Herpes simplex encephalitis: Difference between revisions
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Herpes simplex encephalitis is thought to be caused by the [[Retrograde infection|retrograde transmission]] of virus from a peripheral site on the face to the brain along a nerve [[axon]] following HSV-1 reactivation.<ref name="pmid16675036"/> The virus lies dormant in the [[ganglion]] of the trigeminal or fifth [[cranial nerve]] but the exact pathogenesis remains unknown. The [[olfactory nerve]] may also be involved in herpes simplex encephalitis.<ref>{{cite journal | author = Dinn J | title = Transolfactory spread of virus in herpes simplex encephalitis. | journal = Br Med J | volume = 281 | issue = 6252 | pages = 1392 | year = 1980 | id = PMID 7437807}}</ref> | Herpes simplex encephalitis is thought to be caused by the [[Retrograde infection|retrograde transmission]] of virus from a peripheral site on the face to the brain along a nerve [[axon]] following HSV-1 reactivation.<ref name="pmid16675036"/> The virus lies dormant in the [[ganglion]] of the trigeminal or fifth [[cranial nerve]] but the exact pathogenesis remains unknown. The [[olfactory nerve]] may also be involved in herpes simplex encephalitis.<ref>{{cite journal | author = Dinn J | title = Transolfactory spread of virus in herpes simplex encephalitis. | journal = Br Med J | volume = 281 | issue = 6252 | pages = 1392 | year = 1980 | id = PMID 7437807}}</ref> | ||
== | ==Differential Diagnosis== | ||
==Epidemiology and Demographics== | ==Epidemiology and Demographics== | ||
It is estimated to affect at least 1 in 500,000 individuals per year.<ref name="pmid16675036">{{cite journal |author=Whitley RJ |title=Herpes simplex encephalitis: adolescents and adults |journal=Antiviral Res. |volume=71 |issue=2-3 |pages=141–8 |year=2006 |pmid=16675036 |doi=10.1016/j.antiviral.2006.04.002}}</ref> Approximately 50% of individuals that develop HSE are over 50 years of age.<ref name="pmid11853816">{{cite journal |author=Whitley RJ, Gnann JW |title=Viral encephalitis: familiar infections and emerging pathogens |journal=Lancet |volume=359 |issue=9305 |pages=507–13 |year=2002 |pmid=11853816 |doi=}}</ref> About 1 in 3 cases of HSE result from primary HSV-1 infection predominantly occurring in individuals under the age of 18. Although 2 in 3 cases occur in seropositive persons, few of these individuals have history of recurrent orofacial herpes. | It is estimated to affect at least 1 in 500,000 individuals per year.<ref name="pmid16675036">{{cite journal |author=Whitley RJ |title=Herpes simplex encephalitis: adolescents and adults |journal=Antiviral Res. |volume=71 |issue=2-3 |pages=141–8 |year=2006 |pmid=16675036 |doi=10.1016/j.antiviral.2006.04.002}}</ref> Approximately 50% of individuals that develop HSE are over 50 years of age.<ref name="pmid11853816">{{cite journal |author=Whitley RJ, Gnann JW |title=Viral encephalitis: familiar infections and emerging pathogens |journal=Lancet |volume=359 |issue=9305 |pages=507–13 |year=2002 |pmid=11853816 |doi=}}</ref> About 1 in 3 cases of HSE result from primary HSV-1 infection predominantly occurring in individuals under the age of 18. Although 2 in 3 cases occur in seropositive persons, few of these individuals have history of recurrent orofacial herpes. | ||
==Risk Factors== | |||
==Natural History, Complications and Prognosis== | ==Natural History, Complications and Prognosis== | ||
Without treatment, HSE results in rapid death in around 70% of cases.<ref name="pmid16675036"/> Even with the best modern treatment, it is fatal in around 20% of cases treated, and causes serious long-term neurological damage in over half the survivors. For unknown reasons the virus seems to target the [[temporal lobe]]s of the brain. Only a small population of survivors (2.5%) regain completely normal brain function.<ref name="pmid11853816"/> | Without treatment, HSE results in rapid death in around 70% of cases.<ref name="pmid16675036"/> Even with the best modern treatment, it is fatal in around 20% of cases treated, and causes serious long-term neurological damage in over half the survivors. For unknown reasons the virus seems to target the [[temporal lobe]]s of the brain. Only a small population of survivors (2.5%) regain completely normal brain function.<ref name="pmid11853816"/> | ||
==Diagnosis== | ==Diagnosis== | ||
===History and Symptoms=== | ===History and Symptoms=== | ||
Most individuals with HSE show a decrease in their level of consciousness and an altered mental state presenting as [[Mental confusion|confusion]] and changes in personality. Some patients with HSE will have seizures. | Most individuals with HSE show a decrease in their level of consciousness and an altered mental state presenting as [[Mental confusion|confusion]] and changes in personality. Some patients with HSE will have seizures. | ||
===Physical Examination=== | |||
===Laboratory Findings=== | ===Laboratory Findings=== | ||
Increased numbers of white blood cells can be found in their [[cerebrospinal fluid]] without the presence of [[pathogen]]ic [[bacteria]] and [[fungi]], and they typically have a fever.<ref name="pmid16675036"/> | Increased numbers of white blood cells can be found in their [[cerebrospinal fluid]] without the presence of [[pathogen]]ic [[bacteria]] and [[fungi]], and they typically have a fever.<ref name="pmid16675036"/> | ||
===CT | |||
===MRI=== | |||
===CT=== | |||
[[Computed tomography|CT]] or [[Magnetic resonance imaging|MRI]] scans 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.<ref name="pmid16675036"/> | [[Computed tomography|CT]] or [[Magnetic resonance imaging|MRI]] scans 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.<ref name="pmid16675036"/> | ||
===Other Diagnostic Studies=== | ===Other Diagnostic Studies=== | ||
The electrical activity of the brain (detected using [[Electroencephalography|EEG]] 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.<ref name="pmid16675036"/> | The electrical activity of the brain (detected using [[Electroencephalography|EEG]] 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.<ref name="pmid16675036"/> | ||
==Treatment== | |||
===Medical Therapy=== | |||
===Surgery=== | |||
===Primary Prevention=== | |||
===Secondary Prevention=== | |||
=References== | =References== | ||
Revision as of 17:00, 4 February 2016
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Herpes simplex encephalitis On the Web |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Anthony Gallo, B.S. [3]
Overview
Herpes simplex encephalitis is a severe viral infections of the central nervous system.
Classification
Herpes simplex encephalitis may be classified according to origin of disease into 2 subtypes: oral (HSV-1) and genital (HSV-2).
Pathophysiology
Herpes simplex encephalitis is thought to be caused by the retrograde transmission of virus from a peripheral site on the face to the brain along a nerve axon following HSV-1 reactivation.[1] The virus lies dormant in the ganglion of the trigeminal or fifth cranial nerve but the exact pathogenesis remains unknown. The olfactory nerve may also be involved in herpes simplex encephalitis.[2]
Differential Diagnosis
Epidemiology and Demographics
It is estimated to affect at least 1 in 500,000 individuals per year.[1] Approximately 50% of individuals that develop HSE are over 50 years of age.[3] About 1 in 3 cases of HSE result from primary HSV-1 infection predominantly occurring in individuals under the age of 18. Although 2 in 3 cases occur in seropositive persons, few of these individuals have history of recurrent orofacial herpes.
Risk Factors
Natural History, Complications and Prognosis
Without treatment, HSE results in rapid death in around 70% of cases.[1] Even with the best modern treatment, it is fatal in around 20% of cases treated, and causes serious long-term neurological damage in over half the survivors. For unknown reasons the virus seems to target the temporal lobes of the brain. Only a small population of survivors (2.5%) regain completely normal brain function.[3]
Diagnosis
History and Symptoms
Most individuals with HSE show a decrease in their level of consciousness and an altered mental state presenting as confusion and changes in personality. Some patients with HSE will have seizures.
Physical Examination
Laboratory Findings
Increased numbers of white blood cells can be found in their cerebrospinal fluid without the presence of pathogenic bacteria and fungi, and they typically have a fever.[1]
MRI
CT
CT or MRI scans 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]
Other Diagnostic Studies
The electrical activity of the brain (detected using EEG 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]
Treatment
Medical Therapy
Surgery
Primary Prevention
Secondary Prevention
References=
- ↑ 1.0 1.1 1.2 1.3 1.4 1.5 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.
- ↑ Dinn J (1980). "Transolfactory spread of virus in herpes simplex encephalitis". Br Med J. 281 (6252): 1392. PMID 7437807.
- ↑ 3.0 3.1 Whitley RJ, Gnann JW (2002). "Viral encephalitis: familiar infections and emerging pathogens". Lancet. 359 (9305): 507–13. PMID 11853816.