Abstract
Fluoxetine (Prozacยฎ) is a potent serotonin (5โHT) reuptake inhibitor which has rapidly gained popularity as a firstโline antidepressant due to its favourable sideโeffect profile. However, it has recently been reported to worsen drugโinduced parkinsonism when used in conjunction with neuroleptics (Bouchard et al., 1989; Tate, 1989; Brod, 1989). Since fluoxetine inhibits hepatic microsomal enzymes, a pharmacokinetic interaction cannot be ruled out in such cases โ the drug is known to interact with other psychotropic drugs such as MAO inhibitors (Sternbach, 1988; Feighner et al., 1990) and tricyclic antidepressants (Bell and Cole, 1988; Vaughan, 1988; Goodnick, 1989; Schraml et al., 1989; Kahn, 1990) via this mechanism among others. So far, fluoxetine has not been reported to worsen symptoms in patients with Parkinson's disease (PD) who have never received neuroleptics. Bouchard et al. (1989) observed that other selective 5โHT reuptake inhibitors might exacerbate PD, and Meltzer et al. (1979) described a bipolar patient who developed an acute dystonic reaction, with parkinsonian rigidity and increased serum prolactin when treated with fluoxetine for psychotic depression. Fluoxetine has been implicated in the development of neuroleptic malignant syndrome (Halman and Goldbloom, 1990) and akathisia (Lipinski et al., 1989; Baldwin et al., 1991), which may also be linked to central dopaminergic blockade. A recent review of extrapyramidal tract disorders in association with fluoxetine and fluvoxamine, another selective 5โHT uptake blocker, noted the absence of unambiguous cases and the lack of objective documentation of psychopathological and neurological changes, even though evidence for a causal relationship was compelling (Baldwin et al., 1991).