The status of olfactory function and the striatal dopaminergic system in drug-induced parkinsonism

Abstract

Olfactory impairment has been reported in drug-induced parkinsonism (DIP), but the relationship between dopaminergic dysfunction and smell deficits in DIP patients has not been characterized. To this end, we studied 16 DIP patients and 13 patients affected by Parkinson's disease (PD) using the "Sniffin' Sticks" test and [(123)I] FP-CIT SPECT (single-photon emission computed tomography). DIP patients were divided based on normal (n = 9) and abnormal (n = 7) putamen dopamine transporter binding. Nineteen healthy age- and sex-matched subjects served as controls of smell function. Patients with DIP and pathological putamen uptake had abnormal olfactory function. In this group of patients, olfactory TDI scores (odor threshold, discrimination and identification) correlated significantly with putamen uptake values, as observed in PD patients. By contrast, DIP patients with normal putamen uptake showed odor functions-with the exception of the threshold subtest-similar to control subjects. In this group of patients, no significant correlation was observed between olfactory TDI scores and putamen uptake values. The results of our study suggest that the presence of smell deficits in DIP patients might be more associated with dopaminergic loss rather than with a drug-mediated dopamine receptor blockade. These preliminary results might have prognostic and therapeutic implications, as abnormalities in these individuals may be suggestive of an underlying PD-like neurodegenerative process.

Olfaction in Parkinson's disease and related disorders

“…Of the remaining five, all but one had normal UPSIT scores and all regained normal motor function after medication adjustment. Bovi et al (2010) administered odor identification and detection tests to sixteen DIP patients (7 Haloperidol, 5 Amisulpride, 2 Perphenazine, 1 Fluphenazine, 1 Clomipramine), 13 PD patients, and 19 age- and sex-matched normal controls. The DIP patients were divided based on normal (n=9) and abnormal (n=7) putamen DA transporter binding as determined from 123 I-FP-CIT SPECT imaging.…”

Movement Disorders Induced by Antipsychotic Drugs: Implications of the CATIE Schizophrenia Trial

“…Parkinson’s disease is usually asymmetric in symptom presentation, has a slow progressive course, may have associated dysautonomia, should precede treatment and not resolve after antipsychotic drugs are discontinued, and may show nigrostriatal degeneration on dopamine transporter scans and sympathetic dysregulation on 123 IMIBG cardiac scintigraphy. 44 Interestingly, olfactory deficits have recently been reported in drug-induced parkinsonism 45. The differential diagnosis also includes essential tremor and other causes of parkinsonism, including vascular parkinsonism which also tends to be asymmetric, and parkinsonism caused by other drugs including anti-emetics, tetrabenazine, and reserpine.…”

Drug-induced parkinsonism: diagnosis and management

“…Anosmia and rapid eye movement sleep behavior disorder are not typical of DIP. 34,61 Abnormal olfactory testing in DIP correctly predicted those subjects displaying persistent signs after drug withdrawal 35 or abnormal 123 I-metaiodobenzylguanidine (sympathetic neuron imaging ligand) cardiac scintigraphy suggestive of an underlying neurodegenerative process. …”