Encephalitis

Encephalitis is an inflammation of the substance of the brain. There are primary (tick-borne, Japanese mosquito, Economic encephalitis) and secondary (measles, influenza, post-vaccination) encephalitis. In the case of encephalitis of any etiology, complex therapy is necessary. As a rule, it includes etiotropic treatment (antiviral, antibacterial, antiallergic), dehydration, infusion therapy, anti-inflammatory treatment, vascular and neuroprotective therapy, symptomatic treatment. Patients who have suffered encephalitis also need restorative treatment.

ICD 10

G04.0 G04.8 G04.9

General information

The term “encephalitis” refers to infectious, allergic, infectious-allergic and toxic brain lesions. The group of diseases is very numerous, epidemiological data and etiopathogenetic features of encephalitis are equally diverse. Some of them have seasonal and climatic-geographical specificity, others are widespread and do not depend on the time of year. The study of encephalitis is engaged in infectious diseases and clinical neurology.

Classification

Classification of encephalitis reflects etiological factors, associated clinical manifestations and features of the course.

1. According to the etiology and timing of occurrence, there are:

• primary encephalitis (viral, microbial and rickettsious)
• secondary encephalitis (postexanthemic, postvaccinal, bacterial and parasitic, demyelinating).

2. According to the type of development and course of the disease:

• hyperacute;
• sharp;
• subacute;
• chronic;
• recurrent.

3. According to the localization of the lesion:

• cortical;
• subcortical;
• stem;
• with a lesion of the cerebellum.

4. By prevalence:

• leukoencephalitis (with white matter lesion);
• polyencephalitis (with gray matter lesion);
• panencephalitis.

5. Morphological features:

• necrotic;
• hemorrhagic.

6. According to the severity of the course of the disease, encephalitis is distinguished:

• of moderate severity;
• heavy;
• extremely heavy.

7. Depending on the predominant localization, encephalitis is divided into:

• stem;
• cerebellar;
• mesencephalic;
• diencephalic.

Primary encephalitis

Tick-borne encephalitis (spring-summer)

The disease is caused by the filtering neurotropic tick-borne encephalitis virus. The carriers of the virus and its reservoir in nature are ixode mites. Getting into the human body through a tick bite or alimentary (eating raw milk of infected cows and goats), the virus penetrates the nervous system hematogenically. The duration of the incubation period of the disease developed as a result of a tick bite is from 1 to 30 days (in some cases up to 60 days), in the case of alimentary infection — from 4 days to 1 week. Microscopy of the brain and membranes reveals their hyperemia, infiltrates from poly- and mononuclear cells, mesodermal and gliotic reactions. Localization of inflammatory and degenerative changes of neurons occurs mainly in the nuclei of the medulla oblongata, the anterior horns of the cervical segments of the spinal cord, the bridge of the brain, the cerebral cortex.

For the clinical picture of all forms of tick-borne encephalitis, an acute onset is typical, manifested in the form of an increase in body temperature to 39-40 degrees, aching pains in the lower back, calves. Already in the first days of the disease, pronounced general cerebral symptoms (vomiting, headache), impaired consciousness are noted, in some cases mental disorders (delirium, auditory and sound hallucinations, depression) were observed. There are several clinical forms of tick-borne encephalitis, their difference lies in the prevalence and severity of certain neurological symptoms.:

• polio;
• meningeal;
• encephalitic;
• feverish;
• polyradiculoneuritic;
• two-wave viral meningoencephalitis.

In the diagnosis of tick-borne encephalitis, anamnesis data (stay in an endemic focus, tick bite, the patient’s profession, the use of goat’s milk or cheese) are of great importance. Note that only 0.5-5.0% of all ticks are carriers of viruses, so not every disease that occurs after a tick bite is encephalitis. Verification of the diagnosis of tick-borne encephalitis is carried out using complement binding reactions, neutralization and inhibition of hemagglutination. The isolation of the virus in the blood and cerebrospinal fluid has a certain diagnostic value; in the blood, an increase in ESR, leukocytosis is determined, and in the study of cerebrospinal fluid — lymphocytic pleocytosis and an increase in protein to 1 g / L. Tick-borne encephalitis must be differentiated from typhus, various forms of serous meningitis, acute polio.

Japanese mosquito encephalitis

The disease is caused by a neurotropic virus, the carriers of which are mosquitoes capable of transovarial transmission of the virus. The incubation period lasts from 5 to 14 days. Japanese mosquito encephalitis debuts suddenly, with a sharp increase in body temperature (up to 39-40 degrees), vomiting, intense headache. In addition, the clinical picture of Japanese mosquito encephalitis is characterized by a significant severity of common infectious symptoms (tachycardia, bradycardia, facial hyperemia, herpetic rashes, dry tongue).

There are several forms of Japanese mosquito encephalitis, which differ in the predominance of one or another syndrome:

• meningeal;
• convulsive;
• bulbar;
• hemiparetic;
• hyperkinetic;
• lethargic.

The course of the disease is usually severe. During the first 3-5 days, symptoms increase, high body temperature persists for 10-14 days and decreases lytically. The fatal outcome is most often (up to 70% of cases) observed in the first week of the disease. The onset of death is also possible at a later stage of the disease, as a result of complications that have joined (for example, pulmonary edema). The seasonality of the disease and epidemiological data are of great importance for the diagnosis of Japanese mosquito encephalitis. Verification of the diagnosis is carried out using complement binding and neutralization reactions, antibodies are detected already in the second week of the disease.

Epidemic lethargic encephalitis Economo (encephalitis A)

The disease is not contagious, currently it does not occur in its typical form. The causative agent of epidemic encephalitis Economo has not been detected to this day. Clinically and pathomorphologically, the disease can be divided into two stages — acute, having an inflammatory character, and chronic, for which a progressive degenerative course is typical.

The classic form of epidemic lethargic encephalitis in the acute stage debuts with a rise in body temperature to 39 degrees, moderate headaches, vomiting, feelings of general weakness. The fever lasts about two weeks. At this time, neurological symptoms appear: pathological drowsiness (less often — other sleep disorders), damage to the nuclei of the oculomotor nerves (sometimes ptosis). Extrapyramidal symptoms typical of the chronic stage of epidemic encephalitis Economo are often observed at the acute stage of the disease. They can manifest themselves in the form of hyperkinesis (athetosis, eye cramp, choreoathetosis) and akinetic-rigid syndrome (amymia, akinesis, muscle rigidity).

In some cases, the acute stage of epidemic encephalitis Economo may be accompanied by pronounced psychogenic disorders (visual and / or auditory hallucinations, changes in the perception of the color and shape of surrounding objects). At the acute stage of the disease, pleocytosis (mostly lymphocytic) is detected in the cerebrospinal fluid of most patients, a slight increase in glucose and protein levels; in the blood — an increased level of lymphocytes, eosinophils. The acute stage of epidemic encephalitis Economo can last from 3-4 days to 4 months, after which a full recovery is possible. In 40-50% of cases, the acute stage becomes chronic with the preservation of residual symptoms (persistent insomnia, depression, mild ptosis, convergence insufficiency).

The main clinical manifestation of the chronic stage of epidemic encephalitis Economo is Parkinsonism syndrome, along with which endocrine disorders (infantilism, diabetes insipidus, menstrual disorders, cachexia, obesity) can develop.

Diagnosis of epidemic encephalitis in the acute stage is quite difficult. During this period, diagnosis can be based only on various forms of sleep disorders, accompanied by psychosensory disorders, and symptoms of damage to the nuclei of the oculomotor nerves. Particular attention should be paid to the appearance of the above symptoms against a background of elevated body temperature. Diagnosis of the chronic stage of epidemic encephalitis is economically less difficult and is based on the characteristic Parkinsonism syndrome, endocrine disorders of central genesis, changes in the psyche.

Secondary

Influenza encephalitis

The disease is caused by influenza viruses A1, A2, A3 and B. It occurs as a complication of influenza. Pathogenetic mechanisms of influenza encephalitis — dyscirculatory phenomena in the brain and neurotoxicosis. Lesions of the nervous system are inevitable in any form of influenza, when they manifest themselves in the form of headaches, muscle aches, drowsiness, adynamia, etc. However, in the case of influenza encephalitis, the patient’s well-being deteriorates sharply, there are general cerebral symptoms (dizziness, vomiting). In the cerebrospinal fluid, a moderate increase in protein and a small pleocytosis are detected (during lumbar puncture, the cerebrospinal fluid flows out under increased pressure).

In some cases, at the acute stage of influenza encephalitis, a severe lesion developed in the form of hemorrhagic influenza encephalitis, which debuts with a sharp rise in body temperature, chills and impaired consciousness (up to coma). Traces of blood are found in the liquor. The course of this form of influenza encephalitis is extremely severe, so the fatal outcome occurs quite often, and in the case of a positive outcome of the disease, pronounced neurological disorders persist.

Measles encephalitis

It refers to infectious and allergic encephalitis. It develops acutely, 4-5 days after the appearance of a rash with measles, when the body temperature, as a rule, has already normalized, its new sharp rise to 39-40 degrees is noted. In most cases, there are pronounced disorders of consciousness, hallucinations, psychomotor agitation, generalized convulsions, coordination disorders, hyperkinesis, limb paresis and pelvic organ dysfunction. When examining the cerebrospinal fluid, an increased protein content, pleocytosis is determined. The course of measles encephalitis is extremely severe, the mortality rate reaches 25%.

Postvaccinal encephalitis

They may occur after the introduction of ADS and DPT vaccines, with anti-rabies vaccinations, as well as after measles vaccine (most often). Post-vaccination encephalitis develops acutely, debuting with a sharp increase in body temperature (up to 40 degrees), vomiting, headache, impaired consciousness and generalized seizures. The defeat of the extrapyramidal system is accompanied by the appearance of hyperkinesis and movement coordination disorders.

When examining the cerebrospinal fluid (it flows out under increased pressure), a small lymphocytic cytosis and a slight increase in protein and glucose levels are determined. The peculiarity of the course of encephalitis with anti—rabies vaccinations is the debut of the disease in the form of acute encephalomyelopolyradiculoneuritis, sometimes rapidly progressing, which can lead to death as a result of bulbar disorders.

Treatment

Pathogenetic therapy

Pathogenetic therapy includes several directions:

• dehydration and control of cerebral edema (mannitol 10-20% solution intravenously at 1-1.5 g / kg; furosemide intravenously or intramuscularly 20-40 mg; acetazolamide);
• desensitization (chloropyramine, clemastine, diphenhydramine);
• hormone therapy — has a dehydrating, anti-inflammatory, desensitizing effect, and also protects the adrenal cortex from functional exhaustion (prednisone up to 10 mg / kg / day by pulse therapy for 4-5 days; dexamethasone intravenously or intramuscularly 16 mg / day 4 mg every 6 hours);
• improvement of microcirculation (isotonic dextran solution intravenously drip;
• antihypoxants (ethylmethylhydroxypyridine succinate, etc.);
• maintenance of homeostasis and water-electrolyte balance (parenteral and enteral nutrition, dextrose, dextran, potassium chloride);
• angioprotectors (hexobendine + ethamivan + ethophylline, vinpocetine, pentoxifellin, etc.);
• treatment of cardiovascular disorders (cardiac glycosides, vasopressors, camphor, sulfocamphocaine, glucocorticoids);
• normalization of respiration (preservation of airway patency, hyperbaric oxygenation, oxygen therapy, if necessary, tracheostomy or intubation, ventilator;
• restoration of brain metabolism (vitamins, polypeptides of the cerebral cortex of cattle, piracetam, etc.);
• anti-inflammatory drugs (salicylates, ibuprofen, etc.)

Etiotropic therapy

Etiotropic therapy of viral encephalitis involves the use of antiviral drugs — nucleases that delay the reproduction of the virus. Interferon alpha-2 is prescribed, in severe cases in combination with ribavirin. In RNA and DNA viral encephalitis, the use of tilorone is effective. Corticosteroids (methylprednisolone) are used by pulse therapy up to 10 mg / kg intravenously for 3 days.

Symptomatic therapy

Symptomatic therapy, in turn, involves several directions: anticonvulsant and antipyretic treatment, therapy of delirious syndrome. To relieve the epileptic status, diazepam (5-10 mg intravenously on dextrose solution), 1% sodium thiopental solution intravenously, phenobarbital, primidone, inhalation anesthesia are used. To reduce body temperature, lytic mixtures are used, 2 ml of a 50% solution of sodium metamizole, droperidol, ibuprofen. In the treatment of delirious syndrome, it is advisable to prescribe magnesium sulfate, acetazolamide, and lytic mixtures. Metabolic drugs, biostimulants are used to normalize consciousness, antidepressants, tranquilizers are used to normalize the psyche.

Rehabilitation

Restorative therapy also includes several components: treatment of parkinsonism (levodopa drugs, cholinolytics, muscle relaxants; stereotactic operations are indicated only with increasing rigidity and ineffectiveness of drug treatment); treatment of hyperkinesis (metabolic drugs, neuroleptics, tranquilizers); treatment of Kozhevnikov epilepsy (anticonvulsants, neuroleptics, tranquilizers); treatment of paresis (energy correctors, drugs, stimulating metabolism in the brain and muscle tissues, physical therapy, physiotherapy, massage); treatment of neuroendocrine disorders (metabolic drugs, tranquilizers, desensitizing drugs, neuroleptics).

Prognosis and prevention

Possible outcomes of the disease are recovery, vegetative state, gross focal symptoms. Possible complications are cerebral edema, brain dislocation, cerebral coma, epileptic syndrome, cystic. Preventive measures that can possibly prevent infection with tick-borne and mosquito-borne encephalitis are preventive vaccination of people living and/or working in areas of possible infection. The standard vaccination against tick-borne encephalitis includes 3 vaccinations and gives a stable immunity for 3 years. Prevention of secondary encephalitis implies timely diagnosis and adequate therapy of infectious diseases.