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Cocaine use and stroke
  1. Sean D Treadwell1,
  2. Tom G Robinson2
  1. 1Department of Integrated Medicine, University Hospitals of Leicester NHS Trust, Leicester Royal Infirmary, Leicester, UK
  2. 2Department of Medicine for the Elderly, University Hospitals of Leicester NHS Trust, Leicester General Hospital, Leicester, UK
  1. Correspondence to:
 Dr Sean D Treadwell
 Department of Integrated Medicine, University Hospitals of Leicester NHS Trust, Leicester Royal Infirmary, Leicester, LE1 5WW, UK; seantreadwell{at}hotmail.com

Abstract

Stroke is the third most common cause of death in developed countries. In England and Wales, 1000 people under the age of 30 have a stroke each year. Cocaine is the most commonly used class A drug, and the first report of cocaine-induced stroke was in 1977. Since the development of alkaloidal “crack” cocaine in the 1980s, there has been a significant rise in the number of case reports describing both ischaemic and haemorrhagic stroke associated with cocaine use. Cocaine is a potent central nervous system stimulant, and acts by binding to specific receptors at pre-synaptic sites preventing the reuptake of neurotransmitters. The exact mechanism of cocaine-induced stroke remains unclear and there are likely to be a number of factors involved including vasospasm, cerebral vasculitis, enhanced platelet aggregation, cardioembolism, and hypertensive surges associated with altered cerebral autoregulation. The evidence surrounding each of these factors will be considered here.

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Footnotes

  • Competing interests: None declared

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