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Lupus, Vol. 3, No. 4, 253-257 (1994)
DOI: 10.1177/096120339400300409

Models for Central Nervous System Complications of Antiphospholipid Syndrome

David C. Hess

Neurology Service, V.A. Medical Center, Department of Neurology and Medicine, Medical College of Georgia, Augusta, Georgia, USA

One of the clinical hallmarks of antiphospholipid syndrome is the development of neurological complications, namely cerebral ischaemia, chorea, multi-infarct dementia, amaurosis fugax, migraine and transverse myelitis. An animal model should include the development of measurable neurological deficits and evidence of cerebral infarction. Although there are a number of mouse models for fetal loss, there has been no convincing model for the neurological complications of the antiphosphohpid syndrome. One explanation for the high frequency of neurological events in antiphospholipid syndrome is a vulnerability of the cerebral vasculature to the hypercoagulable state associated with the syndrome. A greater appreciation of the differences in the regulation of coagulation between the systemic and cerebral vasculatures may be key to understanding the apparent predilection for central nervous system involvement in the antiphospholipid syndrome.

Key Words: Antiphospholipid • Animal model • Cerebral infarction • Endothelial


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