HSE is one of the more clearly identified forms of encephalitis and the most common form of non-epidemic encephalitis. HSE is mainly caused by herpes simplex virus type I (HSV-I), and only 4-6% can be caused by HSV-2. Only 1/3 of HSV-infected patients have HSE. Most adults have a history of seropositive indicators indicating HSV infection, but only 6-10% have a history of oral herpes. The annual incidence of HSE reported by Taiwanese scholars in 1992 was 2-4 per million, with 1/3 of the patients being children and adolescents and 2/3 being adults. HSV induces cytolysis and damages neurons. oligodendrocytes and astrocytes. The limbic lobe is the site of greatest concentration of viral antigens, and hemorrhagic necrotic foci of inflammation and intracellular inclusion bodies in this region are pathologically definitive for diagnosis. In this case, the patient’s autopsy brain saw varying degrees of inflammatory response in the bilateral temporal lobes and hippocampus: hemorrhage, necrosis, gliosis, microglial nodules, perivascular inflammatory cell cuff-like infiltration and intracellular inclusion bodies. Pathological changes consistent with HSE. There are clinical features of infectious encephalitis: fever, loss of consciousness, personality changes, epilepsy, and focal signs. aphasia, hemiparesis, and epilepsy are more pronounced and personality changes are more prominent in HSE according to American and Swedish scholars in the early 1980s. The 10 cases we saw were also highlighted by epilepsy, mental retardation, and speech abnormalities, with no significant hemiparesis early on. HSV-DNA testing of the cerebrospinal fluid is the most useful technique for determining the etiology of HSE. The number of HSV detections in the cerebrospinal fluid does not necessarily parallel the clinical and MRI presentation and prognosis. However, quantitative viral analysis can detect antiviral therapy. Negative viral PCR tests have been reported. The negative PCR test for virus in this patient is not a basis for negating the diagnosis of HSE. The cell count, protein, and sugar content of the cerebrospinal fluid can be without significant changes. The main changes on MRI are the same as the pathological features of HSE: easy involvement of the middle temporal lobe, hippocampus, frontal orbital surface, parietal lobe and cingulate limbic system. high signal in these areas seen on T2 images is seen early and more specifically in the imaging diagnosis. In this case, post-mortem fixed brain MRI still showed high signal on T2-weighted images in the bilateral temporal lobes, which is consistent with the MRI findings of HSE. HSE requires rapid diagnosis and early treatment. Early application of acyclovir may greatly improve the prognosis, while the opposite may lead to severe sequelae and death. Our experience is to apply the drug as soon as the diagnosis is made; if the disease progresses despite the drug, the drug can be repeated. We have had cases with 4 d of onset and MRI suggestive of the diagnosis, where acyclovir was applied immediately and no sequelae remained. We have also had the experience of people who came to the clinic with severe mental disorder even after six months of illness in order to get adequate treatment in the early stage of the disease, and the symptoms were significantly reduced by applying acyclovir again. However, the application of acyclovir has not completely prevented death and disability, and the mortality rate of this disease is about 30% to date.