What is tuberculous meningitis. Diagnosis and treatment of neurological manifestations of neuroAIDS Meningitis HIV hepatitis compatible with life

Tuberculous meningitis in children is diagnosed more often as a primary disease, while tuberculous meningitis in adults is a complication of pulmonary tuberculosis.

About pathology

What is tuberculous meningitis? This is an extrapulmonary form of tuberculosis that affects the brain. In other words, meningitis tuberculosis.. It was first identified in 1893. Until recently, it was believed that this type of disease prevails in children and adolescents, but at present, the incidence rate between this age group and adults is almost the same.

Tuberculous meningoencephalitis is more often detected in HIV-infected people (human immunodeficiency virus). Tuberculous meningitis in HIV infection is extremely dangerous.

In addition, the risk group includes:

• frail, retarded children or adults with hypotension;
• drug addicts, alcoholics and people with other similar addictions;
• old men;
• people with other causes of weakened immunity.

In 90% of cases of infection with tuberculous meningitis, the secondary nature of the pathology is diagnosed. The primary focus in 80 cases out of 100 is found in the lungs. If the root cause of tuberculous meningitis is not identified, then it is called isolated.

So, what is it: the spread of Mycobacterium tuberculosis through the blood into the nervous system and structures adjacent to the brain. The causative agent of the disease is strains of tuberculosis bacilli (74 species are known in total, but only a few of them affect humans). Bacteria are highly resistant to external factors and capable of transformation.

How tuberculous meningitis is transmitted: alimentary (fecal-oral) and airborne. The bovine strain is more likely to affect people in rural areas, farm workers. Avian - people with immunodeficiency. The entire population is affected by the human strain.

Which doctors should be contacted: phthisiatrician, pulmonologist, neurologist, pediatrician. The heterogeneity of medical care is due to what happens inside the body during tuberculous meningitis. Tuberculosis is a problem for phthisiatricians and pulmonologists, but neurological disorders are a problem for neurologists, sometimes psychiatrists.

Why the disease develops: penetrating into any organ, the sticks cause a “cold” inflammation that looks like granules. Outwardly, it resembles tubercles. They break up periodically. The disease develops under the condition that phagocytes cannot cope with the pathogen. Meningitis affects the structures and vessels of the brain.

There are some features of the disease in children and adults. Tuberculous meningitis in children and adolescents, as a rule, has a primary character and occurs against the background of generalization of the infection. In some cases, it is a consequence of tuberculosis of the intrathoracic lymph nodes. In early childhood, the disease is extremely difficult. This is due to the weakness of children's immunity and the low density of the barrier between blood and organ tissues.

The weakness of the child's body and the maximum predisposition to infection with dangerous forms of tuberculosis, their rapid progress, which often ends in the death of the child, is the main reason why pediatricians strongly recommend BCG vaccination (BCG-M). It is recommended to vaccinate against tuberculosis during the first month of a child's life.

Despite the severity and rapid progress of the pathology, the clinic of the disease is blurred. In children, swelling of the fontanel is often noted. They are more susceptible to the formation of fluid in the brain. The diagnostic results and methods are the same as in adults.

In adults, the onset of the disease is usually mild. In this age group, meningitis of tuberculous etiology is generally recorded much less frequently. Has a secondary character.

The reasons

The cause of tuberculous meningitis is the penetration of the pathogen (Koch's sticks) into the cortical structures of the brain.

The pathogenesis of the disease originates in the organ-focus of tuberculosis, with blood, mycobacteria penetrate into the choroid plexuses of the pia mater of the brain. Then into the spinal fluid, which causes leptomeningitis. After this, the lesion moves to the base of the brain, called basilar meningitis. Further, the tuberculosis infection spreads to the hemispheres, from them to the gray matter (meningoencephalitis).

Tuberculous meningitis at the cellular level what it is: inflammation of the serous and fibrous tissue with the formation of growths, blockage or atrophy of cerebral vessels, local damage to the gray matter, elements of tissue fusion and scarring, formation and stagnation of fluid (more often in childhood).

Symptoms

Tuberculous meningitis: the symptoms go through several stages in their development. Symptoms of tuberculous meningitis depend on the degree of spread and development of the disease.

1. prodromal stage. Duration - 7-14 days. This is the distinctive period of tuberculous meningitis. For other meningitis, the symptoms of this period are not typical. There is irritability and apathy, in the evenings - a headache. The person feels that “something is not right”. Gradually, cephalgia intensifies, becomes permanent. There is nausea and vomiting. The temperature rises (within degrees). The clinical picture at this stage is unclear, therefore it is extremely difficult to suspect tuberculous meningitis.
2. stage of irritation. Lasts another 8-14 days. A sharp increase in symptoms. The temperature rises to 39 degrees. There is a hypersensitive reaction to external stimuli (light, sound, tactile contact). Periodically, red rashes on the skin appear and disappear (violation of the autonomic function). There is a noticeable weakening and clouding of consciousness. Symptoms characteristic of any meningitis are noted: neck tension, Brudzinsky and Kerning reactions. They grow gradually. By the end of the period, the patient's condition worsens greatly. Often the patient takes a supine position with the head thrown back and the limbs tucked to the chest.
3. Terminal stage (15-24 days of illness). Destruction of the main nervous processes is manifested by convulsions, paralysis and sensory, respiratory and cardiac disorders. The temperature is either very high (up to 41 degrees) or low. Without adequate care at this stage, the situation will end in death due to paralysis of the brain stem.

As mentioned above, meningitis with tuberculosis develops gradually, penetrating into ever deeper layers of the brain. Within the framework of which, based on the mechanism of development of meningitis, three clinical forms of the disease are distinguished: basilar type, meningoencephalitis, spinal type.

The first type develops gradually. The first stage can last up to four weeks. In the second stage, anorexia and gushing vomiting occur. As the disease progresses, the work of the visual and auditory analyzer is disrupted. There is strabismus, omission of the eyelid, asymmetry of the face. By the end of the period, bulbar disturbances are formed. The third stage is coming.

Meningoencephalitis occurs, as a rule, at the third stage of meningitis development. There is a rapid inhibition of all functions and systems of the body. There are spasms, paralysis, rapid and irregular heartbeat, bedsores.

Spinal cord injury is rare. It is manifested by pain, covering like a hoop. In the later stages, it is resistant even to narcotic painkillers. The excretory function is disturbed, disturbances occur during urination and defecation.

The near-death state is characterized by fever (41-42 degrees) or, conversely, hypothermia (35 degrees), tachycardia (beats per minute), arrhythmia, breathing problems (Cheyne-Stokes syndrome). There comes such a state of putting on the course of the disease without treatment or with an incorrectly selected therapy regimen.

Diagnostics

Diagnosis is carried out jointly by a phthisiatrician and a neurologist. It is important to separate pathology from similar diseases, classical meningitis and to differentiate the specific type of disease present. The complexity of diagnosis lies in the non-specificity of symptoms. The main method is lumbar puncture.

1. Spinal fluid (10-12 ml) is taken for analysis. Laboratory research is effective even at the first stage of the disease. Increased pressure is noted (fluid flows out actively). The number of cells per cubic millimeter changes. Normally - three to five units. In case of illness, the figure can reach 600. Chloride and glucose are reduced by 90%. The protein is increased (0.8-2 g/l instead of the normal 0.15-0.45 g/l).
2. Cobweb-like fibrinous film, formed by settling during the afternoon of the day of serum in a test tube.
3. Pandey and Nonne-Apelt syndrome is noted.
4. An increased concentration of protein is detected.
5. It is possible to identify mycobacteria in the liquid in 5-10 cases out of 100. But when working with a fast centrifuge, the percentage approaches 90.

With meningoencephalitis, all indicators are more pronounced, but the number of cells, on the contrary, is less. With the spinal type of pathology, the fluid has a yellow tint, the changes are mild. To differentiate the diagnosis, computed and magnetic resonance imaging of the head is performed.

Diagnostics carried out in the first days from the moment of infection is considered timely. The next step is late diagnosis. But due to the difficulty of detecting the disease in a timely manner, this happens only in 20-25% of cases.

Clinical signs that make it possible to suspect the process are previous tuberculosis, severe intoxication, dysfunction of the pelvic organs (problems with urination and defecation), an even inverted abdomen (a consequence of muscle spasm), impaired consciousness and other consequences of depression of the central nervous system, headaches, migraine, dizziness , nosebleed (sometimes), other clinical symptoms, modified spinal fluid.

When diagnosing, the entire body is examined, a possible primary form of tuberculosis is detected and a complete picture of the existing pathology is compiled. The state of the lymph nodes is assessed, an x-ray of the lungs for a miliary type of disease, an ultrasound examination of the liver and spleen (they are enlarged with meningitis). From the bottom of the eye, choroidal tuberculosis can be detected. Tuberculin test is usually negative.

Treatment of tuberculous meningitis

To eliminate tuberculous meningitis, treatment with first-line anti-tuberculosis drugs (Isoniazid, Rifampicin, Ethambutol, Pyrazinamide) is prescribed.

With the spinal type, drugs are injected directly into the subarachnoid space. At advanced stages of the disease, therapy is supplemented by the use of steroid hormones.

The treatment regimen is selected individually in accordance with the age of the patient and the nature of the disease. If the reception of funds from the main group is not available, then they are replaced by secondary ones. For example, instead of Streptomycin - Kanamycin for children and Viomycin for adults. Instead of Ethambutol and Rifampicin - Para-aminosalicylic acid (PAS), Ethionamide, Prothionamide.

At the time of treatment, a sparing regimen is shown. The first couple of months - strictly bed. Then you are allowed to get up and walk. Monitoring the effectiveness of therapy is carried out using a laboratory study of the spinal fluid.

It is important to follow the basic principles of treatment of tuberculous meningitis (consistency, rest, complexity). From the fifth month of therapy, the inclusion of therapeutic exercises, massage and physiotherapy is indicated.

Treatment of meningitis in children is supplemented by taking Prednisolone (an anti-inflammatory drug) at a dosage of 0.5 mg per kilogram of body weight, once a day. It is taken in the first three months of therapy. At the same time, immunomodulators and vitamin complexes are introduced. To reduce intoxication (including from anti-tuberculosis drugs) - diuretics.

After the main course of therapy, a sanatorium rest is indicated, upon returning from which the patient is observed in the hospital for several more months. First, he is assigned the first accounting group, then the second and third, then they are completely discharged.

In addition to treatment and observation by a phthisiatrician, a course of rehabilitation by an ophthalmologist, speech therapist (if necessary), and a neurologist is indicated. Not the last role is occupied by the social and psychological assistance service.

Prevention and prognosis

After the problem is eliminated, the patient must undergo scheduled diagnostics annually. In the first three years, regular preventive treatment (twice a year for two months) is shown, aimed at preventing relapses and complications.

The consequences of tuberculous meningitis include:

• death (if untreated, inevitable);
• relapse (with late or incorrect treatment, its interruption);
• epilepsy;
• neuroendocrine disorders.

With timely and adequate treatment, a positive outcome is diagnosed in 95% of patients. With late detection of the disease and a prolonged initiation of therapy, the prognosis is less favorable, the risk of developing the consequences of the disease is higher.

As part of the prevention of the development of the disease, it is necessary to undergo an annual examination for tuberculosis (Mantoux, diaskintest, fluorography, x-ray, blood test), children should be vaccinated against tuberculosis infection (BCG) in a timely manner. It is important to select risk groups in time and isolate the infected.

The spread of tuberculosis is influenced by such factors as socio-economic conditions, the level and quality of life, the percentage of migrants, prisoners, the homeless and other disadvantaged groups of the population.

According to statistics, the male part of the population is more susceptible to tuberculosis. Cases of infection in this socio-demographic group occur 3.2 times more often, moreover, the pathology progresses 2.5 times faster. The peak of infections falls on age. The maximum concentration of those infected with Koch's bacillus occurs in places of deprivation of liberty, despite the progressive diagnostic and treatment measures in them.

New developments of a specific vaccine for meningitis caused by tubercle bacilli are currently underway. The H37Rv strain is being investigated. The study is based on the hypothesis that mycobacteria secrete substances that, by binding to certain receptors, provoke and accelerate the process of brain damage. Work is underway to study the resistance of bacteria to drugs and to identify the nature of virulence.

This vaccine also corresponds to another diagnosis - a blood test for immune enzymes (instead of the Mantoux test). This study allows you to diagnose the disease, as well as to suggest the body's response to a new vaccine.

In the selection of treatment methods (medicines), innovative rapid tests based on bacteriophages are successfully used. This allows you to accurately and quickly select the right drug.

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Judging by nutrition, you absolutely do not care about immunity and your body. You are very susceptible to diseases of the lungs and other organs! It's time to love yourself and start getting better. It is urgent to adjust your diet, to minimize fatty, floury, sweet and alcohol. Eat more vegetables and fruits, dairy products. Feed the body with the intake of vitamins, drink more water (precisely purified, mineral). Harden the body and reduce the amount of stress in life.

You are prone to lung diseases at an average level.

So far, it’s good, but if you don’t start taking care of it more carefully, then diseases of the lungs and other organs will not keep you waiting (if there were no prerequisites yet). And frequent colds, intestinal problems and other “charms” of life accompany weak immunity. You should think about your diet, minimize fatty, starchy foods, sweets and alcohol. Eat more vegetables and fruits, dairy products. To nourish the body by taking vitamins, do not forget that you need to drink plenty of water (purified, mineral). Harden your body, reduce the amount of stress in life, think more positively and your immune system will be strong for many years to come.

Congratulations! Keep it up!

You care about your nutrition, health and immune system. Keep up the good work and problems with the lungs and health in general will not bother you for many years to come. Don't forget that this is mainly due to the fact that you eat right and lead a healthy lifestyle. Eat the right and wholesome food (fruits, vegetables, dairy products), do not forget to drink plenty of purified water, harden your body, think positively. Just love yourself and your body, take care of it and it will definitely reciprocate.

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Tuberculous meningitis

What is tuberculous meningitis -

What provokes / Causes of Tuberculous meningitis:

In a bacterial cell, it differentiates:

Microcapsule - a wall of 3-4 layers thick, firmly connected with the cell wall, consists of polysaccharides, protects mycobacteria from environmental influences, does not have antigenic properties, but exhibits serological activity;

Cell wall - limits the mycobacterium from the outside, ensures the stability of the size and shape of the cell, mechanical, osmotic and chemical protection, includes virulence factors - lipids, with the phosphatide fraction of which the virulence of mycobacteria is associated;

Homogeneous bacterial cytoplasm;

Cytoplasmic membrane - includes lipoprotein complexes, enzyme systems, forms an intracytoplasmic membrane system (mesosome);

Nuclear substance - includes chromosomes and plasmids.

Pathogenesis (what happens?) during Tuberculous meningitis:

2. At the second stage, the MBT from the vascular plexuses enter the cerebrospinal fluid, causing a specific inflammation of the soft meninges of the base of the brain - bacillary meningitis.

1. inflammation of the meningeal membranes;

2. formation of a gray jelly-like mass at the base of the brain;

3. inflammation and narrowing of the arteries leading to the brain, which in turn can cause local brain damage.

Symptoms of tuberculous meningitis:

3) terminal (paresis and paralysis).

With blockade of the spinal cord by exudate, weakness of motor neurons or paralysis of the lower extremities may occur.

Diagnosis of tuberculous meningitis:

Timely - within 10 days from the beginning of the irritation period;

Later - after 15 days.

2. Syndrome of intoxication.

3. Functional disorders of the pelvic organs (constipation, urinary retention).

4. Scaphoid belly.

5. Craniocerebral symptoms.

6. The specific nature of the cerebrospinal fluid.

7. Corresponding clinical dynamics.

1) tuberculosis of the lymph nodes;

2) radiographic signs of miliary pulmonary tuberculosis;

3) enlargement of the liver or spleen;

4) choroidal tuberculosis, detected when examining the bottom of the eye.

1. The pressure in the spinal canal is usually increased (liquid

the bone flows out in frequent drops or a jet).

2. Appearance of CSF: initially transparent, later (through

24 h), a fibrin network may form. If there is a blockade

the spinal cord has a yellowish color.

3. Cellular composition: mm3 (norm 3-5).

6. Bacteriological examination of CSF: MBT are found only in 10% if the volume of spinal fluid is sufficient (10-12 ml). Flotation by centrifugation for 30 minutes at high speed can detect MBT in 90% of cases.

Treatment of tuberculous meningitis:

Prevention of tuberculous meningitis:

Carrying out preventive and anti-epidemic measures adequate to the current extremely unfavorable epidemiological situation in tuberculosis.

Early detection of patients and allocation of funds for drug provision. This measure can also reduce the incidence of people who come into contact with patients in the outbreaks.

Carrying out mandatory preliminary and periodic examinations upon admission to work in livestock farms that are unfavorable for tuberculosis in cattle.

An increase in the allocated isolated living space for patients suffering from active tuberculosis and living in multi-occupied apartments and dormitories.

Timely conduct (up to 30 days of life) primary vaccination of newborns.

Which doctors should you contact if you have Tuberculous Meningitis:

Are you worried about something? Do you want to know more detailed information about Tuberculous meningitis, its causes, symptoms, methods of treatment and prevention, the course of the disease and diet after it? Or do you need an inspection? You can make an appointment with a doctor - the Eurolab clinic is always at your service! The best doctors will examine you, study the external signs and help identify the disease by symptoms, advise you and provide the necessary assistance and make a diagnosis. You can also call a doctor at home. The Eurolab clinic is open for you around the clock.

The phone number of our clinic in Kyiv: (+3 (multi-channel). The clinic secretary will select a convenient day and hour for you to visit the doctor. Our coordinates and directions are listed here. Look in more detail about all the services of the clinic on its personal page.

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International Neurological Journal 4 (42) 2011

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Pathomorphosis of tuberculous meningitis in patients with HIV infection

Authors: Bondar V.E., Vetukh I.V., Filimonov Yu.D., Interregional multidisciplinary hospital at the Daryevsk penal colony No. 10 of the Kherson region, Saulkina A.M., Kherson regional TB dispensary

Based on the analysis of literature data and cases from our own clinical practice, the article reveals general patterns characteristic of the course of tuberculous meningitis in patients with HIV infection. The conclusion is made about the change in the classical course (pathomorphosis) of this disease on the background of HIV infection.

Tuberculous meningitis, pathomorphosis, HIV infection, AIDS.

In recent years, epidemics of two socially dangerous diseases - tuberculosis and HIV / AIDS - have been simultaneously developing in Ukraine, which often affect the same population groups. Tuberculosis, as the most common opportunistic disease in HIV infection, has become a major cause of morbidity and mortality in AIDS patients. HIV infection increases the risk of developing active tuberculosis, and vice versa, tuberculosis adversely affects the course of HIV infection. According to statistical studies, severe forms of tuberculosis develop in 30-60% of people infected with HIV. In turn, HIV infection is registered in 40-70% of all patients with tuberculosis. This situation is called an "epidemic within an epidemic". Patients with HIV/AIDS-associated tuberculosis are characterized by high mortality. According to generalized literature data, about 30-40% of patients die from tuberculosis.

High mortality in this case is due to both the severity of the course of tuberculosis against the background of HIV infection, and the untimely detection of severe generalized forms. One of the reasons for the delay in the diagnosis of tuberculosis among HIV-infected and AIDS patients is the atypical course of tuberculosis. In the late stages of HIV infection, tuberculosis in 50–70% of cases has an extrapulmonary localization, often affecting the central nervous system (CNS) and the meninges.

Tuberculosis of the meninges and central nervous system is an infectious and inflammatory disease of the nervous system that occurs primarily or secondarily with the formation of specific granulomas in the membranes (meningitis), the substance of the brain (encephalitis) and spinal cord (myelitis) of the brain, caused by Mycobacterium tuberculosis. This disease is characterized by a rapid increase in clinical signs and their polymorphism, in particular, the presence of 3–4 syndromes: intoxication, meningeal, pathological changes in the cerebrospinal fluid, and dysfunction of the cranial (basal) nerves, often (70%) in combination with encephalitis and very rarely (up to 4%) - with myelitis syndrome. In the absence of etiotropic combined antibiotic therapy, the progressive course of tuberculosis of the meninges and central nervous system leads to death within 3 weeks.

Tuberculosis meningitis (meningoencephalitis), which usually develops when the number of CD4 cells drops to 100 in 1 µl and below (the norm is 500–2000 cells in 1 µl), is of the greatest clinical significance among the forms of CNS damage in tuberculosis in AIDS patients. Tuberculous meningitis is a manifestation of hematogenous disseminated tuberculosis. The primary focus can be localized in the lungs, lymph nodes, bones. In almost half of the cases, the primary focus in AIDS patients cannot be found. Often, meningitis occurs as the primary clinical manifestation of tuberculosis infection.

Mycobacteria penetrate the CNS by the hematogenous route through the choroid plexuses of the ventricles, then from the cavity of the latter they spread to the subarachnoid space, causing an inflammatory process in the pia mater.

As a rule, the initial manifestations of meningitis are nonspecific. Characterized by malaise, apathy, anorexia, subfebrile condition, intermittent headaches, night sweats, weight loss. Then the headache becomes constant, vomiting, drowsiness, meningeal signs appear. Symptoms gradually increase, cognitive disorders intensify, confusion appears, damage to the cranial nerves (often oculomotor, facial, auditory, visual), epileptic seizures, in the later stages - hemiparesis. Less commonly, the process is more acute or more gradual, manifesting itself as a slowly increasing frontal-type dementia with apathy, personality changes, and pelvic disorders. In 20% of cases, severe tuberculous lesions of the meninges in AIDS patients can be erased at normal temperature and in the absence of meningeal symptoms.

An examination of the cerebrospinal fluid reveals moderate pleocytosis (up to 500 cells in 1 μl), which may initially be neutrophilic, but becomes lymphocytic after about a week. A moderate increase in CSF pressure is determined. The liquid is clear or slightly opalescent. The protein content is increased from 1 to 20 g / l, a significant decrease in sugar in the cerebrospinal fluid to 1/5–1/6 of its blood level is characteristic. After 12–24 hours of settling the cerebrospinal fluid in a test tube, a delicate fibrin arachnoid mesh or film falls out, which is one of the pathognomonic signs of tuberculous meningitis. Also a characteristic sign of tuberculous meningitis is the detection of mycobacteria in the cerebrospinal fluid. According to the literature, Mycobacterium tuberculosis in the cerebrospinal fluid is rarely detected (in 15–17% of cases), although it is noted that they can be detected more often in AIDS patients than in individuals with an intact immune system. In some cases, with tuberculous meningitis in HIV-infected patients, cerebrospinal fluid parameters may be normal. The frequency of normal indicators is as follows: for glucose - in 15%, for protein - in 40%, for the number of cells - in 10% of cases.

Recently, more frequent examples of atypical course of tuberculous meningitis in HIV-infected persons, reaching, according to the authors' observations, up to 40% of cases, gave us the opportunity to identify certain patterns that allow us to talk about a change in the classical course (pathomorphosis) of this disease against the background of HIV infection. Below we present an analysis of clinical observations conducted in the penitentiary system on the basis of the infectious diseases department for the treatment of HIV-infected and AIDS patients of the inter-regional multidisciplinary hospital at the Daryevskaya correctional colony No. 10 of the Kherson region in 2009–2010.

Patient M., 24 years old, was admitted to the infectious department on November 20, 2009 with a diagnosis of HIV infection, clinical stage III. Candidiasis of the oral cavity. The purpose of the referral is the appointment of highly active antiretroviral therapy (HAART). History of life: intravenous administration of opiates since 1999. HIV infection was detected in 2005, the level of CD4 is 153 cells. Didn't have tuberculosis. Upon admission - complaints of fever to febrile numbers, general weakness, enlarged inguinal and axillary lymph nodes. Objectively: general condition of moderate severity. Fever up to 38.2 °C. Hypotrophy of skeletal muscles, manifestations of candidiasis of the oral mucosa. Generalized lymphadenopathy. Meningeal signs and signs of organic damage to the central nervous system are absent.

After the examination, which included X-ray of the lungs (an area of ​​pneumosclerosis was found in S4 on the right, Gon's focus in S1-S2 on the left), ultrasound examination of the abdominal organs (signs of diffuse changes in the parenchyma of the liver, pancreas, hepatosplenomegaly), biopsy of peripheral lymph nodes with subsequent pathohistological examination (phenomena of chronic hyperplastic lymphadenitis were found; signs of specific changes in the tissue were not found), the patient was prescribed HAART and symptomatic therapy, against which the condition improved and was regarded as satisfactory, but subfebrile condition persisted. Since December 28, 2009, there was a rise in body temperature to 39.4 °C, complaints of headache, dizziness appeared. In the general blood test: hypochromic anemia (hemoglobin 88 g / l), leukocytosis 22.3 ´ 109 / l, an increase in the erythrocyte sedimentation rate (ESR) up to 65 mm / h, a shift in the leukocyte formula to the left (an increase in the content of stab neutrophils up to 18%, the appearance of myelocytes (2%) and metamyelocytes (6%)). On the repeated X-ray of the lungs, compared with the previous data, there are no dynamics. On December 29, 2009 he was consulted by a neurologist. Meningeal signs were found: slight stiffness of the neck muscles, positive Kernig's symptom on both sides. Focal neurological symptoms, including signs of damage to the cranial nerves, were not detected. Meningitis was suspected and a lumbar puncture was performed. The cerebrospinal fluid is clear, colorless, the pressure is not increased. Positive protein reactions. Protein 0.22 g/l, glucose 1.9 mmol/l (blood glucose 5.3 mmol/l). Cytosis 2 cells (lymphocytes). Microscopy of a smear of cerebrospinal fluid, stained according to Ziehl-Nielsen, revealed Mycobacterium tuberculosis (MBT). 13.01.2010, the patient was referred to the Central Medical Advisory Commission (CMCC) of the Kherson Regional Tuberculosis Dispensary (HOPTD). Diagnosis of CVCC: “newly diagnosed tuberculosis (VDT) of the meninges. MBT +, M + (cerebrospinal fluid), K 0, Resist. 0, Hist. 0, Cat. 1, Cog. 1 (2010)". It is recommended to continue treatment in a specialized tuberculosis facility.

Patient U., aged 31, was admitted to the infectious department on February 1, 2010 for inpatient examination and decision on the appointment of HAART. From the anamnesis: intravenous use of narcotic substances (opiates) since 1996. In 2009, he was treated in a tuberculosis hospital for pulmonary tuberculosis. At the same time, HIV infection was discovered. CD4 level - 154 cells. On admission he was in a state of moderate severity. Fever up to 39.5 °C. Generalized lymphadenopathy, manifestations of candidiasis of the oral mucosa. Doubtful meningeal signs are determined. The diagnosis was established: “HIV infection, clinical stage III (IV?). Tuberculosis of the lungs (2009). Oral candidiasis. Meningitis of tuberculous etiology? The department was further examined: X-ray of the lungs - no pathology, sputum analysis for MBT was three times negative. In the general blood test: anemia (hemoglobin 90 g/l), leukocytosis 11.6 ´ 109/l, an increase in ESR up to 28 mm/h. 03.02.2010, examined by a neurologist. Complains of intermittent headache, general weakness. According to the patient, he has been ill for about 1.5 months, when general weakness and fever appeared. Neurological examination revealed a dissociated meningeal symptom complex: positive Kernig's symptoms, lower Brudzinsky's in the absence of neck stiffness. Focal neurological symptoms were not determined. In order to verify the diagnosis, a lumbar puncture was performed. Liquor is transparent, colorless, flows out under high pressure. Protein reactions are weakly positive. Protein 0.16 g/l, glucose 5.2 mmol/l (blood glucose 6.0 mmol/l). Cytosis 1 cell. Bacterioscopy of a smear of cerebrospinal fluid revealed MBT. Conclusion of the CVCC HOPTD dated February 9, 2010: “relapse of tuberculosis (RTB) of the meninges. MBT +, M + (cerebrospinal fluid), K 0, Resist. 0, Hist. 0, Cat. 2, Cog. 1 (2010)". He was sent to a tuberculosis hospital for further treatment.

Patient V., 29 years old, was hospitalized in the infectious department since October 12, 2009 with a diagnosis of HIV infection, clinical stage III. Oral candidiasis, polymorphic generalized lymphadenopathy. History: injection drug addiction since 1999. HIV infection was detected in 2005. The level of CD4 was not previously determined. Didn't have tuberculosis. After an examination in the hospital, which included determining the level of CD4 (20 cells), the patient was prescribed HAART, against which the level of CD4-lymphocytes increased to 160 cells per 1 μl. On October 27, 2009, due to the occurrence of persistent (for several days) hiccups, he was consulted by a neurologist. At the time of inspection, no complaints. He denies headache, double vision and other symptoms. Traumatic brain injury, inflammatory diseases of the central nervous system in history denies. Objectively: conscious, communicative. There are no meningeal signs. The function of the cranial nerves is not impaired. Active and passive movements in the limbs in full, muscle strength 5 points. Tendon reflexes are alive, D = S, there are no pathological reflexes. Sensitivity is not broken. There are no coordination disorders. On the x-ray of the skull - pronounced signs of hypertension in the form of increased arterial and venous pattern of the cranial vault and osteoporosis of the back of the Turkish saddle. After examination by an ophthalmologist, who ruled out congestion in the fundus, the patient underwent a lumbar puncture for diagnostic purposes. The cerebrospinal fluid is clear, colorless, the pressure is not increased. In the analysis of cerebrospinal fluid: protein reactions are sharply positive. Protein 12 g / l, glucose 4.7 mmol / l (in the blood 7.3 mmol / l). Cytosis 0. Gram stain did not reveal any bacterial flora. MBT were not found. Considering the results of the study (high protein level), the clinic of intracranial hypertension, a volumetric process of the central nervous system is suspected. Additional examination was recommended: magnetic resonance imaging (MRI) of the brain and spinal cord, examination by a neurologist in dynamics. The patient was prescribed diuretics (acetazolamide) and symptomatic therapy (metoclopramide), against which the condition improved, hiccups stopped. MRI was not performed due to the lack of technical feasibility. Starting from January 2010, the patient complained of intermittent headaches of a pressing nature, sometimes nausea, dizziness; febrile fever began to develop. On January 11, 2010, he was repeatedly consulted by a neurologist. On examination, dissociated meningeal signs were determined: in the absence of stiff neck, Kernig's and lower Brudzinsky's symptoms were positive on both sides. No focal neurological symptoms were identified. Due to suspected meningitis, a lumbar puncture was repeated. The cerebrospinal fluid is clear, colorless, the pressure is not increased. Protein reactions are weakly positive. Protein 0.2 g/l, glucose 2.9 mmol/l (in the blood 6.8 mmol/l). Cytosis 1 cell. Bacterioscopy of the smear revealed MBT. Conclusion: tuberculous meningitis. On January 13, 2010, he was sent to the Central Exhibition Center. The diagnosis was established: “VDTB of the meninges, lungs (miliary). Office +, M + (cerebrospinal fluid), K 0, Gist. 0, Resist. 0, Cat. 1, Cog. 1 (2010)". The patient was sent to a tuberculosis hospital.

Patient B., aged 34, was referred to the infectious department in January 2010 for inpatient examination and treatment. History of life: chronic bronchitis for about 15 years, in 2001 he was ill with pulmonary tuberculosis. HIV infection was detected in 2009, the CD4 level was not previously examined. Injection drug addiction since 1990. Upon admission to the department, he was examined by an infectious disease specialist, meningeal signs were detected, in connection with which a neuropathologist was invited for a consultation. On examination, there are no neurological complaints. In general, he considers himself ill for 4 months before admission to the hospital, when he began to notice an increase in body temperature. Objectively: conscious, communicative. Doubtful neck muscle stiffness, Kernig's symptoms, lower Brudzinski's symptoms are positive. There are no focal neurological symptoms. A diagnostic lumbar puncture was performed. Liquor is transparent, colorless. Protein reactions are negative. Protein 0.28 g/l, glucose 4.0 mmol/l (blood glucose 7.2 mmol/l). Cytosis 0. MBT were found in the smear. Additionally examined: X-ray of the lungs - chronic bronchitis, remission phase, sputum analysis for MBT three times negative, CD4 level - 32 cells. On January 20, 2010, he was consulted by a phthisiatrician of the COPTD, the diagnosis was made: “RTB meningitis, active phase. MBT +, M + (cerebrospinal fluid), K 0, Resist. 0, Hist. 0, Cat. 2, Cog. 1 (2010)". The patient was prescribed specific chemotherapy with further continuation of treatment in a specialized institution.

conclusions

Based on our own clinical practice and analysis of literature data, we have identified general patterns in the course of tuberculous meningitis in HIV-infected individuals. In contrast to the classical picture, the disease in this category of patients proceeds in an erased form for a long time, hiding under the guise of a fever of unknown origin. As a rule, there are no complaints in patients, there are no cerebral manifestations (headache, nausea, vomiting, hyperesthesia of the sense organs, etc.). Meningeal syndrome is formed very late, meningeal signs are indistinct, are dissociated: positive symptoms of Kernig, Brudzinsky are noted in the absence of pronounced stiff neck. There were no focal neurological symptoms, including lesions of the cranial nerves pathognomonic for tuberculous meningitis. In 60% of patients, the disease develops in the absence of an active tuberculous process in the lungs. In a cerebrospinal fluid examination, pleocytosis, characteristic of tuberculous meningitis, in combination with the above-described changes in protein and glucose content, is observed in less than 1/3 of patients. In most cases, a peculiar phenomenon is found, consisting in the absence of pleocytosis, normal or increased protein content in the cerebrospinal fluid, the absence of a decrease in glucose levels in the presence of MBT in the cerebrospinal fluid, which are relatively easy to detect by bacterioscopy. Such changes are usually noted in patients on the background of deep immunosuppression at a CD4 level of 100 cells per 1 μl and below. With a higher CD4 count, tuberculous meningitis has a classic course. Thus, we can conclude that the pathomorphism of tuberculous meningitis in HIV-infected individuals against the background of deep immunosuppression. Practitioners caring for this category of patients need to be constantly alert to the possible development of tuberculous meningitis in patients with prolonged fever of unknown origin, CD4 count below 100 cells per 1 µl, complaints of recurrent headache, history of tuberculosis. It should be remembered that tuberculous meningitis is a formidable, but potentially curable disease, the prognosis of which, subject to early detection and timely administration of adequate antimycobacterial therapy, is favorable.

1. The manifestation of VIL / SNID-associated tuberculosis and dispensary care for ailments. Methodological recommendations of the Ministry of Health of Ukraine. - Kiev, 2005. - 21 p.

Primary lesion of the nervous system in HIV infection

What is the primary lesion of the nervous system in HIV infection -

Pathogenesis (what happens?) during the Primary lesion of the nervous system in HIV infection:

Morphologically direct damage to the brain by HIV leads to the development of subacute giant cell encephalitis with areas of demyelination. In the brain tissue, monocytes with a large amount of virus that have penetrated from the peripheral blood can be detected. These cells can merge, forming giant multinucleated formations with a huge amount of viral material, which was the reason for the designation of this encephalitis as giant cell. At the same time, the discrepancy between the severity of clinical manifestations and the degree of pathomorphological changes is characteristic. In many patients with distinct clinical manifestations of HIV-associated dementia, only myelin “blanching” and mild central astrogliosis can be detected pathologically.

Symptoms of the Primary lesion of the nervous system in HIV infection:

Symptoms of direct (primary) damage to the nervous system in HIV infection are classified into several groups.

HIV-associated cognitive-motor complex. This complex of disorders, previously referred to as AIDS dementia, now includes three diseases - HIV-associated dementia, HIV-associated myelopathy and HIV-associated minimal cognitive-motor disorders.

HIV-associated dementia. Patients with these disorders suffer primarily from cognitive impairment. These patients have manifestations of dementia (dementia) of the subcortical type, which is characterized by a slowdown in psychomotor processes, inattention, memory loss, impaired information analysis processes, which complicates the work and daily life of patients. More often this is manifested by forgetfulness, slowness, decreased concentration, difficulty in counting and reading. Apathy, limitation of motivations can be observed. In rare cases, the illness may present with affective disorders (psychosis) or seizures. Neurological examination of these patients reveals tremor, slowing down of fast, repetitive movements, staggering, ataxia, muscle hypertonicity, generalized hyperreflexia, and symptoms of oral automatism. In the initial stages, dementia is detected only with neuropsychological testing. Subsequently, dementia can quickly progress to a serious condition. This clinical picture is observed in 8-16% of AIDS patients, however, taking into account autopsy data, this level rises to 66%. In 3.3% of cases, dementia may be the first symptom of HIV infection.

HIV-associated myelopathy. In this pathology, movement disorders predominate, mainly in the lower extremities, associated with lesions of the spinal cord (vacuolar myelopathy). There is a significant decrease in strength in the legs, increased spastic muscle tone, ataxia. Cognitive impairments are also frequently identified, but weakness in the legs and gait disturbances come to the fore. Movement disorders can affect not only the lower, but also the upper limbs. Sensitivity disturbances of the conductive type are possible. Myelopathy, however, is more diffuse than segmental in nature; therefore, as a rule, there is no "level" of motor and sensory disorders. Characterized by the absence of pain. In the cerebrospinal fluid, nonspecific changes are noted in the form of pleocytosis, an increase in the content of total protein, and HIV may be detected. The prevalence of myelopathy among AIDS patients reaches 20%.

HIV-associated minimal cognitive-motor disorders. This syndrome complex includes the least pronounced disorders. The characteristic clinical symptoms and changes in neuropsychological tests are similar to those of dementia, but to a much lesser extent. Often there is forgetfulness, slowing down of thought processes, reduced ability to concentrate, gait disturbance, sometimes clumsiness in the hands, personality changes with limited motivation.

Diagnosis Primary lesion of the nervous system in HIV infection:

In the initial stages of the disease, dementia is detected only with the help of special neuropsychological tests. Subsequently, a typical clinical picture against the background of immunodeficiency, as a rule, allows an accurate diagnosis. Additional examination reveals symptoms of subacute encephalitis. CT and MRI studies reveal brain atrophy with an increase in sulci and ventricles. On MRI, additional foci of signal enhancement in the white matter of the brain associated with local demyelination can be noted. These studies of cerebrospinal fluid are nonspecific; slight pleocytosis, a slight increase in protein content, and an increase in the level of class C immunoglobulins may be detected.

Other CNS lesions associated with HIV infection. In children, primary CNS involvement is often the earliest symptom of HIV infection and is referred to as progressive childhood HIV-associated encephalopathy. This disease is characterized by developmental delay, muscular hypertension, microcephaly, and calcification of the basal ganglia.

In almost all HIV-infected people, to one degree or another, symptoms of acute aseptic meningitis can be detected, which occurs immediately after infection and is pathogenetically most likely associated with autoimmune reactions during the primary response to virus antigens. This serous meningitis is manifested by symptoms of acute inflammation of the membranes (moderate cerebral and meningeal syndromes), sometimes with damage to the cranial nerves. Clinical manifestations usually regress on their own within 1-4 weeks.

HIV-associated symptoms of damage to the peripheral nervous system. In AIDS patients, inflammatory polyneuropathies are often observed in the form of subacute multifocal multiple polyneuropathy or multiple neuritis with a predominant lesion of the lower extremities. In the etiology of these disorders, in addition to HIV, the role of viruses of the genus Herpesvirus is possible. Less common are severe subacute sensorimotor polyneuropathy or rapidly developing peripheral paralysis with predominantly motor polyneuropathy. Most often, HIV infection is accompanied by distal polyneuropathies with a predominance of sensory disorders in the form of paresthesia and dysesthesia, mainly in the area of ​​​​the arch of the foot and toes, sometimes with mild weakness and decreased knee reflexes.

HIV infection is sometimes accompanied by myopathic syndrome. This syndrome is characterized by subacute development of proximal muscle weakness with myalgias, increased muscle fatigue, and elevated serum creatine kinase levels. EMG changes are close to those observed in poliomyositis, and muscle biopsy reveals de- and regeneration of myofibrils, perivascular and interstitial inflammation.

Treatment of the Primary lesion of the nervous system in HIV infection:

The prevention and treatment strategy provides for the fight against the HIV infection itself, symptomatic treatment for damage to the nervous system, treatment of opportunistic infections and diseases, counseling, health education. Specific treatment includes antiviral and immunotherapy.

More than 30 antiviral drugs for the treatment of HIV infection have been clinically tested. The best known is retrovir (zidovudine, AZT, azidothymidine), which has a proven virostatic effect. Retrovir is a competitive inhibitor of reverse transcriptase responsible for the formation of proviral DNA on a retroviral RNA template. The active triphosphate form of retrovir, being a structural analogue of thymidine, competes with an equivalent thymidine derivative for binding to the enzyme. This form of retrovir does not have the 3 "-OH groups necessary for DNA synthesis. Thus, the proviral DNA chain cannot grow. The competition of retrovir with HIV reverse transcriptase is about 100 times greater than with human cell DNA alpha polymerase. The criterion for prescribing azidothymidine is a decrease in the level of T-helpers below 250-500 per 1 mm² or the appearance of a virus in the blood.The drug is used to treat patients with AIDS in all stages, its beneficial effect on patients with HIV-associated cognitive-motor complex, including AIDS dementia and myelopathy, as well as with HIV-associated polyneuropathies, myopathies.Retrovir is used to prevent the development of neurological manifestations of HIV infection and opportunistic processes.The drug penetrates through the BBB, its level of cerebrospinal fluid is about 50% of the plasma level.As an initial dose for patients with a body weight of about 70 kg, it is recommended to take 200 mg every 4 hours ( 1200 mg per day). Depending on the clinical condition of patients and laboratory parameters, dosages can vary from 500 to 1500 mg per day. The need for selection of individual doses may occur in patients with manifestations of side effects or in severe manifestations of AIDS with depletion of bone marrow resources, which is manifested by leukopenia and anemia. To reduce the severity of hematotoxic effects, the drug is often combined with erythro- or hematopoietin, vitamin B12. Other possible side effects include anorexia, asthenia, nausea, diarrhea, dizziness, headache, fever, sleep disturbances, taste perversions, rash, decreased mental activity, anxiety, increased urination, generalized pain, chills, cough, shortness of breath. Convincing data on the features of acute overdose are not yet available, with the manifestation of side effects with long-term use, hemodialysis may be useful. Currently, retrovir remains the only formally approved antiviral drug for the treatment of AIDS, including primary lesions of the nervous system. Given the large number of severe side effects of retrovir, clinical trials of other nucleoside derivatives are currently underway, in which myelotoxic effects are less pronounced.

Given the role of autoimmune reactions in the development of lesions of the peripheral nervous system in AIDS, corticosteroids and cytostatics, plasmapheresis are effective in some cases. Various immunostimulants are used to correct immunodeficiency. Among them are cytokines (alpha and beta interferons, interleukins, etc.), immunoglobulins, hematopoietic growth factors. Restorative immunotherapy until recently did not give significant clinical effects, allowing only a few slow down the development of the pathological process. In recent years, bone marrow transplantation has rarely been performed due to the large number of adverse reactions and the insignificant effectiveness of this procedure. The use of thymus factors, the soluble recombinant CO4 T-lymphocyte receptor, which is capable of preventing the entry of the virus into the cell, and recombinant and highly purified HIV envelope proteins as vaccines, is being investigated.

In the presence of neurological manifestations of AIDS, as a rule, unfavorable. There are no known cases of cure for HIV infection, although many years of asymptomatic virus carriers are possible. In the fight against HIV infection, the main importance is attached to preventive measures, which have already reduced the rate of growth in the number of infected people.

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Other diseases from the group Diseases of the nervous system:

Human immunodeficiency virus disease can occur in the form of a hidden carrying of the virus, as well as in the form of acquired immunodeficiency syndrome, which is the last stage of HIV.

With the development of HIV and AIDS, almost all systems of the human body are affected and affected. The main pathological changes are concentrated in the nervous and immune systems. The defeat of the nervous system in HIV is called neuroAIDS.

In vivo it is observed in approximately 70% of patients, and postmortem in 90-100%.

Causes and pathogenesis of the disease

The pathogenetic mechanisms of the impact of HIV on the nervous system are still not fully understood. It is believed that neuroAIDS occurs due to direct and indirect effects on the nervous system.

There is also an opinion that the reason lies in the impaired regulation of the response process from the immune system. A direct effect on the nervous system is carried out through penetration into the cells that carry the CD4 antigen, namely the neuroglia of the brain tissue, cells of the lymphocyte membrane.

At the same time, the virus can cross the blood-brain barrier (the physiological barrier between the bloodstream and the central nervous system). The reason for this is that viral infection increases the permeability of this barrier, and the fact that its cells also have CD4 receptors.

There is an opinion that the virus can penetrate into brain cells due to cells that can capture and digest bacteria that easily pass the blood-brain barrier. As a result, only neuroglia are affected, while neurons, due to the fact that they do not have CD4 receptors, are not damaged.

However, due to the fact that there is a connection between glial cells and neurons (the former serve the latter), the function of neurons is also impaired.

As for the indirect impact of HIV, it occurs in various ways:

• as a result of a rapid decrease in immune defense, infections and tumors develop;
• the presence in the body of autoimmune processes that are associated with the production of antibodies to nerve cells that have embedded HIV antigens;
• neurotoxic effects of chemicals that are produced by HIV;
• as a result of damage to the endothelium of cerebral vessels by cytokines, which leads to disturbances in microcirculation, hypoxia, which causes the death of neurons.

At the moment, there is no clarity and consensus on the mechanisms of the origin and development of HIV and neuroAIDS, problems are caused even with the isolation of the virus in the laboratory. This has led to the emergence of a certain number of doctors and specialists who consider HIV to be an incorrect concept, but at the same time do not deny the very existence of HIV infection.

Primary and secondary neuroAIDS

There are two groups of neurological manifestations that are associated with HIV infection: primary and secondary neuroAIDS.

In primary neuroAIDS, HIV directly affects the nervous system. There are several main manifestations of the primary form of the disease:

• vacuolar;
• vascular neuroAIDS;
• plural;
• neuropathy of the facial nerve;
• spicy ;
• damage to the peripheral nervous system;
• sensory polyneuropathy;
• AIDS dementia;
• inflammatory demyelinating polyneuropathy.

Secondary neuroAIDS is caused by opportunistic infections and tumors that develop in an AIDS patient.

Secondary manifestations of the disease are expressed as follows:

Most often, in patients with neuroAIDS, such tumors in the central nervous system are observed:

• disseminated Kaposi's sarcoma;
• Burkitt's lymphoma;
• primary;
• undifferentiated tumors.

Features of the clinical picture

Primary neuroAIDS often occurs without symptoms. In rare cases, neurological symptoms may appear 2-6 weeks after HIV infection. During this period, patients experience fever of unknown origin, swollen lymph nodes, and skin rashes. When this appears:

1. . It occurs in a small number of patients with HIV (about 10%). The clinical picture is similar to. In aseptic meningitis, the level of CD8 lymphocytes increases in the cerebrospinal fluid. When viral meningitis has another cause, the number of CD4 lymphocytes increases. In rare and severe cases, it can lead to mental illness,.
2. Acute radiculoneuropathy. Caused by inflammatory selective damage to the myelin sheath of the roots of the cranial and spinal nerves. This condition manifests itself in sensitivity disorders of the polyneuric type, radicular syndrome, damage to the facial and ophthalmic nerves,. Signs begin to appear and gradually become more intense both after a few days and after a few weeks. With the onset of stabilization of the condition for about 14-30 days, a decrease in the intensity of symptoms begins. Only 15% of patients have sequelae after acute radiculoneuropathy.

Separate forms of neuroAIDS make themselves felt at the open stage of HIV infection:

1. (AIDS dementia). The most common manifestation of neuroAIDS. The presence of behavioral, motor, cognitive disorders is noted. In about 5% of HIV patients, encephalopathy is the primary symptom that indicates the presence of neuroAIDS.
2. HIV myelopathy. It is expressed in dysfunction of the pelvic organs and lower spastic. A feature is the slow flow and differences in the severity of symptoms. The disease is diagnosed in about a quarter of people with HIV.

Establishing diagnosis

NeuroAIDS occurs quite often, in most patients with HIV, so it is recommended that all carriers of the infection undergo regular examination by a neurologist. HIV encephalopathy initially manifests itself in impaired cognitive functions, therefore, in addition to studying the neurological status, it is also necessary to conduct a neuropsychological examination.

In addition to the basic studies that patients with HIV undergo, for the diagnosis of neuroAIDS, it is necessary to turn to tomographic, electrophysiological and liquorological research methods.

Patients may also be referred for consultation with a neurosurgeon, psychiatrist, and other specialists. The effectiveness of the treatment of the nervous system is analyzed for the most part using electrophysical research methods (electromyography,).

Disorders in the nervous system in neuroAIDS, as well as the study of their course, and the results of therapy, are studied using and.

Also, an analysis of cerebrospinal fluid is often prescribed, which is taken with the help of. If, in addition to neurological manifestations, a decrease in the number of CD4 lymphocytes, a patient has an increased protein level in the analysis of cerebrospinal fluid, a reduced glucose concentration, and moderate lymphocytosis, then we are talking about the likelihood of developing neuroAIDS.

Complex treatment

The treatment of neuroAIDS and the relief of its development are inseparable from the treatment of HIV infection, and form its basis. Patients are prescribed antiretroviral therapy with medicines that have the ability to pass through the blood-brain barrier and, as a result, block the development of HIV, stop the increase in immunodeficiency, reduce the intensity and severity of symptoms of neuroAIDS, and reduce the likelihood of infections.

Also effective is the use of plasmapheresis, corticosteroid therapy. Treatment of tumors may require surgery, and consultation with a neurosurgeon is necessary.

In a situation of early detection of neuroAIDS (in the primary stages), and the presence of adequate treatment for the manifestations of the disease of a neurological nature, there is a possibility of slowing down the development of the disease. Often the cause of death in patients with neuroAIDS is a stroke, the presence of opportunistic infections, malignant tumors.

Inflammation of the meninges caused by Mycobacterium tuberculosis that has penetrated into them. It is manifested by a deterioration in the state of health of a patient with hyperthermia, headache, vomiting, disorders of the cranial nerves, a disorder of consciousness, and a meningeal symptom complex that occurs sharply after prodromal phenomena. Tuberculous meningitis is diagnosed mainly by comparing clinical data with the results of a CSF study. A long-term and complex treatment is carried out, consisting of anti-tuberculosis, dehydration, detoxification, vitamin and symptomatic therapy.

ICD-10

A17.0

General information

Morphologically, serous-fibrinous inflammation of the membranes with the presence of tubercles is observed. Changes in the vessels of the membranes (necrosis, thrombosis) can cause circulatory disorders in a separate area of ​​the medulla. In patients treated, the inflammation of the membranes is local in nature, the formation of adhesions and scars is noted. Hydrocephalus often occurs in children.

Symptoms of tuberculous meningitis

Flow periods

prodromal period takes an average of 1-2 weeks. Its presence distinguishes tuberculous meningitis from other meningitis. It is characterized by the appearance of cephalgia (headache) in the evenings, subjective deterioration of well-being, irritability or apathy. Then the cephalgia intensifies, nausea occurs, and vomiting may occur. Subfebrile condition is often noted. When contacting a doctor in this period, it is not possible to suspect tuberculous meningitis due to the non-specificity of this symptomatology.

Irritation period manifests as a sharp increase in symptoms with a rise in body temperature up to 39 ° C. Headache is intense, accompanied by increased sensitivity to light (photophobia), sounds (hyperacusia), touch (skin hyperesthesia). Exacerbation of lethargy and drowsiness. The appearance and disappearance of red spots in various parts of the skin is noted, which is associated with a disorder of the autonomic vascular innervation. There are meningeal symptoms: stiffness (tension) of the neck muscles, symptoms of Brudzinsky and Kernig. Initially, they are fuzzy, then gradually intensify. By the end of the second period (after 8-14 days), the patient is lethargic, his consciousness is confused, and the typical meningeal "pointing dog" posture is typical.

Period of paresis and paralysis(terminal) is accompanied by a complete loss of consciousness, the appearance of central paralysis and sensory disorders. The respiratory and cardiac rhythm is disturbed, convulsions, hyperthermia up to 41 ° C or low body temperature are possible. If untreated in this period, tuberculous meningitis within a week leads to death, the cause of which is paralysis of the vascular and respiratory centers of the brain stem.

Clinical forms

Basilar tuberculous meningitis in 70% of cases it has a gradual development with the presence of a prodromal period, the duration of which varies within 1-4 weeks. In the period of irritation, cephalgia increases, anorexia occurs, vomiting is typical with a “fountain”, drowsiness and lethargy increase. Progressive meningeal syndrome is accompanied by the addition of disorders of the cranial nerves (CNN): strabismus, anisocoria, blurred vision, drooping of the upper eyelid, hearing loss. In 40% of cases, ophthalmoscopy determines stagnation of the optic nerve head. Possible damage to the facial nerve (facial asymmetry). The progression of meningitis leads to the appearance of bulbar symptoms (dysarthria and dysphonia, choking), indicating the defeat of IX, X and XII pairs of cranial nerves. In the absence of adequate therapy, basilar meningitis passes into the terminal period.

Tuberculous meningoencephalitis usually corresponds to the third period of the course of meningitis. Typically, the predominance of symptoms of encephalitis: paresis or paralysis of the spastic type, loss of sensitivity, bilateral or unilateral hyperkinesis. Consciousness is lost. Tachycardia, arrhythmia, respiratory disorders up to Cheyne-Stokes respiration are noted, bedsores are formed. Further progression of meningoencephalitis ends in death.

Spinal tuberculous meningitis rarely observed. As a rule, it manifests with signs of damage to the cerebral membranes. Then, in 2-3 periods, the pains of the girdle type join, due to the spread of tuberculosis to the spinal roots. With the blockade of the liquor pathways, radicular pains are so intense that they are not removed even with the help of narcotic analgesics. Further progression is accompanied by pelvic disorders: first with retention, and then with urinary and fecal incontinence. Peripheral flaccid paralysis, mono- and paraparesis are observed.

Diagnostics

Tuberculous meningitis is diagnosed by a phthisiatrician in conjunction with specialists in the field of neurology. Of paramount importance in the diagnosis is the study of cerebrospinal fluid taken by lumbar puncture. Changes can be detected already in the prodrome. Colorless transparent cerebrospinal fluid flows out with an increased pressure of 300-500 mm of water. Art., sometimes a jet. Cytosis is noted - an increase in cellular elements up to 600 in 1 mm3 (at a rate of 3-5 in 1 mm3). At the onset of the disease, it is neutrophilic-lymphocytic in nature, then it becomes lymphocytic. The concentration of chlorides and glucose decreases. Particular attention is paid to the glucose level indicator: the lower it is, the more serious the prognosis.

A typical sign is the loss of a cobweb-like fibrinous film, which is formed when the cerebrospinal fluid is left in a test tube for 12-24 hours. The Pandey and Nonne-Apelt reactions are positive. The presence of protein-cell dissociation (relatively small cytosis at a high protein concentration) is characteristic of a block in the circulation of cerebrospinal fluid. Detection of Mycobacterium tuberculosis in cerebrospinal fluid currently occurs only in 5-10% of cases, although previously it ranged from 40% to 60%. CSF centrifugation allows to increase the detection of mycobacteria.

Tuberculous meningoencephalitis differs from basilar meningitis in a more pronounced rise in protein levels (4-5 g/l compared to 1.5-2 g/l in the basilar form), not very large cytosis (up to 100 cells per 1 mm3), a large decrease in the concentration glucose. Spinal tuberculous meningitis is usually accompanied by a yellow color of the cerebrospinal fluid (xanthochromia), a slight increase in its pressure, cytosis up to 80 cells per 1 mm3, and a pronounced decrease in glucose concentration.

During the diagnostic search, tuberculous meningitis is differentiated from serous and purulent meningitis, tick-borne encephalitis, meningism associated with some acute infections (flu, dysentery, pneumonia, etc.). For the purpose of differential diagnosis with other cerebral lesions, CT or MRI of the brain may be performed.

Treatment of tuberculous meningitis

Specific anti-tuberculosis treatment is started at the slightest suspicion of a tuberculous etiology of meningitis, since the prognosis directly depends on the timeliness of therapy. The most optimal treatment regimen is considered to include isoniazid, rifampicin, pyrazinamide and ethambutol. Initially, the drugs are administered parenterally, then inside. When the condition improves after 2-3 months. cancel ethambutol and pyrazinamide, reduce the dose of isoniazid. Reception of the latter in combination with rifampicin is continued for at least 9 months.

In parallel, the treatment prescribed by the neurologist is carried out. It consists of dehydration (hydrochlorothiazide, furosemide, acetazolamide, mannitol) and detoxification (dextran infusion, saline solutions) therapy, glutamic acid, vitamins (C, B1 and B6). In severe cases, glucocorticoid therapy is indicated; spinal tuberculous meningitis is an indication for the introduction of drugs directly into the subarachnoid space. In the presence of paresis, neosmtigmine, ATP are included in the treatment regimen; with the development of optic nerve atrophy - nicotinic acid, papaverine, heparin, pyrogenal.

Within 1-2 months. The patient must adhere to bed rest. Then the regimen is gradually expanded and at the end of the 3rd month the patient is allowed to walk. The effectiveness of treatment is assessed by changes in the cerebrospinal fluid. On the day of the control lumbar puncture, bed rest is required. Exercise therapy and massage are recommended no earlier than 4-5 months. diseases. Within 2-3 years after the end of therapy, patients who have had tuberculous meningitis should undergo 2-month anti-relapse courses of treatment 2 times a year.

Forecast and prevention

Without specific therapy, tuberculous meningitis ends in death on the 20-25th day. With timely started and long-term therapy, a favorable outcome is observed in 90-95% of patients. The prognosis is unfavorable with a belated diagnosis and late initiation of therapy. Complications are possible in the form of relapses, the formation of epilepsy and the development of neuroendocrine disorders.

Preventive measures include all known methods of preventing tuberculosis: preventive vaccinations with BCG vaccine, tuberculin diagnostics, annual fluorography, specific blood tests (quantiferon and T-spot tests), early detection of cases, examination of a contact group of persons, etc.

Serous meningitis is a serous inflammation that affects the soft membrane of the brain, accompanied by the formation of serous exudate, which includes some elements of blood cells and 2-2.5% protein.

Serous meningitis most commonly affects children aged 3–6 years

The disease can either be caused by infectious agents (fungi, viruses, bacteria), or be of an aseptic non-infectious nature.

The inflammatory process in serous meningitis does not lead to cell necrosis and is not complicated by purulent tissue fusion. Therefore, this disease, unlike purulent meningitis, has a more favorable prognosis.

Serous inflammation of the meninges most often affects children aged 3-6 years. In adults, serous meningitis is diagnosed extremely rarely, in patients aged 20–30 years.

Causes and risk factors

In 80% of cases, the cause of serous meningitis in adults and children is a viral infection. The causative agents of the disease can be:

• paramyxoviruses.

Much less often, a bacterial infection leads to the development of serous meningitis, for example, infection of a patient with a Koch stick (the causative agent of tuberculosis) or a pale spirochete (the causative agent of syphilis). Very rarely, the disease has a fungal etiology.

Serous meningitis of an infectious nature develops in patients with a weakened immune system, when the body's defenses are unable to cope with the pathogenic microflora.

Ways of infection can be different (water, contact, airborne). The water way of transmission of infection is most characteristic of enteroviruses. That is why serous meningitis of enteroviral etiology is mainly diagnosed at the height of the bathing season, i.e., in the summer months.

Timely treatment of serous meningitis provides a rapid improvement in the condition of patients. The average duration of the disease is 10-14 days.

The development of aseptic serous meningitis is not associated with any infection. The reasons in this case may be:

• systemic diseases (nodular periarteritis, systemic lupus erythematosus);
• tumors of the brain and its membranes.

In clinical practice, there is also a special form of serous meningitis - Armstrong's meningitis (lymphocytic viral choriomeningitis). The causative agent is a virus, and the reservoir of infection is rats and mice. The virus enters the human body through the use of food and water contaminated with the biological secretions of infected rodents (nasal mucus, feces, urine).

Symptoms of serous meningitis

The incubation period for viral serous meningitis is 3 to 18 days. The disease begins with a sudden increase in body temperature to high values ​​​​(40-41 ° C). An intense headache and symptoms of intoxication appear, which include:

• pain in muscles and joints;
• general weakness;
• weakness;
• lack of appetite.

With viral serous meningitis, the temperature curve is often biphasic: the body temperature remains at high values ​​​​for 3-4 days, after which it decreases to subfebrile (below 38 ° C), and after a few days it rises again to 40-41 ° C.

The headache is permanent and is not relieved by the use of conventional painkillers. It is amplified under the influence of external stimuli (noise, harsh sound, bright light).

Other symptoms of serous meningitis of viral etiology are:

• nausea;
• repeated vomiting that does not bring relief;
• hyperesthesia (general and skin), i.e., increased sensitivity to stimuli.

Patients tend to lie in a darkened and quiet room, avoiding unnecessary head movements. To alleviate the condition, they take a forced position, called the “position of a pointing dog” (lying on their side, their head thrown back as much as possible, arms and legs bent at the joints and pressed against the body with force).

Viral serous meningitis in adults and children is in many cases accompanied by the appearance of a symptom complex characteristic of SARS (sore throat, cough, nasal congestion, conjunctivitis).

With damage to the cranial nerves appear:

• drooping of the upper eyelid;
• difficulty swallowing;

A characteristic symptom of serous meningitis is severe rigidity (tension) of the muscles of the back of the neck, due to which the patient cannot reach the sternum with his chin.

Patients may experience drowsiness, slight stupor. More severe disturbances of consciousness, such as stupor or coma, are not typical for serous meningitis and, if present, a different diagnosis should be considered.

In children, against the background of the disease, a whiny and capricious state develops, convulsions can be observed. With unclosed fontanelles, their bulging is clearly visible. If the child is lifted by the armpits and held on weight, then he bends his legs at the knee and hip joints, pulling them to the stomach. This phenomenon is called the suspension symptom or Lessage's symptom.

Some types of serous meningitis have a special clinical picture, we will consider them separately.

Acute lymphocytic choriomeningitis

With this form, not only the pia mater, but also the plexuses of the blood vessels of the ventricles of the brain are drawn into the serous inflammatory process. The incubation period lasts from 6 to 13 days. In about half of patients, the onset is gradual. There is a general malaise, pain and sore throat, nasal congestion, body temperature rises. The manifestation of symptoms of serous meningitis occurs only at the time of the second wave of fever. In the other half of patients, the disease occurs suddenly with a sharp increase in body temperature, cephalgia (headache), severe intoxication, and the appearance of symptoms characteristic of serous meningitis.

Tuberculous meningitis

Serous meningitis, the causative agent of which is Koch's wand, occurs in patients suffering from tuberculosis of various localization (lungs, genitals, kidneys, larynx). Differs in subacute character. Tuberculous meningitis begins with a prodromal period that lasts up to 15-20 days. Characteristic for him:

• loss of appetite;
• subfebrile temperature (37.5-38 ° C);
• moderate headache;
• increased sweating;
• general weakness;
• decrease in physical and mental capacity for work.

Meningeal symptoms develop gradually. Some patients present with mild ptosis, mild strabismus, and reduced visual acuity.

If specific anti-tuberculosis therapy is not carried out, then focal neurological symptoms (paresis, aphasia, dysarthria) appear over time.

Fungal meningitis in patients with HIV infection

Paramyxovirus serous meningitis is characterized by a rapid onset. In patients, the body temperature quickly rises to high values, an intense headache occurs, nausea, vomiting appear, and a pronounced meningeal syndrome develops. In addition, they are characterized by:

• convulsive seizures;
• paresis;
• ataxia (impaired coordination of movements);
• stomach ache;
• signs of damage to the cranial nerves.

The penetration of the mumps virus into other organs is accompanied by the development of adnexitis, orchitis, pancreatitis.

Diagnostics

It is possible to assume the presence of serous meningitis in a patient on the basis of a characteristic clinical picture, in particular the following signs:

• "Position of a pointing dog";
• positive symptoms of Brudzinsky, Kerneg;
• stiffness of the muscles of the back of the neck;
• positive symptom of Lesage (in children of the first years of life).

To establish the cause that caused the development of the inflammatory process in the meninges, it is necessary to collect an anamnesis, paying attention to the features of the onset of the disease, the presence of contact with sick people.

To identify the pathogen, virological studies are carried out using the methods of ELISA, RIF, PCR, and also perform bacterial culture of discharge from the nose and throat.

Confirmation of the diagnosis of serous meningitis is possible according to the results of a laboratory study of cerebrospinal fluid. A sign of serous inflammation is an increased content of protein in the cerebrospinal fluid. With tuberculous and fungal meningitis, a decrease in glucose concentration is noted in the cerebrospinal fluid. The predominance of neutrophils in the CSF is characteristic of bacterial serous meningitis, but if the disease has a viral etiology, then lymphocytes predominate.

In syphilitic and tuberculous serous meningitis, pathogens are detected by microscopy of smears of cerebrospinal fluid, stained in a special way.

As additional diagnostic methods, ophthalmoscopy, RPR test (diagnosis of syphilis), tuberculin tests, ECHO-EG, brain MRI, electroencephalography are used.

Serous meningitis must be differentiated from subarachnoid hemorrhage, arachnoiditis, tick-borne encephalitis, purulent meningitis, meningococcal, pneumococcal, or any other etiology.

Treatment of serous meningitis

If serous meningitis is suspected, the patient is hospitalized. In the hospital begin etiotropic therapy. For herpetic meningitis, acyclovir is prescribed, for other types of viral meningitis - interferons. If the patient has a reduced immune response, then immunoglobulin is used simultaneously with antiviral drugs.

Identification of the causative agent of serous meningitis requires some time. Therefore, after taking the material for bakposev, the patient begins to administer broad-spectrum antibiotics.

Treatment of serous meningitis caused by mycobacterium tuberculosis is carried out with anti-tuberculosis drugs.

In addition, post-syndromic therapy is carried out. Non-steroidal anti-inflammatory drugs are used to lower body temperature. With increased intracranial pressure, diuretics are prescribed for the purpose of dehydration. Relief of convulsive syndrome requires the use of valproic acid, tranquilizers. With a pronounced intoxication syndrome, detoxification therapy is necessary.

To protect brain cells from damage, it is necessary to use neurotropic and neuroprotective drugs (pork brain hydrolyzate, B vitamins, nootropics).

Possible complications and consequences of serous meningitis

After suffering serous meningitis, in some patients, the following persist for several months:

• headache;
• decrease in concentration.

Gradually, these phenomena pass.

The inflammatory process in serous meningitis does not lead to cell necrosis and is not complicated by purulent tissue fusion. Therefore, this disease, unlike purulent meningitis, has a more favorable prognosis.

The consequences of serous meningitis of tuberculous etiology can be much more serious. Untimely start of specific therapy of the disease leads to a chronic inflammatory process, in severe cases, patients die on the 23-25th day from the onset of the first symptoms.

Forecast

Timely treatment of serous meningitis provides a rapid improvement in the condition of patients. The average duration of the disease is 10-14 days. In most cases, serous meningitis ends with complete recovery.

Prevention

Prevention of the development of serous meningitis includes:

• a healthy lifestyle (proper nutrition, exercise, giving up bad habits);
• vaccination against tuberculosis, measles, mumps;
• adequate treatment of infectious diseases;
• compliance with personal hygiene requirements.

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