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Herpes simplex encephalitis
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Herpes simplex encephalitis
Herpes simplex encephalitis (HSE), or simply herpes encephalitis, is encephalitis due to herpes simplex virus. It is estimated to affect at least 1 in 500,000 individuals per year, and some studies suggest an incidence rate of 5.9 cases per 100,000 live births.
About 90% of cases of herpes encephalitis are caused by herpes simplex virus-1 (HSV-1), the same virus that causes cold sores. According to a 2006 estimate, 57% of American adults were infected with HSV-1, which is spread through droplets, casual contact and sometimes sexual contact, though most infected people never have cold sores. The other 10% of herpes encephalitis cases are due to HSV-2, which is typically spread through sexual contact and is the cause of genital herpes.
Two-thirds of HSE cases occur in individuals already seropositive for HSV-1, few of whom (only 10%) have history of recurrent orofacial herpes, while about one third of cases results from an initial infection by HSV-1, predominantly occurring in individuals under the age of 18. Approximately half of individuals who develop HSE are over 50 years of age.
The most common cause for encephalitis in children and adults is HSV-1. However, encephalitis found in newborns and immunocompromised individuals is mainly caused by HSV-2.
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 7–10 days later. Imaging by CT or MRI shows characteristic changes in the temporal lobes (see Figure). After the first symptoms appear, patients might lose their sense of smell. This can also be accompanied by the inability to read, write, or speak coherently, and understand verbal speech.
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. Atypical stroke-like presentation of HSV encephalitis has been described as well and the clinicians should be aware that HSV encephalitis can mimic a stroke.
Herpesviral encephalitis can serve as a trigger of anti-NMDA receptor encephalitis. About 30% of HSE patients develop this secondary immunologic reaction, which is associated with impaired neurocognitive recovery.
The annual incidence of herpesviral encephalitis is from 2 to 4 cases per 1 million population.
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Herpes simplex encephalitis
Herpes simplex encephalitis (HSE), or simply herpes encephalitis, is encephalitis due to herpes simplex virus. It is estimated to affect at least 1 in 500,000 individuals per year, and some studies suggest an incidence rate of 5.9 cases per 100,000 live births.
About 90% of cases of herpes encephalitis are caused by herpes simplex virus-1 (HSV-1), the same virus that causes cold sores. According to a 2006 estimate, 57% of American adults were infected with HSV-1, which is spread through droplets, casual contact and sometimes sexual contact, though most infected people never have cold sores. The other 10% of herpes encephalitis cases are due to HSV-2, which is typically spread through sexual contact and is the cause of genital herpes.
Two-thirds of HSE cases occur in individuals already seropositive for HSV-1, few of whom (only 10%) have history of recurrent orofacial herpes, while about one third of cases results from an initial infection by HSV-1, predominantly occurring in individuals under the age of 18. Approximately half of individuals who develop HSE are over 50 years of age.
The most common cause for encephalitis in children and adults is HSV-1. However, encephalitis found in newborns and immunocompromised individuals is mainly caused by HSV-2.
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 7–10 days later. Imaging by CT or MRI shows characteristic changes in the temporal lobes (see Figure). After the first symptoms appear, patients might lose their sense of smell. This can also be accompanied by the inability to read, write, or speak coherently, and understand verbal speech.
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. Atypical stroke-like presentation of HSV encephalitis has been described as well and the clinicians should be aware that HSV encephalitis can mimic a stroke.
Herpesviral encephalitis can serve as a trigger of anti-NMDA receptor encephalitis. About 30% of HSE patients develop this secondary immunologic reaction, which is associated with impaired neurocognitive recovery.
The annual incidence of herpesviral encephalitis is from 2 to 4 cases per 1 million population.
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