Pargyline reduces/prevents neuroleptic-induced acute dystonia in monkeys

R. Heintz, D. E. Casey

Research output: Contribution to journalArticlepeer-review

5 Scopus citations


The neuropharmacologic mechanisms underlying neuroleptic-induced extrapyramidal syndromes (EPS) were studied using a nonhuman primate model. Twenty-six Cebus albifrons monkeys were given weekly challenges of haloperidol (0.025 mg/kg IM), and half of the animals received the monoamine oxidase (MAO) inhibitor pargyline (5 mg/kg PO) daily for 17 consecutive days during the protocol. Pargyline caused no changes in baseline behaviors, but significantly reduced haloperidol-induced acute dystonia (AD) (-67%, P<0.002) and parkinsonism (-56%, P<0.005). The majority (8 of 13) of the experimental group had complete prevention of neuroleptic-induced EPS during cotreatment with pargyline. Behavioral scores returned to baseline levels after stopping pargyline, and did not show the further sensitization to haloperidol-induced AD that occurred in the control group. The possible mechanisms by which an MAO inhibitor might influence neuroleptic-induced AD were considered. The most likely explanation would appear to involve facilitation of striatal dopamine (DA) neurotransmission by inhibition of intra- and extraneuronal MAO, thus supporting the hypothesis that AD is due to decreased striatal DA function with secondary cholinergic hyperfunction.

Original languageEnglish (US)
Pages (from-to)207-213
Number of pages7
Issue number2
StatePublished - Oct 1987


  • Cebus albifrons monkeys
  • Dystonia
  • Extrapyramidal syndromes
  • Monoamine oxidase
  • Neuroleptics
  • Pargyline
  • Primates

ASJC Scopus subject areas

  • Pharmacology


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