Abstract

ERVICAL spondylosis is a progressive and disabling disease of later life characterized by a variable combination of upper extremity radiculopathy and predominantly motor myelopathy. 2,4,12,~4,~7 The underlying pathologic process seems to begin with degeneration of cervical intervertebral discs, most commonly at the C4-5, C5-6 and C6-7 levels. 2,11,~,*s,2~ Bony hypertrophic changes then develop as ridges or bars along the margins of the affected interspace. How these bony-ligamentous changes produce neurologic deficits has been, and remains, a subject of debate. In all probability the observed radiculopathy results either from direct, mechanical compression of individual nerve roots within their foramina of exit or from stretching of the nerve roots secondary to abnormal angulation of vertebral bodies adjacent to degenerated interspaces, 6 or to a combination of both. z3,~7 The mechanism of production of the myelopathy of cervical spondylosis remains more obscure. Simple mechanical compression of the spinal cord by hypertrophic bars anteriorly, or infoldings of the ligamentum flavum posteriorly, 9 would be expected to produce predominantly sensory myelopathy. Kahn's ingenious theory 1~ implicating the dentate ligaments as stress transmitters has been badly shaken by anatomical studies showing that the tethering effect of these ligaments is restricted to rostro-caudal and lateral displacement of the cord, with anteroposterior movement being relatively unrestricted.6,9,~0,~ Considerable interest has also been devoted to the possible role played by vascular factors in the pathogenesis of the myelopathy of cervical spondylosis. 2'3'7'1~ Demonstrable thrombosis of the anterior spinal artery is rarely found, ~,~ although one might

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