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Departments of Clinical Neuroscience (Dr. Glantz), Brown University School of Medicine, Providence, RI; Pathology (Dr. Burger), Johns Hopkins Medical School, Baltimore, MD; Surgery (Neurosurgery) (Dr. Friedman) and Medicine (Neurology) (Drs. Radtke and Massey), Duke University Medical Center, Durham, NC; and Neurology (Dr. Schold), University of Texas Southwestern, Dallas, TX.
When radiation is used to treat nervous system cancer, exposure of adjacent normal nervous system tissue is unavoidable, and radiation-induced injury may occur. Acute injury is usually mild and transient, but late forms of radiation-induced nervous system injury are usually progressive and debilitating. Treatment with corticosteroids, surgery, and antioxidants is often ineffective. We treated 11 patients with late radiation-induced nervous system injuries (eight with cerebral radionecrosis, one with a myelopathy, and two with plexopathies, all unresponsive to dexa-methasone and prednisone) with full anticoagulation. Some recovery of function occurred in five of the eight patients with cerebral radionecrosis, and all the patients with myelopathy or plexopathy. Anticoagulation was continued for 3 to 6 months. In one patient with cerebral radionecrosis, symptoms recurred after discontinuation of anticoagulation and disappeared again after reinstitution of treatment. We hypothesize that anticoagulation may arrest and reverse small-vessel endothelial injurythe fundamental lesion of radiation necrosisand produce clinical improvement in some patients.
Address correspondence and reprint requests to Dr. Michael Glantz, Department of Neurology (Neuro-Oncology), Memorial Hospital of Rhode Island, 111 Brewster Street, Pawtucket, RI 02860.
Received April 5,1994. Accepted in final form August 24, 1994.
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