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Chapter 6 Biomechanics of the Spinal Motion Segment 113
Level
Load (N)
Compressive loads
A
B
FIG. 6.25 (A) Sagittal view of computational model and (B) stress distributions following total articial disc
placement at L5–S1. (From Knapik GG, Mendel E, Marras WS. Use of a personalized hybrid biomechanical model
to assess change in lumbar spine function with a TDR compared to an intact spine. Eur Spine J. 2012;21[suppl
5]:S641-S652.)
SECTION
I
L1–L2 SUP
L1–L2 INF
L2–L3 SUP
L2–L3 INF
L3–L4 SUP
L3–L4 INF
L4–L5 SUP
L4–L5 INF
L5–S1 SUP
L5–S1 INF
0
–500
–1000
–1500
–2000
–2500
–3000
FIG. 6.26 Average of the peak compression loads on the lumbar spine endplates as a function of intact spine
versus total articial disc replacement (TDR) spine and external loading condition (bending while unloaded
0 kg, lifting 9.5 kg, lifting 19 kg). INF, inferior; SUP, superior. (From Knapik GG, Mendel E, Marras WS. Use of a
personalized hybrid biomechanical model to assess change in lumbar spine function with a TDR compared to
an intact spine. Eur Spine J. 2012;21[suppl 5]:S641-S652.)
–3500
–4000
–4500
T12–L1 SUP
T12–L1 INF
0 kg Intact
0 kg TDR
9.5 kg Intact
9.5 kg TDR
19 kg Intact
19 kg TDR
114 BASIC SCIENCE
Sagittal range of motion
Level
Range of motion (degrees)
16
14
12
10
8
6
4
2
0
L5–S1 L4–L5 L3–L4 L2–L3 L1–L2 T12–L1
FIG. 6.27 Mean sagittal plane range of motion at each lumbar level as
a function of intact spine versus total articial disc replacement (TDR)
spine and external loading condition (bending while unloaded 0 kg, lifting
9.5 kg, lifting 19 kg). (From Knapik GG, Mendel E, Marras WS. Use of a
personalized hybrid biomechanical model to assess change in lumbar spine
function with a TDR compared to an intact spine. Eur Spine J. 2012;21[suppl
5]:S641-S652.)
0 kg Intact
0 kg TDR
9.5 kg Intact
9.5 kg TDR
19 kg Intact
19 kg TDR
is alteration could change the kinematic signature of the
spine.
Finally, a narrowed disc space could compromise the
protection of the nerve root because there is less space for
the nerve root to pass through the intervertebral foramen.
A compromise of the disc could lead to load transmission
irregularities, instability, motion restrictions, and a compromise of the nerve root. is is just one example of how interrelated the components of the spine are from a biomechanical
perspective.
As can be seen from this discussion, biomechanics of the
spine not only can inuence the various dimensions of the
biomechanical system, but it also can inuence the biochemical behavior of the system. Because biomechanical considerations provide an understanding of the forces that are generated
on the system, some authors are beginning to consider the
spine as a mechanobiologic system.
Summary
By nature, the spine is a complex structure that provides
protection for the spinal cord and a structure to support loads
in numerous postures and positions. In addition, the healthy
spine limits physiologic movement to conditions that protect
the structures of the spine. With trauma and degeneration, the
spine loses its ability to achieve these functions adequately.
Biomechanics provides a means to characterize and assess
the status of the spine quantitatively and precisely. Quantication provides a rationale for one to determine “how much is too
much” exposure to the physical conditions that might damage
the spinal system. is chapter has systematically summarized
and characterized the capacity of the spinal motion segments
in terms of kinematic capacity and load tolerance.
e spinal structures themselves are physiologically unique,
and have evolved in such a manner that their functions are
unique. Although this chapter has examined the capacity of
the individual motion segments, this evaluation should make
it clear that the spine is truly a system of components that
act collectively and interactively to achieve the functions of
motion and load support. e kinematic and load support
capacities of the motion segment vary signicantly as a func-
tion of spinal level, direction of motion, direction of load
application, and temporal exposure characteristics.
Although presented as basic information, this information
should be considered the fundamental scientic foundation
for understanding how the spine functions, how disorders
and pain might occur in the spine, how exposure to ADLs
and occupational conditions might aect the spine status, and
what functions need to be restored clinically. Biomechanical
features and function change throughout life. Aging alone
alters the biomechanical properties of the spine. It has also
been well established, however, that various exposures can
greatly accelerate the degenerative process and the biomechanical functioning of the spine.
As knowledge of the spine increases, it is clear that a biomechanical foundation is essential for prevention and treatment of spinal disorders. A better understanding of spine
function can be achieved through a better quantication of
physical attributes, yielding improved sensitivity and specicity of functional understanding and interventions.
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Nerve Root Pain in Disc Herniation and
SECTION
7
CHAPTER
e clinical symptoms associated with lumbar disc herniation
and spinal stenosis are attributed to pathophysiologic changes
in spinal nerve roots. Recent research has dened the basic
pathophysiologic events at the tissue, cellular, or subcellular
levels in relationship to the pathogenesis of sciatica and nerve
root pain. is chapter reviews the current knowledge about
these mechanisms and discusses these mechanisms in relation
to the clinical features of lumbar disc herniation and spinal
stenosis.
Nerve root pain is typically radiating in nature and usually
related to a specic nerve root or adjacent roots. It is associ-
ated with pathologic changes and nerve dysfunction and may
be present in motor and sensory modalities, producing motor
weakness and sensory disturbances. ese changes are tightly
linked through mechanisms that are discussed in this chapter.
Two specic mechanisms at the “tissue level” may be
dened: (1) mechanical deformation of the nerve roots and
(2) biologic or biochemical activity of the disc tissue causing
neuroinammation of nerve roots.
Mechanical Eects on Nerve Roots
Enclosed by the vertebral bones, the spinal nerve roots are
relatively well protected from external trauma, although
somewhat more susceptible to injury than peripheral nerves.
In 1934, Mixter and Barr1 described that intervertebral discs
can rupture and cause mechanical compression of the nerve
roots, leading to sciatica. However, there has been moderate
research interest in the past regarding nerve root compression.
Gelfan and Tarlov2 in 1956 and Sharpless3 in 1975 performed
some initial experiments on the eects of compression on
nerve impulse conduction and showed that nerve roots were
more susceptible to compression than peripheral nerves.
Interest in nerve root pathophysiology has increased more
recently, and numerous studies are reviewed here.
In 1991, a model was presented that allowed for experimental, graded compression of cauda equina nerve roots at
known pressure levels.4 In this model, the cauda equina of pigs
Spinal Stenosis
Robert R. Myers
Björn Rydevik
Kjell Olmarker
Shinichi Kikuchi
was compressed by an inatable balloon xed to the spine
(Fig. 7.1). e cauda equina could also be observed through
the translucent balloon. is model made it possible to study
the ow in the intrinsic nerve root blood vessels at various
pressure levels.5 e average occlusion pressure for the arterioles was found to be slightly below and directly related to the
systolic blood pressure. e blood ow in the capillary networks was intimately dependent on the blood ow of the
adjacent venules. is nding corroborates the assumption
that venular stasis may induce capillary stasis and changes in
the microcirculation of the nerve tissue, which has been suggested as one mechanism in carpal tunnel syndrome.6 e
mean occlusion pressures for the venules showed large variations; however, a pressure of 5 to 10 mm Hg was found to be
sucient for inducing venular occlusion.
Because the nutrition of the nerve root is aected by
ischemia, a compression-induced impairment of the vasculature may be one mechanism for nerve root dysfunction.
e nerve roots also have a considerable nutritional supply
via diusion from the cerebrospinal uid.7 To assess the
compression-induced eects on the total contribution to
the nerve roots, an experiment was performed in which
3
H-labeled methylglucose was allowed to be transported to the
nerve tissue in the compressed segment via the blood vessels
and via the cerebrospinal uid diusion aer systemic injec-
tion.8 e results showed that no compensatory mechanism
from cerebrospinal uid diusion could be expected at low
pressure levels. On the contrary, 10 mm Hg compression was
sucient to induce a 20% to 30% reduction of the transport
of methylglucose to the nerve roots.
It is known from experimental studies on peripheral nerves
that compression may also induce an increase in vascular
permeability, leading to intraneural edema formation.9 Such
edema may increase the endoneurial uid pressure, which
impairs the endoneurial capillary blood ow and nutrition of
the nerve roots.10 Because the edema usually persists for some
time aer the removal of a compressive agent, edema may
negatively aect the nerve root for a longer period than the
compression itself. e presence of intraneural edema is also
I
119
120 BASIC SCIENCE
C
D
B
A
FIG. 7.1 Schematic of an experimental nerve root compression model.
Cauda equina (A) is compressed by an inatable balloon (B) that is xed to
the spine by two L-shaped pins (C) and Plexiglas plate (D). (From Olmarker
K, Holm S, Rosenqvist A-L, et al. Experimental nerve root compression: a
model of acute, graded compression of the porcine cauda equina and an
analysis of neural and vascular anatomy. Spine [Phila Pa 1976]. 1991;16:61-69.)
related to subsequent formation of intraneural brosis,11 a
neuroinammatory response that is seen in some patients
with nerve compression disorders.
Nerve root compression directly aects nerve conduc-
12,13
tion.
more susceptible to compression than the motor bers.
Our data show that the sensory bers are slightly
13,14
One factor that has not been fully recognized in compression trauma of nerve tissue is the onset rate of the compression.
e onset rate (i.e., the time from compression start until full
compression) may vary clinically from fractions of seconds in
traumatic conditions to months or years in association with
degenerative processes.
A rapid-onset rate of less than 1 second has been found to
induce more pronounced pathophysiologic dysfunction. For
the rapid-onset compression, which is likely to be more closely
related to spine trauma or disc herniation than to spinal stenosis, it has been seen that a pressure of 600 mm Hg maintained
only for 1 second is sucient to induce a gradual impairment
of nerve conduction during the 2 hours studied aer the
compression was ended.15 In the case of spinal stenosis, the
rate may be a great deal slower, and pain or nerve dysfunction
may not be seen until aer considerable ischemic injury.
Chronic Experimental Nerve Root Compression
To mimic various clinical situations, compression must be
applied for long periods. In clinical syndromes with nerve root
compression, the onset time may be quite slow and the duration may be quite long. A gradual development of degenerative
changes that induce spinal stenosis leads to an onset time that
can be many years. It is dicult to mimic such a situation in
an experimental model. Chronic models should induce a
controlled compression with a slow-onset time that is easily
reproducible.
Delamarter and colleagues16 introduced a model on the dog
cauda equina in which they applied a constricting plastic band
that was le in place for various times. e band was tightened
around the thecal sac to induce a 25%, 50%, or 75% reduction
of the cross-sectional area. e data indicated that structural
and functional changes were proportional to the degree of
constriction.
To induce a slower onset and more controlled compression,
Corneord and colleagues17 used a constrictor to compress
the nerve roots in the pig. e constrictor consisted of an
outer metal shell that on the inside was covered with a material called ameroid that expands when in contact with uids.
Because of the metal shell, the ameroid expands inward with a
maximum of expansion aer 2 weeks, resulting in a compression of a nerve root placed in the central opening of the
constrictor. Compression of the rst sacral nerve root in the
pig resulted in a signicant reduction of nerve conduction
velocity and axonal injuries.17 It has also been found that
there is an increase in substance P in the nerve root and the
dorsal root ganglion aer such compression.18 Substance P is
a neurotransmitter that is related to pain transmission.
One important aspect in clinical nerve root compression
conditions is that the compression level is probably unstable
and varies as the result of changes in posture and move-
19,20
ments.
In 1995, Konno and colleagues21 introduced a
model in which the pressure could be changed aer some time
of initial chronic compression. An inatable balloon was
introduced under the lamina of the seventh lumbar vertebra
in the dog. By inating the balloon at a known pressure slowly
over 1 hour with a viscous substance that would harden in the
balloon, compression of the cauda equina could be induced
with a known initial pressure level. e compression was veried by myelography. Because the balloon under the lamina
was composed of a twin set of balloons, the second balloon
component could be connected to a compressed air device and
could be used to add compression to the already chronically
compressed cauda equina.
Acute nerve root compression experiments have established
critical pressure levels for interference with various physiologic
parameters in the spinal nerve roots. Studies on chronic
compression may provide knowledge that would be more
applicable to the clinical situation.
Spinal Stenosis: Experimental-Clinical Correlation
Patients with double or multiple levels of spinal stenosis may
have more pronounced symptoms than patients with stenosis
only at one level.22 e mechanism for the dierence between
single and double compression may not simply be based on
the fact that the nerve impulses have to pass more than one
compression zone at double-level compression. ere may
also be a mechanism based on the local vascular anatomy of
the nerve roots. In contrast to peripheral nerves, there are no
regional nutritive arteries from surrounding structures to the
intraneural vascular system in spinal nerve roots.
pression at two levels might induce a nutritionally impaired
region between the two compression sites. In this way the
segment aected by the compression would be widened. Data
23–25
Com-
Chapter 7 Nerve Root Pain in Disc Herniation and Spinal Stenosis 121
from a study on the nutritional transport to the nerve tissue
in double-level compression showed that there is a reduction
of this transport to the uncompressed nerve segment located
between the two compression balloons that was similar to
the reduction within the two compression sites.26 us, there
is experimental evidence that the nutrition to the nerve
segment located between two compression sites in nerve
roots is severely impaired, although this nerve segment itself
is uncompressed.
If nerve compression is of an extremely low onset rate, as
in spinal stenosis, there may be an adaptation of the nerve
tissue to the applied pressure. In cadaveric experiments,
Schönström and colleagues27 found that when a hose clamp
was tightened around a human cadaveric cauda equina specimen there was a critical cross-sectional area of the dural sac
when the rst signs of pressure increase among nerve roots
were recorded by a catheter placed in the compression zone.
is cross-sectional area was approximately 75 mm2, which
was also found to correlate with a corresponding measurement on computed tomography (CT) in patients with spinal
stenosis.28 When the hose clamp was tightened further, the
pressure increased. Owing to creep phenomena in the nerve
tissue, the pressure decreased with time, however. When the
pressure did not normalize within 10 minutes, the “sustained
size” was registered and was found to be in the range of 45 to
50 mm2.27 is study indicates that even in acute compression
there is an adaptation of the nerve tissue to the applied pressure. From a longer perspective, this probably means that the
nerve may also be reorganized in its microstructural elements,
which would result in a nerve with a smaller diameter. Under
such circumstances, with gradually decreasing nerve diameter,
the pressure acting on the nerve would be reduced to some
degree.
ere is a correlation between the experimental animal
observations regarding critical pressures for functional and
nutritional changes in nerve roots under compression and the
measurements of pressure levels among nerve roots in human
cadaveric lumbar spines aer experimental constriction of the
dural sac.
Epidural pressure measurements have been performed,
evaluating the relationship between epidural pressure and
posture.20 It was found that the local epidural pressure at the
stenotic level was low in lying and sitting postures and high
in standing postures. Pressure was increased with extension
but decreased with exion of the spine. e highest epidural
pressure, 117 mm Hg, was found in standing with extension.
Measurements have also been reported regarding changes in
epidural pressure during walking in patients with lumbar
spinal stenosis.29 e pressure changed during walking with a
wave pattern of increasing and decreasing changes. Such
observations correlate with the previously mentioned experimental observations regarding intermittent cauda equina
compression.
19
pain. Howe and colleagues30 found that mechanical stimulation
of nerve roots or peripheral nerves resulted in nerve impulses
of short duration and that these impulses were prolonged if
the nerve tissue had been exposed to mechanical irritation by
a chromic gut ligature for 2 to 4 weeks. Corresponding results
were obtained in an in vitro system using rabbit nerve roots.31
In this setup, it was also evident that the dorsal root ganglion
was more susceptible to mechanical stimulation than the nerve
roots. e dorsal root ganglion has elicited special interest in
this regard, and an increase in the level of neurotransmitters
related to pain transmission has been found in the dorsal root
ganglion in response to whole-body vibration of rabbits.32 A
similar increase has been seen in the dorsal root ganglion and
nerve root aer local constriction of the same nerve root.18
In vivo models of pain behavior have shown that mechanical
nerve deformation superimposed on inammation is painful,
whereas either factor alone might not cause severe pain.
e magnitude of nerve root compression pressure (measured
intraoperatively) correlates with neurologic decit but not
with degree of straight-leg raising test.
31–34
Neuropathologic Changes and Pain
ere is considerable research evidence regarding the relationship of pain to neuropathologic changes.35 Much of what is
known has been studied in relationship to mechanical and
inammatory injury of the sciatic nerve in the rat. Entrapment
of a peripheral nerve produces pathologic change in proportion to the degree of compression and its duration,36 as is
known to be the case for nerve root compression. In an electron microscopic study,36 minor degrees of nerve compression
were associated with ischemic injury to Schwann cells, resulting in their necrosis and in demyelination. Severe nerve
compression was associated with injury to the axon, resulting
in wallerian degeneration.
Subsequent experiments established the relationship of
pain to these forms of neuropathologic change.37 ese studies
established that mild levels of ischemia producing demyelination were generally not painful, whereas severe ischemiaproducing wallerian degeneration resulted in hyperalgesia.
e pathology of the chronic constriction injury model of
neuropathic pain is based on this relationship and the added
insult of inammation caused by the chromic gut ligatures
used to compress the nerve.38 It is now recognized that the
cytokine-driven processes of wallerian degeneration are the
dominant neuropathologic factors linking nerve injury and
37,39,40
pain
eration relate directly to the magnitude and duration of
hyperalgesia.
and that the degree and extent of wallerian degen-
41
Biologic and Biochemical Eects on
Nerve Roots
SECTION
I
Mechanical Nerve Root Deformation and Pain
Some experimental observations indicate that mechanical
nerve root deformation per se may induce impulses that cause
e clinical picture of sciatica with a characteristic distribution of pain and nerve dysfunction in the absence of herniated
disc material at radiologic examination and at surgery has
indicated that mechanical nerve root compression may not be
122 BASIC SCIENCE
the only factor that is responsible for sciatic pain. In 1984 it
was suggested that the disc tissue per se may have some injurious properties.42 It was later conrmed experimentally that
local epidural application of autologous nucleus pulposus in
the absence of mechanical deformation induces signicant
changes in structure and function of the adjacent nerve roots.
43
Biologic Eects of Nucleus Pulposus
In 1993, Olmarker and colleagues43 published a study that
showed that autologous nucleus pulposus can induce a reduction in nerve conduction velocity and light microscopic
structural changes in a pig cauda equina model of nerve root
injury. ese axonal changes had a focal distribution, however,
and the quantity of injured axons was too low to be responsible
for the signicant neurophysiologic dysfunction observed. A
follow-up study of areas of the nerve roots exposed to nucleus
pulposus that appeared to be normal by light microscopy
revealed that there were signicant injuries of Schwann cells
with vacuolization and disintegration of Schmidt-Lanterman
incisures (Fig. 7.2).44 Schmidt-Lanterman incisures are essential for the normal exchange of ions between the axon and the
surrounding tissues. An injury to this structure would be
likely to interfere with the normal impulse conduction properties of the axons, although these models’ changes may not fully
explain the neurophysiologic dysfunction observed.
M
M
A
S
e pathophysiologic potential of the nucleus pulposus was
emphasized further in an experiment using a dog model in
which it was seen that a surgical incision of the anulus brosus,
with minimal leakage of nucleus pulposus, was enough to
induce signicant changes in structure and function of the
adjacent nerve root.45 It has also been seen that epidural
application of the autologous nucleus pulposus within 2 hours
induces an intraneural edema
46,47
that leads to a reduction of
the intraneural blood ow.47 Histologic changes of the nerve
roots are present aer 3 hours,48 and a subsequent reduction
of the nerve conduction velocity starts 3 to 24 hours aer
application.
43,48
e nucleus pulposus may also interfere with
the nutrition to the intraspinal nerve tissue. Aer application
to the dorsal root ganglion, it was found that the intraneural
blood ow was dramatically decreased and that there was a
simultaneous increase of the tissue uid pressure.
47
Methylprednisolone reduces the pathophysiologic events
of the nucleus pulposus–induced nerve root injury if given
within 24 hours. To establish if the presence of autologous
nucleus pulposus could initiate a leukotactic response from
the surrounding tissues, a study was initiated that assessed
the potential inammatogenic properties of the nucleus
pulposus.49 Autologous nucleus pulposus and autologous
retroperitoneal fat were placed in separate perforated titanium
chambers and placed subcutaneously, together with a sham
chamber, in the pig. e number of leukocytes was assessed 7
days later for the chambers. e nucleus pulposus–containing
chambers had a number of leukocytes that exceeded the two
others by 150%. In another experiment, autologous nucleus
pulposus and muscle were placed in Gore-Tex tubes subcutaneously in rabbits.50 Aer 2 weeks, there was an accumulation
of macrophages and T-helper and T-suppresser cells in the
tube with nucleus pulposus that persisted the full observation
time of 4 weeks.
Kawakami and colleagues51 showed that neuropathic pain
in an experimental setting seems to be mediated by inltrating
leukocytes, a nding consistent with the previous observations of neuroimmunologic inammatory changes and pain.52
In rats made leukopenic by using nitrogen mustard, the pain
response was absent aer application of nucleus pulposus,
whereas normal rats with nucleus pulposus application displayed a pathologic response to stimulation. e same group
also showed that inhibition of cyclooxygenase-2 might reduce
nucleus pulposus–induced pain behavior.53 Taken together,
these data further support the impression that autologous
nucleus pulposus may elicit inammatory reactions when
outside the intervertebral disc space and that such reactions
may not be restricted to resorption of the herniated tissue
but also may be intimately involved in the pathophysiology
of sciatica.
FIG. 7.2 Seven days after application of nucleus pulposus. Myelinated
nerve ber with prominent vesicular swelling of Schmidt-Lanterman
incisure. Note mononuclear cell (red M) in close contact with nerve ber.
Arrowheads indicate myelin sheath layers outside Schmidt-Lanterman
incisure. A, well-preserved axon; white M, myelin sheath; S, outer Schwann
cell cytoplasm. (Bar = 2.5 µm.) (From Olmarker K, Nordborg C, Larsson K, et
al. Ultrastructural changes in spinal nerve roots induced by autologous
nucleus pulposus. Spine [Phila Pa 1976]. 1996;21:411-414.)
Nucleus Pulposus and Sciatic Pain
Pain is much more dicult to assess than nerve conduction
in controlled experimental studies. e available literature
indicates that pain may be induced by both mechanical factors
and nucleus pulposus–mediated factors. e role of the
nucleus pulposus in this context is interesting in view of