Timothy C. Yin, BA
MS4
Wake Forest University School of Medicine
Charlotte, North Carolina, United States
Zachary A. Satin, MD
PM&R PGY4
MedStar National Rehabilitation Hospital
Washington, District of Columbia, United States
Ali Jafri, DO
Brain Injury Fellow
Georgetown University
Washington, District of Columbia, United States
Zakariyya Y. Johnson, n/a
OMS-IV
Lake Erie College of Osteopathic Medicine
Grovetown, Georgia, United States
Emma Nally, MD
Brain Injury and Stroke Rehabilitation Assistant Professor
MedStar National Rehabilitation Hospital
Washington, District of Columbia, United States
A 36-year-old male presented with sudden right facial droop and right-sided weakness. Imaging revealed left basal ganglia hemorrhage with intraventricular extension. His course was notable for hydrocephalus status-post external ventricular drain placement, subsequently removed, and left craniotomy. One month later, in acute inpatient rehabilitation, he developed a new fine tremors in his left upper and lower extremities, new tongue fasciculations, and worsening nonfluent aphasia. Amantadine was discontinued. MRI showed ischemic changes in the corpus callosum and left occipital lobe, and evolution of the left basal ganglia hemorrhage into the left corona radiata, prompting acute care transfer. EEG was without epileptiform activity. Neurology attributed symptoms to enhanced physiologic tremor, possibly enhanced by amantadine. The tremors and fasciculations gradually improved over the next two weeks, though the underlying etiology remained unclear.
Discussions: The occurrence of new tremors without clear imaging abnormalities in hemorrhagic stroke patients is rare. Tremors can arise from structural damage to regions including the basal ganglia or cerebellum. In this case, however, the imaging findings were deemed inconsistent with his clinical presentation. Normal EEG findings further complicated the diagnosis, suggesting the cause may involve neural dysfunctions beyond the sensitivity of standard imaging techniques. Amantadine-induced enhanced physiologic tremor was considered, as the abnormal motor activity gradually improved with its stoppage after several days delay, though it is not a well-characterized adverse effect of amantadine, and the patient had been on amantadine for several weeks prior.
Conclusions: This case highlights the complexity of managing post-stroke neurological symptoms, particularly in cases where new abnormal motor behaviors occur without a clear etiology. While an amantadine-induced tremor is possible, it is not a well-known adverse effect of the medication. Further research is needed to improve diagnostic tools and better understand unexplained motor behaviors following hemorrhagic stroke and amantadine initiation in brain injury patients.