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

BackgroundAmantadine 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.

Automated summary

Speech-induced craniofacial myoclonus with stuttering-like dysarthria and speech arrests is a disabling iatrogenic complication in Parkinson's disease that resolves upon amantadine discontinuation. Four of the patients with renal insufficiency were identified as a risk factor.