Encephalitis - causes, signs, symptoms, treatment and consequences for humans. Acute necrotizing encephalitis

Encephalitis is a class of inflammatory disease of the brain (CNS - central nervous system humans) that are caused by certain viruses.

The provocateurs of encephalitis are mainly viruses (measles, rubella, groups of herpes viruses, enteroviruses). You can also add tuberculosis microbes, meningococci, streptococci, microbacteria and protozoan microorganisms.

Severe necrotizing encephalitis, is largely due to the neurotropism of the pathogens. The impact of viruses on the body, possibly food or by airborne droplets, as well as a tick or mosquito bite, as a result of which, if the blood-brain barrier is broken, they penetrate into the central nervous system.

In case of penetration of the encephalitis virus into the body, the following stages are distinguished:

1. The virus is a scavenger on the cell membrane receptor.

2. Maturation of virus particles in the cells of a parenchymal organ.

3. The development of chronic viral pathology, where viral particles are released into the blood. The basis of the effect is the interaction of the viral antigen with the human immune system.

It should be noted that cell damage may occur during development acute infection, as well as the safety of the cell without violations or distortion of genetic codes. During the pathogenesis of encephalitis, swelling and swelling of the brain occurs, which leads to disruption of the functioning of the brain stem, with damage important structures body. Moreover allergic reaction organism - a concomitant factor in most encephalitis.

Encephalitis is classified as:

1. Primary encephalitis, where the pathogen penetrates the central nervous system, further damaging it.

2. Secondary (severe necrotizing encephalitis), where diffuse damage to the gray matter of the central nervous system and leukoencephalitic damage to the white matter usually occurs.

Main symptoms of the disease:

1. Headache in the forehead and eyes.

2. Photophobia.

3. Epileptic seizure.

4. Lethargy and drowsiness.

5. Malaise.

6. Nausea.

7. Temperature.

8. Loose stools.

9. Cramps.

Severe necrotizing encephalitis causes focal damage to the central nervous system, paralysis of the limbs, aphasia, stiff neck, possible herpetic rashes, and subsequently coma. Trepanation of the skull in in this case, shows many necrotic brain lesions.

Symptomatic therapy in the treatment of encephalitis:

1. Antipyretic drugs.

2. Anti-inflammatory drugs (glucocorticoids).

3. Anticonvulsant therapy (difenin, finlepsin, benzonal).

4. Detoxification therapy (protein preparations, saline solutions, plasma substitutes).

5. Resuscitation measures(cardiotropic drugs, mechanical ventilation).

6. Prevention of secondary bacterial complications (broad-spectrum antibiotics).

It is the most common (20% of all viral encephalitis) and the most severe form of sporadic acute encephalitis. Prevalence - from 0.3 to 1.8 per 100,000 population per year (according to other sources - 2-4 per 1,000,000). The causative agent is most often the DNA genomic herpes simplex virus type 1 (HSV-1), which also causes herpetic lesions oral mucosa and various diseases CNS. Less commonly, DNA genomic herpes virus 2 (HSV-2), which causes rashes in the genital area and is sexually transmitted; It is this that causes encephalitis in some newborns; they become infected from a sick mother after rupture of the membranes or during childbirth.

Herpes viruses multiply in the nucleus of neurons of the sympathetic and sensory ganglia, then go into a latent state and remain there during life, periodically leading to relapses herpetic infection in persons with temporary or persistent immunodeficiency of various origins ( poor nutrition, drugs, alcohol, AIDS, heredity, etc.). In the postnatal period, infection can occur through contact with persons who have an exacerbation of cutaneous herpes.

In the first 10 years, the most widespread infection of children with herpes viruses occurs (70–80% of cases). The development of encephalitis is possible during primary infection with HSV (30%) or due to activation of a persistent AI virus (70%). The virus enters the brain hematogenously and through the perineural tract cranial nerves.

When a disease occurs in the brain, pronounced edema, single or multiple foci of hemorrhage, softening, perivascular lymphocytic infiltration and liquefaction necrosis, mainly in the temporal and frontal lobes brain and underlying white matter. Edema can lead to dislocation and herniation of brain structures, in particular, infringement of the uncus of the hippocampal gyrus or brain stem, which is a common cause fatal outcome. In subacute and chronic GE, along with fresh areas of necrosis with perifocal and perivascular infiltration, cystic cavities and foci of gliosis are found.

The incubation period of GE lasts from 2 to 26 days, more often – 9–14 days. Symptoms of HE in newborns appear at 2–4 weeks of life, and with generalized herpetic infection - in the first 10 days after birth. When the infection generalizes, both the brain and other organs are affected, and jaundice, collapse, and shock are possible. GE often develops against the background of ARVI, influenza, aphthous stomatitis, laryngotracheitis, gastrointestinal diseases. In children, especially newborns, typical herpetic rashes on the skin and mucous membranes (in adults - in 10–15% of cases). There are 4 stages of GE: early, culminating, reverse development and residual phenomena.

The disease begins acutely, less often - subacutely, with a rise in body temperature to 39–40°C (sometimes low-grade fever), headache, general weakness, vomiting. The febrile period lasts up to several weeks, sometimes it is fleeting or even absent. Sometimes there are two febrile waves separated by a “clear” interval, with focal neurological symptoms occurring during the second wave. Neurological and psychiatric symptoms may develop acutely or gradually.

Its nature depends on the predominant localization of the lesion in the temporal or frontal lobe. Violations of higher brain functions (motor, sensory, amnestic and other forms of aphasia), amnesia, agnosia, apraxia, behavioral disorders, pathology of smell and taste (anosmia, olfactory and gustatory hallucinations), confusion, depression of consciousness (up to coma) are observed. hemiparesis, hemianopsia, cranial nerve lesions, autonomic disorders, complex partials epileptic seizures. Often already at early stage generalized epileptic seizures occur, possible development status epilepticus(with seizures different types). In most cases, it is detected meningeal symptoms, sometimes stagnant discs are detected optic nerves, herpetic rashes on the lips. It should be noted: herpes labialis can occur in any febrile state, not only with GE.

Without treatment, the condition steadily worsens, coma develops, and death occurs in 50–70% of cases. Death can occur in the first 24–72 hours of illness due to swelling and herniation of the brain due to respiratory arrest, cardiac activity, and destruction of other vital centers of the brainstem. For example, in the USA, 5,000 cases of HE are registered annually, with 1/3 of patients dying, and 1/3 of patients developing persistent neuropsychiatric disorders.

IN last years describe atypical forms of GE with erased subacutely developing symptoms, with predominant defeat brain stem (brainstem encephalitis, as well as forms simulating acute psychiatric pathology, in particular delirious stupefaction). A recurrent form of GE with exacerbations 2–10 years after the next remission is rare. Occurs in middle-aged and elderly people chronic form GE with gradual increase neuropsychiatric disorders and mnestic-intellectual decline.

The stage of residual phenomena is formed within 1–2 years or more after the end of the manifest stage of HE.

Diagnosis. When examining the cerebrospinal fluid, increased pressure, lymphocytic or lymphocytic-neutrophilic pleocytosis (on average 50–100, sometimes up to 1000 cells per 1 μl), a moderate increase in protein concentration, are detected. normal content glucose (in 25% of cases the glucose level is reduced, this creates certain difficulties in differential diagnosis with tuberculous or fungal meningitis). In more than 40% of patients, red blood cells and xanthochromia are found in the cerebrospinal fluid - an indication of the hemorrhagic nature of the lesion. In 5–10% of cases, during the first examination of the cerebrospinal fluid, no changes are detected in it.

On the EEG against the background of diffuse slowing electrical activity In 85% of patients, focal changes are recorded in the anterior parts of the brain (frontotemporal region) in the form of slow-wave activity or periodic high-amplitude epileptiform discharges. At the beginning of the disease, they can be in one hemisphere, but later they are detected on both sides.

CT scan may not detect changes in the first 3–5 days. Later, most patients develop lesions low density with mass effect, primarily in the frontotemporal region, cingulate gyrus, insular zone on one or both sides. Sometimes hyperdense (superdense) areas of hemorrhage are found. Lesions may accumulate peripheral contrast, reflecting disruption of the blood-brain barrier.

MRI allows you to identify focal hyperintense zones in T2 mode at a time when they are not yet visible on CT; in the first two days they may not be visible even on MRI (but with a brain abscess, tumor, subdural empyema, they are detected very early).

Due to the widespread prevalence of herpes infection, the detection of specific antibodies does not have of great importance(even with a high titer). The results of the study of paired sera become too late (on the 10th–12th day). The fastest and most reliable method for recognizing HE is now polymerase chain reaction. It becomes positive already on the 1st day after appearance neurological symptoms. The probability of error during PCR does not exceed 5%.

Therapy. Usually performed in a department setting intensive care. The drug of choice is acyclovir (Virolex, Zovirax), which selectively inhibits viral DNA synthesis. The main condition for the success of treatment is its early start (at least before the development of stupor or coma). Treatment with acyclovir is recommended to begin at the slightest suspicion of the herpetic nature of encephalitis, i.e. in almost every case of severe encephalitis. Only after eliminating the possibility of GE, treatment with acyclovir is stopped and another one is prescribed, corresponding to the etiology of the disease. Acyclovir is administered intravenously in a single dose of 10 mg/kg 3 times a day, slowly over at least 1 hour (to prevent precipitation of the drug in the renal tubules). The course of treatment is at least 10–14 days.

Pathogenetic and symptomatic therapy aimed at maintaining respiratory functions and cardiovascular activity, water and electrolyte balance, prevention and treatment of secondary bacterial and trophic complications ( aspiration pneumonia, bedsores, urinary infection), thrombosis of deep veins of the leg. To reduce ICH, osmodiuretics and mechanical ventilation in hyperventilation mode are prescribed, especially severe cases– barbiturates. Corticoids do not significantly reduce ICP in GE, and their administration is believed to be of little value. In the presence of seizures, as well as for their prevention (when paroxysmal island-wave activity appears on the EEG), anticonvulsants are prescribed.

Very important early start rehabilitation activities.

Forecast. The use of acyclovir reduces mortality to 28%, and among surviving patients increases from 5 to 28% the proportion of those who recover completely or with minor residual neuropsychiatric disorders. Approximately half of the patients develop a persistent residual defect in the form of amnesia, aphasia, dementia, personality changes, epilepsy, and other mental and neurological disorders.

Encephalitis is a group of inflammatory diseases of the brain substance that are infectious, allergic or toxic in nature. If a patient is diagnosed with a disease, he should be hospitalized immediately. In case of encephalitis, a person is placed in an infectious diseases or specialized neurological department and is prescribed the strictest bed rest and constant surveillance.

What is encephalitis

Encephalitis (lat. encephalitis - inflammation of the brain) is the name the whole group inflammatory processes, affecting the human brain, appearing against the background of exposure infectious agents and allergic agents, toxic substances.

Changes in nerve tissue with encephalitis they are quite stereotypical, and only in some cases can signs of a specific disease be detected (rabies, for example). The significance for the body and the consequences of any inflammatory changes in the brain are always serious, so there is no need to once again remind us of their danger.

IN acute stage in the substance of the brain it causes an inflammatory process, affecting the hypothalamus, basal ganglia, nuclei oculomotor nerves. IN chronic stage a toxic-degenerative process develops, most pronounced in the substantia nigra and globus pallidus.

The incubation period for encephalitis ranges from one to two weeks.

In case of encephalitis of any etiology, it is necessary complex therapy. As a rule, it includes etiotropic treatment (antiviral, antibacterial, antiallergic), dehydration, infusion therapy, anti-inflammatory treatment, vascular and neuroprotective therapy, symptomatic treatment.

Classification

The classification of encephalitis reflects etiological factors related to them clinical manifestations and flow features.

Depending on the presence of inflammation of the meningeal membranes (linings of the brain), the following forms of encephalitis are distinguished:

• isolated - in the clinic there are symptoms only of encephalitis;
• meningoencephalitis - symptoms of inflammation of the meninges are also present in the clinic.

By localization:

• cortical;
• subcortical;
• stem;
• cerebellar damage.

According to the pace of development and flow:

• fast;
• spicy;
• subacute;
• chronic;
• recurrent.

By severity:

• moderate severity;
• heavy;
• extremely heavy.

Causes

Most often, encephalitis is caused by viruses - neuroinfections; sometimes it also occurs as complications of various infectious diseases.

A common cause of progression is neuroinfection. It is worth noting that the etiology of the disease directly depends on its type. Thus, the reasons for the progression of viral encephalitis are: the bite of infected insects (usually carried by mosquitoes or ticks), the penetration of influenza, herpes, and rabies viruses into the body.

Ways the virus enters the human body:

• insect bite (hematogenous route);
• with direct contact;
• nutritional route;
• airborne route.

Anyone can develop the disease, but older people and children are at greatest risk. People whose immune systems are suppressed or weakened by other factors, such as cancer treatment, HIV infection, or long-term use of steroids, are also prone to the disease.

Symptoms of encephalitis

The disease usually begins with fever and headache, then the symptoms increase sharply and worsen - convulsions (fits), confusion and loss of consciousness, drowsiness and even coma are observed. Encephalitis can be seriously life-threatening.

Symptoms of encephalitis depend on many factors: the causative agent of the disease, its pathology, course and localization.

The disease in many situations manifests itself as aches and pain. At the same time, these unpleasant symptoms affect the whole body: joints, muscles.

However, there are symptoms common to all types of encephalitis:

• headache - it is most often expressed in all areas of the head (diffuse), can be pressing, bursting;
• nausea and vomiting that does not bring relief;
• torticollis, tremor, seizures;
• The main symptom of encephalitis is sudden jump temperatures up to high values ​​(39–40°C);
• oculomotor disorders: ptosis (drooping of the upper eyelid), diplopia (double vision), ophthalmoplegia (lack of eyeball movements);
• Defeat is rarely possible facial nerve with the development of paresis of facial muscles, trigeminal nerve with pain in the face, isolated convulsions are possible.

Depending on the type of pathogen, the time interval between infection and the appearance of the first symptoms lasts from 7 to 20 days. During the latent period, the infection does not reveal itself; the presence of the pathogen can only be detected in a laboratory setting.

Other possible signs of encephalitis:

• increased muscle tone;
• involuntary movements (hyperkinesis);
• strabismus, impaired movements of the eyeballs (ophthalmoparesis);
• diplopia (double vision);
• ptosis (drooping) of the upper eyelid;

Another characteristic feature- These are muscle twitches in humans. These twitches occur involuntarily. It is important to note that sometimes a person is bothered by numbness of the skin, which manifests itself in different parts bodies.

Types of encephalitis

Despite all the variety of causes and types, its manifestations are quite stereotypical when severe course disease, but if inflammation of the nervous tissue accompanies other ailments, then recognizing encephalitis as such is not so easy.

Epidemic encephalitis Economo(lethargic encephalitis A)

The causative agent is a filterable virus that has not been isolated to date. This type of virus is transmitted by airborne droplets.

Signs of developing epidemic encephalitis:

• temperature rise to 38-39 degrees;
• chills;
• increased drowsiness;
• fatigue;
• lack of appetite;
• headache.

In this case, urgent hospitalization is necessary. Exact duration unknown incubation period, therefore, everyone who has been in contact with a sick person should be under observation for three months.

Tick-borne encephalitis

Herpetic

Herpetic encephalitis is caused by the herpes simplex virus. The cortex and white matter big brain. A necrotic process occurs (focal or widespread).

Polyseasonal

Multiseasonal encephalitis is usually caused by ECHO. The disease can develop at any time of the year, is manifested by headache, moderate fever, paresis may develop for a short time (partially impaired motor function individual muscles).

Toxoplasmosis

Toxoplasmosis encephalitis is a leading cause of morbidity and mortality in patients with AIDS. The gateway of infection is often the digestive organs, although there are known cases of intra-laboratory infections with highly virulent strains of Toxoplasma when the skin is damaged (with a pipette or syringe with a Toxoplasma culture). TO frequent signs include: chills, fever, headache, seizures, depression and neurological disorders.

Japanese (encephalitis B)

This type of encephalitis is especially common in Asian countries. The reservoir and source of infection are wild and domestic animals, birds, and rodents. Animals carry the infection in a latent form with rapid elimination of the pathogen from the blood. A sick person, if there are carriers, can also be a source of infection.

In general, Japanese encephalitis is diagnosed very rarely; there have never been epidemics. The onset of the disease is characterized by elevated temperature body, headaches and chills.

Complications and consequences for humans

The consequences of encephalitis are very severe - the inflammatory process affects the central nervous system, which can lead to disability of the patient.

The main complications of encephalitis:

• cerebral edema;
• cerebral coma;
• development of epilepsy;
• lifelong carriage of the virus;
• impaired vision, speech, hearing;
• memory impairment;
• flaccid paralysis;
• cystosis;
• mental disorders;
• risk of death.

Encephalitis poses a danger to full life patient, it can cause not only disability, but also death of the patient.

Diagnostics

To diagnose encephalitis, it is carried out spinal tap. To clarify the diagnosis and differential diagnosis, the fundus of the eye is examined, electroencephalography, echoencephalography, tomography, etc. are performed. Once the diagnosis is established, the patient must be hospitalized in the infectious diseases or neurological department.

Also needed:

• general and biochemical tests blood tests, urine tests,
• blood culture for sterility,
• puncture with obtaining cerebrospinal fluid,
• conducting REG or EEG, fundus examination,
• carrying out CT or MRI,
• if necessary, a biopsy is performed.

Treatment of encephalitis

An infectious disease doctor diagnoses and treats the disease in children and adults. If the diagnosis has been confirmed, the patient is immediately admitted to a hospital, infectious diseases department. Strict bed rest is indicated. The patient's condition is constantly monitored.

When treating encephalitis, specialists may be faced with the need to restore proper metabolism within the brain. For this purpose, the use of special vitamins, piracetam or polypeptides is prescribed. Among the anti-inflammatory drugs, salicylates and ibuprofen are often prescribed.

Symptomatic therapy:

• Antipyretic drugs
• Anti-inflammatory (glucocorticoids)
• Anticonvulsant therapy (benzonal, difenin, finlepsin)
• Detoxification therapy (saline solutions, protein preparations, plasma substitutes)
• Resuscitation measures (ventilation, cardiotropic drugs)
• Secondary warning bacterial complications(broad spectrum antibiotics)

To restore the normal functioning of the nervous system and rehabilitate consciousness, all kinds of biostimulants, antidepressants or tranquilizers are prescribed.

If the disease leads to impairment respiratory function, then carry out artificial ventilation lungs. In addition, they are appointed anticonvulsants and analgesics.

Vaccines are the most effective way to reduce the risk of developing the disease. Wherein we're talking about not only about vaccinations tick-borne encephalitis, but also about the prevention of pathologies such as measles, etc.

Therefore, you should not neglect vaccination (vaccination) against certain types of encephalitis when traveling to areas with unfavorable conditions for this disease.

All encephalitis is treated in infectious diseases hospitals. In the chronic stage, it is necessary to regularly visit a neurologist, as well as take courses of medications aimed at improving brain activity and restoring ataxic and motor defects.

Prevention

Preventive measures taken to prevent different types of encephalitis differ and are represented by the following activities:

1. Preventive measures that can, if possible, prevent infection with tick-borne and mosquito-borne encephalitis are preventive vaccination people living and/or working in the zones possible infection. Standard vaccination against tick-borne encephalitis includes 3 vaccinations and provides lasting immunity for 3 years.
2. Prevention of secondary encephalitis involves timely diagnosis and adequate treatment of infectious diseases.
3. Limiting tourist travel to countries where infection with viral encephalitis through mosquito bites is possible.

001.Acute necrotizing encephalitis is caused by viruses

a) Coxsackie

V b) herpes simplex

d) mumps

002. Treatment of mumps meningitis includes all of the following except

a) corticosteroids

V b) deoxyribonuclease

c) trypsin

d) ascorbic acid

e) glycerol

003. The development of Waterhouse-Friderichsen syndrome (acute adrenal insufficiency) is typical for severe cases

a) staphylococcal meningitis

b) pneumococcal meningitis

c) meningitis caused by the Coxsackie virus

V d) meningococcal meningitis

e) lymphocytic choriomeningitis

004.K rare syndromes Economo's encephalitis is classified as

a) oculomotor disorders

V b) pathological foot signs

c) sleep disorders

d) autonomic disorders

005.Not typical for acute tick-borne encephalitis

b) meningoencephalitic syndrome

c) increased intracranial pressure

d) flaccid paresis and paralysis of the muscles of the shoulder girdle

e) fever at the onset of the disease

006. Viral two-wave meningoencephalitis is not characterized by the presence

a) fever

V b) atrophic spinal palsy

c) pleocytosis in the cerebrospinal fluid

d) radiculoneuritis

007. Herpetic encephalitis is not characterized by the presence

a) general cerebral symptoms and disturbances of consciousness

b) intracranial hypertension and fundus congestion

c) seizures

d) hemiparesis

V e) hemiataxia

008.When viral encephalitis not observed in the liquor

a) lymphocytic pleocytosis

b)increasing protein content

V c)increased glucose content

d) a) and b) are correct

d) true b) and c)

009.Characteristic electroencephalographic signs of focal necrotic brain damage during herpetic encephalitis are

a) diffuse decrease in wave voltage

b) the appearance of d- and q-waves

V c) the presence of peaks (spikes) and sharp waves

d) the presence of asymmetric giant waves

d) presence of sleep spindles

b) polymyalgia

c) meningeal hypertensive syndrome

d) lymphocytic pleocytosis

V d) severe course and severe residual symptoms

016. A significant decrease in sugar levels in the cerebrospinal fluid (up to 0.1 g/l) is characteristic of meningitis

a) flu

b) pneumococcal

c) mumps

V d) tuberculosis

d)syphilitic

017.If the causative agent of bacterial purulent meningitis is not identified, it is advisable to use

a) cephalexin (ceporex)

b) clindamycin (dalacin)

c) erythromycin (erythran)

V g)cefotaxime (claforan)

018.For the treatment of meningococcal meningitis, you should choose

a) clindamycin

b) tetracycline

c) erythromycin

d) kanamycin

V d) chloramphenicol

019. Subarachnoid hemorrhage as a complication of the underlying disease occurs with meningitis caused

a) pneumococcus

b) mumps virus

c) klebsiella

d) Afanasyev-Pfeiffer wand

V d)streptococcus

020.Brain abscesses as a complication of the underlying disease are more common with meningitis caused

a) Afanasiev-Pfeiffer wand

b) staphylococcus

V c) pneumococcus

d) leptospira

021.Rare pathogens of serous meningitis include

a) lymphocytic choreomeningitis virus

b) Mycobacterium tuberculosis

V c) parainfluenza virus

d) mumps virus

022. Purulent meningitis is not caused

a) staphylococci

b) meningococci

c) pneumococci

d) proteus vulgaris

V d) Leptospira

023.Acute lymphocytic choriomeningitis is not characterized by the presence

a) high fever

b) intracranial hypertension

c) cell-protein dissociation in the cerebrospinal fluid

V d) reducing the level of glucose in the cerebrospinal fluid

024. Acute (primary) disseminated encephalomyelitis is rarely accompanied by the development

a) lower spastic paraplegia

b) bulbar disorders

V c) extrapyramidal disorders

d) Brown-Séquard syndrome

025.Morphological substrate pyramidal symptoms in acute disseminated encephalomyelitis are

b) death of axial cylinders

c) myelin breakdown

d) a) and b) are correct

V e) correct b) and c)

026.Brain abscess is relatively rare complication meningitis caused

a) pneumococcus

b) staphylococcus

c) Afanasiev-Pfeiffer wand

V d)meningococcus

d) streptococcus

027. High contagiousness is characteristic of meningitis caused by

a) Pseudomonas aeruginosa

b) staphylococci

c) herpes simplex virus

V d) Coxsackie and ECHO viruses

028. Acute focal transverse myelitis at the lower thoracic level is not characterized by the presence

a) lower paraplegia

b) conduction type sensitivity disorder

c) dysfunction of the pelvic organs

V d) blockade of the subarachnoid space

029. Motor and sensory disorders in acute disseminated encephalomyelitis are caused by damage

a) brain

b) spinal cord

c) roots and peripheral nerves

d) a) and b) are correct

V d)all of the above

030.Decreased visual acuity in acute disseminated encephalomyelitis is caused by damage

a) retina

V b) optic nerve

c) the primary visual center in the external geniculate body

d) corona radiata of Graziole in the occipital lobe

e) cortical part of the visual analyzer in the occipital lobe

031. In the treatment of acute disseminated encephalomyelitis, it is used to correct autoimmune disorders

a) non-steroidal anti-inflammatory drugs

b) anabolic steroid drugs

V c) synthetic glucocorticoids

d) estrogenic steroid drugs

032.Motor disturbances during the second attack of acute epidemic anterior poliomyelitis, occurring after a “minor illness” and subsequent latent period, are characterized by the presence

a) muscle cramps

b) fibrillar twitching

c) flaccid paralysis

d) all of the above

V d) a) and b) are correct

033. Acute poliomyelitis is not characterized by damage to motor neurons

V a) cerebral cortex

b) motor nuclei of the trunk

c) cervical thickening of the spinal cord

d) thoracic spinal cord

e) lumbar enlargement of the spinal cord

034. In the cerebrospinal fluid in the second week of the paralytic stage of acute polio (unlike the first week)

a) normal glucose level

V b) protein-cell dissociation

c) normal chloride level

d) eosinophilic cytosis

035.Features of residual motor disorders after suffering from polio, they are determined

a) asymmetrical damage to the muscles of the limbs and trunk

b) growth retardation and impaired trophism of the limbs

c) violation of coordination and statics

V d) a) and b) are correct

d) a) and c) are correct

036. Differential diagnosis of the non-paralytic form of acute polio should be carried out

a) with viral serous meningitis

b) with bacterial serous meningitis

c) with acute demyelinating polyradiculoneuropathy Guillain-Barré

d) with the anterior horn form of tick-borne encephalitis

V d) with all of the above

037. Suspicion of a brain abscess arises if the disease is characterized by signs

a) increasing intracranial hypertension

b) focal cerebral lesion

c) general cerebral symptoms

d) a) and b) are correct

V d)all of the above

038. When diagnosing a brain abscess using contrast methods, you can obtain a direct image of a round-shaped pathological focus using

a) pneumoencephalography

b) ventriculography

c) angiography

V g)g-scintigraphy

e) all of the above

e) increased cerebrospinal fluid pressure

047.For neurological disorders Botulism has all the symptoms except

a) paresis of accommodation

b) paresis of the oculomotor muscles

c) dysphonia, dysphagia, dysarthria

V d) hypersalivation

e)myasthenic-like symptoms

048. The high risk of fatal polyneuropathy in diphtheria is determined by the lesion

a)bulbar cranial nerves

b) diaphragm

c) myocardium

d) a) and b) are correct

V d)all of the above

049.For the treatment of generalized painful muscle spasms and seizures in tetanus, the drug of first choice is

a) chloral hydrate

b) thiopental

c)phenobarbital

V g)seduxene

e) tubocurarine

050.For clinical picture lesions of the nervous system in acquired toxoplasmosis (toxoplasma meningoencephalitis) are not characterized by the presence

a)chorioretinitis

b) atrophy of the optic nerves

c) neurogenic deafness

V d) convulsive seizures

e) positive serological tests in high dilutions

051. All of the following findings contribute to the diagnosis of cerebral cysticercosis, except

a) detection of cysts using computed tomography in the tissue and ventricles of the brain

b) unstable syndrome of intracranial hypertension

V c) atrophy of the optic nerves and neurogenic deafness

d) aversion to fatty and sweet foods

052. Cerebral cysticercosis is characterized by pleocytosis

a) neutrophilic

b) neutrophilic-lymphocytic

c) lymphocytic-basophilic

d) lymphocytic

V d) lymphocytic-monocyte

053.Clinical and morphological features immune-dependent measles encephalitis are

a) the appearance of neurological symptoms on the 3-6th day after the appearance of the rash

b) the appearance of neurological symptoms in the 2-3rd week after the onset of the rash

c) substrate-perivenous demyelination with destruction of fibers

d) substrate-perivenous hemorrhages

V e) correct a) and c)

054. Meningoencephalitis after rabies vaccination is not characterized by the presence

a) acute onset with high fever

b) paresis of oculomotors

c) spastic paresis and paralysis

V d) choreoathetosis

e) convulsive syndrome

055.For syphilitic lesions auditory nerves typical

V a)decrease bone conduction while maintaining air

b) decrease in air conduction while maintaining bone

c) decreased bone and air conduction

d) preservation of bone and air conduction

056.Morphological substrate early forms neurosyphilis are

a) inflammatory changes in the membranes of the brain and spinal cord

b) inflammatory changes in the vessels of the central nervous system

c) degenerative changes in the parenchyma of the brain and spinal cord

d) foci of demyelination in the central nervous system

V d) a) and b) are correct

057. For damage to the optic nerves in syphilitic basal meningitis, it is characteristic

a) change in visual fields

b) color vision disturbance

V d) a) and b) are correct

058.Late forms of neurosyphilis occur in the form

a) brain gumma

b) tabes dorsalis

c) meningovascular (or vascular) syphilis

d) asymptomatic membrane damage

V d)all of the above

059. The diagnosis of neurosyphilis is confirmed using the following methods Cerebrospinal fluid examinations, with the exception of

a) Wasserman reaction with three dilutions of cerebrospinal fluid

b) colloidal Lange reaction

V c) colloidal reaction Takata - Ara

d) immobilization reactions of Treponema pallidum

060.Impaired statics and gait with tabes dorsalis is caused by

a) flaccid paralysis of the legs

b) cerebellar ataxia

V c) sensitive ataxia

d) decreased vision with tabetic atrophy of the optic nerves

e) tabetic arthropathy

061.The term “tabetic crises” in patients with tabes dorsalis refers to

a) paroxysms of tachycardia

b) blood pressure fluctuations

V c) paroxysms of tearing pain

d) episodes of profuse sweating and general weakness

d) all of the above

062.Primary tabetic atrophy of the optic nerves with tabes dorsalis is characterized by the following changes in the fundus

a) blanching of the temporal halves of the discs

b) gray color of disks

c) swelling of the discs

d) preservation of clear disc boundaries

V e) correct b) and d)

063. The morphological substrate of arachnoiditis is a chronic productive process in the arachnoid, as well as

a) in the pia mater

b) in the ependyma of the ventricles

c) in the choroid plexuses

d) a) and b) are correct

V d) all of the above

064. Plays a decisive role in the pathogenesis of symptoms of arachnoiditis

a)increased cerebrospinal fluid production

b) disturbance of cerebrospinal fluid circulation

c) impaired absorption of cerebrospinal fluid

d) a) and b) are correct

V e) correct b) and c)

065. Disturbances in the circulation of cerebrospinal fluid are most pronounced when arachnoiditis is localized

a) in the optochiasmal region

b) in the cisterns of the base of the brain

c) in the area cerebellopontine angle

d) a) and b) are correct

V e) correct b) and c)

066. Opticochiasmatic arachnoiditis is characterized by

a) decreased visual acuity

b) concentric narrowing of visual fields

c) swelling of the optic disc

V d)all of the above

e) a) and b) are correct

067. Opticochiasmatic arachnoiditis may be misdiagnosed

a) with retrobulbar neuritis

b) with neuromyelitis optica

c) with multiple sclerosis

d) with hereditary atrophy Leber's optic nerves

V d) with all of the above

068. Arachnoiditis of the posterior cranial fossa must be differentiated

a) from a tumor of the same location

b) from Arnold-Chiari syndrome

c) from Klippel-Feil syndrome

V d) from all of the above

e) a) and b) are correct

069. Arachnoiditis of the cerebellopontine angle should be differentiated

a) from neuroma of the VIII nerve

b) from arachnoidendothelioma of the posterior cranial fossa

c) from syringobulbia

d) from all of the above

V d) a) and b) are correct

070. Among the physiotherapeutic methods of treatment for cerebral arachnoiditis, the most effective

a) electrophoresis of novocaine according to Bourguignon

b) nasal electrophoresis of calcium chloride

V c) nasal electrophoresis of lecozyme

d) true b) and c)

d) a) and c) are correct

071. Acute purulent epiduritis can be a complication of such inflammatory processes as

a) abscesses and phlegmon of organs and tissues

b) osteomyelitis

c) pansinusitis

V d) a) and b) are correct

d) all of the above

072. The pathogenesis of neurological symptoms of acute epiduritis is due to

a) inflammatory-toxic influence of the focus

b) compression of the spinal cord roots

c) impaired blood circulation in the membranes

V d) a) and b) are correct

d) all of the above

073. Neurological symptoms of acute spinal epiduritis are presented

a) radicular pain

b) spinal cord compression syndrome

c) loss of consciousness

V d) a) and b) are correct

a)aminalon

b)phenibut

V c)baclofen

d) pantogam

086. Sign of deficiency cellular immunity during exacerbation multiple sclerosis is

a) T-lymphopenia

b) B-lymphocytosis

c)increase in the number of T-killers

d) all of the above

V d) a) and b) are correct

087. The phenomenon of “clinical dissociation” in multiple sclerosis is characterized by the presence

a) horizontal nystagmus in combination with the absence of abdominal reflexes

b) central paresis in the limbs and the absence of sensitivity disorders

c) sensitivity disorders of segmental or conduction type against the background lung central limb paresis

V d) central paresis in the limbs in combination with muscle hypotonia

088. When performing computed tomography diagnostics of multiple sclerosis, it should be taken into account that plaques, as a rule, are not localized

a) in the periventricular white matter

V b) in the subcortical white matter

c) in the pons of the brain

d) in the cerebellum

089. The morphological substrate for restoration of the functions of neuronal systems and clinical remission in multiple sclerosis is

a) resorption of fibrous sclerotic plaque

b) restoration of the ability to synthesize neurotransmitters in affected neurons

c) restoration of the normal circulation of neurotransmitters in interneuronal synapses

V d) periaxonal remyelination in affected neurons

090. To prevent and treat exacerbations of multiple sclerosis, it is advisable to prescribe

a) a-interferon

b) b-interferon

c) g-interferon

d) all of the above

V d) a) and b) are correct

091.In case of remission of multiple sclerosis, the use of

V a)immunostimulants

b) plasmapheresis

c) glucocorticoids

d) cytostatics

092.Argyll Robertson syndrome is called

V a) absence of pupillary reaction to light with intact reaction to convergence and accommodation

b) absence of a direct reaction to light with a preserved friendly reaction

c) lack of reaction of the pupils to convergence with intact reaction to light

d) lack of reaction to accommodation in combination with mydriasis

e) lack of reaction to convergence and accommodation in combination with anisocoria

093. Subacute sclerosing panencephalitis is not classified as a single disease

V a) Schilder's leukoencephalitis

b) subacute leukoencephalitis of Van Bogart

c) Pette-Döring nodular panencephalitis

d) encephalitis with Dawson's inclusions

094. Differential diagnosis of subacute sclerosing panencephalitis is carried out

a) with Schilder’s periaxial leukoencephalitis

b) with multiple sclerosis

c) with a brain tumor

d) true b) and c)

V d) with all of the above

095.In case of exacerbation of multiple sclerosis (T-lymphopenia, B-lymphocytosis), it is preferable to prescribe

V a) glucocorticoid drugs

b) cytostatics (azathioprine, cyclophosphamide)

c) stimulators of B-lymphocytes (propermil, zymosan, pyrogenal)

d) complex treatment with these drugs

096. The following clinical forms of Schilder’s encephalitis are distinguished:

a) psychoorganic (hallucinations, dementia)

b) paralytic (pyramidal paresis)

c) convulsive (epileptic syndrome)

d) occipito-parietal (decreased vision, visual field defects)

V d) all of the listed forms are available

097. Anti-rabies allergic post-vaccinationathy, which occurs months after vaccination, is characterized by the following symptoms, except

a) onset without general infectious signs

b) moderate damage to the central and peripheral nervous system

c) protein-cell dissociation in the cerebrospinal fluid

d) marginal swelling of the optic nerve nipples

V e) correct c) and d)

098.Decreased vision in Schilder’s periaxial encephalitis is caused by

a) atrophy of the optic nerves

b) damage to the primary visual centers

c) defeat visual pathways in the white matter of the occipital lobe

d) all of the above

V e) correct a) and c)

099.At hereditary disease Guam islands amyotrophic lateral sclerosis syndrome combined

a) with parkinsonism

b) with dementia

c) with amaurosis

d) with all of the above

V d) a) and b) are correct

100. With amyotrophic lateral sclerosis, all of the listed formations are affected, except

a) neurons of the anterior horns of the gray matter of the spinal cord

V b) neurons of the lateral horns of the gray matter of the spinal cord

c) pyramidal conductors in the lateral cords

d) nuclei of motor cranial nerves

e) neurons of the cortex of the anterior central gyrus

101. Amyotrophic lateral sclerosis with a predominant lesion of the cervical enlargement of the spinal cord must be differentiated

a) with vertebrogenic myelopathy

b) with the anterior horn form of syringomyelia

c) with intramedullary tumor

d) a) and b) are correct

V d) with all of the above

102. The clinical picture of subacute spongy Creutzfeldt-Jakob encephalopathy is not characterized by the presence

a) pyramidal syndrome

b) cerebellar ataxia

c) extrapyramidal syndrome

V d) sensitive ataxia

e) epileptiform syndrome

103. Features of dyscirculatory measles encephalopathy are due to

a) perivascular ischemic foci

b) perivascular hemorrhagic foci

c) thrombosis of cerebral veins and sinuses

d) a) and c) are correct

V e) correct b) and c)

104. The clinical picture of subacute polio in adults (Duchenne disease) includes all of the following, except

a) atrophy of the muscles of the distal limbs

b) muscle hypotonia

c) fascicular twitching

d) extinction of reflexes

V e) pathological pyramidal symptoms

105. Decisive importance in the differential diagnosis of cerebral echinococcosis from other space-occupying lesions of the brain belongs to

a) features of the clinical picture

b) computed tomography data

c) anamnestic data

V d) features of serological reactions

106.AIDS is transmitted in all of the following ways, except

a) sexual (hetero- and homosexuality)

V b) airborne

c) parenteral injections and infusions

d) organ and tissue transplantation

e) from mother to fetus (in utero)

107.The human immunodeficiency virus (HIV) has all of the following properties except

V a) high resistance to thermal influences

b) the ability to persist in the body

c) pronounced tropism for macrophages and lymphocytes

d) significant tropism for brain cells

e) long incubation period

108. The clinical picture of tabes dorsalis is characterized by all of the following, except

a) pain syndrome

b) sensitive ataxia

V c) pathological foot signs

d) decreased tendon reflexes

109. General somatic manifestations of AIDS include

a) prolonged fever and night sweats

b)diarrhea and weight loss

c) generalized lymphadenopathy

d) a) and c) are correct

V d) all of the above

110. Characteristic disorders of the immune system in AIDS, detected by laboratory means, are

a) decrease in the number of T-helpers

b) decrease in the T-helper/T-suppressor ratio

c) decrease in B-lymphocytes

V d) a) and b) are correct

d) all of the above

111. Symptoms not typical for tick-borne encephalitis:

1. “dangling head”

2. bulbar disorders

5. Kozhevnikov epilepsy

112. Symptoms not typical for the acute stage of epidemic encephalitis:

1. accommodation paresis, diplopia

4. periodic urinary incontinence

1. hypokinesia

4. bilateral ptosis

114. Symptoms not typical for mosquito encephalitis:

1. seasonality
2. epileptic seizures
3. increase in body temperature up to 40 degrees

4.meningeal symptoms

5. paralysis of accommodation
115. Symptoms not typical for acute myelitis:
1. general infectious syndrome
+2. disorder of consciousness
3. radicular pain
4. paresis of the lower extremities
5. conduction sensitivity disorders

116. Symptoms not typical for tuberculous meningitis:

2. symptoms of intoxication

3. prodromal period 2-3 weeks

4. neutrophilic pleocytosis in the cerebrospinal fluid

5. lymphocytic pleocytosis in the cerebrospinal fluid with high content squirrel

117. The basic treatment regimen for tuberculous meningitis does not include:

1. isoniazid 15 mg/kg body weight per day
2. rifampicin 600 mg per day

3. streptomycin 1g per day

118. The causative agents of primary serous meningitis include:

2. mumps virus