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Related Concept Videos

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...
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...
Hyperthyroidism I: Introduction01:25

Hyperthyroidism I: Introduction

Hyperthyroidism is a type of thyrotoxicosis characterized by the thyroid gland's overproduction of the thyroid hormones triiodothyronine (T3) and thyroxine (T4). This hormone excess increases the basal metabolic rate and enhances sensitivity to catecholamines.DiagnosisDiagnosis is based on clinical features and biochemical testing. It typically shows suppressed thyroid-stimulating hormone (TSH) levels below 0.4 mIU/L, with elevated free T3 and/or T4. Additional tests, including thyroid...
Goiter01:27

Goiter

Goiter refers to an abnormal enlargement of the thyroid gland that may appear as a diffuse goiter (uniform enlargement) or nodular (single or multiple nodules). Functionally, it is classified as nontoxic (normal/low hormone levels) or toxic (excess hormone production).PathophysiologyDiffuse thyroid enlargement typically results from prolonged stimulation by thyroid-stimulating hormone (TSH) or TSH-like agents, commonly seen in hypothyroidism or iodine deficiency. In contrast, in hyperthyroid...

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Related Experiment Video

Updated: Jul 2, 2026

Imaging CD19+ B Cells in an Experimental Autoimmune Encephalomyelitis Mouse Model using Positron Emission Tomography
09:41

Imaging CD19+ B Cells in an Experimental Autoimmune Encephalomyelitis Mouse Model using Positron Emission Tomography

Published on: January 20, 2023

Steroid-responsive encephalopathy associated with autoimmune thyroiditis presenting with diffusion MR imaging

C Grommes1, C Griffin, K A Downes

  • 1Department of Neurology, University Hospitals Case Medical Center, Cleveland, OH 44106, USA.

AJNR. American Journal of Neuroradiology
|August 15, 2008
PubMed
Summary

Steroid-responsive encephalopathy associated with autoimmune thyroiditis (SREAT) can show MR imaging abnormalities. This case highlights diffusion-weighted imaging changes in SREAT, improving with steroids and plasmapheresis, supporting inflammatory causes.

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Diffusion Tensor Magnetic Resonance Imaging in the Analysis of Neurodegenerative Diseases
09:33

Diffusion Tensor Magnetic Resonance Imaging in the Analysis of Neurodegenerative Diseases

Published on: July 28, 2013

Related Experiment Videos

Last Updated: Jul 2, 2026

Imaging CD19+ B Cells in an Experimental Autoimmune Encephalomyelitis Mouse Model using Positron Emission Tomography
09:41

Imaging CD19+ B Cells in an Experimental Autoimmune Encephalomyelitis Mouse Model using Positron Emission Tomography

Published on: January 20, 2023

Diffusion Tensor Magnetic Resonance Imaging in the Analysis of Neurodegenerative Diseases
09:33

Diffusion Tensor Magnetic Resonance Imaging in the Analysis of Neurodegenerative Diseases

Published on: July 28, 2013

Area of Science:

  • Neurology
  • Immunology
  • Radiology

Background:

  • Steroid-responsive encephalopathy associated with autoimmune thyroiditis (SREAT) is an inflammatory neurological condition.
  • It is characterized by encephalopathy and often associated with autoimmune thyroid disease.

Observation:

  • A patient with SREAT presented with specific changes on diffusion-weighted magnetic resonance (MR) imaging.
  • These MR imaging findings were observed during a subacute exacerbation of the condition.

Findings:

  • The patient's diffusion-weighted MR imaging abnormalities showed improvement following treatment.
  • Treatment included corticosteroid therapy and plasmapheresis.
  • These clinical and imaging outcomes support the hypothesis of inflammatory processes in SREAT exacerbations.

Implications:

  • Diffusion-weighted MR imaging may be a valuable tool for diagnosing and monitoring SREAT.
  • The findings reinforce the role of inflammatory mechanisms in the pathophysiology of SREAT.
  • Aggressive immunomodulatory treatments like plasmapheresis may be beneficial in managing SREAT exacerbations.