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Autoimmune disorders that can be mistaken for viral illness
Published in Avindra Nath, Joseph R. Berger, Clinical Neurovirology, 2020
Maxwell Greene, Eric Lancaster
Hashimoto encephalopathy is a poorly understood disorder consisting of a steroid-responsive encephalopathy, seizures, and/or movement disorders that are associated with thyroid autoantibodies, particularly thyroid peroxidase (TPO) antibodies. These antibodies are normally found in the serum and rarely found in the CSF. Thyroid function is generally not sufficiently abnormal to explain the neurological symptoms. It is unclear whether these thyroid antibodies have a pathogenic role or are the marker of another form of autoimmunity that has not been identified. This disorder may cause repeated attacks of encephalopathy that respond to steroid treatment [56–58].
Thyroid disorders, dementia and Down syndrome
Published in Vee P. Prasher, Down Syndrome and Alzheimer’s Disease, 2018
It is not known whether antithyroid antibodies cause thyroid disease, whether thyroid disease causes the antibodies, or whether the antibodies’ functions are physiologically beneficial.127 Rarely, elderly people with autoimmune hypothyroidism have a condition called Hashimoto’s encephalopathy, which features cognitive abnormalities (usually a delirium state but sometimes a stroke-like syndrome).65 Thyroid hormones are unlikely to be directly involved in this condition, which may respond to corticosteroid treatment.
Hypothyroidism
Published in David S. Cooper, Jennifer A. Sipos, Medical Management of Thyroid Disease, 2018
Steroid Responsive Encephalopathy Associated with Autoimmune Thyroid Disease (SREAAT) is an acute encephalopathy of unknown cause that typically presents with symptoms of impaired mental status, somnolence, multiple stroke-like episodes, and seizures (101, 102). Because many affected patients have been found to have positive antithyroid antibodies in the serum and also in the cerebrospinal fluid (CSF), it was initially believed that these antibodies might play a pathophysiological role in causing the encephalopathy, possibly by promoting an antibody-mediated cerebritis; the condition was therefore termed “Hashimoto’s Encephalopathy.” However, it remains unclear if there is a pathogenic role for these antibodies in this condition. Reported cases have been hypothyroid, euthyroid, or even hyperthyroid, and treatment of hypothyroid patients with thyroid hormone replacement has produced no beneficial effects on the encephalopathy. Moreover, a substantial number of patients have experienced significant improvement following a course of intravenous or oral glucocorticoid therapy. Because the encephalopathy does not appear to be related to thyroid antibodies or to thyroid dysfunction but does respond well to glucocorticoid therapy, the term “Hashimoto’s Encephalopathy” fell out of favor and the condition has become more accurately referred to as steroid-responsive encephalopathy associated with autoimmune thyroid disease (SREAAT) (101, 102).
Diagnosing autoimmune encephalitis based on clinical features and autoantibody findings
Published in Expert Review of Clinical Immunology, 2019
To summarize, the term ‘autoimmune encephalitis’ is the superordinate term of choice. If such a condition is strongly epilepsy-dominated, one may say instead ‘autoimmune epilepsy’. ‘Limbic encephalitis’ is a syndromic subcategory. ‘Paraneoplastic encephalitis’ is one causally defined form of autoimmune encephalitis. ‘Hashimoto encephalopathy/SREAT’ is no longer a condition of its own but rather helps identifying immune-mediated cases which are negative for more specific antibodies.