Viral encephalitis is a primary encephalitis caused by direct viral invasion of the brain parenchyma. The disease occurs throughout the year and is therefore also known as sporadic encephalitis. The common viruses that cause encephalitis are enterovirus, cytomegalovirus, mucovirus and some other viruses. The main clinical manifestations are symptoms of brain parenchymal damage and signs of intracranial hypertension, such as fever, headache, vomiting, convulsions, and in severe cases, coma. However, the severity of the disease can vary depending on the location and extent of virus invasion.
Many viruses can cause encephalitis, the most common of which are coxsackieviruses and echoviruses, and others are herpes simplex virus, varicella-virus, mumps virus, rubella virus, measles virus, and EBV. Most of the megaviruses are intrauterine infections and acquired only in immunocompetent children. Enteroviruses replicate in local lymphoid tissues, and herpesviruses, measles and rubella viruses invade the blood stream after mucosal reactions and spread to multiple organs. Replication in organ tissues is massive and re-enters causing a second viraemia. The varicella-zoster virus, on the other hand, can follow the neurons directly to the nervous system. Viral invasion of brain tissue with massive replication and proliferation can directly disrupt the main mechanisms of neurological injury, which can also stimulate host responses to damage the nervous system, such as perivasculitis, avascular necrosis and endothelial hyperplasia.
Clinical manifestations.
The clinical manifestations of acute viral encephalitis caused by various viruses vary widely and are determined by.
1, the site of neurological involvement.
2, the intensity of viral pathogenesis.
3. the immune response of the affected child, etc.
Therefore, even if the infection is caused by the same virus, the clinical manifestations may vary.
(i) Prodromal symptoms.
Symptoms of the upper respiratory tract or gastrointestinal tract, such as fever, headache, sore throat, vomiting, diarrhea, loss of appetite, etc.
(ii) Neuropsychiatric symptoms.
1. Disorders of consciousness.
In mild cases, indifference, sluggishness or irritability and drowsiness to the outside world; in severe cases, delirium and coma.
2. Increased intracranial pressure.
Headache, vomiting, dizziness or even brain herniation, full fontanelle in infants.
3, Convulsions.
It can be limited, generalized or in a continuous state.
4.Motor dysfunction.
Depending on the site of damage, it can be central or peripheral paralysis of one side or one limb; it can also be extra-pyramidal movement disorders such as choreiform movements and muscle ankylosis; it can also be strabismus, facial paralysis or swallowing disorder due to cerebral nerve paralysis.
5. Mental disorders.
Such as memory loss, disorientation, hallucinations, hallucinations; mood changes, irritability, and sometimes suspicion, which are often mistaken for psychosis or frontal lobe tumor.
Viral infections are systemic diseases, but each virus has its own unique clinical manifestations. For example, Echovirus and Coxsackie virus infections often present with a small measles-like rash or concurrent myocarditis or pericarditis. In mumps, the parotid glands are enlarged (and may be preceded by encephalitis). In herpes simplex virus infection, a herpes rash appears around the mouth and lips. The course of the disease is usually about 2 weeks, and most cases can recover completely; only a few remain with sequelae of epilepsy, visual and hearing impairment, limb paralysis, and varying degrees of mental retardation.
Clinical diagnosis.
It is mainly based on clinical manifestations and laboratory tests.
(I) Clinical manifestations.
As mentioned above, if the lesion involves the meninges (meningoencephalitis), meningeal irritation such as cervical tonicity, positive Kernig’s sign and Brookinski’s sign appears.
(ii) Laboratory tests.
1. Cerebrospinal fluid examination.
When there are the above clinical manifestations and acute viral encephalitis is suspected, a lumbar puncture should be performed and the cerebrospinal fluid sent for laboratory tests. It may show typical viral encephalitis changes. (In special cases, even if the cerebrospinal fluid does not change can not be ruled out)
2. Pathogenetic diagnosis.
① cerebrospinal fluid sent for virus isolation.
② Cerebrospinal fluid cells for immunofluorescence antibody examination.
③Serological examination, the antibody titer is more than 4 times higher in the recovery period than in the acute period for diagnosis. Antibodies in the cerebrospinal fluid can also be measured.
3.Electroencephalogram.
Early in the course of the disease, there are obvious changes in the EEG. Although the above changes are not specific, they are still of some value for diagnosis and prognosis estimation in combination with the clinic.
Differential diagnosis.
The disease needs to be differentiated from septic meningitis (including those not thoroughly treated), tuberculous meningitis, fungal meningitis and brain abscess.
Treatment measures.
(i) Strengthening nursing care.
Nursing care should be strengthened during the course of the disease to prevent the occurrence of decubitus ulcers. Supply a certain amount of water, nutrition and electrolytes. Prevent accidents in sick children with psychiatric symptoms. Observe for precursors of brain herniation.
(ii) Anti-viral treatment.
Although there are no effective antiviral drugs, the following drugs can be used: iodoside (herpes net), triazolyl nucleoside (virazole), aprotinin, others such as transfer factor, interferon can improve the body’s resistance to the virus, can be applied.
(C) symptomatic treatment.
1, antipyretic, antispasmodic.
High fever can cause convulsions. Use physical cooling or Chinese and Western drugs to reduce fever. Phenobarbital or Valium can prevent or control convulsions.
2. Reduce cerebral edema.
20% mannitol. Hydrocortisone or dexamethasone can also be used.
Prognosis.
The prognosis of viral encephalitis is closely related to the infecting agent. Herpes simplex virus has a poor prognosis. Many surviving patients have varying degrees of sequelae.