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Updated: Mar 31, 2026

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Limb-shaking transient ischemic attacks: Two case reports with unusual pathogenesis.

M Yeung1, D W Gross2, A Shuaib1

  • 1Saskatchewan Stroke Research Centre, Department of Medicine, Royal University Hospital, University of Saskatchewan, Saskatoon, Saskatchewan, Canada; (Division of Neurology), Royal University Hospital, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.

Journal of Stroke and Cerebrovascular Diseases : the Official Journal of National Stroke Association
|October 22, 2015
PubMed
Summary
This summary is machine-generated.

Limb-shaking transient ischemic attacks (TIAs) can stem from causes beyond carotid stenosis. Our findings highlight essential thrombocytosis and severe anemia as potential triggers for these neurological events.

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Area of Science:

  • Neurology
  • Vascular Medicine
  • Hematology

Background:

  • Limb-shaking transient ischemic attacks (TIAs) are typically linked to severe carotid stenosis causing transient regional cerebral hypoperfusion.
  • The established pathogenesis involves focal cerebral ischemia due to significant occlusive vascular disease.

Purpose of the Study:

  • To investigate and report on unusual pathogenic mechanisms underlying limb-shaking TIAs.
  • To highlight alternative causes of cerebral hypoperfusion contributing to limb-shaking TIAs.

Main Methods:

  • Case report analysis of two patients presenting with limb-shaking TIAs.
  • Review of patient histories, diagnostic imaging (carotid angiography), and laboratory findings (platelet count, hemoglobin levels).

Main Results:

  • Patient 1: A 73-year-old woman with essential thrombocytosis experienced resolved limb-shaking TIAs after antiplatelet therapy.
  • Patient 2: A 56-year-old woman with severe anemia and bilateral carotid stenoses (>70%) had her limb-shaking TIAs cease after anemia correction.

Conclusions:

  • Limb-shaking TIAs can arise from factors affecting oxygen delivery beyond carotid stenosis, such as platelet disorders and severe anemia.
  • These cases broaden the understanding of TIA pathogenesis, emphasizing the role of systemic conditions impacting cerebral blood flow.