Etiology, pathophysiology, and imaging of tardive dyskinesia

Chanoch Miodownik, Vladimir Lerner

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review


This chapter summarizes the current data concerning the etiology, pathophysiology, and results of imaging studies: computed tomography, magnetic resonance imaging, positron emission tomography and dopamine transporter scan. Tardive dyskinesia may be caused by medications from a variety of chemical groups and classes with sundry therapeutic purposes. The pathophysiology of tardive dyskinesia is complicated, only partly explained and remains unclear. Multiple models have been suggested to explain this unpleasant and sometimes disabling side effect. To date, several neurochemical hypotheses have been proposed for the explanation of TD development. These theories include: dopamine postsynaptic hypersensitivity; a disturbed balance between dopamine and cholinergic systems; noradrenergic dysfunction; dysfunctions of striatonigral, γ-aminobutric acid (GABA)ergic neurons; neurodegenerative hypothesis; synaptic plasticity, and genetic predisposition. The results of imaging studies concerning TD are not consistent and need further investigation.

Original languageEnglish
Title of host publicationTardive Dyskinesia
Subtitle of host publicationCurrent Approach
PublisherNova Science Publishers, Inc.
Number of pages27
ISBN (Print)9781536137774
StatePublished - 10 Jul 2018


  • Etiology
  • Genetics
  • Pathophysiology
  • Plasticity
  • Tardive dyskinesia

ASJC Scopus subject areas

  • General Medicine


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