Herpes simplex virus (HSV) is thought to be the most common cause of acute fatal, sporadic viral encephalitis in the United States, comprising about 10-20% of all cases. HSV-I accounts for more than 95% of cases. HSV-II mostly causes diffuse encephalitis in newborns whose mothers are infected with genital herpes. The most common symptoms include headache and fever, particularly early in the illness. Other signs and symptoms include seizures, expressive or receptive aphasia, and paresthesia. Rapid progression to confusion, disorientation and coma can occur within a few days. Early diagnosis is essential since decreased mortality and morbidity have been shown with early initiation of antiviral therapy (Patient A). Blood and CSF antibody titers against HSV do not increase until the second or third week of illness. Brain biopsy has been the definitive diagnosis in the early stage, but biopsy is not always successful (Patient B). MRI has been shown to be superior to CT in detecting edema changes in HSV encephalitis. This is due to the high sensitivity of the T2-weighted spin-echo technique to increased brain water content, and has been advocated as the first diagnostic step when there is a clinical suspicion of HSV encephalitis (2). Appreciation of low-attenuation abnormalities in the temporal lobe with CT may be delayed following the onset of symptoms (1).

There are two hypotheses for the pathogenesis of HSV-I encephalitis: 1) reactivation of trigeminal or autonomic nerve root HSV infection may be associated with extension of the virus into the CNS via sensory nerves of the middle cranial fossa; 2) primary HSV results in encephalitis. HSV-I encephalitis is characterized by hemorrhagic necrosis involving particularly the temporal lobes. Bilateral temporal lobe involvement is highly characteristic of HSV-I infection. Involvement of adjacent frontal and parietal lobes can also be found.