OBJECTIVE: There is increasing evidence for olfactory deficits in patients with extrapyramidal disorders, but little is known about their occurrence in patients with drug-induced extrapyramidal symptoms (EPS). The present study was performed to investigate olfactory function in depressed patients with drug-induced parkinsonism under treatment with D2-blocking neuroleptic drugs compared to depressed controls on similar neuroleptic dose without EPS (no-EPS), and neuroleptic-naive depressed controls (no-NL). METHODS: A total of 79 depressed patients with (N = 59) and without psychotic features (N = 20) were included in the study. Psychotic patients were treated with D2 blocking neuroleptic drugs. Of the neuroleptic-treated patients, 15 developed EPS. In all patients psychophysical olfactory testing was performed using "Sniffin' Sticks" which included assessment of odor thresholds for phenylethylalcohol (PEA), odor identification, and odor discrimination. RESULTS: Patients in the EPS group had significantly lower olfactory scores than patients in the no-EPS or no-NL groups. Patients in the no-NL and no-EPS groups were not significantly different from each other in terms of olfactory function. Using partial correlations controlling for the patients' age, significant correlations were observed for EPS patients between severity of EPS and odor thresholds and odor identification, but not for odor discrimination. This indicated that olfactory function decreased with increasing severity of EPS symptoms. CONCLUSIONS: Our data show that olfactory deficits may be drug-induced in patients with primary affective disorder with a sensitivity toward developing EPS.
OBJECTIVE: There is increasing evidence for olfactory deficits in patients with extrapyramidal disorders, but little is known about their occurrence in patients with drug-induced extrapyramidal symptoms (EPS). The present study was performed to investigate olfactory function in depressedpatients with drug-induced parkinsonism under treatment with D2-blocking neuroleptic drugs compared to depressed controls on similar neuroleptic dose without EPS (no-EPS), and neuroleptic-naive depressed controls (no-NL). METHODS: A total of 79 depressedpatients with (N = 59) and without psychotic features (N = 20) were included in the study. Psychoticpatients were treated with D2 blocking neuroleptic drugs. Of the neuroleptic-treated patients, 15 developed EPS. In all patients psychophysical olfactory testing was performed using "Sniffin' Sticks" which included assessment of odor thresholds for phenylethylalcohol (PEA), odor identification, and odor discrimination. RESULTS:Patients in the EPS group had significantly lower olfactory scores than patients in the no-EPS or no-NL groups. Patients in the no-NL and no-EPS groups were not significantly different from each other in terms of olfactory function. Using partial correlations controlling for the patients' age, significant correlations were observed for EPSpatients between severity of EPS and odor thresholds and odor identification, but not for odor discrimination. This indicated that olfactory function decreased with increasing severity of EPS symptoms. CONCLUSIONS: Our data show that olfactory deficits may be drug-induced in patients with primary affective disorder with a sensitivity toward developing EPS.
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