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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...
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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...
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Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre- and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
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Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
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Related Experiment Video

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A Simple Cell-based Immunofluorescence Assay to Detect Autoantibody Against the N-Methyl-D-Aspartate (NMDA) Receptor in Blood
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Late-onset anti-NMDA receptor encephalitis.

Maarten J Titulaer1, Lindsey McCracken, Iñigo Gabilondo

  • 1From the Department of Neurology (M.J.T., I.G., M.R.R., F.G., J.D.), Hospital Clinic, Universitat de Barcelona/Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Spain; Department of Neurology and Neurosciences (M.J.T., L.M., M.R.R., R.B.-G., J.D.), Perelman School of Medicine, Hospital of the University of Pennsylvania, Philadelphia; Department of Neurology (T.I.), Kitasato University School of Medicine, Sagamihara; Department of Neurology (I.K.), Brain Research Institute, Niigata University, Japan; Department of Neurology (L.B.), Hospital Universitario La Fe, Valencia; Biostatistics and Data Management Platform (A.T.), IDIBAPS, Hospital Clinic; and Institució Catalana de Recerca i Estudis Avançats (ICREA) (J.D.), Barcelona, Spain.

Neurology
|August 16, 2013
PubMed
Summary

Older adults with anti-NMDA receptor encephalitis experience delayed diagnosis and poorer outcomes compared to younger individuals. Early immunotherapy is crucial for improving recovery in this patient group.

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Area of Science:

  • Neurology
  • Immunology
  • Clinical Medicine

Background:

  • Anti-NMDA receptor (NMDAR) encephalitis is a severe autoimmune neurological disorder.
  • Clinical features and outcomes in older adults (≥45 years) are not well-characterized.

Purpose of the Study:

  • To delineate the clinical characteristics and prognosis of anti-NMDAR encephalitis in patients aged 45 and older.
  • To compare outcomes between older and younger adult patients.

Main Methods:

  • Observational cohort study.
  • Analysis of 661 patients with anti-NMDAR encephalitis, with a focus on 31 patients aged ≥45 years.
  • Comparison of demographic, clinical, treatment, and outcome data between age groups.

Main Results:

  • Older patients (≥45 years) were more frequently male and had a lower incidence of tumors (often carcinomas, not teratomas) compared to younger adults.
  • A significant delay in diagnosis (median 8 vs. 4 weeks) and treatment (median 7 vs. 4 weeks) was observed in older patients.
  • Older patients had less favorable outcomes at 2 years (60% vs. 80% with modified Rankin Scale score 0-2), though 60% achieved full or substantial recovery by 24 months.
  • Multivariable analysis identified younger age, early treatment, and absence of intensive care as predictors of good outcome.
  • Rituximab and cyclophosphamide showed efficacy in patients refractory to first-line therapies.

Conclusions:

  • Anti-NMDAR encephalitis presents differently in older adults, with delayed diagnosis and treatment contributing to poorer outcomes.
  • Tumor frequency is lower in older patients, with a different tumor type profile.
  • Prompt and aggressive immunotherapy is recommended to improve clinical outcomes in this demographic.