Anti-neuronal autoantibody in Hashimoto's encephalopathy: neuropathological, immunohistochemical, and biochemical analysis of two patients

Oide, Takashi; Tokuda, Takahiko; Yazaki, Masahide; Watarai, Megumi; Mitsuhashi, Shigeaki; Kaneko, Kazuma; Hashimoto, Takao; Ohara, Shuichi; Ikeda, Shu‐ichi

doi:10.1016/j.jns.2003.08.005

Cited by 93 publications

(63 citation statements)

References 27 publications

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“…4 Another study identified antineuronal antibodies in the serum of a patient with HE that reacted with human brain tissue, but none from a control nor a patient with Hashimoto thyroiditis without encephalopathy. 5 Therefore, the presence of antithyroid antibodies should be viewed as a diagnostic marker rather than the etiologic agent.…”

Section: Viral Encephalitismentioning

confidence: 99%

Pearls & Oy-sters: Hashimoto encephalopathy

Afshari¹,

Afshari²,

Schuele³

2012

Neurology

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PEARLS• A diagnosis of Hashimoto encephalopathy (HE) should be considered when a combination of encephalopathy and elevated antithyroid antibody levels are seen in a patient in whom other more common infectious, metabolic, and toxic causes of encephalopathy have been thoroughly excluded. Diagnosis should prompt early corticosteroid therapy, which leads to favorable outcomes in the majority of cases.• The presentation of HE is highly variable with fulminant, acute, subacute, and even chronic patterns of altered mental status across pediatric, adult, and elderly patient populations. Commonly reported clinical manifestations of HE include stroke-like symptoms, dementia, focal or generalized seizures, status epilepticus, myoclonus, tremor, and neuropsychiatric symptoms. OY-STERS• HE should not be confused with myxedema coma and the neurologic complications associated with Hashimoto thyroiditis, although the name suggests a connection. There is no conclusive evidence that HE represents a state of dysthyroidism. However, the majority of evidence today and patients' clinical response to corticosteroids does suggest that the underlying pathogenesis of HE is autoimmune.• The clinical picture of a relapsing and remitting encephalopathy characterized by stroke-like episodes, seizures, myoclonus, tremor, and neuropsychiatric disturbances particularly in a young female patient should warrant investigation into HE. An encephalopathic EEG with normal neuroimaging and nonspecific inflammatory CSF findings supports the diagnosis, and detection of antithyroid antibodies confirms the diagnosis.• Early diagnosis of HE and prompt institution of corticosteroid therapy can often lead to seizure control where antiepileptic drug therapy is ineffective.CASE REPORT A 30-year-old previously healthy, right-handed woman was admitted to an outside hospital for new-onset seizures preceded by a flu-like prodrome for a week. After admission, she was noted to have frequent events consisting of a sudden blank stare with associated hand fumbling, lip smacking, and postictal confusion and amnesia. She experienced occasional tonic-clonic seizures, preceded by these staring events with head version to the left or right side. An estimated 100 seizures occurred during her first 4 days of admission. She was placed on video EEG monitoring which demonstrated bitemporal electrographic seizure onset. Apart from persistent disorientation and lethargy, her general and neurologic examination including vital signs were normal. Initial workup showed normal blood counts, electrolytes, and liver and renal function panels, and negative urine toxicology. Mild hypothyroidism with a serum thyroid-stimulating hormone of 7.25 mIU/mL (normal range 0.350 -5.500 mIU/mL) but normal free thyroxine fT 4 (1.0; normal range 0.9 -1.8 ng/dL) was noted. Basic CSF analysis on the first day of admission showed 3-4 white blood cells (WBCs) with normal pressure, glucose, and protein, and without erythrocytes or other atypical cells. A repeat analysis on day 4 was normal except for a ly...

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Section: Viral Encephalitismentioning

confidence: 99%

Pearls & Oy-sters: Hashimoto encephalopathy

Afshari¹,

Afshari²,

Schuele³

2012

Neurology

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“…These antibodies, however, are not believed to be pathogenic. The exact mechanism of disease is unknown, but is speculated to by either vasculitis or direct neuronal/glial recognition by autoantibodies (but not anti-thyroperoxidase or ant-thyroglobulin antibodies) [254,255]. The CSF may show a slight pleocytosis and mild-moderate elevation of protein.…”

Section: Steroid Responsive Encephalopathy Associated With Autoimmunementioning

confidence: 99%

Immune Mediated Diseases and Immune Modulation in the Neurocritical Care Unit

Geldern¹,

McPharlin

Becker

2012

Neurotherapeutics

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This chapter will review the spectrum of immunemediated diseases that affect the nervous system and may result in an admission to the neurological intensive care unit. Immunomodulatory strategies to treat acute exacerbations of neurological diseases caused by aberrant immune responses are discussed, but strategies for long-term immunosuppression are not presented. The recommendations for therapeutic intervention are based on a synthesis of the literature, and include recommendations by the Cochrane Collaborative, the American Academy of Neurology, and other key organizations. References from recent publications are provided for the disorders and therapies in which randomized clinical trials and large evidenced-based reviews do not exist. The chapter concludes with a brief review of the mechanisms of action, dosing, and side effects of commonly used immunosuppressive strategies in the neurocritical care unit.

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“…10 Again, as with the other auto antibodies that have been detected in patients with this condition, it is not yet known whether they are the cause of the disease or whether they merely coexist with the autoantibodies that are directly involved in the disease's pathogenesis. The roles of these newly discovered autoantibodies, as well as those of the previously described antithyroid antibodies, require further clarification.…”

Section: Practicementioning

confidence: 99%