Case Report Delirious Mania Associated with Autoimmune Gastrothyroidal Syndrome of a Mid-Life Female: The Role of Hashimoto Encephalopathy and a 3-Year Follow-Up including Serum Autoantibody Levels Udo Bonnet, 1 Claudia Selle, 1 and Ralf Kuhlmann 2 1 Department of Psychiatry, Psychotherapy, and Psychosomatic Medicine, Evangelisches Krankenhaus Castrop-Rauxel, Academic Teaching Hospital of the University of Duisburg-Essen, Essen, Germany 2 Department of Neurology, Evangelisches Krankenhaus Castrop-Rauxel, Academic Teaching Hospital of the University of Duisburg-Essen, Essen, Germany Correspondence should be addressed to Udo Bonnet; udo.bonnet@uni-due.de Received 11 June 2016; Revised 5 August 2016; Accepted 9 August 2016 Academic Editor: Toshiya Inada Copyright © 2016 Udo Bonnet et al. Tis is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. We report the case study of a 57-year-old Caucasian female with steroid-responsive encephalopathy associated with autoimmune thyroiditis (SREAT), commonly termed Hashimoto encephalopathy (HE). Tis presentation includes one of the longest lasting follow-up studies of HE considering the neuropsychiatric symptoms (here delirium, mania, and EEG-slowing) and their relation to serum autoantibody levels. Antithyroid-peroxidase autoantibodies, the hallmark of autoimmune thyroiditis, were found in the serum and also in the cerebrospinal fuid. Diagnostic analyses found no evidence of limbic encephalopathies characterized by serum antibodies against intracellular, synaptic, or further cell surface antigenic targets, neoplasm, and connective tissue or vasculitis diseases. A potential contribution of bipolar disorder and metabolic encephalopathies due to severe hypothyroidism, glucocorticoid treatment, accelerated thyroid hormone replacement therapy, or vitamin B defciency is critically discussed. Another special feature of this case report is the linkage of HE to an autoimmune polyendocrine syndrome (type 3B) afecting the gastroduodenum in addition to the thyroid gland. 1. Introduction Hashimoto encephalopathy (HE) is a rare pathological con- dition with an estimated prevalence of 2/100,000 and vari- ous neuropsychiatric symptoms (NPS) combined with posi- tive serum antithyroid-peroxidase autoantibodies (TPO-Abs, usually >200 U/mL) [1, 2]. Tese antibodies are a hallmark of Hashimoto thyroiditis that occurs in 1–5% of the general population [1, 2]. Most patients with HE are euthyroid or have subclinical hypothyroidism, and 20% of them have overt hypothyroidism while hyperthyroidism is rare [1, 2]. HE’s clinical onset is usually subacute and its clinical presentation is multifaceted including neuropsychiatric symptoms (NPS), such as cognitive decline, behavioral symptoms, depression, psychosis, cerebral ischemia, seizure, myoclonus, tremors, and fuctuating levels of consciousness [1, 2]. Abnormalities in neuroimaging, electroencephalogram (EEG), and cere- brospinal fuid (CSF) are not required to diagnose HE although being present in more than 50% of the cases (usually elevated CSF protein, generalized slowing of EEG-waves, and T2-hyperintense foci on brain MR imaging) [1, 2]. HE is characterized by a remission of NPS, followed by normalization of neuroimaging and EEG afer corticosteroid (glucocorticoid) therapy (steroid-responsiveness) or, if resis- tant, escalating immunosuppression [1, 2]. However, cases with partial remission or progression even up to death were described [1]. Data regarding the course of HE are scarce and rely on clinical follow-ups which usually lasted from 6 to 24 months. A review of the 82 cases reported in literature revealed that, in this time span, most HE patients (>50%) had not relapsed while 30% had relapsed afer glucocorticoid discontinuation, 5% of whom had died [1]. Te etiology of Hindawi Publishing Corporation Case Reports in Psychiatry Volume 2016, Article ID 4168050, 7 pages http://dx.doi.org/10.1155/2016/4168050