A 57-year-old female developed dizziness and forgetfulness several days before admission. She was admitted to our hospital because of a headache and nausea. On admission, she had a mild disturbance of consciousness and right hemiparesis. Initial MR imaging revealed multiple infarctions in the acute-to-subacute phases in the right cerebellum, left occipital lobe, and bilateral parietal lobes. Her electrocardiogram showed atrial fibrillation and transesophageal echocardiography revealed the presence of a thrombus at the left atrial appendage, suggesting that she suffered from cardioembolic stroke. Laboratory testing showed elevated free T4 levels and low thyroid stimulating hormone (TSH) levels with positive anti-TSH receptor antibodies, indicating untreated Basedow disease. Although treatment with anticoagulants and methimazole was initiated, her postural tremor, tachycardia, and psychosis deteriorated. On the 8th day of admission, thyrotoxic crisis was confirmed. Despite increased doses of methimazole, as well as treatments with inorganic iodine, steroids, and β-blockers, her psychosis prolonged even after her thyroid function was normalized. Long-term use of antipsychotic medications was required to treat her psychosis. In this case, neurotoxicity of the anti-TSH antibodies related to Basedow disease may have caused prolonged psychosis because of the extensive damage to the blood-brain-barrier function following multiple ischemic strokes. Careful observation and treatment are required for psychotic symptoms, in addition to the treatment for acute stroke in such cases, where thyrotoxic crisis is associated with ischemic stroke.