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. 1996 Aug;47(2):321-30.
doi: 10.1212/wnl.47.2.321.

Spinal cord infarction: etiology and outcome

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Spinal cord infarction: etiology and outcome

W P Cheshire et al. Neurology. 1996 Aug.

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.

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Comment in

  • Spinal cord watershed.
    Jellinger KA. Jellinger KA. Neurology. 1997 May;48(5):1474-5. doi: 10.1212/wnl.48.5.1474-b. Neurology. 1997. PMID: 9153506 No abstract available.
  • Spinal cord infarction.
    Leite I, Monteiro L. Leite I, et al. Neurology. 1997 May;48(5):1478. doi: 10.1212/wnl.48.5.1478. Neurology. 1997. PMID: 9153513 No abstract available.

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