Pathophysiology

Encephalitis is an inflammatory process in the brain parenchyma. It is associated with clinical evidence of brain dysfunction due to infective (usually viral) or non-infective processes. The pattern of brain involvement depends on the specific pathogen, the immunological state of the host, and a range of environmental factors. In viral encephalitis the virus initially gains entry and replicates in local or regional tissue, such as the GI tract, skin, urogenital system, or respiratory system. Subsequent dissemination to the CNS occurs by haematogenous routes (enterovirus, arboviruses, HSV, HIV, mumps) or via retrograde axonal transport as with the herpes or rabies virus. Depending on the interactions between the neurotropic properties of the virus and the host immune response (mediated by humoral antibodies, cytotoxic T cells and cytokines), infection and inflammation of brain parenchyma occur. In these cases, neuronal involvement occurs along with evidence of a productive viral infection. Autoimmune processes, with antibodies directed against normal brain components (e.g., myelin), play a role in acute disseminated encephalomyelitis (ADEM). Prominent perivascular inflammation and demyelination are seen. If the aetiological agent is unknown it is presumed that the inflammatory reaction in the brain parenchyma is directed against, or is mediated by, this elusive agent.