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We describe two patients, aged 3.5 years and 15 years, with a mild form of herpes simplex encephalitis (HSE). The disease was characterized by convulsions and lymphocytic pleocytosis in the cerebrospinal fluid (CSF). Involvement of herpes simplex virus (HSV) was established by antibody measurements in serum and CSF. Recovery was complete with no antiviral drug administration. It appears that scrutinized serological work-up would widen our concept of mild forms of HSE, with a better prognosis and complete recovery.

Survivors of herpes simplex encephalitis (HSE) experience intellectual impairment and an inability to store and recall information. Because the temporal lobes and associated limbic structures are central to storage and retrieval of memories, and are predominantly affected in adult HSE, injury to these areas is postulated to cause behavioral and learning disabilities. A previous study (Beers et al., 1993) demonstrated that intranasal inoculation of Lewis rats with herpes simplex virus type-1 (HSV-1) induced acute partial complex seizures, and hemorrhagic and inflammatory lesions of the hippocampus and entorhinal cortex. Consequently, it was of interest to determine whether rats that had recovered from HSE had limbic system-associated memory impairments. Therefore, rats were evaluated when signs and symptoms of encephalitis were no longer apparent using an eight arm radial maze to assess the acquisition and retention of learned information. An allocentric-spatial location paradigm revealed HSV-1 infected rats performed at chance levels on both acquisition and retention which were statistically different from sham-inoculated controls. However, using an egocentric-spatial left/right discrimination task, infected rats performed statistically similar to sham-inoculated controls. Furthermore, HSV-1 nucleic acids were detected in the nuclei of neurons within the hippocampus and entorhinal cortex using in situ hybridization techniques. Of interest was the observation that rats with learning and memory deficits had no apparent histopathological or immunocytochemical evidence of antecedent CNS infection. This is the first experimental demonstration that HSV-1 can cause behavioral impairments in the absence of obvious inflammatory injury to the temporal lobe memory system.

Retrograde amnesia for autobiographical material in the absence of anterograde amnesia or other memory disturbances was found in a patient with acute viral encephalitis. Memory loss showed a temporal gradient, but new learning was spared. Both brain perfusion imaging with 99mTc-HMPAO SPECT, and EEG localized the lesion in the left temporal lobe while CT and MRI were normal. This observation supports the anatomical differentiation between the different memory functions. The uncommon combination of isolated retrograde amnesia without other neuropsychological findings may raise the doubt of psychogenic aetiology, which in this case was refuted.

The clinical features of infectious mononucleosis are variable. The course is often asymptomatic and/or atypical. Serious complications are rare. The prognosis is often good, even though there may have been serious neurological symptoms. However, as in the case history presented here, persistent sequelae may be seen.

Amnesic subjects suffering from Korsakoff's syndrome and post-viral encephalitis were assessed on their ability to estimate short temporal durations using two quite different tasks. In the first experiment subjects were required to reproduce and estimate intervals of between 3 and 96 sec. In the second experiment subjects carried out an automated Fixed Interval task using intervals of 15 and 30 sec. On both tasks the Korsakoff group were impaired at all intervals compared to an alcoholic control group, whereas the post-encephalitic subjects were unimpaired compared to a normal control group. The results suggest that temporal estimation can be independent of memory function. There was, however, evidence of a relationship between the ability to estimate time intervals and performance on a particular test of frontal lobe function, cognitive estimation. The results are discussed in relation to these findings and to theories of temporal perception.

Prior to the onset of immunodeficiency disease, neurochemical and neuropathological events associated with motor and/or cognitive impairment can be identified in rhesus monkeys infected with simian immunodeficiency virus (SIV). These are astrocytosis, up-regulation of mRNA encoding the neuropeptide somatostatin (SRIF) and an increased expression of MHC Class II antigen. End-stage immunodeficiency disease has been associated with robust viral expression in the CNS frequently observed as multinucleated giant cell formation. SIV encephalitis has not been observed in animals whose only clinical signs of SIV disease were motor and/or cognitive impairment. These data suggest that neuronal dysfunction discernable as altered neuropeptide expression in cortical neurons precedes frank structural damage to the CNS in SIV encephalopathy. This model is consistent with the mechanism of neuropathogenesis in human HIV encephalopathy that can be partially inferred from neurochemical and neuropathological examination of autopsy material in HIV disease.