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Herpesviral encephalitis
coronal T2-weighted MR image shows high signal in the temporal lobes including
hippocampal formations and parahippogampal gyrae, insulae, and right inferior
frontal gyrus. A brain biopsy was performed and the histology was consistent with
encephalitis. PCR was repeated on the biopsy specimen and was positive for HSV
ICD-10
B00.4
ICD-9
054.3
eMedicine
article/1165183 article/341142
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Contents
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1 Pathophysiology
2 Presentation
3 Treatment
4 References
5 External links
Pathophysiology[edit]
HSE is thought to be caused by the retrograde transmission of virus from a peripheral site on the
face following HSV-1 reactivation, along a nerve axon, to the brain. The virus lies dormant in
the ganglion of the trigeminal cranial nerve, but the reason for reactivation, and its pathway to gain
access to the brain, remains unclear, though changes in the immune system caused by stress
clearly play a role in animal models of the disease. The olfactory nerve may also be involved in HSE,
which may explain its predilection for the temporal lobes of the brain, as the olfactory nerve sends
branches there. In horses, a single-nucleotide polymorphism is sufficient to allow the virus to cause
neurological disease; but no similar mechanism has been found in humans.
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Presentation[edit]
Most individuals with HSE show a decrease in their level of consciousness and an altered mental
state presenting as confusion, and changes in personality. Increased numbers of white blood cells
can be found in patient's cerebrospinal fluid, without
the presence of pathogenic bacteria and fungi. Patients typically have a fever and may have
seizures. The electrical activity of the brain changes as the disease progresses, first showing
abnormalities in one temporal lobe of the brain, which spread to the other temporal lobe 710 days
later. Imaging by CT or MRI shows characteristic changes in the temporal lobes (see Figure).
Definite diagnosis requires testing of the cerebrospinal fluid (CSF) by a lumbar puncture (spinal tap)
for presence of the virus. The testing takes several days to perform, and patients with suspected
Herpes encephalitis should be treated with acyclovir immediately while waiting for test results.
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Treatment[edit]
Herpesviral Encephalitis can be treated with high-dose intravenous aciclovir. Without treatment, HSE
results in rapid death in approximately 70% of cases; survivors suffer severe neurological damage.
When treated, HSE is still fatal in one-third of cases, and causes serious long-term neurological
damage in over half of survivors. Twenty percent of treated patients recover with minor damage.
Only a small population of survivors (2.5%) regain completely normal brain function. Earlier
treatment (within 48 hours of symptom onset) improves the chances of a good recovery. Rarely,
treated individuals can have relapse of infection weeks to months later. While the herpes virus can
be spread, encephalitis itself is not infectious. Other viruses can cause similar symptoms of
encephalitis, though usually milder (human herpes virus-6, varicella zoster virus, EpsteinBarr, cytomegalovirus, coxsackievirus, etc.).
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