Amantadine‐Induced Craniofacial Myoclonus: Distinctive Iatrogenic Dysarthria in Parkinson's Disease

Abstract

ABSTRACTBackgroundAmantadine is a widely prescribed medication in Parkinson's disease (PD). A distinctive craniofacial distribution of myoclonus with speech impairment is an underrecognized iatrogenic complication in amantadine‐treated patients with PD.CasesWe report 7 patients with idiopathic PD (disease duration, 6–21 years) who developed speech‐induced craniofacial‐predominant myoclonus with “stuttering‐like” dysarthria and speech arrests days to months after amantadine initiation or dose increase. Renal insufficiency was identified as a risk factor in 4 cases. In all cases, reduction or discontinuation of amantadine markedly attenuated the myoclonus and restored speech intelligibility.Literature ReviewAmantadine can induce subcortical segmental or generalized myoclonus. A report in 1996 of “vocal myoclonus” in an amantadine‐treated patient with PD was the first observation of a focal distribution of myoclonus, particularly affecting speech. Since then, few cases of craniofacial myoclonus with speech impairment have been reported, none with accompanying video. With 1 exception, the craniofacial distribution was part of a generalized pattern of amantadine‐induced myoclonus. Comorbid renal insufficiency is a recognized risk factor.ConclusionsSpeech‐induced craniofacial myoclonus, with marked “stuttering‐like” dysarthria and speech arrests, is a disabling iatrogenic complication in PD that resolves upon amantadine discontinuation.