It is an inflammation of the brain parenchyma caused by a virus.
It is the most common type of encephalitis and often coexists with viral meningitis. Viruses invade the host outside the central nervous system (CNS) and then reach the spinal cord and brain hematogenously or retrograde from nerve endings.
In addition, in rarer cases, long-term illnesses may develop changes in the heart, serositis, microscopic enteritis, and, occasionally, meningitis.
Causes of viral encephalitis
In etiology, infectious encephalitis can be viral, bacterial, fungal, protozoal, or helminthic.
The etiology of many cases of encephalitis remains unknown despite extensive study. Viruses are the most common identified cause, accounting for approximately 70% of confirmed encephalitis cases.
In the United States, the most common causes of viral encephalitis are herpes simplex virus (HSV), West Nile virus, and enteroviruses.
Some of the other viral etiologic agents include a varicella-zoster virus, Epstein-Barr virus (EBV), cytomegalovirus (CMV), human herpesvirus type 6 and 7, measles virus, virus mumps, rubella virus, St. Louis virus, eastern equine virus, western equine virus, dengue virus, and rabies virus.
The incidence of viral encephalitis is 3.5 to 7.5 per 100,000 people, with the highest incidence in the young and the elderly. The epidemiology of specific viral causes of encephalitis has changed over time.
For example, vaccination has led to a decrease in measles and mumps encephalitis. On the other hand, EBV and CMV encephalitis are seen more frequently because they occur in immunocompromised individuals, such as AIDS, transplant, and chemotherapy patients.
Other important epidemiological factors include the time of year, geography, and animal or insect exposure.
For example, arboviruses (i.e., eastern equine, western equine, San Luis, Venezuelan equine, Zika, and West Nile) cause illness during the summer months when mosquitoes are active.
St. Louis encephalitis is seen primarily in the Midwest and South.
Viruses invade the host at a site outside the CNS and replicate. Most then reach the spinal cord and brain hematogenous. HSV, rabies, and the herpes zoster virus are significant exceptions.
They travel to the CNS from nerve endings in a retrograde manner. Once in the brain, the virus and the host’s inflammatory response disrupt neuronal cell function.
Brain histology of individuals with viral encephalitis shows dead neurons with nuclear dissolution and hypereosinophilia in the cytoplasm on light microscopy.
Because encephalitis is an inflammatory process, perivascular inflammatory cells such as microglia, macrophages, and lymphocytes are also seen.
Virions within neurons can be visualized with electron microscopy, which allows for much higher magnification than light microscopy.
Symptoms of viral encephalitis
The most common signs and symptoms are fever, headache, seizures, and altered mental status.
Neuropsychiatric features, such as behavioral changes, hallucinations, and cognitive impairment, are seen often. Patients may also have other symptoms or test findings that are more specific to a given virus.
For example, rashes and skin blisters are seen with herpes zoster encephalitis, whereas lymphadenopathy and splenomegaly are often associated with EBV.
HSV encephalitis affects the frontal and temporal lobes. Therefore it is often characterized by psychiatric features, memory deficits, and aphasia.
On the other hand, motor symptoms, such as choreoathetosis and parkinsonian movements, are seen with some arboviruses because they predominantly affect the basal ganglia.
Neuroimaging and lumbar puncture (LP) are essential initial diagnostic studies to evaluate patients with viral encephalitis.
Computed tomography (CT) or magnetic resonance imaging (MRI) helps exclude increased intracranial pressure and the risk of nail herniation before performing LP.
MRI is also the most sensitive imaging modality to show findings consistent with HSV encephalitis, such as frontal and temporal lobe involvement.
Cerebrospinal fluid (CSF) should be tested for opening pressure, cell count, glucose, and protein.
CSF evaluation should also include polymerase chain reaction (PCR) tests for HSV-1, HSV-2, and enteroviruses. Additional tests, such as arbovirus serology and HIV testing, may also be performed depending on the history and clinical presentation.
A broad differential diagnosis, both infectious and non-infectious, should be considered for encephalitis.
These alternatives include malignant, autoimmune, or paraneoplastic diseases (e.g., anti-NMDA receptor encephalitis), brain abscess, drug-induced tuberculosis or delirium, neurosyphilis, or bacterial, fungal, protozoal, or helminthic encephalitis.
Treatment and management of viral encephalitis
Treatment of viral encephalitis is primarily supportive, as there is no specific medical therapy for most viral infections of the central nervous system. A significant exception to this is HSV encephalitis.
When started early, acyclovir has been shown to significantly decrease mortality and morbidity and limit the severity of HSV encephalitis’s long-term cognitive and behavioral impairment.
Therefore, empirically, it is recommended that clinicians initiate all patients with suspected encephalitis with acyclovir.
The recommended dose is 10 mg/kg intravenously (IV) every 8 hours for 14 to 21 days.
Although not as effective with HSV, nucleoside analogs are also used for other herpes viruses. Acyclovir 10 to 15 mg/kg IV every 8 hours for 10 to 14 days, with possible adjuvant corticosteroids in immunocompetent patients, is recommended for varicella-zoster virus.
The recommended treatment for CMV encephalitis is a combination of ganciclovir 5 mg/kg IV every 12 hours and foscarnet 60 mg/kg IV every 8 hours or 90 mg/kg IV every 12 hours 21 days.
Another critical component of managing patients with viral encephalitis is serial intracranial pressure (ICP) monitoring. Elevated ICP is associated with a poor prognosis.
Although there is limited data on its efficacy in viral encephalitis, steroids and mannitol can be given to alleviate increased ICP.
Most patients with viral encephalitis recover without sequelae. Those who remain symptomatic have difficulty concentrating, behavioral and speech disorders, and memory loss.
In rare cases, patients can remain in a vegetative state.
- Deterioration in intelligence.
- Changes in mood and behavior.
- Residual neurological deficits.
- Extrapyramidal symptoms (JE).
- Hyponatremia (especially St. Louis encephalitis).
- Flaccid paralysis.
Patients with viral encephalitis should be admitted to the hospital for supportive care and antiviral therapy intravenously. They may require intensive care for frequent neurological examinations and respiratory assistance.