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Clomethiazole protects against hemineglect in a primate model of stroke

J W Marshall1, A J Cross, D M Jackson

  • 1MRC Comparative Cognition Team, Department of Experimental Psychology, University of Cambridge, Cambridge, United Kingdom. jwbm2@cus.cam.ac.uk

Insights

Clomethiazole, a drug modulating GABA(A) receptors, significantly reduced spatial neglect in a marmoset stroke model. While not improving motor deficits, it lessened brain damage, suggesting potential for treating stroke-related neglect in humans.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Primate Models of Stroke

Background:

  • Middle cerebral artery occlusion (MCAO) in marmosets causes functional deficits like motor and spatial neglect.
  • Clomethiazole is a drug that modulates gamma-aminobutyric acid(A) receptors.

Purpose of the Study:

  • To investigate if clomethiazole reduces hemineglect and other deficits in a primate stroke model.
  • To assess clomethiazole's efficacy in mitigating stroke-induced brain damage and functional impairments.

Main Methods:

  • Permanent M1 segment of the middle cerebral artery occlusion (pMCAO) was induced in nine marmosets.
  • Four monkeys received clomethiazole treatment via injection and osmotic mini-pumps for 48 hours.
  • Behavioral tasks were administered pre-surgery and at 3 and 10 weeks post-surgery; brain damage was analyzed postmortem.

Main Results:

  • Clomethiazole treatment significantly reduced spatial neglect severity at 3 weeks post-pMCAO compared to controls.
  • The drug did not improve severe contralesional motor impairment but showed efficacy in a prior M2 occlusion model.
  • Postmortem brain analysis revealed clomethiazole significantly reduced damage in parts of the parietal cortex.

Conclusions:

  • Clomethiazole demonstrates potential in reducing spatial neglect following stroke.
  • The drug's efficacy may be dependent on stroke severity and location.
  • These findings suggest clomethiazole could be a therapeutic option for managing debilitating neglect symptoms in human stroke patients.

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