METHODS: Eleven patients with paralysis, secondary to rheumatoid arthritis of the cervical spine were analyzed postmortem. Neurologic classification (Ranawat) included one Class 2, four Class IIIA, and six Class IIIB. Rheumatologic changes included atlantoaxial subluxation, basilar invagination, and subaxial subluxation. During autopsy the entire cervical spine was removed, including the occiput and foramen magnum. The spinal cord and medulla oblongata were removed en toto and examined histologically by a neuropathologist. RESULTS: Nine of the eleven cases revealed abnormal histology of the spinal cord, and in two patients, the spinal cords were normal. Three histologic types of spinal cord compression were identified. In Type 1 (four cases) severe chronic mechanical compression revealed marked mechanical distortion, flattening, and destruction of the cord with secondary Wallerian degeneration of the ascending and descending tracts without anoxicischemic neuron changes. In Type 2 (three cases), there was vascular compression showing ischemic damage to the cord with necrosis of the lateral columns in the ischemic watershed regions supplied by anterior and posterior spinal arteries. In Type 3 (two cases), there was mild mechanical compression showing focal gliosis at the site of compression without ascending or descending tract injury. Two of the eleven cases had thrombosis of the vertebral arteries. Of the eleven cases analyzed, two had normal spinal cords. CONCLUSION: This autopsy analysis of rheumatoid cervical spine suggests that paralysis can be due to both mechanical neural compression and/or vascular impairment.
METHODS: Eleven patients with paralysis, secondary to rheumatoid arthritis of the cervical spine were analyzed postmortem. Neurologic classification (Ranawat) included one Class 2, four Class IIIA, and six Class IIIB. Rheumatologic changes included atlantoaxial subluxation, basilar invagination, and subaxial subluxation. During autopsy the entire cervical spine was removed, including the occiput and foramen magnum. The spinal cord and medulla oblongata were removed en toto and examined histologically by a neuropathologist. RESULTS: Nine of the eleven cases revealed abnormal histology of the spinal cord, and in two patients, the spinal cords were normal. Three histologic types of spinal cord compression were identified. In Type 1 (four cases) severe chronic mechanical compression revealed marked mechanical distortion, flattening, and destruction of the cord with secondary Wallerian degeneration of the ascending and descending tracts without anoxicischemic neuron changes. In Type 2 (three cases), there was vascular compression showing ischemic damage to the cord with necrosis of the lateral columns in the ischemic watershed regions supplied by anterior and posterior spinal arteries. In Type 3 (two cases), there was mild mechanical compression showing focal gliosis at the site of compression without ascending or descending tract injury. Two of the eleven cases had thrombosis of the vertebral arteries. Of the eleven cases analyzed, two had normal spinal cords. CONCLUSION: This autopsy analysis of rheumatoid cervical spine suggests that paralysis can be due to both mechanical neural compression and/or vascular impairment.