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C H A P T E R 2 Applied Anatomy of the Normal and Aging Spine
References
1. J.P.J. Van Schaik, H. Verbiest, et al., The orientation of the laminae and facet joints in the
lower lumbar spine, Spine 10 (1985) 59–63.
2. W.R. Francis, J.W. Fielding, Traumatic spondylolisthesis of the axis, Orthop. Clin. North
Am. 9 (1978) 1011–1027.
3. J.A. McColloch, E.E. Transfelt, Macnab’s backache, Williams & Wilkins, Baltimore, 1997.
4. E.C. Benzel, Anatomic consideration of the C2 pedicle screw placement (letters to the
editor), Spine 21 (1996) 2301–2301.
5. P.V. Scoles, A.E. Linton, B. Latimer, et al., Vertebral body and posterior element morphology:
the normal spine in middle life, Spine 13 (1988) 1082–1086.
6. B.L. Riggs, L.J. Melton III, Evidence for two distinct syndromes of involutional osteoporosis,
Am. J. Med. 75 (1983) 899–901.
7. G. Lyons, S.M. Eisenstein, M.B. Sweet, Biochemical changes in intervertebral disc degeneration, Biochim. Biophys. Acta 673 (1981) 443–453.
8. Y. Kawaguchi, M. Kanamori, H. Ishihara, et al., The association of lumbar disc disease with
vitamin D receptor gene polymorphism, J. Bone Joint Surg. Am. 84 (2002) 2022–2028.
9. T. Kimura, K. Nakata, N. Tsumaki, et al., Progressive generation of the articular cartilage and
intervertebral discs: an experimental study in transgenic mice bearing a type IX collagen mutation,
Int. Orthop. 20 (1996) 177–181.
10. G. Dommissee, Morphological aspects of the lumbar spine and lumbosacral regions, Orthop.
Clin. North Am. 6 (1975) 163–175.
11. N.A. Ebraheim, R. Xu, M. Darwich, et al., Anatomic relations between the lumbar pedicle
and the adjacent neural structures, Spine 15 (1997) 2338–2341.
12. J.A. McCulloch, P.H. Young, Essentials of spinal microsurgery, Lippincott-Raven, Philadelphia, 1998.
13. M.D. Humzah, R.W. Soames, Human intervertebral disc: structure and function, Anat. Rec.
229 (1988) 337–356.
14. M.T. Milen, D.A. Bloom, J. Culligan, et al., Albert Adamkiewicz (1850-1921)—his artery
and its significance for the retroperitoneal surgeon, World J. Urol. 17 (1999) 168–170.
15
F IG UR E 2 -1 2 Diffuse Idiopathic Skeletal Hyperostosis
Histological Changes in the Aging Spine
Kiran F. Rajneesh, G. Ty Thaiyananthan, David A. Essig, and Wolfgang Rauschning
k e y p o i n t s
e aging spine is predisposed to various disorders, with back pain being the
primary complaint.
Intervertebral disk degeneration is the commonest pathology in the aging
spine.
Osteoporosis of the vertebral bodies is a preventable cause of back pain.
Facet joint degeneration can lead to painful facet joint syndrome.
Back pain in older patients is amenable to treatment with a better
understanding of the disease pathogenesis.
3
INTRODUCTION
Back pain is one of the most common reasons for office visits to a physician. It accounts for 2% of all visits, surpassed only by routine examinations,
diabetes, and hypertension.
affects the older population. Increased survival rates, better health care outcomes, and improved economic status will increase the number of older
people in our society. At present, persons older than 65 years constitute 13%
of our population. In 30 years, they will constitute 30% of the United States
population, and by the year 2050 they will makeup 60% of the population.
It is of paramount importance to recognize this trend of aging in the population and plan how best to fulfill the health needs of this growing part of
our society.
Aging is a natural, inevitable, physiological change that leads to compromises in physical, mental, and functional abilities. At a cellular level, it represents decreased regeneration and repair, and increased catabolic changes that
gradual deterioration in function. The spine, composed of the framework of
vertebral columns and intervertebral disks encasing the spinal cord, is not
insensitive to the onslaught of changes that occur during aging. The aging of
the spinal cord results in decreased strength and agility and increased reflex
times. However, the predominant effects of aging in the spine involve the
mechanical components of the spine. Histologically, they can be classified
as aging of the disks, the vertebral bodies, the facet joints, and the muscles
and ligaments.
1
Back pain is a condition that predominantly
INTERVERTEBRAL DISK
The intervertebral disks are remnants of the notochord and are interspersed
between adjacent vertebral bodies of the spine except between the fused bodies of the sacrum and the coccyx. The intervertebral disks are composed of a
circular ring of more resilient annulus fibrosus, which holds a central core of
gelatinous material called the nucleus pulposus (Figure 3-1). Biochemically,
both the annulus fibrosus and the nucleus pulposus contain proteoglycans
in addition to water. The amount of water varies and is responsible for their
varied characteristics and, consequently, their functions. The intervertebral
disks derive their nutrition by diffusion across vertebral endplates. As the
rate of permeability decreases with aging, the health of the disk is threatened.
The intervertebral disks are primarily shock absorbers and are resistant
to compressive forces. During the process of aging, the daily wear and tear
16
F IG UR E 3 - 1 Intervertebral disk. Outer annulus fibrosus surrounding
inner nucleus pulposus. (Courtesy of Wolfgang Rauschning, MD.)
2
F IG UR E 3 - 2 Neovascularization at periphery of an annular tear.
(Courtesy of Wolfgang Rauschning, MD.)
damage of years of mechanical stress compounded by decreased nutrition
and water predispose the disks to degeneration. Associated with these local
changes, systemic changes of aging such as decreased structural protein synthesis, impaired water metabolism, and decreased physical activity serve as
additional insults to the fragile microenviroment of the aging disks.
The pathophysiology of disk degeneration involves a multitude of cellular and biochemical changes. Proteoglycans, responsible for the osmotic
gradient and thus the hydration of the disk, are lost. There is overall fragmentation of type I and type II collagen within the disk, with an increase in
the ratio of type I to type II collagen fibers. Furthermore, there is an increase
in degradative enzymatic activity including cathepsins and matrix metalloproteinases (MMPs). As a result, there is a decrease in the biomechanical
and load-sharing ability of the disk.
Due to decreased turgor and nutrition of the disks, radial and concentric
fissures appear in the initial phases of degeneration. The normal avascular
disks may develop microvascular capillaries at the periphery of the annulus
fibrosus as a compensatory mechanism for decreased nutrition (Figure 3-2).
C H A P T E R 3 Histological Changes in the Aging Spine
BA
FI G U RE 3- 3 Degenerative changes on T2-weighted MRI. Note the decreased brightness of the intervertebral disk,
the annular fissures, and the disk-space narrowing.
17
A
D
F IG UR E 3 -4 Cascade of disk degeneration. A, Healthy disk with an intact nucleus pulposus and annulus fibrosus. Weakening of or injury to the annulus
coupled with loss of hydration and proteoglycans of the nucleus can lead to loss of disk height and subsequent endplate changes (B-E) (Courtesy of Wolfgang
Rauschning, MD.)
B
E
C
However, this impaired neovascularization is detrimental, contributes to
microedema, and exposes the disks to the body’s immune cells for the first
time in adult life. Also, there is dissection of the microstructural organization of the annulus fibrosus. The radial fissures eventually enlarge and follow the path of least resistance posterolaterally in relation to the vertebral
bodies and overlying the intervertebral foramina. In the late stages of disk
degeneration, the nucleus pulposus tracks out over the intervertebral foramina and can compress the exiting spinal nerve, potentially causing symptoms
of radiculopathy.
Plain x-ray films show decreased intervertebral spaces, accompanied by
deformed endplates and osteophyte formation. However, these are terminal
changes and not helpful from an early diagnostic point of view. Magnetic
resonance imaging (MRI) is regarded as the gold standard for early detection of disk degeneration. Disk desiccation (unhealthy disks are darker due
to lesser water content), disk bulge due to deformed annulus fibrosus, and
radial tears within the disk are early makers of disk degeneration
3
(Figures
F IG UR E 3 -5 The vertebral body is composed of cancellous bone.
3-3, 3-4). Novel imaging techniques such as MR spectroscopy to measure
lactic acid within the disk (an early sign of disk degeneration), diffusion tensor imaging (DTI) for measuring water content within the disk, and functional MRI (fMRI) for task dependent signal intensity changes have been
proposed and warrant further study.
same property predisposes the cancellous bones to accelerated changes
during aging. They are supplied by a rich network of vascular channels
at low pressure, compared to cortical bones found elsewhere in the body
which have haversian canals with high-pressure vascular channels. The
increased vascularity in vertebral bodies, coupled with a low pressure
VERTEBRAL BODIES
The vertebral bodies are the primary support of the spinal cord and are
osseous in nature. They differentiate from the segmental sclerotomes in
embryological life and form the framework to support the spinal cord and
its vascular supply. Vertebral bodies are composed of cancellous bone and
are best adapted to resist compressive loads (Figure 3-5). However, this
system, increases their surface area ratio and sensitizes them to minute
changes in hormones and other factors in the extracellular fluids. On a
biochemical level, the cancellous bone is a lattice network composed of collagen and noncollagen proteins and calcium hydroxyapatite. The osteoid
framework is laid down by osteoblasts and resorbed and restructured by
osteoclasts, both of which are under the influence of parathyroid hormone
(PTH) and calcitonin.
18
P A R T I Introduction to the Aging Spine
F IG UR E 3 -6 Compression fracture.
The bone density is maximal at 25 years of age and decreases with aging.
Osteoporosis is characterized by decreased bone formation and mineralization as well as decreased bone density.
4
This effect is multifactorial in nature.
During aging, there is a decrease in absorption and assimilation of nutrients
including calcium and vitamin D. Decreased conversion of vitamin D
vitamin D
in kidneys decreases the mineralized components of the bone.5
3
2
to
There is also a general decline in production of various hormones influencing bone formation including PTH, estrogen, and glucocorticoids, which
decrease osteoblastic activity. Furthermore, there is an increase in IL-6,
TNF-α, and other chemokines due to impaired immunity which increases
osteoclastic activity. In addition, there is usually an overall decline in physical activity and exercise and decreased quality of diet in the elderly. All these
factors together precipitate an osteopenic state.
Patients usually present with overwhelming back pain brought on after
sudden physical activity, after lifting objects, or after coughing or bending.
Plain radiographs show a decreased vertebral body height, decreased bone
density (a 30% reduction in mineralization from baseline is required to visualize osteopenia on plain radiographs), and compression fractures (Figure 3-6).
The bone density scan, also known as the dual energy x-ray absorptiometry
(DEXA) scan, is an enhanced form of x-ray technology and the gold standard for imaging osteoporosis. The results of a DEXA scan are expressed as a
T-score, which is an index of standard deviation. A T-score of less than −2.5 is
significant for osteoporosis. Quantitative CT is an alternative imaging modality but requires high-resolution CT scanners and may not be available at all
6
centers.
High-resolution MR imaging has been proposed and is focused on
assessing bone structure directly rather than only assessing mineralization.
7
F IG UR E 3 - 7 Facet joints are composed of synovial joints lined with
synovium and articular cartilage. (Courtesy of Wolfgang Rauschning, MD.)
F IG UR E 3 -8 The three-column motion segment. 70% of the axial load
is borne by the intervertebral disk, while up to 30% may be borne by the facet
complex.
FACET JOINTS
Facet joints are the only true synovial joints within the vertebral column. The
facet joint is located between two adjacent vertebral bodies with the upper
facet facing downwards and medially and the lower facet facing upward
and laterally. The facets articulate with a thin interspersed cartilage and are
surrounded by a synovial sac and innervated by rich nerve endings (Figure
3-7). In a healthy young individual, the intervertebral disk is the anterior
load-bearing structure and the facet is the posterior load-bearing structure.
Hence facet joints are referred to as the three-joint complex, with two facets
and the intervertebral disk (Figure 3-8). These joints allow flexion-extension
and some torsion of the spine.
secondary to disk degeneration. Increased load is subsequently transferred
to the facet joints, which were designed for small load-bearing capacity. This
increased load causes facet joint degeneration. The cartilage is the first structure to be affected, with resultant synovial inflammation, joint space narrowing, and osteophyte formation resulting in central or foraminal stenosis and
spondylolisthesis (Figures 3-9, 3-10). The resulting inflammation causes
irritation of the nociceptive nerve endings, causing back pain sometimes
referred to as “facet joint syndrome.”
8
During aging, facet joint pathology is always
9
F IG UR E 3 -9 Degenerative cascade. Disk degeneration leading to
increased facet loading and degeneration resulting in instability and spondylolisthesis.
On plain radiographs, sclerosis and osteophyte formation can be visualized in facet joints, demonstrating late stages of degeneration. MR imaging of the cartilage revealing focal erosions may be the earliest sign of facet
C H A P T E R 3 Histological Changes in the Aging Spine
FI G U RE 3- 1 0 MRI and CT evidence of foraminal and central stenosis as a result of facet osteophyte development.
19
degeneration and may be amenable to rescue measures. Facet hypertrophy,
apophyseal malalignment, and osteophyte formation may be recognized on
CT scans.
10
MUSCLES AND LIGAMENTS
The intrinsic and extrinsic muscles, along with the ligaments, maintain the
spine at optimal tension and maintain the normal physiological primary
curvatures.
11
The ligamentum flavum connects adjacent vertebrae along
the anterior edge of the lamina. It is primarily composed of elastin, and
allows flexion and extension. The elastin content is responsible for the tensile strength of the ligamentum flavum. During aging, the muscles lose the
ability to attain tetanic contractions, have decreased contractile force, and
undergo atrophy. This atrophy is due to a decline in nutrition and hormonal
status, in addition to decreased physical activity. Microscopically the muscles show decreased collagen fiber content and increased fatty infiltration.
The ligamentum flavum has decreased elastin content and becomes lax and
bulging, destabilizing the vertebral column.
12
These changes predispose the
aging spine to disk degeneration, compression fractures, and spinal stenosis
by altering the normal curvature and the normal tension within the spine.
Plain x-ray studies may show calcifications and altered curvatures of the
spine. However, MR imaging may show atrophy of specific muscles, fatty
infiltration. and impaired architecture of ligaments in aging.
SUMMARY
Aging results in irreversible, permanent changes to the spinal column. The
findings of disk, facet, vertebral body, and ligamentous pathology play an
interrelated role in the aging spine. Thus, the management of these patients
must take into account all of these interrelated elements. Future treatment
challenges will not only center on treating end-stage disease, but also in preventing disease progression.
References
1. B.I. Martin, R.A. Deyo, S.K. Mirza, et al., Expenditures and health status among adults with
back and neck problems, Jama 299 (2008) 656–664.
2. V. Turkulov, N. Madle-Samardzija, O. Niciforovic-Surkovic, C. Gavrancic, [Demographic
aspects of aging], Med Pregl 60 (2007) 247–250.
3. W. Johannessen, J.D. Auerbach, A.J. Wheaton, et al., Assessment of human disc degeneration and proteoglycan content using T1rho-weighted magnetic resonance imaging, Spine 31
(2006) 1253–1257.
4. Y.L. Lee, K.M. Yip, The osteoporotic spine, Clinical orthopaedics and related research (1996)
91–97.
5. T.L. Nickolas, M.B. Leonard, E. Shane, Chronic kidney disease and bone fracture: a growing
concern, Kidney international, 2008.
6. H. Shi, W.C. Scarfe, A.G. Farman, Three-dimensional reconstruction of individual cervical
vertebrae from cone-beam computed-tomography images, Am J Orthod Dentofacial Orthop
131 (2007) 426–432.
7. A. Zaia, R. Eleonori, P. Maponi, R. Rossi, R. Murri, MR imaging and osteoporosis: fractal
lacunarity analysis of trabecular bone, IEEE Trans Inf Technol Biomed 10 (2006) 484–489.
8. A. Fujiwara, K. Tamai, M. Yamato, et al., The relationship between facet joint osteoarthritis
and disc degeneration of the lumbar spine: an MRI study, Eur Spine J 8 (1999) 396–401.
9. P.P. Raj, Intervertebral disc: anatomy-physiology-pathophysiology-treatment, Pain Pract 8
(2008) 18–44.
10. M. Barry, P. Livesley, Facet joint hypertrophy: the cross-sectional area of the superior articular
process of L4 and L5, Eur Spine J 6 (1997) 121–124.
11. M. Yamada, Y. Tohno, S. Tohno, et al., Age-related changes of elements and relationships
among elements in human tendons and ligaments, Biological trace element research 98
(2004) 129–142.
12. H. Kosaka, K. Sairyo, A. Biyani, et al., Pathomechanism of loss of elasticity and hypertrophy
of lumbar ligamentum flavum in elderly patients with lumbar spinal canal stenosis, Spine 32
(2007) 2805–2811.
Natural History of the Degenerative Cascade
Ali Araghi and Donna D. Ohnmeiss
4
k e y p o i n t s
For many years, the mechanics of the spine and how spinal tissues respond
to the demands placed upon them has been studied, as well as the role of
mechanical loading in impacting degeneration of spinal structures.
e body of knowledge continues to grow, giving us greater insight into the
complicated biochemistry of the intervertebral disc.
Degeneration of the spinal segment is a very complex process, which is
complicated by the high degree of interrelationship of the various spinal
structures.
e specific details of disc-related pain mechanisms resulting in a patient’s
clinical symptoms remain elusive.
Along with disc degeneration, the posterior elements also degenerate, which
may produce pain arising from the facet joints and, often, pain related to
central or foraminal stenosis.
NATURAL HISTORY OF THE DEGENERATIVE
CASCADE
The degenerative process encompasses every element of the spine: the ligamentous structures, facet joints, intervertebral discs, endplates, and vertebral
bodies. Changes occur in a sequential fashion on a multitude of levels,
including the gross visual level, the radiographic level, the biomechanical
level, and the biochemical level. Unfortunately, the changes seen in the normal aging spine are very similar to the changes seen in the pathologic and
symptomatic spine. Hence, it becomes extremely difficult to differentiate the
symptomatic conditions from the manifestations of a normal aging spine. It
is only after understanding the normal changes associated with aging that
we may be able to identify some of the pathologic changes.
The natural history of degenerative disc disease has been studied for
many years. Lees and Turner, in 1963, followed 51 patients with cervical
radiculopathy for 19 years and found that 25% had worsening of the symptoms, 45% had no recurrence, and 30% had what they classified as mild
symptoms.
cervical myelopathy over 20 years.
presented with early symptoms did not progress, and approximately 66%
of patients with moderate to severe symptoms did not progress either. The
patients who progressed tended to be the younger patients.
1
Nurick studied the nonsurgical treatment of 36 patients with
2
Sixty-six percent of the patients who
ANATOMY AND GENERAL MECHANISMS OF PAIN
In order to understand the degenerative cascade of the spine, it is of paramount importance to understand the normal function of the different structures and how they interrelate with each other. The facet joints are designed
to bear approximately 10% to 30% of the load in the lumbar spine, depending on the patient’s position. The articular cartilage that bears such loads is
supported by the subchondral bone. The subchondral bone also serves to
20
provide nutrition to the articular cartilage. The facet joints are diarthrodial
synovial joints that have a capsule. The capsules together with the ligaments constrain joint motion. The medial and anterior capsule is formed
bya lateral extension of the ligamentum flavum. The capsules and ligaments
are innervated by primary articular branches from larger peripheral nerves
and accessory articular nerves. Such nerves consist of both proprioceptive
and nociceptive fibers. They are monitored by the central nervous system,and may perceive excessive joint motion (potentially due to instability
or an injury) as a noxious stimulus and mediate a muscular reflex to counteract such excursions. Nociceptive free nerve endings and mechanoreceptors have been isolated in the human facet capsules and synovium. Such
nerve endings may perceive chemical stimuli or mechanical stimuli such as
instability, trauma, or capsular distention as noxious stimuli. Joint effusions,
commonly seen on MRIs, may prevent such reflexes due to capsular distention, similar to a distended knee joint and absent patellar reflex. Substance
P, a pain-related neuropeptide, has been identified in synovium. Higher concentrations have been found in arthritic joints. Additionally, capsular free
nerve endings have been found to become sensitized in arthritic joints. This
has caused otherwise dormant nerve endings to become reactive to motion
that was perceived as normal in nonarthritic conditions.
The intervertebral disc is another significant component of the degenerative cascade. The sinuvertebral nerve innervates the posterior and posterolateral aspect of the intervertebral disc, as well as the posterior longitudinal
ligament (PLL) and the ventral aspect of the thecal sac. The lateral and
anterior aspect of the disc is innervated by the gray ramus communicans.
These free nerve endings have been found primarily in the outer one third
of the annulus, and have been found to be immunoreactive for painful neuropeptides. Some complex endings have been identified within the annulus
as well. The considerable overlap of the descending and ascending nerve
endings with branches of the sinuvertebral nerves of the adjacent one to two
discs makes identifying the exact pain generator even more difficult when
performing clinical diagnostic tests. Leakage of such neuropeptides out of
the disc in the presence of annular tears, onto the nearby dorsal root ganglion (DRG), can cause irritation of the DRG and become another source
of pain. The PLL fibers are closely intertwined with the posterior annulus.
The PLL has been identified to contain a variety of free nerve endings.
Hence any irritation of the posterior annulus and disc can cause irritation
of these nerve endings. Such irritation can be mechanical secondary to pressure from a herniated disc, abnormal motion from instability, or mechanical incompetence of the annulus. Irritants can also be chemical such as low
pH fluids, cytokines, or neuropeptides that can leak out from the disc via
annular tears.
Cortical bone, bone marrow, and periosteum have been found to be
innervated by nerves containing nociceptive neuropeptides such as calcitonin, gene-related peptides, and substance P. Periosteal elevation, such as
in cases of infection, tumor, or hematoma, can be painful. Periosteal tears
incases such as fractures, inflammation, or subsidence (e.g., in osteoarthritic
conditions) can cause pain. Vascular congestion from bone infarcts or sickle
cell can cause the intramedullary nerve fibers to initiate a painful response.
C H A P T E R 4 Natural History of the Degenerative Cascade
21
Nociceptive nerve fibers have been identified in varying concentrations
within the fibrous tissue of spondylolytic pars defects as well.
The spine is covered with muscles and tendons in which the main
nociceptive nerve endings are unencapsulated. Pain may be mediated by
chemical or mechanical conditions or both. The mechanonociceptive units
may respond to disruption, stretch, or pressure. Direct injury can cause
damage to the intrafascicular nerve fibers or cause a hematoma and edema,
which can lead to a chemically mediated pathway. Such a pathway can begin
by release of nociceptive sensitizing chemicals such as histamine, potassium,
and bradykinin from the damaged tissues. This, in turn, can lead to altered
vascular permeability and an influx of the inflammatory cells. It is through
such neuropeptides that sensitization of the receptors occurs and, in combination with interstitial edema, this can cause primary muscular pain. At
times, the mechanical effect of spasm of a major muscle group in and of itself
can cause further trauma to the muscle, and potentiate the pain cascade.
PATHOGENESIS OF LUMBAR DEGENERATION
During childhood and the first two decades of life, the spinal motion segments generally function in a physiologic manner and the disc maintains its
hydrostatic properties. Hence, the disc maintains its height and its normal
relationship with the facets, allowing the facets to experience normal loads
and physiologic motion. The canal and the foramen are usually patent and
the ligamentum flavum is only a few millimeters thick. Invagination of the
disc into the endplates (Schmorl nodes) and some facet asymmetry may
be seen, but are generally not symptomatic. In the next 20 years, however,
degeneration does occur and annular tears occur that lead to disc bulging
and protrusion, which can then cause loss of disc space height and loss of
hydrostatic properties. This, in turn, will cause increased loads on the facets
and initiate facet hypertrophy and neural encroachment. Such hypertrophy,
when present in combination with loss of disc height, potentiates foraminal compromise. Ligamentum flavum hypertrophy occurs as well, which
together with facet hypertrophy potentiates central canal compromise. Loss
of disc height can certainly cause loss of stature in the elderly population.
BIOCHEMICAL CHANGES
Numerous biochemical changes occur in the disc as a result of aging. The
gelatinous nature of the disc degenerates into a more fibrotic state due to
loss of water content. It is important to understand that a normal disc is
composed of 80% water and 20% collagen and proteoglycans. The negatively
charged glycosaminoglycans are what allows the nucleus to retain its water
content and osmotic pressure. The actual cascade of nucleus degeneration
occurs in the following order. First, there is loss of distinction between
the nuclear and annular fibers and an increase in the collagen content of
the disc, followed by the loss of the negative charges mentioned earlier
and loss of water content, greatly reducing the proteoglycan aggregates. In
fact, during the breakdown of the glycosaminoglycans, there is also a significant loss of chondroitin sulfate in comparison to keratin sulfate. The
annulus degenerates by a decrease in cellularity and metabolic activity. The
annulus is the only portion of the disc that in its healthy state has vascularity. This vascularity decreases with degeneration, which may hinder
the healing process. Proteoglycan content decreases and large collagen fibrils
appear. The large fibrils when present in a biomechanically vulnerable portion of the annulus may increase the likelihood of annular tears. Such tears
generally occur due to a rotational force and occur in the posterolateral
annulus. With annular disruption, changes take place within the disc itself.
Vascularized granulation tissue forms along the margins of the annular ruptures and may pass as far as into the nucleus.
tomatic subjects, among discs taken from back pain patients, nerve endings
extended deep into the annulus and in some cases into the nucleus. Such
nerves produced substance P.
4
These changes within the disc likely play a
role in discogenic pain. Also, such changes may challenge disc regeneration
as a pain-relieving intervention.
The cartilaginous endplate serves as a nutrition gradient for the healthy
disc. Degeneration of the disc has been associated with a decrease in the diffusion capability across the endplate and sclerosis of the endplate, which in
turn negatively affects the nutrition of the disc.
have a negative impact on the biochemical medium within the disc, if it is
3
Unlike discs from asymp-
5
This is thought to at least
not the actual cause. These types of degenerative and nutritional changes
within the disc will likely pose a significant challenge to disc regenerative
therapies.
Kirkaldy-Willis et al. inspected 50 lumbar cadaveric specimens and also
analyzed morphologic changes in 161 patients’ lumbar spines intraopera-
6
tively.
It is such observations that have provided links between the different
aspects of the degenerative cascade, leading to a better understanding of the
transformation of a healthy level in the spine to a stenotic level with spondylolisthesis and instability.
BIOMECHANICAL CHANGES
The theory of the three joint complex, and the interdependence of these
elements, was recognized and described by Farfan and co-workers.
interdependence and sequence of degeneration is outlined in Figure 4-1.
Furthermore, the increased risk of the lower two levels for degeneration, secondary to their increased lordotic shape of the disc as well as their increased
vulnerability to rotational injuries due to the exaggerated obliquity of their
facet joints, was recognized. The two mechanisms of propagation of degeneration that were described consisted of a minor rotational injury causing
facet injuries and annular tears and a repetitive compressive injury causing
minor damage to the cartilage plate, which would serve as an early stimulus
for progressive disc degeneration over time. Additionally, it was postulated
that the abnormal stresses of a degenerated segment will affect the adjacent
levels. The biochemical changes are accompanied and potentiated by biomechanical factors. The healthy disc has hydrostatic properties that allow the
nucleus to convert axial compressive forces to tensile strain on the annular
fibers as well as evenly share the load over the endplates. The oblique
arrangement of the crossing collagen fibrils in the annulus allow it to convert
the axial loads to tensile strains. In fact, the annulus is largely made of type
I collagen which provides the tensile strength seen in tendons, whereas the
nucleus is largely made of type II collagen. In the degenerative cascade, loss
of hydrostatic properties occurs in the annulus and nucleus, and the osmotic
pressure of the disc decreases, allowing an increase in creep by a factor of two.
The disc loses its ability to imbibe water and to evenly distribute the loads
that it is under. This is due to changes in the molecular meshwork of the
proteoglycan collagens. Annular fissures occur, and, as a result of repetitive
trauma, coalesce together and become radial tears. Radial tears render the
disc even more incompetent. Such factors, particularly when potentiated by
biochemical changes, cause resorption of disc material, and facilitate adjacent endplate sclerosis. Rarely may resorption lead to spontaneous fusion
of the disc. Herniations are generally more likely in the earlier stages of
degeneration when the intradiscal pressures are higher than in the more
advanced stages. Offending osteophytes, however, are more likely in the
more advanced stages of degeneration.
The medial and anterior facet joint capsules are made of approximately
80% elastin and 20% collagen. Degeneration starts by a synovial inflammatory response and fibrillation of the articular cartilage of the joint. This
progresses to gross irregularity of the articular cartilage and formation of
osteophytes. Eventually, one of the articular processes may fracture and
become a loose body as well as contribute to capsular laxity, which will allow
excessive motion of the joint and instability. The facet and discchanges cause
mechanical incompetence of a motion segment and may lead to abnormal
sagittal translation, further compromising the neural elements (Figure 4-2).
Compensatory posturing is observed in the elderly with spinal stenosis as
a forward flexed posture in an attempt to put the spine into flexion and
increase the space available for the neural elements. This posturing will
offload the degenerated facets and potentially decrease facet pain as well.
7
This
THE THREE STAGES OF INSTABILITY
The theory of biomechanical degenerative instability was described by
Kirkaldy-Willis and Farfan in 1982.
entity when the patient changes from mild symptoms to severe symptoms
acutely with minimal activity or provocation. This was explained as abnormal joint deformation with stress, which produces a symptomatic reaction
in the affected area, hence causing pain. The factors that affect such instability are primarily the increased motion of the joint and, secondarily, the
physical changes that occur within the joint with repetitive trauma. They
8
They defined instability as a clinical
22
P A R T 1 Introduction to the Aging Spine
Posterior joints
Synovial reaction
Cartilage destruction
Osteophyte formation
Capsular laxity
Subluxation
Enlargement articular
process (and laminae)
Effect of recurrent strains at levels above and below the original lesion
Herniation
One-level
central stenosis
Intervertebral discThree-joint complex
Circumferential tears
Radial tears
Internal disruption
Loss of disk heightInstability
Disc resorptionLateral nerve entrapment
Osteophytes at back of
vertebral bodies
F IG UR E 4 - 1 Overview of the interrelation
of disc and posterior element degeneration.
(From Kirkaldy-Willis WH, et al: Pathology and pathogenesis of lumbar spondylosis and stenosis, Spine
3:320, 1978.)
Multilevel degenerative lesions
Multilevel spinal stenosis
A B
C D
F IG UR E 4 -2 As the spinal segment progresses from normal (A) to
degenerative, positional changes may become more pronounced such as nerve
root compression in extension (B), or patients leaning forward to increase
the narrowed foramen (C). Eventually, the segment collapses and osteophytes
form (D).
divided the clinical symptoms into three phases. First, a stage of temporary
dysfunction, second, an unstable phase, and lastly, a stabilization phase. In
the temporary dysfunction stage, the increased abnormal motion may actually manifest itself as decreased overall motion secondary to acute inflammation, muscle spasm, or guarding. The spinous processes may be held in
midline or to one side secondary to spasm and hence limit lateral bending
and rotation. Vertebral tilting and rotation are coupled in the spine and
produce lateral bending. Abnormal excursion of the facets may be seen on
lateral flexion and extension radiographs. Generally, significant abnormal
shear or translation does not occur if there is a healthy disc present. In
the second stage, the changes become more constant and long-lasting, yet
the spine still has increased motion present. As stage two progresses the
changes become more irreversible. Stage three is accompanied by advanced
degeneration and loss of disc height as well as the presence of stabilizing
osteophytes. This stage is generally more stable and less prone to instability.
Some of the key clinical findings of each stage are summarized in Table 4-1.
In this context, injury is defined as any force that is too great for the joint
to withstand. Such forces do not necessarily have to be from a significant
traumatic episode or from lifting a heavy object, but simply from uncoordinated muscle activity supporting the patient’s body weight. Injury can cause
trauma to the articular surface and capsule of the facets, as well as to the endplates and disc annulus. . However, much larger external trauma is required
for injury to the other ligamentous tissues and muscles. Facet joint articular
surface injuries will start with fibrillation and progress to erosion and eburnation. Finally, subchondral fractures can lead to complete fractures and
loose bodies as alluded to earlier in this chapter. By the same token, the
synovial membrane will thicken through this inflammatory process and
develop an effusion, which can become exudative and create fibrosis. If
capsular tears occur, they may cause initial instability. Recovery with minor
trauma is usually complete, though it can lead to a more prolonged vulnerable (unstable) phase.
C H A P T E R 4 Natural History of the Degenerative Cascade
23
With major traumatic episodes, the damage is different in that endplate
fractures or detachment of peripheral annulus from the endplate can occur.
This is especially likely if the segment is already in a more unstable phase.
The body’s reparative process consists of microvascular invasion and loss
of normal annular and nuclear cells. This, in turn, will lead to loss of discheight. Such changes generally occur at the same time as when the facets
begin to fragment, hypertrophy, and override. This, in combination with
the thickening of the ligamentum flavum, will lead to central and foraminal
stenosis. Repetitive injuries cause fibrosis and scar formation, but can also
prolong the unstable phase. In cases of prolonged instability, the eventual
loss of disc space height and formation of endplate osteophytes will stabilize the segment. Depending on the mode of impact of the forces, different
parts of the spine will be injured and the reparative process will vary. Such
variations are the determining factor for whether the reparative process will
further destabilize the segment. Such instabilities may occur after multiple
traumatic episodes or after only one.
The different modes of injury can induce episodic severe dysfunction by their interaction with the pathologic processes already present in
the spine. The forces can be applied as direct axial compression. These
forces are typically less damaging to the discs or facets when they are in
their healthier phase, but further down the degenerative cascade, when
there are more degenerative changes in the discs and annulus, the effects
of such forces can become more damaging. Injury can also be directed in a
torsional direction. Such injuries tend to put more stress on the facets and
outer annular fibers. Facet injuries are even more pronounced in the lower
TA BL E 4 1 Clini cal o bservatio ns se en in the Kirk aldy -
Willis c lassification stage s of spinal
degene rati on
Phase I Dysfunction II Unstable III Stabilization
Symptoms
Signs Local tenderness
Radiological
changes
From Bertilson BC, et al: Inter-examiner reliability in the assessment of low back pain (LBP)
using the Kirkaldy-Willis classification (KWC), Europ Spine J 2006:1696.
Low back pain
Often localized
Sometimes
referred
Movement painful
Muscle contracted
Hypomobility
Extension painful
Seldom neurology
Abnormal
decreased
movement
Spinous processes
malaligned
Irregular facets
Early disc changes
ose of dysfunction
Giving way of
back: “catch”
Pain on coming to
standing position
after flexion
Detection of
abnormal movement (inspection,
palpation)
Observation of
“catch,” sway, or
shift when coming
erect after flexion
Anteroposterior:
Lateral shift
Rotation
Abnormal tilt
Malaligned
spinous processes
Oblique:
Opening facets
Lateral:
Spondylolisthesis
(in flexion)
Retrospondylolisthesis (in
extension)
Abnormal opening
of disc
Abnormal change
in pedicle height
CT changes:
Disc bulging
Less low back
pain
Mainly leg pain
Muscle
tenderness
Stiffness
Reduced
movement
Scoliosis
Some neurology
Enlarged facets
Loss of disc
height
Osteophytes
Small foramina
Reduced
movement
Scoliosis
lumbar and lumbosacral spine where the facets are more coronally oriented
and more prone to torsional injuries. Additionally, forces can cause a creep
effect over time. Axial creep may cause bulging of the disc and loss of discheight, especially at the lumbosacral junction where the forces are applied
at an angle. Also important to note is that the erect patient adds extension
to the lumbosacral junction which further narrows the canal and foramen.
Injuries occurring with the patient in a semi-prone position can cause the
segment to experience further unilateral foraminal narrowing, which, along
with preexisting axial creep, can cause dynamic foraminal nerve entrapment.
Torsional creep will cause rotation of one vertebra on the other, which can
cause bulging of the posterolateral corner of the annulus. This, along with
the rotated posterior facet and lamina, can lead to lateral recess and foraminal narrowing.
CLINICAL INSTABILITY AND DIAGNOSTIC IMAGING
Instability can be suspected based on symptoms of recurrent low back pain
and sciatica without any neurologic deficit that starts with minimal trauma
and is relieved by rest and bracing. Repetitive recurrence in a short period of
time is typical. Another suspicious sign of instability is symptoms of pain,
temporarily relieved by manipulation or mobilization of the spine, recurring with minimal activity. Pain on forward bending with a painful clunk on
trunk extension is a sign of instability. Rotoscoliosis may be present as well.
Most of such injuries occur in the lower lumbar region (L4-5 greater than
L5-S1, in a 2:1 ratio). However, the presence of a deep-seated L5 within the
pelvis (intercrestal line being at L4-5 disc or upper portion of L5 vertebral
body) and elongated L5 transverse processes, protects the L5-S1 level and
increases the chances of injury to the L4-5 level. Conversely, a high position
of the L5 vertebral body (intercrestal line at lower portion of L5 vertebral
body or the L5-S1 disc space) along with short L5 transverse processes
increases the chances of L5-S1 injury.
Careful attention to x-rays can identify signs of instability, such as
McNab traction spurs, which occur below the rims of the endplates, or the
presence of gas in the disc space, sometimes referred to as Knutsson sign.
Lateral flexion/extension x-rays can help identify instability by revealing a
dynamic spondylolisthesis or retrolisthesis. Such malalignments can cause
narrowing of the neural foramen, especially in the presence of decreased
F IG UR E 4 -3 Different stages of degeneration present in the same
lumbar spine. (From Kirkaldy-Willis WH, et al: Pathology and pathogenesis of
lumbar spondylosis and stenosis, Spine 3:324, 1978.)
24
F IG UR E 4 -4 Stages I through V of degeneration in the lumbar spine,
based on the Thompson classification. (From Thompson JP, et al: Preliminary
evaluation of a scheme for grading the gross morphology of the human intervertebral disc, Spine 15:411-415, 1990.)
P A R T 1 Introduction to the Aging Spine
I
II
III
IV
V
discspace height. If flexion/extension radiographs demonstrate an exaggerated increase in posterior heights of the disc along with decreased anterior
height of the disc of one level in comparison to the other levels, this may
also be a sign of instability. This finding is sometimes referred to as “rockering.” Less commonly evaluated radiographic modalities include anterior/
posterior side bending films, which may demonstrate asymmetric tilting
of the vertebral body, or decreased bending to one side (which stems from
decreased tilt and rotation in a coupled fashion) with a paradoxical increase
in disc height on the side to which the patient is bending. Exaggerated closure of the disc on the ipsilateral side as the bending can also occur. Lateral
listhesis is due to abnormal rotation of the vertebral body during side bending, which is yet another sign of instability. Spinous process malalignment
and pedicle asymmetry are important to be noted on the AP films as well.
CT scanning a patient while rotated to the left and right side (with similar positioning to that of Judet views) can show gapping of the facet joint
on the side opposite to the rotation of the vertebral body. This causes the
superior articulating process to shift anteriorly and narrow the lateral recess
on the ipsilateral side as the gapping. Such a finding can be consistent with
dynamic nerve entrapment in the lateral recess.
CONCLUSION
In summation, we have to compile the degenerative changes of each of the
different parts of the spine, and apply them to the theory of the interrelated three-joint (tripod) complex. Injury to one part of the spine can cause
abnormal motion and load transfers, and hence affect the other parts of the
spine over time. Loss of disc height causes the posterior facets to sublux
and the superior articular process of the level below to migrate upward and
anteriorly, hence narrowing the lateral recess and possibly impinging on the
traversing root. This is especially true when there is concomitant hypertrophy of the superior articular process. Depending on the amount of loss of
disc height, the neural foramen can be narrowed as well and cause exiting
root impingement. If the initial injury was asymmetric with respect to one
facet joint, then that facet can degenerate, hypertrophy, stretch the capsule,
and become more lax than the other side. In such a case scenario, a rotational
deformity begins to occur which can simultaneously cause eccentric bulging
of the disc due to its rotational instability, and cause unilateral lateral recess
stenosis. Experimental work supports the concept that abnormal motion
at one level causes nonphysiologic strains at the adjacent levels which can
lead to multi-level involvement. This can explain why degeneration is typically seen in multiple adjacent levels of the spine in different stages of the
cascade (Figure 4-3). Posterior element laxity and increased motion can
exert additional forces on an already partially degenerated disc, render the
segment incompetent to physiologic loads, and cause a degenerative spondylolisthesis. Certainly the reverse order of events can occur as well, possibly
more often. When formulating a surgical treatment plan for a patient, it is
of paramount importance to diagnose which of the stages of instability best
fits the patient’s spine at the time of treatment (Figure 4-4). Most stage I and
early stage II will respond to conservative treatment. However, decompression alone for late stage II can lead to further instability and may be better
accompanied by a fusion. Stage III, on the other hand, may best be treated
with decompression alone without fusion.
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