From Wikipedia, the free encyclopedia
Herpesviral encephalitis is encephalitis
associated with herpes simplex virus.
Herpes simplex encephalitis (HSE) is a severe viral
infection of the human central nervous system. It is
estimated to affect at least 1 in 500,000 individuals per year.[1]
About 1 in 3 cases of HSE result from primary HSV-1 infection,
predominantly occurring in individuals under the age of 18; 2 in 3
cases occur in seropositive persons, few of whom have history of
recurrent orofacial herpes. Approximately 50% of individuals that
develop HSE are over 50 years of age.[2]
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.[1]
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. The olfactory nerve may also be involved in HSE,[3] which
may explain its prediliction 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;[4] but no
similar mechanism has been found in humans.
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.[1]
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 7–10 days
later.[1]
Without treatment, HSE results in rapid death in approximately
70% of cases.[1]
HSE is fatal in around 20% of cases treated, and causes serious
long-term neurological damage in over half of survivors. Only a
small population of survivors (2.5%) regain completely normal brain
function.[2]
References
- ^ a
b
c
d
e
Whitley RJ (2006). "Herpes simplex
encephalitis: adolescents and adults". Antiviral Res.
71 (2-3): 141–8. doi:10.1016/j.antiviral.2006.04.002. PMID 16675036.
- ^ a
b
Whitley RJ, Gnann JW (2002). "Viral
encephalitis: familiar infections and emerging pathogens".
Lancet 359 (9305): 507–13. doi:10.1016/S0140-6736(02)07681-X. PMID 11853816.
- ^
Dinn J (1980). "Transolfactory
spread of virus in herpes simplex encephalitis.". Br Med J
281 (6252): 1392. PMID 7437807.
- ^
van de Walle GR, Goupil R, Wishon C,
et al. (2009). "A single‐nucleotide polymorphism in a
herpesvirus DNA polymerase is sufficient to cause lethal
neurological disease". J Infect Dis 200
(1): 20–25. doi:10.1086/599316.
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Pathology of the nervous system, primarily CNS (G04–G47,
323–349) |
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Inflammation |
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Brain/
encephalopathy |
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autoimmune
( Multiple
sclerosis, Neuromyelitis optica, Schilder's
disease) · hereditary
( Adrenoleukodystrophy, Alexander,
Canavan, Krabbe, ML, PMD, VWM, MFC,
CAMFAK
syndrome) · Central pontine
myelinolysis · Marchiafava-Bignami
disease · Alpers'
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Other
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Spinal cord/
myelopathy |
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Both/either |
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| central nervous system navs:
anat/physio/dev, noncongen/congen/neoplasia,
symptoms+signs/eponymous, proc |
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