Hashimoto’s Encephalopathy: A Review

Abstract

The condition "Hashimoto's encephalopathy" (HE) refers to a cerebral dysfunction syndrome with elevated antithyroid peroxidase antibody titers that is thought to have an autoimmune cause. Similar to autoimmune thyroid illness, women are more likely than men to develop HE. It has been documented in adult, geriatric, and pediatric populations worldwide. The clinical appearance may be recurrent and remitting, with myriad symptoms involving myoclonus, seizures, episodes resembling strokes, cognitive deterioration, and neuropsychiatric symptoms. Clinically and biochemically, thyroid function is often normal. Although HE seems to be a rare disorder, it should be taken into consideration when treating "investigation negative encephalopathies" because it responds to corticosteroid treatment. The results of neuroimaging frequently do not help to clarify the diagnosis. High titers of antithyroid antibodies, specifically antithyroid peroxidase antibodies, are diagnosed in the setting of the usual clinical picture. Corticosteroid treatment is nearly always successful, although relapses are common. Other immunomodulatory treatments, like intravenous immunoglobulin and plasma exchange, are often effective as well. Despite a statistical correlation to autoimmune thyroid illness, the cause of HE is not well understood. Research is still needed to fully understand the connections between clinical images, thyroid disease, auto-antibody pattern, and brain pathology. It's possible that over time, a class of nonvasculitic autoimmune inflammatory meningoencephalopathies will include HE. Some writers have proposed severing all connections to Hashimoto and calling the illness, SREAT - "steroid responsive encephalopathy associated with autoimmune thyroiditis".