Viral Encephalitis

2021-03-23 12:00 AM

Suspected cases of HSV viral encephalitis can detect HSV glycoprotein antigens in CSF.


Viral encephalitis is an inflammatory pathological process that occurs in the brain parenchyma, caused by a variety of viruses that have an affinity for nerve cells. Clinical characteristics are diverse, but mainly acute encephalopathy causes consciousness disorders with many different degrees.

The causes of viral encephalitis

There are many ways to classify viral etiologies for encephalitis. The classification below according to the mechanism of pathogenesis.

Viruses that cause primary encephalitis

Primary encephalitis viruses are viruses whose target cells are nerve cells, causing direct damage to these cells. The primary encephalitis viruses are:

Family Togaviridae: Eastern Horses, Western Horses, Venezuelan Horses.

Family Flaviviridae: St. Louis, Murray Valley, West Nile River, Japanese encephalitis virus, Dengue, Tick-borne complex.

Family Bunyaviridae: La Crosse, Rift valley, Toscana.

Family Paramyxoviridae: Mumps, Measles, Hendra, Nipah.

Họ Arenaviridae: Lymphocytic choriomeningitis, Machupo, Lassa, Junin.

Family Piconaviridae: Polio, Coxsackie, ECHO, Hepatitis A.

Family Reoviridae: Colorado tick fever.

Family Rhabdoviridae: Lyssa, Wild bats.

Họ Filoviridae: Ebola, Marburg.

Family Retroviridae: HIV.

Họ Herpesviridae: Herpes simplex typ 1 và 2, VZV (Varicella-zoster), EBV (Epstein-Barr virus), CMV (Cytomegalovirus).

Họ Adenoviridae: Adenovirus.

Viruses cause secondary encephalitis

Secondary encephalitis viruses cause damage to glial cells:

Family Togaviridae: Rubella.

Family Orthomyxoviridae: Flu.

Family Paramyxoviridae: Mumps, Measles.

Family Poxviridae: Cowpea (Cowpox -Vaccinia virus).

Family Herpesviridae: CMV, VZV.

General clinical and subclinical features of viral encephalitis

Syndrome of infection - intoxication

There are often many different manifestations, depending on the cause. However, most of them have a fever. Some cases have increased peripheral leukocytes and the rate of polymorphonuclear leukocytes increased (common in Arbovirus encephalitis).

Mental - neurological disorders

Usually very diverse with the following major disorders:

Change in consciousness: Depending on the severity of the illness, drowsiness, lethargy, semi-coma and lethargy may occur.

Mental disorders: Delirium, disorientation, hallucinations, psychosis, behavioural and personality disorders ...

Seizure type seizures: Common in 50% of critically ill patients, possible local or systemic convulsions.

Localized nerve damage: Loss of speech, ataxia, paralysis or mild paralysis, increased tendon reflexes, pyramidal (+) pathological reflexes, muscle tremors, paralysis of the optic nerve, wire VII ...

Symptoms due to damage to the hypothalamus-pituitary (plant neurological disorders) such as: disorders of body temperature regulation, increased sweating, diabetes mellitus ...

Test of cerebrospinal fluid

Cells in the cerebrospinal fluid

Most (85% of cases) have a slight increase in cells (more than 5 to several dozen cells / mm3), mainly lymphocytes. However, at the first lumbar lumbar puncture (early stage) or in immunocompromised patients ... there was no increase in cells in the cerebrospinal fluid. Approximately 10% of patients have lymphocytes in cerebrospinal fluid greater than 500 / mm3, few can be> 1000 / mm3 (common in Eastern equine encephalitis, California encephalitis, mumps virus encephalitis and by LCMV ...)

Some encephalitis viruses do not increase lymphocytes, commonly caused by EBV, CMV and HSV.

Some encephalitis with neutropenia in cerebrospinal fluid (common in Eastern equine encephalitis, ECHO 9 virus encephalitis, some other intestinal VR). However, in cases where the CSF test has a slow rise in neutrophils (after> 48 hours), it should be distinguished from bacterial etiologies or other etiologies.

Some cases (about 20% of viral encephalitis cases caused by HSV, CTFV and California encephalitis) in DNT may have red blood cells> 500 cells / mm3.

Biochemical test in cerebrospinal fluid

Protein: Usually slightly increased.

Glucose: Usually normal, sometimes slightly increased.

Sequelae due to viral encephalitis

If the patient with viral encephalitis does not die, it can leave many different types of sequelae, most of which are neurological sequelae.

80% of Eastern equine encephalitis has severe neurological sequelae.

Viral encephalitis causes less sequelae: EBV, California, VN Venezuelan horse.

The rate and degree of sequelae depend on the age, the cognitive status of the patient when admitted to the hospital. In patients with deep coma, Glasgow ≤ 6 points, it is easy to die or leave serious sequelae. Patient ≤ 30 years old with little consciousness disorder: Usually cured, mild sequelae ...      

Tests to diagnose the etiology of viral encephalitis

Tests to find the cause in the cerebrospinal fluid

Isolation of the virus in cerebrospinal fluid: Usually no result.

PCR (viral nuclear acid amplification) technique in cerebrospinal fluid: Currently being widely used and considered as a basic technique in diagnosing viral encephalitis in advanced countries, especially viral encephalitis due to CMV, EBV, chicken pox virus and intestinal virus.

Searching for the antigen in the CSF: In suspected cases of HSV viral encephalitis, HSV glycoprotein antigens can be found in cerebrospinal fluid. But this test should be done early in the first week of illness.

Detects anti-virus specific antibodies in cerebrospinal fluid and in serum. These tests need to be done twice, 2 weeks apart to determine antibody variation. When detecting specific antibodies to anti-virus type IgM in cerebrospinal fluid and in serum, it also has diagnostic value. The specific antibody index against the virus in the cerebrospinal fluid compared with the serum when ≥ 1.5 times is also valid for diagnosis.

Electroencephalography (EEG), computed tomography (CT) and magnetic resonance imaging (MRI)

These techniques are only valuable for directing brain damage to be diffuse or local. Therefore, it is only possible to support the direction of a suspected diagnosis of viral encephalitis, not of decisive diagnostic value. However, these techniques can be very valuable in differential diagnosis from other brain diseases (such as tumours, abscesses, cerebral haemorrhage...). In patients with viral encephalitis, EEG, CT, MRI techniques can see the following images:

EEG: The acute phase may have spiky waves appear cyclic against the slow, low amplitude thorny background. These waves are common in the temporal lobe. In the subacute phase, delta and theta waves appear.

CT: Uneven density reduction areas, unknown boundaries, slow absorption, large diffusion size, large brain coils ... Lesions are usually scattered in the two hemispheres, but they are many in the temporal lobe.

MRI: You can see signs of hyperemia in the frontal lobes, temples ...

Brain biopsy

Before PCR, brain biopsy was considered the "gold standard" for the definitive diagnosis of viral encephalitis, especially viral encephalitis caused by HSV. Currently, this technique is less applicable. The brain organization after the biopsy is examined for histopathology and superstructure. The results are over 95% accurate. But this technique causes many complications: 0.5 - 2% (bleeding, local oedema, local epilepsy, infection ...) and can be fatal due to technology (0.2%) .

They come not from virut Arbo

Mechanism of pathogenesis - pathology

The Arboviruses that cause encephalitis generally have similar pathogenesis. Insects, when sucking on human blood, carry the virus into the body. The virus travels through the bloodstream to invade and damage the central nervous system, especially the epithelial cells of the olfactory system and the peripheral vasculature.

Common pathological images are neuronal necrosis, inflammation of glial cells and perivascular infiltration of lymphocytes. Neighbourhoods show an "increased perfusion" phenomenon with manifestations of increased blood vessels and decreased oxygen consumption.

General clinical manifestations of Arbovirus encephalitis

The clinical manifestations of Arbovirus encephalitis usually differ by age group. However, there are usually the following main symptoms:

Onset: Usually fever, skin and mucous membranes are often congested, dizziness; some can be sore throat and manifestations of respiratory tract inflammation or abdominal pain ... in children: often onset suddenly with high fever, often with convulsions (systemic or local) ... in For adults, the onset is usually less sudden, the fever is not as high as a child, with symptoms of headache (in the forehead or diffuse ...), nausea, vomiting ...

Thereafter: Headache, vomiting, meningeal signs (+), photophobia. More severe may be drowsiness, confusion, disorientation, semi-coma and lethargy ...

The common symptoms are muscle tremors, loss of abdominal reflexes, paralysis of the cranial nerves, mild hemiplegia or local paralysis in one limb, difficulty swallowing ... Frequent convulsions and also early symptoms. .

The acute phase of encephalitis usually ranges from a few days to 2-3 weeks. The recovery phase usually lasts weeks to months.

Treatment of viral encephalitis

Specific treatment

With antiviral drugs. However, at present, there are not really drugs that work well with viruses and there is also a phenomenon that the virus is resistant to antiviral drugs. Some of the drugs that have been used are:


Absolutely indicated in HSV viral encephalitis, in addition: severe viral encephalitis due to EBV and VZV. Acyclovir has an inhibitory effect on viral DNA polymerase.

Dosage: 10mg / kg x 3 times / day for 14 days, dilute in slow intravenous infusion. Acyclovir has an alkaline pH, so when infusion, it must be closely monitored, not to let the drug escape (due to a rupture of a vein or a bias needle ...). When the drug deviates out, it will cause local inflammation. Do not inject under the skin or capture meat.

Side effects of acyclovir: Intramuscular or subcutaneous injection causes local inflammation (9%), increases urea and blood creatinine (5%), thrombocytopenia (6%), digestive disturbances (7%: nausea , vomiting, diarrhoea), neurotoxicity (1%: lethargy, loss of pain sensation, disorientation, confusion, agitation, hallucinations, muscle tremors and convulsions).

Currently, there has been an expression of the acyclovir-resistant virus due to thymidine-kinase-modifying virus and DNA polymerase, especially in immunocompromised patients.

Ganciclovir and Foscarnet

Are drugs that are indicated for the treatment of viral encephalitis caused by CMV. Ganciclovir and Foscarnet have competitive inhibitory effects with viral DNA polymerase.

Dosage of Ganciclovir: 5 mg/kg heavy x 2 times/day, diluted in slow intravenous fluid (attack dose). Thereafter, the dose is maintained at 5 mg/kg/day. When there is kidney failure to reduce the dose, when there is a decrease in granulocytes and platelets, the drug must be stopped.

Foscarnet dose: 60 mg / kg weight x 3 times / day, slow intravenous infusion x 14-21 days. Then reduce to a maintenance dose: 60-120 mg/kg heavy/day. Foscarnet can cause kidney damage, reduce calcium, magnesium, and potassium, and may disturb heart rate and seizures.

Symptomatic treatment

Patients must be treated and monitored in resuscitation emergency rooms. Special attention should be paid to follow-up and emergency management of respiratory and circulatory systems.

Positive anti-oedema with the measures.

Lower the temperature when the fever is high.

Sedative, anticonvulsant.

Patient immobilization, monitoring, preventive care for pneumonia, ulcers, thrombophlebitis, and catheter site infections.