Tardive dyskinesia: possible involvement of free radicals and treatment with vitamin E

A M Elkashef1, R J Wyatt

  • 1Medications Development Division, National Institute on Drug Abuse, Bethesda, MD 20892-9551, USA. ae8a@nih.gov

Schizophrenia Bulletin
|February 10, 2000
PubMed

Insights

Free radicals generated by neuroleptic treatment may cause tardive dyskinesia (TD). Studies suggest vitamin E could be an effective treatment for this condition.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Oxidative Stress

Background:

  • A hypothesis proposed a decade ago suggests free radicals contribute to tardive dyskinesia (TD) development following neuroleptic treatment.
  • Subsequent preclinical and clinical research has explored this link, investigating the role of oxidative stress in TD pathogenesis.

Purpose of the Study:

  • To review and synthesize evidence regarding the involvement of free radicals in tardive dyskinesia.
  • To evaluate the potential therapeutic efficacy of vitamin E in managing TD.

Main Methods:

  • Literature review of preclinical and clinical studies.
  • Analysis of research investigating the relationship between neuroleptic-induced free radicals and TD.
  • Assessment of studies examining vitamin E's effects on TD.

Main Results:

  • Evidence suggests a probable role for free radicals in the pathogenesis of tardive dyskinesia.
  • Preclinical and clinical data indicate that vitamin E may be a beneficial treatment for TD.

Conclusions:

  • The free radical hypothesis for tardive dyskinesia is supported by accumulated research.
  • Vitamin E shows promise as a therapeutic agent for tardive dyskinesia, warranting further investigation.

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