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NEUROLOGY 1988;38:1012
© 1988 American Academy of Neurology

Cerebral infarction in sickle cell anemia

Mechanism based on CT and MRI

R. J. Adams, MD, F. T. Nichols, MD, V. McKie, MD, K. McKie, MD, P. Milner, MD and T. E. Gammal, MD

From the Departments of Neurology (Drs. Adams and Nichols), Cell and Molecular Biology, Pediatrics, and Comprehensive Sickle Cell Center (Drs. V. McKie and K. McKie), Pathology and Medicine (Dr. Milner), and Radiology (Dr. Gammal), Medical College of Georgia, Augusta, GA.

We studied 25 patients with sickle cell anemia and cerebral infarction. We classified lesions as to probable mechanism (large versus small vessel disease) based on the CT/MRI appearance of established infarction. Most patients had CT/ MRI patterns of major cerebral vessel occlusion (41%) or borderzone (distal insufficiency) infarcts (31%) best explained by large cerebral vessel vasculopathy. Seven of 25 (28%) had either isolated subcortical (12%) or small cortical branch occlusion (16%) consistent with other mechanisms such as small vessel occlusion or embolism. These results suggest that most clinically recognized cerebral infarctions in sickle cell anemia are caused by large vessel disease, but this mechanism may not account for symptoms of cerebral ischemia in all cases.

Address correspondence and reprint requests to Dr. Adams, Department of Neurology, Section of Cerebrovascular Disease, BD-241, Medical College of Georgia, Augusta, GA 30912–2366.

Received August 12, 1987. Accepted for publication in final form December 1,1987.

Supported in part by the Medical College of Georgia Research Institute and NIH grant HL 29554 awarded to the Medical College of Georgia Comprehensive Sickle Cell Center, Titus H.J. Huisman, Director.




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