Anti-NMDA receptor encephalitis pathophysiology

Anti-NMDA receptor encephalitis Microchapters
Home
Patient Information
Overview
Historical Perspective
Classification
Pathophysiology
Causes
Differentiating Anti-NMDA receptor encephalitis from Other Diseases
Epidemiology and Demographics
Risk Factors
Natural History, Complications, and Prognosis
Diagnosis
History and Symptoms
Physical Examination
Laboratory Findings
Electrocardiogram
Chest X Ray
CT
MRI
Echocardiography or Ultrasound
Other Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Surgery
Primary Prevention
Secondary Prevention
Cost-Effectiveness of Therapy
Future or Investigational Therapies
Case Studies
Case #1
Anti-NMDA receptor encephalitis pathophysiology On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
American Roentgen Ray Society Images of Anti-NMDA receptor encephalitis pathophysiology All Images X-rays Echo & Ultrasound CT Images MRI
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA on Anti-NMDA receptor encephalitis pathophysiology
CDC on Anti-NMDA receptor encephalitis pathophysiology
Anti-NMDA receptor encephalitis pathophysiology in the news
Blogs on Anti-NMDA receptor encephalitis pathophysiology
Directions to Hospitals Treating Anti-NMDA receptor encephalitis
Risk calculators and risk factors for Anti-NMDA receptor encephalitis pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; AE Dheeraj Makkar, M.D.[2]

Pathophysiology

Approximately sixty percent of individuals have tumors that contain nerve tissue. Majority of women have ovarian teratoma, while men have tumors like (testicular teratoma and small-cell lung carcinoma).

Anti-NMDA receptor encephalitis is predominantly caused by autoantibodies directed against the GluN1 component of the receptor.

In the acute phase of brain diseases, B cells, plasma cells, CD4 T cells, and, less frequently, CD8 T cells have been detected.

Crossing the blood-brain barrier enables systemically produced antibodies to crosslink NMDA receptors. This leads to their internalization and a severe disruption of synaptic plasticity and NMDA receptor network function.

• A model for the condition proposes that a decrease in NMDARs in inhibitory GABA neurons and glutamate synapses results in numerous effects, including dysregulation of glutamate release, elevated glutamate levels and excitatory circuits.

The clinical syndrome disinhibits the frontostriatal network, resulting in psychotic, catatonic, stiffness, dystonia, and mutistic symptoms. The brainstem central-pattern generator is disinhibited, resulting in complicated movement problems, and the brainstem respiratory network is also disinhibited, leading to respiratory dysfunction. NMDAR Dysregulation Proposed Symptoms Agonist effect on NMDARs Seizures Synaptic NMDAR hypofunction Amnesia, psychosis, hypoventilation Extrasynaptic NMDAR hyperfunction Catatonia, dyskinesias, seizures Neuronal network imbalance with impaired intraneuronal activity

NMDAR Dysregulation	Proposed Symptoms
Agonist effect on NMDARs	Seizures
Synaptic NMDAR hypofunction	Amnesia, psychosis, hypoventilation
Extrasynaptic NMDAR hyperfunction	Catatonia, dyskinesias, seizures
Neuronal network imbalance with impaired intraneuronal activity	Seizures