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- •The Lumbar Spine
- •Contents
- •Contributing Authors
- •Preface
- •Acknowledgments
- •Epidemiology and the Economics of Low Back Pain
- •Pathophysiology of Nerve Root Pain in Disc Herniation and Spinal Stenosis
- •Biomechanical Considerations of Disc Degeneration
- •Clinical Spinal Instability Resulting from Injury and Degeneration
- •Morphologic Changes of End Plates in Degenerative Disc Disease
- •Spinal Instrumentation
- •Fracture and Repair of Lumbar Vertebrae
- •Genetic Transmission of Common Spinal Disorders
- •Genetic Applications to Lumbar Disc Disease
- •Clinical Neurophysiologic and Electrodiagnostic Testing in Disorders of the Lumbar Spine
- •Sensorimotor Control of the Lumbar Spine
- •Outcomes Assessment: Overview and Specific Tools
- •The Role of Outcomes and How to Integrate Them into Your Practice
- •Manual Therapy in Patients with Low Back Pain
- •Acupuncture and Reflexology
- •Returning Workers to Gainful Employment
- •Occupational Ergonomics
- •Preparation for Surgery
- •Surgical Approaches to the Thoracolumbar Spine
- •Surgical Approaches to the Lumbar Spine: Anterior and Posterior
- •Posterior and Anterior Surgical Approaches to the Lumbosacral Junction
- •Endoscopic Anterior Lumbar Procedures
- •Biology of Bone Grafting: Autograft and Allograft
- •Bone Graft Substitutes in Spinal Surgery
- •Spinal Instrumentation Overview in Lumbar Degenerative Disorders: Cages
- •Translaminar Screw Fixation
- •Lumbar Disc Disorders
- •Facet Joint Denervation: A Minimally Invasive Treatment for Low Back Pain in Selected Patients
- •Intradiscal Electrothermal Therapy
- •Operative Management of the Degenerative Disc: Posterior and Posterolateral Procedures
- •Posterior Lumbar Interbody Fusion
- •Operative Treatment of Anterior Procedures
- •Operative Treatment of Anterior and Posterior Fusion
- •Degenerative Disc Disease: Fusion Cages and Dowels
- •Minimally Invasive Procedures for Anterior Column Fusion and Reconstruction
- •Degenerative Disc Disease: Complications of Surgery
- •Dynamic Stabilization in the Treatment of Low Back Pain Due to Degenerative Disorders
- •Lumbar Artificial Disc Replacement: Rationale and Biomechanics
- •Lumbar Disc Replacement: Current Model, Results, and the Future
- •Disc Herniation: Definition and Types
- •Disc Herniation: Imaging
- •Disc Herniation: Nonoperative Treatment
- •Operative Treatment of Disc Herniation: Natural History and Indications for Surgery
- •Operative Treatment of Disc Herniation: Laminotomy
- •Chymopapain and Chemonucleolysis
- •Microscopic Lumbar Discectomy
- •Classification, Natural History, and Clinical Evaluation
- •Imaging of Spinal Stenosis and Degenerative Lumbar Spondylolisthesis with Stenosis

CHAPTER 11/SENSORIMOTOR CONTROL OF THE LUMBAR SPINE / 123
joints, are responsible for mechanical guidance of the
motion segment (35). The inferior articular processes of
one lumbar vertebra with the superior articular processes
of the low er adjacent v ertebra form the lumbar facet joints.
The joints exhibit features typical of synovial joints and the
articulating surfaces are covered by articular cartilage. The
amount of weight bearing has been difficult to calculate,
but is estimated to range from 0 to 20% (36,37).
Sensory innervation of the facet joints is derived from
the posterior ramus of the spinal nerves, with each joint
receiving branches from the level above, the same level,
and the level below. These branches supply filaments to
the capsule surrounding the facet joint, which is attached
to the articular cartilage. Anteriorly, the f ibrous capsule
of the joint is replaced entirely by the ligamentum
flavum, which attaches close to the articular margin. The
enclosing joint capsule is thick dorsally and is reinforced
by some of the deep fibers of the multif idus muscle. The
consensus is that the facet joint is a possible source of low
back pain (38). Marked degenerative changes can often
be demonstrated on imaging. Attempts ha v e been made to
establish the “facet joint syndrome” as a clinical entity,
but this remains questionable (10).
The Ligaments
The different ligaments provide substantial stability of
the spine. The anterior and posterior longitudinal ligaments resist separation between adjacent as well as multiple vertebral bodies. Posteriorly, ligamentous str uctures
provide resistance to flexion or axial separation between
adjacent laminae (ligamentum flavum) and spinous
processes (interspinous and supraspinous ligaments). The
iliolumbar ligament provides a strong resistance to forward displacement between the L5 vertebra and the
ilium. The intertransverse ligament, w hich spans between
consecutive transverse processes, is considered part of
the fascial system, which separates different muscular
compartments within the spine (24).
Apart from ligamentum flavum, all ligaments seem to
be innervated (39). The ligaments around the disc receive
their innervation from the same nerves as the disc. The
dorsal longitudinal ligament is more densely innervated
than the anterior longitudinal ligament, receiving nerve
endings from both sides. The more lateral and posteriorly
located ligaments receive their innervation mainly from
the posterior branch of the spinal nerve (24).
ments are self-tightening with increasing load. Roentgen
stereophotogrammetric analysis has sho wn the amount of
SIJ motion to range from 0.5 to 1.6 mm for translation
and up to 4° for rotation (40).
The SIJ appears to be richly innervated, although there
seems to be some uncertainty as to the exact innervation
patterns (Fig. 11-4). Solonen found the SIJ to be predominantly innervated by the L4-S1 nerve roots, with
some contribution from the superior gluteal nerve, but
with a lesser contribution from S2, and rarely from L3
nerve roots (41). Grob et al. (42), in a study on adult
human cadavers, found the SIJ to be innervated by f ine
nerve branches derived exclusively from dorsal rami of
the S1-S4 spinal nerves. Ikeda reported that the upper
ventral portion of the SIJ was mainly supplied b y the ventral ramus of the fifth lumbar nerve, while the lower ventral portion was mainly supplied by the ramus of the S2
nerve (43). Thick, thin, and unmyelinated nerve fibers
have been reported, which are compatible with a broad
repertoire of sensory receptors, including encapsulated
mechanoreceptors (42,43).
In search of causes of low back pain, the SIJ has gained
renewed interest as a possible pain generator (44,45).
There is a special aw areness of the SIJ as a source of pain
in pregnant and postpartum women, and although the
mechanism is not understood, relaxation of the SIJ before
childbirth is believed to play a role (9). Instability or subluxation has most often been suggested as mechanisms
behind sacroiliac dysfunction (7,46). Despite any proven
clinical findings or clearly def ined function of the joint,
The Sacroiliac Joint
The sacroiliac joint (SIJ) is a true synovial joint with
an auricular shape and a very limited amount of motion.
The joint is relatively small, considering the large forces
transmitted across it. The SIJ does, however, have an
extensive network of strong ligaments that helps maintain
stability and is constructed in such a way that the liga-
FIG. 11-4. Representation showing the sacroiliac joint, stabilizing ligaments, and innervation.

124 /SECTION I/BASIC SCIENCE
“sacroiliac dysfunction” has been established as a clinical
entity (5,7,46,47).
The Supporting Musculature
The system responsible for muscle coordination around
a joint is called the “myotactic unit.” Muscle spindle afferents make direct connections to motor neurons responsible for activation of synergist muscles and to interneurons
inhibiting motor neurons of antagonist muscles. Through
these divergent connections to the different muscles
around a joint, a strong neural network is established so
that muscles do not act independently of each other. Such
arrangements are responsible for joint stiffness.
Neural control on multiple levels is required to maintain normal locomotion. In order to support the body
against gravity, maintain posture, and to propel it forward, muscle contractions must be well coordinated for
several joints. At the same time, the nervous system must
exert active control to maintain balance of the moving
body, and it must adapt the locomotion patterns to the
environment and to the overall behavioral goals. The
spinal circuits activated by descending signals from
higher centers accomplish this. Neural circuits in the
spinal cord play an essential role in motor coordination.
Spinal reflexes, w here the “m yotactic units” are the building blocks, provide the nervous system with a set of elementary patterns of coordination that can be activated,
either by sensory stimuli or by descending signals from
the brainstem and cerebral cortex.
The lumbar musculature exerts various forces on the
spinal motion segments. Each muscle not only acts as a
moment-producer, but also generates compressive and
shear forces. The functions of these muscles are to stabilize the spine while providing mobility (21,48,49). The
recruitment patterns for these muscles are not well established. The multifidus muscles are the longest and most
medial of the lumbar back muscles. They consist of
repeating series of fascicles that originate from the laminae and the spinous processes of the lumbar vertebrae
and display consistent patterns of attachments caudally
(24). The key feature of the morphology of the lumbar
multifidus is that its f ascicles are arranged polysegmentally (Fig. 11-5). Each lumbar vertebra is supplied with a
group of fascicles that radiate from its spinous process,
anchoring it below to mammillary processes. The f ibers
of the multifidus are designed to act together on a single
spinous process of two to four levels. All the fascicles
originating from the spinous processes of a given vertebra are innervated by the medial branch of the dorsal
ramus that originates from below that vertebra. The muscles that act directly on a particular vertebral segment
are innervated by the nerve of that segment (50–52).
Although the paraspinal musculature has been studied
quite extensively, its role in the formation of low back
pain is far from clear (53). Electromyographic evaluations of various back lesions have contributed to the current understanding of low back pain (54–58). The clinical
picture often seen is one of tense and painful paraspinal
muscles and reduced flexibility in the lumbar spine. This
A B
FIG. 11-5. A: Schematic of the interspinales, intertransversarii mediales and laterales, and parts of the
multifidus muscles. B: Schematic showing the polysegmental attachments of the multifidus fascicles
originating from L1 vertebra. (From Holm S, Indahl A, Solomonow M.Sensorimotor control of the spine.
J EMG Kinesiol 2002;12:219–234, with permission.)

CHAPTER 11/SENSORIMOTOR CONTROL OF THE LUMBAR SPINE / 125
is thought to be caused by reflex stabilization by the
paraspinal muscles.
SENSORIMOTOR CONTROL
The innervation patterns of the active and passive structures of the lumbar spine have, for the most part, been
experimentally determined. The spinal nerve roots (dorsal
and ventral), which exit from the spinal canal, connect the
central nervous system and the peripheral nerves. The dorsal nerve root contains sensory f ibers and the ventral root
contains motor and some sensory f ibers. The nerve roots
join to form a spinal nerve. For each lumbar vertebra, there
is an associated lumbar spinal nerve. Peripherally, each
lumbar spinal nerve divides into a dorsal and ventral ramus,
which branch further to provide innervation to the various
passive and active structures (Fig. 11-6). Three branches
stem from the dorsal ramus: lateral, intermediate, and
medial. The lateral and intermediate branches innervate
iliocostalis lumborum and the longissimus thoracis muscles, respectively. The medial branch provides innervation
to a number of structures which lie posteriorly: muscles
(interspinales, intertransversarii mediales, and multif idus),
ligaments (interspinous and perhaps the supraspinous), and
the zygapophysial joint capsules. The ventral ramus provides innervation to structures that lie anteriorly: muscles
(intertransversarii laterales, psoas major), the intertransverse ligament, and the lateral aspects of the intervertebral
disc. The gra y ramus communicans, which is an autonomic
root from the sympathetic trunk, also provides innervation
to the lateral aspects of the intervertebral disc and to the
intervening anterior longitudinal ligament.
The control of movement depends on the sensory system working together with the motor system. Sensory
information influences motor output in many wa ys and at
all levels of the motor system. Sensory input to the spinal
cord directly triggers reflex responses. The reflexes are
involuntary and relatively stereotyped responses to certain sensory stimuli. Reflexes in which the sensory stimuli arise from receptors in muscles, joints, and skin, and
in which the neural circuitry is entirely contained within
the spinal cord are called spinal reflexes (Fig. 11-1).
In muscle and tendon, the motor and sensory functions
of the neural structures for controlling posture and movements are well established. The load-sensitive nerve endings, or mechanoreceptors, found in muscle (muscle
spindles) and tendon (Golgi tendon organs), provide proprioceptive information regarding tension levels, essen-
FIG. 11-6. Schematic drawing of the bilateral active and passive structural arrangement and sensory
innervation on the L3-L4 level. (From Holm S, Indahl A, Solomonow M. Sensorimotor control of the
spine. J EMG Kinesiol 2002;12:219–234, with permission.)

126 /SECTION I/BASIC SCIENCE
tial for controlling muscle tone, and therefore joint stability (Fig. 11-7).Although the presence of nerve endings
in passive structures (ligaments, intervertebral disc,
zygapophysial joint capsule) in the spinal column has
been documented, their role is not clearly defined.
Regarding the articular structures, the outer annulus of
the intervertebral disc and the capsules of the zygapophysial joint contain both free nerve endings and
mechanoreceptors. In addition to being potential sources
of pain, these structures may act as transducers for monitoring the position and movements in the motion segment. The neurologic feedback from passive structures
provides sensory information needed to regulate muscle
tension, and hence, the stability in the lumbar spine.
Normal locomotion requires multiple levels of neural
control. To support the body against gravity, maintain posture and to transport it forward, the nervous system must
coordinate muscle contractions. At the same time, the nervous system must exert active control to maintain balance
of the moving body and adapt the locomotion patterns.
FIG. 11-7. Neuromuscular feedback system depicting the
afferent sensory information from joint receptors, muscles spindles, and Golgi tendon organs for regulating muscle tension.
Neural circuits in the spinal cord play an essential role in
motor coordination. Spinal reflexes provide the nervous
system with a set of basic patterns of coordination that can
be activated, either by sensory stimuli or by descending
signals from the brainstem and cerebral cortex.
Functioning of the motor system is strongly related to
that of the sensory system. Proper functioning of the
motor system depends on a continuous inflow of sensory
information. Sensory input to the spinal cord directly
triggers reflexes. It is also essential for determining the
parameters of programmed voluntary responses. Finally,
both feedback and feed-forward mechanisms provide
flexibility in the control of motor output (Fig. 11-8).
Although the same sensors may provide information for
both feedback and feed-forward control, the manner in
which the information is processed varies. Biologic feedback processes generally operate continuously but slowly
and are therefore used to maintain posture and regulate
slow movements, while feed-forward systems, with an
intermittent mode, operate more quickly.
FUNCTION AND D YSFUNCTION
In low back pain, where no pathoanatomic findings can
be demonstrated, the cause of the pain may mainly be a
functional disturbance. In order to be able to describe
possible functional disturbances, the normal function
must first be described. However, this is not always the
case in medicine. For e xample, sacroiliac dysfunction w as
described 90 years ago, but the function of this joint has
not yet been established. The hypothesis laid out below
takes into account the muscular, ligamentous, and nervous
networks, and their various interactive processes (Fig. 11-
1). It builds upon what is known about neural control of
other joints, and it is reasonable to believe that the same
mechanisms apply to the spinal motion segments.
To understand the nature of a functional disturbance and
how this can occur, it is necessary to first describe normal
function. The nerve endings in the outer annulus fibrosus
of the disc, in the capsule of the facet joints, and in the ligaments are most likely part of a proprioceptive system
responsible for optimal recruitment of the paraspinal muscles (29,31). Mechanoreceptors are thought to play an
important role in monitoring position and joint movement
by regulating and modifying muscle tension. These different nerve endings can record the loading on the different
spinal structures. The descending signals that initiate muscle action are modified by the sensory input from the proprioceptive nerve endings. Recruitment of the paraspinal
muscles may thus be coordinated in such a manner that the
forces applied to the various structures are properly distributed regardless of position. In such a system, the action
of the muscles can provide the different spinal structures
with the support needed in order to counteract detrimental
forces and avoid injury. Overload of specific structures can
be detected by high threshold nerve endings, and in due

CHAPTER 11/SENSORIMOTOR CONTROL OF THE LUMBAR SPINE / 127
FIG. 11-8. Flowchart showing the functioning of the motor system involving feed-forw ard control in relation to feedback compensatory corrections. (From Ghez C. The control of movement. In: Kandel ER,
Schwartz JH, Jessel TM, eds. Principles of neural science, 3rd ed. Norwalk, CT: Appleton & Lange,
1991:536, with permission.)
process inhibit muscle actions responsible for increasing
the loading, and thereby prevent injury. This may be a reason why heavy physical loading does not seem to have the
impact on degeneration of the spine as earlier assumed
(59–61).
The common clinical finding of decreased range of
motion of the spine in patients with low back pain points to
increased muscle activity presumably caused by alterations
in the recruitment system. The origin of such a change in
paraspinal muscle recruitment is thought to be a lesion of
some kind in one or more spinal structures. The intervertebral disc is the spinal structure where lesions are most readily detected. Even if it is not yet known exactly why disc
lesions occur, since the time w hen Mixter and Barr demonstrated herniation of the nucleus pulposus and its effect on
the nerve root as a mechanism behind sciatic pain, there has
been mounting evidence for disc pathology and disc
changes (4). Some of these changes can be seen on imaging, but others may only be demonstrated through histologic methods. In most cases, the likely site of the lesion is
probably the annulus fibrosus of a lumbar disc. Such a
lesion must occur in an innervated region of the annulus
fibrosus (Fig. 11-3). Depending on the size of the lesion,
the density of the neural structures, and the damage done to
them, the firing patter ns from these nerve endings may be
altered in such a manner to cause increased activation of the
paraspinal muscles. This muscle activation may occur in a
“bracing” fashion and subject the muscles to static work,
which is believed to be responsible for muscle pain (62).
Toward the latter part of trunk flexion, there is a spontaneous reduction in the muscle electric activity in certain
paraspinal muscles. This behavior is known as flexionrelaxation and was first recognized by Floyd and Silv er in
1951 (63). Paquet et al. (64) have demonstrated altered
muscle activation patterns in patients with a former history of back pain compared to similar back patients without previous back pain experience. Haig et al. (65) have
shown changes in the flexion-relaxation phenomenon in
a patient with acute disc herniation, and Sihvonen et al.
(17) have demonstrated increased muscle activation and
lack of flexion-relaxation in patients with chronic low
back pain. Pain, for whatever reason, lasting for some
time may lead to the establishment of a more “bracing”
pattern as the dominating strategy for muscle activation.
Even though it is not known which processes are
responsible for muscle pain, it is a common human experience that muscles can be painful (66). There is no suitable experimental evidence supporting the hypothesis
that a “pain-spasm-pain” cycle can exist in the back.
Studies have shown that experimental pain in muscles
does not increase the firing of γ-motor units, but it does
increase the stretch reflex (67). Increase in such reflexes
may result in inappropriate muscle activation.
NEUROMUSCULAR REFLEX SYSTEM
A thorough description of reflex systems essential for
sensorimotor control has been provided by Gordon (68).

128 /SECTION I/BASIC SCIENCE
A summary, in part, is provided in this section. The
stretch reflex is the only known monosynaptic reflex in
the mammalian nervous system. Because the participating afferent and efferent axons have large diameters and
are among the most rapidly conducting neurons in the
nervous system, the stretch reflex pathway is adapted for
speed of operation. The economy of the neural circuit for
the stretch reflex allows muscle tone to be regulated
quickly and efficiently without direct intervention by
higher centers. Descending control signals adjust the gain
of the reflex loops, adapting them to the requirements of
specific motor acts.
A characteristic aspect of muscle tone is that the tension produced by the muscle increases approximately in
proportion to the amount of stretch. Moreover, when
muscle is released from a stretch, the tension decreases
progressivel y to its resting lev el. This symmetric response
is present whether the muscle is stretched slowly or
abruptly and is due to a combination of the mechanical
properties of muscle and the neural components provided
by the stretch reflex. In slowly imposed stretches, this
springlike behavior occurs because of the intrinsic
length-tension properties of muscle. In rapid stretches,
however, the intrinsic mechanical response is an initial
increase in tension followed by a transient collapse even
as the muscle continues to be stretched.
The increased focus on the innervation of different
spinal structures has led to a new understanding and
awareness that they may play an important role in a complex regulating system (20,24–26,42). Reflexes from ligaments in many of the joints of the extremities have previously been established (69–71). Spasms and elevated
activity of the lumbar paraspinal muscles are common in
patients with low back pain. In the spine, several ligaments are associated with each motion segment, thus
comprising a complex proprioceptive measurement system, particularly when combined with the sensory inputs
from nearby discs and capsules. The existence of sensory
receptors in the various spinal ligaments has been established (51,72–75). Solomonow et al. have experimentally
investigated whether or not a ligament-muscular reflex
exists from the spinal ligaments to related muscles (76).
Furthermore, it has been demonstrated that static constant load applied to the lumbar spine through the
supraspinous ligament results in spasm of the multifidus
muscles, although the stretching was below the physiologic range limit and spasms were evident regardless of
the loading magnitude (22). A conclusion drawn from
these studies is that there exists a clear chain of events
consisting of viscoelastic tissue damage, pain, and muscular spasm. The spasms are most likely triggered by
nerve endings, which are found in the spinal ligamentous
tissues. These receptors monitor tissue injury and trigger
responses such as pain and probably its associated
spasms. The finding that the viscoelastic structures were
stretched, although the applied load was constant was
very interesting as this indicates that the tension developed may be a stimulus that elicits reflexive activity in
the muscles (22). These two separate sensory feedback
mechanisms are probably in synergy with each other to
protect the spinal structures from instability and injury.
Possible muscle activation because of damage to passive viscoelastic spinal structures is difficult to detect.
Painful stimuli seem to have an inhibitory effect on muscle activation. But damage done to ligaments and perhaps
other passive structures does not necessarily have to
result in a lot of pain. Depending on the size of the lesion,
the density of the neural structures, and damage done to
them, and the degree of irritation to the surrounding
nerve endings, the firing patter n from these nerve endings may be altered in such a manner so as to cause
increased activation of the paraspinal muscles. Studies
have shown that experimental pain in muscles does not
increase the firing of γ-motor units, but it does increase
the stretch reflex (67). Increase in such reflexes may
result in inappropriate muscle activation.
In muscle and tendon, the motor and sensory functions
of the neural structures for controlling posture and movements are well established (77); however, until recently,
this has not been the case for the spinal structures. Stimulation of the outer annulus of the disc or zygapophysial
joint, both of which have been shown to contain nerve
endings, causes activation of paraspinal musculature.
This not only occurs on the same segmental le vel but also
on different levels, indicating a complex interaction (15).
Such an interaction is necessary in order to stabilize different segments, not only in relation to each other, but
also in the process of maintaining posture. However, a
lesion at one location may cause alterations in muscle
activation at a location other than the actual segment and
even on the contralateral side. Avramov et al. (78) have
shown that loading excites three patterns of nerve discharges from the zygapophysial joints: short duration
bursts during changes in loading, prolonged discharges at
low levels, and prolonged discharges at high load levels.
These results indicate that different units in the joint capsule have different levels of stress threshold.
The range of motion and innervation of the SIJ seems
well suited for detecting various loading patterns during
locomotion. In humans, the slanted position of the L5-S1
motion segment and the relative position of the SIJ appear
to have physiologic importance for load detection. The
afferent input from SIJ receptors, as well as mechanoreceptors in the intervertebral disc and zygapophysial joints,
will contribute to different degrees of muscle activation
and may constitute an integral regulatory system (79).
Changes in loading on the SIJ may result in altered activation of the stabilizing muscles, and thus play an important
regulatory function in stabilization and movement of the
upper body during postural changes.
Instability of a spinal motion segment, as a result of
degeneration of the disc or zygapophysial joints, is

CHAPTER 11/SENSORIMOTOR CONTROL OF THE LUMBAR SPINE / 129
believed to be manifested as “slipping” because of laxity
in the motion segment. Kaigle et al. (21) have shown that
this kind of hypermobility does not seem to occur, but
that the segmental motion pattern is greatly altered. The
change in length and loading of the spinal ligaments may
cause alterations in the firing patter ns and consequently,
coordination of the muscle activity. With decreased disc
height as a result of degeneration, adaptation of the surrounding nerve endings may be less efficient and thus
result in less optimal neuromuscular reflexes. Better
knowledge of the sensory function of the passive spinal
structures should influence the manner in which these
structures are treated clinically.
In healthy persons, the paraspinal muscles display the
flexion-relaxation phenomenon (i.e., muscle activity
decreases as flexion of the trunk increases), and the muscles become silent in the fully bent posture (15,63,79). In
a patient with a herniated nucleus pulposus, Haig et al.
found that the flexion-relaxation phenomenon was absent
(65). It may be assumed that in patients in w hom the phenomenon is absent, there is an imbalance between nerve
discharges to the muscles from a pathologic structure and
inhibitory discharges from the zygapophysial joint capsule in forward bending. Conversely, inhibitory discharges from the joint capsule can explain why manipulative treatment and mobilization of the zygapophysial
joint provide relief in some cases.
Using an experimental model, it has been demonstrated by Indahl et al. (15) that stimulation of nerve endings in the intervertebral disc and zygapophysial joint
capsule elicited responses in the paraspinal muscles,
thereby demonstrating neuromuscular interaction exists
between these structures. Stretching on the zygapophysial
joint capsule inhibited the muscular response, thus suggesting the existence of a complex reflex system that is
responsible for the motion and stabilization of the lumbar
spine.
Stretching of more than one joint can increase inhibition and make the treatment more effective. Muscle
spasm is a common clinical feature in patients with back
problems, and manipulation of the zygapophysial joints
may elicit a stretch reflex from the capsule, contributing
to an inhibitory action on muscle spasm, thereby relieving pain (Fig. 11-9). Thus, it appears that there is a delicate interaction between the different parts of the spinal
motion segments, and proprioceptive nerve endings may
play a vital part in load distribution during movements.
In addition to the lumbar motion segments, the SIJ is
of great importance in stabilization of the lumbosacral
area. Despite this, there have been surprisingly few
experimental studies investigating SIJ function. The
results of mapping studies (80), the innervation of the SIJ
(41–43), its position and range of motion (81), altogether
give reason to believe that the SIJ also plays a regulatory
FIG. 11-9. Schematic representation of patient pain and how it relates to muscle activation (left) and
disc herniation (right).

130 /SECTION I/BASIC SCIENCE
function involving reflex muscle activation responsible
for stabilization and movement of the upper body during
locomotion. Furthermore, it was shown by Indahl et al.
(15) that stimulation of nerve and nerve endings in the
deep part of the ventral SIJ, as well as in the superf icial
part of the dorsal capsule, elicits motor action potentials
in different muscles. Interesting patterns were revealed.
Stimulation of nerve elements in the ventral area of the
SIJ produced predominant contractions in the gluteus
medius and quadratus lumborum muscles. However,
stimulation of the superficial dorsal layer of the SIJ capsule elicited responses predominantly in the medially
located multifidus f ascicles. It is possible that the different areas of the SIJ play different roles in regulating the
locomotion system and the response may therefore vary
depending on the stimulation site.
SUMMARY
Despite a pathophysiologic understanding of the involved structures, no single group of patients can, with
certainty, be identif ied at an early stage and be given a
specific treatment. This seems to support the basic notion
that low back pain is multicausal, and that the prognosis
depends on a variety of factors. Furthermore, this suggests that movement-related pain should be considered as
a complex behavior, and not solely as a psychiatric or a
neurologic problem, but rather as a prob lem related to the
integration of nervous and biomechanical mechanisms.
This involves the sensorimotor control, with feedback
from muscles, discs, and joints, all in a complex interaction with the central nervous system, as well as the traditional peripheral pain mechanisms.
REFERENCES
1. Albee FH. A study of the anatomy and the clinical importance of the
sacroiliac joint. JAMA 1909;53:1273–1276.
2. Ghormley RK. Low back pain with special reference to the articular
facets, with presentation of an operative procedure. JAMA 1933;101:
1773–1777.
3. Mooney V. Facet syndrome. In: Wiesel SW, Weinstein JN, Herkowitz
HN, et al., eds. The lumbar spine. Philadelphia: WB Saunders, 1996:
538–558.
4. Mixter WJ, Barr JS. Rupture of the intervertebral disc with involvement of the spinal canal. N Engl J Med, 1934;2A:210–215.
5. Bernard PN, Cassidy JD. Sacroiliac joint syndrome: pathophysiology,
diagnosis and management. In: Frymoyer JW, ed. The adult spine: principles and practice. New York: Raven Press, 1991:2107–2131.
6. Daum WJ. The sacroiliac joint: an underappreciated pain generator.
Am J Orthop 1995;24:475–478.
7. DonTigny RL. Dysfunction of the sacroiliac joint and its treatment. J
Orthop Sports Phys Ther 1979;1:23–35.
8. Wiberg G. Back pain in relation to the nerve supply of the intervertebral discs. Acta Orthop Scand 1947;19:211–221.
9. MacLennan AH, Green RC, Nicolson R, et al. Serum relaxin and
pelvic pain of pregnancy. Lancet 1986;2:243–245.
10. Mooney V. Evaluation and treatment of sacroiliac dysfunction. In:
Wiesel SW, Weinstein JN , Herk owitz HN, et al., eds. The lumbar spine.
Philadelphia: WB Saunders, 1996:559–569.
11. Anderson J. Pathogenesis of back pain. In: Grahame R, Andersson
JAD, eds. Low back pain. Vol 2. Westmount, Montreal, Canada: Eden
Press, 1980:23–32.
12. Nachemson A. The lumbar spine: an orthopaedic challenge. Spine
1976;1:59–71.
13. Swezey RL, Clements PJ. Conservative treatment of back pain. In:
Jayson MIV, ed. The lumbar spine and back pain, 3rd ed. Edinburgh:
Churchill Livingstone, 1987:299–314.
14. Indahl A, Kaigle A, Reikerås O, et al. Electromyographic response of
the porcine multifidus musculature after nerve stimulation. Spine
1995;20:2652–2658.
15. Indahl A, Kaigle A, Reikerås O, et al. Interaction between the porcine
lumbar intervertebral disc, zygapophysial joints, and paraspinal muscles. Spine 1997;22:2834–2840.
16. Lamb DW. The neurology of spinal pain. Phys Ther 1979;59:971–973.
17. Sihvonen T, Partanen J, Hanninen O, et al. Electric behavior of low
back muscles during lumbar pelvic rhythm in low back pain patients
and healthy controls. Arch Phys Med Rehabil 1991;72:1080–1087.
18. Taylor JR, Twomey LT. Innervation of lumbar intervertebral discs. Med
J Aust 1979;2:701–702.
19. Wyke B. The neurolo gy of low back pain. In: Jayson MIV, ed. The lumbar spine and back pain, London: Longman, 1987:58–99.
20. Yamashita T, Minaki Y, Oota I, et al. Mechanosensitiv e af ferent units in
the lumbar intervertebral disc and adjacent muscle. Spine 1993;18:
2252–2256.
21. Kaigle AM, Holm S, Hansson T. Experimental instability in the lumbar
spine. Spine 1995;20:421–430.
22. Solomonow M, Zhou B, Baratta RV, et al. Neuromuscular disorders
associated with static lumbar flexion: a feline model. J EMG Kinesiol
2002;12:81–90.
23. Kaigle AM, Holm SH, Hansson TH. Kinematic behavior of the porcine
lumbar spine—a chronic lesion model. Spine 1997;22:2796–2806.
24. Bogduk N, Tynan W, Wilson AS. The nerve supply to the human lumbar intervertebral discs. J Anat 1981;132:39–56.
25. Cavanaugh JM, El-Bohy AA, Hardy WH, et al. Sensory innervation of
soft tissues of lumbar spine in the rat. J Orthop Res 1989;7:389–397.
26. Kojima Y, Maeda T, Arai R, et al. Nerve supply to the posterior longitudinal ligament and the intervertebral disc of the rat vertebral column
as studied by acetylcholinesterase histochemistry. J Anat 1990;169:
237–255.
27. Basmajian JV. Acute back pain and spasm. A controlled multicenter trial
of combined analgesic and antispasm agents. Spine 1989;14:438–439.
28. Holm S. Pathophysiology of disc degeneration. Acta Orthop Scand
Suppl 1993;251:13–15.
29. Malinsky J. The ontogenetic development of nerve terminations in the
intervertebral disc of man. Acta Anat 1959;38:96–113.
30. Kumar S, Davis PR. Lumbar intervertebral innervation and intraabdominal pressure. J Anat 1973;114:47–53.
31. Roberts S, Eisenstein SM, Menage J, et al. Mechanoreceptors in intervertebral discs. Spine 1995;20:2645–2651.
32. Ohtori S, Takahashi K, Chiba T, et al. Sensor y innervation of the dorsal portion of the lumbar intervertebral discs in rats. Spine 2001;26
(8):946–950.
33. Kuslich SD, Ulstrom CL, Michael CJ. The tissue origin of low back
pain and sciatica: a report of pain response to tissue stimulation during
operations on the lumbar spine using local anesthesia. Orthop Clin
North Am 1991;22:181–189.
34. Wyke B. The neurolo gy of low back pain. In: Jayson MIV, ed. The lumbar spine and back pain. London: Longman, 1987:58–99.
35. Stokes IAF. Mechanical function of facet joints in the lumbar spine.
Clin Biomech 1988;3:101–105.
36. Adams MA, Hutton WC, Stott JRR. The resistance to flexion of the
lumbar intervertebral joint. Spine 1980;5:245–253.
37. Lorentz M, Patwardhan A, Vanderby R. Load-bearing characteristics of
lumbar facets in normal and surgically altered spinal segments. Spine
1983;8:122–130.
38. Ashton IK, Ashton BA, Gibson SJ, et al. Morphological basis for back
pain: the demonstration of nerve fibers and neuropeptides in the lumbar zygapophysial joint capsule, but not in the ligamentum flavum. J
Orthop Res 1992;10:72–78.
39. Buckmill A T, Covard K, Plumton C, et al. Nerve fibers in lumbar
spine structures, and injured spinal roots express the sensory neuron
specific sodium channels SNS/PN3 and NaN/SNS2. Spine 2002;27:
135–140.

CHAPTER 11/SENSORIMOTOR CONTROL OF THE LUMBAR SPINE / 131
40. Sturesson B, Selvik G, Uden A. Movements of the sacroiliac joints: a
roentgen stereophotogrammetric analysis. Spine 1989;14:162–165.
41. Solonen KA. The sacroiliac joint in the light of anatomical, roentgenological and clinical studies. Acta Orthop Scand Suppl 1957;27:1–27.
42. Grob KR, Neuberger WL, Kisslig RO. Die innervation des sacroiliacgelenkes beim menschen. Zeitschrift fur Rheumatologie 1995;54:
117–122.
43. Ikeda R. Innervation of the sacroiliac joint. Macroscopical and histological studies [in Japanese]. J Nippon Med Sch 1991;58:587–596.
44. Daum WJ. The sacroiliac joint: an underappreciated pain generator.
Am J Orthop 1995;24:475–478.
45. Schwarzer AC, Apprill CN, Bogduk N. The sacroiliac joint in chronic
low back pain. Spine 1995;20:31–37.
46. Mooney V. Understanding, examining for, and treating sacroiliac pain.
J Musculoskel Med 1993;37–49.
47. Dreyfuss P, Michalsen M, Pauza K, et al. The value of medical history
and physical examination in diagnosing sacroiliac joint pain. Spine
1996;21:2594–2602.
48. Bogduk N, Macintosh JE, Pearcy MJ. A universal model of the lumbar
back muscles in the upright position. Spine 1992;17:897–913.
49. Bogduk N, Twomey L. Clinical anatomy of the lumbar spine. New
York: Churchill Livingstone, 1987.
50. Bogduk N. The myotomes of the human multifidus. J Anat 1983;136:
148–149.
51. Bogduk N, Wilson A, Tynan W. The human lumbar dorsal rami. J Anat
1982;134:383–397.
52. Macintosh JE, Valencia F, Bogduk N, et al. The morphology of the lumbar multifidus muscles. Clin Biomech 1986;1:196–204.
53. Cailliet R. Low back pain syndrome, 4th ed. Philadelphia: FA Davis,
1988:63–75.
54. Eisen A, Hoirch M. The electrodiagnostic evaluation of spinal root
lesion. Spine 1983;8:98–116.
55. Haldeman S. The electrodiagnostic evaluation of nerve root function.
Spine 1984;9:42–48.
56. Jacobsen RE. Lumbar stenosis. An electromyographic evaluation. Clin
Orthop 1976;115:68–71.
57. Johnson EW, Melvin JL. Value of electromyography in lumbar radiculopathy. Arch Phys Med Rehabil 1971;52: 239–243.
58. Wise CS, Ardizzone I. Electromyography in intervertebral disc protr usions. Arch Phys Med Rehabil 1954;35:442–446.
59. Battie MC, Videman T, Gibbons LE, et al. Determinants of lumbar disc
degeneration: a study relating lifetime exposures and magnetic resonance imaging findings in identical twins. Spine 1995;20:2601–2612.
60. Lundberg U, Mardberg B, Frankenhauser M. The total work load of
male and female white collar workers as related to age, occupational
level, and number of children. Scand J Psychol 1994;35:315–337.
61. Nachemson AL. The load on lumbar discs in different positions of the
body. Clin Orthop 1966;45:107–122.
62. Edwards RHT. Hypotheses of peripheral and central mechanisms
underlying occupational muscle pain and injury. Eur J Appl Physiol
1988;57:275–281.
63. Floyd WF, Silver PHS. Function of the erectors spinae muscles in flexion of the trunk. Lancet 1951;15:133–143.
64. Paquet N, Malouin F, Richards C. Hip-spine movement interaction and
muscle activation patterns during sagittal trunk movements in low back
pain patients. Spine 1994;19:596–603.
65. Haig AJ, Weismann G, Haugh LD, et al. Prospective evidence for
change in paraspinal muscle activity after herniated nucleus pulposus.
Spine 1993;18:926–930.
66. Ursin H, Endresen I, Ursin G. Psychological factors and self-reports of
muscle pain. Eur J Appl Physiol 1988;57:282–290.
67. Matre DA, Sinkjr T, Svensson P, et al. Experimental muscle pain
increases the human stretch reflex. Pain 1998;75:331–339.
68. Gordon G. Spinal mechanisms of motor coordination. In: Kandel ER,
Schwartz JH, Jessel TM, eds. Principles of neural science, 3rd ed. Norwalk, CT: Appleton & Lange, 1991:581–595.
69. Knatt T, Guanche C, Solomonow M, et al. The glenohumeral-biceps
reflex in the feline. Clin Orthop 1995;314:247–252.
70. Phillips D, Petrie S, Solomonow M, et al. Ligamento-muscular protective reflex in the elbow. J Hand Surg 1997;22:473–478.
71. Solomonow M, Baratta RV, Zhou B, et al. The synergistic action of the
ACL and thigh muscles in maintaining knee stability. Am J Sports Med
1987;15:207–213.
72. Hirsch C, Inglemark B, Miller M. The anatomical basis for low back
pain: study on presence of sensory nerve endings in ligaments, capsular and disc structures in human lumbar spine. Acta Orthop Scand
1963;33:1–17.
73. Jackson H, Winkleman R, Bickel W. Nerve endings in the human lumbar spinal column and related structures. J Bone Joint Surg Am 1966;
48:1272–1281.
74. Rhalmi W, Yahia H, Newman N, et al. Immunohistochemical study of
nerves in lumbar spine ligaments. Spine 1993;18:264–267.
75. Yahia H, Newman N. Innervation of spinal ligaments of patients with
disc herniation. Pathol Res Pract 1991;187:936–938.
76. Solomonow M, Zhou B, Harris M, et al. The ligamento-muscular stabilizing system of the spine. Spine 1998;23:2552–2562.
77. Ghez C, Gordon J. The control of movement. In: Kandel ER, Schwartz
JH, Jessel TM, eds. Principles of neural science, 3rd ed. Norwalk, CT:
Appleton & Lange, 1991:533–547.
78. Avramov AI, Cavanaugh JM, Ozaktay CA, et al. The effects of controlled mechanical loading on group II, III, and IV afferent units from
the lumbar zygapophysial joint and surrounding tissue. An in vitro
study. J Bone Joint Surg Am 1992;74:1464–1471.
79. Indahl A, Kaigle A, Reikerås O, et al. Sacroiliac joint involvement in
activation of the porcine spinal and gluteal musculature. J Spinal Disord 1999;12:325–330.
80. F ortin JD , Dwy er AP, West S, Pier J. Sacroiliac joint: pain referral maps
upon applying a new injection—arthrography technique. Part I: asymptomatic volunteers. Spine 1994;19:1475–1482.
81. Vleeming A, Volkers ACW, Snijders CJ, et al. Relation between form
and function in the sacroiliac joint. Part II: biomechanical aspects.
Spine 1990;15:133–135.

CHAPTER 12
Outcomes Assessment: Overview and Specific Tools
Kevin F. Spratt
Clinical outcomes were often what clinicians said they
were in the days before 1982. “My doctor says I’m doing
very well.” Since the early 1980s, in spine care and many
other disciplines where pain and suffering are major
symptoms associated with the complaints that bring the
patient to health care providers, outcomes have become
more strongly associated with patient self-report. The
argument is clear: Who but the patient is in a position to
accurately recount symptom magnitude and quality?
In spine care, the 1982 Spine publications of the Million et al. pain interference scale (1) (popularly called the
Million Visual Analogue Scale) and the 1983 Roland and
Morris Disability Questionnaire (2) signaled the beginning of legitimizing patient self-report for spine-related
disease outcomes.
THE NOTION OF CLINICAL OUTCOMES
The universe of outcome instruments potentially
applicable to the spine care professional is reasonably
large. Gattchel (3) edited a compendium of outcome
instruments for assessment and research of spinal disorders, where he categorized such biopsychosocial measures as the following:
1. Physical or “hard” measures
a. Range of motion: using inclinometers or Isosta-
tion B-200 equipment (Isotechnologies, Hillsborough, NC)
b. Spine strength: using Cybex (a division of
Lumex Corporation, Ronkonkoma, NY) or Isostation B-200 equipment
c. Lifting capacity functional measures: using
Cybex and MedX (MedX Corporation, Altamonte Springs, FL) equipment
d. Other tests of human performance capacity: aer-
obic capacity and treadmill tolerance
2. Psychological or “soft” measures
a. Psychological tests: depression, MMPI-2,
Symptom Checklist 90-Revised (4–7)
b. Self-report measures of pain and disability: the
SF-36, Chronic Pain Coping Inventory, Coping
Strategies Questionnaire, McGill Pain Questionnaire, Oswestry Disability Index, Roland and
Morris Disability Questionnaire, Multidimensional Pain Inventory (MPI), Quebec Back Pain
Disability Scale, Sickness Impact Profile, and
Activities of Daily Living (ADL) scales (8–24)
c. Clinical interview: the structured clinician inter-
view for the DSM-IV (SCID) (25)
d. Clinical ratings of overt pain behavior: the Wad-
dell Non-Organic Signs Test (26)
The clinical outcomes chapter by Spratt and Weinstein
(27) in The Lumbar Spine, vol. 2, provides greater detail
regarding the types of outcomes as well as classification
schemes for a wide variety of outcomes measures.
RELIABILITY AND VALIDITY
For any outcome measure, whether based on patient
self-report or a laboratory test, the psychometric properties
of primary interest are the same: reliability or precision
and validity or accuracy. Methods for ev aluating reliability
and validity are major topics in measurement theory and
are beyond the scope of this chapter. Impressive o v ervie ws
of the concepts of reliability are provided by Feldt and
Brennan (28), and for validity by Cronbach (29).
As a brief primer of reliability in the clinical setting,
reliability considerations are usually evaluated in two
ways, internal consistence of items, and test-retest reliability. Typically internal consistency is of primary importance when considering scale construction and test-retest
or stability of the score is of primary importance when
considering clinical value. With test-retest reliability the
object of measurement (a patient) is assessed on multiple
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