Encefalitis II: Pathofysiologie

The pathophysiology of infectious encephalitis begins when pathogens, such as viruses, infiltrate the CNS through the bloodstream, the olfactory bulb, the choroid plexus, or peripheral nerves.

For instance, herpes simplex virus type 1, or HSV-1, may invade the brain via the olfactory or trigeminal routes.

After crossing the blood–brain barrier, viruses infect neurons and glial cells. This disrupts their function and triggers inflammation, leading to perivascular lymphocytic infiltration, capillary congestion, and cerebral edema.

Within the brain, gray matter is often more affected than white matter because it has a higher density of neuronal receptors that viruses bind to. This regional tropism reflects viral preference for specific receptor-rich brain regions, such as HSV-1’s affinity for the inferior and medial temporal lobes.

In autoimmune encephalitis, antibodies target neuronal antigens and disrupt neural signaling.

For example, anti-NMDAR encephalitis involves an immune-mediated attack on NMDARs, causing inflammation and neurological symptoms.