Drug-induced parkinsonism

Drug-induced parkinsonism (DIP) is the second cause of akinetic rigid syndrome in the Western world and its prevalence is increasing and approaching that of idiopathic Parkinson’s disease due to the ageing of the population and to the rising of polypharmacotherapy. DIP was initially reported as a complication of neuroleptics in psychiatric patients, but it has also been described with a great diversity of compounds such as antiemetics, drugs used for the treatment of vertigo, antidepressants, calcium channel antagonists, antiarrythmics, antiepileptics, cholinomimetics and other drugs. Although traditionally considered reversible, DIP may persist after drug withdrawal. At least 10% of patients with DIP develop persistent and progressive parkinsonism in spite of the discontinuation of the causative drug. Irreversible or progressive DIP has been considered as an indication of presymptomatic parkinsonian deficit, unmasked but not caused by the offending drug, but it could be explained by persistent toxicity of the responsible pharmacological agents on the nigrostriatal dopamine pathway. The best treatment of DIP is prevention, including the avoidance of prescription of causative drugs whenever it is not strictly necessary. In patients who require potentially risky medication, it is necessary to perform adequate monitoring for early parkinsonian deficits and early discontinuation if these deficits appear. Atypical neuroleptics are associated with lower risk than first generation antipsychotic drugs. Special precautions are needed in elderly subjects, in patients treated with multiple drugs for prolonged periods of time and in those with familial risk factors including familial parkinsonism or tremor, or in those with genetic variants of genes involved in idiopathic Parkinson’s disease.