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The first account of the description of cervical degenerative disk disease (DDD) appeared in 1911. Since then, most published studies on cervical DDD have been related to spinal surgery. Although DDD is common in the cervical spine, it manifests later than in the lumbar spine. The quantity of water decreases in the nucleus pulposus as a person ages, and this loss reduces the cushioning effect of the disk. This change further decreases the dynamic function of the disk by directing more mechanical forces to the zygapophyseal joints and reducing the height of the intervertebral space. Not all the degenerative changes are seen on magnetic resonance imaging (MRI), but they can be noted histologically. In addition to the disk, the cartilage end plates of the vertebrae are degenerated, causing blood vessels to grow into the disk and thereby triggering disk ossification. Cervical disk disease encompasses a spectrum of disorders, ranging from diskogenic neck pain to myelopathy. Degenerative disease of the cervical spine can manifest with a variety of clinical signs and symptoms. Nonoperative treatment is the cornerstone of management in the majority of cases. Operative treatment is indicated in patients with neural compression and spinal instability. This chapter presents an overview of cervical DDD.
Epidemiology
Cervical DDD is an age-related phenomenon, as it is in the lumbar spine. Disk degeneration is a natural aging phenomenon, and its prevalence increases with age whether symptoms are present or not. In an MRI study, Boden and associates showed that the disk was degenerated or narrowed at one level or more in 25% of subjects who were less than 40 years old and in almost 60% of subjects who were more than 40 years old. Lehto and colleagues, in another MRI study, showed that abnormalities were found in 62% of subjects who were more than 40 years old, whereas no abnormalities were found in subjects who were less than 30 years old. Among asymptomatic Japanese study subjects, 20% of participants in their 20s and almost 90% of participants who were more than 60 years old had cervical disk degeneration. The most commonly involved disk level in patients who were more than 30 years old was C5-C6. A study by Lawrence and co-workers similarly showed that the C5-C6 and C6-C7 disks were most often degenerated, and the prevalence of cervical disk degeneration increased with age. No differences were found among male and female study subjects. Matsumoto and associates reported that cervical disks were degenerated in 17% and 12% of asymptomatic men and women in their twenties, respectively. In subjects more than 60 years old, the prevalence rose to 86% in men and 89% in women. Moderate to severe cervical degeneration was associated with a past episode or repeated episodes of pain in the neck-shoulder-brachial region. Moderate to severe cervical disk degeneration was associated significantly with lumbar degeneration in both sexes. Although disk degeneration is common in the cervical spine, it appears to begin later in the cervical spine than in the lumbar region.
Pathophysiology
The intervertebral disk is the largest avascular tissue in the human body. Disk nutrition derives from diffusion across the cartilaginous end plates. The intervertebral disk consists of the central nucleus pulposus and the peripherally encircling annulus fibrosus. These structures are important shock absorbers of the spine to body motion. The nucleus pulposus is a remnant of the notochord and consists of the loose network of collagen fibers in a gelatinous fluid that is composed of 85% to 90% water in a young individual. The rest of the matrix is composed of 25% to 35% collagen and 60% to 65% proteoglycans. Aging causes the water content of the nucleus pulposus to decrease, thus resulting in a relative increase of proteoglycan and collagen. The annulus fibrosus is predominantly composed of water (60% to 70%) and, to a lesser degree, collagen (20% to 30%). Unlike in the nucleus pulposus, however, the water content of the annulus fibrosus does not change with age.
Biochemical changes of the spinal unit begin in the nucleus pulposus. With aging, the nucleus pulposus begins to desiccate and loses its mechanical competence. Effective load transmission is no longer possible when this occurs because the normal nucleus pulposus is similar to a contained fluid. Axial loads to the spine are converted to tensile strain on annular fibers and are then transmitted to the vertebral end plates. With continuous loading, creep occurs in the nucleus pulposus. Eventually, the gel structure degenerates. The collagen content of the disk increases while glycoprotein content decreases after the second decade of life. The loss of glycoproteins decreases imbibition pressure. In its relaxed state, the degenerated disk imbibes fluid.
Loading, genetics, and local autocrine factors all influence the rate and degree of disk degeneration. The significant effect of axial loading is evidenced by the high rates of disk degeneration in the lordotic area of the spine. When static compressive stress exceeds the pressure in the disk, water is forced out, thus causing altered intradiskal stress distribution and resulting in a number of harmful, dose-dependent responses. These include apoptosis of the nuclear cells, loss of cellularity, down-regulation of the collagen II and aggrecan gene expression, and increasingly disorganized annulus fibrosis. Cells of the intervertebral disk are metabolically active and are capable of responding to biochemical stimuli. These autocrine factors function as local cellular signals that affect disk degeneration.
The percentage of matrix metalloproteinase-3 (MMP-3)–positive cells correlates with the degree of degeneration on MRI and osteophyte size. Degenerated disks exhibit MMP-3 but no metalloproteinase tissue inhibitor. Disk degeneration is suggested to be caused by an imbalance of MMP-3 and tissue inhibitor of metalloproteinase-1. Cathepsins and other proteolytic enzymes can separate disks from vertebral bodies, thereby affecting the rate of disk degeneration.
The mature annulus fibrosus contains degenerated cells and necrotic debris. Collagen types I and II predominate in the disk. Type I collagen is suited to withstand tensile-type loading and is located in the annulus fibrosus. Type II collagen can sustain tensile loads and is found in the nucleus pulposus. The proteoglycan content of the disk decreases with age. The normal disk contains enzymes active against type II collagen, whereas in the prolapsed disk, the enzyme systems are active against type I collagen. The prolapsed disk contains elastin-degrading enzymes, which are not found in the normal disk. Elastic fibers are located in the annulus fibrosus at the interface of the disk and the vertebral body. The increased presence of elastin- and type I collagen–degrading enzymes in the annulus fibrosus is likely one mechanism for disk herniation. The histologic changes in disk degeneration are seen in adjacent cartilaginous end plates, where neovascularization, capillary wall thickening, and calcification are found.
The normal functions of the annulus fibrosus are to contain the nucleus pulposus and to convert compressive stress to tangential stress. When the nucleus pulposus fails to maintain hydration, strain changes occur at the nucleus-annulus interface. The mechanical effectiveness of the disk decreases with decreasing states of hydration. The disk is no longer able to generate increased intradiskal pressures and is therefore unable to distribute force effectively. The central annular lamellae buckle under constant compressive loading. The disk collapses and causes external concentric bands of annulus fibrosus to bulge outward.
Increased annular stress leads to fibrillation and tearing of annular fibers. In younger patients, disk material prolapses through tears in the annulus fibrosus and causes nerve root or spinal cord impingement. The soft disk herniation causes nerve dysfunction both directly and through vascular compromise of radicular feeder arteries. The exiting nerve root is most commonly affected by disk protrusion. Acute disk herniation and annular degeneration and protrusion are part of a continuum of degeneration that leads to advanced spondylosis. Disk collapse translates into excess motion in the zygapophyseal (facet) joints posteriorly and increased strain in the supporting ligaments. With loss of disk height, the facets begin to override, and uncovertebral joints come into contact, thus forming osteophytes. Decreasing facet competence and increased segmental motion hasten the rate of disk degeneration. Ten years after the disk begins to degenerate, the mechanical competence of the motion segment becomes evident, with facet and uncovertebral joint degeneration. True disk protrusion or a hard disk (osteophytes) can also compress the nerve root and lead to radiculopathy. With continued degeneration, osteophytes along with other pathologic processes, such as disk protrusion or ossification of the posterior longitudinal ligament (OPLL), may compress the central spinal canal. Spinal cord function is affected by vascular insufficiency, and direct mechanical pressure on the neural elements results from central spinal canal stenosis, which may lead to cervical myelopathy.
Risk Factors
DDD has several possible mechanisms, such as decreased proteoglycan and water content, inflammation induced by cytokines such as interleukin-1 and tumor necrosis factor-α, genetics, smoking, occupational load, atherosclerosis, and history of surgery. However, a longitudinal study could not support all suggested DDD theories such as smoking. In addition, the role of body mass index, gender, sports, and alcohol consumption is not certain in the development of DDD of the cervical spine. Smoking was not found to be related to cervical DDD on lateral plain radiographs in a cross-sectional case-control study. No increased risk for herniation was found for sedentary jobs or jobs requiring twisting of the neck, and no increased risk was noted for any sport including weightlifting. In fact, sport activity has been suggested to be protective of the cervical spine. Hence, causal factors for DDD have not been fully established.
Genetics
Hereditary factors could affect disk degeneration through several mechanisms, such as an influence on the size and shape of spinal structures that affect the mechanical properties of the spine and its vulnerability to external forces. Biologic processes associated with the synthesis and breakdown of structural and biochemical constituents of the disk could be partly genetically predetermined, thus leading to vulnerability to accelerated degenerative changes in some persons. The identification of specific genetic influences may eventually provide key insights into underlying mechanisms. Furthermore, for specific genes and some environmental factors, gene-gene interactions and gene-environment interactions may exist.
Another factor that must be considered is age. A particular gene may possibly be associated with DDD only at a certain age. Some genes have been associated with disk degeneration in human beings, including genes coding for collagen type I ( COL1A1 ), collagen type IX ( COL9A2 and COL9A3 ), collagen type XI ( COL11A2 ), interleukin-1, aggrecan, vitamin D receptor (VDR), MMP-3, and cartilage intermediate-layer protein (CILP). At present, only an association of the COL1A1, COL9A2, MMP-3, and VDR genes with DDD has been verified in different ethnic populations. The annulus fibrosus consists mainly of collagen type I, and the nucleus pulposus contains approximately 50% proteoglycans, mainly aggrecan, and 20% collagen type II. Both contain small amounts of collagen types IX and XI. Studies based on a mouse model indicated that mutations in collagen type IX and aggrecan can cause age-related disk degeneration and herniation. Collagen types IX and XI are attractive candidates for lumbar disk degeneration because they serve as minor components in both the annulus fibrosus and the nucleus pulposus ; however, their roles in the cervical spine warrant further investigation. Nonetheless, various genetic studies have noted concomitant cervical and lumbar degenerative changes, findings suggesting that these two regions share common risk factors.
Collagen Type I
The collagen type I α1 gene ( COLIA1; chromosomal location, 17q21.3-q22) encodes a part of type I collagen, which is the major protein in bone and in the outer layer of the annulus fibrosus. Pluijm and colleagues evaluated 517 older Dutch individuals (65 to 85 years old) and showed that people with the TT genotype had a higher risk of DDD than did those with the GG and GT genotypes (odds ration [OR], 3.6; 95% confidence interval [CI], 1.3 to 10). The frequencies of the GG, GT, and TT genotypes were 66%, 30%, and 4% in men, and 70%, 27%, and 3% in women, respectively.
Collagen Type IX
A subsequent study of Finnish families revealed that family members who carry the Trp2 allele have a greater degree of degeneration in the vertebral disk and end plate. Jim and co-workers found that the Trp2 allele was present in 20% of the population and was associated with a fourfold increase in the risk of developing annular tears at age 30 to 39 years and a 2.4-fold increase in the risk of developing DDD and end plate herniations at age 40 to 49 years. Affected Trp2 individuals had more severe degeneration. The Trp3 allele was absent from the southern Chinese population. This study demonstrated that the association between this gene and DDD was age dependent because it was more prevalent in some age groups than in others.
Trp2 was common in the Japanese population, but no association with DDD was found. However, the researchers found an association of a COL9A2- specific haplotype with DDD ( P = 0.025; permutation test); this association was more significant in patients with severe DDD ( P = 0.011). In another Japanese study of 84 patients (mean age, 43.4 years) who underwent lumbar diskectomy, 21.4% had the Trp2 allele, and no patients had the Trp3 allele. Patients with the Trp2 allele who were less than 40 years old showed more severe disk degeneration at the surgical level than did those without the Trp2 allele (OR, 6.00; P = 0.043). In contrast, patients 40 years old or older did not show a significant association between disk degeneration and collagen type IX genotype.
Collagen Type XI, Matrix Metalloproteinase-3, Vitamin D Receptor, and Cartilage Intermediate-Layer Protein
In a study of 164 Finnish men (40 to 45 years old), Solovieva and associates found that the carriers of the COL11A2 (chromosomal location 6p21.3) minor allele had an increased risk of disk bulges (OR, 2.1; 95% CI, 1.0-4.2) compared with noncarriers. MMP-3 (stromelysin-1) is a potent proteoglycan-degrading enzyme that has an important role in the degeneration of intervertebral disks. Gene polymorphisms of the VDR are thought to contribute to disorders such as osteoporosis, osteoarthritis, and DDD. Furthermore, Seki and colleagues concluded that the extracellular matrix protein CILP regulates transforming growth factor-β signaling and that this regulation plays a crucial role in the etiology and pathogenesis of DDD.
Symptoms and Natural Course of Disease
Pain Generator
In the lumbar spine, disk degeneration is associated with low back symptoms. Studies indicate that a higher degree of lumbar disk degeneration is related to a higher likelihood of symptoms; moreover, the presence of moderate disk degeneration or degenerative changes at multiple levels increases the likelihood of pain. A tissue or structure can generate pain only if it is innervated. Pain generators of the spine have been studied mostly in the lumbar region, but the physiology of nociception in cervical disks is identical to that in lumbar disks. The intervertebral disk is innervated mainly by the sinuvertebral nerve, although it receives direct branches in its posterolateral aspect from the ramus communicans or the ventral ramus. In a normal lumbar disk, nerve endings can be found in the periphery of the outer annulus fibrosus and central end plate but not in the inner annulus fibrosus or nucleus pulposus. The facet joints, the posterior synovial joints, are compromised with advancing disk degeneration. Disk degeneration with reduction of disk height is considered to be the initiating event that leads to secondary deterioration of the posterior elements, such as in the facet joints, most of the time.
Diskographic studies have shown that only annular ruptures, which extend to the outer annulus fibrosus, as expected on the basis of histologic studies on innervation, produce pain. In the lumbar spine, pain among young subjects is more likely to be diskogenic, whereas in older subjects the probability of pain related to the facet joint increases. Although diskography is regarded as the gold standard in the diagnosis of diskogenic pain, this procedure is invasive and may enhance progression of disk degeneration, as noted in the lumbar spine.
Neck Pain
Most cases of cervical DDD can be diagnosed by history and physical examination alone, but patients with concerning signs (red flags) should be screened with neurologic examination for signs of radiculopathy and myelopathy. Cervical disk disease typically manifests with axial neck pain and loss of range of motion of the cervical spine. Headaches have been reported by 2.5% of patients, and 71% of patients experience unilateral or bilateral shoulder pain. The burden and determinants of neck pain in the general population were estimated in a best evidence synthesis of the published literature; the 12-month prevalence of any neck pain ranged between 30% and 50%, and activity-limiting pain ranged between 1.7% and 11.5%. Neck pain was more prevalent among women, and prevalence peaked in middle age. In the state of North Carolina, the prevalence of chronic neck pain was 2.2% among noninstitutionalized individuals, and it was also more common in middle age and among women. In Finland, the prevalence of physician-diagnosed chronic neck syndrome was 5.5% among male patients and 7.3% among female patients, and the highest prevalence was in older age groups.
Risk factors for neck pain include genetics, poor psychological health, and smoking, whereas higher education decreases the risk of chronic neck pain. Disk degeneration was not identified as a risk factor of chronic neck pain. In one retrospective study of patients with chronic neck pain, the most common tissue sources of neck pain were the facet joints (55% of those with completed investigations), followed by diskogenic pain (16%) and lateral atlantoaxial pain (9%). Most episodes of neck and arm pain resolve spontaneously. Underlying cervical degeneration likely increases the time course of healing for minor neck strains. Patients with neck pain usually have difficulty with persistent static positioning (sitting, writing, computer use, driving) and with upper extremity activities (reaching, pushing over the shoulder).
Radiculopathy
Occipital pain, pain in the mastoid-maxillary area, and pain in the supraorbital area can also occur. Interscapular and upper brachial dermatomal pain radiation is also common. Radicular syndromes may result from a wide variety of pathologic conditions. A Rochester, Minnesota, study looked at patients from 13 to 91 years of age and found that the mean age for onset of radicular complaints was similar for men (48.2 years) and women (47.7 years). The most common causes are posterolateral soft disk herniations and spondylotic osteophytes at the neural foramen, with resulting unilateral radiculopathy.
Neurologic problems include specific nerve root signs of weakness, atrophy, decreased deep tendon reflexes, paresthesias, or hypesthesias. The largest intersegmental flexion-extension motion occurs between C4 and C5 and, in particular, between C5 and C6. Thus, the C5-C6 interspace exhibits the earliest and greatest degree of degeneration, and the C6 root is the most commonly affected by disk protrusion. Henderson and co-workers showed that 98.7% of 846 cases of cervical radiculopathy occurred at C5-C6 or C6-C7. These patients complain of radiating pain down the biceps into the radial forearm. Other complaints include weakness of the wrist extensors, biceps, and triceps. Diminution of the brachioradialis reflex may also be noted. More than half of these patients have a normal dermatomal pattern of pain and paresthesia. Herniations more commonly cause reflex loss, cervical muscle spasm, restricted motion, a positive Spurling sign, and pain or motor deficit in a single dermatomal or myotomal distribution. Radicular pain from soft disk protrusion may be intensified with a Valsalva maneuver, rotation and flexion of the head toward the side of symptoms, and axial compression of the skull. Abduction of the shoulder often eases radicular pain.
The spinal nerve root, which consists of secondary motor neurons, has a capacity for recovery. Radiculopathies tend to improve with time. For approximately half of patients with cervical radiculopathy, symptoms resolve after 6 to 12 weeks. Only 10% to 15% of patients have residual impairment. However, the evidence supporting nonoperative management is not strong, and studies have reported contrasting findings. Gore and associates showed that 79% of patients treated nonoperatively improved or were asymptomatic at follow-up; however, one third of these patients still rated their pain as moderate to severe. Another series showed that symptoms persisted in more than 50% of patients treated nonoperatively.
Myelopathy
Cervical spondylotic myelopathy arises from cervical spondylosis, OPLL, or soft disk herniation. The average age of patients is reported to be in the middle to late 50s. Myelopathy usually has a less favorable natural history. Symptoms evolve slowly and insidiously, but some patients experience periods of stability interspersed with episodes of deterioration. In 44 patients, Lees and Turner showed that symptoms and disability were rapidly progressive in only 5% of cases. In 20% of these patients, symptoms were slowly progressive. Duration of symptoms ranges from several months to several years before patients require surgery.
Large central disks can cause myelopathy and usually require decompression. This disorder usually causes problems with the posterior column function of the upper extremities. Patients describe sensory complaints such as numbness or tingling in the hands. These symptoms start in the fingertips, and the usual feeling is described as being gloved. Thus, the symptoms do not follow a dermatomal distribution that suggests radicular symptoms unless specific nerve roots are involved. Patients have difficulty in fine motor function, such as writing. Hyperreflexia is commonly found in patients with a positive Hoffmann sign, reverse supinator and scapulohumeral reflexes, Babinski reflex, and ankle clonus. Gait deterioration usually follows the severity of the disease and is generally attributable to spasticity rather than weakness. Stiff-knee gait is the usual description for these gait patterns. Patients may require walking aids or even a wheelchair if the condition is severe. Other severe symptoms include sphincter and sexual dysfunction. Soft disk herniation usually produces radicular symptoms along with myelopathy, and pure myelopathy is seen in fewer than 10% of patients. Symptoms usually progress more rapidly than in spondylosis or OPLL.
Vertebral Artery Compression
Vertebral artery compression and vertebrobasilar insufficiency have also been described as caused by degenerative disorders of the cervical spine. Symptoms include headaches, dizziness, vertigo, tinnitus, visual symptoms, facial pain, or numbness. More severe compressions can cause transient ischemic attacks. External compression is rare, however, and these vessels are usually compressed by osteophytes or unstable vertebral elements rather than by herniations.
Imaging
Radiographic changes exhibit a linear increase with age. In the mid-20s, the prevalence of disk degeneration is 10%, and it increases through the age of 65 years, when it approaches 95%. By the sixth decade, more than three fourths of individuals have degenerative changes but may nevertheless be asymptomatic. Lawrence and colleagues found radiographic changes in more than 90% of their patients who were more than 65 years old, but the peak prevalence of pain was only 9%. In another study, 25% of asymptomatic patients in their fifth decade, as opposed to 75% of patients in their seventh decade, demonstrated cervical degeneration. The clinical implications are not clear. Brain and co-workers found no consistent association between radiographs and symptoms. Gore and associates followed 205 patients with neck complaints and failed to identify a relationship between the degree of spinal degeneration and the patients’ symptoms. An MRI study of the cervical spine in 497 asymptomatic volunteers between 1993 and 1996 found that the incidence of degenerative changes in the cervical spine on MRI increased with age. For example, a decrease in the signal intensity of the intervertebral disks was observed in 17% and 12% of the disks in men and women, respectively, in their 20s, whereas a decrease was observed in 86% and 89% of the disks in men and women, respectively, after 60 years of age. In general, the quantity of water decreases in the nucleus pulposus as Keep it “as” person ages, and the disk becomes a dry, crumbly, grayish-white, or dark brown mass. This condition can be seen in T2-weighted MRI images as lost signal intensity, as well as decrement of intervertebral space.
Although MRI is widely considered the gold standard for the diagnosis and assessment of cervical DDD, important information can also be gathered from plain radiographs and computed tomography (CT) scans. On plain radiographs, cervical DDD can be diagnosed on the basis of narrowed disk spaces and osteophyte formation. Dynamic scans are also useful to assess the integrity of the cervical disk and the severity of degeneration leading to instability of spinal segments ( Fig. 12-1 ). Findings noted on dynamic scans can drive the decision about whether fusion is required to stabilize the spine. CT scans are useful to distinguish between soft and hard disk disorders ( Fig. 12-2 ). CT can also assess the severity of involvement and the location of osteophyte formation, as well as establish the diagnosis of OPLL or ossified yellow ligament.
Disk spaces on MRI have moderately high signal intensity in the inner region and are surrounded by a rim of low signal intensity that represents the annulus fibrosus. Herniation that is central or paracentral can be recognized on sagittal images by an area of medium-intensity signal posterior to the disk space. On gradient-echo or T1-weighted sequences, disk material has a higher signal than the dense cortical bone of a ridge. Disk protrusion or herniation can be adequately assessed on MRI scans ( Fig. 12-3 ). Further evidence of myelopathy can be observed by hyperintensity or enhancement of the spinal cord at the level of the compression, thus indicating spinal cord damage. This is important for the diagnosis and location of the lesion for surgical planning.
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