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Related Concept Videos

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...
Arboviral Encephalitis01:25

Arboviral Encephalitis

Arboviral encephalitis refers to brain inflammation caused by arthropod-borne viruses, particularly those transmitted through mosquito vectors. Among these, West Nile virus (WNV), a member of the Flaviviridae family, is a significant public health concern. WNV is an enveloped, positive-sense, single-stranded RNA virus. Human infection typically begins when an infected mosquito introduces the virus into the dermis during feeding. The primary transmission cycle involves birds as amplifying hosts...
Viral Meningitis01:18

Viral Meningitis

Viral meningitis is the most common form of meningitis and is often referred to as aseptic meningitis to indicate the absence of bacterial involvement. It is generally milder than bacterial meningitis, with symptoms including fever, headache, stiff neck, drowsiness, nausea, photophobia, and vomiting. Rarely, more severe manifestations or death may occur. Common causative agents include enteroviruses, particularly coxsackie A and B viruses and echoviruses, all members of the Enterovirus genus...
Bacterial Meningitis II: Pathophysiology01:26

Bacterial Meningitis II: Pathophysiology

Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...

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Related Experiment Video

Updated: May 11, 2026

Induction and Clinical Scoring of Chronic-Relapsing Experimental Autoimmune Encephalomyelitis
26:48

Induction and Clinical Scoring of Chronic-Relapsing Experimental Autoimmune Encephalomyelitis

Published on: July 4, 2007

Rasmussen encephalitis.

Tiziana Granata1, Frederick Andermann

  • 1Department of Pediatric Neuroscience, Carlo Besta Neurological Institute, Milan, Italy.

Handbook of Clinical Neurology
|April 30, 2013
PubMed
Summary
This summary is machine-generated.

Rasmussen encephalitis (RE) is a rare inflammatory brain disease causing progressive neurological decline and severe seizures. Treatment requires personalized strategies, balancing surgery for seizure control with immunotherapy to slow disease progression.

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Area of Science:

  • Neurology
  • Immunology
  • Neuroinflammation

Background:

  • Rasmussen encephalitis (RE) is a rare, unilateral, inflammatory brain disorder.
  • Characterized by progressive neurological deficits and intractable seizures, often epilepsia partialis continua.
  • Distinctive MRI findings include unilateral atrophy and focal cortical/subcortical signal changes.

Purpose of the Study:

  • To summarize the key features, diagnostic challenges, and therapeutic approaches for Rasmussen encephalitis.
  • To highlight the need for tailored treatment strategies based on individual patient needs.

Main Methods:

  • Review of clinical, neuroimaging (MRI), and histopathological findings in Rasmussen encephalitis.
  • Analysis of treatment outcomes for antiepileptic drugs, surgery, and immunotherapy.
  • Emphasis on differential diagnosis to exclude other causes of focal encephalitis and seizures.

Main Results:

  • Histopathology reveals T-cell dominated inflammation, microglial activation, neuronal loss, and astrogliosis.
  • Surgical hemispherectomy offers high seizure freedom but causes permanent deficits.
  • Immunotherapy can slow disease progression but has limited impact on seizure burden.

Conclusions:

  • Diagnosis of RE is challenging, especially early on, requiring exclusion of other conditions.
  • Treatment must be individualized, considering the trade-offs between seizure control and neurological deficits.
  • A multidisciplinary approach is crucial for managing this complex neuroinflammatory disease.