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August 01, 1996; 47 (2) VIEWS AND REVIEWS

Spinal cord infarction

Etiology and outcome

William P. Cheshire, Cesar C. Santos, E. Wayn Massey, James F. Howard
First published August 1, 1996, DOI: https://doi.org/10.1212/WNL.47.2.321
William P. Cheshire
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Cesar C. Santos
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E. Wayn Massey
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James F. Howard Jr.
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Citation
Spinal cord infarction
Etiology and outcome
William P. Cheshire, Cesar C. Santos, E. Wayn Massey, James F. Howard
Neurology Aug 1996, 47 (2) 321-330; DOI: 10.1212/WNL.47.2.321

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Abstract

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

  • Copyright 1996 by Advanstar Communications Inc.
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