Encephalitis

Treatment

Pathogenetic therapy:

•    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 (prednisolone 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;
•    Antihypoxants (ethylmethylhydroxypyridine succinate, etc.);
•    Maintaining homeostasis and water and electrolyte balance (parenteral and enteral nutrition, dextrose, dextran, potassium chloride);
•    Angioprotectors (hexobendin + etamivan + etofillin, vinpocetine, pentoxifylline, etc.);
•    Treatment of cardiovascular disorders (cardiac glycosides, vasopressors, camphor, sulfocamphocaine, glucocorticoids);
•    Normalization of breathing (preservation of airway patency, hyperbaric oxygenation , oxygen therapy , if necessary, tracheostomy or intubation, mechanical ventilation;
•    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. Assign interferon alpha-2, in severe cases in combination with ribavirin. With RNA and DNA viral encephalitis, the use of tilorone is effective. Corticosteroids (methylprednisolone) are used according to the method of pulse therapy up to 10 mg/kg intravenously for 3 days.

Symptomatic therapy:

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

Rehabilitation:

Rehabilitation therapy also includes several components: treatment of parkinsonism (levodopa drugs, anticholinergics, muscle relaxants; stereotaxic operations are indicated only with an increase in rigidity and ineffectiveness of drug treatment); treatment of hyperkinesis (metabolic drugs, antipsychotics, tranquilizers); treatment of epilepsy (anticonvulsants, neuroleptics, tranquilizers); treatment of paresis (energy correctors, drugs that stimulate metabolism in the brain and muscle tissues, physiotherapy exercises , physiotherapy, massage ); treatment of neuroendocrine disorders (metabolic drugs, tranquilizers, desensitizing drugs, antipsychotics).
 

Useful info

Tick-borne encephalitis (spring-summer)

The disease is caused by a filtering neurotropic tick -borne encephalitis virus.. The carriers of the virus and its reservoir in nature are ixodid ticks. Entering the human body through a tick bite or alimentary (eating raw milk of infected cows and goats), the virus enters the nervous system hematogenously.

The duration of the incubation period of the disease that has 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. Microscopic examination of the brain and membranes reveal their hyperemia, infiltrates from poly- and mononuclear cells, mesodermal and gliosis reactions. Localization of inflammatory and degenerative changes in neurons occurs mainly in the nuclei of the medulla oblongata, the anterior horns of the cervical segments of the spinal cord, the brain bridge, and the cerebral cortex.

For the clinical picture of all forms of tick-borne encephalitis,
an acute debut is typical, manifested in the form of an increase in body temperature to 39-40 degrees, aching pain in the lower back, calves. Already in the first days of the disease, pronounced cerebral symptoms (vomiting, headache ), impaired consciousness, in some cases, mental disorders (delusions, auditory and auditory hallucinations, depression) were observed.

There are several clinical forms of tick-borne encephalitis, their difference lies in the predominance and severity of certain neurological symptoms.:

•    Polio;
•    Meningeal;
•    Encephalitic;
•    Feverish;
•    Polyradiculoneuritic;
•    Two-wave viral meningoencephalitis .
In diagnosing tick-borne encephalitis, 
Anamnesis data (stay in an endemic focus, tick bite, patient's profession, consumption 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 fixation reactions, neutralization and inhibition of hemagglutination. Of certain diagnostic value is the isolation of the virus in the blood and cerebrospinal fluid; in the blood, an increase in ESR, leukocytosis is determined, and in the study of cerebrospinal fluid - lymphocytic pleocytosis and an increase in protein up to 1 g / l. 

Tick-borne encephalitis must be differentiated from typhus , various forms of serous meningitis ,acute poliomyelitis .

2.    Japanese mosquito encephalitis

The disease is caused by a neurotropic virus, which is carried by 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, and intense headache. In addition, the clinical picture of Japanese mosquito encephalitis is characterized by a significant severity of general infectious symptoms ( tachycardia , bradycardia , facial flushing, herpetic eruptions , 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 there is an increase in symptoms, high body temperature persists for 10-14 days and decreases lytically. The lethal outcome most often (up to 70% of cases) is observed in the first week of the disease. The onset of death is also possible in the later stages of the disease, as a result of associated complications (for example, pulmonary edema ). Of great importance for the diagnosis of Japanese mosquito encephalitis are the seasonality of the disease and epidemiological data. Verification of the diagnosis is carried out using complement fixation and neutralization reactions, antibodies are determined already in the second week of the disease.

3.    Economo epidemic lethargic encephalitis (encephalitis A)

The disease is slightly contagious, currently it does not occur in a typical form. The causative agent of epidemic encephalitis Ekonomo has not been found to this day. Clinically and pathomorphologically, the disease can be divided into two stages - acute, which has an inflammatory nature, and chronic, for which a progressively 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, and a feeling 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 Economo epidemic encephalitis, are often observed in the acute stage of the disease. They can manifest themselves in the form of hyperkinesis ( athetosis , gaze spasm, choreoathetosis) and akinetic-rigid syndrome (amimia, akinesis, muscle rigidity).

In some cases, the acute stage of Economo epidemic encephalitis may be accompanied by severe 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 in the cerebrospinal fluid in most patients, pleocytosis (mostly lymphocytic), a slight increase in glucose and protein levels are detected; in the blood - an increased level of lymphocytes, eosinophils. The acute stage of Economo epidemic encephalitis 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 residual symptoms (persistent insomnia , depression , mild ptosis, convergence insufficiency).

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

Diagnosis of epidemic encephalitis in the acute stage is quite difficult. During this period, diagnosis can be based only on various forms of sleep disturbance, 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 the background of elevated body temperature. Diagnosis of the chronic stage of Economo epidemic encephalitis is less difficult and is based on the characteristic syndrome of parkinsonism , endocrine disorders of central origin, and mental changes.

Secondary encephalitis:

1.    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 are dyscirculatory phenomena in the brain and neurotoxicosis. Damage to the nervous system is inevitable with any form of influenza, when they manifest themselves as headaches, muscle pains, drowsiness, weakness, etc. 

However, in the case of the development of influenza encephalitis, the patient's state of health deteriorates sharply, there are cerebral symptoms (dizziness, vomiting). In the cerebrospinal fluid, a moderate increase in protein and a slight pleocytosis are found (during a lumbar puncture , the cerebrospinal fluid flows out under high 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 cerebrospinal fluid. The course of this form of influenza encephalitis is extremely severe, so death occurs quite often, and in the case of a positive outcome of the disease, pronounced neurological disorders persist.

2.    Measles encephalitis

Refers to infectious-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 returned to normal, its new sharp rise to 39-40 degrees is noted. In most cases, there are severe disorders of consciousness , hallucinations, psychomotor agitation , generalized convulsions, coordination disorders, hyperkinesis, paresis of the limbs and dysfunction of the pelvic organs. In the study of cerebrospinal fluid, an increased content of protein, pleocytosis is determined. The course of measles encephalitis is extremely severe, mortality reaches 25%.

3.    Post-vaccination encephalitis

May occur after the introduction of DTP and DTP vaccines , with anti-rabies vaccinations, and also after the 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 convulsions. The defeat of the extrapyramidal system is accompanied by the appearance of hyperkinesis and impaired coordination of movement.

In the study of cerebrospinal fluid (flows out under high pressure), a small lymphocytic cytosis and a slight increase in the level of protein and glucose are determined. A feature of the course of encephalitis with anti-rabies vaccinations is the onset of the disease in the form of acute encephalomyelopolyradiculoneuritis, sometimes rapidly progressing, capable of leading to death as a result of bulbar disorders.