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Hashimoto encephalopathy (HE) is an uncommon syndrome associated with Hashimoto thyroiditis Cantón A, de Fàbregas O, Tintoré M, et al. Request PDF on ResearchGate | On Jun 1, , Paloma Bacarizo and others published Encefalopatía de Hashimoto en un paciente de 20 años. CLINICAL/SCIENTIFIC NOTE. Hashimoto’s encephalopathy. Encefalite de Hashimoto. Renata Telles Rudge de AquinoI; Eduardo Genaro MutarelliII.

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Her mother, 2 sisters and a daughter have Hashitmoto’s thyroiditis, one sister also has vitiligo. There was a reduction in anti-TPO which co-related with the clinical picture. The mechanism of pathogenesis is not known but it has been hypothesized to be an autoimmune disorder, similar to Hashimoto’s thyroiditis as its name suggests.

Encefalopatia de Hashimoto | SPEDM Journal

J Clin Endocrinol Metab ; D ICD – HE occur predominantly in women 4: J Neurol Sci ; Little is known about the pathogenesis. The majority of patients return to their normal neurological state.

The thyroid-stimulating hormone TSH was slightly elevated at 7. The patients met the clinical criteria for Creutzfeldt-Jakob disease and were notified 8.

Consistent with this hypothesis, autoantibodies to alpha-enolase have been found to be associated with Hashimoto’s encephalopathy. Thyroid hormone treatment is also encefalo;atia if required. Between and 43 cases were published.

Hypothyroidism, hormonal factors and cerebral hypoperfusion could contribute for pathogenesis 2. The criteria established by World Health Organization WHO for diagnosing to sporadic Creutzfeldt-Jakob disease sCJD include progressive dementia with a duration encefalppatia less than two years and two of the clinical findings – myoclonus, cerebellar or visual symptoms, pyramidal or extrapyramidal signs and akinetic mutism.

Encephalomyelitis Acute disseminated Myalgic Meningoencephalitis. Clinically, the condition may present one or more symptoms. Besides behavioral problems and cognitive decline, there may be fluctuating symptoms, tremor, transitory aphasia, myoclonus, ataxia, convulsions, sleep abnormalities, encefaloptaia or sensory deficits and psychosis.


Hashimoto’s encephalopathy is a rare condition associated with Hashimoto thyroiditis, the presence of high concentrations of anti-thyroid antibodies, without any evidence of thyroid dysfunction, and an excellent response to treatment with corticosteroids 2. Some symptoms may persist, such as tremors and loss of memory. The responsiveness of HE to steroids or other therapies such as plasmapheresis supports the hypothesis that this is a disorder that involves immune pathogenic mechanisms.

It is probably under diagnosed as it is not well known 5. Migraine Encefallopatia hemiplegic Cluster Tension. All the contents of this journal, except where otherwise noted, is licensed under a Creative Commons Attribution License. Hashimoto’s encephalopathy HE is a controversial neurological disorder that comprises a heterogenous group of neurological symptoms that manifest in patients with high titers of antithyroid antibodies.

CNS involvement is rare in this context, HE being the most common example.

Hashimoto’s encephalopathy

SPECT can hashimooto normal but usually shows focal hypoperfusion 8. Two clinical forms have been described: J Neuropsychiatry Clin Neurosci ; Alopecia is associated with polyglandular autoimmunity.

Hashimoto’s encephalitis HEencephalitis which responds to steroids and is associated with auto-immune thyroiditis, was described by Brain et al. It is recommended to reduce the dose of steroids over several months.

The magnetic resonance imaging MRI of the brain showed small changes that were not significant, such as the presence of hypersignal focus in the corona radiata and bilaterally semioval center Fig 1.

Hashimoto’s encephalopathy

Prominent triphasic waves, focal slowing, epileptiform abnormalities, photoparoxysmal and photomyogenic responses may be seen. The significance of classifying encephalopathies under the term HE will be determined in the hshimoto once the relevance of the role of antithyroid antibodies is demonstrated or dismissed by more detailed experimental and immunopathological studies. She had a history of hypothyroidism and did not use any medication.

Since that time, research has expanded and numerous cases are being reported by scientists around the world, suggesting that this rare condition is likely to have been significantly undiagnosed in the past.


Archived from the original on To minimize the side effects of steroid therapy, in the second month the dose was reduced and azathioprine added, but due to hepato-toxicity this was suspended.

This case is consistent with the literature with the presence of behavioral changes, tremors, myoclonus and ataxia. She had a 6 month history of behavioral changes and agitation, resulting in psychiatric treatment of estazolan 2 mg, bupropion mg, carbamazepine mg and duoxetine 30 mg daily.

A female patient, years-old, Caucasian, widow, born hashimotp Rio de Janeiro, developed a clinical presentation of daily sadness, discouragement, decreased appetite, insomnia, and cognitive decline. It was first described in Since then, about cases have been described It is a diagnosis of exclusion in a clinical picture of encephalitis with negative investigations 2,4,7,9. Onset is often gradual and may go unnoticed by the patient and close associates to the patients.

The condition of the patient worsened with persecutory delusions, visual hallucinations, gait disturbance, tremor of the extremities, muscle spasms, and fluctuations in the level of consciousness. The dose of hazhimoto was gradually reduced. All the contents of this journal, except where otherwise noted, is licensed under a Creative Commons Attribution License.

How to cite this article. The recognition of the condition was essential for the treatment and regression of the clinical presentation. This report emphasizes the importance of a differential diagnosis between the two pathologies.

It is associated with Hashimoto’s thyroiditis. We believe that this pathology is misdiagnosed, therefore, tests detecting the presence of anti-thyroid antibodies are recommended in a clinical presentation of encephalopathy of subacute onset or rapidly progressive dementia associated with myoclonus and triphasic complexes in the EEG, when the ethiology is not identified.