AbstractFluoxetine (Prozac®) is a potent serotonin (5‐HT) reuptake inhibitor which has rapidly gained popularity as a first‐line antidepressant due to its favourable side‐effect profile. However, it has recently been reported to worsen drug‐induced parkinsonism when used in conjunction with neuroleptics (Bouchardet al., 1989; Tate, 1989; Brod, 1989). Since fluoxetine inhibits hepatic microsomal enzymes, a pharmacokinetic interaction cannot be ruled out in such cases — the drug is known to interact with other psychotropic drugs such as MAO inhibitors (Sternbach, 1988; Feighneret al., 1990) and tricyclic antidepressants (Bell and Cole, 1988; Vaughan, 1988; Goodnick, 1989; Schramlet 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. Bouchardet al.(1989) observed that other selective 5‐HT reuptake inhibitors might exacerbate PD, and Meltzeret 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 (Lipinskiet al., 1989; Baldwinet 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 5‐HT 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 (Baldwi