Herpes simplex encephalitis

An uncommon but potentially catastrophic manifestation of herpes simplex virus infection.

The most common acute sporadic focal encephalitis in the US.

About 1-2 per 1,000,000 persons per year in the US.

May be caused either by a primary infection or reactivation of latent virus.

The route of spread to brain is not fully understood.

With primary oropharyngeal disease, it is hypothesized that the virus spreads along the olfactory or trigeminal nerves.

Reactivation of latent virus may occur by other neuronal pathways.

Infection or reactivation of the viral infection leads to focal information, often in the temporal lobe, with associated neurological deficits.

Patients present with fever, focal neurologic abnormalities including seizures which are common.

Meningitis may occur.

Usually associated with frontotemporal signs, including behavior changes, amnesia, aphasia, seizures, and hemiparesis.

Can be fatal and can manifest in a clinical fashion similar to the cute bacterial meningitis with a rapid onset, marked severity of headache, fever, and focal neurologic signs.

CSF analysis typically shows lymphocytic predominance with an elevated protein level, and elevated red cell counts may also be present.

Rarely associated with intracranial hemorrhage, either initially or as a late complication.

Brain MRI may show edema, mass effect, inflammation, and temporal lobe involvement is common.

Brain MRI characteristically shows signal hyperintensity in the orbitofrontal and temporal lobes.

EEG may show periodic lateralizing epileptiform discharges or focal slowing.

EEG changes are often localized to the temporal lobe.

Brain biopsy is the standard for the diagnosis of herpes simplex encephalitis.

Brain biopsy is infrequently performed because of it’s invasive nature.

Histopathology of the brain may show hemorrhagic necrosis, mononuclear infiltrate, perivascular cuffing, and gliosis.

50% of cases reveal intranuclear inclusions.

Diagnosis is usually established on the basis of nucleic acid amplification such as PCR testing of the CSF.

Viral culture of the CSF is low sensitivity of less than 10%.

PCR testing for herpes simplex virus is positive with at least 98% sensitivity and 94% specificity on the CSF, and maybe positive as early as 24 hours after the initial symptomatology.

A false negative result with PCR may result from the presence of inhibitor levels of viral nucleic acid in the CSF or from mutations in the HSV genome.

Initially CSF PCR assay for HSV may be negative, a repeat testing becomes positive after 4 days in many cases.

Treatment is with acyclovir treated intravenously at a dose 10 mg per kilogram every eight hours for 14-21 days.

Treatment with acyclovir results in a reduction of the mortality from more than 70% to approximately 25%.

Almost 50% of patients have moderate to severe neurological deficit at six months.

Risk factors associated with the poor prognosis include: age of more than 30 years, Glascow coma scale of six or less, treatment initiation more than four days after symptom onset, more than 100 copies of HSV DNA from microliter by PCR assay of initial CSF sample, and detection of focal lesions on the initial brain CT scan.

This will prognosis a brave 30 years, for the lesson Glasgow coma scale and treatment initiation more than four days if symptom onset, more than 100 copies of age if the car microliter by PCR assay on the initial CSF sample section of focal lesion on the initial fee instead of brain.

Acyclovir resistant disease is seen primarily in immunocompromise patients with substantial previous exposure to acyclovir.

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