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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...
Neural Regulation01:37

Neural Regulation

Digestion begins with a cephalic phase that prepares the digestive system to receive food. When our brain processes visual or olfactory information about food, it triggers impulses in the cranial nerves innervating the salivary glands and stomach to prepare for food.
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...
Multiple Sclerosis l: Introduction01:19

Multiple Sclerosis l: Introduction

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Nephrotic Syndrome II : Assessment and Medical Management01:26

Nephrotic Syndrome II : Assessment and Medical Management

IntroductionNephrotic syndrome is a kidney disorder marked by excessive protein loss in the urine, leading to various systemic complications. This condition often results from damage to the glomeruli—the kidney's filtering units—causing proteinuria, low blood protein levels, and fluid retention. Understanding the assessment, diagnosis, and management of nephrotic syndrome is essential for effective treatment and prevention of further kidney damage.AssessmentPatient History: Document any history...
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Related Experiment Video

Updated: Jul 19, 2026

Visualizing Impairment of the Endothelial and Glial Barriers of the Neurovascular Unit during Experimental Autoimmune Encephalomyelitis In Vivo
10:50

Visualizing Impairment of the Endothelial and Glial Barriers of the Neurovascular Unit during Experimental Autoimmune Encephalomyelitis In Vivo

Published on: March 26, 2019

[Neuropsychiatric lupus erythematosus].

M Vadacca1, F Buzzulini, A Rigon

  • 1Dipartimento di Medicina Clinica, Immunologia, Reumatologia, Università Campus Bio-Medico, Roma, Italia.

Reumatismo
|October 3, 2006
PubMed
Summary

Diagnosing neuropsychiatric systemic lupus erythematosus (NPSLE) is challenging due to varied symptoms and prevalence. Early identification of brain involvement is crucial for effective treatment and avoiding complications.

Related Experiment Videos

Last Updated: Jul 19, 2026

Visualizing Impairment of the Endothelial and Glial Barriers of the Neurovascular Unit during Experimental Autoimmune Encephalomyelitis In Vivo
10:50

Visualizing Impairment of the Endothelial and Glial Barriers of the Neurovascular Unit during Experimental Autoimmune Encephalomyelitis In Vivo

Published on: March 26, 2019

Area of Science:

  • Rheumatology
  • Neurology
  • Immunology

Background:

  • Neuropsychiatric involvement (NPSLE) in Systemic Lupus Erythematosus (SLE) presents diagnostic challenges.
  • NPSLE has a wide prevalence (14-80%) and diverse manifestations, from seizures to cognitive dysfunction.
  • Pathogenic mechanisms include antibodies, vasculitis, thrombosis, and cytokine-mediated damage.

Purpose of the Study:

  • To highlight the complexity in diagnosing NPSLE.
  • To emphasize the need for integrated diagnostic approaches.
  • To underscore the importance of early detection for patient outcomes.

Main Methods:

  • Review of diagnostic challenges and pathogenic mechanisms in NPSLE.
  • Discussion of current diagnostic tools, including immunoserology and neuroimaging.
  • Analysis of therapeutic strategies for CNS lupus.

Main Results:

  • NPSLE diagnosis is complex due to variable prevalence and broad spectrum of manifestations.
  • Morphological neuroimaging often shows minimal, non-specific changes.
  • No single diagnostic tool exists; a combination of tests is required.

Conclusions:

  • Accurate NPSLE diagnosis requires integrating immunoserological tests, functional/anatomical neuroimaging, and standardized criteria.
  • Current management involves symptomatic, immunosuppressive, and anticoagulant therapies tailored to individual needs.
  • Advancements in neuroimaging and understanding disease mechanisms are anticipated to improve early detection and treatment, preventing severe complications.