To the Editor: Hashimoto's encephalopathy is a rare neurological syndrome characterized by high levels of antithyroid antibodies, good responsiveness to corticosteroid treatment, and neuropsychiatric symptoms, including seizures, stroke-like episodes, dementia, and psychosis (1). In one report, (2) one woman was found to have Hashimoto's encephalopathy 15 months after a diagnosis of bipolar disorder; the authors suggested that Hashimoto's encephalopathy may have caused her psychiatric symptoms. We report a case of Hashimoto's encephalopathy with manic symptoms as a dominant clinical feature.

A 52-year-old woman with no family or personal history of psychiatric illness was admitted to our psychiatric unit for manic symptoms that had begun 1 month earlier. She had exhibited unusual elation, mood lability, decreased need for sleep, and hyperactivity, and was giving her money away to strangers. On admission, she demonstrated irritability, distractibility, talkativeness, psychomotor agitation, and flight of thought. At 30 years old, she had received a partial thyroidectomy for a hyperthyroid goiter but no T4 therapy. Initial laboratory examinations were normal except for hypothyroidism with high thyroid-stimulating hormone (50.71 μIU/ml, reference range: 0.47–4.64 μIU/ml). She was prescribed olanzapine (20 mg/day) and valproate (1,000 mg/day) for mania and T4 for hypothyroidism. At 4 weeks, she remained manic and episodically disoriented. Hashimoto's encephalopathy was suspected when thyroid function study showed euthyroidism with increases in thyroglobulin antibodies (296 IU/ml, normal value: <25 IU/ml) and thyroperoxidase antibodies (1652 IU/ml, normal value: <25 IU/ml). A psychiatrist, neurologist, and endocrinologist jointly evaluated her reports and diagnosed her with Hashimoto's encephalopathy. Oral prednisolone (1 mg/kg/day) was added to her regimen. At 45 days, her manic symptoms and antithyroid antibodies had decreased markedly (thyroglobulin antibodies: 35.8 IU/ml, thyroperoxidase antibodies: 408 IU/ml). Four weeks later, she was prescribed prednisolone (40 mg/day) and valproate (500 mg/day) and discharged. Her psychiatric symptoms continued improving. By 6 months, she was completely weaned from prednisolone but continued taking valproate.

Review of the literature suggests that possible explanations for our case's manic symptoms could have been secondary mania, a direct pathophysiological effect of Hashimoto's encephalopathy, or a latent/preexisting bipolar disorder precipitated by Hashimoto's encephalopathy. Secondary mania is found to begin at a later age in people with comorbid neurological disorders and no family history of the illness, while bipolar disorder may be triggered by Hashimoto's encephalopathy because Hashimoto's thyroiditis was suspected to be involved in deterioration of bipolar disorder,³ and there is a high prevalence of autoimmune thyroiditis in patients with bipolar disorder and their female offspring.⁴ Findings from a twin study have also shown autoimmune thyroiditis to possibly contribute to genetic vulnerability to bipolar disorder.⁵

To our knowledge, this is the first reported case of Hashimoto's encephalopathy leading to mania. Her remarkable response to adjunctive corticosteroid treatment but not to antimanic medications or T4 therapy confirmed the diagnosis and suggested more would be needed to effectively treat her mania than just treating the symptoms themselves. Therefore, clinicians treating patients with a history of thyroid disease for atypical bipolar mania should be aware of the possibility of Hashimoto's encephalopathy and know of its treatment options.