Anti-NMDA receptor encephalitis pathophysiology: Difference between revisions
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{{Anti-NMDA receptor encephalitis}} | {{Anti-NMDA receptor encephalitis}} | ||
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==Overview== | ==Overview== | ||
Revision as of 22:08, 20 December 2022
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Anti-NMDA receptor encephalitis Microchapters |
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Differentiating Anti-NMDA receptor encephalitis from Other Diseases |
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Diagnosis |
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Treatment |
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Anti-NMDA receptor encephalitis pathophysiology On the Web |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; AE Dheeraj Makkar, M.D.[2]
Overview
Pathophysiology
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.