Herpes simplex encephalitis (HSE) is a life-threatening condition with
high mortality as well as significant morbidity in survivors. In most
cases herpes simplex virus type 1 (HSV-I) is responsible for the dise
ases, however, the type 2 virus (HSV-2) is involved in 4-6% of cases.
Primary HSV infection is identified in only one-third of patients with
HSE. The majority of cases are recorded in adults with recurrent HSV
infection who are already seropositive for HSV at the onset of symptom
s, but only 6-10% of these patients have a history of labial herpes. A
cute focal, necrotizing encephalitis with inflammation and swelling of
the brain tissue are consistent features of the pathology of HSE. HSV
-induced cytolysis certainly damages neurones, oligodendrocytes and as
trocytes, but the role of cellular and humoral immunopathology is impo
rtant. A complex network of cytokines seems to be active in regulating
the local immune response and inflammation during and after HSE. Brai
n biopsy, serological analysis of intrathecal HSV antibodies and detec
tion of HSV-DNA in the cerebrospinal fluid (CSF) are all useful techni
ques to confirm the aetiology of HSE. Neurodiagnostic tests which supp
ort a presumptive diagnosis of HSE include: CSF analysis, electroencep
halography, computer-assisted tomography and magnetic resonance imagin
g. Although aciclovir is the treatment of choice in HSE, mortality and
morbidity still remain problematic. Long-term follow-up indicates tha
t intrathecal cellular and humoral activation persist in HSE.