Deterioration of preexisting myoclonus following nifedipine use in parkinsonian syndrome: A case report.

L-type calcium channel antagonists are uncommon causes of myoclonus, and the underlying mechanism remains unclear. Here, we report a case of parkinsonian syndrome with deterioration of preexisting myoclonus after nifedipine use. A 96-year-old woman was administered a single dose of sustained-release nifedipine for chest pain.  One hour later, the patient developed shock-like jerky movements in the trunk and upper and lower limbs. Neurological examination revealed myoclonus, intention tremor in both hands, facial hypomimia, stooped posture, short stride length, absent arm swing during walking, and muscle rigidity in the neck, left arm, and both legs. Brain magnetic resonance imaging showed no causative lesions, suggesting a nifedipine-induced movement disorder. Myoclonic movements almost completely resolved within 24 h. Despite no further administration of nifedipine, a neurological examination one week later revealed parkinsonism with mild myoclonus and intention tremor. It appeared that preexisting myoclonus and intention tremor transiently worsened with nifedipine use. The patient was diagnosed with parkinsonian syndrome with deterioration of myoclonus due to nifedipine administration. This case suggests that the corticostriatal pathways may have already been impaired and were further affected by nifedipine. Nifedipine-induced alterations in dopaminergic and serotonergic systems may have contributed to the deterioration of myoclonus and intention tremor. When patients present with myoclonus after taking an L-type calcium channel antagonist, underlying neurological disorders should be carefully investigated.