Herpes simplex encephalitis
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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]
Causes
Differentiating Herpes simplex encephalitis from Other Diseases
Herpes simplex encephalitis must be differentiated from other diseases that cause fever, headache, and altered mental status, such as:[3]
menengitis, and other viral and bacterial encephalitis cases
| Disease | Findings |
|---|---|
| Encephalopathy | Presents with steady depression, generalized seizures. Generally absent are fever, headache, leukocytosis, and pleocytosis. MRI often appears normal. |
| Brain abscess | Presents with an abscess in the brain caused by the inflammation and accumulation of infected material from local or remote infectious areas of the body; the infectious agent may also be introduced as a result of head trauma or neurological procedures. |
| Bacterial meningitis | Presents with inflammation of the meninges, which may develop in the setting of an infection, physical injury, cancer, or certain drugs; it may have an indolent evolution, resolving on its own, or may present as an rapidly evolving inflammation, causing neurologic damage and possible mortality. |
| Viral encephalitis | Presents with acute inflammation of the brain, caused by a viral infection; it may complicate into severe brain damage as the inflamed brain pushes against the skull, potentially leading to mortality. |
| Epidural abscess | Presents with an abscess in the epidural space, between the vertebrae and the dura mater of the spinal canal; it may complicate into spinal cord dysfunction, leading to paralysis. |
| Cerebral thrombophlebitis | Presents with inflammation of a cerebral vein, related to a blood clot or thrombus; it can cause chronic pain, leg swelling, and pulmonary embolism. |
| Superior sagittal sinus thrombosis | Presents with thrombosis affecting the dural venous sinuses, which drain blood from the brain; it can cause headaches, fever, and increased intracranial pressure. |
| Acute disseminated encephalomyelitis | Presents with scattered foci of demyelination and perivenular inflammation; it can cause focal neurological signs and decreased ability to focus. |
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.[4] 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.[4]
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.
- ↑ Kennedy PG (2004). "Viral encephalitis: causes, differential diagnosis, and management". J Neurol Neurosurg Psychiatry. 75 Suppl 1: i10–5. PMC 1765650. PMID 14978145.
- ↑ 4.0 4.1 Whitley RJ, Gnann JW (2002). "Viral encephalitis: familiar infections and emerging pathogens". Lancet. 359 (9305): 507–13. PMID 11853816.