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Encephalitis ll: Pathophysiology

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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Related Experiment Video

Updated: Jun 13, 2026

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

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

Published on: March 26, 2019

Optic neuritis: A mechanistic view.

Erik V Burton¹, Benjamin M Greenberg, Elliot M Frohman

¹Department of Neurology, University of Texas Southwestern Medical Center at Dallas, United States.

Pathophysiology : the Official Journal of the International Society for Pathophysiology

|May 18, 2010

Summary

This summary is machine-generated.

Acute demyelinating optic neuritis involves optic nerve inflammation and damage, often linked to multiple sclerosis. Advanced imaging and biomarkers aid in understanding neurodegeneration and developing new treatment strategies.

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Bioluminescence and Near-infrared Imaging of Optic Neuritis and Brain Inflammation in the EAE Model of Multiple Sclerosis in Mice

Bioluminescence and Near-infrared Imaging of Optic Neuritis and Brain Inflammation in the EAE Model of Multiple Sclerosis in Mice

Published on: March 1, 2017

Area of Science:

Neuroscience
Ophthalmology

Background:

Acute demyelinating optic neuritis affects the optic nerves, causing inflammation, demyelination, and neurodegeneration.
Optic neuritis is a frequent demyelinating condition closely associated with multiple sclerosis (MS).

Purpose of the Study:

To explore the pathological and pathophysiological mechanisms of optic neuritis and MS.
To investigate novel strategies for neuroprotection and neurorestoration in optic neuritis.

Main Methods:

Utilized clinical assessments.
Employed radiographic and retinal imaging techniques.
Applied electrophysiologic methods.

Main Results:

Gained significant insights into the mechanisms of optic neuritis and MS.
Identified validated biomarkers in the anterior visual system.

Conclusions:

Biomarkers facilitate research into axonal loss and neurodegeneration.
Future research can focus on neuroprotection and neurorestoration strategies for optic neuritis.