Objective: We describe a patient who developed amantadine-induced craniofacial myoclonus with speech impairment. Few cases have been reported [1], thus we offer an additional case of a patient who developed craniofacial myoclonus with speech impairment and arrest after exposure to amantadine. 

Background: Amantadine is a commonly prescribed medication for people with Parkinson’s disease who have developed levodopa-induced dyskinesia. Common side effects include hallucinations, peripheral edema, orthostatic hypertension, and livedo reticularis. A rare side effect associated with amantadine is craniofacial myoclonus with speech impairment and arrest. Given that amantadine is widely used in Parkinson’s disease treatment, providers should be aware of this less common side effect.

Method: MB, a 77-year-old female, with a 14-year history of idiopathic Parkinson’s disease. As is common with Parkinson’s patients after exposure to oral levodopa for more than 10 years, she developed levodopa-induced dyskinesia (LID) and motor fluctuations. She was given 137 mg of extended-release amantadine to alleviate both issues. After titrating up to 2 capsules of 137mg, she began to experience speech arrest and craniofacial myoclonus. Despite decreasing back to one capsule, she continued to exhibit these symptoms. Therefore, she was given instructions to wean off the medication and the involuntary movements and speech arrests resolved 10 days after her last dose of extended-release amantadine. Concomitant medications included carbidopa/levodopa 25/100 mg (650 mg in divided doses daily), carbidopa/levodopa controlled release 50/200 mg (1 tablet at bedtime), rasagiline 0.5 mg, and melatonin 5 mg.

Results: In consultation, MB demonstrated frequent speech arrests and myoclonic movements of the lower face. There was no protrusion of her tongue, and her blink rate was normal. After the extended-release amantadine had been weaned off, the speech arrest and myoclonus resolved. The diagnosis we suggest is amantadine-induced craniofacial myoclonus with speech arrest.

Conclusion: This case study adds to the existing literature from Lin et al. to highlight the uncommon side effect of amantadine-induced craniofacial myoclonus. We caution prescribers to observe patients with Parkinson’s disease who take amantadine to be aware of these symptoms.

References: 1. Lin, I., Armengou-Garcia, L., Sasikumar, S., Kuhlman, G., Fox, S.H., Lang, A.E. and Espay, A.J. (2023), Amantadine-Induced Craniofacial Myoclonus: Distinctive Iatrogenic Dysarthria in Parkinson’s Disease. Mov Disord Clin Pract, 10: 1408-1413. https://doi.org/10.1002/mdc3.13828

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MDS Abstracts - https://www.mdsabstracts.org/abstract/craniofacial-myoclonus-a-disabling-complication-of-amantadine-therapy/