BackgroundThe encephalopathy associated with autoimmune thyroid disease (EAATD) is characterized by neurological/psychiatric symptoms, high levels of anti-thyroid antibodies, increased cerebrospinal fluid protein concentration, non-specific electroencephalogram abnormalities, and responsiveness to the corticosteroid treatment in patients with an autoimmune thyroid disease. Almost all EAATD patients are affected by Hashimoto's thyroiditis (HT), although fourteen EAATD patients with Graves' disease (GD) have been also reported.MethodsWe have recorded and analyzed the clinical, biological, radiological, and electrophysiological findings and the data on the therapeutic management of all GD patients with EAATD reported so far as well as the clinical outcomes in those followed-up in the long term.ResultsTwelve of the fourteen patients with EAATD and GD were women. The majority of GD patients with EAATD presented with mild hyperthyroidism at EAATD onset or shortly before it. Active anti-thyroid autoimmunity was detected in all cases. Most of the patients dramatically responded to corticosteroids. The long term clinical outcome was benign but EAATD can relapse, especially at the time of corticosteroid dose tapering or withdrawal. GD and HT patients with EAATD present with a similar clinical, biological, radiological, and electrophysiological picture and require an unaffected EAATD management.ConclusionsGD and HT equally represent the possible background condition for the development of EAATD, which should be considered in the differential diagnosis of all patients with encephalopathy of unknown origin and an autoimmune thyroid disease, regardless of the nature of the underlying autoimmune thyroid disease.

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[123I]N,N,N'-trimethyl-N'-(2 hydroxy-3-methyl-5-123I-iodobenzyl)- 1,3-propane-diamine 2HCl single-photon-emission computed tomography (HIPDM-SPECT) brain imaging in one patient with periodic lateralized epileptiform discharges (PLEDs) on the EEG demonstrated increased regional cerebral perfusion in the PLEDs focus suggesting that PLEDs are the manifestation of abnormally enhanced neuronal activities. This may explain the frequent association of mental confusion, focal neurologic signs, and occurrence of seizures in association with PLEDs.