Focal Upper Limb Mononeuropathies in Patients with Diabetes Mellitus

*Tayir Alon and Vera Bril*

#### **Abstract**

In this chapter, we describe the prevalence, diagnostic methods, and treatment efficacy of compressive neuropathies of the median and the ulnar nerves in patients with diabetes mellitus (DM). Median neuropathy at the wrist is found in up to onethird of patients with DM, when demonstrated electrophysiologically, but is symptomatic as carpal tunnel syndrome (CTS) in a smaller proportion of these patients. It is clear that diabetes increases the risk of having clinical CTS. Diagnosis of CTS using nerve conduction studies is difficult in patients with DM and diabetic sensorimotor polyneuropathy (DSP) as median nerve conduction studies are affected predominantly by the diabetes state. We will discuss different electrodiagnostic and ultrasonography techniques for diagnosis and the outcomes of carpal tunnel release decompressive surgery in this special patient population. It is controversial whether DM is a risk factor for cubital tunnel syndrome or ulnar neuropathy at the elbow (UNE) or at the wrist (UNW). In this chapter, we will review the ultrasonographic and electrophysiological diagnostic techniques used in UNE and UNW and the efficacy of cubital tunnel release in DM patients.

**Keywords:** mononeuropathy, diabetes mellitus, carpal tunnel syndrome, nerve compression, diabetic sensorimotor polyneuropathy, median nerve, ulnar nerve, carpal tunnel syndrome, cubital tunnel syndrome

#### **1. What causes the increased vulnerability to entrapment neuropathies in patients with DM**

Entrapment neuropathies are more prevalent among patients with DM, and carpal tunnel syndrome (CTS) can guide a better understanding of the pathophysiology of entrapment neuropathies in this patient population. CTS is the most commonly studied entrapment syndrome and changes in the small arteries, such as vascular hypertrophy and intimal thickening, and noninflammatory fibroses of connective tissue are key pathologic features as discussed earlier in this book. In patients with DM, the reasons for the higher susceptibility to entrapment neuropathies are likely the combination of increased vulnerability of the nerves to compression arising from underlying diffuse DM-related nerve fiber injury and the presence of altered connective tissue structures within the carpal tunnel causing additional compression [1]. These two mechanisms are most likely relevant to all entrapment neuropathies in DM. Axonal, metabolic, and structural changes in DM that can

lead to higher susceptibility to external injury are well-known. Less information on altered connective tissue structure in areas of nerve compression is available in this patient population. Deger et al. found a statistically significant increase in neoangiogenesis in subsynovial connective tissue in DM CTS cases, correlating with greater expression of vascular endothelial growth factor (VEGF), in subsynovial connective tissue in DM than what is present in CTS in patients without DM [2, 3]. These findings are consistent with the findings of Tekin et al., showing DM CTS patients, when compared with non-DM CTS patients, have higher rates of synovial edema and vascular proliferation and increased vascular wall thickness [4]. Thus the increased neovascularization, arising from a proposed ischemia-reperfusion mechanism, and more apparent in patients with DM, impinges the tissue compartment space within the carpal tunnel. In their recently published review, Sharma and Jaggi summarize the current knowledge regarding the role of transforming growth factor (TGF-β), VEGF, and interleukins in the subsynovial connective tissue in CTS patients, with and without diabetes [5].

#### **2. Median compressive neuropathy at the wrist in patients with diabetes mellitus (DM)**

The high prevalence of DM among patients with clinical CTS was first noted in 1962 by Blodgett et al. who reported DM in 59/915 or 6.4% of consecutive patients diagnosed with CTS [6]. A higher prevalence of DM among patients with CTS was described in 1972 by Phalen, who reported DM in 14.6% or in 56/384 consecutive patients diagnosed with CTS [7]. Subsequent studies demonstrated a similar prevalence with the calculated odds ratio (OR) of 3.02 for CTS in DM [8, 9]. The risk of CTS is further increased in DM patients with neuropathic symptoms, as shown by Perkins et al., who found a similar frequency of clinical CTS in 14% of nonneuropathic DM subjects, increasing to 30% in those with diabetic sensorimotor polyneuropathy (DSP) of varying severity [10]. This prospective cohort study evaluated clinical CTS, defined rigorously, across a broad spectrum of DSP patients (**Table 1**). Pourmemari and Shiri performed a meta-analysis including over 90,000 subjects and examined DM as a risk factor for CTS. They found the association to be more modest with an unadjusted OR estimate of about 2 and less when controlling for potential confounding factors with a pooled estimate OR was 1.59 [11, 12]. This outcome may be related to varying definitions of CTS within different studies included in the meta-analysis.

Comi et al. examined the prevalence of median neuropathy in patients with DM using electrophysiological studies, but not symptoms and signs of CTS.


**5**

78% sensitivity in another study [21].

*Focal Upper Limb Mononeuropathies in Patients with Diabetes Mellitus*

11.2% showed electrophysiology indicating focal median neuropathy. The prevalence was higher (16.1%) among patients with DSP [13]. Other studies have shown even higher rates, up to 23%, of asymptomatic median compressive neuropathy at the wrist in patients with DM [14]. The issue with this approach is that CTS is a clinical diagnosis, and the Perkins study showed that electrophysiological changes at the carpal tunnel are related to DSP and not indicative of the presence of CTS [10]. All of these studies indicate that although median neuropathy at the wrist is relatively common in patients with DM when tested by nerve conduction studies, clinical CTS is not found in a similar proportion. Symptomatic CTS was described in 9% of DM subjects in an early study [15], and the lifetime risk of symptomatic CTS in type 1 diabetes was calculated more

**2.1 Electrophysiologic and ultrasonographic diagnostic techniques used in median compressive neuropathy at the wrist in patients with DM**

ological parameters to CTS rather than DM with or without DSP.

There have been attempts to establish electrodiagnostic methods that might distinguish CTS from DSP but doubt about the results which arise from the Perkins study [10]. For example, the median nerve distal motor latency or the median nerve sensory distal onset latency when stimulating at the palm or at the wrist crease has been reported to show differences between DM patients with CTS and idiopathic CTS in a small study [17], but those same parameters were not reliable in larger studies [10, 18]. Additional studies have reported other parameters that may be useful in diagnosis such as the median-radial sensory latency difference from the thumb, which showed 94% sensitivity in one study [19], and for a cutoff of 0.55, 82% sensitivity and 80% specificity in another study [18]. As the ulnar nerve is also susceptible to entrapment, a comparison of median nerve parameters to radial nerve parameters was thought to be preferable. Other studies have suggested using the median-ulnar sensory latency difference measured from the ring finger with 86% sensitivity in one study [19], and for a cutoff of 0.35, 90% sensitivity and 85% specificity in another study [18], although this sensory latency difference could not identify those with CTS in a larger study [10]. The lumbrical-interosseous latency difference was significantly different between CTS patients with and without DM, with sensitivity of up to 88.4% in two studies [17, 20], and for a cutoff of 1 ms had

Small studies have examined the feasibility of using ultrasonography to distinguish CTS with DM cases from DSP alone. Kim et al. found that all the crosssectional areas (CSA) of the median nerve were larger in DSP patients compared with healthy controls, and the CSA of the median nerve at the wrist revealed no significant differences among DSP patients with and without CTS; however,

DSP symptoms might mimic those of CTS in clinical practice. Nonetheless, clear symptoms for a diagnosis of CTS can be established even in those with advanced DSP [10]. Establishing the diagnosis of CTS based solely on electrophysiological diagnostic criteria is unreliable in DM patients, since the changes in electrophysiological parameters are due to DSP rather than CTS [10]. Various electrophysiological parameters are thought to distinguish CTS from DSP in subjects with DM, but none were found to be different in those with and without CTS in a population of subjects with DM [10]. Parameters such as median nerve distal motor or sensory latency, comparison of ratios of median (ulnar latencies or amplitudes or sensory conduction velocities), and others failed to differentiate those patients who had clinical CTS from those who did not in subjects with DM [10]. Consequently, in subjects with DM, it is prudent to be cautious in attributing changes in electrophysi-

*DOI: http://dx.doi.org/10.5772/intechopen.84839*

recently to be as high as 85% by Singh et al. [16].

#### **Table 1.**

*Clinical criteria for the diagnosis of carpal tunnel syndrome in diabetes patients.*

*Focal Upper Limb Mononeuropathies in Patients with Diabetes Mellitus DOI: http://dx.doi.org/10.5772/intechopen.84839*

*Peripheral Nerve Disorders and Treatment*

patients, with and without diabetes [5].

**mellitus (DM)**

lead to higher susceptibility to external injury are well-known. Less information on altered connective tissue structure in areas of nerve compression is available in this patient population. Deger et al. found a statistically significant increase in neoangiogenesis in subsynovial connective tissue in DM CTS cases, correlating with greater expression of vascular endothelial growth factor (VEGF), in subsynovial connective tissue in DM than what is present in CTS in patients without DM [2, 3]. These findings are consistent with the findings of Tekin et al., showing DM CTS patients, when compared with non-DM CTS patients, have higher rates of synovial edema and vascular proliferation and increased vascular wall thickness [4]. Thus the increased neovascularization, arising from a proposed ischemia-reperfusion mechanism, and more apparent in patients with DM, impinges the tissue compartment space within the carpal tunnel. In their recently published review, Sharma and Jaggi summarize the current knowledge regarding the role of transforming growth factor (TGF-β), VEGF, and interleukins in the subsynovial connective tissue in CTS

**2. Median compressive neuropathy at the wrist in patients with diabetes** 

The high prevalence of DM among patients with clinical CTS was first noted in 1962 by Blodgett et al. who reported DM in 59/915 or 6.4% of consecutive patients diagnosed with CTS [6]. A higher prevalence of DM among patients with CTS was described in 1972 by Phalen, who reported DM in 14.6% or in 56/384 consecutive patients diagnosed with CTS [7]. Subsequent studies demonstrated a similar prevalence with the calculated odds ratio (OR) of 3.02 for CTS in DM [8, 9]. The risk of CTS is further increased in DM patients with neuropathic symptoms, as shown by Perkins et al., who found a similar frequency of clinical CTS in 14% of nonneuropathic DM subjects, increasing to 30% in those with diabetic sensorimotor polyneuropathy (DSP) of varying severity [10]. This prospective cohort study evaluated clinical CTS, defined rigorously, across a broad spectrum of DSP patients (**Table 1**). Pourmemari and Shiri performed a meta-analysis including over 90,000 subjects and examined DM as a risk factor for CTS. They found the association to be more modest with an unadjusted OR estimate of about 2 and less when controlling for potential confounding factors with a pooled estimate OR was 1.59 [11, 12]. This outcome may be related to varying definitions of CTS within different studies included in the meta-analysis. Comi et al. examined the prevalence of median neuropathy in patients with DM using electrophysiological studies, but not symptoms and signs of CTS.

Paresthesiae in hands or marked preponderance of sensory symptoms in the hands

Upper limb sensory loss solely within the distribution of the median nerve *4/6 criteria required to diagnose CTS in those with DM with or without DSP [10] Electrodiagnostic criteria for CTS unreliable in the presence of DM [10]*

*Clinical criteria for the diagnosis of carpal tunnel syndrome in diabetes patients.*

Symptoms precipitated by activities such as holding a newspaper or driving a car and relieved by hand

Nocturnal hand symptoms awakening the patient

**4**

**Table 1.**

shaking

Predilection for radial digits Weak thenar muscles

11.2% showed electrophysiology indicating focal median neuropathy. The prevalence was higher (16.1%) among patients with DSP [13]. Other studies have shown even higher rates, up to 23%, of asymptomatic median compressive neuropathy at the wrist in patients with DM [14]. The issue with this approach is that CTS is a clinical diagnosis, and the Perkins study showed that electrophysiological changes at the carpal tunnel are related to DSP and not indicative of the presence of CTS [10]. All of these studies indicate that although median neuropathy at the wrist is relatively common in patients with DM when tested by nerve conduction studies, clinical CTS is not found in a similar proportion. Symptomatic CTS was described in 9% of DM subjects in an early study [15], and the lifetime risk of symptomatic CTS in type 1 diabetes was calculated more recently to be as high as 85% by Singh et al. [16].

#### **2.1 Electrophysiologic and ultrasonographic diagnostic techniques used in median compressive neuropathy at the wrist in patients with DM**

DSP symptoms might mimic those of CTS in clinical practice. Nonetheless, clear symptoms for a diagnosis of CTS can be established even in those with advanced DSP [10]. Establishing the diagnosis of CTS based solely on electrophysiological diagnostic criteria is unreliable in DM patients, since the changes in electrophysiological parameters are due to DSP rather than CTS [10]. Various electrophysiological parameters are thought to distinguish CTS from DSP in subjects with DM, but none were found to be different in those with and without CTS in a population of subjects with DM [10]. Parameters such as median nerve distal motor or sensory latency, comparison of ratios of median (ulnar latencies or amplitudes or sensory conduction velocities), and others failed to differentiate those patients who had clinical CTS from those who did not in subjects with DM [10]. Consequently, in subjects with DM, it is prudent to be cautious in attributing changes in electrophysiological parameters to CTS rather than DM with or without DSP.

There have been attempts to establish electrodiagnostic methods that might distinguish CTS from DSP but doubt about the results which arise from the Perkins study [10]. For example, the median nerve distal motor latency or the median nerve sensory distal onset latency when stimulating at the palm or at the wrist crease has been reported to show differences between DM patients with CTS and idiopathic CTS in a small study [17], but those same parameters were not reliable in larger studies [10, 18]. Additional studies have reported other parameters that may be useful in diagnosis such as the median-radial sensory latency difference from the thumb, which showed 94% sensitivity in one study [19], and for a cutoff of 0.55, 82% sensitivity and 80% specificity in another study [18]. As the ulnar nerve is also susceptible to entrapment, a comparison of median nerve parameters to radial nerve parameters was thought to be preferable. Other studies have suggested using the median-ulnar sensory latency difference measured from the ring finger with 86% sensitivity in one study [19], and for a cutoff of 0.35, 90% sensitivity and 85% specificity in another study [18], although this sensory latency difference could not identify those with CTS in a larger study [10]. The lumbrical-interosseous latency difference was significantly different between CTS patients with and without DM, with sensitivity of up to 88.4% in two studies [17, 20], and for a cutoff of 1 ms had 78% sensitivity in another study [21].

Small studies have examined the feasibility of using ultrasonography to distinguish CTS with DM cases from DSP alone. Kim et al. found that all the crosssectional areas (CSA) of the median nerve were larger in DSP patients compared with healthy controls, and the CSA of the median nerve at the wrist revealed no significant differences among DSP patients with and without CTS; however,

patients with CTS (with and without DM) had larger CSAs at the wrist and a higher wrist/forearm ratio compared with DSP patients. The cutoff value for the CSA at the wrist that yielded the highest sensitivity and specificity was 11.6 mm [22]. A smaller study found no ultrasound measurement (distal median CSA, wrist-forearm ratio, wrist-forearm difference) reached significance to detect CTS in patients with DSP [17].

#### **2.2 Treatment efficacy for CTS in patients with DM**

The outcome of open decompression of the median nerve by sectioning the carpal transverse ligament in DM patients has been evaluated in many studies. Several studies, with a post-procedure follow-up of up to 2 years, showed similar beneficial outcomes, in nerve conduction studies and symptoms, for patients with and without DM [23–29]. Some studies found that electrodiagnostic findings and assessment of symptoms and clinical signs improved significantly in both DM patients and in non-DM patients but that the improvement was less in the diabetic group [30–33]. Zhang et al. demonstrated an association of DM with an increased risk for secondary surgery following carpal tunnel decompression. They tested a total of 904 patients with and without DM, for a median follow-up length of less than a year [34]. Gulabi et al. compared the symptomatic outcome at 6 months and 10 years after decompression of 27 patients with DM and 42 patients with idiopathic CTS. They found that at 6 months, the outcomes were similar for the DM and non-DM groups, but at 10 years the DM group had poor outcomes possibly due to progression of DSP in the DM group [35]. Recently published results of a randomized controlled prospective study comparing the outcome of endoscopic carpal tunnel release versus open carpal tunnel release in DM patients suggest that the endoscopic approach is more beneficial for patients with diabetes. In this study, the patients who underwent endoscopic carpal tunnel release had better relief of symptoms and better function scores, less pillar pain and tenderness at 12 weeks after surgery, faster regain of grip and pinching functions, significantly faster return to work and significant improvement in wound healing, as well as reduction in wound infection and complications [36].

The evidence to date indicates that surgery in DM patients with CTS leads to an improvement in symptoms and signs of CTS that is very similar to non-DM patients with CTS. Given this background, it is reasonable to offer surgical therapy to DM patients with CTS when conservative treatments have failed, as is the case for idiopathic CTS, i.e., in those without DM.

#### **3. Compressive ulnar neuropathy at the elbow in patients with DM**

There is controversy over whether or not cubital tunnel syndrome is more common in those with DM. Stamboulis et al. found 12.2% of patients with cubital tunnel syndrome had DM [37]. In other studies, the prevalence of DM was the same in patients with cubital tunnel syndrome as in the general population, i.e., 6% in both groups, when the diagnosis of cubital tunnel syndrome was established on the combination of symptoms, objective clinical findings, and electrodiagnostic tests [38], and the severity of symptoms was also similar between those with and without DM [39]. In a case-control study, including only patients who had undergone ulnar nerve decompression, DM was not found to be a risk factor for ulnar neuropathy at the elbow [40]. The question of whether DM is a risk factor for cubital tunnel syndrome remains uncertain.

**7**

*Focal Upper Limb Mononeuropathies in Patients with Diabetes Mellitus*

**3.1 Electrophysiologic and ultrasonographic diagnostic techniques used in compressive ulnar neuropathy at the elbow in patients with DM**

Rota et al. tested DM patients for ulnar neuropathy at the elbow irrespective of clinical symptoms and found that 34% had electrodiagnostic features of ulnar dysfunction due to chronic compression at the elbow. Most of the patients with neurophysiological abnormalities were asymptomatic, and only 6% had sensory symptoms and showed clinical signs of cubital tunnel

It has been demonstrated in large cohorts that sensory nerve conduction velocity and amplitudes of sensory nerve action potentials are markedly lower in DM patients than in healthy controls, even more so in DM patients with known DSP [38, 42–45]. As asymptomatic ulnar nerve entrapment at the elbow (UNE) is relatively common among patients with DM, possibly due to the underlying DSP similar to CTS, when the diagnosis of cubital tunnel syndrome in patients with DM with or without DSP is in question, we rely mainly on changes in the motor conduction electrophysiologic parameters. Schady et al. studied 20 DM patients with cubital tunnel syndrome, demonstrated by hand wasting and weakness. All patients also had signs of DSP in the lower limbs. The nerve conduction studies in this cohort showed markedly reduced ulnar nerve compound muscle action potential (CMAP) amplitudes with a mean value of 1.2 versus 7.4 mV in controls and also reduced ulnar/median CMAP amplitude ratios. Less sensitive than the CMAP amplitudes was the ulnar nerve motor conduction velocity. This was disproportionately slowed across the elbow segment in only 8 of 34 affected ulnar

Only two studies have used ultrasonography for the diagnosis of ulnar compressive neuropathy at the elbow in patients with DM. Kang et al. had demonstrated that the cross-sectional area (CSA) of the ulnar nerve at the cubital tunnel outlet was significantly greater in patients with DSP than in healthy controls, with no correlation to nerve conduction study results [46]. It is possible that the larger CSA is a marker of DM and not specific for DSP or of ulnar compressive neuropathy at the elbow in patients with DM, as might be inferred from the second study. Chen et al. tested DM patients with and without confirmed DSP. They found that CSA of the ulnar nerve at the cubital tunnel outlet was greater in DM patients than that in the healthy control group, yet no difference was detected in the CSA of the ulnar nerve between DM patient with and without DSP [47]. These studies found no correlation between the cubital tunnel syndrome and the CSA or even between asymptomatic

**3.2 Treatment efficacy for ulnar compressive neuropathy at the elbow in patients** 

A recent US national database review of more than 15,000 patients who underwent ulnar nerve decompression at the cubital tunnel found a low incidence of failure of cubital tunnel release requiring ipsilateral revision, but the presence of DM was an independent risk factor for revision with an adjusted odds ratio of 1.27 [48]. The presence of DM did not increase the risk for infection following cubital tunnel release [49]. Other smaller studies have found that DM is not associated with a poor surgical result, either clinically or electrophysiologically [50], or with a greater likelihood of revision surgery [51–53]. When satisfaction with treatment was assessed, having DM was not associated with a higher likelihood of dissatisfac-

*DOI: http://dx.doi.org/10.5772/intechopen.84839*

syndrome [41].

nerves [43].

UNE and the CSA.

**with DM**

tion with treatment [54].

*Peripheral Nerve Disorders and Treatment*

**2.2 Treatment efficacy for CTS in patients with DM**

in wound infection and complications [36].

idiopathic CTS, i.e., in those without DM.

syndrome remains uncertain.

in patients with DSP [17].

patients with CTS (with and without DM) had larger CSAs at the wrist and a higher wrist/forearm ratio compared with DSP patients. The cutoff value for the CSA at the wrist that yielded the highest sensitivity and specificity was 11.6 mm [22]. A smaller study found no ultrasound measurement (distal median CSA, wrist-forearm ratio, wrist-forearm difference) reached significance to detect CTS

The outcome of open decompression of the median nerve by sectioning the carpal transverse ligament in DM patients has been evaluated in many studies. Several studies, with a post-procedure follow-up of up to 2 years, showed similar beneficial outcomes, in nerve conduction studies and symptoms, for patients with and without DM [23–29]. Some studies found that electrodiagnostic findings and assessment of symptoms and clinical signs improved significantly in both DM patients and in non-DM patients but that the improvement was less in the diabetic group [30–33]. Zhang et al. demonstrated an association of DM with an increased risk for secondary surgery following carpal tunnel decompression. They tested a total of 904 patients with and without DM, for a median follow-up length of less than a year [34]. Gulabi et al. compared the symptomatic outcome at 6 months and 10 years after decompression of 27 patients with DM and 42 patients with idiopathic CTS. They found that at 6 months, the outcomes were similar for the DM and non-DM groups, but at 10 years the DM group had poor outcomes possibly due to progression of DSP in the DM group [35]. Recently published results of a randomized controlled prospective study comparing the outcome of endoscopic carpal tunnel release versus open carpal tunnel release in DM patients suggest that the endoscopic approach is more beneficial for patients with diabetes. In this study, the patients who underwent endoscopic carpal tunnel release had better relief of symptoms and better function scores, less pillar pain and tenderness at 12 weeks after surgery, faster regain of grip and pinching functions, significantly faster return to work and significant improvement in wound healing, as well as reduction

The evidence to date indicates that surgery in DM patients with CTS leads to an improvement in symptoms and signs of CTS that is very similar to non-DM patients with CTS. Given this background, it is reasonable to offer surgical therapy to DM patients with CTS when conservative treatments have failed, as is the case for

**3. Compressive ulnar neuropathy at the elbow in patients with DM**

There is controversy over whether or not cubital tunnel syndrome is more common in those with DM. Stamboulis et al. found 12.2% of patients with cubital tunnel syndrome had DM [37]. In other studies, the prevalence of DM was the same in patients with cubital tunnel syndrome as in the general population, i.e., 6% in both groups, when the diagnosis of cubital tunnel syndrome was established on the combination of symptoms, objective clinical findings, and electrodiagnostic tests [38], and the severity of symptoms was also similar between those with and without DM [39]. In a case-control study, including only patients who had undergone ulnar nerve decompression, DM was not found to be a risk factor for ulnar neuropathy at the elbow [40]. The question of whether DM is a risk factor for cubital tunnel

**6**

#### **3.1 Electrophysiologic and ultrasonographic diagnostic techniques used in compressive ulnar neuropathy at the elbow in patients with DM**

Rota et al. tested DM patients for ulnar neuropathy at the elbow irrespective of clinical symptoms and found that 34% had electrodiagnostic features of ulnar dysfunction due to chronic compression at the elbow. Most of the patients with neurophysiological abnormalities were asymptomatic, and only 6% had sensory symptoms and showed clinical signs of cubital tunnel syndrome [41].

It has been demonstrated in large cohorts that sensory nerve conduction velocity and amplitudes of sensory nerve action potentials are markedly lower in DM patients than in healthy controls, even more so in DM patients with known DSP [38, 42–45]. As asymptomatic ulnar nerve entrapment at the elbow (UNE) is relatively common among patients with DM, possibly due to the underlying DSP similar to CTS, when the diagnosis of cubital tunnel syndrome in patients with DM with or without DSP is in question, we rely mainly on changes in the motor conduction electrophysiologic parameters. Schady et al. studied 20 DM patients with cubital tunnel syndrome, demonstrated by hand wasting and weakness. All patients also had signs of DSP in the lower limbs. The nerve conduction studies in this cohort showed markedly reduced ulnar nerve compound muscle action potential (CMAP) amplitudes with a mean value of 1.2 versus 7.4 mV in controls and also reduced ulnar/median CMAP amplitude ratios. Less sensitive than the CMAP amplitudes was the ulnar nerve motor conduction velocity. This was disproportionately slowed across the elbow segment in only 8 of 34 affected ulnar nerves [43].

Only two studies have used ultrasonography for the diagnosis of ulnar compressive neuropathy at the elbow in patients with DM. Kang et al. had demonstrated that the cross-sectional area (CSA) of the ulnar nerve at the cubital tunnel outlet was significantly greater in patients with DSP than in healthy controls, with no correlation to nerve conduction study results [46]. It is possible that the larger CSA is a marker of DM and not specific for DSP or of ulnar compressive neuropathy at the elbow in patients with DM, as might be inferred from the second study. Chen et al. tested DM patients with and without confirmed DSP. They found that CSA of the ulnar nerve at the cubital tunnel outlet was greater in DM patients than that in the healthy control group, yet no difference was detected in the CSA of the ulnar nerve between DM patient with and without DSP [47]. These studies found no correlation between the cubital tunnel syndrome and the CSA or even between asymptomatic UNE and the CSA.

#### **3.2 Treatment efficacy for ulnar compressive neuropathy at the elbow in patients with DM**

A recent US national database review of more than 15,000 patients who underwent ulnar nerve decompression at the cubital tunnel found a low incidence of failure of cubital tunnel release requiring ipsilateral revision, but the presence of DM was an independent risk factor for revision with an adjusted odds ratio of 1.27 [48]. The presence of DM did not increase the risk for infection following cubital tunnel release [49]. Other smaller studies have found that DM is not associated with a poor surgical result, either clinically or electrophysiologically [50], or with a greater likelihood of revision surgery [51–53]. When satisfaction with treatment was assessed, having DM was not associated with a higher likelihood of dissatisfaction with treatment [54].

#### **4. Ulnar compressive neuropathy at the wrist in patients with diabetes mellitus (DM)**

Ulnar entrapment at the wrist is far less common, and thus less studied, than ulnar nerve entrapment at the elbow. The prevalence of DM among patients with ulnar tunnel syndrome at the wrist is yet to be determined, as no large-scale study has assessed the presence of this potential entrapment. In fact, the only relevant data comes from a single retrospective study of 31 patients who had an ulnar nerve palsy treated by ulnar tunnel (Guyon's canal) release, and 6 patients or 19% had DM [55].

#### **4.1 Electrophysiologic and ultrasonographic diagnostic techniques used in ulnar compressive neuropathy at the wrist in patients with DM**

The diagnosis of ulnar tunnel syndrome at the wrist is routinely based on the motor nerve conduction study parameters. Rota et al. tested DM patients for ulnar neuropathy at the wrist, and their electrodiagnostic study demonstrated relevant neurophysiological abnormalities in 11% of the patients, all of whom had DSP as well. The paper does not state how many of the patients presenting with these electrophysiological abnormalities were symptomatic [41].

There is a single paper regarding the use of ultrasonography for the diagnosis of ulnar compressive neuropathy at the wrist in patients with DM. Chen et al., who tested DM patients with and without confirmed DSP, showed that the CSA of the ulnar nerve at Guyon's canal was greater in DM patients than in the healthy control group, yet no difference was detected in the CSA of ulnar nerves between DM patients with and without DSP. No potential relationship to clinical signs or symptoms of ulnar tunnel syndrome was examined in this study [47].

#### **5. Summary**

Upper limb mononeuropathies are common in patients with DM with the most common being CTS. The diagnosis of CTS in DM is a clinical diagnosis as the electrophysiologic and ultrasonographic parameters do not reliably distinguish between CTS and DSP. Treatment can be highly effective in CTS patients with DM whether or not DSP is present. Asymptomatic ulnar nerve electrophysiological abnormalities are common in DM, but it is unclear if clinical entrapment syndromes at the elbow are more common or not. The success of surgical decompression of the ulnar nerve at the elbow in those with DM is similar to that in non-DM patients. Ulnar nerve entrapment at the wrist is infrequent, and data on diagnosis and treatment is limited or unavailable.

#### **Acknowledgements**

No funding was received for preparation of this manuscript.

#### **Conflict of interest**

All authors declare that they have no conflict of interest pertinent to this work.

**9**

**Author details**

Toronto, Toronto, Canada

University, Dammam, Saudi Arabia

Tayir Alon1

provided the original work is properly cited.

and Vera Bril2,3\*

1 Edith Wolfson Medical Center, Holon, Israel

\*Address all correspondence to: vera.bril@utoronto.ca

© 2019 The Author(s). Licensee IntechOpen. 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,

2 Ellen and Martin Prosserman Centre for Neuromuscular Diseases, Division of Neurology, Department of Medicine, University Health Network, University of

3 Institute for Research and Medical Consultations, Imam Abdulrahman Bin Faisal

*Focal Upper Limb Mononeuropathies in Patients with Diabetes Mellitus*

*DOI: http://dx.doi.org/10.5772/intechopen.84839*

*Focal Upper Limb Mononeuropathies in Patients with Diabetes Mellitus DOI: http://dx.doi.org/10.5772/intechopen.84839*

### **Author details**

*Peripheral Nerve Disorders and Treatment*

**mellitus (DM)**

19% had DM [55].

**5. Summary**

limited or unavailable.

**Acknowledgements**

**Conflict of interest**

**4. Ulnar compressive neuropathy at the wrist in patients with diabetes** 

Ulnar entrapment at the wrist is far less common, and thus less studied, than

**4.1 Electrophysiologic and ultrasonographic diagnostic techniques used in ulnar** 

The diagnosis of ulnar tunnel syndrome at the wrist is routinely based on the motor nerve conduction study parameters. Rota et al. tested DM patients for ulnar neuropathy at the wrist, and their electrodiagnostic study demonstrated relevant neurophysiological abnormalities in 11% of the patients, all of whom had DSP as well. The paper does not state how many of the patients presenting with these

There is a single paper regarding the use of ultrasonography for the diagnosis of ulnar compressive neuropathy at the wrist in patients with DM. Chen et al., who tested DM patients with and without confirmed DSP, showed that the CSA of the ulnar nerve at Guyon's canal was greater in DM patients than in the healthy control group, yet no difference was detected in the CSA of ulnar nerves between DM patients with and without DSP. No potential relationship to clinical signs or symp-

Upper limb mononeuropathies are common in patients with DM with the most common being CTS. The diagnosis of CTS in DM is a clinical diagnosis as the electrophysiologic and ultrasonographic parameters do not reliably distinguish between CTS and DSP. Treatment can be highly effective in CTS patients with DM whether or not DSP is present. Asymptomatic ulnar nerve electrophysiological abnormalities are common in DM, but it is unclear if clinical entrapment syndromes at the elbow are more common or not. The success of surgical decompression of the ulnar nerve at the elbow in those with DM is similar to that in non-DM patients. Ulnar nerve entrapment at the wrist is infrequent, and data on diagnosis and treatment is

All authors declare that they have no conflict of interest pertinent to this work.

**compressive neuropathy at the wrist in patients with DM**

electrophysiological abnormalities were symptomatic [41].

toms of ulnar tunnel syndrome was examined in this study [47].

No funding was received for preparation of this manuscript.

ulnar nerve entrapment at the elbow. The prevalence of DM among patients with ulnar tunnel syndrome at the wrist is yet to be determined, as no large-scale study has assessed the presence of this potential entrapment. In fact, the only relevant data comes from a single retrospective study of 31 patients who had an ulnar nerve palsy treated by ulnar tunnel (Guyon's canal) release, and 6 patients or

**8**

Tayir Alon1 and Vera Bril2,3\*

1 Edith Wolfson Medical Center, Holon, Israel

2 Ellen and Martin Prosserman Centre for Neuromuscular Diseases, Division of Neurology, Department of Medicine, University Health Network, University of Toronto, Toronto, Canada

3 Institute for Research and Medical Consultations, Imam Abdulrahman Bin Faisal University, Dammam, Saudi Arabia

\*Address all correspondence to: vera.bril@utoronto.ca

© 2019 The Author(s). Licensee IntechOpen. 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.

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[2] Deger AN, Deger H, Taser F. The role of neoangiogenesis and vascular endothelial growth factor in the development of carpal tunnel syndrome in patients with diabetes. Nigerian Journal of Clinical Practice. 2016;**19**(2):189-195. Available from: http://www.ncbi.nlm.nih.gov/ pubmed/26856279

[3] Taser F, Deger AN, Deger H. Comparative histopathologic evaluation of diabetic, hypothyroid and idiopathic carpal tunnel syndrome. Turkish Neurosurgery. 2016;**27**(6):991-997. Available from: http://www.ncbi.nlm. nih.gov/pubmed/27651338

[4] Tekin F, Sürmeli M, Şimşek H, Ceran C, Tezcan S, Taner ÖF, et al. Comparison of the histopathological findings of patients with diabetic and idiopathic carpal tunnel syndrome. International Orthopaedics. 2015;**39**(12):2395-2401. Available from: http://link.springer.com/10.1007/ s00264-015-2790-y

[5] Sharma D, Jaggi AS, Bali A. Clinical evidence and mechanisms of growth factors in idiopathic and diabetesinduced carpal tunnel syndrome. European Journal of Pharmacology. 2018;**837**:156-163. Available from: http://www.ncbi.nlm.nih.gov/ pubmed/30125568

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[9] Eversmann WW, Ritsick JA. Intraoperative changes in motor nerve conduction latency in carpal tunnel syndrome. The Journal of Hand Surgery. 1978;**3**(1):77-81. Available from: http:// linkinghub.elsevier.com/retrieve/pii/ S0363502378801191

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**11**

mus.23677

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c9ec9e4c72c8d4003dd59

[20] Yagci I, Gunduz OH, Sancak S, Agirman M, Mesci E, Akyuz G. Comparative electrophysiological techniques in the diagnosis of carpal tunnel syndrome in patients with diabetic polyneuropathy. Diabetes Research and Clinical Practice. 2010;**88**(2):157-163. Available from: https://ac.els-cdn. com/S0168822710000872/1 s2.0-S0168822710000872-main. pdf?\_tid=84d8434e-ce77-11e7-95a9- 00000aacb361&acdnat=1511240018\_2b 24f72b235788bf9cf0425a9e54c009

[21] Vogt T, Mika A, Thömke F, Hopf HC. Evaluation of carpal tunnel syndrome in patients with polyneuropathy. Muscle & Nerve. 1997;**20**(2):153-157. Available from: http://www.ncbi.nlm.nih.gov/

[22] Kim L-N, Kwon H-K, Moon H-I, Pyun S-B, Lee H-J. Sonography of the median nerve in carpal tunnel syndrome with diabetic neuropathy. American Journal of Physical Medicine & Rehabilitation. 2014;**93**(10):897- 907. Available from: http://content. wkhealth.com/linkback/open url?sid=WKPTLP:landingpage &an=00002060-201410000-00007

[23] Thomsen NOB, Cederlund R, Rosén I, Björk J, Dahlin LB. Clinical outcomes of surgical release among diabetic patients with carpal tunnel syndrome: Prospective follow-up with matched

pubmed/9040652

*DOI: http://dx.doi.org/10.5772/intechopen.84839*

diabetes duration and polyneuropathy.

1985;**22**(3):259-262. Available from: https://link.springer.com/content/ pdf/10.1007%2FBF02590778.pdf

[14] Albers JW, Brown MB, Sima AAF, Greene DA. Frequency of median mononeuropathy in patients with mild diabetic neuropathy in the early diabetes intervention trial (EDIT). Muscle and Nerve. 1996;**19**(2):140-146. Available from: http://www.ncbi.nlm.nih.gov/

[15] Mulder DW, Lambert EH, Bastron JA, Sprague RG. The neuropathies associated with diabetes mellitus. A clinical and electromyographic study of 103 unselected diabetic patients. Neurology. 1961;**11**(4 Pt 1):275-284. Available from: http://www.ncbi.nlm.

nih.gov/pubmed/13773672

[16] Singh R, Gamble G, Cundy T. Lifetime risk of symptomatic carpal tunnel syndrome in type 1 diabetes. Diabetic Medicine. 2005;**22**(5):625-630. DOI: 10.1111/j.1464-5491.2005.01487.x

[17] Hassan A, Leep Hunderfund AN, Watson J, Boon AJ, Sorenson EJ. Median nerve ultrasound in diabetic peripheral neuropathy with and without carpal tunnel syndrome. Muscle and Nerve. 2013;**47**(3):437-439. DOI: 10.1002/

[18] Gazioglu S, Boz C, Cakmak VA. Electrodiagnosis of carpal tunnel syndrome in patients with diabetic polyneuropathy. Clinical Neurophysiology. 2011;**122**(7):1463- 1469. Available from: https://

ac.els-cdn.com/S1388245711000137/1 s2.0-S1388245711000137-main. pdf?\_tid=455fa08c-ce76-11e7-a88e-00000aacb362&acdnat=1511239482\_ ed527fcb50dc5e024b4a4b1ea89ad6ee

[13] Comi G, Lozza L, Galardi G, Ghilardi MF, Medaglini S, Canal N. Presence of carpal tunnel syndrome in diabetics: Effect of age, sex,

Acta Diabetologica Latina.

pubmed/8874414

*Focal Upper Limb Mononeuropathies in Patients with Diabetes Mellitus DOI: http://dx.doi.org/10.5772/intechopen.84839*

[13] Comi G, Lozza L, Galardi G, Ghilardi MF, Medaglini S, Canal N. Presence of carpal tunnel syndrome in diabetics: Effect of age, sex, diabetes duration and polyneuropathy. Acta Diabetologica Latina. 1985;**22**(3):259-262. Available from: https://link.springer.com/content/ pdf/10.1007%2FBF02590778.pdf

[14] Albers JW, Brown MB, Sima AAF, Greene DA. Frequency of median mononeuropathy in patients with mild diabetic neuropathy in the early diabetes intervention trial (EDIT). Muscle and Nerve. 1996;**19**(2):140-146. Available from: http://www.ncbi.nlm.nih.gov/ pubmed/8874414

[15] Mulder DW, Lambert EH, Bastron JA, Sprague RG. The neuropathies associated with diabetes mellitus. A clinical and electromyographic study of 103 unselected diabetic patients. Neurology. 1961;**11**(4 Pt 1):275-284. Available from: http://www.ncbi.nlm. nih.gov/pubmed/13773672

[16] Singh R, Gamble G, Cundy T. Lifetime risk of symptomatic carpal tunnel syndrome in type 1 diabetes. Diabetic Medicine. 2005;**22**(5):625-630. DOI: 10.1111/j.1464-5491.2005.01487.x

[17] Hassan A, Leep Hunderfund AN, Watson J, Boon AJ, Sorenson EJ. Median nerve ultrasound in diabetic peripheral neuropathy with and without carpal tunnel syndrome. Muscle and Nerve. 2013;**47**(3):437-439. DOI: 10.1002/ mus.23677

[18] Gazioglu S, Boz C, Cakmak VA. Electrodiagnosis of carpal tunnel syndrome in patients with diabetic polyneuropathy. Clinical Neurophysiology. 2011;**122**(7):1463- 1469. Available from: https:// ac.els-cdn.com/S1388245711000137/1 s2.0-S1388245711000137-main. pdf?\_tid=455fa08c-ce76-11e7-a88e-00000aacb362&acdnat=1511239482\_ ed527fcb50dc5e024b4a4b1ea89ad6ee

[19] Imada M, Misawa S, Sawai S, Tamura N, Kanai K, Sakurai K, et al. Median-radial sensory nerve comparative studies in the detection of median neuropathy at the wrist in diabetic patients. Clinical Neurophysiology. 2007;**118**(6):1405- 1409. Available from: https://ac.els-cdn. com/S1388245707000946/1-s2.0- S1388245707000946-main.pdf?\_ tid=496688fa-ce79-11e7-85fb-00000aac b362&acdnat=1511240786\_8144071cb3d c9ec9e4c72c8d4003dd59

[20] Yagci I, Gunduz OH, Sancak S, Agirman M, Mesci E, Akyuz G. Comparative electrophysiological techniques in the diagnosis of carpal tunnel syndrome in patients with diabetic polyneuropathy. Diabetes Research and Clinical Practice. 2010;**88**(2):157-163. Available from: https://ac.els-cdn. com/S0168822710000872/1 s2.0-S0168822710000872-main. pdf?\_tid=84d8434e-ce77-11e7-95a9- 00000aacb361&acdnat=1511240018\_2b 24f72b235788bf9cf0425a9e54c009

[21] Vogt T, Mika A, Thömke F, Hopf HC. Evaluation of carpal tunnel syndrome in patients with polyneuropathy. Muscle & Nerve. 1997;**20**(2):153-157. Available from: http://www.ncbi.nlm.nih.gov/ pubmed/9040652

[22] Kim L-N, Kwon H-K, Moon H-I, Pyun S-B, Lee H-J. Sonography of the median nerve in carpal tunnel syndrome with diabetic neuropathy. American Journal of Physical Medicine & Rehabilitation. 2014;**93**(10):897- 907. Available from: http://content. wkhealth.com/linkback/open url?sid=WKPTLP:landingpage &an=00002060-201410000-00007

[23] Thomsen NOB, Cederlund R, Rosén I, Björk J, Dahlin LB. Clinical outcomes of surgical release among diabetic patients with carpal tunnel syndrome: Prospective follow-up with matched

**10**

*Peripheral Nerve Disorders and Treatment*

[1] Dyck PJ, Giannini C. Pathologic alterations in the diabetic neuropathies of humans. Journal of Neuropathology

1962;**182**(7):814-815. Available from: http://jama.jamanetwork. com/article.aspx?doi=10.1001/ jama.1962.03050460106017a

[7] Phalen GS. The carpal-tunnel syndrome. Clinical evaluation of 598 hands. Clinical Orthopaedics and Related Research. 1972;**83**:29-40. Available from: http://www.ncbi.nlm.

nih.gov/pubmed/5014825

pubmed/11862031

S0363502378801191

pubmed/11874948

dme.12855

[8] Karpitskaya Y, Novak CB,

[9] Eversmann WW, Ritsick JA. Intraoperative changes in motor nerve conduction latency in carpal tunnel syndrome. The Journal of Hand Surgery. 1978;**3**(1):77-81. Available from: http:// linkinghub.elsevier.com/retrieve/pii/

[10] Perkins BA, Olaleye D, Bril V. Carpal tunnel syndrome in patients with diabetic polyneuropathy. Diabetes Care. 2002;**25**(3):565-569. Available from: http://www.ncbi.nlm.nih.gov/

[11] Pourmemari MH, Shiri R. Diabetes as a risk factor for carpal tunnel syndrome: A systematic review and meta-analysis. Diabetic Medicine. 2016;**33**(1):10-16. DOI: 10.1111/

[12] Geoghegan JM, Clark DI,

The Journal of Hand Surgery. 2004;**29**(4):315-320. Available from: http://journals.sagepub.com/ doi/10.1016/J.JHSB.2004.02.009

Bainbridge LC, Smith C, Hubbard R. Risk factors in carpal tunnel syndrome.

Mackinnon SE. Prevalence of smoking, obesity, diabetes mellitus, and thyroid disease in patients with carpal tunnel syndrome. Annals of Plastic Surgery. 2002;**48**(3):269-273. Available from: http://www.ncbi.nlm.nih.gov/

and Experimental Neurology. 1996;**55**(12):1181-1193. Available from: https://academic.oup.com/jnen/ article-lookup/doi/10.1097/00005072-

[2] Deger AN, Deger H, Taser F. The role of neoangiogenesis and vascular endothelial growth factor in the development of carpal tunnel syndrome in patients with diabetes. Nigerian Journal of Clinical Practice. 2016;**19**(2):189-195. Available from: http://www.ncbi.nlm.nih.gov/

[3] Taser F, Deger AN, Deger H.

nih.gov/pubmed/27651338

s00264-015-2790-y

pubmed/30125568

[6] Blodgett RC, Lipscomb PR, Hill RW. Incidence of hematologie disease in patients with carpal tunnel syndrome. Journal of the American Medical Association.

[4] Tekin F, Sürmeli M, Şimşek H, Ceran C, Tezcan S, Taner ÖF, et al. Comparison of the histopathological findings of patients with diabetic and idiopathic carpal tunnel syndrome. International Orthopaedics.

2015;**39**(12):2395-2401. Available from: http://link.springer.com/10.1007/

[5] Sharma D, Jaggi AS, Bali A. Clinical evidence and mechanisms of growth factors in idiopathic and diabetesinduced carpal tunnel syndrome. European Journal of Pharmacology. 2018;**837**:156-163. Available from: http://www.ncbi.nlm.nih.gov/

Comparative histopathologic evaluation of diabetic, hypothyroid and idiopathic carpal tunnel syndrome. Turkish Neurosurgery. 2016;**27**(6):991-997. Available from: http://www.ncbi.nlm.

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199612000-00001

pubmed/26856279

controls. The Journal of Hand Surgery. 2009;**34**(7):1177-1187. Available from: http://linkinghub.elsevier.com/retrieve/ pii/S0363502309003451

[24] Mondelli M, Padua L, Reale F, Signorini AM, Romano C. Outcome of surgical release among diabetics with carpal tunnel syndrome. Archives of Physical Medicine and Rehabilitation. 2004;**85**(1):7-13. Available from: http://www.archives-pmr.org/article/ S0003-9993(03)00770-6/pdf

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[28] Ozer K, Malay S, Toker S, Chung KC. Minimal clinically important difference of carpal tunnel release in diabetic and nondiabetic patients. Plastic and Reconstructive Surgery. 2013;**131**(6):1279-1285. Available from: http://content.wkhealth.com/linkback/ openurl?sid=WKPTLP:landingpage &an=00006534-201306000-00008

[29] Watchmaker JD, Watchmaker GP. Independent variables affecting outcome of carpal tunnel release surgery. The Hand. 2018;**13**(3):285-291. Available from: http://journals.sagepub. com/doi/10.1177/1558944717703739

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[31] Isik C, Uslu M, Inanmaz ME, Karabekmez FE, Kose KC. The effects of diabetes on symptoms of carpal tunnel syndrome treated with miniopen surgery. Acta Orthopaedica Belgica. 2013;**79**(4):381-385. Available from: http://www.ncbi.nlm.nih.gov/ pubmed/24205766

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[35] Gulabi D, Cecen G, Guclu B, Cecen A. Carpal tunnel release in patients with diabetes result in poorer outcome in long-term study. European Journal of Orthopaedic Surgery and Traumatology. 2014;**24**(7):1181-1184. Available from: http://link.springer.com/10.1007/ s00590-014-1418-z

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mononeuropathies in diabetic patients: Increased or not? Journal of Neurology. 2005;**252**(4):448-452. Available from: http://link.springer.com/10.1007/

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*Focal Upper Limb Mononeuropathies in Patients with Diabetes Mellitus DOI: http://dx.doi.org/10.5772/intechopen.84839*

[36] Ismail M, Schuh A, Ibrahim M. Outcome of Endoscopic Carpal Tunnel Release Versus Open Carpal Tunnel Release in Diabetic Patients: A Randomized Controlled Prospective Double Blinded Study. 2018. Available from: http://www.oatext.com/ pdf/GMT-1-108.pdf [Accessed: 27 September 2018]

*Peripheral Nerve Disorders and Treatment*

[24] Mondelli M, Padua L, Reale F, Signorini AM, Romano C. Outcome of surgical release among diabetics with carpal tunnel syndrome. Archives of Physical Medicine and Rehabilitation. 2004;**85**(1):7-13. Available from: http://www.archives-pmr.org/article/

S0003-9993(03)00770-6/pdf

pii/S1388245710003020

jbjsbr/94-B/6/811.full.pdf

[27] Zyluk A, Puchalski P. A comparison of outcomes of carpal tunnel release in diabetic and nondiabetic patients. Journal of Hand Surgery. 2013;**38**(5):485-488. Available from: http://journals.sagepub.com/ doi/10.1177/1753193412469781

[28] Ozer K, Malay S, Toker S, Chung KC. Minimal clinically important difference of carpal tunnel release in diabetic and nondiabetic patients. Plastic and Reconstructive Surgery. 2013;**131**(6):1279-1285. Available from: http://content.wkhealth.com/linkback/ openurl?sid=WKPTLP:landingpage &an=00006534-201306000-00008

[29] Watchmaker JD, Watchmaker GP. Independent variables affecting outcome of carpal tunnel release surgery. The Hand. 2018;**13**(3):285-291.

[25] Thomsen NOB, Rosén I, Dahlin LB. Neurophysiologic recovery after carpal tunnel release in diabetic patients. Clinical Neurophysiology. 2010;**121**(9):1569-1573. Available from: http://linkinghub.elsevier.com/retrieve/

[26] Jenkins PJ, Duckworth AD, Watts AC, McEachan JE. The outcome of carpal tunnel decompression in patients with diabetes mellitus. Journal of Bone and Joint Surgery. 2012;**9494**(6):811-814. Available from: http://bjj.boneandjoint.org.uk/content/

pii/S0363502309003451

controls. The Journal of Hand Surgery. 2009;**34**(7):1177-1187. Available from: http://linkinghub.elsevier.com/retrieve/ Available from: http://journals.sagepub. com/doi/10.1177/1558944717703739

[30] Ozkul Y, Sabuncu T, Kocabey Y, Nazligul Y. Outcomes of carpal tunnel release in diabetic and nondiabetic patients. Acta Neurologica Scandinavica. 2002;**106**(3):168-172. Available from: http://www.ncbi.nlm.

nih.gov/pubmed/12174177

pubmed/24205766

pubmed/8409659

[33] Yucel H. Factors affecting symptoms and functionality of patients with carpal tunnel syndrome: A retrospective study. Journal of Physical Therapy Science. 2015;**27**(4):1097-1101. Available from: https://www.jstage.jst.go.jp/article/ jpts/27/4/27\_jpts-2014-727/\_pdf

[31] Isik C, Uslu M, Inanmaz ME, Karabekmez FE, Kose KC. The effects of diabetes on symptoms of carpal tunnel syndrome treated with miniopen surgery. Acta Orthopaedica Belgica. 2013;**79**(4):381-385. Available from: http://www.ncbi.nlm.nih.gov/

[32] Haupt WF, Wintzer G, Schop A, Löttgen J, Pawlik G. Long-term results of carpal tunnel decompression.

Assessment of 60 cases. Journal of Hand Surgery. 1993;**18**(4):471-474. Available from: http://www.ncbi.nlm.nih.gov/

[34] Zhang D, Blazar P, Earp BE. Rates of complications and secondary surgeries of mini-open carpal tunnel release. The Hand. 2018:155894471876522. Available from: http://journals.sagepub.com/ doi/10.1177/1558944718765226

[35] Gulabi D, Cecen G, Guclu B, Cecen A. Carpal tunnel release in patients with diabetes result in poorer outcome in long-term study. European Journal of Orthopaedic Surgery and Traumatology. 2014;**24**(7):1181-1184. Available from: http://link.springer.com/10.1007/

s00590-014-1418-z

**12**

[37] Stamboulis E, Vassilopoulos D, Kalfakis N. Symptomatic focal mononeuropathies in diabetic patients: Increased or not? Journal of Neurology. 2005;**252**(4):448-452. Available from: http://link.springer.com/10.1007/ s00415-005-0672-8

[38] Mondelli M, Aretini A, Rossi S. Ulnar neuropathy at the elbow in diabetes. American Journal of Physical Medicine & Rehabilitation. 2009;**88**(4):278-285. Available from: http://content.wkhealth.com/linkback/ openurl?sid=WKPTLP:landingpage &an=00002060-200904000-00006

[39] Naran S, Imbriglia JE, Bilonick RA, Taieb A, Wollstein R. A demographic analysis of cubital tunnel syndrome. Annals of Plastic Surgery. 2010;**64**(2):177-179. Available from: http://content.wkhealth.com/linkback/ openurl?sid=WKPTLP:landingpage &an=00000637-201002000-00016

[40] Bartels RHMA, Verbeek ALM. Risk factors for ulnar nerve compression at the elbow: A case control study. Acta Neurochirurgica. 2007;**149**(7): 669-674. Discussion 674. Available from: http://link.springer.com/10.1007/ s00701-007-1166-5

[41] Rota E, Zavaroni D, Parietti L, Iafelice I, De Mitri P, Terlizzi E, et al. Ulnar entrapment neuropathy in patients with type 2 diabetes mellitus: An electrodiagnostic study. Diabetes Research and Clinical Practice. 2014;**104**(1):73-78. Available from: https://www.sciencedirect.com/science/ article/pii/S0168822714000540

[42] Zhang Y, Li J, Wang T, Wang J. Amplitude of sensory nerve action potential in early stage diabetic peripheral neuropathy: An analysis of 500 cases. Neural Regeneration Research. 2014;**9**(14):1389-1394. Available from: http://www.ncbi.nlm. nih.gov/pubmed/25221597

[43] Schady W, Abuaisha B, Boulton AJM. Observations on severe ulnar neuropathy in diabetes. Journal of Diabetes and its Complications. 2017;**12**(3):128-132. Available from: https://ac.els-cdn.com/ S1056872797000949/1-s2.0- S1056872797000949-main.pdf?\_ tid=69558916-c9b2-11e7-b816-00000aac b362&acdnat=1510715557\_4d8fa0a0aab 177eeab422e8a99981877

[44] Rota E, Quadri R, Fanti E, Isoardo G, Poglio F, Tavella A, et al. Electrophysiological findings of peripheral neuropathy in newly diagnosed type II diabetes mellitus. Journal of the Peripheral Nervous System. 2005;**10**(4):348-353. DOI: 10.1111/j.1085-9489.2005.00046.x

[45] Jang JE, Kim YT, Park BK, Cheong IY, Kim DH. Subclinical ulnar neuropathy at the elbow in diabetic patients. Annals of Rehabilitation Medicine. 2014;**38**(1):64-71. Available from: https://synapse.koreamed.org/ DOIx.php?id=10.5535/arm.2014.38.1.64

[46] Kang S, Kim SH, Yang SN, Yoon JS. Sonographic features of peripheral nerves at multiple sites in patients with diabetic polyneuropathy. Journal of Diabetes and its Complications. 2016;**30**(3):518-523. Available from: https://ac.els-cdn. com/S1056872715004900/1-s2.0- S1056872715004900-main.pdf?\_ tid=1eb9bf84-c959-11e7-82af-00000aab 0f6b&acdnat=1510677206\_8d523dc643 7dc142dedade48e77373c7

[47] Chen J, Wang C-L, Wu S, He S, Ren J. The feasibility of using

high-resolution ultrasonography to assess ulnar nerve in patients with diabetes mellitus. Journal of Ultrasonography. 2017;**17**:160-166. Available from: http://jultrason.pl/ uploads/dm\_artykuly/jou-2017-0024. pdf

[48] Camp CL, Ryan CB, Degen RM, Dines JS, Altchek DW, Werner BC. Risk factors for revision surgery following isolated ulnar nerve release at the cubital tunnel: A study of 25,977 cases. Journal of Shoulder and Elbow Surgery. 2017;**26**(4):710-715. Available from: http://linkinghub.elsevier.com/retrieve/ pii/S1058274616305730

[49] Camp CL, Tebo CC, Degen RM, Dines JS, Altchek DW, Werner BC. Patient-related risk factors for infection following ulnar nerve release at the cubital tunnel: An analysis of 15,188 cases. Orthopaedic Journal of Sports Medicine. 2018;**6**(5). Available from: http://www.pearldiverinc.com

[50] Friedman RJ, Cochran TP. A clinical and electrophysiological investigation of anterior transposition for ulnar neuropathy at the elbow. Archives of Orthopaedic and Trauma Surgery. 1987;**106**(6):375-380. Available from: http://www.ncbi.nlm.nih.gov/ pubmed/3435238

[51] Krogue JD, Aleem AW, Osei DA, Goldfarb CA, Calfee RP. Predictors of surgical revision after in situ decompression of the ulnar nerve. Journal of Shoulder and Elbow Surgery. 2015;**24**(4):634-639. Available from: https://www.sciencedirect.com/science/ article/pii/S105827461400682X

[52] Gaspar MP, Kane PM, Putthiwara D, Jacoby SM, Osterman AL. Predicting revision following in situ ulnar nerve decompression for patients with idiopathic cubital tunnel syndrome. The Journal of Hand Surgery. 2016;**41**(3):427-435. Available from:

http://linkinghub.elsevier.com/retrieve/ pii/S0363502315015889

[53] Gaspar MP, Jacoby SM, Osterman AL, Kane PM. Risk factors predicting revision surgery after medial epicondylectomy for primary cubital tunnel syndrome. Journal of Shoulder and Elbow Surgery. 2016;**25**(4):681- 687. Available from: https://www. sciencedirect.com/science/article/pii/ S1058274615005959

[54] Roh YH, Kim S, Gong HS, Baek GH. Clinical features affecting the patient-based outcome after minimal medial epicondylectomy for cubital tunnel syndrome. Journal of Plastic, Reconstructive & Aesthetic Surgery. 2018. Available from: https://www. sciencedirect.com/science/article/pii/ S174868151830192X

[55] Murata K, Shih JT, Tsai TM. Causes of ulnar tunnel syndrome: A retrospective study of 31 subjects. The Journal of Hand Surgery. 2003;**28**(4):647-651. Available from: https://ac.els-cdn. com/S0363502303001473/1 s2.0-S0363502303001473-main. pdf?\_tid=5f7bde2c-c9ad-11e7-8e60- 00000aab0f01&acdnat=1510713393\_4d 6ab2b3c461d4f88fc3ee4bc6b97c1f

**15**

**Chapter 2**

*and Leonel Garcia Valdés*

**1. General considerations**

bilateral affection [5].

compress itself [6, 7].

tendon and the nerve [7].

tions is an average of 35 mmHg [6].

Introductory Chapter: Current

*Leonel García Benavides, Miriam Méndez del Villar*

cubital nerves at the forearm, present in 5–10% of the population [1].

State of Carpal Tunnel Syndrome

The carpal tunnel is a fibrous extension that connects the anterior compartment of the forearm with the palm of the hand. It is delimited by the pisiform bone medially, by the hamate bone laterally, and the base of the scaphoid and trapezoid bone and the roof by the dorsal radiocarpal ligaments of the carpus. Through the carpal tunnel, various anatomical structures pass, such as the median nerve (NM), the nine flexor tendons of the fingers and the thumb, the nerve is located on a superficial plane over the tendons and medial to the radio palmar artery, although its trajectory and division has numerous anatomical variant, which present with a frequency of 11% approximately in general population. The principal anatomical variants are the presence of a residual median artery (5% of the population) and the anastomosis of Martin-Gruber, a motor communication between the median and

The American Association of Orthopedic Surgery (AAOS) defines carpal tunnel syndrome as the most common mononeuropathy [2]. It has a prevalence of 3.8% in general population, and has an incidence of 276 for every 100,000 citizens [3, 4]. It affects women in major proportions than men, and 50–60% of all patients have

CTS can be divided into primary or idiopathic, which is associated with repeti-

Other studies have established that idiopathic CTS is caused by a spaced conflict

Other studies have encountered morphological changes in the synovial tissue that surrounds the tendons. The principal findings have been inflammation, edema and fibrosis [7]. Multiple biochemical changes in the proteoglycans have also been reported, which causes a decrease in the capacity of the tendon to deform and

These findings suggest that the changes in the tendons and the synovial tissues caused by repetitive manual activity and aging degeneration, increase the volume of content inside the tunnel, resulting in the compression of the MN, leading eventually to CTS [8]. Another suggested mechanism of lesion is through repetitive microtrauma of the MN caused by alterations on the kinetic movement of the

tive manual activity and secondary, which is associated to other pathologies.

between the limits of the tunnel and the content that passes through it, which increases the pressure inside the tunnel and consequently alters the blood flow to the MN, provoking an inflammatory response and epineural edema. In healthy individuals, the pressure inside the tunnel (with the hand at neutral position) varies from 3 to 5 mm/hg. However, in patients with CTS, this pressure in the same condi-

#### **Chapter 2**

*Peripheral Nerve Disorders and Treatment*

high-resolution ultrasonography to assess ulnar nerve in patients with diabetes mellitus. Journal of Ultrasonography. 2017;**17**:160-166. Available from: http://jultrason.pl/ uploads/dm\_artykuly/jou-2017-0024. http://linkinghub.elsevier.com/retrieve/

[53] Gaspar MP, Jacoby SM, Osterman AL, Kane PM. Risk factors predicting

epicondylectomy for primary cubital tunnel syndrome. Journal of Shoulder and Elbow Surgery. 2016;**25**(4):681- 687. Available from: https://www. sciencedirect.com/science/article/pii/

[54] Roh YH, Kim S, Gong HS, Baek GH.

patient-based outcome after minimal medial epicondylectomy for cubital tunnel syndrome. Journal of Plastic, Reconstructive & Aesthetic Surgery. 2018. Available from: https://www. sciencedirect.com/science/article/pii/

pii/S0363502315015889

S1058274615005959

S174868151830192X

revision surgery after medial

Clinical features affecting the

[55] Murata K, Shih JT, Tsai TM. Causes of ulnar tunnel syndrome: A retrospective study of 31 subjects. The Journal of Hand Surgery. 2003;**28**(4):647-651. Available from: https://ac.els-cdn. com/S0363502303001473/1 s2.0-S0363502303001473-main. pdf?\_tid=5f7bde2c-c9ad-11e7-8e60- 00000aab0f01&acdnat=1510713393\_4d 6ab2b3c461d4f88fc3ee4bc6b97c1f

[48] Camp CL, Ryan CB, Degen RM, Dines JS, Altchek DW, Werner BC. Risk factors for revision surgery following isolated ulnar nerve release at the cubital tunnel: A study of 25,977 cases. Journal of Shoulder and Elbow Surgery. 2017;**26**(4):710-715. Available from: http://linkinghub.elsevier.com/retrieve/

[49] Camp CL, Tebo CC, Degen RM, Dines JS, Altchek DW, Werner BC. Patient-related risk factors for infection following ulnar nerve release at the cubital tunnel: An analysis of 15,188 cases. Orthopaedic Journal of Sports Medicine. 2018;**6**(5). Available from: http://www.pearldiverinc.com

[50] Friedman RJ, Cochran TP. A clinical and electrophysiological investigation of anterior transposition for ulnar neuropathy at the elbow. Archives of Orthopaedic and Trauma Surgery. 1987;**106**(6):375-380. Available from: http://www.ncbi.nlm.nih.gov/

[51] Krogue JD, Aleem AW, Osei DA, Goldfarb CA, Calfee RP. Predictors of surgical revision after in situ decompression of the ulnar nerve. Journal of Shoulder and Elbow Surgery. 2015;**24**(4):634-639. Available from: https://www.sciencedirect.com/science/

article/pii/S105827461400682X

[52] Gaspar MP, Kane PM, Putthiwara D, Jacoby SM, Osterman AL. Predicting revision following in situ ulnar nerve decompression for patients with idiopathic cubital tunnel syndrome. The Journal of Hand Surgery. 2016;**41**(3):427-435. Available from:

pii/S1058274616305730

pubmed/3435238

pdf

**14**

## Introductory Chapter: Current State of Carpal Tunnel Syndrome

*Leonel García Benavides, Miriam Méndez del Villar and Leonel Garcia Valdés*

#### **1. General considerations**

The carpal tunnel is a fibrous extension that connects the anterior compartment of the forearm with the palm of the hand. It is delimited by the pisiform bone medially, by the hamate bone laterally, and the base of the scaphoid and trapezoid bone and the roof by the dorsal radiocarpal ligaments of the carpus. Through the carpal tunnel, various anatomical structures pass, such as the median nerve (NM), the nine flexor tendons of the fingers and the thumb, the nerve is located on a superficial plane over the tendons and medial to the radio palmar artery, although its trajectory and division has numerous anatomical variant, which present with a frequency of 11% approximately in general population. The principal anatomical variants are the presence of a residual median artery (5% of the population) and the anastomosis of Martin-Gruber, a motor communication between the median and cubital nerves at the forearm, present in 5–10% of the population [1].

The American Association of Orthopedic Surgery (AAOS) defines carpal tunnel syndrome as the most common mononeuropathy [2]. It has a prevalence of 3.8% in general population, and has an incidence of 276 for every 100,000 citizens [3, 4]. It affects women in major proportions than men, and 50–60% of all patients have bilateral affection [5].

CTS can be divided into primary or idiopathic, which is associated with repetitive manual activity and secondary, which is associated to other pathologies.

Other studies have established that idiopathic CTS is caused by a spaced conflict between the limits of the tunnel and the content that passes through it, which increases the pressure inside the tunnel and consequently alters the blood flow to the MN, provoking an inflammatory response and epineural edema. In healthy individuals, the pressure inside the tunnel (with the hand at neutral position) varies from 3 to 5 mm/hg. However, in patients with CTS, this pressure in the same conditions is an average of 35 mmHg [6].

Other studies have encountered morphological changes in the synovial tissue that surrounds the tendons. The principal findings have been inflammation, edema and fibrosis [7]. Multiple biochemical changes in the proteoglycans have also been reported, which causes a decrease in the capacity of the tendon to deform and compress itself [6, 7].

These findings suggest that the changes in the tendons and the synovial tissues caused by repetitive manual activity and aging degeneration, increase the volume of content inside the tunnel, resulting in the compression of the MN, leading eventually to CTS [8]. Another suggested mechanism of lesion is through repetitive microtrauma of the MN caused by alterations on the kinetic movement of the tendon and the nerve [7].

The pathologies with a higher prevalence associated to CTS are diabetes mellitus; with a prevalence of 14–30% of the patients, in which a dysfunction of The Schwann cells, alterations of the immune system and microangiopathy have been associated. Pregnancy is associated to diverse alterations of the peripheral nervous system. Amyloidosis through a direct lesion to the MN by amyloid deposits [5]. This book describes not only the prevalence, but also diagnostic methods and treatment efficacy of compressive neuropathies of the median and the ulnar nerves in patients with diabetes mellitus.

The clinical manifestations can be classified into three stages according its severity: first stage: nocturnal paresthesia and pain in the carpal region [3]. The sensorial symptoms and the pain continue through the day and the sensation of a having clumsy hand is added, presenting difficulties to perform precise activities with the hand. Atrophy of the thenar eminence and weakness are present in the final stage [4].

It is common that the patients mention the necessity to shake the hand to try to diminish the symptoms, which is known as Flick's sign [9], which reflects the presence of abnormalities in nerve conduction studies; it has a sensibility and specificity of 93 and 96%, respectively. Due to the variety in the clinical manifestations, we should focus on the new evaluation instruments used with the intent of identifying symptomatology and evolution, such as the Boston questionnaire [10, 11].

Provocative tests are numerous maneuvers that exist to detect CTS, these include Phalen's test, which has a sensibility of 57–91% and a specificity of 33.86%; Reversed Phalen's test, which has a sensibility of 23–60% and a specificity of 64–87%; Tinel's Sign, which has a sensibility of 67% and a specificity of 55–87% and Durkan's Test; which has a sensibility of 64% and a specificity of 83% [12, 13].

To quantitatively establish the electrophysiological state of the nerve and select the definitive treatment, it is required to perform nerve conduction studies, which have a sensibility and specificity of 85 and 94%, respectively, and are realized comparing the findings of the MN to another nerve [2, 14].

#### **2. New approaches to be followed**

This book will approach the current treatment regarding CTS, which can be classified into surgical and non-surgical. The decision of which treatment to follow is difficult and the severity of the symptoms must be taken into consideration. In patients with moderate to severe manifestations, surgical treatment must be considered as the first choice. Non-surgical treatment includes different therapeutic actions such as steroid injections or use of drugs with antioxidant and anti-inflammatory properties. Splinting is recommended before any option of treatment; surgical or non-surgical; the proper application of orthotic splinting is analyzed as well in this book as a special chapter to show the clinical convenience of a novel light guided medical device.

**17**

**Author details**

Leonel García Benavides1,2\*, Miriam Méndez del Villar1

\*Address all correspondence to: drleonelgb@hotmail.com

provided the original work is properly cited.

1 Division of Health Sciences, Cutonala, University of Guadalajara, Jalisco, México

2 Hospital Civil de Guadalajara "Fray Antonio Alcalde", Guadalajara, Jalisco, México

© 2020 The Author(s). Licensee IntechOpen. 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,

and Leonel Garcia Valdés2

*Introductory Chapter: Current State of Carpal Tunnel Syndrome*

*DOI: http://dx.doi.org/10.5772/intechopen.87253*

*Introductory Chapter: Current State of Carpal Tunnel Syndrome DOI: http://dx.doi.org/10.5772/intechopen.87253*

*Peripheral Nerve Disorders and Treatment*

with diabetes mellitus.

final stage [4].

The pathologies with a higher prevalence associated to CTS are diabetes mellitus; with a prevalence of 14–30% of the patients, in which a dysfunction of The Schwann cells, alterations of the immune system and microangiopathy have been associated. Pregnancy is associated to diverse alterations of the peripheral nervous system. Amyloidosis through a direct lesion to the MN by amyloid deposits [5]. This book describes not only the prevalence, but also diagnostic methods and treatment efficacy of compressive neuropathies of the median and the ulnar nerves in patients

The clinical manifestations can be classified into three stages according its severity: first stage: nocturnal paresthesia and pain in the carpal region [3]. The sensorial symptoms and the pain continue through the day and the sensation of a having clumsy hand is added, presenting difficulties to perform precise activities with the hand. Atrophy of the thenar eminence and weakness are present in the

It is common that the patients mention the necessity to shake the hand to try to diminish the symptoms, which is known as Flick's sign [9], which reflects the presence of abnormalities in nerve conduction studies; it has a sensibility and specificity of 93 and 96%, respectively. Due to the variety in the clinical manifestations, we should focus on the new evaluation instruments used with the intent of identifying

Provocative tests are numerous maneuvers that exist to detect CTS, these include Phalen's test, which has a sensibility of 57–91% and a specificity of 33.86%; Reversed Phalen's test, which has a sensibility of 23–60% and a specificity of 64–87%; Tinel's Sign, which has a sensibility of 67% and a specificity of 55–87% and Durkan's Test;

To quantitatively establish the electrophysiological state of the nerve and select the definitive treatment, it is required to perform nerve conduction studies, which have a sensibility and specificity of 85 and 94%, respectively, and are realized

This book will approach the current treatment regarding CTS, which can be classified into surgical and non-surgical. The decision of which treatment to follow is difficult and the severity of the symptoms must be taken into consideration. In patients with moderate to severe manifestations, surgical treatment must be considered as the first choice. Non-surgical treatment includes different therapeutic actions such as steroid injections or use of drugs with antioxidant and anti-inflammatory properties. Splinting is recommended before any option of treatment; surgical or non-surgical; the proper application of orthotic splinting is analyzed as well in this book as a special chapter to show the clinical convenience of a novel

symptomatology and evolution, such as the Boston questionnaire [10, 11].

which has a sensibility of 64% and a specificity of 83% [12, 13].

comparing the findings of the MN to another nerve [2, 14].

**2. New approaches to be followed**

light guided medical device.

**16**

#### **Author details**

Leonel García Benavides1,2\*, Miriam Méndez del Villar1 and Leonel Garcia Valdés2

1 Division of Health Sciences, Cutonala, University of Guadalajara, Jalisco, México

2 Hospital Civil de Guadalajara "Fray Antonio Alcalde", Guadalajara, Jalisco, México

\*Address all correspondence to: drleonelgb@hotmail.com

© 2020 The Author(s). Licensee IntechOpen. 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.

## **References**

[1] Herrera E, Anaya C, Abril AM, Lozano Wilson M, Avellaneda YC, Cruz AM. Anastomosis Martin-Gruber: Aspectos anatómicos y electrofisiológicos. Revista de la Universidad Industrial de Santander. Salud. 2009;**41**(2):157-168. Available from: http://www.scielo.org.co/ scielo.php?script=sci\_arttext&pid=S0121 08072009000200007&lng=en [Accessed: 01 June 2019]

[2] American Academy of Ortopedic Surgeons. Clinical Practice Guidelines on Diagnosis of Carpal Tunnel Syndrome. 1st ed. Rosemont, Illinois: American Academy of Orthopedic Surgeons; 2007. p. 5

[3] Mondelli M, Giannini F, Giacchi M. Carpal tunnel syndrome incidence in a general population. Neurology. 2002;**58**(2):289-294

[4] Bland JD, Rudolfer SM. Clinical surveillance of carpal tunnel syndrome in two areas of the United Kingdom, 1991-2001. Journal of Neurology, Neurosurgery, and Psychiatry. 2003;**74**(12):1674-1679

[5] Le Blanc K, Cestia W. Carpal tunnel syndrome. American Family Physician. 2011;**83**(8):952-958

[6] Werner R, Armstrong T. Carpal tunnel syndrome: Ergonomic risk factors and intracarpal canal pressure, carpal tunnel syndrome. Physical Medicine and Rehabilitation Clinics of North America. 1997;**8**:555-569

[7] Copplieters MW, Alshami AM. Longitudinal excursion and strain in the median nerveduring novel nerve gliding exercises for carpal tunnel syndrome. Journal of Orthopaedic Research. 2007;**25**:972-980

[8] Rojviroj S, Sirichativapee W, Kowsuwon W, Wongwiwat-tananon J, Tamnanthong N, Jeeravipoolvarn P. Pressures in the carpal tunnel. A comparison between patients with carpal tunnel syndrome and normal subjects. Journal of Bone and Joint Surgery. British Volume (London). 1990;**72**:516-518

[9] Pryse-Phillips WE. Validation of a diagnostic sign in carpal tunnel syndrome. Journal of Neurology, Neurosurgery, and Psychiatry. 1984;**47**(8):870-872. DOI: 10.1136/jnnp.47.8.870

[10] Levine DW, Simmons BP, Koris MJ, Daltroy LH, Hohl GG, Fossel AH, et al. A self-administered questionnaire for the assessment of severity of symptoms and functional status in carpal tunnel syndrome. The Journal of Bone and Joint Surgery. American Volume. 1993;**75**(11):1585-1592

[11] Miyamoto Meirelles L, Gomes dos santos JB, Leonel dos santos LL, Branco MA, Faloppa F, Mattioli Leite V, Fernandes CH. Evaluation of Boston questionnaire applied at late postoperative period of carpal tunnel syndrome operated with the Paine retinaculatome through palmar port. Acta Ortopédica Brasileira. 2006;**14**(3):126-132

[12] D'Arcy CA, McGee S. Does this patient have carpal tunnel syndrome? Journal of the American Medical Association. 2000;**283**(23):3110-3117. DOI: 10.1001/jama.283.23.3110

[13] Mac Dermid JC, Wessel J. Clinical diagnosis of carpal tunnel syndrome: A systematic review. Journal of Hand Therapy. 2004;**17**:309-319. DOI: 10.1197/j.jht.2004.02.015

[14] de Jesus Filho AG, do Nascimento BF, Amorim Mde C, Naus RA, Loures Ede A, Moratelli L. Comparative study between physical examination, electroneuromyography and ultrasonography in diagnosing carpal tunnel syndrome. Revista Brasileira de Ortopedia. 2014;**49**(5):446-451. DOI: 10.1016/j.rboe.2014.09.002

**19**

**Chapter 3**

**Abstract**

**1. Introduction**

sized and difficult nerves [2].

**2. Magnetic resonance imaging**

on Sonography

Peripheral Nerve Imaging: Focus

*Mohamed A. Bedewi, Daniele Coraci and Sherine Swify*

comparison with the contralateral side at the same setting.

**Keywords:** peripheral, ultrasound, imaging, peripheral nerves

The diagnosis of different peripheral nerve disorders is basically established by electrodiagnostic tests; the assessment of the function of peripheral nerve disorders is estimated by nerve conduction tests (NCT) and electromyography (EMG). The need for more information about nerve morphology mandated the usage of more diagnostic tools. This role is now achieved by means of peripheral nerve imaging consisting mainly of magnetic resonance imaging (MRI) and ultrasonography. In this chapter we will clarify the role of imaging in the diagnosis of peripheral nerve disorders, concentrating more on the role of modern high-resolution ultrasound, considering its advantages like cheap price, dynamic ability, and possibility of

Diseases of the peripheral nerves are common in the setting of clinical practice. The traditional way of the diagnosis of peripheral nerve disorders is made by neurophysiology and clinical assessment. These tools give information about the functional status of the involved nerve, the presence of nerve damage, and the degree of demyelination [1]; however, the need for more information about nerve morphology mandated the usage of more diagnostic tools. This role is now enhanced by means of peripheral nerve imaging consisting mainly of magnetic resonance imaging (MRI) and ultrasonography, with special ability to assess small-

Magnetic resonance imaging is a noninvasive imaging technique that has the ability to differentiate pathological peripheral nerves from healthy ones. MRI is also useful in the demonstration of the topographic anatomy of the peripheral nerves. MRI uses a strong magnetic field to create a net magnetization in the involved tissues, then disruption of this magnetization with pulse, and change of direction resulting in T1- and T2-weighted images. Basic MRI study of the peripheral nerves uses T2-weighted images (with fat suppression) detecting the site of injury as sharp hyperintense (as a result of local edema), in comparison to the nearby healthy nerves which appear as isointense. As nerve regeneration resumes, the degree of hyperintensity will gradually return to isointesntiy. Fat suppression is used for

#### **Chapter 3**
