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John P. Allen, MD
Dept of Med Univ of Texas Health Science Center 7703 Floyd Curl Dr San Antonio, TX 78284

Joseph V. McDonald, MD
Dept of Neurosurg

Frederick A. Horner, MD
Dept of Pediatr and Neurol Univ of Rochester School of Med Strong Memorial Hosp Rochester, NY

Arch Neurol. 1979;36(7):455.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.—

The most common consequence of these embryologic abnormalities is gradual progression from paraparesis to paraplegia.¹ Less common is the acute onset of hematomyelia, thrombosis of the malformation, or subarachnoid hemorrhage with associated deficits in function.

Report of a Case.—

A 6-year-old boy had progressive thoracic back pain of one month's duration, with an acute spastic paraparesis. Mental status, cranial nerve function, coordination of his arms and anal tone were normal. There was impairment to light touch and proprioception in the legs. Myelography showed a complete obstruction at the T-6 level due to an intramedullary mass lesion with dilated and tortuous vessels. The spinal fluid was discolored but not xanthochromic, acellular, with a protein content of 500 mg/dl and a glucose level of 52 mg/dl. At operation, distended tortuous vessels were seen between T-9 and T-12 typical of an arteriovenous malformation (AVM) of the spinal cord.

At . . . [Full Text PDF of this Article]

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