Not all drug-induced parkinsonism are the same: the effect of drug class on motor phenotype

• Published in: Neurological sciences Vol. 38; no. 2; pp. 319 - 324
• Main Authors: Munhoz, Renato P., Bertucci Filho, Delcio, Teive, Hélio A. G.
• Format: Journal Article
• Language: English
• Published: Milan Springer Milan 01.02.2017; Springer Nature B.V
• Subjects: Aged; Aged, 80 and over; Antipsychotic Agents - adverse effects; Calcium Channel Blockers - adverse effects; Female; Humans; Male; Medicine; Medicine & Public Health; Middle Aged; Neurology; Neuroradiology; Neurosciences; Neurosurgery; Original Article; Parkinson Disease, Secondary - chemically induced; Parkinson Disease, Secondary - physiopathology; Phenotype; Psychiatry; Parkinsonism; Dopamine receptor blocker; Antipsychotics; Neuroleptics; Drug-induced parkinsonism; Calcium channel blocker
• ISSN: 1590-1874; 1590-3478
• DOI: 10.1007/s10072-016-2771-y

Drug-induced parkinsonism (DIP) is classically described as acute/subacute, bilateral symmetric syndrome in which tremor is infrequent compared to Parkinson’s disease. Most DIP cases are caused by classic (CN) and second-generation neuroleptics (SN), and calcium channel blockers (CCB). We evaluated potentially distinctive demographic and clinical features in DIP among different drug classes. This was a prospective study of reversible DIP related to single selected drugs on each class. Baseline assessment included demographic, clinical data, and scales for staging, severity of motor signs of parkinsonism, tremor, and other involuntary movements. Six months after medication withdrawal, patients were reassessed. Those with no parkinsonian signs were included in the final sample. 157 cases were included after strict criteria were applied. Most common agents were haloperidol, levomepromazine, and chlorpromazine for the CN-DIP group, flunarizine and cinnarizine for the CCB-DIP group, and risperidone and olanzapine for the SN-DIP group. Drug exposure was shorter for CN-DIP cases; duration of parkinsonism was longer in the CCB-DIP group. CN-DIP had worse bradykinesia, rigidity, axial, total motor, and disease stage scores, with higher frequency of rigid-akinetic parkinsonism. Tremor scores were worse for CCB-DIP cases. SN-DIP presented as a less severe but similar form of CN-DIP. Tardive-type involuntary movements were less common in the SN-DIP group. DIP profile differs significantly depending on drug class involved, not only in terms of severity, but also regarding the differential combination of signs. These findings may help guiding clinicians in screening and diagnosing DIP in patients exposed to these drugs.