1646 - Unveiling the Unexpected: Amantadine-induced Myoclonus in a Chronic Hypoxic-Ischemic Brain Injury

Amantadine-induced myoclonus in a chronic hypoxic-ischemic brain injury (HIBI)

Case Description: A 36-year-old male with HIBI due to cardiac arrest secondary to COVID-19 hypoxic respiratory failure. For two years, the patient experienced multiple readmissions due to infection and gastrotomy tube dysfunction, while suffering a notable decline in functional status and arousal. In 2024, he was placed on amantadine 50 mg BID at a skilled nursing facility for arousal, but reduced dosage to 50 mg daily due to worsening agitation. He was subsequently admitted to an inpatient rehabilitation facility with amantadine on hold. Shortly into his rehabilitation course, the patient was restarted on amantadine 50 mg BID which he tolerated well without any side effects. The amantadine dose was increased to 100 mg BID. One day later, the patient developed myoclonus in both upper and lower extremities affecting his ability to transfer. In response, the amantadine dosage was reduced to 50 mg BID, effectively preventing further episodes of myoclonus while maintaining arousal.

Discussions:

Amantadine can cause myoclonus in HIBI patients. Current research suggests that amantadine induced myoclonus occurs in patients with Parkinson's disease and/or supranuclear palsy. This case highlights that standard amantadine dosing can induce myoclonus in young patients with chronic HIBI. However, by reducing the dose, patients can continue to benefit from neurostimulation without experiencing unwanted myoclonus. 

Conclusions:

Though uncommon, physiatrists should consider amantadine as a potential cause of myoclonus in patients with HIBI. Careful monitoring for this rare side effect is essential when initiating neurostimulation with amantadine. Given the limited existing literature, further research is warranted to better understand the mechanisms of amantadine-induced myoclonus and optimal dosing in this population.