biomechanics_of_the_cns.pdf

Journal of Manipulative and Physiological TherapeuticsVolume 22 • Number 6 • July/August 1999

0161-4754/99/$8.00 + 0 76/1/99793 © 1999 JMPT

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INTRODUCTIONIn Part II of this review, neural tissue strains resulting

from postural loads were discussed.1 Considering theamount of deformation that can occur in some areas of thecentral nervous system (CNS) and related structures, it isapparent that adaptive mechanisms are needed to maintainadequate perfusion so that normal neural physiology mayproceed unimpaired. As examples, the area where the car-diac and respiratory nuclei are located (brainstem) deformsmore than the entire thoracic spinal cord during posturalrotations and axial translations and some nerve roots canhave strains up to 30% during spinal canal lengthening.1

Although spinal movement and the consequent tissuedeformations are imperative for the function and health ofall spinal tissues, long-term consequences may result ifaltered positions or stresses are maintained for prolonged

periods. Long-term stresses have been associated with theformation and occurrence of ligament hypertrophy and ossi-fication.2,3 Altered alignment of the spine, abnormal rota-tion, and translation of human posture (see Figs 4 and 5 inPart I of this Review), are known to increase the rate of boneformation and can lead to osteophyte formation4,5 and earlydisk degeneration.6 There is reason to believe that the samephenomenon of tissue loading and degenerative changes isapplicable to the nervous system.7 Consequently, an under-standing of the effects of neural and vascular stresses andstrains that occur during canal changes with postural loadsand their relationship to physiology and myelopathy is clini-cally relevant. This review will address these issues.However, the reader should realize that there are severalstudies providing descriptive anatomy of the spinal cord, butthere is a complete lack of detailed quantitative anatomy.

DISCUSSIONCirculatory Supply to the Cord

Neural tissue needs oxygen and various other nutrients tomaintain optimum structure and function.8,9 The spinal cordrequires large amounts of energy, even under resting condi-tions. Energy consumption is required for “cellular biosyn-thesis and neurotransmitter metabolism, maintenance ofionic pumps, and axoplasmic transport.”8 The CNS is sup-plied via intrinsic vasculature and by diffusion from thecerebrospinal fluid (CFS) system. There is evidence to sug-gest in scoliosis that altered alignment of the spinal column

aPrivate practice, Elko, Nevada.bProfessor emeritus, chairman emeritus, Department of Rehabili-

tation & Physical Medicine, University of Southern California Med-ical School, Pacific Palisades, California.

cCBP Nonprofit, Inc, Harvest, Alabama.dPrivate practice, Normal, Illinois.Submit reprint requests to: Deed E. Harrison, DC, 123 Second

St, Elko, NV 89801.Paper submitted February 27, 1998; in revised form April 13,

1998.Supported by CBP Nonprofit, Inc, Harvest, AL.

REVIEWS OF THE LITERATURE

A Review of Biomechanics of the Central Nervous System—Part III: Spinal Cord Stresses fromPostural Loads and Their Neurologic EffectsDeed E. Harrison, DC,a Rene Cailliet, MD,b Donald D. Harrison, PhD, DC,c Stephan J.Troyanovich, DC,d and Sanghak O. Harrison, DCc

ABSTRACTObjective: To review literature pertaining to

neurologic disorders stemming from abnor-mal postures of the spine.

Data Collection: A hand search of availablereference texts and a computer search of lit-erature from Index Medicus sources was per-formed, with special emphasis placed onspinal cord stresses and strains caused by vari-ous postural rotations and translations of the skull,thorax, and pelvis.

Results: Spinal postures will often deform the neural ele-ments within the spinal canal. Spinal postures can be brokendown into four types of loading: axial, pure bending, torsion,and transverse, which cause normal and shear stresses andstrains in the neural tissues and blood vessels. Prolonged stress-es and strains in the neural elements cause a multitude of dis-ease processes.

Conclusion: Four types of postural loads create avariety of stresses and strains in the neural tis-sue, depending on the exact magnitude and di-rection of the forces. Transverse loading is themost complex load. The stresses and strains inthe neural elements and vascular supply aredirectly related to the function of the sensory,

motor, and autonomic nervous systems. Theliterature indicates that prolonged loading of

the neural tissue may lead to a wide variety of de-generative disorders or symptoms. The most offen-

sive postural loading of the central nervous system andrelated structures occurs in any procedure or position requir-

ing spinal flexion. Thus flexion traction, rehabilitation positions,exercises, spinal manipulation, and surgical fusions in any posi-tion other than lordosis for the cervical and lumbar spines shouldbe questioned. (J Manipulative Physiol Ther 1999;22:399-410)

Key Indexing Terms: Spinal Canal; Myelopathy; Multiple Scle-rosis; Posture; Biomechanics; Nerve

will directly impair the blood flow to the spinal cordmeningeal complex.10

The vascular system of the spinal cord is extensive.Briefly, the vessels include the anterior spinal artery, twoposterior spinal arteries, transverse or circumferential pialplexus (arising from the anterior and posterior arteries), andcentral arteries (running anterior to posterior from the ante-rior and posterior spinal arteries). The nerve roots are sup-plied by the anterior and posterior medullary arteries and theanterior and posterior radicular arteries.8 The above arteriesare also accompanied by their associated veins (Fig 1).

The spinal cord has perivascular spaces, shaped in rhom-boid networks, which act like spinal cord lymph ducts.These spaces channel CSF in and out of the spinal cord tis-sue. The deformations that these channels undergo duringspinal canal and, hence, spinal cord lengthening and short-ening act as a mechanical pump for fluid flow.7,11 Spinal

movements act to pump a new supply of oxygen, and nutri-ent-enriched CSF is brought in around the cellular compo-nents, and metabolic waste products are carried away to berecycled or discarded. This is a normal mechanical event inthe pons-cord tract that occurs with respiration, with pulsa-tions of the vascular tissue, and during healthy movementsof the spinal column.7,11

Blood Vessel and Cerebrospinal Space DeformationsThe vascular components of the pons-cord tract are subject

to the similar physiological forces that the neural tissue ele-ments are. The elongation of the spinal cord from flexion ofthe spine results in increased strain of the longitudinal vesselsof the cord. The anterior vessels will be drawn out and havea slightly decreased lumen size, whereas the posterior spinalarteries tend to zigzag and are put under slight tension whenelongation of the cord takes place in cervical flexion.


CNS Deformations III • Harrison et al

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Fig 1. Circulatory system of the spinal cord. Starting from the outside the circulatory system for thecord and nerve roots is depicted. The surface of the dura is drained by the internal vertebral venousplexus. The space between the dura mater and the arachnoid contains only small capillaries, butbetween the arachnoid and pia mater is the arachnoid space for the CSF. There are vertical anteriorand posterior arteries and veins, AP sulcal arteries and veins (some texts call these “central” arter-ies and veins), and transverse arteries and veins. The spinal arteries originate at the level of eachspinal nerve and have branches of the medullary and radicular arteries that connect with the cir-cumferential arterial vasocorona. Different combinations of these vessels and arachnoid space canbe deformed in different postural loads and pathologic conditions.

Breig7 demonstrated that extension of the skull caused allthe vessels to be wavy, relaxed in form, and full of blood. Withflexion the vessels have a straightened course and appear tohave a decreased blood supply because of a narrowing of thelumen. The transverse or circumferential pial vessels becomesignificantly stretched because the transverse dimension ofthe cord is increased with increasing tension in the cord. Thismight seem contradictory in that tension in the y-axis direc-tion should narrow the dimension in the transverse plane.However, the dentate ligaments, situated bilaterally, restrictx-axis narrowing, which causes anterior-posterior (AP) nar-rowing and tension left to right (Fig 2).

The spinal pial vessels, however, have slightly differentforces acting on them.7 There is a direct stretch acting (alongthe long axis of the vessel) in the lateral direction, whichwill reduce the cross-sectional area. Additionally, there is atensile force exerted on either side of the short axis (AP andsuperior to inferior directions resulting from Poisson’seffect) as a result of longitudinal elongation of the cord. Fig2 illustrates the reduction in cross-sectional area affectingthese vessels during flexion. This second component is addi-tive to the reduction in the lumen size of the vessel becauseit tends to force the lumen walls together from outside toinside. With increasing tension from increasing flexion, thepial vessels may become completely occluded. Examples ofthese vessels would be the lateral branches of the centralarteries and the transverse pial plexus.

In contrast the vessels running primarily in the AP dimen-sion of the cord will have an increased lumen size and berelaxed in form on flexion and will be slightly tensed inextension.7 The central arteries and veins are examples ofAP vessels. Fig 1 illustrates that these vessels are in linewith the narrowing cross-section, which is due to Poisson’seffect during flexion, because the dentate ligaments hold thecord side-to-side. Poisson’s effect directly applies to the bio-mechanics of the spinal cord in flexion/extension. Whenrelaxed, the cord has a larger cross-section (AP dimension).When stretched, the cord has a reduced AP dimension.12

The blood vessels of the dorsal and ventral roots will alsodeform with postural changes. The radicular and medullaryarteries and veins will be under tension and thus narrowed,with an increase in spinal canal length and will be relaxed inthe extended posture of the pons-cord tract.7,13-15 However,depending on the level, as well as which components of thespine are flexed, individual nerve roots and their vessels maybe strained more than others.

The vast majority of the cerebrospinal fluid pulse waveoriginates from pulsations of the arteries and veins supply-ing the spinal cord and canal.11 The pulsation wave and thepumping action of the cord resulting from respiration maydecrease or diminish such that it is no longer visible withincreasing tension in the cord from flexion.7,16 When anabnormal static posture is maintained, such as kyphosis ofthe cervical or lumbar spines or increased kyphosis of thethorax, then this normal pumping action of the cord isimpaired as a result of the inability of the pons-cord tissue torelax.

Adverse Tension and Neural DysfunctionBreig7 stated that increased tension in the spinal cord tis-

sues might be a primary mechanism leading to neurologicdysfunction. It has been found that neural axoplasm hasthixotropic properties, which indicates that lack of motion orincreased constant strain will increase the viscosity of fluidflow and may slow or impair neural transport mechanisms.17

Several investigators have studied spinal column/spinal corddistraction to clarify the relation between tension and neu-ronal dysfunction.14,15,18-22 Fujita and Yamamoto19 studiedthe effect of lumbosacral traction in 50 dogs. Here tractionwas applied to the filum terminale externum, internum, duraltube, and conus medullaris. All areas where traction was ap-plied showed an initial augmentation of spinal-evoked po-tentials suggestive of early stages of cord impairment. Othershave shown and verified this finding.23 The amplitude ofspinal-evoked potentials changed earlier and were larger forthe filum terminale internum traction than for filum terminale



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Fig 2. During traction of the cord, the cross-section of the cord isreduced. Poisson’s ratio is the absolute value of the lateral andaxial strains during axial loading and is between 0 and 1/2. Thisratio being close to 0.5 is indicative of incompressibility. Becausesoft tissues of the body are mostly water, such structures as thespinal cord tend to conserve volume when stretched by reducing thecross-sectional area. A, Poisson’s effect is depicted as if the cordwas a homogeneous material without lateral supports. B, However,the dentate ligaments attach to the cord laterally and do not allowthe cord cross-sectional area to reduce in that direction. Thus thecord reduces in the AP dimension when tractioned longitudinally,and tension develops along the x-axis in the cord because of thedentate ligaments.

B

A

externum. Traction of the dural tube and the conus showedsimilar tendencies. Traction on these structures altered theevoked potentials of the upper cervical cord function anddysfunction was also found in the nerve root potentials (thesefindings correlate with the posture-dependent biomechanicaldeformations discussed in Part II of this Review1).

Yamada et al21,22 used human beings and animals in anattempt to clarify the effect of traction on the filum and lum-bosacral cord and its relationship to the pathophysiology oftethered cord syndrome. The underlying mechanism of thisdisorder was found to be a derangement of neural tissuemetabolism caused by longitudinal tensile stress. Specifi-cally, the oxidative metabolism of the mitochondria wasfound to be impaired. Because neurons and glial cells relyentirely on energy derived from converting intramitochondr-ial adenosine diphosphate phosphorylation to adenosine tri-phosphate (ATP), any change in the metabolic efficiency ofcellular mitochondria is likely to lead to progressive neu-ronal dysfunction.8,21

The pons-cord tract (mesencephalon, pons, medullaoblongata, spinal cord, nerve roots and associated cranialnerves 5-12) will develop increased intramedullary pressure,increased CSF pressure, and increased intrafascicular pres-sure (inside the neural cell) because of stretch or tensileloads.7,24-28 Laplace’s law predicts that cord interstitial pres-sure (CIP) will elevate during spinal cord elongation, and, infact, this linear relationship has been demonstrated.25

Increased CIP is a known cause of compartment syndrome,a hypoperfusion syndrome, and is related to spinal cord per-fusion pressure by the equation (Perfusion = Mean arteriolepressure – CIP).25 From this equation, it is apparent that asthe CIP is increased, the perfusion of the cord (the exchangeof oxygen and metabolic materials to and from the cord) isreduced. This correlates well with the above findings ofYamada et al21,22 concerning the reduced mitochondrialmetabolism in tethered cord syndrome.

Increased pressure in or around the cord is known to causea decrease of afferent and efferent impulse conduction andwill increase the risk of damage to the neural and supportingtissues.25,29,30 Jarzem et al25 measured spinal cord blood flowand somatosensory-evoked potentials (SSEP) during spinalcord distraction in dogs. Distraction was carried out with stepincrements by use of a Harrington rod. Each step was held for20 to 30 minutes and was associated with a 10 mm Hg in-crease in CIP. Significantly, a fall in the SSEP did not occuruntil 20 to 30 minutes of maintained distraction (note: the 20-to 30-minute time frame is crucial because most of the stress-relaxation and creep occurs in this period, thus implying thatany remaining pressure increase and loss of evoked poten-tials will be present until tensile load is released).31 At thepressure of 47 mm Hg (average pressure), a simultaneous de-crease in spinal cord blood flow and somatosensory evokedpotentials occurred. Close scrutiny, however, reveals that theauthors define a significant fall in the SSEP as 50% orgreater; 47 mm Hg was the pressure that was required to de-crease the spinal cord blood flow to 27% of the original valueand to completely abolish the evoked potentials. Smaller

changes in blood flow occurred at much lower pressures,with its significance unknown.

Altering the cerebrospinal fluid pressure is known toaffect spinal cord blood flow. Raising the cerebrospinal fluidpressure by 15 mm Hg and 35 mm Hg was found to cause a25% and 40% reduction in the spinal cord blood flow,respectively.32

Kwan et al31 applied axial tensile loads to the peripheralnerves of rabbits. The nerves were stretched 6% and 12%beyond the resting length and held for 1 hour while com-pound nerve action potentials (CNAP) were recorded. At alongitudinal strain of 6%, the amplitude of the CNAPremained stable for 20 minutes, after which they decreasedto 60% of baseline by 1 hour. At a strain of 12%, the CNAPdecreased to 65% of baseline by 10 minutes and to near zeroby 1 hour. These numbers are slightly less than the 8% and15% found by Lundborg and Rydevik33 in a similar study. Itis noted that the peripheral nerves contain perineurium,which is the primary load carrying structure. This structureis absent from the CNS, indicating that lower strains mayadversely affect the CNS in comparison to the peripheralnervous system (PNS). The posture-dependent deformationsof the pons-cord system, discussed earlier, are well withinand may be above the 6% to 12% strain level (describedabove) depending on which posture is maintained and atwhich segmental level.

Postural Changes and Neural DysfunctionNow, the question must be asked, do changes in posture

or spinal canal length impart enough stress and strain to thepons-cord tract to increase pressure and decrease blood flowand cord perfusion? Several studies are relevant to this issue.It is well documented that distraction instrumentation, suchas those used in surgery or traction devices, produces signif-icant losses of lumbar and cervical curvatures.34 In addition,spinal column distraction results in a reduction of afferentand efferent impulse conduction, detected by somatosenso-ry-evoked potentials and neurogenic motor-evoked poten-tials.18 Significantly, in the baboon, Lew et al35 showed thatthe spinal cord elongation and displacement caused by trac-tion forces are consistently less than that produced by cervi-cal flexion. Breig’s7 case studies suggest that prolonged pos-tural deformities, such as cervical kyphosis, may result inthe same neuronal dysfunctions that occur with distractioninstrumentation applied to the spine, spinal cord, or thosethat occur in tethered cord syndrome. Although relativelyfew studies exist on this information besides Breig’s7 stud-ies, they are worth discussing.

Physiological changes are known to occur in astronautsexposed to microgravity conditions (space flight).20 Underthese conditions the spine is decompressed, which results inheight increases of up to 7 cm. This increase in spinal col-umn length occurs as a result of straightening of the sagittalplane curves and an increase in disk height. We note that 7cm is the maximum range of spinal cord lengthening duringflexion of the spine.7 This results in considerable longitudi-nal stress and strain of the spinal cord and was proposed as a



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mechanism to explain the neurologic dysfunctions found inastronauts, referred to as “microgravity-related physiologicphenomena.” Microgravity-related physiologic phenomenaconsists of nutritional, metabolic, cardiovascular, neuro-vestibular, and otolith-spinal reflex changes; sensory, motor,and autonomic dysfunctions such as hyperreflexia, backpain, paresthesia, and muscle atrophy were also associated.

Others have studied intramedullary cord pressure changesresulting from postural changes in dogs.26-28 The intra-medullary pressure measurements were recorded at C5 andC6 levels in three head positions: extension, neutral, and flex-ion. There were no significant increases in intramedullarypressure between the neutral and the extended neck postures.Flexion of the neck, in contrast, resulted in an increase of in-tramedullary pressure of 16 mm Hg. Furthermore, the in-crease in the intramedullary pressure disappeared after thedura, cord, and C7 root were transected, proving that the in-crease in pressure was due to actual stretching of the cord.26

Intramedullary pressure is related to the sum of the 3-dimensional stresses within the pia of the spinal cord. This

pressure is caused by the combination of two or more forces:a longitudinal one causing elongation/stretching of the cordand a transverse compressive force (which causes a combi-nation of three stresses) pressing the cord against the anteri-or wall of the spinal canal.10,24,26-28 Fig 3 illustrates shearforces and shear stresses created by cord contact with theposterior vertebral body. Attempts have been made to sepa-rate the effect of each of these loads (traction and transverse)to examine their individual contributions to the overall pres-sure increase in the spinal cord.

Three-dimensional Stress Patterns in the Spinal Cord and IntramedullaryPressure Tension

To fully appreciate the effects of stresses acting on thespinal cord, each one will need to be identified and exam-ined. The first of these stresses has already been described,axial tensile stresses. Axial tensile loads will cause adecrease in the cross-sectional area of the spinal cord andwill cause uniformly distributed tensile stresses throughoutthe cord. In addition, shear stresses are generated that are



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Fig 3. Anteroposterior shearing force applied to the cord. (A) A shearing force is applied to the ante-rior of the cord. This results in shearing stress in the cross-section of the cord (B). Note that for, illus-tration purposes only, one side of the shearing force about z is illustrated and on only one side of thecord. The magnitude of the shear force at any point is represented by the length of the vectors andshearing stress at any point is represented by the area under the curve (integral in calculus).Engineers often use contour lines to illustrate the magnitude of shear in a cross-section (C).

B C

A

directed inward from and perpendicular to the cord’s wallsduring elongation. This is described as Poisson’s effect36,37

(Fig 2). Breig7 believed that the CNS followed Saint-Venants law: A tensile force will be distributed so that itbecomes uniformly distributed around the circumferencewithin a distance (lengthwise) equal to three times the diam-eter. In Part I, it was demonstrated that tension in the spinalcord is transmitted several segments distal to the generatedstress and, if large enough, will be distributed throughout theentire spinal cord and nerve roots.

In an additional position, Kitahara et al27 studied the effectof tension in the spinal cord on intramedullary pressure inadult dogs. Although the head was placed into three differentpostures, neutral, extension, and flexion, this time the middleto lower cervical spine was kept in the neutral positionwhereas the upper cervical spine was placed in flexion,which is similar to a second harmonic buckling mode.38,39

Pressures were measured at C2, C4, and C6 vertebral levelsby use of three different balloons. No significant differencesin the pressures between the extended and neutral postureswere found at any level. In contrast, the mean pressure wassignificantly increased at all levels with upper cervical flex-ion. The mean pressure increases were 15.3 mm Hg at C2,9.4 mm Hg at C4, and 6.2 mm Hg at the C6 level. The largerincrease in pressure at the C2 level was believed to be due totwo factors: a larger flexion angle and, hence, greater cord

stretching and possible posterior body contact, creating atransverse component of force. However, the pressure in-creases at C4 and C6 were the result of the longitudinal trans-mission of force alone.27 To help visualize the complicatedstresses resulting from posterior vertebral body contact withthe cord during flexion, Fig 4 demonstrates stress contours ina cross-section of the cord for the loads of axial tension, purebending, and anterior compression (transverse loading).

Transverse LoadingThe second load to be discussed is transverse loading (Fig

3, D in Part I of this review). This can exist in normal canalconditions, as well as in many degenerative and pathologiccanal conditions. A transverse load is caused by an anteriordisplacement of the cord against an osteophyte as flexion isincreased. This forces the cord to ride over the posterior wallof the vertebral bodies or the anterior aspect of the spinalcanal during spinal flexion or in kyphotic configurations ofthe cervical and lumbar spines. Breig,7,40 Reid,41 and Ruch42

have demonstrated this in the cadaver. Reid41 states the fol-lowing:

Where stretch was exerted over a convexity, as normally inthe thoracic spine, or in the neck after conversion of the nor-mal lordosis to a flexion kyphosis, it appeared that there mustbe a considerable component of force directed anteriorly andholding the cord against the ventral wall of the canal.



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Fig 4. Stress contours during flexion in the cervical spine. Three cross-sectional areas of the cervicalspinal cord are shown for the postural load of flexion. A, The shear stresses are maximum at the cen-ter and minimum toward the periphery. B, Axial tension in flexion causes the cord to move anterior inthe canal and be compressed against the posterior vertebral, resulting in larger stresses at the ante-rior, which diminish toward the posterior. C, Tension is shown at the posterior one half of the cordwith compression at the anterior from the longitudinal force of tension induced by the flexion.

B

C

A

Several other investigators have observed the samething.26,27,43,44

Penning et al45 claimed that the transverse load dependedon the specific configuration of the individual’s canal. Thisdirectly applies to individuals with kyphotic changes of thenormal lordotic lumbar and cervical spines or to people whohad whiplash-type injuries. In whiplash-type injuries, buck-ling or snap-through of the cervical spine occurs that altersthe configuration of the spinal column creating kyphoticregions where a lordosis should be. Snap-through is a sud-den change in equilibrium of a curve column into a newshape such as an S curve. In these cases, the curve is neithercompletely lordotic nor kyphotic, even though curve mea-surements (modified Cobb or Ruth Jackson’s lines) may bewithin normal limits.39 Spinal cord stretching and contactwith the canal wall most commonly occurs at the apex ofthis altered curve configuration, but often adjacent levels areaffected as well. Ruch’s42 cadaveric dissections thoroughlydemonstrate this effect.

Many investigators, in fact most of them, erroneously usethe term compression to describe this transverse loading ofthe neural tissue.46 Compression stress is only one of thestresses caused by transverse loading; compression of thenervous system is a rare occurrence and only exists when thetissue is clamped between two opposing structures such asin a congenitally narrowed spinal canal.

Transverse loads act perpendicular to the long axis of thecord, and several different types of stress conditions in thecord are generated. The magnitude of the transverse loaddepends on the amount of flexion generated at each individ-ual segment and the size of the canal protrusion. Transverseloads can be equivalently broken down into two compo-nents: (1) a shear force and (2) a bending moment.36 Fig 5illustrates the moment, shear forces, and shear stressesinvolved in transverse loads.

The shear force (load) is applied parallel to the z-axis in ananteroposterior direction. The magnitude of the inducedshear stresses is largest at the anterior of the cord and de-

creases in value until it reaches a zero value at the center ofthe cord directly away from the point of application. To com-pletely analyze stress, engineers use a 3 × 3 array, with ele-ments consisting of all normal and shear stresses, called astress tensor. Because the stress tensor is symmetric aboutthe diagonal of the tensor (matrix), it is well known in the me-chanics of materials that transverse loads are associated withlongitudinal or y-axis shear force, which is exactly equal tothe AP or z-axis shear force. The induced longitudinal shearstress is largest in value at the anterior of the cord and also de-creases to zero in the center of the cord directly behind orposterior to the applied z-axis shear force. This longitudinalor y-axis shearing stress could potentially affect horizontalinterneurons connecting the longitudinal tracts of the cordand the horizontal AP blood vessels. Additionally, there is anassociated lateral or x-axis shear stress. This lateral shearingstress is largest in the center of the cord directly posterior tothe applied z-axis shear. Concerning the lateral shearingstress, White and Panjabi24 state, “It is interesting to note thatthe maximum shear stresses occur in the region where thecentral venules are located. These venules are thought to bethe structures in the spinal cord least resistant to mechanicaldamage.”

The bending moment has two components: compressionand tension, separated by a longitudinal neutral axis.Compression, –Ty, is largest at the anterior of the cord, andtension, +Ty, is largest at the posterior aspect of the spinalcord and dura. It is important to realize that the posteriorportion of the spinal cord will be highly loaded in tensionbecause the tensile stress from the bending moment is addi-tive to the tensile stress from canal lengthening, that is, fromflexion of the neck. For a thorough understanding of thestresses and their effects on the neural tissue, the interestedreader is referred to references 7, 24, and 46. Fig 6 illustratesa posterior vertebral body osteophyte causing transverseloading on the spinal cord during neck flexion or kyphosis.

The effects of transverse loads on the spinal cordintramedullary pressure have been demonstrated in dogs.28



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Fig 5. Forces and stresses in transverse loading. A, A transverse load (F) is shown. It can be equiva-lently broken down into a shear force (V) and a bending moment. B, The bending moment causescompression on the concavity and tension on the convexity of the deformed structure. The shear force(V) causes cross-sectional shear stresses in B and longitudinal shear stresses in C.

B

C

A

Two latex balloons were inserted into the cord, one at the C5level and the other at C6. A small plastic saddle was placedanterior to the cord at the C5 level in the extradural space.The neck was maintained in the neutral position while atraction load was applied in an anterior-to-posterior (a nega-tive translatory pull on the z-axis) direction. A linear rela-tionship between cord transverse pull and increase inintramedullary pressure at both C5 and C6 levels werefound. Loads of 50 to 75 g resulted in an approximate dou-bling of the intramedullary pressure at the C5 level. Becausethe intramedullary pressures at C5 and C6 were significantlycorrelated, this documents that a transverse-directed force atone level causes increased pressures at adjacent levels notexposed directly to the force. This transmission of force toadjacent levels is consistent with the mechanical engineer-

ing principles concerning force applications to structuresdiscussed previously.

Significantly, Reid41 calculated that for a 3-mm protrusioninto the anterior portion of the spinal canal (disk, osteophyte,retrospondylolisthesis, or an ossified posterior longitudinalligament [PLL]), the force of contact between the spinal cordand the protrusion during neck flexion was approximately 30to 40 psi. This is much greater than the force (50 to 75 g) usedby Lida and Tachibana28 and would be expected to drasticallyincrease the cord intramedullary pressure.

Recently, the effects of neck flexion in patients with atro-phy of the distal upper extremity were demonstrated.16 Neckflexion was found to flatten the cervical cord and “com-press” it against the anterior of the canal at C5-C7 vertebrallevels; the measured spinal cord evoked potentials were sig-



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Fig 6. Stress caused by a posterior-lateral osteophyte during kyphosis. (A) A cervical kyphosis (flex-ion) causes the tensed cord to come in contact with a posterior-lateral vertebral body osteophyte.This is a very complicated loading with horizontal transverse shear stresses (B), horizontal sagittalshear forces (C), compression of the anterior cord between the vertebral body and dentate ligaments(D), and longitudinal tension stresses (E), horizontal shear stresses resulting from torsion (F), andvertical shear forces (G) associated with the transverse load.

B

C

D

E

F

G

A

nificantly reduced compared with the neutral posture.Harrison46 suggested that this was actually transverse load-ing of the neural tissue and that the stresses acting on thespinal cord were probably the cause of the patient’s muscu-lar atrophy and pathologic findings.

TorsionThere is one last load that needs to be discussed. The

above analysis of the transverse force was with the forcedirected along the z-axis at the center of the cord. Anotherforce is generated when the force is applied lateral to thecenter or if the force is applied in an oblique direction.Examples of this would be a posterolateral osteophyte ordisk herniation. Similarly, if the head or thorax is rotatedaround the y-axis and flexed simultaneously, the same forcewould result. This load is termed torsion. Torsion generatesAP cross-sectional shear stress that is largest in value at theperiphery of the spinal cord and will decrease in magnitudetowards the center.36,47 In the examples given above (pos-terolateral disk or osteophyte), the posterior columns wouldbe under high torsional stresses, as well as tensile stresses.Raynor and Koplik47 state, “Torsional stresses may produceinteresting variations especially in sensory patterns.” Fig 3,B in Part I of this review depicts that stresses are greater inthe outer cord from an applied torsion load.

Transverse Loads and NeuropathologyDegenerative or pathologic structures located at or near

the anterior aspect of the canal will drastically add to thepreexisting state of decreased potential and function createdby tension in the spinal cord resulting from altered align-ment. The transverse component of force may be due to sev-eral factors, including a herniated disk, tumor, a bony pro-trusion such as that seen in cervical spondylosis, and ahypertrophied or ossified posterior longitudinal ligament.

Flexion or distraction of any part of the spinal column willincrease the contact force between the canal and the pons-cord tract.* The three part series from Tencer et al49-51 dem-onstrated this. However, two of their conclusions were notsupported by their data, which has been incorrectly acceptedby others as well.37 An in vitro model was developed to mea-sure the strains in the dura under varying conditions, includ-ing combinations of anterior canal encroachment, segmentalflexion angulations, distraction, compression, extension,laminectomy, and resection of anterior dural ligaments andnerve roots.49-51 Their findings were as follows. The anteriordura can be deformed by AP protrusion 8 to 10 mm beforethe posterior wall is displaced; thus laminectomy is not war-ranted for canal occlusions of this size.51 Distraction or ten-sile loads increased the contact force between the dura andanterior canal protrusion, whereas compression or shorteningthe motion segment did not alter the contact force comparedto the neutral canal position. Flexion of T11-T12 motion seg-ment did not increase the dura and canal contact force.49 Thislast conclusion, together with the statement “flexion of the

head and neck increases the resistance of the spinal cord andmeninges (SCM) to penetration due to an anterior mass,” isvery misleading.

For example, these two conclusions lead one to believethat kyphotic deformities at the segmental level of up to 20degrees do not lead to increased stress in the dura, and thatflexion may be beneficial in that it increases the spinal cord’sresistance to damage from transverse loading. These find-ings are far from correct. The technique used to simulate asegmental kyphotic deformity was removal of 75% of theanterior vertebral body of T11. This creates a condition, towhich the authors alluded, where the axis of rotation mayshift into the spinal canal and no deformation of the dura isexpected.51 Thus this model is not applicable to anythingother than severe vertebral body fractures, which is whatprompted the study to begin with.

In flexion, tensile loads create a smaller point of cord con-tact with any offending structure. Although, in this posture,the dura and nerve roots are less deflected, this small contactpoint results in stresses that are large.* If the cord is relaxed(lordosis or extension), then it has a larger contact area andis able to fold around the structure. Thus there will be largerstress concentrations per unit area for a smaller cord contactthat will cause large increases in internal stresses and inter-nal pressure. This information may explain the posture-dependent relief associated with back and referred leg painwith nerve root involvement.52-55 We suggest that mostpathologic and neurologic disorders of the spinal cord canbe ascribed to the combination of both spinal cord tensionand transverse loading caused by altered spinal configura-tions and degenerative conditions. Our engineering analysisof loads applied to the neural tissue and those of previousauthors support this point of view.7,37,46-48 Figs 3, 4, and 6provide examples of normal and shear stresses in combina-tion loading on the cord.

There are several studies concerning the effects on neuralelements caused by transverse loading. Some authors havesuggested the AP compression ratio (AP diameter/transversediameter) as an indicator of cord dysfunction.56 The spinalcord’s AP dimension will decrease by 2 to 3 mm as a resultof neck flexion.12 Significantly, a transverse protrusion willdiminish this further. Shinomiya et al57,58 discussed the pos-terior epidural ligaments in relation to flexion or kyphoticconfigurations of the cervical spine. These ligaments attachthe posterior dura mater to the ligamentum flavum and func-tion to prevent large anterior displacement of the posteriordura and spinal cord. When these ligaments are damaged incervical spine injuries or surgical procedures, such aslaminectomies, one side of or the entire cervical spinal cordcan be severely flattened against the anterior canal wall oragainst any anterior protrusion. These phenomena have beenlinked to myelopathies and specifically motor deficiencywith atrophy.44,46,57,58

The pathologic changes in the spinal cord caused by trans-verse loads are ascribed to the varying degrees of ischemia



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*References 12, 19, 26-28, 41, 48-53. *References 12, 19, 26-28, 41, 48, 52, 53.

associated with the different types and magnitudes of thestresses in the neural tissue (review the stress patterns in thecord in Fig 6). Venous congestion in the spinal cord and nerveroots has been demonstrated with pressures as low as 5 to 10mm Hg. Arterioles may be completely blocked at 108 mmHg, capillaries at 36 mm Hg, and venules at 23 mm Hg.59,60

The previously presented information suggests pressurechanges in neural tissue resulting from postural changes arewell within and may be above these ranges. Once this processoccurs, it may set up a positive feedback loop, like a com-partment syndrome. The blood/nerve barrier may be com-promised by the stresses and increased permeability results,leading to edema and further increased intraneural pressure.8

This process may not lead to immediately obvious patho-logic conditions and neuronal dysfunction instantaneously.Several studies indicate that the process of neuronal dys-function and progressive pathology may take anywhere from17 weeks to 30 or 40 years.61-64 For example, Wilberger andPang62 followed up on 108 symptom-free patients with herni-ated disks. Within 3 years, symptoms of lumbosacral radicu-lopathy developed in 64% of the patients.

The stresses and strains in the neural tissues and concomi-tant altered oxidation may cause longitudinal progressivecellular disruption and degeneration.65 Many diseaseprocesses may result from these abnormal stresses andstrains. Breig7 discussed this in relation to the developmentof multiple sclerosis (MS). Postmortem evaluation of spinalcords of individuals with MS revealed “deformed blood ves-sels with hyalinization, organized thrombi and or completeocclusion, leading to myelomalacia, gliosis and local shrink-ing.”7 These processes are consistent with known effects ofadverse stress in neural tissue. Burgerman et al66 discussedthe relationship between cervical spondylosis and MS. Theysuggested that at least two types of MS may exist, an auto-immune response of unknown cause and one caused by orassociated with “myelin breakdown due to chronic or recur-rent cord compression,”66 leading to an autoimmune re-sponse. This latter form may follow from the processesdescribed above in this review.

Many other conditions have been linked to spinal cordstresses and strains. These include periradicular, epidural,and subarachnoid adhesions,7,9,42 amyotrophic lateral sclero-sis, urinary incontinence, cerebral palsy,7 intramedullary neo-plasms and syringomylia,26-28 paraplegia, and tetraplegia.67

There is suggestive evidence that progressive neuronaldysfunction and degenerative changes may be counteracted,slowed, or even reversed.7,29,66-71 This is only true if thestresses and strains are alleviated or eliminated. Regenera-tion of the injured spinal cord has been described as “theHoly Grail” for neurobiologists.72 Although not yet success-fully achieved, it may be in sight according to Young.72 Iron-ically, no one seems to be paying attention to the work ofBreig et al,29 who more than a decade ago demonstrated suc-cessful healing of hemisectioned spinal cords in dogs. Thiswas done by surgically fixing the dogs in an extended spinalposture, which allowed the wound surfaces of the hemisec-tioned spinal cord to be approximated and thus heal, result-

ing in dramatic neurologic recovery and verified repair bypostmortem histologic examination.29

What Breig et al29 described as common sense has beenmostly overlooked with the exception of one study. Chen73

examined the stress distribution in the spinal cord meningealcomplex after injury during flexion/extension and axial rota-tion of the cervical spine and concluded, “Strict immobiliza-tion and keeping the cervical spine in the natural-extensionposition [are] recommended for the injury of the cervicalspine.” If the cervical and lumbar regions of the spine are al-lowed freedom of movement in the presence of severe neu-ronal trauma, then the stresses and strains associated withspinal postures (especially flexion) will separate the woundsurfaces. This will allow glial and pial scar formation andconcomitant fluid-filled cavities, syringomyelia. Thus lordo-sis of the cervical and lumbar spines are paramount for theproper growth, repair, and function of the pons-cord tract.Other surgical studies are verifying the importance of cervi-cal lordosis for successful neurologic outcomes.67,69-71,74-78

Many procedures deeply rooted in the physicians’ treatmentregimens for spinal disorders and neural derangements needto be reevaluated. These include flexion or longitudinal dis-traction traction, manipulation in flexed postural positions,surgical fusion in straight or flexed segmental positions in thelateral view, laminectomy, and surgical procedures that placethe spine in any position other than the neutral position,which is lordosis for the cervical and lumbar areas.

CONCLUSIONWith a knowledge of the four types of loads that are

applied to the neural tissue and to which regions of the cordthe stresses are localized, a pathomechanical picture can bepainted concerning degenerative states of the spinal columnand their adverse neuronal consequences. The four types ofloads are associated with abnormal postural rotations andtranslations and cause altered stresses in static positions andin dynamic spinal motions. These stress patterns in thespinal cord have been shown to correlate clinically withabnormal neurologic signs and symptoms after trauma andnonacute cord injuries.24,46,47,65

Prolonged flexion is the most offensive postural loading onspinal structures. Flexing the upper cervical spine alone re-sults in a significant increase in the intramedullary cord pres-sure, which is in the range, 10 to 20 mm Hg, required to re-duce spinal cord blood flow and cord perfusion (actually anyincrease in CIP will reduce the perfusion of the cord, accord-ing to the equation Perfusion = MAP – CIP). Prolonged load-ing of the neural tissue may result in impaired oxidative me-tabolism in the mitochondria. Kyphotic configurations of thecervical and lumbar curves are types of flexed spinal posi-tions, that is, buckling modes. These types of configurationsare associated with transverse loading of the neural tissue.Thus flexion traction, longitudinal traction, and braces or sur-gical fusions that fix the spine in flexed or military (straight)configurations should be questioned.

Although combinations of postures have not been studiedfor their effects on cord stresses and strains and the conse-



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quent increase in interstitial pressure, it should be intuitivelyobvious to the reader that individuals who adopt a combina-tion of two postures of the skull, thorax, and pelvis, or whohave them present in their upright static stance, may havelarge increases in stresses and strains of their cords. Thiscould theoretically cause a significant increase in the CIP (alinear relationship) compared with single postural positions.

We suggest, in addition to symptomatic improvement orresolution, rehabilitative and surgical procedures shouldstrive for an anatomic outcome of improved posture in theAP and lateral views. In the lateral view, the lordosis of thecervical and lumbar regions should be restored as close aspossible to their normal configuration: an arc of a circle inthe cervical spine39,79-81 and an elliptical shape with increas-ing distal curve in the lumbar spine.82-84 Ultimately, thismay improve the outcomes of patients with a wide variety ofneurologic disorders.

ACKNOWLEDGEMENTSSanghak O. Harrison, DC, and Shirlene Ching, DC, for

artwork.

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