Hashimoto's encephalopathy mimicking a brain tumor and its pathological findings: A case report

Uwatoko, Hisashi; Yabe, Ichiro; Sato, Sunao; Abe, Masataka; Shirai, Shinichi; Takahashi, Ikuko; Matsushima, Masaaki; Kano, Takahiro; Yamaguchi, Shigeru; Hatanaka, Kanako C.; Yoneda, Makoto; Sasaki, Hidenao

doi:10.1016/j.jns.2018.09.008

Cited by 9 publications

(3 citation statements)

References 10 publications

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“…noted that hyperperfusion was clearly detected in the right hippocampus on continuous arterial spin labeling imaging at the incipient stage . A few patients showed nodular lesions and a tumor‐like lesion …”

Section: Neuroimagingmentioning

confidence: 96%

Hashimoto encephalopathy

Matsunaga

Ikawa

Yoneda

2019

Clinical & Exp Neuroim

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Hashimoto encephalopathy (HE) is an autoimmune encephalopathy associated with autoimmune chronic thyroiditis. The clinical entity and nosology of HE have long been debated. Recently, new autoantibodies associated with autoimmune encephalitis have been discovered. With accumulated reported cases, and our discovery of serum autoantibody against NH2‐terminal of alpha‐enolase as a specific diagnostic marker, HE has been recognized as a distinct clinical entity. The condition appears dominant in females. The clinical features of HE are characterized by various neuropsychiatric symptoms, such as altered consciousness, psychosis and seizures, the presence of serum anti‐thyroid antibodies, normal or non‐specific changes in brain magnetic resonance imaging, diffuse slow wave activities in electroencephalogram and responsiveness to immunotherapy. A few pathological studies showed a lymphocytic infiltration of the small and medium‐sized vessels of the brain, which suggested vasculitis. Non‐specific neurological symptoms, laboratory findings and neuroimaging of HE make its diagnosis an oversight and difficult, whereas antibodies against NH2‐terminal of alpha‐enolase can be useful as a diagnostic biomarker for HE. In this review, we describe the current state of knowledge about HE and discuss progress in the diagnosis of HE.

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Section: Neuroimagingmentioning

confidence: 96%

Hashimoto encephalopathy

Matsunaga

Ikawa

Yoneda

2019

Clinical & Exp Neuroim

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“…In subsequent years, postmortem examination in HE patients demonstrated “ mild perivascular lymphocytic infiltration throughout the brain and leptomeninges plus diffuse gliosis of gray matter in the cortex, basal ganglia, thalami, hippocampi, and, to a lesser extent, the parenchymal white matter ” [16] . Biopsy of other HE patients revealed: [i] “ patchy myelin pallor, scant perivascular chronic inflammation, mild gliosis, and microglial activation ” [17] ; [ii] primary vasculitis of the CNS [18] ; [iii]“ diffuse gliosis and perivascular lymphocyte infiltration with CD3 + T-cell predominance, … with no signs of a brain tumor ” in a patient with a tumor-like lesion of the left caudate nucleus, “ suggesting cerebral vasculitis as an underlying etiology ” [19] ; [iv] non-vasculitic autoimmune inflammatory meningoencephalitis [20] ; [v] reactive gliosis, angiogenesis, swollen vascular endothelial cells, mild lymphocyte infiltration (almost exclusively T cells) around small vessels [21] .…”

Section: Introductionmentioning

confidence: 99%

Amino acid sequence homology between thyroid autoantigens and central nervous system proteins: Implications for the steroid-responsive encephalopathy associated with autoimmune thyroiditis

Benvenga

Antonelli

Fallahi

et al. 2021

Journal of Clinical & Translational Endocrinology

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“…1 After Brain et al’s initial publication of HE in 1966, 2 SREAT has been reported to cause seizures, 3 epilepsia partialis continua (EPC), 3–5 status epilepticus, tremor, 3 myoclonus, 3 stroke-like episode, 3 dementia, stupor/coma, psychosis, 6 headache, ataxia, and myelopathy. 7 SREAT image findings include normal appearance, tumor-like lesions, 5,8 and focal or diffuse pathology. 3,4…”

Section: Introductionmentioning

confidence: 99%

SREAT presenting as decades of intractable seizures and isolated delusional episodes with clinical, laboratory, and EEG confirmation of treatment response

Tjong

Gardner

Peng

2019

SAGE Open Medical Case Reports

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We report a case of a 60-year-old woman with a history of intractable seizures and isolated delusional psychosis who was later diagnosed with steroid-responsive encephalopathy associated with autoimmune thyroiditis. The patient underwent right temporal lobectomy (epilepsy surgery) 15 years before coming to this clinic, but continued to have focal seizures, resulting in frequent emergency room visits thereafter. After admission for intensive inpatient video electroencephalogram monitoring and subsequent 7 months of close follow-up, both the electroencephalogram abnormalities and isolated delusional psychosis were found to be responsive to immunotherapy. This suggests that her epilepsy may be autoimmune in nature. Steroid-responsive encephalopathy associated with autoimmune thyroiditis was diagnosed after 26 years since the onset of seizures. Performing invasive epilepsy surgery in patients with autoimmune epilepsy cannot reverse the inflammatory process; therefore, it is reasonable to test for autoimmune etiologies before excision surgery on patients with medically intractable epilepsy. This case demonstrates the clinical use of quantitative electroencephalogram in assisting with the diagnosis of steroid-responsive encephalopathy associated with autoimmune thyroiditis and supports that it is a spectrum disorder with protean manifestations.

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Hashimoto's encephalopathy mimicking a brain tumor and its pathological findings: A case report

Cited by 9 publications

References 10 publications

Hashimoto encephalopathy

Hashimoto encephalopathy

Amino acid sequence homology between thyroid autoantigens and central nervous system proteins: Implications for the steroid-responsive encephalopathy associated with autoimmune thyroiditis

SREAT presenting as decades of intractable seizures and isolated delusional episodes with clinical, laboratory, and EEG confirmation of treatment response

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