Dopamine Antagonist-Induced Parkinsonism

Abstract

Abstract Drug-induced parkinsonism (DIP) can be defined as parkinsonism (at least two of four cardinal features) occurring in temporal relationship to medications known to lessen dopaminergic functioning. In fact, one of the first suggestions that dopamine may be involved in the pathogenesis of Parkinson’s disease was based on observing the effects of reserpine, a dopamine depleter, on movements. Individual susceptibility, genetic factors, older age, female sex, and higher doses of offending drugs that have more affinity to D2/D3 receptor for longer durations are known risk factors. However, the pathophysiology is likely more complex than simply blocking dopamine receptors. It’s nearly impossible to differentiate between DIP and idiopathic Parkinson’s disease based on clinical manifestations alone. DaTscan and other dopamine imaging modalities, transcranial sonography of the midbrain, and cardiac sympathetic imaging are more reliable in differentiating the two conditions and, in some cases, can predict which patients have underlying degenerative parkinsonism. Treatments of DIP include withdrawal of the offending drug or decreasing the dose, switching to a drug with less risk, and adding pharmacological agents such as amantadine, anticholinergics, and electroconvulsive therapy (ECT).