Cervical spondylotic myelopathy (CSM) is a clinical condition characterized by symptomatic dysfunction of the cervical spinal cord resulting from pathoanatomical changes associated with spinal degeneration. The condition currently represents the most common cause of spinal cord dysfunction in adults worldwide, and is the most common cause of acquired spastic paresis in those older than 55. Clinical presentation is extremely variable due to the possibility that any or all of the tracts of the spinal cord can be affected. Signs and symptoms can vary from axial neck pain and subtle hyperreflexia to florid neurologic decompensation with quadriparesis. Although an accurate estimate of the incidence of CSM has not been easy to make—a likely result of the variable nature of the condition—several epidemiologic findings have been reported.

The rate of CSM increases with age, with clinical symptoms most often presenting in the latter half of the seventh decade of life. A Japanese study of patients hospitalized with symptoms of CSM reported a rate of 29 hospital admissions per 100,000 person-years for men and 15 per 100,000 person-years for women. Given the high prevalence of CSM, it is very likely that an orthopedic surgeon in any subspecialty of practice will encounter this condition. There is often a delay in the diagnosis of CSM, and it can be misdiagnosed as carpal tunnel syndrome or cervical radiculitis. The medical community should have a high index of suspicion for CSM, given the importance of early diagnosis and treatment, and the potential for irreversible neurologic decline. The purpose of this chapter is to summarize the current understanding of the pathophysiology of disease, presentation, and treatment of CSM.

The clinical manifestations of CSM result from an interplay of structure and function of the cervical spine. The spinal cord, after exiting the foramen magnum, travels through the cervical spinal canal en route to the thoracic and lumbar segments. For the spinal cord to be properly protected both statically and with physiologic motion of the cervical spine, ample space is required. The typical midsagittal diameter of the spinal canal in the subaxial cervical spine is 17 to 18 mm. The spinal cord is approximately 10 mm in sagittal diameter, with the dura mater and cerebrospinal fluid (CSF) each occupying approximately 1 mm both anterior and posterior to the spinal cord. Spinal stenosis is, therefore, diagnosed when the sagittal diameter is reduced below 14 mm. Stenosis is considered “relative” if the spinal canal diameter is between 10 and 13 mm and “absolute” if the canal diameter is less than 10 mm (the spinal cord is “absolutely” compressed because the diameter of the cord itself is approximately 10 mm). Any structural or dynamic compromise to the space within the spinal canal may cause cord compression. Furthermore, a patient with a congenitally narrow cervical spinal canal is at a higher risk of developing cord compression and myelopathy from less severe degenerative changes at an earlier age (Fig. 15.1).

The clinical signs and symptoms of CSM result from age-associated degenerative changes to structures about the spinal cord. Clarke and Robinson classically described the degenerative process of the cervical spine as the “basic etiological feature” of cervical myelopathy. As the spine ages, the nucleus pulposus desiccates as a result of proteoglycan breakdown, leading to a loss of disk height. This in turn leads to bulging of the annulus fibrosus and buckling of the ligamentum flavum into the spinal canal, both of which encroach upon the space available for the cord. The compromise of disk integrity results in an increase in the loading forces on the facet joints and uncovertebral joints (also known as the joints of Lushka), leading to additional degeneration and osteophyte formation. Degeneration of these joints contributes to narrowing of the neural foramina and the lateral aspect of the spinal canal, further reducing space available for the cord. With the loss of disk height,
the cervical spine may also lose its normal lordotic posture. Kyphotic cervical alignment can also contribute to myelopathy, as the spinal cord becomes effectively “draped” over the degenerative, hypertrophic anterior structures. Finally, in association with the increased rigidity associated with spinal degeneration, adjacent motion segments may become hypermobile, leading to “compensatory pseudosubluxation.” This segmental hypermobility may result in dynamic compression of the cervical spinal cord and can be studied with flexion and extension radiographs.

The pathophysiologic effects of cord compression are thought to be a combination of direct mechanical effects on the neural tissue, as well as impairment in cord blood supply. Histologic specimens from autopsies of patients with documented myelopathy show destruction of both gray matter and white matter and ascending and descending demyelination. Sudden vascular insufficiency is associated with acute changes in symptomatology. Compression of the primary blood supply to the spinal cord—the anterior spinal artery, radicular arteries, and posterior spinal arteries—can produce diffuse ischemia of the spinal cord with rapid and diffuse loss of neurologic function. The transverse intramedullary arterioles, however, are the most susceptible to compression. Focal cord ischemia resulting from compromise of these arterioles is the most likely explanation of the classic stepwise, irreversible loss of function seen in CSM.

Ossification of the posterior longitudinal ligament (OPLL) is another well-described cause of myelopathy. In Japanese and other Asian populations, OPLL is observed with an incidence of 4% in individuals older than 50 years of age. The diagnosis of OPLL is made by the observation of hypertrophic ossification dorsal to the vertebral bodies (Fig. 15.2). A spectrum of disease in OPLL exists; the condition may be as focal as ossification dorsal to a single vertebral body, or as diffuse as continuous ossification spanning the dorsal aspects of multiple vertebrae. It is important to identify OPLL because the surgical plan will often need to be altered to avoid the ossified area which is often densely adherent to the dura.

Since CSM is characterized by symptomatic dysfunction of the spinal cord, the diagnosis of CSM is made clinically. A thorough history and neurologic examination should be performed on all patients suspected of CSM. This evaluation should elicit the severity and distribution of sensory and motor function changes, reflex abnormalities, and provocative neurologic tests. Importantly, the neurologic examination should focus
on differentiating between the findings associated with dysfunction of individual nerve roots (monoradicular patterns) and peripheral nerves (characteristic motor and sensory patterns), from spinal cord dysfunction. A patient’s symptoms may include pain, paresthesia, sensory changes, weakness, or dyscoordination depending on which of the spinal cord tracts are affected. Upper extremity paresthesia is the most common presenting complaint. Neurologic symptoms typically present diffusely in a polyradicular pattern, even with a single level of spinal cord compression. This is a result of dysfunction of the entire spinal cord tract distal to the site of compression. Extension or flexion of the neck, which effectively decreases the space available for the spinal cord, may exacerbate the polyradicular symptoms in the arms or legs (L’hermitte’s sign), again in distinction to the exacerbation of symptoms seen with compression of a single nerve root (Spurling’s sign). Despite the differences between the neurologic patterns of myelopathy, radiculopathy, and peripheral neuropathy, the overlap of these clinical conditions often leads to a delay in the management of CSM, with a mean time from onset of symptoms to diagnosis of about 2 years.

Motor weakness, when present, can be seen in a polyradicular pattern and may affect ipsilateral upper and lower extremities or even all four extremities. If proprioception is impaired, coordination will be affected. This manifests as dysfunction of fine motor skills in the upper extremity, with patients complaining of trouble fastening buttons or noticing changes in the coordination of handwriting. Lower extremity signs and symptoms include gait dysfunction or dyscoordination. Patients often ambulate with spasticity and a broad-based, uneven stride. These findings should be easily elicited from the patient history and observed during physical examination. More subtle findings, however, must be specifically sought. Weakness may manifest only as fatigue with prolonged muscular activity. This may not be observed on a physical examination, which typically elicits only brief provocation of each muscle group. Older patients may often dismiss fatigue as an undesirable but inevitable sign of their advancing age.