values of body mass index (BMI, kg/m2

not significant vs. controls, which is a finding in line with the literature [10, 37]. Neverthe‐ less, Gupta et al demonstrated the usefulness of BMI as an indicator of obesity [38]. Whether the criteria of BMI may assess obesity in people with spinal cord injury the latest studies show the opposite [39]. The applicability of conventional BMI cut off values is into question [40, 41]. Another critical issue is that the relationship between BMI and disease is typical‐ ly U-or J-shaped with those in the middle categories of BMI having the lowest risk compared to the lowest extreme and upper levels of BMI. It is under question if the cut-points for underweight, normal, overweight, and obese used in able-bodied populations can be applied to disabled subjects [42]. Not many studies investigated BMI in patients with MS. Nevertheless, BMI was found statistically less compared to age comparable controls [43]. Anthropometric standards such as the ideal body weight (IBW), the triceps skin fold thickness and the middle arm circumference which are common tools for assessment of nutrition may not be valid for disabled subjects due to water changes, atrophy of mus‐ cles because of immobility, increased body fat, and the inevitable weight loss beyond the normal. Patients' early weight loss is mainly due to loss of muscle rather than fat which bias the results of validity. In chronic paraplegics, the ideal weight has been estimated to be 4.5 to 6.5 kg below their respective controls finding which is in line with our recently published results [37]. Indeed, height and weight measurements are the key elements in nutritional assessment. The IBW is determined by the height. No matter which method of

Underweight <18.5 - Normal 18.5-24.9 - Overweight 25.0-29.9 - Obesity 30, 0-34, 9 I Moderate obesity 35.0-39.9 II Extreme obesity > 40.0 III

), which is a very practical and useful measure that

and extreme

) were

and obesity as a BMI of ≥30.0 kg/m<sup>2</sup>

takes in more calories than the body needs or uses [33, 34].

using the equation weight (Kg)/height (m2

weight is defined as a BMI of 25–29.9 kg/m2

(Table 1) [35, 36].

obesity≥40 kg/m<sup>2</sup>

132 Topics in Paraplegia

Dionyssiotis Y. [36])

As with the visceral and somatic visceral proteins, non-dietary factors (i.e. blood loss, chronic infections, and fluid overload) should be considered as potential reasons for the reduction of serum concentrations [1]. Proteins are essential for tissue growth, mainte‐ nance and rebuilding their synthesis of hormones, enzymes, antibodies and cells trans‐ port molecules. In cases of protein excess protein is either metabolized for energy or stored as fat. The recommendations for protein intake in patients with spinal cord injury vary with respect to acute or chronic phase of the lesion and the presence of decubitus ulcers or not. Specific proteins (albumin, transferrin, and pre-albumin) are biochemical indicators used for assessing nutritional status [44].

The level of serum albumin is not a definitive measure of visceral protein status, but reflects the complex relationship between synthesis, degradation, and distribution. Given the long half-life of 21 days, serum albumin cannot be effectively used for monitoring the acute response to nutritional therapy. Therefore, albumin levels should be included in the initial profile for food control and monitoring purposes during hospitalization for measuring trends of visceral protein or as an indicator of chronic nutritional status. Beside this limitation there are many non-dietary factors that reduce the levels of albumin, regard‐ less of nutritional status (inadequate composition: acute stress, hypoxia, impaired diges‐ tion, as in malabsorption, modified status as edematous fluid status and fluid overload, chronic loss of protein) (Table 2) [36].


**4. Malnutrition screening tools**

tools investigated (sensitivity 96%, specificity 77%) [52, 54].

malnutrition.eu/fight-malnutrition/screening-tools/

Screening is important for the early detection of patients who are undernourished or at risk of developing malnutrition. Since January 2010, the Dutch Health Care Inspectorate (HCI) has defined under nutrition as a main care problem in rehabilitation centres, by establishing it as a Performance Indicator for Risk Steering Supervision. Dutch rehabilitation centres are now obligated to screen all rehabilitants for under nutrition on admission The Short Nutritional Assessment Questionnaire (SNAQ) is the recommended screening tool in this benchmark (Figure 1) [50]. However, various screening tools have been developed to detect a patient's nutritional status in many healthcare settings, but not in the rehabilitation setting. In the Netherlands, the SNAQ [51] and the Malnutrition Universal Screening Tool (MUST) are used for the hospital situation [52, 53]. The HCI advises the use of the SNAQ for under nutrition screening in rehabilitation centres [51]. Our results suggest the use of the SNAQ65+as a screening tool. This tool showed the best diagnostic accuracy of the quick and easy screening

Malnutrition in Paraplegia http://dx.doi.org/10.5772/58382 135

**Figure 1.** The Short Nutritional Assessment Questionnaire (SNAQ). Published with permission from: http://www.fight‐

**Table 2.** Basic levels of albumin and nutritional status distribution (published with permission from Dionyssiotis Y. [36])

Due to the lower half-life (8-9 days) and the smaller size as a constituent body, transferrin is a better indicator of nutritional status of visceral protein from albumin. Normal levels of transferrin are between 200-400 mg/dl, and 150 mg/dl are considered nutritionally decision point or a point where nutritional support should be revised or adjusted. The transferrin levels are reduced in impaired synthesis as chronic infections, increased secretion, fluid overload, increased iron stores and increased in reduced iron stores as iron deficiency anemia and chronic blood loss, increased protein synthesis on estrogen therapy and oral contraception and dehydration. The serum concentration of transferrin is approximately 0.8 times the total iron binding capacity (TIBC). If direct measurement of transferrin is not possible due to the high cost and limited availability of equipment required, the level of transferrin can be easily calculated from TIBC, using the following formula: TIBC x 0.8-43=transferrin [45].

The third protein biochemical indicator is pre-albumin, which has very short half-life (2 days), making it an excellent nutritional index and due to this reason is increasingly used as an indicator of response to nutritional therapy. Reference values for pre-albumin are 16-35 mg/dl. A value of dietary intervention is 11 mg/dl because a value below this level means malnutrition. The failure of patients to increase pre-albumin above 11 mg/dl with dietary therapy is an indication that nutritional needs are not met. Concentrations should increase about 1 mg/dl per day or twice a week when the treatment is the appropriate. Non-dietary factors that reduce pre-albumin include stress, inflammation [46, 47, 48].

Physical measurements include protein nitrogen balance studies and measurement of creati‐ nine / height index (CHI). Nitrogen balance studies measure the net change in total body protein. An assessment of nitrogen balance can be achieved by measurement of urinary urea (UUN) and compare it with the intake of nitrogen at the same time. The nitrogen balance is calculated as follows: N2=balance intake N2-N2 elimination or=[protein (gr)]-(24 hour UUN+3) [6.25 gr nitrogen]. An "agent" of 3 is added to the equation for nitrogen losses in feces, skin, and the drainage of body fluids. When calculating the nitrogen balance a value of 0 meaning nitrogen balance (healthy adults), nitrogen balance> 0 (protein anabolism exceeds catabolism, usually consistent with pregnancy, growth, and recovery from disease or may indicate nutrient saturation, the goal in nutrition replenishment is a positive nitrogen balance of 4-6 grams per day and nitrogen balance <0 (the protein catabolism exceeds protein anabolism, occurs in situations of famine, increased catabolism due to trauma or surgery, and inadequate nutrition therapy), respectively. CHI measures the 24-hour creatinine excretion in urine and compares with an optimum value based on the ideal weight for height [49].

#### **4. Malnutrition screening tools**

**Albumin (g/dl) 3.5-5 3-3.5 <3.5 <3.0 <2.5**

**Table 2.** Basic levels of albumin and nutritional status distribution (published with permission from Dionyssiotis Y.

calculated from TIBC, using the following formula: TIBC x 0.8-43=transferrin [45].

factors that reduce pre-albumin include stress, inflammation [46, 47, 48].

with an optimum value based on the ideal weight for height [49].

The third protein biochemical indicator is pre-albumin, which has very short half-life (2 days), making it an excellent nutritional index and due to this reason is increasingly used as an indicator of response to nutritional therapy. Reference values for pre-albumin are 16-35 mg/dl. A value of dietary intervention is 11 mg/dl because a value below this level means malnutrition. The failure of patients to increase pre-albumin above 11 mg/dl with dietary therapy is an indication that nutritional needs are not met. Concentrations should increase about 1 mg/dl per day or twice a week when the treatment is the appropriate. Non-dietary

Physical measurements include protein nitrogen balance studies and measurement of creati‐ nine / height index (CHI). Nitrogen balance studies measure the net change in total body protein. An assessment of nitrogen balance can be achieved by measurement of urinary urea (UUN) and compare it with the intake of nitrogen at the same time. The nitrogen balance is calculated as follows: N2=balance intake N2-N2 elimination or=[protein (gr)]-(24 hour UUN+3) [6.25 gr nitrogen]. An "agent" of 3 is added to the equation for nitrogen losses in feces, skin, and the drainage of body fluids. When calculating the nitrogen balance a value of 0 meaning nitrogen balance (healthy adults), nitrogen balance> 0 (protein anabolism exceeds catabolism, usually consistent with pregnancy, growth, and recovery from disease or may indicate nutrient saturation, the goal in nutrition replenishment is a positive nitrogen balance of 4-6 grams per day and nitrogen balance <0 (the protein catabolism exceeds protein anabolism, occurs in situations of famine, increased catabolism due to trauma or surgery, and inadequate nutrition therapy), respectively. CHI measures the 24-hour creatinine excretion in urine and compares

Due to the lower half-life (8-9 days) and the smaller size as a constituent body, transferrin is a better indicator of nutritional status of visceral protein from albumin. Normal levels of transferrin are between 200-400 mg/dl, and 150 mg/dl are considered nutritionally decision point or a point where nutritional support should be revised or adjusted. The transferrin levels are reduced in impaired synthesis as chronic infections, increased secretion, fluid overload, increased iron stores and increased in reduced iron stores as iron deficiency anemia and chronic blood loss, increased protein synthesis on estrogen therapy and oral contraception and dehydration. The serum concentration of transferrin is approximately 0.8 times the total iron binding capacity (TIBC). If direct measurement of transferrin is not possible due to the high cost and limited availability of equipment required, the level of transferrin can be easily

associated with poor outcome of surgery, rising costs of hospitalization and prolonged stay in ICU

severe malnutrition

increased morbidity and mortality

point that dietary intervention should be revised or adjusted

nutritional status normal

[36])

134 Topics in Paraplegia

Screening is important for the early detection of patients who are undernourished or at risk of developing malnutrition. Since January 2010, the Dutch Health Care Inspectorate (HCI) has defined under nutrition as a main care problem in rehabilitation centres, by establishing it as a Performance Indicator for Risk Steering Supervision. Dutch rehabilitation centres are now obligated to screen all rehabilitants for under nutrition on admission The Short Nutritional Assessment Questionnaire (SNAQ) is the recommended screening tool in this benchmark (Figure 1) [50]. However, various screening tools have been developed to detect a patient's nutritional status in many healthcare settings, but not in the rehabilitation setting. In the Netherlands, the SNAQ [51] and the Malnutrition Universal Screening Tool (MUST) are used for the hospital situation [52, 53]. The HCI advises the use of the SNAQ for under nutrition screening in rehabilitation centres [51]. Our results suggest the use of the SNAQ65+as a screening tool. This tool showed the best diagnostic accuracy of the quick and easy screening tools investigated (sensitivity 96%, specificity 77%) [52, 54].

**Figure 1.** The Short Nutritional Assessment Questionnaire (SNAQ). Published with permission from: http://www.fight‐ malnutrition.eu/fight-malnutrition/screening-tools/

#### **5. Monitoring**

Healthcare professionals with relevant skills and training should review the indications, route, risks, benefits and goals of nutrition support at regular intervals. The time between reviews depends on the patient, care setting and duration of nutrition support. Intervals may increase as the patient is stabilised on nutrition support [55]. (NICE Clinical Guideline 32 Feb.2006 Nutrition Support in Adults: Oral Nutrition Support, Enteral Tube Feeding and Parenteral Nutrition, the whole guideline can be downloaded from: http://www.nice.org.uk/nicemedia/ live/10978/29979/29979.pdf)

decreased lipoprotein lipase activity, and impaired clearance of triglycerides [63]. Glucose is the preferred energy molecule for the central nervous system, red blood cells, the cellular tissue, etc. A minimum quantity of 100-150 gr glucose per day is required for these functions and prevents the consumption of endogenous protein. The normal rate at which the body metabolizes carbohydrates or glucose is approximately 2-4 mg/ Kg/min. In times of severe stress, glucose metabolism may be increased to 3-5 mg/Kg/min. In most patients, administra‐ tion of more than 400-500 gr glucose per day, exceeding the body's ability to metabolize and stored as energy. Sources of glucose include not only the liquid diet and peritoneal fluid filtration. Excess glucose is converted into fat (lipogenesis) and leads to an increased ratio of

Malnutrition in Paraplegia http://dx.doi.org/10.5772/58382 137

The provision of lipids as a source of increased calories can facilitate protein maintenance, reduce the risk of excessive carbohydrates and reduce the total volume of liquid. Lipids are required to account for 30% of total calories supplied. In the acute phase after injury, large amounts of fat, especially as linoleic or omega-6 fatty acids have an immunosuppressive effect by triggering the release of arachidonic acid. This leads to synthesis of prostaglandins and then compresses the delayed hypersensitivity cell-regulated, proliferation of lymphocytes. In the presence of sepsis, high levels of serum triglycerides (250 gr/ml) indicate limited tolerance and decreased need for intravenous fluid delivery. A minimum of 4% of total energy requirements is necessary for the essential fatty acids to avoid deficiencies [65]. Unfortunately, although the hormonal cataract through increases in glycogenolysis and gluconeogenesis, is enhancing lipolysis, which provides endogenous glucose, amino acids, and free fatty acids that are required for cellular and organ function and wound healing and certain plasma levels of substrates are increased (i.e., glutamine) they could be insufficient to meet metabolic needs due to limited availability for use by peripheral tissues (because of factors such as insulin

Acute post-traumatic nitrogen requirements are much higher than in normal state. Another serious metabolic issue is negative nitrogen balance, due to excessive secretion of nitrogen because of protein use by the body to meet energy needs in the first week, with a peak at 3 weeks and can last for a period of 7 weeks. This imbalance will respond only slightly increased protein intake and may be non-modifiable as a process during the acute phase. The more severe the injury the greater the amount of nitrogen excreted. The accelerated catabolism of muscle mass results in a supply of amino acids for the acute-phase of protein synthesis, gluconeo‐ genesis, and the healing of wounds. Moreover, administration of glucocorticosteroids after injury may increase the catabolism of protein. The losses of nitrogen in the urine, mainly due to muscle atrophy because of paralysis, are increasing with the severity of the injury. On the other side, Cooper and Hoen stated that the secretion of more than 25 gr/day of nitrogen in the urine during the first two weeks after the injury is insufficient prognostic indicator for functional recovery of paralyzed muscles. The nitrogen losses after an injury are always present and last at least 7 weeks. In cases of acute injury, despite the provision of sufficient quantities of calories and protein usually occurs a negative nitrogen balance (NB), which peaks during the third week after injury. The same phenomenon has been observed in cases of severe poisoning with botulinum toxin (botulism) which resulted in paralysis of muscles. Negative

VCO2/VO2 (or RQ) [64].

resistance and inhibition of lipoprotein lipase) [60, 61].

#### **6. Physiopathological mechanisms of malnutrition**

#### **6.1. Malnutrition in the acute phase of paraplegia**

Pathophysiological mechanisms of malnutrition in paraplegia are multifactorial. There is a dramatic increase in energy expenditure, endogenous protein catabolism and nitrogen excretion after lesion-injury. Extensive multiple organ trauma, soft tissue injuries and frac‐ tures, may further increase hyper catabolic reactions. Also, the body temperature and energy expenditure increases due to pulmonary infections or urinary tract infractions, and pancrea‐ titis. The metabolic rate does not seem to be affected by the small reductions in thyroxin levels in plasma observed after the injury [56, 57].

Metabolic changes are also present with the elevated catabolic hormonal and cytokine responses including increased blood levels of counter regulatory hormones (e.g., cortisol, catecholamines, and glucagon), increased blood and tissue levels of proinflammatory cyto‐ kines (i.e., interleukin-1, interleukin-6, interleukin-8, and tumor necrosis factor α), and peripheral-tissue resistance to endogenous anabolic hormones (i.e., insulin and insulin-like growth factor 1) to be primarily responsible for the initial changes in metabolism [58-61].

Glucose intolerance, which cannot be readily apparent during the acute phase, but may be caused by complications and physiological processes of acute care such as the initial hyper metabolic-catabolic stress response, administration of steroids, the parenteral / enteral nutrition, and atrophy as a consequence of aponeurosis which results in gluconeogenesis [62]. Glucose and lipid metabolism disrupt in acute post-traumatic phase. Increased hepatic gluconeogenesis and regional response to insulin result in hyperglycemia. The metabolism of glucose in combination with acute nerve injury has been studied extensively, especially as related to ischemia. These studies suggest that hyperglycemia which follows immediately after head injury or spinal cord may worsen the outcome. High serum glucose levels increase the availability of substrate for anaerobic glycolysis, and thus the production of lactic acid, which may have the reverse effect on neurological recovery from injury. The prevention of hyper‐ glycemia, particularly during the first 2 to 8 hours after injury, seems to be very critical for optimal recovery. After 2 to 8 hours after injury, elevated glucose levels may be beneficial, allowing the beginning of intestinal or parenteral feedings in a short time after the injury. It is also likely the serum triglyceride levels to be found elevated due to the accelerated lipogenesis, decreased lipoprotein lipase activity, and impaired clearance of triglycerides [63]. Glucose is the preferred energy molecule for the central nervous system, red blood cells, the cellular tissue, etc. A minimum quantity of 100-150 gr glucose per day is required for these functions and prevents the consumption of endogenous protein. The normal rate at which the body metabolizes carbohydrates or glucose is approximately 2-4 mg/ Kg/min. In times of severe stress, glucose metabolism may be increased to 3-5 mg/Kg/min. In most patients, administra‐ tion of more than 400-500 gr glucose per day, exceeding the body's ability to metabolize and stored as energy. Sources of glucose include not only the liquid diet and peritoneal fluid filtration. Excess glucose is converted into fat (lipogenesis) and leads to an increased ratio of VCO2/VO2 (or RQ) [64].

**5. Monitoring**

136 Topics in Paraplegia

live/10978/29979/29979.pdf)

**6. Physiopathological mechanisms of malnutrition**

**6.1. Malnutrition in the acute phase of paraplegia**

in plasma observed after the injury [56, 57].

Healthcare professionals with relevant skills and training should review the indications, route, risks, benefits and goals of nutrition support at regular intervals. The time between reviews depends on the patient, care setting and duration of nutrition support. Intervals may increase as the patient is stabilised on nutrition support [55]. (NICE Clinical Guideline 32 Feb.2006 Nutrition Support in Adults: Oral Nutrition Support, Enteral Tube Feeding and Parenteral Nutrition, the whole guideline can be downloaded from: http://www.nice.org.uk/nicemedia/

Pathophysiological mechanisms of malnutrition in paraplegia are multifactorial. There is a dramatic increase in energy expenditure, endogenous protein catabolism and nitrogen excretion after lesion-injury. Extensive multiple organ trauma, soft tissue injuries and frac‐ tures, may further increase hyper catabolic reactions. Also, the body temperature and energy expenditure increases due to pulmonary infections or urinary tract infractions, and pancrea‐ titis. The metabolic rate does not seem to be affected by the small reductions in thyroxin levels

Metabolic changes are also present with the elevated catabolic hormonal and cytokine responses including increased blood levels of counter regulatory hormones (e.g., cortisol, catecholamines, and glucagon), increased blood and tissue levels of proinflammatory cyto‐ kines (i.e., interleukin-1, interleukin-6, interleukin-8, and tumor necrosis factor α), and peripheral-tissue resistance to endogenous anabolic hormones (i.e., insulin and insulin-like growth factor 1) to be primarily responsible for the initial changes in metabolism [58-61].

Glucose intolerance, which cannot be readily apparent during the acute phase, but may be caused by complications and physiological processes of acute care such as the initial hyper metabolic-catabolic stress response, administration of steroids, the parenteral / enteral nutrition, and atrophy as a consequence of aponeurosis which results in gluconeogenesis [62]. Glucose and lipid metabolism disrupt in acute post-traumatic phase. Increased hepatic gluconeogenesis and regional response to insulin result in hyperglycemia. The metabolism of glucose in combination with acute nerve injury has been studied extensively, especially as related to ischemia. These studies suggest that hyperglycemia which follows immediately after head injury or spinal cord may worsen the outcome. High serum glucose levels increase the availability of substrate for anaerobic glycolysis, and thus the production of lactic acid, which may have the reverse effect on neurological recovery from injury. The prevention of hyper‐ glycemia, particularly during the first 2 to 8 hours after injury, seems to be very critical for optimal recovery. After 2 to 8 hours after injury, elevated glucose levels may be beneficial, allowing the beginning of intestinal or parenteral feedings in a short time after the injury. It is also likely the serum triglyceride levels to be found elevated due to the accelerated lipogenesis,

The provision of lipids as a source of increased calories can facilitate protein maintenance, reduce the risk of excessive carbohydrates and reduce the total volume of liquid. Lipids are required to account for 30% of total calories supplied. In the acute phase after injury, large amounts of fat, especially as linoleic or omega-6 fatty acids have an immunosuppressive effect by triggering the release of arachidonic acid. This leads to synthesis of prostaglandins and then compresses the delayed hypersensitivity cell-regulated, proliferation of lymphocytes. In the presence of sepsis, high levels of serum triglycerides (250 gr/ml) indicate limited tolerance and decreased need for intravenous fluid delivery. A minimum of 4% of total energy requirements is necessary for the essential fatty acids to avoid deficiencies [65]. Unfortunately, although the hormonal cataract through increases in glycogenolysis and gluconeogenesis, is enhancing lipolysis, which provides endogenous glucose, amino acids, and free fatty acids that are required for cellular and organ function and wound healing and certain plasma levels of substrates are increased (i.e., glutamine) they could be insufficient to meet metabolic needs due to limited availability for use by peripheral tissues (because of factors such as insulin resistance and inhibition of lipoprotein lipase) [60, 61].

Acute post-traumatic nitrogen requirements are much higher than in normal state. Another serious metabolic issue is negative nitrogen balance, due to excessive secretion of nitrogen because of protein use by the body to meet energy needs in the first week, with a peak at 3 weeks and can last for a period of 7 weeks. This imbalance will respond only slightly increased protein intake and may be non-modifiable as a process during the acute phase. The more severe the injury the greater the amount of nitrogen excreted. The accelerated catabolism of muscle mass results in a supply of amino acids for the acute-phase of protein synthesis, gluconeo‐ genesis, and the healing of wounds. Moreover, administration of glucocorticosteroids after injury may increase the catabolism of protein. The losses of nitrogen in the urine, mainly due to muscle atrophy because of paralysis, are increasing with the severity of the injury. On the other side, Cooper and Hoen stated that the secretion of more than 25 gr/day of nitrogen in the urine during the first two weeks after the injury is insufficient prognostic indicator for functional recovery of paralyzed muscles. The nitrogen losses after an injury are always present and last at least 7 weeks. In cases of acute injury, despite the provision of sufficient quantities of calories and protein usually occurs a negative nitrogen balance (NB), which peaks during the third week after injury. The same phenomenon has been observed in cases of severe poisoning with botulinum toxin (botulism) which resulted in paralysis of muscles. Negative nitrogen balance following injury, has been associated with further findings. During the first weeks after injury, many patients experience a transient positive nitrogen balance, possibly due to initial delays in the loss of nitrogen [66]. Four conscientious objectors were immobilized on pelvic corset and leg casts for 6 to 7 weeks in a metabolic chamber. All 4 subjects showed an increase in nitrogen excretion and negative nitrogen balance. However, it took 4 to 5 days to develop. In conclusion, acute immobilization of paralyzed patients contributes to increased excretion of nitrogen which starts about a week after the injury [67].

Serum hemoglobin and hematocrit may reflect a general state of malnutrition. Anemia, defined by low hemoglobin levels (<14 mg/dl) and hematocrit (<36%) reduces the oxygen in the blood and impedes the wound healing. Anemia may be due to a preexisting condition or as the result of unbalanced production and distribution of blood cells as a result of reaction to stress, gastrointestinal bleeding or obvious bleeding due to other trauma [76]. Low levels of total serum protein (<6.4 mg/dl) and protein (<3.5 mg/dl), accelerate the development of edema, which causes a decrease in skin elasticity and prevent the transfer of oxygen and nutrients from the blood to the skin. Also, the swelling may increase local tissue pressure, causing loss of regional blood flow and tissue damage. The loss of protein and protein secretion in pressure ulcers increases the deficiencies in proteins. The paralytic ileus occurs as a result of disturbance of the autonomic and simultaneous or ischemia as a complication of hypokalemia, abdominal trauma or sepsis, generally persists for 72 hours-1 week and may restrict the movement of the diaphragm [77]. Parenteral nutrition is indicated if paralytic ileus persists for more than 3-5 days. Ulcers and bleeding, which occur as a result of paralytic vasodilatation with ischemia, steroids, nasogastric tube irritation, and other causes should be treated with oral or enteral

Malnutrition in Paraplegia http://dx.doi.org/10.5772/58382 139

During aging with paraplegia other complications are added in the physiopathological context

A neglected factor is muscle tonus: hypotonia (low muscle tone, floppiness) results in a lower resistance to muscle movement. The lower the resistance, the fewer calories burned during movement. Furthermore, hypertonia (high muscle tone, spasticity) is limiting muscle move‐ ment and reduces caloric needs. Lack of movement results in muscle atrophy and a lower lean

In spinal cord injured subjects is mainly central or abdominal obesity leading to metabolic, cardiovascular issues etc. There is conflicting evidence about the contribution of visceral and subcutaneous adipose tissue to different metabolic disorders after SCI. Moreover subjects with longstanding disabilities (i.e. spinal cord injury) are at increased risk for cardiovascular disease and cardiopulmonary disease because of extensive fat intake and limiting activities. In generally, subjects with disabilities are prone to developing vitamin D deficiency. Earlier work by Bauman et al suggested that approximately 32% of veterans with spinal cord injury (SCI) were absolutely deficient in vitamin D (25 hydroxyvitamin D [25(OH)D]). Most subjects have a high incidence of vitamin D deficiency as defined by levels of 25(OH)D<20 ng/mL. The reasons might be due to a combination of low dietary vitamin D intake and avoiding sun exposure because of depression or sensitivity in drugs i.e. dantrolene [80]. The low intake of vitamin D, which is supplied by food either in vitamin D2 (ergocalciferol, activated ergosterol), found in yeast, or vitamin D3 (cholecalciferol), found in fish, can be bypassed through

Moreover, reduced mobility and immobilization for long period cause pressure ulcers of the skin and the wound but can be prevented by adequate intake of quantity of protein, vitamin

body mass, which in turn reduces the number of calories burned even at rest [79].

feeding as soon as possible but may require parenteral nutrition [78].

of "malnourished paraplegics".

supplements [81].

E, zinc, and fluids to maintain skin integrity [82].

**6.2. Malnutrition in the chronic phase of paraplegia and during aging**

Deficiencies in zinc and vitamin C have been associated with poor wound healing. The provision of these micronutrients supplementation in patients with these deficits enhances the healing. Adequate quantities of salts and vitamins are usually provided in a balanced diet. The supplemental micro-nutrient dietary substances are necessary if we suspect shortcomings intake or increased requirements because of circumstances specific diseases. Zinc is often prescribed to improve stress ulcers, is known to be involved in structural integrity of collagen. However, zinc levels in serum is similar in patients taking supplements that contain sulfur (220 mg daily) and do not affect the healing process of ulcers sprawling over a period of 2-3 months. Opposite physiological effects, such as metabolism of copper, copper deficiency and anemia may be caused by long-term supplementation of large amounts of zinc [68]. The role of vitamin C in collagen synthesis is crucial. Although the supplementation with vitamin C did not accelerate the healing of decubitus ulcers in patients, dietary intake of vitamin C has not been associated with the development of decubitus ulcers. Moreover, given that the subclinical deficiencies are difficult to show up, the minimum recommended dietary intake is proposed to 60mg [69]. Excessive excretion of potassium and abnormal hyponatremia; hypercalcemia, due to immobilization, particularly in young men and hypercalciuria exceed the normal range in 4 weeks, with higher values at 16 weeks, which can persist for a long time. Hypercalcemia occurs with anorexia, abdominal cramps, nausea, vomiting, constipation, polydipsia, polyuria, dehydration and did not respond to diets which restrict the intake of calcium and need to be treated with medication, hydration, and mobilization [70].

Finally the effect of drugs such as analgesics and barbiturates is crucial. Drugs that are frequently administered to acute paraplegic patients may themselves increase skeletal-muscle breakdown (corticosteroids), decrease splanchnic blood flow (pressor agents), or increase urinary loss of electrolytes, minerals, and water-soluble vitamins (diuretics). Infection, operative trauma, and other stresses may increase energy expenditure and protein and micronutrient needs [71-74]. The average daily dietary needs are modified because of the altered physiology of each body system and psychological integrity of a patient susceptible to an injury, potentially at any age, which cannot exclude the possibility of a pre-existing disease causing nutritional problems [75].

Moreover, the frequent coexistence of injuries from other systems, such as brain injury, maxillofacial injuries, fractures, etc., disturbs the normal physiology further. Studies in malnourished patients stated that malnutrition before a spine stabilization surgery is leading to postoperative complications, hyperthermia, which increases the caloric needs of the patient, and denervation, leading to atrophy and paralysis, which supply amino acids for gluconeo‐ genesis, which, in turn, supplies glucose to meet caloric needs [1].

Serum hemoglobin and hematocrit may reflect a general state of malnutrition. Anemia, defined by low hemoglobin levels (<14 mg/dl) and hematocrit (<36%) reduces the oxygen in the blood and impedes the wound healing. Anemia may be due to a preexisting condition or as the result of unbalanced production and distribution of blood cells as a result of reaction to stress, gastrointestinal bleeding or obvious bleeding due to other trauma [76]. Low levels of total serum protein (<6.4 mg/dl) and protein (<3.5 mg/dl), accelerate the development of edema, which causes a decrease in skin elasticity and prevent the transfer of oxygen and nutrients from the blood to the skin. Also, the swelling may increase local tissue pressure, causing loss of regional blood flow and tissue damage. The loss of protein and protein secretion in pressure ulcers increases the deficiencies in proteins. The paralytic ileus occurs as a result of disturbance of the autonomic and simultaneous or ischemia as a complication of hypokalemia, abdominal trauma or sepsis, generally persists for 72 hours-1 week and may restrict the movement of the diaphragm [77]. Parenteral nutrition is indicated if paralytic ileus persists for more than 3-5 days. Ulcers and bleeding, which occur as a result of paralytic vasodilatation with ischemia, steroids, nasogastric tube irritation, and other causes should be treated with oral or enteral feeding as soon as possible but may require parenteral nutrition [78].

#### **6.2. Malnutrition in the chronic phase of paraplegia and during aging**

nitrogen balance following injury, has been associated with further findings. During the first weeks after injury, many patients experience a transient positive nitrogen balance, possibly due to initial delays in the loss of nitrogen [66]. Four conscientious objectors were immobilized on pelvic corset and leg casts for 6 to 7 weeks in a metabolic chamber. All 4 subjects showed an increase in nitrogen excretion and negative nitrogen balance. However, it took 4 to 5 days to develop. In conclusion, acute immobilization of paralyzed patients contributes to increased

Deficiencies in zinc and vitamin C have been associated with poor wound healing. The provision of these micronutrients supplementation in patients with these deficits enhances the healing. Adequate quantities of salts and vitamins are usually provided in a balanced diet. The supplemental micro-nutrient dietary substances are necessary if we suspect shortcomings intake or increased requirements because of circumstances specific diseases. Zinc is often prescribed to improve stress ulcers, is known to be involved in structural integrity of collagen. However, zinc levels in serum is similar in patients taking supplements that contain sulfur (220 mg daily) and do not affect the healing process of ulcers sprawling over a period of 2-3 months. Opposite physiological effects, such as metabolism of copper, copper deficiency and anemia may be caused by long-term supplementation of large amounts of zinc [68]. The role of vitamin C in collagen synthesis is crucial. Although the supplementation with vitamin C did not accelerate the healing of decubitus ulcers in patients, dietary intake of vitamin C has not been associated with the development of decubitus ulcers. Moreover, given that the subclinical deficiencies are difficult to show up, the minimum recommended dietary intake is proposed to 60mg [69]. Excessive excretion of potassium and abnormal hyponatremia; hypercalcemia, due to immobilization, particularly in young men and hypercalciuria exceed the normal range in 4 weeks, with higher values at 16 weeks, which can persist for a long time. Hypercalcemia occurs with anorexia, abdominal cramps, nausea, vomiting, constipation, polydipsia, polyuria, dehydration and did not respond to diets which restrict the intake of

calcium and need to be treated with medication, hydration, and mobilization [70].

causing nutritional problems [75].

Finally the effect of drugs such as analgesics and barbiturates is crucial. Drugs that are frequently administered to acute paraplegic patients may themselves increase skeletal-muscle breakdown (corticosteroids), decrease splanchnic blood flow (pressor agents), or increase urinary loss of electrolytes, minerals, and water-soluble vitamins (diuretics). Infection, operative trauma, and other stresses may increase energy expenditure and protein and micronutrient needs [71-74]. The average daily dietary needs are modified because of the altered physiology of each body system and psychological integrity of a patient susceptible to an injury, potentially at any age, which cannot exclude the possibility of a pre-existing disease

Moreover, the frequent coexistence of injuries from other systems, such as brain injury, maxillofacial injuries, fractures, etc., disturbs the normal physiology further. Studies in malnourished patients stated that malnutrition before a spine stabilization surgery is leading to postoperative complications, hyperthermia, which increases the caloric needs of the patient, and denervation, leading to atrophy and paralysis, which supply amino acids for gluconeo‐

genesis, which, in turn, supplies glucose to meet caloric needs [1].

excretion of nitrogen which starts about a week after the injury [67].

138 Topics in Paraplegia

During aging with paraplegia other complications are added in the physiopathological context of "malnourished paraplegics".

A neglected factor is muscle tonus: hypotonia (low muscle tone, floppiness) results in a lower resistance to muscle movement. The lower the resistance, the fewer calories burned during movement. Furthermore, hypertonia (high muscle tone, spasticity) is limiting muscle move‐ ment and reduces caloric needs. Lack of movement results in muscle atrophy and a lower lean body mass, which in turn reduces the number of calories burned even at rest [79].

In spinal cord injured subjects is mainly central or abdominal obesity leading to metabolic, cardiovascular issues etc. There is conflicting evidence about the contribution of visceral and subcutaneous adipose tissue to different metabolic disorders after SCI. Moreover subjects with longstanding disabilities (i.e. spinal cord injury) are at increased risk for cardiovascular disease and cardiopulmonary disease because of extensive fat intake and limiting activities. In generally, subjects with disabilities are prone to developing vitamin D deficiency. Earlier work by Bauman et al suggested that approximately 32% of veterans with spinal cord injury (SCI) were absolutely deficient in vitamin D (25 hydroxyvitamin D [25(OH)D]). Most subjects have a high incidence of vitamin D deficiency as defined by levels of 25(OH)D<20 ng/mL. The reasons might be due to a combination of low dietary vitamin D intake and avoiding sun exposure because of depression or sensitivity in drugs i.e. dantrolene [80]. The low intake of vitamin D, which is supplied by food either in vitamin D2 (ergocalciferol, activated ergosterol), found in yeast, or vitamin D3 (cholecalciferol), found in fish, can be bypassed through supplements [81].

Moreover, reduced mobility and immobilization for long period cause pressure ulcers of the skin and the wound but can be prevented by adequate intake of quantity of protein, vitamin E, zinc, and fluids to maintain skin integrity [82].

Pneumonia and paralysis of respiratory muscles through malnutrition may further weaken the respiratory muscles. On the other site excessive feeding may lead to increased oxidation of glucose and production of carbon dioxide to be eliminated and further stress on the respiratory system. The fluid overload or aggressive implementation of parenteral support can lead to pulmonary edema. The reduced hydration can lead to reduced drainage of secretions, atelectasis, and pneumonia. Abdominal distension due to unabsorbed food by mouth or enteral feeding or swallowing air during feeding can lead to compromise the functioning of the diaphragm and predisposes to hypoventilation or aspiration [83]. Neuro‐ genic bowel requires the right amount of food, fiber and fluids in order to be successful retraining of the bowel, and prevent constipation, diarrhea, incontinence, and autonomic dysreflexia as a result of fecal impaction. Bowel function may be compromised by hyperos‐ molar feeding through a tube, lactose intolerance or pseudomembranous colitis, prolonged treatment with antibiotics, which can cause diarrhea and require parenteral nutritional support. For neurogenic bladder vitamin C and other supplements are necessary for the acidification of urine and prevention of infection of the urinary tract.

#### **7. The nutritional support**

The provision of a nutritional supplement is definitely not a frontline management technique for poor oral intake. Supplements when administered correctly to patients can easily optimize nutrition and should be an adjunctive to nutrition.

Per os feeding is recommended for patients who are weaned from tracheal tubes, which are awakened, may follow commands and have good swallowing and intestinal function. Patients with central nervous system (CNS) acute diseases are frequently in coma or have their swallowing reflexes impaired and need parenteral nutrition or enteral tube feeding [84, 85]. Enteral nutrition (EN) is recommended for patients who are tubed, not able to swallow or to receive adequate diet orally but have good bowel function.

Early nutrition support through the enteral route has been shown to blunt catabolism, reduce complications and reduce length of stay in a number of patient populations, including both surgical and non-surgical neuro patients [86, 87]. However, nutrition support must be initiated within the 48-to 72-hour period immediately following injury or surgical insult to achieve these benefits. Clinicians are often hesitant to feed critically ill neuro patients too soon. However, studies indicate patients with severe neurological deficits and clinically silent abdomens can tolerate low-rate jejunal feedings within 36 hours of injury with a gradual increase in feeding rate to meet initial caloric goals within two to four days [88, 89]. If jejunal feedings are initiated prior to induction of pentobarbital infusion, even patients in pentobarbital coma can be fed enterally [90].

where enteral feeding is expected to be required for longer than 2–4 weeks, for example in patients with acute stroke [91]. Although complications of PEG tube feeding are rare in stable patients, they become increasingly common in critically ill and debilitated patients. One of most feared complication of enteral feeding: aspiration hypoxia/ pneumonia. Clinically, gastric residual volume (GRV) measurement was frequently used as marker to predict aspiration & pneumonia. Elevated GRV: associated with comorbidities such as vasopressor use, sedation sepsis, vomiting. GRV: no significance between GRV> 200ml and GRV> 400ml, low sensitivity

**Figure 2.** The enteral feeding pump type COMPAT (unpublished photo courtesy of Dionyssiotis Y). The system is a rel‐ atively simple, lightweight, easy to use for managing all types of enteral feeding. Have an audible and visual alarm that alerts you when each of the following conditions: empty container feeding, low battery, change the dose, or the existence of j free flow out of the system (waste). The memory of the pump retains infusion rate, volume delivered, dose limit even after turning it off. It is designed to provide precision dosing. Start enteral feeding schedule and prog‐

Malnutrition in Paraplegia http://dx.doi.org/10.5772/58382 141

With increasing frequency, nasogastric feeding tubes are replaced by PEG to provide semilong-term enteral nutrition because of various advantages of a PEG in daily use [93-95]. In contrast to a nasogastric feeding tube, PEG does not interfere with the swallowing mechanism, which reduces the possibility of choking, especially when oral feeding is initiated during

as a marker of aspiration [92].

ress.

Νasogastric or nasoenteric feeding tubes should not be used for periods longer than 4 weeks because of discomfort and the risk of nasal injury and sinusitis. Placement of a percutaneous endoscopic gastrostomy (PEG) tube should be considered for patients who continue to require enteral feeding beyond 4 weeks[90]. PeG is also indicated as firstline intervention in conditions

Pneumonia and paralysis of respiratory muscles through malnutrition may further weaken the respiratory muscles. On the other site excessive feeding may lead to increased oxidation of glucose and production of carbon dioxide to be eliminated and further stress on the respiratory system. The fluid overload or aggressive implementation of parenteral support can lead to pulmonary edema. The reduced hydration can lead to reduced drainage of secretions, atelectasis, and pneumonia. Abdominal distension due to unabsorbed food by mouth or enteral feeding or swallowing air during feeding can lead to compromise the functioning of the diaphragm and predisposes to hypoventilation or aspiration [83]. Neuro‐ genic bowel requires the right amount of food, fiber and fluids in order to be successful retraining of the bowel, and prevent constipation, diarrhea, incontinence, and autonomic dysreflexia as a result of fecal impaction. Bowel function may be compromised by hyperos‐ molar feeding through a tube, lactose intolerance or pseudomembranous colitis, prolonged treatment with antibiotics, which can cause diarrhea and require parenteral nutritional support. For neurogenic bladder vitamin C and other supplements are necessary for the

The provision of a nutritional supplement is definitely not a frontline management technique for poor oral intake. Supplements when administered correctly to patients can easily optimize

Per os feeding is recommended for patients who are weaned from tracheal tubes, which are awakened, may follow commands and have good swallowing and intestinal function. Patients with central nervous system (CNS) acute diseases are frequently in coma or have their swallowing reflexes impaired and need parenteral nutrition or enteral tube feeding [84, 85]. Enteral nutrition (EN) is recommended for patients who are tubed, not able to swallow or to

Early nutrition support through the enteral route has been shown to blunt catabolism, reduce complications and reduce length of stay in a number of patient populations, including both surgical and non-surgical neuro patients [86, 87]. However, nutrition support must be initiated within the 48-to 72-hour period immediately following injury or surgical insult to achieve these benefits. Clinicians are often hesitant to feed critically ill neuro patients too soon. However, studies indicate patients with severe neurological deficits and clinically silent abdomens can tolerate low-rate jejunal feedings within 36 hours of injury with a gradual increase in feeding rate to meet initial caloric goals within two to four days [88, 89]. If jejunal feedings are initiated prior to induction of pentobarbital infusion, even patients in pentobarbital coma can be fed

Νasogastric or nasoenteric feeding tubes should not be used for periods longer than 4 weeks because of discomfort and the risk of nasal injury and sinusitis. Placement of a percutaneous endoscopic gastrostomy (PEG) tube should be considered for patients who continue to require enteral feeding beyond 4 weeks[90]. PeG is also indicated as firstline intervention in conditions

acidification of urine and prevention of infection of the urinary tract.

**7. The nutritional support**

140 Topics in Paraplegia

enterally [90].

nutrition and should be an adjunctive to nutrition.

receive adequate diet orally but have good bowel function.

**Figure 2.** The enteral feeding pump type COMPAT (unpublished photo courtesy of Dionyssiotis Y). The system is a rel‐ atively simple, lightweight, easy to use for managing all types of enteral feeding. Have an audible and visual alarm that alerts you when each of the following conditions: empty container feeding, low battery, change the dose, or the existence of j free flow out of the system (waste). The memory of the pump retains infusion rate, volume delivered, dose limit even after turning it off. It is designed to provide precision dosing. Start enteral feeding schedule and prog‐ ress.

where enteral feeding is expected to be required for longer than 2–4 weeks, for example in patients with acute stroke [91]. Although complications of PEG tube feeding are rare in stable patients, they become increasingly common in critically ill and debilitated patients. One of most feared complication of enteral feeding: aspiration hypoxia/ pneumonia. Clinically, gastric residual volume (GRV) measurement was frequently used as marker to predict aspiration & pneumonia. Elevated GRV: associated with comorbidities such as vasopressor use, sedation sepsis, vomiting. GRV: no significance between GRV> 200ml and GRV> 400ml, low sensitivity as a marker of aspiration [92].

With increasing frequency, nasogastric feeding tubes are replaced by PEG to provide semilong-term enteral nutrition because of various advantages of a PEG in daily use [93-95]. In contrast to a nasogastric feeding tube, PEG does not interfere with the swallowing mechanism, which reduces the possibility of choking, especially when oral feeding is initiated during neurological recovery. The cosmetic advantage of a PEG, which can be worn invisibly underneath the patients' clothes, may play a psychological role during recovery. PEG place‐ ment is associated with a mortality rate of 1-3 per cent, major complication rates of 3-9 per cent and minor complication rates of 5-45 per cent. The risk of aspiration, frequently associated with nasogastric feeding tubes, has not been eliminated with PEG placement [96-100].

hyperglycemia, an increased risk of infectious complications and increased mortality rates in

Malabsorption and maldigestion must be recognized early in the decision making process in the use of enteral nutrition. Weight loss, signs of macronutrient (i.e., decreased visceral protein status, hypoglycemia, and steatorrhea) and micronutrient (electrolytes, trace elements, and vitamins) abnormalities suggest that the intestine may not be optimally functioning [107].

The European Society for Clinical Nutrition and Metabolism guidelines recommends that: "All patients receiving less than their targeted enteral feeding after 2 days should be considered for

Despite considerable controversy in this field, physicians generally agree on two key aspects: firstly, the enteral route is preferable whenever possible, and secondly, if possible, enteral nutritional support should be started early (within 24–48 h after admission) [101, 108, 109].

The American Society for Parenteral and Enteral Nutrition (ASPEN) and Society of Critical Care Medicine (SCCM) guidelines recommend that parenteral nutrition be initiated after 1 week, unless the patient is severely malnourished. By contrast, the European Society of Enteral and Parenteral (ESPEN) guidelines recommend consideration of a combination of enteral and parenteral nutrition after only 2–3 days in the ICU if enteral nutrition alone is insufficient at

In the early phase of rehabilitation enteral feeding solutions with low osmolarity (<300 mOsm/ l) to prevent hyperosmolar diarrhea (appeared in case of long time left unfeeded intestine, and

> **Nutricia Pre-nutrison 500ml**

**g/100ml** 2, 5 30% 1, 95 35% 0, 2 2% 1, 5 13, 3% **Fibers** 0, 5 0 0 0 **Osmolarity** 250 140 N.A. 269

**Energy Kcal/ml** 0, 75 0, 5 0, 5 1 **Protein g/100ml** 5 27% 2 16% 8, 5 68% 5, 2 20, 8% **Gluamine g/100ml** 1 N.A. 6 1, 4

**Fresenius Intestamin 500ml**

8 43% 6, 1 49% 17, 7 54% 16, 4 64, 9%

**Abbott Osmolite HP**

Malnutrition in Paraplegia http://dx.doi.org/10.5772/58382 143

**8. Transition from parenteral to enteral feeding and vice versa**

critically ill patients [104, 105].

supplementary parenteral nutrition" [108].

low calorie <1Kcal/ml) are usually used (Table 3).

**Novartis Novasource start 500ml**

that time [108, 110].

**Products**

**Carbohydrates g/100ml**

**Fat**

**Table 3.** Starters for enteral nutrition

Another interesting issue is early compared with late introduction of the feed. With data limited to ICU patients there was no overall difference in mortality rates with either EN or PN with no apparent difference in mortality rates across groups receiving EN or PN (RR 1.08; 95% CI 0.70 to 1.65). As suggested compared with PN, EN was associated with a significant reduction in infectious complications (RR 0.61; 95% CI 0.44 to 0.84; p=0.003). The early compared with late introduction of enteral feed only suggested that early EN was associated with a trend toward a reduction in mortality (RR 0.52; 95% CI 0.25 to 1.08; p=0.08) when compared with delayed nutrient intake and infection risk was not different [101]. The compi‐ lation of 11 high quality studies comparing enteral and parenteral nutrition revealed a significant effect in favor of parenteral nutrition [odds ratio (OR) 0.51, 95% confidence interval (CI) 0.27–0.97]. A subgroup analysis of trials comparing parenteral nutrition with early or late enteral feeding showed that there was no survival benefit in parenteral nutrition when enteral nutrition was provided early. The benefit of parenteral nutrition was confined to trials comparing it with late enteral nutrition. Therefore, this metaanalysis confirms at least a finding already reported in earlier metaanalyses: there is no increased mortality risk with parenteral nutrition! [102].

A major concern with EN is the discrepancy between prescribed and delivered amount of nutrient, the major causes of which are diarrhea, vomiting or gastric stasis. Furthermore, enteral nutrient delivery is gradually increased in critically ill patients in order to avoid the possibility of gastrointestinal intolerance, so that a few days are required to achieve the caloric target. Administering the total nutritional requirement of mechanically ventilated medical patients starting on day 1 was associated with greater infectious complications and prolonged length of hospital stay compared to patients in whom a gradual approach was implemented [103]. Despite the caloric deficiency, EN is still superior to PN so that nonenergetic effects of EN, such as immune modulation or protection of the intestinal mucos‐ al barrier, seem to be of greater value in the critically ill than the mere energetic supply. The issue of the better enteral access (gastric vs. post-pyloric route) is not yet settled. However, available evidence does not support the routine insertion of post-pyloric tubes as long as the gastric route is effective [104, 105, 106].

Aside from the potential problems associated with receiving in adequate or excessive nutrition or medication therapy, additional injury to the patient may result from using the gut that is at risk for bacterial or candidal translocation. Therefore, enteral nutrition should be started only if the potential benefits outweigh the risks [107, 108].

However, nutritional support is not without adverse effects and risks. Early EN may be associated with high gastric residuals, bacterial colonization of the stomach, and increased risk of aspiration pneumonia. PN has been associated with gut mucosal atrophy, overfeeding, hyperglycemia, an increased risk of infectious complications and increased mortality rates in critically ill patients [104, 105].

#### **8. Transition from parenteral to enteral feeding and vice versa**

Malabsorption and maldigestion must be recognized early in the decision making process in the use of enteral nutrition. Weight loss, signs of macronutrient (i.e., decreased visceral protein status, hypoglycemia, and steatorrhea) and micronutrient (electrolytes, trace elements, and vitamins) abnormalities suggest that the intestine may not be optimally functioning [107].

The European Society for Clinical Nutrition and Metabolism guidelines recommends that: "All patients receiving less than their targeted enteral feeding after 2 days should be considered for supplementary parenteral nutrition" [108].

Despite considerable controversy in this field, physicians generally agree on two key aspects: firstly, the enteral route is preferable whenever possible, and secondly, if possible, enteral nutritional support should be started early (within 24–48 h after admission) [101, 108, 109].

The American Society for Parenteral and Enteral Nutrition (ASPEN) and Society of Critical Care Medicine (SCCM) guidelines recommend that parenteral nutrition be initiated after 1 week, unless the patient is severely malnourished. By contrast, the European Society of Enteral and Parenteral (ESPEN) guidelines recommend consideration of a combination of enteral and parenteral nutrition after only 2–3 days in the ICU if enteral nutrition alone is insufficient at that time [108, 110].

In the early phase of rehabilitation enteral feeding solutions with low osmolarity (<300 mOsm/ l) to prevent hyperosmolar diarrhea (appeared in case of long time left unfeeded intestine, and low calorie <1Kcal/ml) are usually used (Table 3).


**Table 3.** Starters for enteral nutrition

neurological recovery. The cosmetic advantage of a PEG, which can be worn invisibly underneath the patients' clothes, may play a psychological role during recovery. PEG place‐ ment is associated with a mortality rate of 1-3 per cent, major complication rates of 3-9 per cent and minor complication rates of 5-45 per cent. The risk of aspiration, frequently associated with nasogastric feeding tubes, has not been eliminated with PEG placement [96-100].

Another interesting issue is early compared with late introduction of the feed. With data limited to ICU patients there was no overall difference in mortality rates with either EN or PN with no apparent difference in mortality rates across groups receiving EN or PN (RR 1.08; 95% CI 0.70 to 1.65). As suggested compared with PN, EN was associated with a significant reduction in infectious complications (RR 0.61; 95% CI 0.44 to 0.84; p=0.003). The early compared with late introduction of enteral feed only suggested that early EN was associated with a trend toward a reduction in mortality (RR 0.52; 95% CI 0.25 to 1.08; p=0.08) when compared with delayed nutrient intake and infection risk was not different [101]. The compi‐ lation of 11 high quality studies comparing enteral and parenteral nutrition revealed a significant effect in favor of parenteral nutrition [odds ratio (OR) 0.51, 95% confidence interval (CI) 0.27–0.97]. A subgroup analysis of trials comparing parenteral nutrition with early or late enteral feeding showed that there was no survival benefit in parenteral nutrition when enteral nutrition was provided early. The benefit of parenteral nutrition was confined to trials comparing it with late enteral nutrition. Therefore, this metaanalysis confirms at least a finding already reported in earlier metaanalyses: there is no increased mortality risk with parenteral

A major concern with EN is the discrepancy between prescribed and delivered amount of nutrient, the major causes of which are diarrhea, vomiting or gastric stasis. Furthermore, enteral nutrient delivery is gradually increased in critically ill patients in order to avoid the possibility of gastrointestinal intolerance, so that a few days are required to achieve the caloric target. Administering the total nutritional requirement of mechanically ventilated medical patients starting on day 1 was associated with greater infectious complications and prolonged length of hospital stay compared to patients in whom a gradual approach was implemented [103]. Despite the caloric deficiency, EN is still superior to PN so that nonenergetic effects of EN, such as immune modulation or protection of the intestinal mucos‐ al barrier, seem to be of greater value in the critically ill than the mere energetic supply. The issue of the better enteral access (gastric vs. post-pyloric route) is not yet settled. However, available evidence does not support the routine insertion of post-pyloric tubes

Aside from the potential problems associated with receiving in adequate or excessive nutrition or medication therapy, additional injury to the patient may result from using the gut that is at risk for bacterial or candidal translocation. Therefore, enteral nutrition should be started only

However, nutritional support is not without adverse effects and risks. Early EN may be associated with high gastric residuals, bacterial colonization of the stomach, and increased risk of aspiration pneumonia. PN has been associated with gut mucosal atrophy, overfeeding,

as long as the gastric route is effective [104, 105, 106].

if the potential benefits outweigh the risks [107, 108].

nutrition! [102].

142 Topics in Paraplegia

The rate of early products' infusion is shown in the Table 4. Moreover, Table 5 depicts most used enteral products according to categories and their characteristics.

**Categories Products Characteristics** Novasource Forte (Novartis) Nutrison Energy (Nutricia) Nutridrink (Nutricia)

The goal of rehabilitation is to return through a gradual transition from the feeding tube back in swallowing if possible. The steps for neurocognitive and neuromuscular patients are based

The initial (preparatory) phase focuses on physiologic readiness for oral nutrition and incorporates medical and nutrition stability (normal swallowing function and nutrition values in normal range), and includes implementation of intermittent tube feeding, and swallowing assessment. The second (weaning) phase is described as a graduated increase in oral feeding, with corresponding decreases in tube feeding. In a patient able to consume more than 75% of his nutrition requirements consistently by mouth for 3 days, all tube feedings are discontinued. Subjects during weaning phase are being continuously evaluated for specific clinical param‐ eters including weight, hydration, and swallowing ability, focusing on respiratory complica‐

1 Rehabilitation Center "Aghios Loukas o Iatros", Trikala Thessaly, Greece

ting. http://emedicine.medscape.com/article/318180-overview

2 University of Athens, 1st Department of Orthopaedics, General University Hospital Attikon,

[1] Dawodu TS, Scott DD, Chase M. Nutritional management in the rehabilitation set‐

Perative (Abbott) 1, 31 kcal/ml

Malnutrition in Paraplegia http://dx.doi.org/10.5772/58382 145

Fresubin HP Energy (Fresenius) 1, 5 kcal/ml Intestamin (Fresenius) 0.5 kcal/ml) Infatrini (Nutricia 1 kcal/ml

**Hyperprotein**

tions [111, 112].

**Author details**

Athens, Greece

**References**

Yannis Dionyssiotis1,2\*

**Table 5.** Most used enteral solution products per company

in a clinical algorithm proposed by Buchholz [111].


**Table 4.** Starting enteral nutrition rate



**Table 5.** Most used enteral solution products per company

The goal of rehabilitation is to return through a gradual transition from the feeding tube back in swallowing if possible. The steps for neurocognitive and neuromuscular patients are based in a clinical algorithm proposed by Buchholz [111].

The initial (preparatory) phase focuses on physiologic readiness for oral nutrition and incorporates medical and nutrition stability (normal swallowing function and nutrition values in normal range), and includes implementation of intermittent tube feeding, and swallowing assessment. The second (weaning) phase is described as a graduated increase in oral feeding, with corresponding decreases in tube feeding. In a patient able to consume more than 75% of his nutrition requirements consistently by mouth for 3 days, all tube feedings are discontinued. Subjects during weaning phase are being continuously evaluated for specific clinical param‐ eters including weight, hydration, and swallowing ability, focusing on respiratory complica‐ tions [111, 112].

#### **Author details**

The rate of early products' infusion is shown in the Table 4. Moreover, Table 5 depicts most

**1** 30ml/h 10 max 500ml **2** 40ml/h 10 max 1000ml **3** 60ml/h 20 max 1500ml

**<sup>4</sup>** 90ml/h <sup>30</sup> max

**<sup>5</sup>** 100ml/h <sup>30</sup> max

**Categories Products Characteristics**

Jevity FOS (Abbott) 1 kcal/ml Fresubin Energy Fibre (Fresenius) 1, 5 kcal/ml Fresubin Original Fibre (Fresenius) 1 kcal/ml Novasource Forte (Novartis) 1, 5 kcal/ml Novasource Gl Control (Novartis) 1, 1 kcal/ml Cubison (Nutricia) 1 kcal/ml

Stresson Multi Fibre (Nutricia) 1 kcal/ml

Fresubin Energy (Fresenius) 1, 5 kcal/ml

Osmolite HN (Abbott)

Pediasure (Abbott) Frebini (Fresenius) Fresubin Original (Fresenius) Isosource Standard (Novartis) Nutrison Standard (Nutricia) Nutrini Standard (Nutricia) Tetrini Standard (Nutricia)

Nutrison Multifibre (Nutricia)

Ensure Plus (Abbott)

Fresubin HP Energy (Fresenius)

**per minute (20 drops=1ml)**

**Total Volume**

2000ml

2000ml

1 kcal/ml

used enteral products according to categories and their characteristics.

**Day Rate Drops**

**Table 4.** Starting enteral nutrition rate

144 Topics in Paraplegia

**Isotonic**

**Enriched with fibers**

**Hypercaloric**

Yannis Dionyssiotis1,2\*

1 Rehabilitation Center "Aghios Loukas o Iatros", Trikala Thessaly, Greece

2 University of Athens, 1st Department of Orthopaedics, General University Hospital Attikon, Athens, Greece

#### **References**

[1] Dawodu TS, Scott DD, Chase M. Nutritional management in the rehabilitation set‐ ting. http://emedicine.medscape.com/article/318180-overview

[2] Leistra E, Neelemaat F, Evers AM, van Zandvoort MH, Weijs PJ, van Bokhorst-de van der Schueren MA, Visser M, et al. Prevalence of undernutrition in Dutch hospital outpatients. Eur J Intern Med 2009;20(5):509-13.

[15] Williams RR, Fuenning CR. Circulatory indirect calorimetry in the critically ill. JPEN

Malnutrition in Paraplegia http://dx.doi.org/10.5772/58382 147

[16] Long CL, Schaffel N, Geiger JW, Schiller WR, Blakemore WS. Metabolic response to injury and illness: estimation of energy and protein needs from indirect calorimetry

[17] Mifflin MD, St Jeor ST, Hill LA, et al. A new predictive equation for resting energy

[18] Harris JA, Benedict FG. A Biometric Study of Human Basal Metabolism. Proc Natl

[19] Cerra FB, Benitez MR, Blackburn GL, Irwin RS, Jeejeebhoy K, Katz DP, et al. Applied nutrition in ICU patients. A consensus statement of the American College of Chest

[20] Faisy C, Guerot E, Diehl JL, Labrousse J, Fagon JY. Assessment of resting energy ex‐ penditure in mechanically ventilated patients. Am J Clin Nutr 2003;78(2):241-9. [21] Ireton-Jones CS, Turner WW, Liepa GU, Baxter CR. Equations for estimation of ener‐ gy expenditures in patients with burns with special reference to ventilator status. J

[22] Ireton-Jones CS, Turner WW. Actual or ideal body weight: which should be used to

[23] Frankenfield DC, Coleman A, Alam S, Cooney RN. Analysis of estimation methods for resting metabolic rate in critically ill adults. JPEN J Parenter Enteral Nutr

[24] Frankenfield DC. Validation of an equation for resting metabolic rate in older obese,

[25] Frankenfield DC, Ashcraft CM, Galvan DA. Longitudinal prediction of metabolic rate in critically ill patients. JPEN J Parenter Enteral Nutr 2012;36(6):700-12.

[26] Hamwi GL. Therapy: changing dietary concepts. In: Danowski TS, ed. Diabetes Mel‐ litus: Diagnosis and Treatment. New York, NY: American Diabetes Association; 1964.

[27] Frankenfield DC, Hise M, Malone A, Russell M, Gradwell E, Compher C.Prediction of resting metabolic rate in critically ill adult patients: results of a systematic review

[28] Campbell CG, Zander E, Thorland W. Predicted vs. measured energy expenditure in

[29] Kearns PJ, Thompson JD, Werner PC, Pipp TL, Wilmot CB. Nutritional and metabol‐ ic response to acute spinal-cord injury. JPEN J Parenter Enteral Nutr 1992;16(1):11-5.

[30] Jeejeebhoy KN. Total parenteral nutrition at home. Can J Surg 1976;19(6):477-8.

critically ill, underweight patients. Nutr Clin Pract 2005;20(2):276-80.

predict energy expenditure? J Am Diet Assoc 1991;91(2):193-5.

critically ill patients. JPEN J Parenter Enteral Nutr 2011;35:264-9.

of the evidence. J Am Diet Assoc 2007;107(9):1552-61.

and nitrogen balance. JPEN J Parenter Enteral Nutr 1979;3(6):452-6.

expenditure in healthy individuals. Am J Clin Nutr 1990;51(2):241-7.

J Parenter Enteral Nutr 1991;15(5):509-12.

Acad Sci USA 1918;4(12):370-3.

Physicians. Chest 1997;111(3):769-78.

Burn Care Rehab 1992;13(3):330-3.

2009;33(1):27-36.


[15] Williams RR, Fuenning CR. Circulatory indirect calorimetry in the critically ill. JPEN J Parenter Enteral Nutr 1991;15(5):509-12.

[2] Leistra E, Neelemaat F, Evers AM, van Zandvoort MH, Weijs PJ, van Bokhorst-de van der Schueren MA, Visser M, et al. Prevalence of undernutrition in Dutch hospital

[3] Harris D, Haboubi N. Malnutrition screening in the elderly population. J R Soc Med

[4] Stratton RJ, Green CJ, Elia M. Disease Related Malnutrition: an Evidence Based Ap‐

[5] Anson CA, Shepherd C. Incidence of secondary complications in spinal cord injury.

[6] Chen YM, Ho SC, Lam SS, Chan SS. Validity of body mass index and waist circum‐ ference in the classification of obesity as compared to percent body fat in Chinese

[7] Liang H, Chen D, Wang Y, Rimmer JH, Braunschweig CL. Different risk factor pat‐ terns for metabolic syndrome in men with spinal cord injury compared with ablebodied men despite similar prevalence rates. Arch Phys Med Rehabil 2007;88(9):

[8] Dufoo M Jr., Oseguera AC, Dufoo-Olvera M, Lopez OG, Palacios JL, Trejo AA, Tole‐ do GC, et al. Metabolic changes and nutritional status in the spinal cord injured pa‐ tient ASIA A. Evaluation and monitoring with routine laboratories, a feasible option.

[9] Rodriguez D. Nutritional Assessment and Management in spinal cord injury pa‐ tients. In Charles Tator and Edward Benzel (Eds). Contemporary Management of Spinal Cord Injury: From Impact to Rehabilitation.), 2nd edition, Publisher: Thieme /

[10] Dionyssiotis Y. Body Composition in Disabilities of Central Nervous System. In: El Maghraoui, Editor. Dual Energy X-Ray Absorptiometry, Rijeka: InTech; 2012.p 75-94.

[12] Peiffer SC, Blust P, Leyson JF. Nutritional assessment of the spinal cord injured pa‐

[13] McClave SA, Martindale RG, Vanek VW, et al. Guidelines for the provision and as‐ sessment of nutrition support therapy in the adult critically ill patient: Society of Critical Care Medicine (SCCM) and American Society for Parenteral and Enteral Nu‐

[14] Pinheiro Volp AC, Esteves de Oliveira FC, Duarte Moreira Alves R, Esteves EA, Bres‐ san J. Energy expenditure: components and evaluation methods. Nutr Hosp

[11] Shetty P. Malnutrition and Under nutrition. Medicine.2003;31(4):18-22.

trition (A.S.P.E.N.). JPEN J Parenter Enteral Nutr 2009;33(3):277-316.

outpatients. Eur J Intern Med 2009;20(5):509-13.

proach to Treatment. Oxford: CABI, 2003

middle-aged women. Int J Obes (Lond) 2006;30(6):918-25.

Int J Rehabil Res 1996;19(1):55-66.

Acta Ortop Mex 2007;21(6):313-7.

tient. J Am Diet Assoc 1981;78(5):501-5.

2005;98(9):411-4.

146 Topics in Paraplegia

1198-204.

AANS; 2000.

2011;26(3):430-40.


[31] Cerra FB, Shronts EP, Raup S, Konstantinides N. Enteral nutrition in hypermetabolic surgical patients. Crit Care Med 1989;17(7):619-22.

[45] Ingenbleek Y, Van Den Schrieck HG, De Nayer P, De Visscher M. Albumin, transfer‐ rin and the thyroxinebinding prealbumin/retinol-binding protein (TBPARBP) com‐

Malnutrition in Paraplegia http://dx.doi.org/10.5772/58382 149

[46] Devoto G, Gallo F, Marchello C, Racchi O, Garbarini R, Bonassi S, et al. Prealbumin serum concentrations as a useful tool in the assessment of malnutrition in hospital‐

[47] Mears E. Linking serum prealbumin measurements to managing a malnutrition clini‐

[48] Robinson MK, Trujillo EB, Mogensen KM, Rounds J, McManus K, Jacobs DO. Im‐ proving nutritional screening of hospitalized patients: the role of prealbumin. JPEN J

[49] Frankenfield D. Energy expenditure and protein requirements after traumatic injury.

[50] Hertroijs D, Wijnen C, Leistra E, Visser M, van der Heijden E, Kruizenga H. Rehabili‐ tation patients: undernourished and obese? J Rehabil Med 2012;44(8):696-701.

[51] [Set Performance Indicator rehabilitation centers.] Commissie Prestatie-indicatoren, Revalidatie Nederland en Nederlands Vereniging van Revalidatieartsen 2011 (in

[52] Kruizenga HM, Seidell JC, de Vet HCW, Wierdsma NJ, van Bokhorst-de van der Schueren. Development and validation of a hospital screening tool for malnutrition: the short nutritional assessment questionnaire (SNAQ). Clin Nutr 2005; 24(1):75–82.

[53] Stratton RJ, Hackston A, Longmore D, Dixon R, Price S, Stroud M. Malnutrition in hospital outpatients and inpatients: prevalence concurrent validity and ease of use of the 'Malnutrition Universal Screening Tool' ('MUST') for adults. Br J Nutr 2004;

[54] Kruizenga HM, de Vet HC, Van Marissing CM, Stassen EE, Strijk JE, Van Bokhorstde Van der Schueren MA, et al. The SNAQ(RC), an easy traffic light system as a first step in the recognition of undernutrition in residential care. J Nutr Health Aging

[55] National Collaborating Centre for Acute Care (UK). Nutrition Support for Adults: Oral Nutrition Support, Enteral Tube Feeding and Parenteral Nutrition. London: Na‐

[56] Kolpek JH, Ott LG, Record KE, Rapp RP, Dempsey R, Tibbs P, Young B. Comparison of urinary urea nitrogen excretion and measured energy expenditure in spinal cord injury and nonsteroid-treated severe head trauma patients. JPEN J Parenter Enteral

tional Collaborating Centre for Acute Care (UK); 2006 Feb.

plex in assessment of malnutrition. Clin Chim Acta 1975;63(1):61-7.

ized patients. Clin Chem 2006;52(12):2281-5.

Parenter Enteral Nutr 2003;27(6):389-95;

Nutr Clin Pract 2006;21(5):430-7.

Dutch).

92(5): 799–808.

2010;14(2):83-9.

Nutr 1989 ;13(3):277-80.

cal pathway. J Clin Ligand Assay 1999;22:296-303.


[45] Ingenbleek Y, Van Den Schrieck HG, De Nayer P, De Visscher M. Albumin, transfer‐ rin and the thyroxinebinding prealbumin/retinol-binding protein (TBPARBP) com‐ plex in assessment of malnutrition. Clin Chim Acta 1975;63(1):61-7.

[31] Cerra FB, Shronts EP, Raup S, Konstantinides N. Enteral nutrition in hypermetabolic

[32] Owen OE, Kavle E, Owen RS, et al. A reappraisal of caloric requirements in healthy

[33] Jeejeebhoy KN, Baker JP, Wolman SL, Wesson DE, Langer B, Harrison JE, et al. Criti‐ cal evaluation of the role of clinical assessment and body composition studies in pa‐ tients with malnutrition and after total parenteral nutrition. Am J Clin Nutr 1982 ;

[34] Klein JD, Hey LA, Yu CS, Klein BB, Coufal FJ, Young EP, et al. Perioperative nutri‐ tion and postoperative complications in patients undergoing spinal surgery. Spine

[35] Alpers DH, Klein S. Approach to the patient requiring nutritional supplementation. In Yamada T, ed. Textbook of Gastroenterology, 4th edn. Baltimore: Lippincott Wil‐

[36] Dionyssiotis Y. Malnutrition in spinal cord injury: more than nutritional deficiency. J

[37] Dionyssiotis Υ, Petropoulou Κ, Rapidi CA, Papagelopoulos PJ, Papaioannou N, Gal‐ anos A, Papadaki P, and Lyritis GP. Body Composition in Paraplegic Men. Journal of

[38] Gupta N, White KT, Sandford PR. Body mass index in spinal cord injury – a retro‐

[39] McDonald CM, Abresch-Meyer AL, Nelson MD, Widman LM. Body mass index and body composition measures by dual x-ray absorptiometry in patients aged 10 to 21

[40] Jones LM, Legge M, Goulding A Healthy body mass index values often underesti‐ mate body fat in men with spinal cord injury. Arch Phys Med Rehab 2003;84(7):

[41] Buchholz AC, Bugaresti JM. A review of body mass index and waist circumference as markers of obesity and coronary heart disease risk in persons with chronic spinal

[42] Laughton GE, Buchholz AC, Martin Ginis KA Lowering body mass index cutoffs bet‐ ter identifies obese persons with spinal cord injury. Spinal Cord 2009;47(10):757-62.

[43] Formica CA, Cosman F, Nieves J, Herbert J, Lindsay R. Reduced bone mass and fatfree mass in women with multiple sclerosis: effects of ambulatory status and gluco‐

[44] Charney P. Nutrition assessment in the 1990s: where are we now? Nutr Clin Pract.

years with spinal cord injury. J Spinal Cord Med. 2007;30:S97-104.

surgical patients. Crit Care Med 1989;17(7):619-22.

women. Am J Clin Nutr 1986;44(1):1-19.

(Phila Pa 1976). 1996;21(22):2676-82.

35(5 Suppl):1117-27.

148 Topics in Paraplegia

liams & Wilkins, 2003.

1068-71

1995;10(4):131-9.

Clin Med Res 2012;4(4):227-36.

Clinical Densitometry 2008;11(3):437-43.

spective study. Spinal Cord. 2006;44(2):92-4.

cord injury. Spinal Cord. 2005;43(9):513-8.

corticoid Use. Calcif Tissue Int 1997;61(2):129-33.


[57] Claus-Walker J, Halstead LS. Metabolic and endocrine changes in spinal cord injury: IV. Compounded neurologic dysfunctions. Arch Phys Med Rehabil 1982;63(12):632-8.

[73] Shaw JH, Wildbore M, Wolfe RR. Whole body protein kinetics in severely septic pa‐ tients: the response to glucose infusion and total parenteral nutrition. Ann Surg

Malnutrition in Paraplegia http://dx.doi.org/10.5772/58382 151

[74] Streat SJ, Beddoe AH, Hill GL. Aggressive nutritional support does not prevent pro‐ tein loss despite fat gain in septic intensive care patients. J Trauma 1987 ;27(3): 262-6.

[75] Monroe MB, Tataranni PA, Pratley R, Manore MM, Skinner JS, Ravussin E. Lower daily energy expenditures as measured by a respiratory chamber in subjects with spinal cord injury compared with control subjects. American Journal of Clinical Nu‐

[76] Perkash A, Brown M. Anaemia in patients with traumatic spinal cord injury. Paraple‐

[77] Blissitt PA. Nutrition in acute spinal cord injury. Crit Care Nurs Clin North Am

[78] Braunschweig C, Levy P. Sheean P, Wang X. Enteral compared to parenteral nutri‐ tion: a meta analysis American Journal of Clinical Nutrition 2001;74(4):534-42.

[79] Yin L, McLennan M, Bellou TF. Overweight in children with intellectual disabilities: No Simple Matter. ICAN: Infant, Child, & Adolescent Nutrition April 2013 5: 92-6. [80] Bauman WA, Zhong YG, Schwartz E. Vitamin D deficiency in veterans with chronic

[81] Dionyssiotis Y. Bone loss and fractures in multiple sclerosis: focus on epidemiologic

[82] Maklebust J, Magnan MA. Risk factors associated with having a pressure ulcer: a sec‐

[83] Fishburn MJ, Marino RJ, Ditunno JF Jr. Atelectasis and pneumonia in acute spinal

[84] Endersbe LA. Nutrition Support in Neurologic Impairment. In: Shronts, Eva P, edi‐ tors. Nutrition support dietetics. Maryland, Aspen: Silver Spring, p.107-18, 1989. [85] Jacksic T, Blakburn GL. Nutrition and CNS disease, the unconscious patient. In: Jee‐ jeebhoy KN, editor. Current therapy in nutrition. Toronto, Philadelphia: B C Decker

[86] Minard G, Kudsk K A. Is early feeding beneficial? How early is early? New horizons

[87] Nyswonger GD, Helmchen RH. Early enteral nutrition and length of stay in stroke

ondary data analysis. Adv Wound Care 1994;7(6):25, 27-8, 31-4 passim.

spinal cord injury Metabolism 1995; 44(12):1612–6.

and physiopathological features. Int J Gen Med 2011;4:505-9.

cord injury. Arch Phys Med Rehabil 1990;71(3):197-200.

1987;205(3):288-94.

trition 1998; 68(6):1223-7.

gia 1982;20(4):235-6.

1990;2(3):375-84.

Inc., p.269-78, 1988.

(Baltimore, Md.), 2(2), p. 156-63, 1994.

patients. J Neurosci Nurs 1992; 24(4):220-3.


[73] Shaw JH, Wildbore M, Wolfe RR. Whole body protein kinetics in severely septic pa‐ tients: the response to glucose infusion and total parenteral nutrition. Ann Surg 1987;205(3):288-94.

[57] Claus-Walker J, Halstead LS. Metabolic and endocrine changes in spinal cord injury: IV. Compounded neurologic dysfunctions. Arch Phys Med Rehabil 1982;63(12):632-8.

[58] Wilmore DW. Catabolic illness: strategies for enhancing recovery. N Engl J Med

[59] Burnham EL, Moss M, Ziegler TR. Myopathies in critical illness: characterization and

[60] Bongers T, Griffiths RD, McArdle A. Exogenous glutamine: the clinical evidence. Crit

[61] Cree MG, Wolfe RR. Postburn trauma insulin resistance and fat metabolism. Am J

[62] Thibault-Halman G, Casha S, Singer S, Christie S. Acute management of nutritional

[63] Robertson CS, Grossman RG. Protection against spinal cord ischemia with insulin-in‐

[64] Burr RG, Clift-Peace L, Nuseibeh I. Haemoglobin and albumin as predictors of length of stay of spinal injured patients in a rehabilitation centre. Paraplegia

[65] Gottschlich MM, Matarese LE, Shronts EP. Nutrition Support Dietetics Core Curricu‐

[66] Cooper IS, Hoen TI. Metabolic disorders in paraplegics. Neurology 1952;2(4):332-40.

[67] Whedon GD, Dietrick JE, Shorr E. Modification of the effects of immobilization upon metabolic and physiologic functions of normal men by the use of an oscillating bed.

[68] Eleazer GP, Bird L, Egbert J, Ryan C, Wei M, Guest K. Appropriate protocol for zinc

[69] ter Riet G, Kessels AG, Knipschild PG. Randomized clinical trial of ascorbic acid in

[70] Peruzzi WT, Shapiro BA, Meyer PR Jr, Krumlovsky F, Seo BW. Hyponatremia in

[71] De Jonghe B, Appere-De-Vechi C, Fournier M, Tran B, Merrer J, Melchior JC, et al. A prospective survey of nutritional support practices in intensive care unit patients:

[72] Nardo P, Dupertuis YM, Jetzer J, Kossovsky MP, Darmon P, Pichard C. Clinical rele‐ vance of parenteral nutrition prescription and administration in 200 hospitalized pa‐

therapy in long term care facilities. J Nutr Elder 1995;14(4):31-8.

acute spinal cord injury. Crit Care Med 1994;22(2):252-8.

tients: a quality control study. Clin Nutr 2008;27(6):858-64.

the treatment of pressure ulcers. J Clin Epidemiol 1995;48(12):1453-60.

what is prescribed? What is delivered? Crit Care Med 2001;29(1):8-12.

demands after spinal cord injury. J Neurotrauma 2011;28(8):1497-507.

1991;325(10):695-702.

150 Topics in Paraplegia

1993;31(7):473-8.

Am J Med 1949;6(6):684-711.

nutritional aspects. J Nutr 2005;135(7):1818S-23S.

Care Med 2007;35(9 Suppl):S545-52.

Physiol Endocrinol Metab 2008;294(1):E1-9.

duced hypoglycaemia. J Neurosurg 1987;67(5):739-44.

lum. 2 ed. Silver Springs, MD: A.S.P.E.N., 1993.


[88] Kirby DF, Clifton GL, Turner H, Marion DW, Barrett J, Gruemer HD. Early enteral nutrition after brain injury by percutaneous endoscopic gastrojejunostomy. JPEN J Parenter Enteral Nutr 1991;15(3):298-302.

[102] Simpson F, Doig GS. Parenteral vs. enteral nutrition in the critically ill patient: a meta-analysis of trials using the intention to treat principle. Intensive Care Med

Malnutrition in Paraplegia http://dx.doi.org/10.5772/58382 153

[103] Kudsk KA, Croce MA, Fabian TC, Minard G, Tolley EA, Poret HA, et al. Enteral ver‐ sus parenteral feeding. Effects on septic morbidity after blunt and penetrating ab‐

[104] Heyland DK, Konopad E, Alberda C, Keefe L, et al. How well do critically ill patients tolerate early, intragastric enteral feeding? Results of a prospective, multicenter trial.

[105] Rello J, Quintana E, Ausina V, Castella J, Luquin M, Net A, et al. Incidence, etiology, and outcome of nosocomial pneumonia in mechanically ventilated patients. Chest

[106] Heyland DK, Macdonald S, Keefe L, Drover JW. Total parenteral nutrition in the crit‐

[107] Baumgartner TG, Cerda JJ, Somogyi L, Baumgartner SL. Enteral Nutrition in Clinical

[108] Singer P, Berger MM, Van den Berghe G, Biolo G, Calder P, Forbes A, Griffiths R, Kreyman G, Leverve X, Pichard C, ESPEN. ESPEN Guidelines on Parenteral Nutri‐

[109] Martindale RG, McClave SA, Vanek VW, McCarthy M, Roberts P, Taylor B, et al. American College of Critical Care Medicine; A.S.P.E.N. Board of Directors. Guide‐ lines for the provision and assessment of nutrition support therapy in the adult criti‐ cally ill patient: Society of Critical Care Medicine and American Society for Parenteral and Enteral Nutrition: Executive Summary. Crit Care Med 2009;37(5):

[110] Vincent JL, Preiser JC. When should we add parenteral to enteral nutrition? Lancet

[111] Buchholz AC. Weaning patients with dysphagia from tube feeding to oral nutrition:

[112] Crary MA, Groher ME. Reinstituting oral feeding in tube-fed adult patients with dys‐

a proposed algorithm. Can J Diet Pract Res 1998;59(4):208–14.

dominal trauma. Ann Surg 1992;215(5):503-11; discussion 511-3.

ically ill patient: a meta analysis. JAMA 1998; 280(23):2013-9.

2005;31(1):12-23.

1991;100(2):439-44.

1757-61.

2013;381(9864):354-5.

Nutr Clin Pract 1999;14(1):23-8.

Practice Croatian Med J 1999;40(4):515-27.

phagia. Nutr Clin Pract 2006;21(6):576-86.

tion: intensive care. Clin Nutr 2009;28(4):387-400.


[102] Simpson F, Doig GS. Parenteral vs. enteral nutrition in the critically ill patient: a meta-analysis of trials using the intention to treat principle. Intensive Care Med 2005;31(1):12-23.

[88] Kirby DF, Clifton GL, Turner H, Marion DW, Barrett J, Gruemer HD. Early enteral nutrition after brain injury by percutaneous endoscopic gastrojejunostomy. JPEN J

[89] Grahm TW, Zadrozny DB, Harrington T: The benefits of early jejunal hyperalimenta‐

[90] Magnuson B, Hatton J, Zweng TN, Young B. Pentobarbital coma in neurosurgical pa‐

[91] O'Keefe SJ. A guide to enteral access procedures and enteral nutrition. Nat Rev Gas‐

[92] Zaloga GP. The myth of the gastric residual volume. Crit Care Med 2005;33(2):449-50. [93] Park RH, Allison MC, Lang J, Spence E, Morris AJ, Danesh BJ, et al.Randomised comparison of percutaneous endoscopic gastrostomy and nasogastric tube feeding in

[94] Wicks C, Gimson A, Vlavianos P, Lombard M, Panos M, Macmathuna P, et al. As‐ sessment of the percutaneous endoscopic gastrostomy feeding tube as part of an inte‐

[95] Allison MC, Morris AJ, Park RH, Mills PR. Percutaneous endoscopic gastrostomy tube feeding may improve outcome of late rehabilitation following stroke. J R Soc

[96] Larson DE, Burton DD, Schroeder KW, DiMagno EP. Percutaneous endoscopic gas‐

[97] Miller RE, Castlemain B, Lacqua FJ, Kotler DP. Percutaneous endoscopic gastrosto‐ my. Results in 316 patients and review of literature. Surg Endosc 1989;3(4):186-90. [98] Burtch GD, Shatney CH. Feeding gastrostomy. Assistant or assassin? Am Surg

[99] Fay DE, Poplausky M, Gruber M, Lance P. Long-term enteral feeding: a retrospective comparison of delivery via percutaneous endoscopic gastrostomy and nasoenteric

[100] Marik PE, Zaloga GP. Early enteral nutrition in acutely ill patients: a systematic re‐ view. Crit Care Med 2001;29(12):2264-70. Erratum in: Crit Care Med 2002;30(3):725.

[101] Heyland DK, Dhaliwal R, Drover JW, Gramlich L, Dodek P; Canadian Critical Care Clinical Practice Guidelines Committee. Canadian clinical practice guidelines for nu‐ trition support in mechanically ventilated, critically ill adult patients. JPEN J Parenter

patients with persisting neurological dysphagia. BMJ 1992;30:(304):1406-9.

tion in the head-injured patient. Neurosurgery 1989; 25(5):729-35.

tients: nutrition considerations. Nutr Clin Pract 1994;9(4):146-50.

grated approach to enteral feeding. Gut 1992;33(5):613-6.

trostomy. Gastroenterology, 1987; 93(1), 48-52.

tubes. Am J Gastroenterol 1991;86(11):1604-9.

Enteral Nutr 2003;27(5):355-73.

Parenter Enteral Nutr 1991;15(3):298-302.

152 Topics in Paraplegia

troenterol Hepatol 2009;6(4):207-15.

Med 1992;85(3):147-9.

1985;51(4):204-7.


**Chapter 7**

**Body Composition in Paraplegia**

Additional information is available at the end of the chapter

of aging, and muscle-wasting diseases [8, 9].

spinal cord injury (SCI) [14].

ambulatory subjects with paraplegia.

Paraplegia leads to immobilisation associated with profound changes in body composition. The potential risks involved with these changes i.e. loss of lean tissue mass (LM) and bone mineral density (BMD) vs. gain in fat mass (FM) in body composition have implications for the health of the disabled individuals [1]. Body fat has been identified as a significant predictor of mortality in humans making body composition measurement to quantify nutritional and health status an important issue for human health [2-4]. Moreover, some disorders such as carbohydrate intolerance, insulin resistance, lipid abnormalities, and heart disease occur prematurely and at a higher prevalence in disabled populations may be related to adverse changes in body composition that result from immobilization and skeletal muscle denervation [5]. To standardize or index physiological variables, such as resting metabolic rate and power fat free mass (FFM) is usually used [4]. Skeletal muscle represents 50% of the non fat component in the total body [6, 7] and exact quantification of the amount of skeletal muscle is important to assess nutritional status, disease risk, danger of illnesses, physical function, atrophic effects

A paraplegic subject could be wheelchair bound, may have an alternated walking gait pattern but may also be unable to walk at all [10, 11]. In addition to these differences and according to osteoporosis the role of factors which do not change, such as race or gender of patients has not been yet clarified, although there are few studies in women debating that bone mass in women with paraplegia is more affected than men [12, 13]. Similar findings of reduced muscle mass and increased intramuscular fat have been also published in individuals with incomplete

Therefore, the purpose of this chapter was to present the bone-mineral density, bone-mineral content, and bone-mineral-free lean and fat tissue mass alterations of ambulatory and non-

> © 2014 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Yannis Dionyssiotis

**1. Introduction**

http://dx.doi.org/10.5772/58539

#### **Chapter 7**

### **Body Composition in Paraplegia**

Yannis Dionyssiotis

Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/58539

#### **1. Introduction**

Paraplegia leads to immobilisation associated with profound changes in body composition. The potential risks involved with these changes i.e. loss of lean tissue mass (LM) and bone mineral density (BMD) vs. gain in fat mass (FM) in body composition have implications for the health of the disabled individuals [1]. Body fat has been identified as a significant predictor of mortality in humans making body composition measurement to quantify nutritional and health status an important issue for human health [2-4]. Moreover, some disorders such as carbohydrate intolerance, insulin resistance, lipid abnormalities, and heart disease occur prematurely and at a higher prevalence in disabled populations may be related to adverse changes in body composition that result from immobilization and skeletal muscle denervation [5]. To standardize or index physiological variables, such as resting metabolic rate and power fat free mass (FFM) is usually used [4]. Skeletal muscle represents 50% of the non fat component in the total body [6, 7] and exact quantification of the amount of skeletal muscle is important to assess nutritional status, disease risk, danger of illnesses, physical function, atrophic effects of aging, and muscle-wasting diseases [8, 9].

A paraplegic subject could be wheelchair bound, may have an alternated walking gait pattern but may also be unable to walk at all [10, 11]. In addition to these differences and according to osteoporosis the role of factors which do not change, such as race or gender of patients has not been yet clarified, although there are few studies in women debating that bone mass in women with paraplegia is more affected than men [12, 13]. Similar findings of reduced muscle mass and increased intramuscular fat have been also published in individuals with incomplete spinal cord injury (SCI) [14].

Therefore, the purpose of this chapter was to present the bone-mineral density, bone-mineral content, and bone-mineral-free lean and fat tissue mass alterations of ambulatory and nonambulatory subjects with paraplegia.

© 2014 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

#### **2. Body composition measurements**

#### **2.1. Anthropometric and various techniques of body composition measurements**

Similar body mass indices were found between paraplegics and controls; although there were significant decreases in the lean muscle mass of the paraplegics (16% less). The analysis of body composition with dual-energy X-ray absorptiometry (DXA) has also revealed large increases in fat in people who do not appear to be obese, yet they carry large amounts of fat tissue and in the group of paraplegic subjects fat mass was 47% higher [15]. Furthermore, where authors performed a research in the usage of the body mass index (BMI) in anthropometric measure‐ ments, the conclusion was that BMI, widely used as an obesity measurement tool, is not capable of distinguishing the weight components among people so that the fat percentage is degraded in the population of paraplegic in comparison to the control group [16].

BMI of the male paraplegic group was slightly greater than that of the male tetraplegic group

with SCI and that observed in men in the US general population. Distribution of BMI by level of injury was similar with 37.5% and 40.5% of the male tetraplegic and male paraplegic groups, respectively, falling into the recommended BMI range. Approximately 50% in each male group were overweight by BMI, and 12.5% and 10.8%, respectively, were classified as obese. Overall, when compared with the general population-observed distribution by BMI, a greater propor‐ tion of men with SCI fell into the desirable BMI range and fewer fell into the obese category [26].

No differences were found in BMI between paraplegics in the acute phase of injury and controls, which is a finding in accordance with other studies reported in chronic paraplegic patients and controls, in which despite the same BMI the body composition and the distribu‐ tion of fat and fat free mass were alterated in patients with spinal cord damage, with the fat free mass being statistically significantly lower in paraplegic patients in total body composition and in the lower, but not the upper limbs. As far as the fat mass is concerned, it was statistically significantly higher (kilograms and %) in the total body composition in the upper and lower

These findings show that using the BMI does not contribute substantially in determining the body composition of paraplegics and lowers the percentage of fat in this population, finding that agrees with other studies and shows that the anthropometric measurement with BMI in paraplegics, underestimates fat in body composition when measurements are compared with

Changes in body composition in spinal cord injured subjects can be assessed with various techniques including isotope-labelled water [1] total body potassium counting (Lussier et al 1983; Spungen et al 1992) anthropometric measures [16] hydrodensitometry [28] dual photon absorptiometry (DPA) [29] and dual energy X-ray absorptiometry (DXA) [1]. However, some

The hydrodensitometric model was regarded as the "gold standard" for body composition assessment. This model partitions the body into two compartments of constant densities [fat

components [water, protein, protein, bone mineral (BM), and non-BM] are fixed [4]. Hydro‐ densitometry is clearly inappropriate for individuals who deviate from these fixed and/or assumed values (e.g., children, elderly, blacks, obese), and its application is, therefore,

Bioelectrical impedance analysis has been used to measure cerebral palsy subjects. However, the inclusion of weight in the BIA predictive equation may reduce its accuracy in determining change in lean body mass. The inability of BIA to accurately predict percentage body fat in the sample may be related to several factors. In the BIA method where the impedance of a geometrical system (i.e., the human body) is dependent on the length of the conductor (height) and its configuration, it is almost impossible to measure accurately height in subjects with CP because of their muscle contractures. An over-or underestimation of height by 2.5 cm can result in a l.0-L error in the estimation of TBW, producing a small error in the estimation of percentage

] and assumes that the relative amounts of the FFM

of these methods are not particularly suitable for use in the SCI population.

; p<0.01). Proportion of overweight or obese was comparable between men

Body Composition in Paraplegia http://dx.doi.org/10.5772/58539 157

(25.2 vs. 24.7 kg/ m2

limbs [27].

healthy subjects [1].

mass: 0.9007 g/cm3 and FFM: 1.100 g/cm3

somewhat limited [30, 31].

In a study which investigated a chronic paraplegic population the values of BMI did not present statistical significance in relation to the controls, which is a finding in line with the literature [17, 18, 19]. Moreover, the values of BMI in both paraplegics and controls were below values consider to signify obesity (BMI>27.8) [19, 20, 21]. This finding could be acceptable for the population of the controls, but raises questions regarding the paraplegics. It is known from literature that paraplegics are obese [22]. Nevertheless, there are studies which demonstrate the usefulness of BMI as an indicator of obesity, in body composition in people with spinal cord injury [23]. These studies, however, included in their sample both tetraplegics and middle-aged people unlike the Greek one which included relatively young individuals [19]. Whether the criteria of BMI may assess obesity in people with spinal cord injury the latest studies show the opposite [24].

Similarly to the healthy population values of BMI are positively correlated with obesity. This emerged from a study, conducted by whole body DXA Norland X-36, only when the findings of total fat in paraplegics were correlated with BMI. Employing whole body DXA Norland XR-36 it was found that the total fat mass was statistically significantly higher for any given BMI value in paraplegics compared with controls [19], finding that strongly supports the studies held by the whole body DXA Hologic QDR-2000 method [5, 25].

The studies illustrated statistically significantly higher total fat mass and fat percentages for any given unit of body mass index in paraplegics in comparison to controls. Increased fat per body mass index unit was found in a study of monozygotic twins, one with SCI compared with a non-SCI co-twin by the above authors also [25]. Adjustments in classifications of normal, overweight, obese, and morbid obesity by BMI are needed for persons with SCI [26].

In addition, by analysis between paraplegics with high and low neurological level injuries not statistically significant differences in BMI were highlighted. However, when data from the analysis undertaken in areas measured by the method of whole body DEXA were compared in the same patients there were differences between paraplegics with high and low neurolog‐ ical level of injury. This finding is new and reinforces those views on the inability of BMI usage in the analysis of body composition of paraplegics [19].

BMI of the male paraplegic group was slightly greater than that of the male tetraplegic group (25.2 vs. 24.7 kg/ m2 ; p<0.01). Proportion of overweight or obese was comparable between men with SCI and that observed in men in the US general population. Distribution of BMI by level of injury was similar with 37.5% and 40.5% of the male tetraplegic and male paraplegic groups, respectively, falling into the recommended BMI range. Approximately 50% in each male group were overweight by BMI, and 12.5% and 10.8%, respectively, were classified as obese. Overall, when compared with the general population-observed distribution by BMI, a greater propor‐ tion of men with SCI fell into the desirable BMI range and fewer fell into the obese category [26].

**2. Body composition measurements**

156 Topics in Paraplegia

studies show the opposite [24].

**2.1. Anthropometric and various techniques of body composition measurements**

in the population of paraplegic in comparison to the control group [16].

studies held by the whole body DXA Hologic QDR-2000 method [5, 25].

in the analysis of body composition of paraplegics [19].

Similar body mass indices were found between paraplegics and controls; although there were significant decreases in the lean muscle mass of the paraplegics (16% less). The analysis of body composition with dual-energy X-ray absorptiometry (DXA) has also revealed large increases in fat in people who do not appear to be obese, yet they carry large amounts of fat tissue and in the group of paraplegic subjects fat mass was 47% higher [15]. Furthermore, where authors performed a research in the usage of the body mass index (BMI) in anthropometric measure‐ ments, the conclusion was that BMI, widely used as an obesity measurement tool, is not capable of distinguishing the weight components among people so that the fat percentage is degraded

In a study which investigated a chronic paraplegic population the values of BMI did not present statistical significance in relation to the controls, which is a finding in line with the literature [17, 18, 19]. Moreover, the values of BMI in both paraplegics and controls were below values consider to signify obesity (BMI>27.8) [19, 20, 21]. This finding could be acceptable for the population of the controls, but raises questions regarding the paraplegics. It is known from literature that paraplegics are obese [22]. Nevertheless, there are studies which demonstrate the usefulness of BMI as an indicator of obesity, in body composition in people with spinal cord injury [23]. These studies, however, included in their sample both tetraplegics and middle-aged people unlike the Greek one which included relatively young individuals [19]. Whether the criteria of BMI may assess obesity in people with spinal cord injury the latest

Similarly to the healthy population values of BMI are positively correlated with obesity. This emerged from a study, conducted by whole body DXA Norland X-36, only when the findings of total fat in paraplegics were correlated with BMI. Employing whole body DXA Norland XR-36 it was found that the total fat mass was statistically significantly higher for any given BMI value in paraplegics compared with controls [19], finding that strongly supports the

The studies illustrated statistically significantly higher total fat mass and fat percentages for any given unit of body mass index in paraplegics in comparison to controls. Increased fat per body mass index unit was found in a study of monozygotic twins, one with SCI compared with a non-SCI co-twin by the above authors also [25]. Adjustments in classifications of normal,

In addition, by analysis between paraplegics with high and low neurological level injuries not statistically significant differences in BMI were highlighted. However, when data from the analysis undertaken in areas measured by the method of whole body DEXA were compared in the same patients there were differences between paraplegics with high and low neurolog‐ ical level of injury. This finding is new and reinforces those views on the inability of BMI usage

overweight, obese, and morbid obesity by BMI are needed for persons with SCI [26].

No differences were found in BMI between paraplegics in the acute phase of injury and controls, which is a finding in accordance with other studies reported in chronic paraplegic patients and controls, in which despite the same BMI the body composition and the distribu‐ tion of fat and fat free mass were alterated in patients with spinal cord damage, with the fat free mass being statistically significantly lower in paraplegic patients in total body composition and in the lower, but not the upper limbs. As far as the fat mass is concerned, it was statistically significantly higher (kilograms and %) in the total body composition in the upper and lower limbs [27].

These findings show that using the BMI does not contribute substantially in determining the body composition of paraplegics and lowers the percentage of fat in this population, finding that agrees with other studies and shows that the anthropometric measurement with BMI in paraplegics, underestimates fat in body composition when measurements are compared with healthy subjects [1].

Changes in body composition in spinal cord injured subjects can be assessed with various techniques including isotope-labelled water [1] total body potassium counting (Lussier et al 1983; Spungen et al 1992) anthropometric measures [16] hydrodensitometry [28] dual photon absorptiometry (DPA) [29] and dual energy X-ray absorptiometry (DXA) [1]. However, some of these methods are not particularly suitable for use in the SCI population.

The hydrodensitometric model was regarded as the "gold standard" for body composition assessment. This model partitions the body into two compartments of constant densities [fat mass: 0.9007 g/cm3 and FFM: 1.100 g/cm3 ] and assumes that the relative amounts of the FFM components [water, protein, protein, bone mineral (BM), and non-BM] are fixed [4]. Hydro‐ densitometry is clearly inappropriate for individuals who deviate from these fixed and/or assumed values (e.g., children, elderly, blacks, obese), and its application is, therefore, somewhat limited [30, 31].

Bioelectrical impedance analysis has been used to measure cerebral palsy subjects. However, the inclusion of weight in the BIA predictive equation may reduce its accuracy in determining change in lean body mass. The inability of BIA to accurately predict percentage body fat in the sample may be related to several factors. In the BIA method where the impedance of a geometrical system (i.e., the human body) is dependent on the length of the conductor (height) and its configuration, it is almost impossible to measure accurately height in subjects with CP because of their muscle contractures. An over-or underestimation of height by 2.5 cm can result in a l.0-L error in the estimation of TBW, producing a small error in the estimation of percentage body fat (< 5%). The second major problem is body asymmetry which renders the assumption of a symmetrical configuration of the human body invalid in this case [20, 32].

Isotope dilution measures the water compartment of the whole body rather than a single area assumed to mimic the composition of the whole body. Thus, the use of a stable isotope to measure body composition is ideal for people with CP because it is non-invasive, does not require the subject to remain still for the measurement, and is independent of height and body symmetry. However, the prohibitive cost of the isotopes and the need for a mass spectrometry facility and highly trained technicians make this method impractical for routine clinical use [32].

To determine whether bioelectrical impedance analysis (BIA) and anthropometry can be used to determine body composition for clinical and research purposes in children with cerebral palsy 8 individuals (two female, mean age=10 years, mean gross motor function classifica‐ tion=4.6 [severe motor impairment]) recruited from an outpatient tertiary care setting under‐ went measurement of fat mass, fat-free mass, and percentage body fat using BIA, anthropometry (two and four skinfold equations), and dual-energy x-ray absorptiometry. Correlation were excellent for determination of fat-free mass for all methods (i.e., all were above 0.9) and moderate for determination of fat mass and percent body fat (range=0.4 to 0.8). Moreover, skinfolds were better predictors of percent body fat, while bioelectrical impedance was a better predictor for fat mass [33]. On the contrary another study investigated the pattern of body composition in 136 subjects with spastic quadriplegic cerebral palsy, 2 to 12 years of age, by anthropometric measures, or by anthropometric and total body water (TBW) measures (n=28), compared with 39 control subjects. Body composition and nutritional status indicators were significantly reduced. Calculation of body fat from two skinfolds correlated best with measures of fat mass from TBW [34].

Figure 1. Whole body and regional distribution of fat mass, lean mass, bone mineral content (BMC) and bone mineral density (BMD) from paraplegic subject thoracic 6 (left picture) using whole body DXA (Norland X-36, Fort Atkinson, Wisconsin, USA) and values of measured parameters. Modified and translated with permission from: Dionyssiotis Y. (2008a). Doctoral Dissertation, Laboratory for Research of the Musculoskeletal System,

Body Composition in Paraplegia http://dx.doi.org/10.5772/58539 159

**Figure 1.** Whole body and regional distribution of fat mass, lean mass, bone mineral content (BMC) and bone mineral density (BMD) from paraplegic subject thoracic 6 using whole body DXA (Norland X-36, Fort Atkinson, Wisconsin, USA) and values of measured parameters. Modified and translated with permission from Dionyssiotis Y, Doctoral Dis‐

DXA analyzes differently the dense pixels in body composition. Soft tissue pixels are analyzed for two materials: fat and fat-free tissue mass. Variations in the fat mass/fat free tissue mass composition of the soft tissue produce differences in the respective attenua‐ tion coefficients at both energy levels. The ratio at the two main energy peaks is automat‐ ically calculated of the X-ray attenuation providing separation of the soft tissue compartment into fat mass and fat-free tissue mass (lean mass) [40, 41]. A bone-contain‐ ing pixel is analyzed for "bone mass" (bone mineral content, BMC) and soft tissue as the two materials. Thus, the fat mass/fat free tissue mass of the soft tissue component of the

The important issue on this the investigation of distribution of bone mineral, fat and mass throughout the body. These changes induce the risk for diseases such as diabetes, coronary heart disease, dyslipidaimias and osteoporosis [22, 43, 44, 45]. There is a need to quantify the alterations in body composition to prevent these diseases and their complications. Studies also reported that bone density measurements at one site cannot usefully predict the bone density elsewhere [46] because different skeletal regions, even with similar quantities of trabecular or

In disabled conditions the accuracy of skeletal muscle measured by DXA may be compro‐ mised when muscle atrophy is present. A lower ratio of muscle to adipose-tissue-free mass indicates a lower proportion of muscle in the fat-free soft tissue mass. Cross-sectional area of skeletal muscle in the thighs after SCI is extensively reduced [48]. If this is the case

cortical bone, may respond variably in different physiopathological conditions [47].

sertation, Laboratory for Research of the Musculoskeletal System, University of Athens, 2008 [39].

University of Athens, Greece,

bone pixels cannot be measured, but only estimated [42].

Magnetic resonance imaging (MRI) provides remarkably accurate estimates of skeletal muscle in vivo [7]. MRI and also quantitative computed tomography (QCT) have been validated in studies of humancadavers in the assessment of regional skeletal muscle [35]. Although, these devices have disadvantages of high radiation exposure and are expensive.

#### **2.2. Dual-energy X-ray absorptiometry (DXA)**

Recently, dual-energy X-ray absorptiometry (DXA) has gained acceptance as a reference method for body composition analysis [36, 37]. Originally designed to determine bone density, DXA technology has subsequently been adopted for the assessment of whole body composi‐ tion and offers estimation rapidly, non-invasively and with minimal radiation exposure [4, 19]. Moreover, is well tolerated in subjects who would be unable to tolerate other body composition techniques, such as underwater weighing (hydro-densitometry). DXA software determines the bone mineral and soft tissue composition in different regions of the body being a three-compartment model that quantifies: (i) bone mineral density and content (BMD, BMC), (ii) fat mass (FM); and (iii) lean mass (LM), half of which is closely correlated with muscle mass and also yields regional as well as total body values [38] for example in the arms, legs, and trunk (figure 1).

body fat (< 5%). The second major problem is body asymmetry which renders the assumption

Isotope dilution measures the water compartment of the whole body rather than a single area assumed to mimic the composition of the whole body. Thus, the use of a stable isotope to measure body composition is ideal for people with CP because it is non-invasive, does not require the subject to remain still for the measurement, and is independent of height and body symmetry. However, the prohibitive cost of the isotopes and the need for a mass spectrometry facility and highly trained technicians make this method impractical for

To determine whether bioelectrical impedance analysis (BIA) and anthropometry can be used to determine body composition for clinical and research purposes in children with cerebral palsy 8 individuals (two female, mean age=10 years, mean gross motor function classifica‐ tion=4.6 [severe motor impairment]) recruited from an outpatient tertiary care setting under‐ went measurement of fat mass, fat-free mass, and percentage body fat using BIA, anthropometry (two and four skinfold equations), and dual-energy x-ray absorptiometry. Correlation were excellent for determination of fat-free mass for all methods (i.e., all were above 0.9) and moderate for determination of fat mass and percent body fat (range=0.4 to 0.8). Moreover, skinfolds were better predictors of percent body fat, while bioelectrical impedance was a better predictor for fat mass [33]. On the contrary another study investigated the pattern of body composition in 136 subjects with spastic quadriplegic cerebral palsy, 2 to 12 years of age, by anthropometric measures, or by anthropometric and total body water (TBW) measures (n=28), compared with 39 control subjects. Body composition and nutritional status indicators were significantly reduced. Calculation of body fat from two skinfolds correlated best with

Magnetic resonance imaging (MRI) provides remarkably accurate estimates of skeletal muscle in vivo [7]. MRI and also quantitative computed tomography (QCT) have been validated in studies of humancadavers in the assessment of regional skeletal muscle [35]. Although, these

Recently, dual-energy X-ray absorptiometry (DXA) has gained acceptance as a reference method for body composition analysis [36, 37]. Originally designed to determine bone density, DXA technology has subsequently been adopted for the assessment of whole body composi‐ tion and offers estimation rapidly, non-invasively and with minimal radiation exposure [4, 19]. Moreover, is well tolerated in subjects who would be unable to tolerate other body composition techniques, such as underwater weighing (hydro-densitometry). DXA software determines the bone mineral and soft tissue composition in different regions of the body being a three-compartment model that quantifies: (i) bone mineral density and content (BMD, BMC), (ii) fat mass (FM); and (iii) lean mass (LM), half of which is closely correlated with muscle mass and also yields regional as well as total body values [38] for example in the arms, legs, and

devices have disadvantages of high radiation exposure and are expensive.

of a symmetrical configuration of the human body invalid in this case [20, 32].

routine clinical use [32].

158 Topics in Paraplegia

measures of fat mass from TBW [34].

trunk (figure 1).

**2.2. Dual-energy X-ray absorptiometry (DXA)**

Figure 1. Whole body and regional distribution of fat mass, lean mass, bone mineral content (BMC) and bone mineral density (BMD) from paraplegic subject thoracic 6 (left picture) using whole body DXA (Norland X-36, Fort Atkinson, Wisconsin, USA) and values of measured parameters. Modified and translated with permission from: Dionyssiotis Y. (2008a). Doctoral Dissertation, Laboratory for Research of the Musculoskeletal System, University of Athens, Greece, **Figure 1.** Whole body and regional distribution of fat mass, lean mass, bone mineral content (BMC) and bone mineral density (BMD) from paraplegic subject thoracic 6 using whole body DXA (Norland X-36, Fort Atkinson, Wisconsin, USA) and values of measured parameters. Modified and translated with permission from Dionyssiotis Y, Doctoral Dis‐ sertation, Laboratory for Research of the Musculoskeletal System, University of Athens, 2008 [39].

 DXA analyzes differently the dense pixels in body composition. Soft tissue pixels are analyzed for two materials: fat and fat-free tissue mass. Variations in the fat mass/fat free tissue mass composition of the soft tissue produce differences in the respective attenua‐ tion coefficients at both energy levels. The ratio at the two main energy peaks is automat‐ ically calculated of the X-ray attenuation providing separation of the soft tissue compartment into fat mass and fat-free tissue mass (lean mass) [40, 41]. A bone-contain‐ ing pixel is analyzed for "bone mass" (bone mineral content, BMC) and soft tissue as the two materials. Thus, the fat mass/fat free tissue mass of the soft tissue component of the bone pixels cannot be measured, but only estimated [42].

The important issue on this the investigation of distribution of bone mineral, fat and mass throughout the body. These changes induce the risk for diseases such as diabetes, coronary heart disease, dyslipidaimias and osteoporosis [22, 43, 44, 45]. There is a need to quantify the alterations in body composition to prevent these diseases and their complications. Studies also reported that bone density measurements at one site cannot usefully predict the bone density elsewhere [46] because different skeletal regions, even with similar quantities of trabecular or cortical bone, may respond variably in different physiopathological conditions [47].

In disabled conditions the accuracy of skeletal muscle measured by DXA may be compro‐ mised when muscle atrophy is present. A lower ratio of muscle to adipose-tissue-free mass indicates a lower proportion of muscle in the fat-free soft tissue mass. Cross-sectional area of skeletal muscle in the thighs after SCI is extensively reduced [48]. If this is the case muscle mass would be overestimated by prediction models that assume that muscle represents all or a certain proportion of the fat-free soft tissue mass, i.e. in spinal cord injured subjects [7]. DXA technique has been used in assessment of SCI and appears to be tolerated well by this population [49, 50, 51]. Fort Atkinson, Wisconsin, USA) and values of measured parameters. Modified and translated with permission from: Dionyssiotis Y. (2008a). Doctoral Dissertation, Laboratory for Research of the Musculoskeletal System, University of Athens, Greece, 

Figure 1. Whole body and regional distribution of fat mass, lean mass, bone mineral content (BMC) and bone mineral density (BMD) from paraplegic subject thoracic 6 (left picture) using whole body DXA (Norland X-36,

> paraplegics 1 year post injury. With reliance on the upper limbs to provide movement for activities of daily living in the SCI population, this area could be subjected to greater sitespecific loading, and thus increasing osteogenesis, than in the corresponding able-bodied population. At the lumbar spine, the trabecular bone demineralization remains relatively low compared to the cortical bone demineralization of long bones [56]. Normal [52, 57] or even higher than normal [58] values of BMD in the lumbar spine have been reported a phenomenon is named "dissociated hip and spine demineralization" [54]. One reason for preservation of bone mass in the vertebral column is because of its continued weight-bearing function in paraplegics. In a cross-sectional study of 135 SCI men, BMD in the lumbar spine was found to be stable with an insignificant decline in the tetraplegic population at 1±5 years post injury in the 20–39-year age group, whereas in the 40-59-year age group and the 60+-year age group, bone mass in the lumbar spine remained unchanged or even increased with age [49]. However, several factors may affect the results of BMD measurement: lumbar spine arthrosis, bone callus, vertebral fracture, aortic calcification, osteosynthesis material, etc. Degenerative changes in the spine may be the most possible reason to give falsely higher values of BMD [56]. An interesting question is why we don't see osteoporotic vertebral fractures in SCI patients to the

Body Composition in Paraplegia http://dx.doi.org/10.5772/58539 161

extent it occurs in post-menopausal osteoporotic women or senile osteoporotic men?

explained in the paper of Dionyssiotis et al. [19].

0

and translated from Dionyssiotis Y [39].

0.2

0.4

0.6

mean value in grcm-2

0.8

1

1.2

1.4

Figure 3 depicts the analysis of bone mineral density (BMD) in high and low level paraple‐ gics and controls. A statistically significant reduction in total BMD (p<0.001) and lower limbs BMD in body composition compared to able-bodied males was observed. On the con‐ trary, upper limbs BMD was higher in low paraplegics and controls, an unexpected finding

BMD ANALYSIS

High paraplegics Low paraplegics Controls \* \* \* \*

\* p < 0,05 vs control # p < 0,05 vs high
