Herpes Simplex Encephalitis Patofisiology

HSE pathogenesis has not been understood. Part of the brain affected by ptekie very diffuse and scattered necrosis of the medial lobe asymmetry in the inferior temporal and frontal lobes. The exact mechanism is not clear cell damage and affects either directly or indirectly virus immune mediated process.
Brain infection is often a primary infection because of direct transmission of virus through neuronal path from the peripheral to the brain via nerve trigeminus or olfactorius. Factors that accelerate the HSE is not known. Although HSE is often found in patients with decreased immune system, most people have never experienced immune system suppression.
In one third of cases of HSE is a complication of primary HSV infection, while the remainder are caused by reinfection. In some cases the HSE is a reactivation of latent infection in the brain. Asymptomatic HSV often encountered by the high prevalence of antibodies to HSV in the population. Latent HSV infection in the brain is the biggest part of neurological disease are asymptomatic. From the autopsy results, HSV is found in the brain in 35% of the population without neurological symptoms until the patient dies.
In most cases, the HSE developed progressive neurological disorder that begins with. With the development of non-invasive diagnostic methods are extremely sensitive, patients with mild and atypical symptoms can be diagnosed. These cases reached 20% of total cases and includes patients with immuno suppressants, temporal lobe abnormalities non-dominan or HSV-2 infection.

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Herpes Simplex Encephalitis Clinical Manifestation