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The authors thank Dr. Saxena for the cervical disc replacement operative photographs. Operative video is available on Expert Consult.
Although great progress has occurred on the biomechanical aspects and significant progress on the clinical aspects of spinal arthroplasty, it should still be considered a work in progress. Surgeons should not forget that there are very acceptable alternatives to arthroplasty within the surgical armamentarium and should feel no compulsion to undertake the latest techniques.
The intervertebral disc is composed of a central nucleus pulposus (containing predominantly type 1 collagen fibrils) and a peripheral annulus fibrosis (which can consist of up to 25 lamellae of mostly type 1 collagen) that provides support, allows some movement, resists excessive movement, and, according to some, absorbs shock. The ability to resist axial stresses is considerable but decreases with age. With normal loading, the normal nucleus pulposus is transposed by vertebral body pressure to tighten the annulus and produce ligamentous intervertebral stability. With heavy loading, the rigid, spherical normal nucleus pulposus gains stable seating in the nuclear recesses, where it acts as a piston to depress the cribriform plates, bend the trabeculae, and produce the necessary stability. With return of normal loading, the vertebral body rebounds, the nucleus pulposus resumes its normal locus, and the annulus tightens. Therefore it has been recognized that the vertebral bodies are very significant contributors to the shock-absorption function of the spinal column.
It is fairly well accepted that the degenerative changes that result from aging of the vertebral body, the annulus fibrosis, and the nucleus pulposus are likely to begin with infarction of the cribriform cartilage end plates and subsequent nutritional failure of the nucleus pulposus. Calcification of the end plates occurs in adulthood, and the nutrient uptake and waste elimination within the disc then becomes dependent on diffusion. This leads to anaerobic metabolism taking a more prominent role, leading to lactate production and an acidic environment. The proteinases become more active, resulting in further disc degeneration. Indeed, it has been shown that when heavy loads are applied to the intervertebral disc, the normal disc biology can be disrupted, leading to an increase in catabolic enzymes and an acceleration of intervertebral disc degeneration. Studies have noted increased rates of degenerative disc disease in siblings of affected persons and strong correlation in twins.
The pathophysiology of the degenerative disease process has been described by Kirkaldy-Willis. The progressive disease is divided into three stages based on the amount of damage or degeneration to the disc and facet joints at a given point in time. However, the cascade of individual motion segment degeneration is best thought of as a continuous process rather than as three clearly definable and separate stages.
The first stage is described as the dysfunctional stage. It develops as the initial changes of intervertebral disc degeneration begin. This can occur between 20 and 30 years of age. There is circumferential fissuring or tearing of the outer annulus fibrosis. This can result from repetitive vertebral end plate injury, which leads to a disruption of the intervertebral vascular supply and therefore impairment of the normal disc metabolism. It is thought that these pathophysiologic changes might result from years of repetitive microtrauma and can manifest as acute mechanical back pain episodes. These clinical episodes tend to be self-limiting and improve with minimal intervention. Occasionally, the pain is debilitating because of the large innervations to the outer third of the annulus fibrosis via the sinuvertebral nerves.
With the passage of time, the circumferential annular tears can coalesce, forming larger radial tears, while the nucleus pulposus shrinks owing to the loss of its water-retaining properties resulting from a decrease in the amount and organization of its proteoglycans. Magnetic resonance imaging (MRI) studies at this stage can reveal a high-intensity zone (HIZ) in the posterior outer annular fibrosis and decreased signal intensity on T2-weighted images, suggesting disc desiccation with or without disc bulging but without disc herniation.
The second stage is described as the instability stage. It represents more significant tissue damage and tends to occur later in life, typically between 30 and 50 years of age. Multiple annular tears and delamination of the annulus fibrosis accelerates the intervertebral disc degeneration to a point where vertebral segment instability occurs. This results in a further decline in the nuclear proteoglycan composition, with a further resulting deterioration in the water content. Collapse of the nucleus pulposus leads to increased force transfer to the annulus fibrosis. The clinical episodes now tend to be periods of back pain that are usually more intense, often last longer, and tend to require more aggressive intervention. The MRI reveals loss of intervertebral disc height, a darker disc on T2-weighted imaging, and sometimes a disc herniation.
The third stage is described as the stabilization stage. It is exemplified by end-stage tissue damage and attempts at repair. Further nucleus pulposus resorption occurs with increasing intervertebral disc space narrowing fibrosis, end plate irregularities, and the formation of osteophytes. The stage typically occurs later and in the lumbar spine can manifest with symptoms of neurogenic claudication or radiculopathy from any combination of central, lateral recess, or foraminal stenosis. At this stage the lower limb symptoms can prevail over low back pain.
However, MRI is positive in asymptomatic patients at least 40% of the time. Approximately 30% of adults without low back pain have evidence of protruded disc on MRI; more than half have bulging or degenerative discs, and a fifth have annular fissures. Therefore the relationship among disc degeneration, the MRI appearance, and spine-related pain remains controversial, and the decision to undertake surgical management of a degenerative spinal condition is a large one and is very much patient specific. The presurgical work-up must include a thorough history relating to any spinal complaints including neurologic compromise, a diligent physical examination that leads to a working diagnosis, and the appropriate subsequent confirmatory radiologic imaging. Although simple radiography is an inexpensive and readily accessible starting point, its utility is severely limited by its inability to visualize neural structures directly or indirectly, and therefore the presence or absence of neural compression is indeterminable. , Nonetheless, all our potential arthroplasty patients undergo plain flexion-extension radiographs of the appropriate spinal segment to look for instability of the potential operative or another segment and to confirm that there is still movement of the proposed operative segment. In addition, if there is going to be any delay in obtaining true confirmatory imaging, routine spinal radiography should be undertaken to exclude other disease processes, such as malignancy, infection, or arthritis. Interestingly, when Friedenberg and Miller compared 92 asymptomatic patients with those complaining of neck and arm pain, no difference was found between the two groups in radiographic findings, with the exception of a greater incidence of disc degeneration at C5–6 and at C6–7 in the symptomatic group.
All patients undergo MRI of the appropriate spinal area unless a contraindication exists. Virtually all patients now undergo supplementary computed tomography (CT) scanning, which allows excellent visualization of bony osteophytes and the foraminal architecture including the facet joints, especially with the reconstructed (three-dimensional) CT imaging. CT scanning in flexion and extension can allow an enhanced appreciation of subtle instability or spinal canal or foraminal encroachment (especially by the ligamentum flavum if CT myelography is undertaken). The CT imaging also allows the surgeon to assess the disc size before surgery.
Electromyography and nerve conduction studies can be useful in diagnostic evaluation, providing additional objective evidence of root compression in patients with relatively minor neurologic findings. Moreover, they are useful in differentiating root, plexus, peripheral nerve, and muscle disorders that might mimic cervical or lumbar radiculopathy. They can also help to uncover a second problem that coexists with the radiculopathy, such as carpal tunnel syndrome, ulnar neuropathy, or compression of the lateral cutaneous nerve of the thigh causing meralgia paresthetica.
We also occasionally request the radiologists to undertake a provocative discogram, which should include a normal control level above or below the degenerative disc in question.
None of our groups have been provided with the resources to undertake psychological profiling of prospective patients. Nonetheless, we try to avoid operating on patients with outstanding litigation claims.
Interbody stabilization procedures using the standard fusion techniques including techniques reported by our groups and others account for the majority of our interbody operations.
The elimination of motion at the functional spinal unit (two vertebral bodies, the intervertebral disc, and associated facet joints) has been the mainstay of treatment since the 1960s. Anterior cervical discectomy and fusion is the standard of care for relief of pain and stabilization associated with radiculopathy and myelopathy, with excellent long-term results. However, lest we forget, very satisfactory results have been reported with the placement of nothing at all in the disc space after anterior cervical discectomy. , It was the significant concerns raised by Hillibrand , and others who noted, in various series of patients who had undergone anterior cervical arthrodesis, that between 25% and 89% who were followed for a lengthy period developed new degenerative changes at adjacent levels.
The debate is complex because much of the biomechanical and clinical evidence about the cause of adjacent segment disease is anecdotal and inconsistent. Although intradiscal pressure and motion alterations have been found at the adjacent levels following a single-level anterior lumbar interbody fusion (ALIF) in a calf model, it is recognized that longer fusions, both in the lumbar spine and in the cervical spine, have not been associated with higher rates of adjacent segment disease. ,
Indeed, the recent enthusiasm for the application of cervical plates to aid fusion might actually be related to the increase in adjacent segment degeneration. Anterior plate impingement upon an adjacent disc is likely to accelerate adjacent level changes. An association between adjacent level ossification and the plate-to-disc distance has been established in a retrospective review of 118 patients undergoing anterior cervical discectomy and fusion. We should not forget that a patient who has already developed cervical spondylosis at the most common level (C5–6) to such a degree that surgery is warranted may be predisposed to develop degeneration at an adjacent level (C6–7 or C4–5) because of the natural history of the spondylosis and independent of whether or not a fusion is performed at the original level.
Moreover, despite the frequent reference to Hillibrand’s paper by those promoting arthroplasty, the authors later indicated that the paper suggested that the development of adjacent segment disease may be related to the natural history of cervical spondylosis. Similar findings have been documented in the lumbar spine by Ghiselli and colleagues, who found no correlation between the length of fusion and the rate of reoperation in 215 patients following posterior lumbar fusion. They noted that segments that were adjacent to a single-level fusion had a three times higher risk for developing disease than did those adjacent to a multiple-level fusion.
Contraindications to cervical disc replacement include ankylosing spondylitis, rheumatoid arthritis, a history or cervical infection, ossification of the posterior longitudinal ligament, and diffuse idiopathic skeletal hyperostosis. We avoid an arthroplasty in the presence of severe spondylosis at the proposed level (significant or bridging osteophytes, disc height loss of greater than 70%, absence of motion). Similarly, radiologic suggestion of cervical instability including translation of more than 3 mm or more than 11 degrees of rotational difference to that of either adjacent level is a contraindication. We would be very reluctant to undertake an arthroplasty in a morbidly obese patient (body mass index [BMI] >40) or in insulin-dependent diabetic patients (for fear of infection). At present we will not consider an arthroplasty for treatment of isolated axial neck pain. Clearly, allergy to any of the components of the implant is a definite contraindication.
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