Viral encephalitis is diffuse or focal inflammatory changes in the structures of the brain caused by the penetration of viral agents into them. The clinical picture is variable, it depends on the type of virus and the state of the patient’s immune system; it consists of general infectious, cerebral and focal manifestations. The diagnostic algorithm includes EEG, Echo-EG, CT or MRI of the brain, lumbar puncture and cerebrospinal fluid analysis, PCR studies to identify the pathogen. Combined treatment: antiviral, decongestant, anticonvulsant, antihypoxant, neuroprotective, psychotropic.
ICD 10
A83 A84 A85 A86
General information
Viral encephalitis is an inflammatory lesion of the brain substance of viral etiology. When the cerebral membranes are involved in the process, they talk about meningoencephalitis, when inflammation spreads to the spinal cord, encephalomyelitis. Depending on the genesis, primary and secondary viral encephalitis are distinguished. The first is caused by direct penetration of the virus into the cerebral tissues, the second by secondary brain damage against the background of an acute infectious disease (influenza, measles, rubella, herpes zoster) or as a result of post—vaccination complications.
The prevalence of viral encephalitis of various etiologies varies significantly climatically and geographically. Thus, Japanese mosquito encephalitis is most common in Japan and Asian countries, St. Louis encephalitis is observed mainly in the USA, lethargic encephalitis Economo – in Western Europe, tick—borne encephalitis — in the forest areas of Eastern Europe. Given the complexity of the diagnosis and identification of the pathogen, the risk of serious complications, the problem of viral encephalitis continues to be an urgent issue of practical neurology.
Causes
Among the neurotropic viruses that cause encephalitis, the herpes simplex virus is the most common. The cause of damage to the cerebral substance can also be other herpes viruses: cytomegalovirus, chickenpox virus, the causative agent of infectious mononucleosis (Epstein-Barr virus). Enteroviruses (including polio virus), adenoviruses, mumps virus, influenza A, rubella, measles, rabies, arboviruses, reoviruses, arena and bunyaviruses are also etiofactors of viral encephalitis.
Transmission of infection occurs directly from the patient by airborne, contact, fecal-oral routes or transmissive – with the bite of a vector (mosquito, tick). In the latter case, birds and animals can be the reservoir of infection. The entry of a neurotropic virus into the body may be a consequence of vaccination with a live weakened vaccine (for example, anti-rabies, anti-polio, anti-inflammatory).
Of no small importance in the development of the infectious process when viruses enter the human body is the state of its immune system, reactivity at the time of infection. In this regard, factors that increase the likelihood of encephalitis and cause the severity of its course include infancy and old age, the presence of immunodeficiency diseases or immunosuppression conditions. So, HIV itself usually does not act as a direct cause of the disease, but causes an immunodeficiency condition, in which the likelihood of viral encephalitis increases.
Classification
According to etiology, primary viral encephalitis is divided into seasonal, polyseasonal and caused by an unknown virus. Seasonal encephalitis is transmissible, their incidence is observed strictly at certain times of the year. This group includes tick-borne encephalitis, Japanese encephalitis, St. Louis encephalitis and Murray Valley encephalitis (Australian). Polyseasonal encephalitis does not have a clear seasonality (for example, influenza, enterovirus, herpetic encephalitis and encephalitis in rabies). Encephalitis of presumably viral etiology with an undetected pathogen includes leukoencephalitis, lethargic encephalitis. Secondary viral encephalitis is classified into those associated with a common viral infection (with chickenpox, measles, etc.) and post-vaccination.
According to the predominant localization of inflammatory changes, leukoencephalitis with predominance of inflammation of the white medulla, polyoencephalitis with predominant inflammation of the gray matter (lethargic encephalitis) and panencephalitis with diffuse involvement of cerebral structures (Japanese, tick-borne, St. Louis, Australian) are distinguished.
Viral encephalitis symptoms
The clinical picture depends on the type of encephalitis and the characteristics of its course. The debut is usually characterized by general infectious manifestations: fever, malaise, myalgia, sore throat or loosening of the stool and abdominal discomfort. Then, against their background, general cerebral symptoms appear: cephalgia (headache), nausea without food, vomiting, hypersensitivity to light, dizziness, epileptic paroxysms, etc. Cephalgia usually affects the frontal area and eye sockets. Possible psychosensory disorders, meningeal syndrome, various types of disorders of consciousness (inhibition, sopor, coma), psychomotor agitation, delirium, amentia.
In parallel with the increase of the above-mentioned manifestations, a focal neurological deficit occurs. There may be combined with hypesthesia spastic paresis, ataxia, aphasia, signs of damage to the cranial nerves (hearing loss, visual acuity and visual field changes, oculomotor disorders, bulbar paralysis), cerebellar syndrome (discoordination, swinging gait, swinging, muscular hypotension, intentional tremor, dysarthria).
The above manifestations can be observed in encephalitis of any etiology. However, individual viral encephalitis have specific clinical symptoms or a characteristic combination of signs that allow them to be distinguished from many other similar diseases. Thus, hypersomnia is typical for lethargic encephalitis, severe disorders of consciousness are typical for Japanese encephalitis, hallucinations and psychomotor agitation are typical for measles encephalitis, cerebellar ataxia is typical for chickenpox, and moderate disorders of consciousness and meningeal syndrome are typical for St. Louis encephalitis.
According to its course, viral encephalitis can be typical, asymptomatic, abortive or lightning-fast. Asymptomatic forms occur with periodic cephalgia, fever of unknown origin, transient dizziness and /or episodic diplopia. With abortive variants, neurological manifestations are not observed, symptoms of gastroenteritis or respiratory infection are possible. The lightning-fast course is characterized by the rapid development of coma and death.
Diagnostics
The absence of specific clinical symptoms and similarity with other CNS lesions (acute encephalopathy, acute multiple encephalomyelitis, bacterial encephalitis, etc.) makes the diagnosis of viral encephalitis a difficult task. In the course of its solution, the neurologist should rely on anamnestic and epidemiological data, clinic features and the results of additional studies.
Echo-encephalography usually determines cerebrospinal hypertension, EEG — diffuse changes with the dominance of slow-wave activity, in some cases with the presence of epiactivity. Ophthalmoscopy reveals changes in the optic nerve discs. When performing a lumbar puncture, there is an increased pressure of cerebrospinal fluid (CSF), its color is not changed. A distinctive feature of encephalitis of viral genesis is the detection of lymphocytic pleocytosis in the study of cerebrospinal fluid. However, initially such changes may be absent, so after a day it is necessary to re-take the cerebrospinal fluid for analysis.
CT and MRI scans of the brain allow to confirm the presence of encephalitis, determine the prevalence and predominant localization of inflammatory changes. CT of the brain visualizes the affected area of cerebral tissues as having a reduced density, MRI in T1 mode — as hypointensive, MRI in T2 mode — as hyperintensive. MRI has greater sensitivity, which is especially important in the initial stages of the disease.
Verification of the pathogen is often a difficult and sometimes impossible task. Serological methods involve the study of paired sera with an interval of 3-4 weeks and therefore have only retrospective significance. In practice, detection of DNA or RNA of the virus using PCR examination of cerebrospinal fluid is used for early identification of the pathogen. However, this method is not able to detect all viruses.
Treatment
The therapy is complex and consists of etiotropic, pathogenetic, symptomatic and rehabilitative treatment. The etiotropic component involves the appointment of antiviral pharmaceuticals: acyclovir and ganciclovir for herpetic encephalitis, ribavirin for arboviruses. In parallel, therapy with interferon and its analogues is carried out. It is possible to use a specific immunoglobulin.
The pathogenetic component consists in the correction of vital functions (according to indications — cardiac glycosides, vasoactive drugs, oxygen therapy, ventilator), the use of decongestants (mannitol, furosemide, acetazolamide), antihypoxants (ethylmethylhydroxypyridine succinate, meldonium), neuroprotectors (oxymethylethylpyridine succinate, piracetam, glycine, scopolamine). There is often a need for the appointment of glucocorticoids, which have a pronounced anti-inflammatory and decongestant effect. Symptomatic therapy involves the use of anticonvulsants (carbamazepine, valproates, diazepam), antiemetics (metoclopramide), psychotropic drugs (neuroleptics, tranquilizers) as needed.
Restorative treatment involves vascular and neuroprotective therapy in order to restore cerebral structures and their functions as soon as possible and as completely as possible. In the presence of paresis, massage and physical therapy are mandatory components of rehabilitation; it is possible to use physiotherapy — electrophoresis, electromyostimulation, reflexotherapy. In case of mental disorders, it is necessary to consult a psychiatrist with the implementation of correctional therapy, psychotherapy, social adaptation.
Prognosis and prevention
Encephalitis of a viral nature can have a number of serious complications. First of all, this is cerebral edema and the occurrence of dislocation syndrome with compression of the brain in the trunk area, which can cause death. The development of a cerebral coma threatens the formation of a vegetative state of the patient. The death of the patient may be associated with the addition of an intercurrent infection, the development of cardiac or respiratory failure. Against the background of encephalitis, the formation of epilepsy, persistent neurological deficit, intracranial hypertension, hearing loss, mental disorders is possible.
In general, the prognosis of encephalitis depends on its type, the severity of the course, the patient’s condition (according to the Glasgow scale) at the time of initiation of therapy. With tick-borne, herpetic and lethargic encephalitis, the mortality rate reaches 30%, with St. Louis encephalitis — less than 7%. Japanese encephalitis is characterized by a high mortality rate and a large percentage of residual events in those who have been ill. Postvaccinal encephalitis usually has a favorable course. The exception is viral encephalitis, which develops after anti-rabies vaccination according to the type of ascending paralysis of Landry and is accompanied by a risk of death due to bulbar disorders.
Measures for the prevention of transmissible encephalitis are protection from insect vectors, specific vaccination of the population of endemic foci and people who are going to visit them. Prevention of the development of secondary encephalitis against the background of a viral disease is timely and adequate treatment of infection, maintaining a high level of functioning of the immune system. Prevention of post-vaccination encephalitis consists in adequate selection of persons for vaccination, proper dosing and administration of vaccines.
