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Related Concept Videos

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...
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...
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...
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...
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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Hippocampal Neuronal Cultures to Detect and Study New Pathogenic Antibodies Involved in Autoimmune Encephalitis
08:20

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Limbic encephalitis associated with elevated antithyroid antibodies.

Yael Hacohen1, Sonia Joseph2, Rachel Kneen3

  • 1Children's Neurosciences Center, Evelina Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, King's Health Partners Academic Health Sciences Centre, London, UK Nuffield Department of Clinical Neurosciences, West Wing, John Radcliffe Hospital, University of Oxford, Oxford, UK.

Journal of Child Neurology
|March 23, 2013
PubMed
Summary
This summary is machine-generated.

Children with limbic encephalitis and elevated thyroid antibodies often require aggressive immunotherapy beyond corticosteroids. This study highlights a need for tailored treatment approaches for this specific patient group.

Keywords:
Hashimotoautoantibodiesencephalitisencephalopathyepilepsylimbic system

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Area of Science:

  • Neurology
  • Immunology
  • Pediatrics

Background:

  • Immune-mediated limbic encephalitis (IML) affects adults and children, presenting with seizures and memory deficits.
  • Commonly associated with antibodies to leucine-rich glioma-inactivated 1 (LGI1).
  • Elevated antithyroid antibodies are linked to encephalopathy, termed Hashimoto encephalopathy, often responsive to corticosteroids.

Observation:

  • This study details three pediatric cases of limbic encephalitis with elevated thyroid antibodies.
  • These patients did not respond to corticosteroid treatment alone.

Findings:

  • The children required more aggressive immunotherapy for treatment.
  • Treatment response was slower, similar to other immune-mediated limbic encephalitis forms.

Implications:

  • Suggests a subset of limbic encephalitis with thyroid antibodies may need intensified immunotherapy.
  • Highlights the importance of considering varied treatment strategies beyond corticosteroids for pediatric IML.
  • Further research into the specific mechanisms and optimal treatments for this presentation is warranted.