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From the Department of Neurology (Drs. Cheshire and Howard), University of North Carolina, Chapel Hill, NC; and the Division of Neurology (Drs. Santos and Massey), Department of Medicine, Duke University, Durham, NC.
Presented in part at the 42nd annual meeting of the American Academy of Neurology, Miami, FL, May 1990.
Received August 29, 1994. Accepted in final form February 2, 1996.
Address correspondence and reprint requests to Dr. William P. Cheshire, Department of Neurology, Mayo Clinic Jacksonville, 4500 San Pablo Road, Jacksonville, Florida 32224.
We reviewed 44 cases of ischemia and infarction of the spinal cord at two university hospitals.Three patients experienced transient ischemic attacks. Etiologies of completed strokes were diverse and included rupture and surgical repair of aortic aneurysms, aortic dissection, aortic rupture and thrombosis, global ischemia, anterior spinal artery embolism, repair and thrombosis of spinal arteriovenous malformations, hematomyelia, epidural hematoma, cervical osteophytosis, celiac plexus block, systemic lupus erythematosus, coagulopathy, and decompression sickness. Motor function improved in 12 patients, was substantial in only one, and occurred largely within the first 2 to 4 weeks. Favorable ambulatory outcome correlated with improving neurologic examinations and relatively preserved strength in hip abductors and knee extensors. More extensive deficits without initial improvement portended a more severe prognosis. Autonomic dysfunction, pain, paresthesia, and depression were common and impeded recovery in some patients. The mean level of deficit was at T-8 and in cases of global ischemia was at T-9, which leads us to dispute the classical view of a midthoracic watershed zone of ischemic vulnerability near T-4.
NEUROLOGY 1996;47: 321-330
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