What is encephalitis?
We currently believe that encephalitis is inflammation of the brain due to infection, infection and allergy, allergy and toxins.
What types of encephalitis are known?
Several classifications of encephalitis are based on various principles. According to the principal classification, clinical manifestations and features of the course depend on the etiological factor (possible reason).
Viral encephalitis appears in epidemic form and has a seasonal distribution. By the pathological prevalence, they differentiate between leukoencephalitis (inflammation of the white matter of the brain), polioencephalitis (inflammatory disease of the gray matter of the brain, for instance, acute poliomyelitis), and panencephalitis (diffuse lesions of nerve cells and conduction tracts, for instance, tick-borne encephalitis). Depending on the predominant localization of the pathological process, there are hemispheric, brainstem and cerebellar encephalitis. If some portions of the spinal cord are affected along with the brain matter, we deal with encephalomyelitis. Encephalitis can be diffuse and focal or purulent and non-purulent (by the type of inflammation).
How does encephalitis occur?
In viral encephalitis, brain penetration is mediated by the hematogenous pathway (spread by blood). In mosquito-borne and tick-borne encephalitis, a virus reaches blood vessels through a bite and is spread by blood to different organs including the brain. The most vulnerable structures in the brain are located at the bottom of the III ventricle. They also include basal ganglia, cerebral cortex, and cell formations in the brain stem and spinal cord. Contact, alimentary and droplet spread of infection from a man or from an animal to a man is also possible.
Tick-borne encephalitis (TBE) belongs to the type of encephalitis most typical of our climatic area. TBE is caused by the tick-borne encephalitis virus which is well preserved in low temperatures and easily destroyed when temperature exceeds 70 °C. Ixodic ticks are carriers and reservoir of the virus. Seasonal variations are explained by the biology of ticks that appear in huge amounts in spring or summer. The disease is widely spread in Siberia, in the Far East, and in the Urals. However, lately it is often met in more southern regions.
There are various ways through which the virus can enter the human body: through a tick bite or sometimes through the mouth. Alimentary infection occurs when drinking uncooked milk and eating dairy products made from the milk of infected cows and goats. After a tick bite the virus goes into the blood immediately. The virus is found in the brain tissue 2–3 days after the bity. Its highest concentration in the brain is reached by day 4. During the first days of the disease, the virus can be isolated from the blood and cerebrospinal fluid. The incubation period is 8–20 days in a tick bite, and 4–7 days when the virus enters the body through the mouth. The duration of incubation and severity of the disease depend on the amount of viruses and immune reactivity of the body. Numerous tick bites are more dangerous than solitary ones.
Prevention consists in combating ticks and vaccination of people. Immunization is done thrice. Revaccination is received in 4.12 months.
How is encephalitis manifested?
Clinical symptoms of encephalitis present with the following triad:
- Prodromal period of all infectious diseases lasts from several hours to several days. It is manifested through fever, symptoms of lesions of the upper respiratory tract or gastrointestinal tract (syndrome of infectious disease)
- Cerebral symptoms: headache, usually in the area of forehead and orbits, vomiting, photophobia, epileptic seizures. Impairment of consciousness, from mild impairment (apathy, somnolence) to coma. Psychic excitement and mental disorders are possible
- Focal symptoms of brain affection depending on the localization of a pathological process and form of encephalitis. They can be manifested as loss of functions (movement, coordination, speech, etc.) and cerebral cortex irritation (epileptic seizures)
Apart from typical forms of encephalitis, asymptomatic, abortive (reduced) are common whereas fulminant forms are rare. Asymptomatic forms are manifested through moderate headache and fever of uncertain origin, mild and transient neurological symptoms such as double vision, dizziness, skin sensitivity disorders, etc. The disease nature can be specified using changes in the cerebrospinal fluid.
An abortive form lacks any neurological symptoms. The disease is manifested through the symptoms of acute respiratory or gastrointestinal infection. Rigidity of cervical muscles along with moderate headache and a slightly elevated temperature indicate that a spinal puncture is necessary.
Fulminant encephalitis lasts from several hours to several days. The outcome is usually tragic. In this case, the disease starts with high temperature, and intense diffuse headache. Consciousness is quickly impaired, the patients are lapsed into coma. Rigidity (tension and shortening) of posterior cervical muscles is pronounced. A person dies due to respiratory disturbance or cardiac insufficiency.
How is encephalitis diagnosed?
The most important and diagnostically valuable tool is an examination of cerebrospinal fluid with a considerably increased number of lymphocytes (20 to 100 cells per 1 uL), and moderately increased level of protein. Fluid goes out under increased pressure. Leukocytosis and elevated ESR develop. EEG (during examination of brain cortex electrical activity) shows slow wave forms (theta and delta waves). In case of cramps, seizure patterns are registered. CT and MRI can show centers of different density in the brain matter.
Papilledema is sometimes found during an examination of the fundus of the eye.
Exact diagnosis is based on typical clinical manifestations and results of bacteriological (virology) examinations and blood analyses. However, it is difficult or sometimes impossible to identify the virus.
As soon as a patient’s condition is relatively stabilized and nothing threatens a patient’s life any more, restoration of neurological deficiency must be predicted. Medicinal products that produce a neurotrophic effect are used to increase the stability of the nervous system towards damaging infectious and immune effects and to improve the extent and rate of restoration of functions in complex therapy of meningitis, encephalitis and encephalomyelitis. In particular, these are peptide drugs that launch internal compensation mechanisms and produce a positive effect on metabolic processes in the nervous system.
What is postvaccinal encephalitis/or postvaccinal encephalomyelitis? How must it be treated?
Postvaccinal encephalitis is based on cross-protective autoimmune reaction to vaccine antigens and brain antigens manifested as inflammatory lesion of the brain.
The first symptoms usually occur on days 7–12 postvaccination, sometimes even earlier. Postvaccinal encephalitis (or encephalomyelitis) often occurs in children who underwent primary vaccination (especially in late vaccination) and rare in revaccination. At the onset of the disease, the temperature elevates to 39–40 °C. Patients have headaches, vomiting, uncommon loss of consciousness and generalized cramps. Meningeal symptoms, central paresis, hyperkinesis (excessive movements), disturbed coordination of movements can be found occasionally. Increased pressure of the cerebrospinal fluid, mild cytosis due to lymphocytes (or normal levels of cell elements), mildly increased levels of protein and glucose.
The course is favorable. In the majority of cases, complete convalescence results. Paresis and paralysis can be preserved for some time. They tend to progression. After an antirabic vaccination encephalomyelitis typically presents with an ascending paralysis. It can be fatal as disturbances in swallowing and respiration are developed.
Immunosupressors (frequent corticosteroids, rare cytostatic agents), antisensitizers (dimedrol, pipolphen, suprastin), dehydrating, anticonvulsive, and antipyretic agents are used to treat postvaccinal encephalitis.
K. R. Badalyan
Department of Neurology, Faculty of Additional Professional Education
of Pirogov Russian National Research Medical University
