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Related Concept Videos

Hepatic Encephalopathy01:29

Hepatic Encephalopathy

DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic shunting—including...
Encephalitis ll: Pathophysiology01:26

Encephalitis ll: Pathophysiology

Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...
Graves' Disease I: Introduction01:28

Graves' Disease I: Introduction

Graves' disease is an autoimmune disorder that causes hyperthyroidism, or overactivity of the thyroid gland. It results from autoantibodies called thyroid-stimulating immunoglobulins (TSIs), which bind to thyroid-stimulating hormone (TSH) receptors, leading to overstimulation of hormone production and a hypermetabolic state.EtiologyAlthough considered idiopathic, Graves’ disease has well-established contributing factors. There is a strong genetic component, with increased prevalence in...
Graves Disease II: Pathophysiology01:24

Graves Disease II: Pathophysiology

Graves’ disease is an autoimmune disorder characterized by the production of thyroid-stimulating immunoglobulins (TSI) that activate TSH receptors, leading to excessive synthesis and release of thyroid hormones (T3 and T4) and resulting in hyperthyroidism.Among all causes of hyperthyroidism, Graves’ disease is the most common and can happen at any age, though it is more frequent in women. It produces a hypermetabolic state with features such as weight loss, tachycardia, tremor, and heat...
Encephalitis l: Introduction01:19

Encephalitis l: Introduction

Encephalitis is inflammation of the brain parenchyma, most often due to infections or autoimmune processes. It presents with neuropsychiatric features such as fever, altered mental status, behavioral changes, cognitive dysfunction, seizures, focal deficits, and sometimes autonomic instability. In some cases, the meninges are also involved, resulting in meningoencephalitis.Infectious CausesInfectious encephalitis is most commonly viral but can also result from bacterial, fungal, or parasitic...
Hyperthyroidism II: Pathophysiology01:27

Hyperthyroidism II: Pathophysiology

Hyperthyroidism is a hypermetabolic state caused by elevated levels of thyroid hormones, triiodothyronine (T3) and thyroxine (T4). It results from dysregulation at the thyroid, pituitary, or immune system level and affects multiple organ systems.PathophysiologyThe most common cause of hyperthyroidism is Graves’ disease, an autoimmune disorder in which antibodies, specifically thyroid-stimulating antibodies (TSAb), a subtype of TSH receptor antibodies (TRAb), bind to and activate TSH receptors...

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Related Experiment Video

Updated: Jun 28, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

Hashimoto's encephalopathy.

Nicoline Schiess1, Carlos A Pardo

  • 1Department of Neurology, Division of Neuroimmunology and Neuroinfectious Disorders, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA.

Annals of the New York Academy of Sciences
|November 8, 2008
PubMed
Summary
This summary is machine-generated.

Hashimoto's encephalopathy (HE) involves neurological symptoms linked to high antithyroid antibody levels. Steroid treatment suggests immune involvement, but further research is needed to confirm the role of antibodies in HE pathogenesis.

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Preparation of Mouse Pituitary Immunogen for the Induction of Experimental Autoimmune Hypophysitis
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Last Updated: Jun 28, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

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Published on: March 17, 2023

Preparation of Mouse Pituitary Immunogen for the Induction of Experimental Autoimmune Hypophysitis
10:52

Preparation of Mouse Pituitary Immunogen for the Induction of Experimental Autoimmune Hypophysitis

Published on: December 17, 2010

Area of Science:

  • Neurology
  • Immunology
  • Endocrinology

Background:

  • Hashimoto's encephalopathy (HE) presents diverse neurological symptoms in individuals with elevated antithyroid antibodies.
  • Key features include seizures, psychiatric changes, movement disorders, and coma.
  • While associated with Hashimoto's thyroiditis, the primary immunological marker is high antithyroglobulin or anti-TPO antibody titers.

Purpose of the Study:

  • To investigate the controversial nature of Hashimoto's encephalopathy.
  • To explore the potential pathogenic role of antithyroid antibodies in HE.
  • To assess the implications of HE classification pending further immunopathological studies.

Main Methods:

  • Review of clinical manifestations and immunological features of HE.
  • Analysis of patient responses to treatments like steroids and plasmapheresis.
  • Discussion of the need for experimental and immunopathological studies.

Main Results:

  • HE is characterized by neurological dysfunction and high antithyroid antibody titers.
  • The exact relationship between antibodies and encephalopathy (causal vs. epiphenomenal) remains uncertain.
  • HE shows responsiveness to immunosuppressive therapies, suggesting immune-mediated mechanisms.

Conclusions:

  • The pathogenic role of antithyroid antibodies in HE requires further elucidation through detailed studies.
  • Therapeutic responses support an immune basis for HE.
  • Future controlled trials are essential to confirm the role of antibodies in HE's pathogenesis.