It has been stated that spondylotic myelopathy may simulate amyotrophic lateral sclerosis (amyotrophy of arms and spastic weakness of the legs). This has seldom been a diagnostic problem. Although brachial and shoulder fasciculations with muscle atrophy may be combined with hyperreflexia in spondylosis, the widespread denervation and progressive course of ALS are not in evidence. We have observed only a few patients with spondylotic myelopathy who exhibited an absolutely pure motor syndrome, that is, one in which there was no cervical or brachial pain and no sensory symptoms in the arms or impairment of vibratory or position sense in the legs. Likewise, a pure spastic paraparesis is more likely to be a manifestation of MS, hereditary spastic paraplegia, motor neuron disease (primary lateral sclerosis type), HTLV-I myelopathy, or the carrier state of adrenoleukodystrophy or other intrinsic myelopathy.
When imbalance, both perceived by the patient and observed in tests of walking, is a major symptom, spondylosis must be differentiated from a number of acquired large-fiber polyneuropathies, particularly inflammatory or immune types and the more benign sensory neuropathy of the aged (see discussion of this entity in Chap. 43). Loss of tactile sensation in the feet and loss of tendon reflexes are characteristic of the latter; examination of the tendon reflexes distinguishes neuropathy from myelopathy. Subacute combined degeneration of the spinal cord because of vitamin B12 deficiency or low serum copper, AIDS and HTLV-I myelopathy, ossification of the posterior longitudinal ligament, and spinal cord tumor (discussed further on) are usually listed among the conditions that might be confused with spondylotic myelopathy. The gait abnormality produced by spondylotic myelopathy may also be mistaken for that of normal-pressure hydrocephalus; a marked increase of imbalance with removal of visual cues (Romberg sign) is a feature of spondylosis but not of hydrocephalus, and the short-stepped and magnetic quality of walking, that is, characteristic of hydrocephalus is not seen in cervical myelopathy (see Chap. 29 for discussion of NPH). Incontinence occurs only in advanced cases of spondylotic myelopathy but usually follows soon after gait deterioration in hydrocephalus.
The special problems of spondylotic radiculopathy, which may accompany or occur independently of the myelopathy, are discussed in Chap. 10.
The slow, intermittently progressive course of cervical myelopathy with long periods of relatively unchanging symptomatology makes it difficult to evaluate the effects of treatment. Assuming that the prevailing view of the mechanism of cord and root compression is correct, the use of a soft collar to restrict anteroposterior motions of the neck seems reasonable. This form of immobilization may be sufficient to reduce discomfort in the neck and arms; only exceptionally in our experience, however, has arm and shoulder pain alone been sufficiently severe and persistent to require surgical decompression unless there is in addition a laterally protruded disc or osteophytic constriction of a root foramen. Many patients have been dissatisfied with the results of this passive approach and are unable to wear a collar for prolonged periods.