What is the pathophysiology of encephalitis?

Updated: Aug 07, 2018
  • Author: David S Howes, MD; Chief Editor: Barry E Brenner, MD, PhD, FACEP  more...
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Portals of entry are virus specific. Many viruses are transmitted by humans, though most cases of HSE are thought to be reactivation of HSV lying dormant in the trigeminal ganglia. Mosquitoes or ticks inoculate arbovirus, and rabies virus is transferred via an infected animal bite or exposure to animal secretions. With some viruses, such as varicella-zoster virus (VZV) and cytomegalovirus (CMV), an immune-compromised state is usually necessary to develop clinically apparent encephalitis.

In general, the virus replicates outside the CNS and gains entry to the CNS either by hematogenous spread or by travel along neural pathways (eg, rabies virus, HSV, VZV). The etiology of slow virus infections, such as those implicated in the measles-related subacute sclerosing panencephalitis (SSPE) and progressive multifocal leukoencephalopathy (PML), is poorly understood.

Once across the blood-brain barrier, the virus enters neural cells, with resultant disruption in cell functioning, perivascular congestion, hemorrhage, and a diffuse inflammatory response that disproportionately affects gray matter over white matter. Regional tropism associated with certain viruses is due to neuron cell membrane receptors found only in specific portions of the brain, with more intense focal pathology in these areas. A classic example is the HSV predilection for the inferior and medial temporal lobes.

In contrast to viruses that invade gray matter directly, acute disseminated encephalitis and postinfectious encephalomyelitis (PIE), most commonly due to measles infection and associated with Epstein-Barr virus (EBV) and CMV infections, are immune-mediated processes that result in multifocal demyelination of perivenous white matter.

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