Stroke
Brijesh Sharma, DO
Resident
Stanford University
Fremont, California, United States
Matthew Kaufman, MD
Resident
Stanford University
Redwood City, California, United States
Royce Le, BS
MS4
University of Virginia
Chalottesville, Virginia, United States
Henry Huie, MD
Chief of Brain Injury Medicine, Vice Chair of PM&R
Santa Clara Valley Medical Center
San Jose, California, United States
Brijesh Sharma, DO
Stanford University
Fremont, California, United States
57-year-old male who experienced hypoactive delirium in the setting of right basal ganglia hemorrhage with intraventricular extension secondary to hypertensive emergency.
Case Description:
A 57-year-old male who sustained a right basal ganglia hemorrhage developed hypoactive delirium. He was treated with amantadine for neurological stimulation prior to his IRF stay. Amantadine was titrated up to 100mg BID and resulted in improved alertness. In rehab, he was continued on the same dose of amantadine but subsequently developed an acute on chronic kidney injury followed by neurological changes including agitation, tremulousness, visual hallucinations, and confusion. Amantadine was discontinued due to concern for toxicity in the setting of new renal impairment. The patient's mental status and tremors improved significantly over the following week with return to baseline nine days after cessation of amantadine.
Discussions:
Amantadine has been used as a neurostimulant that has been shown to improve functional recovery in patients following a cerebrovascular accident. Few studies have described amantadine toxicity in IRF. Amantadine is primarily renally excreted, and its clearance is significantly reduced with renal impairment leading to drug accumulation and increased risk of neuropsychiatric toxicity. The most common neuropsychiatric manifestations of amantadine toxicity include delirium, visual hallucinations, agitation, myoclonus, and psychosis. In this case, the patient received amantadine for hypoactive delirium but then developed agitation, tremulousness, and visual hallucinations after a recent acute kidney injury (AKI). Despite stable dosing, the patient's symptoms coincided with his AKI, resulting in decreased amantidine clearance, amantadine toxicity was suspected and the drug promptly was discontinued. The patient's AKI was concurrently treated with resolution of the patient’s encephalopathy.
Conclusions: Amantadine toxicity is a rare, but significant concern in rehabilitation patients with renal impairment. Careful dose adjustment and monitoring of renal function can minimize toxicity risks.
