An Overview of Hashimoto’s Encephalopathy


TH [email protected] 1 , * , FJ Muzaffar 2 , RK Ghaddar 3

1 687 Pine Avenue West, Room M9.05, Montreal, Quebec, H3A 1A1, Canada

2 Pathology Department, Mcmaster University, Hamilton, Ontario, Canada

3 Department of Internal Medicine, Al-Amiri Hospital, Kuwait,

How to Cite: [email protected] T, Muzaffar F, Ghaddar R. An Overview of Hashimoto’s Encephalopathy, Iran Red Crescent Med J. 2009 ; 11(2):e95877.


Iranian Red Crescent Medical Journal: 11 (2); e95877
Published Online: April 30, 2009
Article Type: Letter
Received: July 01, 2019
Accepted: April 30, 2009



Hashimoto's encephalopathy is a rare complication of autoimmune thyroid disease with an estimated prevalence of 2.1/100,000.1 It is also known as steroid responsive encephalopathy associated with autoimmune thyroiditis, SREAT.2 The pathogenesis is still unknown, but the possible mechanism could be due to cerebral vasculitis with or without immune complex deposition.3 It is an inflammatory condition proposed by the presence of elevated TPO,4 elevated CSF protein,4 histological feature of vasculitis of venules, and lymphocytic perivascular cuff.1

Patients may present with encephalopathy (100%) which usually develop over 1 to 7 days, tremor (84%), transient aphasia (73%), seizure (66%), gait ataxia (63%), hypersomnolence (63%), myoclonus (38%), neuropsychiatric symptoms (36%), and stroke-like symptoms (27%).1,5 Variable thyroid function tests could be seen in patients with Hashimoto’s encephalopathy despite similar neurological findings. Goiter was found in 63% of the reported cases, subclinical hypothyroidism in 35%, normal thyroid function in 30%, overt hypothyroidism in 20%, and hyperthyroidism in 7% of cases.1,6 Lab tests in patients with Hashimoto’s encephalopathy usually show elevated TPO antibodies (100% of reported cases) and  elevated thyroglobulin antibodies in 73% of the reported cases.1,7Upon CSF examination, 78% of the reported cases had elevated protein, and normal leukocyte count in 76% of cases.1,7 The minority of patients, about 15%, had elevated ESR and CRP. Most of the patients (about 98%) with Hashimoto’s encephalopathy had abnormal EEG.7 EEG abnormalities could be generalized slowing, focal slowing, prominent triphasic waves, epileptiform abnormalities, and frontal intermittent rhythmic delta activity.50% of the patients with Hashimoto’s encephalopathy had abnormal imaging in CT and MRI, in the form of cerebral atrophy, abnormalities in the white matter and diffused subcortical or focal cortical abnormalities.7,8 Single photon emission computed tomography (SPECT) showed focal hypoperfusion in 73% of cases, global hypoperfusion in 9%, and 18% of cases had normal SPECT. Treatment options include steroids.6 Steroids could be given as oral prednisone (50-100 mg/day), or intravenous methylprednisolone (1 g/day). Thyroid hormone replacement therapy with steroid was administered for patients presenting with hypothyroidism and Hashimoto’s encephalopathy, and there was 92% improvement of reported cases using this combination therapy, and 67% improvement in patients taking levothyroxine alone. There has been only one case having been reported to recover from Hashimoto’s encephalopathy after thyroidectomy.8

Hashimot’s encephalopathy is a rare complication of autoimmune thyroid disease, which is most of the time underdiagnosed. The pathogenesis is still unknown. Steroid is considered the mainstay of treatment.

© 2009, Author(s). This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License ( which permits copy and redistribute the material just in noncommercial usages, provided the original work is properly cited.



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