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reflexes in both hands. Parkinsonism symptoms, such as rigidity, were mild, but she could not stand or walk. Brain computed tomography showed no apparent ischemic changes, and electroencephalography showed no obvious paroxysmal discharges or triphasic waves. Her plasma amantadine hydrochloride level was high (4,900 ng/ml), and she was eventually diagnosed with amantadine toxicity. After cessation of oral amantadine hydrochloride, all of her symptoms and signs gradually improved; about 3 weeks later she was able to walk without aid. Patient 2: A 74-year-old woman had a right cerebellar hemorrhage in 1991. She subsequently developed apathy, depression, and gait disturbance, and was treated with 200 mg amantadine hydrochloride and 200 mg droxidopa per day. In March 2005, she began to have visual disturbances, e.g., ‘the floor looks crooked’. In April 2005, she developed fever, vomiting, and myoclonic jerks in her limbs, and became unable to stand independently. On May 18, 2005, she was referred to our hospital. She did not speak voluntarily and was bound to her wheelchair. Neurological examinations revealed myoclonic jerks in limbs and marked grasp reflexes in both hands. There was no apparent motor paresis or cerebellar ataxia. Assessment of muscular tone was difficult because of declined auditory comprehension. Electroencephalography showed no obvious paroxysmal discharges or triphasic waves. Dear Sir, Amantadine hydrochloride is widely used to treat Parkinson’s disease. In Japan, amantadine is also commonly used to treat post-stroke depressive states and influenza A virus infection. There are a few reports describing amantadine toxicity in aged patients with renal dysfunction, but the neurological features of amantadine toxicity are not well recognized and thus might be misdiagnosed. Here, we present 3 patients with amantadine toxicity.

Severe Reversible Neurological Complications following Amantadine Treatment in Three Elderly Patients with Renal Insufficiency