**3. Biomechanics of the central nervous system**

The brainstem (mesencephalon, pons, medulla oblongata), cranial nerves V-XII, spinal cord, cauda equina, and nerve roots may collectively be referred to as the pons-cord tissue tract. The static and dynamic characteristics of the pons-cord tract constitutes a self-contained compartment of biomechanics [8, 9, 67]. This results from the way the cord is maintained within the canal by its many attachments: from above (being continuous with the brainstem), from below (sacral and coccyx attachment through the cauda equina and filum terminale), as well as throughout its length (intermittent dural attachments to the posterior longitudinal ligament,

**53**

**Figure 4.**

*The Influence of Sagittal Plane Spine Alignment on Neurophysiology and Sensorimotor Control…*

ventral attachments of the nerve root sleeves exiting the intervertebral foramina, and bilateral dentate ligament attachments ranging from the upper cervical region down to the level of L1). Under relatively normal static posture without pathological processes, spine dynamics produce normal or 'physiologic' tension as transmitted by its constraining elements, and without neurological compromise (**Figure 4**) [8, 9, 68]. Only when normal neurodynamic aspects of the so-called pons-cord tract are understood can neuropathology from adverse tensions be fully understood. As Breig states "Internal deformation of the tissue cannot be ruled out as a factor in any disease of the nervous system even in inflammatory and degenerative conditions of the hindbrain, cord and associated nerves, and in some cases it will be of primary pathologic significance" [8] (p. 12). A key concept is that under normal circumstances, normal movements of the spine involve physiologic unfolding and folding of the cord and nerve roots. Head flexion causes instantaneous unfolding and normal elasticity of the neural tissues and head extension causes elastic rebound and a re-folding of the cord and nerve roots (**Figure 4**). In this way the CNS can preserve normal function while accommodating differing spinal positions. Breig also found that movements of the cord occur at the location of movement as well as throughout the entire pons-cord tract; cervical motions produce strains (deformations) caudally down to the cauda equina and movements of the lower spine cause strains as far up as the cervical cord and brainstem. In fact, deformation of the brain tissue below the tentorium (which can affect cranial nerves V-XII [8]) within the cerebellum occurs to accommodate spine movements (particularly maximal

All ventral flexion movements throughout the spine (i.e. cervical, thoracic, lumbar) cause a lengthening of the spinal canal, and therefore, a transmission of axial tension onto the cord. Pathological processes, such as disc herniations and bone spurs, if severe enough, interfere with the pons-cord tract biomechanics [69, 70], where the normal tension transmitted by the pons-cord restraining elements may then be referred to as 'pathological' tension [71]. Independent but equally as significant, abnormal spinal postures may create adverse tension within the neural elements as well. For instance, Stein found that "in a deformed kyphotic cervical spine, even a 'normal' amount of movement in the cervical spine may cause compression of the spinal cord" [72]. This is because the spinal cord adopts the

*Left: Physiologic folding of the cord and nerve roots in normal lordosis. Right: A forward flexion in those with normal lordosis causes normal unfolding and elasticity of the pons, cord and nerve roots that remain 'physiologic' or within tolerable tensions that do not overload the nervous system (Courtesy CBP Seminars).*

*DOI: http://dx.doi.org/10.5772/intechopen.95890*

functional positions).

length of the bony canal [73].

### *The Influence of Sagittal Plane Spine Alignment on Neurophysiology and Sensorimotor Control… DOI: http://dx.doi.org/10.5772/intechopen.95890*

ventral attachments of the nerve root sleeves exiting the intervertebral foramina, and bilateral dentate ligament attachments ranging from the upper cervical region down to the level of L1). Under relatively normal static posture without pathological processes, spine dynamics produce normal or 'physiologic' tension as transmitted by its constraining elements, and without neurological compromise (**Figure 4**) [8, 9, 68].

Only when normal neurodynamic aspects of the so-called pons-cord tract are understood can neuropathology from adverse tensions be fully understood. As Breig states "Internal deformation of the tissue cannot be ruled out as a factor in any disease of the nervous system even in inflammatory and degenerative conditions of the hindbrain, cord and associated nerves, and in some cases it will be of primary pathologic significance" [8] (p. 12). A key concept is that under normal circumstances, normal movements of the spine involve physiologic unfolding and folding of the cord and nerve roots. Head flexion causes instantaneous unfolding and normal elasticity of the neural tissues and head extension causes elastic rebound and a re-folding of the cord and nerve roots (**Figure 4**). In this way the CNS can preserve normal function while accommodating differing spinal positions. Breig also found that movements of the cord occur at the location of movement as well as throughout the entire pons-cord tract; cervical motions produce strains (deformations) caudally down to the cauda equina and movements of the lower spine cause strains as far up as the cervical cord and brainstem. In fact, deformation of the brain tissue below the tentorium (which can affect cranial nerves V-XII [8]) within the cerebellum occurs to accommodate spine movements (particularly maximal functional positions).

All ventral flexion movements throughout the spine (i.e. cervical, thoracic, lumbar) cause a lengthening of the spinal canal, and therefore, a transmission of axial tension onto the cord. Pathological processes, such as disc herniations and bone spurs, if severe enough, interfere with the pons-cord tract biomechanics [69, 70], where the normal tension transmitted by the pons-cord restraining elements may then be referred to as 'pathological' tension [71]. Independent but equally as significant, abnormal spinal postures may create adverse tension within the neural elements as well. For instance, Stein found that "in a deformed kyphotic cervical spine, even a 'normal' amount of movement in the cervical spine may cause compression of the spinal cord" [72]. This is because the spinal cord adopts the length of the bony canal [73].

### **Figure 4.**

*Left: Physiologic folding of the cord and nerve roots in normal lordosis. Right: A forward flexion in those with normal lordosis causes normal unfolding and elasticity of the pons, cord and nerve roots that remain 'physiologic' or within tolerable tensions that do not overload the nervous system (Courtesy CBP Seminars).*

*Therapy Approaches in Neurological Disorders*

that proper assessment of the spine includes the whole spine, that is, the cervical, thoracic and lumbar regions and femur heads. This is because spine balance and compensation mechanisms involve the whole spine; thus, regional X-rays to the 'problem area' can mislead treatment and not account for distal spinopelvic compensations that need to be considered prior to initiating a trial of spine care by these

*Three patients demonstrating dramatically different spine alignment patterns. Left: Excessive lumbar hyperlordosis, L4 anterolisthesis, and excessive anterior sagittal balance in a mid-aged female with disabling low back pain; Middle: Excessive thoracolumbar kyphosis and early degenerative changes in a mid-aged male; Right: Excessive thoracic hyperkyphosis in a young male with Scheuermann's disease. Red line is contiguous with posterior vertebral body margins; green line represents Harrison normal spinal model (Courtesy PAO).*

The brainstem (mesencephalon, pons, medulla oblongata), cranial nerves V-XII,

spinal cord, cauda equina, and nerve roots may collectively be referred to as the pons-cord tissue tract. The static and dynamic characteristics of the pons-cord tract constitutes a self-contained compartment of biomechanics [8, 9, 67]. This results from the way the cord is maintained within the canal by its many attachments: from above (being continuous with the brainstem), from below (sacral and coccyx attachment through the cauda equina and filum terminale), as well as throughout its length (intermittent dural attachments to the posterior longitudinal ligament,

**3. Biomechanics of the central nervous system**

**52**

methods.

**Figure 3.**

Further, as suggested by Harrison et al. [74] static neutral postures or dynamically adopted combinations of postures; that is, rotations and translations of the head, thorax, or pelvis (**Figures 5** and **6**) [36], exert larger stresses and strains onto the pons-cord tissue tract. Thus, it can be deduced that the combination of pathological processes (bone spurs, disc herniations, etc.) and aberrations in posture (forward head posture, thoracic hyperkyphosis, etc.) may disrupt normal CNS biomechanics, and at levels below that at which either factor acting alone would elicit neurological symptoms. As it can be presumed when a patient has an accumulation of forward flexed spine positions, such as severe thoracic hyperkyphosis (THK) posture for example, the amount of spinal canal lengthening can be great and supersede the 'normal' or physiologic amount of unfolding and elastic deformation available within the pons-cord system. In this situation, normal physiologic tensions transition to become pathologic tensions causing intermittent over-stretching and over-straining of the tissues and ultimately, causing or exacerbating neurologic symptoms.

### **Figure 5.**

*If the head, thoracic cage, and pelvis are considered rigid bodies, then the possible rotations in 3-dimensions are illustrated. Flexion and extension are rotations on the x-axis, axial rotation is about the y-axis, and lateral flexion is rotation about the z-axis (Courtesy CBP Seminars).*

**55**

**Figure 6.**

*The Influence of Sagittal Plane Spine Alignment on Neurophysiology and Sensorimotor Control…*

**4. Pathophysiologic mechanisms from adverse CNS tension**

Understanding the normal biomechanics of the CNS lays the foundation for the understanding of postural-induced neurological signs and symptoms. As discussed, two main events may individually, or in combination, lead to excessive stresses (longitudinal, torsional, pure bending, shear) and strains (longitudinal cross-sectional) that are sufficient to produce symptoms. In words, poor postures (lengthened spinal canal via forward flexed spinal positions) and space occupying lesions (bone spurs, intervertebral disc prolapse, etc.) combine to produce symptomatology. The greater the spinal canal is flexed, or as discussed, the presence of combinations of rotations and translations in posture, the greater the forced

*If the head, thoracic cage, and pelvis are considered rigid bodies, then the possible translations in 3-dimensions are illustrated. Lateral translations occur along the x-axis, vertical translations occur along the y-axis, and anterior–posterior translations (protraction-retraction) occurs along the z-axis (Courtesy CBP Seminars).*

*DOI: http://dx.doi.org/10.5772/intechopen.95890*

*The Influence of Sagittal Plane Spine Alignment on Neurophysiology and Sensorimotor Control… DOI: http://dx.doi.org/10.5772/intechopen.95890*

**Figure 6.** *If the head, thoracic cage, and pelvis are considered rigid bodies, then the possible translations in 3-dimensions are illustrated. Lateral translations occur along the x-axis, vertical translations occur along the y-axis, and anterior–posterior translations (protraction-retraction) occurs along the z-axis (Courtesy CBP Seminars).*

### **4. Pathophysiologic mechanisms from adverse CNS tension**

Understanding the normal biomechanics of the CNS lays the foundation for the understanding of postural-induced neurological signs and symptoms. As discussed, two main events may individually, or in combination, lead to excessive stresses (longitudinal, torsional, pure bending, shear) and strains (longitudinal cross-sectional) that are sufficient to produce symptoms. In words, poor postures (lengthened spinal canal via forward flexed spinal positions) and space occupying lesions (bone spurs, intervertebral disc prolapse, etc.) combine to produce symptomatology. The greater the spinal canal is flexed, or as discussed, the presence of combinations of rotations and translations in posture, the greater the forced

*Therapy Approaches in Neurological Disorders*

symptoms.

Further, as suggested by Harrison et al. [74] static neutral postures or dynamically adopted combinations of postures; that is, rotations and translations of the head, thorax, or pelvis (**Figures 5** and **6**) [36], exert larger stresses and strains onto the pons-cord tissue tract. Thus, it can be deduced that the combination of pathological processes (bone spurs, disc herniations, etc.) and aberrations in posture (forward head posture, thoracic hyperkyphosis, etc.) may disrupt normal CNS biomechanics, and at levels below that at which either factor acting alone would elicit neurological symptoms. As it can be presumed when a patient has an accumulation of forward flexed spine positions, such as severe thoracic hyperkyphosis (THK) posture for example, the amount of spinal canal lengthening can be great and supersede the 'normal' or physiologic amount of unfolding and elastic deformation available within the pons-cord system. In this situation, normal physiologic tensions transition to become pathologic tensions causing intermittent over-stretching and over-straining of the tissues and ultimately, causing or exacerbating neurologic

*If the head, thoracic cage, and pelvis are considered rigid bodies, then the possible rotations in 3-dimensions are illustrated. Flexion and extension are rotations on the x-axis, axial rotation is about the y-axis, and lateral* 

*flexion is rotation about the z-axis (Courtesy CBP Seminars).*

**54**

**Figure 5.**

unfolding and elastically stretched pons-cord tract (**Figure 7**). With the addition of space occupying lesions, patients having deviations in postural alignment become much more likely to succumb to various pressure mechanisms, or how the nervous tissue is compressed upon certain positions and movements.

It is important to realize that those patients with poor spinal posture may at times be in positions that are tolerable by the pons-cord tract (i.e. not overstretched), and at other times perform movements that dynamically lengthen the spinal canal causing a pivotal transition to over-stress and over-strain the system (i.e. dynamic stress and strain). Therefore, successful symptomatic relief resulting from postural correction to a patient suffering from neurological complaints may be elucidated. Although some spinal pathologies will not change (e.g. bone spurs), the reduction of forward flexion of the neutral postural position (e.g. increasing cervical/lumbar hypo-lordosis; reducing thoracic hyper-kyphosis) will change the resting, and therefore the dynamic tensions throughout the pons-cord tract sufficiently enough to reduce the tensions from surpassing some pathological tension threshold (maintaining physiologic or normal tensions), and therefore alleviate neurologic symptomatology [74, 75].

How does adverse mechanical tensions within the CNS produce symptoms? Ultimately, pathological CNS tensions affect the vascular supply and therefore the perfusion of the neural tissues or they may affect the actual nerve conduction ability of the nerve cells (causing hyper or hypo function). Mathematically, perfusion = mean arteriole pressure (MAP) – cord interstitial pressure (CIP) [76]. Thus, for perfusion to remain adequate, the MAP must remain greater than CIP. However, as discussed by Harrison et al. [77], an increase in CIP can be caused by at least two forces, a longitudinal force causing unfolding and elastic elongation of the cord, and a transverse force usually by the cord being thrust into the posterior margin of the vertebral body at the anterior portion of the spinal canal. As stated, Stein found that cervical kyphosis, posture subluxation alone is enough to interfere with cord conduction [72], but with an accompanying space occupying lesion the likelihood for a transverse cord/nerve compression pressure mechanism to limit perfusion and compromise neural function is much greater.

### **Figure 7.**

*Left: Cervical kyphosis subluxation in neutral posture results in the unfolding and elastic pre-tension present prior to flexion. Right: Forward flexion of a kyphotic neck may result in 'pathologic' or pons-cord-nerve root tensions that exceed physiologic limits and results in neurologic symptoms; particularly in the presence of a space-occupying lesion such as a bone spur or intervertebral disc prolapse (Courtesy CBP Seminars).*

**57**

**Figure 8.**

*showed no improvement in central conduction time.*

*The Influence of Sagittal Plane Spine Alignment on Neurophysiology and Sensorimotor Control…*

There have been several clinical controlled trials documenting the association with improved postural parameters (e.g. increasing cervical lordosis, increasing lumbar lordosis, decreasing thoracic hyperkyphosis) translating into improved physiological measures including specific tests indicative of neurologic function

• Dermatomal somatosensory evoked potentials (DSSEPs) (**Figures 9** and **10**);

*Central conduction time (N13-N20) also known as spinal cord velocity. In the top figure, a representative example of central conduction time (N13-N20) at three intervals of measurement: baseline, following 10-weeks of treatment, and 1-year follow-up. This is from the study by Moustafa et al. [13] on symptomatic patients with cervical spine disc herniation. Follow correction of the cervical lordosis, a 20% change in central conduction speed is shown in milliseconds (m sec) indicating a faster more efficient response. In the bottom graph a representative sample from the study of Moustafa et al. [78] is shown. Here, in asymptomatic participants, correction of the cervical lordosis and anterior head posture was found to result in a 10% faster response in the central conduction time potential. Comparative and placebo control groups not attaining spine correction* 

**5. Postural correction to treat neurologic disorders by reducing** 

• Central somatosensory conduction time N13-N20 (**Figure 8**);

• Sensorimotor control measures (**Figures 11** and **12**);

• Sympathetic skin resistance response (**Figure 13**).

*DOI: http://dx.doi.org/10.5772/intechopen.95890*

**pons-cord tensions**

[10–16]. These measures include:

• H-reflex;

*The Influence of Sagittal Plane Spine Alignment on Neurophysiology and Sensorimotor Control… DOI: http://dx.doi.org/10.5772/intechopen.95890*
