Background: Amantadine is widely used to improve reduced spontaneity and prevent aspiration pneumonia. There are few reports on cases of amantadine intoxication in the field of rehabilitation. Cases: Case 1 involved an 83-year-old man with a history of a lacunar infarction who was transferred to our rehabilitation hospital after a left femoral neck fracture and a left upper arm fracture. He had mild renal dysfunction. Although he was started on oral amantadine 150 mg/dayto reverse a decline in spontaneity, he could not begin rehabilitation therapy because of hallucinations and myoclonus. Furthermore, he developed aspiration pneumonia as a result of a consciousness disorder. After stopping amantadine, his toxic symptoms disappeared completely. Case 2 involved a 53-year-old man who was transferred to our hospital for rehabilitation after a brain contusion. He was started on oral amantadine 100 mg/day to reverse a decline in spontaneity. After amantadine was increased to 150 mg/day, myoclonus and hallucinations developed. At that time, his renal function was mildly impaired. The concentration of amantadine in his blood serum was found to be 4783 ng/dl. After amantadine was stopped, his spontaneity decline recurred. After restarting amantadine at 50 mg/day, his toxic symptoms did not reappear, and the decline in his spontaneity improved. Discussion: Amantadine is a renally excreted drug that may cause toxic symptoms as a result of decreased renal function. It is necessary to monitor renal function and toxic symptoms when amantadine is administered in rehabilitation hospitals.