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Models for Central Nervous System Complications of Antiphospholipid Syndrome

*Corresponding author for this work
Scholary Output:
Contribution to journal
Article
Peer-review

Abstract

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.

Publication Information

Output type

Scholary Output:
Contribution to journal
Article
Peer-review

Original language

English (US)

Pages from-to (Number of pages)

Pages 253-257 (5 pages)

Journal (Volume, Issue Number)

Lupus (Volume 3, Issue 4)

Publication milestones

  • Published - 08/1994

Publication status

Published - 08/1994

ISSN

0961-2033

Publication IDs

  • Scopus: 0028123166
  • PubMed: 7804311

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