• I A Awad and G H Barnett.
• Department of Neurological Surgery, Cleveland Clinic Foundation, Ohio.
• J. Neurosurg. 1990 Apr 1; 72 (4): 650-3.

AbstractThe mechanism of nonhemorrhagic neurological deterioration from spinal arteriovenous malformation (AVM) and the role of acute surgical intervention in this setting are not well understood. The case is described of a 65-year-old man who presented with a 2-year history of mild gait spasticity and vague sensory complaints affecting both lower extremities. Following a diagnostic lumbar puncture, these symptoms progressed painlessly over a 4-day period to total motor paraplegia, urinary retention, and hypesthesia in all modalities with a midthoracic sensory level. Magnetic resonance imaging showed a probable spinal AVM but no evidence of hemorrhage or cord compression. Spinal angiography confirmed the diagnosis of spinal AVM fed by radicular branches of left T-7 and T-8 segmental intercostal arteries. Drainage was via long dorsal veins caudally. Emergency laminectomy with intradural exploration was performed. There was no evidence of prior hemorrhage or focal mass effect, although the cerebrospinal fluid pressure was elevated. The dural component of the spinal AVM was excised, and its communications with the spinal cord were disconnected intradurally. Neurological function started improving within 6 hours of the patient awakening from anesthesia. He had achieved antigravity strength in every muscle group of the lower extremities by the time of discharge to a rehabilitation center 10 days after surgery. Three months postoperatively, he was ambulating with a walker and was continent of urine and stool. Possible pathophysiological mechanisms are discussed in light of the favorable response to timely surgical intervention.

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