Tuberculous meningitis is a long time a person lives. The complexity of the treatment of tuberculous meningitis

Tuberculous meningitis

What is tuberculous meningitis -

Hematogenous dissemination of MBT into the nervous system, into the structures surrounding the brain or spinal cord, causes meningitis.

Tuberculous meningitis is an inflammation of the meninges. Up to 80% of patients with tuberculous meningitis have either traces of previous tuberculosis of other localizations, or active tuberculosis of another localization at the moment.

What provokes / Causes of Tuberculous meningitis:

The causative agents of tuberculosis are mycobacteria - acid-fast bacteria of the genus Mycobacterium. A total of 74 species of such mycobacteria are known. They are widely distributed in soil, water, among people and animals. However, tuberculosis in humans causes a conditionally isolated M. tuberculosis complex, which includes Mycobacterium tuberculosis(human species), Mycobacterium bovis (bovine species), Mycobacterium africanum, Mycobacterium bovis BCG (BCG strain), Mycobacterium microti, Mycobacterium canetti. Recently, Mycobacterium pinnipedii, Mycobacterium caprae, phylogenetically related to Mycobacterium microti and Mycobacterium bovis, have been assigned to it. The main species characteristic of Mycobacterium tuberculosis (MBT) is pathogenicity, which manifests itself in virulence. Virulence can vary significantly depending on environmental factors and manifest itself differently depending on the state of the macroorganism that is subjected to bacterial aggression.

Tuberculosis in humans most often occurs when infected with human and bovine species of the pathogen. The isolation of M. bovis is observed mainly in rural areas, where the route of transmission is mainly alimentary. Avian tuberculosis is also noted, which occurs mainly in immunodeficient carriers.

MBT belong to prokaryotes (in their cytoplasm there are no highly organized organelles of the Golgi apparatus, lysosomes). There are also no plasmids characteristic of some prokaryotes, which provide the dynamics of the genome for microorganisms.

Shape - slightly curved or straight stick 1-10 µm × 0.2-0.6 µm. The ends are slightly rounded. They are usually long and thin, but bovine pathogens are thicker and shorter.

MBT are immobile, do not form microspores and capsules.
In a bacterial cell, it differentiates:
- microcapsule - a wall of 3-4 layers 200-250 nm 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.

Proteins (tuberculoproteins) are the main carriers of antigenic properties of MBT and show specificity in delayed-type hypersensitivity reactions. These proteins include tuberculin. The detection of antibodies in the blood serum of patients with tuberculosis is associated with polysaccharides. Lipid fractions contribute to the resistance of mycobacteria to acids and alkalis.

Mycobacterium tuberculosis is an aerobe, Mycobacterium bovis and Mycobacterium africanum are aerophiles.

In organs affected by tuberculosis (lungs, lymph nodes, skin, bones, kidneys, intestines, etc.), a specific "cold" tuberculosis inflammation develops, which is predominantly granulomatous in nature and leads to the formation of multiple tubercles with a tendency to disintegrate.

Pathogenesis (what happens?) during Tuberculous meningitis:

The hematogenous route of MBT penetration into the meninges is recognized as the main one. In this case, the damage to the meninges occurs in two stages.

1. At the first stage, with primary tuberculosis, sensitization of the body develops, a breakthrough of the MBT through the blood-brain barrier and infection of the choroid plexuses of the pia mater.
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.

During the spread of MBT from the primary tuberculosis focus or as a manifestation of miliary tuberculosis, microscopic tubercles appear in the brain tissue and meningeal membranes. Sometimes they can form in the bones of the skull or spine.

Tubercles can cause:
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.

These three processes form the clinical picture of tuberculous meningitis.

Not only the membranes of the brain and spinal cord, but also the vessels are involved in the pathological process. All layers of the vascular wall suffer, but the intima is the most affected. These changes are considered by pathologists as a manifestation of hyperergic inflammation. So, with tuberculous meningitis, the membranes and vessels of the brain are primarily affected. The brain parenchyma is involved in the process to a much lesser extent. In the cortex, subcortex, trunk, spinal cord, foci of specific inflammation are found mainly near the affected vessels.

Symptoms of tuberculous meningitis:

Meningitis affects mainly children, especially infants of early age, much less often - adults.

By localization, the main forms of tuberculous meningitis are distinguished: basilar meningitis; meningoencephalitis; spinal meningitis.

There are 3 periods of development of tuberculous meningitis:
1) prodromal;
2) irritation;
3) terminal (paresis and paralysis).

prodromal period characterized by gradual (within 1-8 weeks) development. First, there is a headache, dizziness, nausea, sometimes vomiting, fever. There is a delay in urine and stool, the temperature is subfebrile, less often - high. However, cases of the development of the disease and at normal temperatures are known.

Irritation period: 8-14 days after the prodrome, there is a sharp increase in symptoms, body temperature 38-39 ° C, pain in the frontal and occipital region of the head. Growing drowsiness, lethargy, oppression of consciousness. Constipation without distention - scaphoid abdomen. Photophobia, skin hyperesthesia, noise intolerance. Vegetative-vascular disorders: persistent red dermographism, red spots appear spontaneously and quickly disappear on the skin of the face and chest.

At the end of the first week of the irritation period (on the 5-7th day), an indistinctly pronounced meningeal syndrome appears (stiff neck, symptom of Kernig and Brudzinsky).

Characteristic manifestations of symptoms appear in the second period of irritation, depending on the localization of the inflammatory tuberculous process.

With inflammation of the meningeal membranes, headaches, nausea, and stiff neck are observed.

With the accumulation of serous exudate at the base of the brain, irritation of the cranial nerves may occur with the following symptoms: visual impairment, eyelid paralysis, strabismus, unequally dilated pupils, deafness. Fundus papilla edema is present in 40% of patients.

Involvement of the cerebral arteries in the pathological process can lead to loss of speech or weakness in the limbs. This can damage any area of ​​the brain.

With hydrocephalus of varying severity, exudate blocks some of the cerebrospinal connections with the brain. Hydrocephalus is the main cause of loss of consciousness. Pathological manifestations can be permanent and indicate a poor prognosis for patients who are unconscious.
With blockade of the spinal cord by exudate, weakness of motor neurons or paralysis of the lower extremities may occur.

Terminal period(period of paresis and paralysis, 15-24th day of illness). The clinical picture is dominated by signs of encephalitis: lack of consciousness, tachycardia, Cheyne-Stokes respiration, body temperature of 40 ° C, paresis, paralysis of a central nature.

In the spinal form in the 2nd and 3rd periods there are girdle, very strong radicular pain, flaccid paralysis, bedsores.

Diagnosis of tuberculous meningitis:

Diagnosis:
- timely - within 10 days from the beginning of the irritation period;
- later - after 15 days.

The simultaneous presence of the following diagnostic features indicates a high probability of tuberculous meningitis:
1. Prodrome.
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.

Since tuberculosis infection can be located anywhere in the body, it is necessary to pay attention to the presence of:
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.

The tuberculin test may be negative, especially in advanced stages of the disease (negative anergy).

Diagnostic signs of tuberculous meningitis in the analysis of cerebrospinal fluid:
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. Cell composition: 200-800 mm3 (norm 3-5).
4. The protein content is increased (0.8-1.5-2.0 g / l), the norm is 0.15-
0.45 g/l.
5. Sugar: reduced by 90%, but may be normal in early disease or AIDS. This indicator is important for differential diagnosis with viral meningitis, in which the sugar content in the spinal fluid is normal.
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.

Tuberculosis of the meninges, central nervous system in adults remains the main cause of death.

It is necessary to carry out differential diagnosis with bacterial meningitis, viral meningitis and HIV-cryptococcal meningitis. The first two are characterized by an acute onset. Cryptococcosis meningitis develops relatively slowly. The presence of tuberculosis in the family or the detection of tuberculous lesions of any organ makes the tuberculous origin of meningitis more likely. However, a reliable indication is the collection of cerebrospinal fluid (CSF) by lumbar puncture.

Treatment of tuberculous meningitis:

If there is a suspicion of the presence of tuberculous meningitis, the patient must be urgently hospitalized in a specialized medical institution, where X-ray examination, spinal puncture, laboratory examination, and specific methods of anti-tuberculosis therapy can be performed.

If left untreated, the outcome is fatal. The earlier the diagnosis is made and treatment is started, the clearer the patient's consciousness at the time of treatment, the better the prognosis.

Prevention of tuberculous meningitis:

Tuberculosis is one of the so-called social diseases, the occurrence of which is associated with the living conditions of the population. The causes of the epidemiological trouble for tuberculosis in our country are the deterioration of socio-economic conditions, the decline in the living standards of the population, the increase in the number of people without a fixed place of residence and occupation, and the intensification of migration processes.

Men in all regions suffer from tuberculosis 3.2 times more often than women, while the incidence rate in men is 2.5 times higher than in women. The most affected are persons aged 20-29 and 30-39 years.

The morbidity of contingents serving sentences in institutions for the execution of sentences of the system of the Ministry of Internal Affairs of Russia is 42 times higher than the average Russian indicator.

In order to prevent it is necessary to carry out the following measures:
- 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 hostels.
- 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 book an appointment with a doctor– clinic Eurolaboratory 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 also can call a doctor at home. Clinic Eurolaboratory open for you around the clock.

How to contact the clinic:
Phone of our clinic in Kyiv: (+38 044) 206-20-00 (multichannel). The secretary of the clinic will select a convenient day and hour for you to visit the doctor. Our coordinates and directions are indicated. Look in more detail about all the services of the clinic on her.

(+38 044) 206-20-00

If you have previously performed any research, be sure to take their results to a consultation with a doctor. If the studies have not been completed, we will do everything necessary in our clinic or with our colleagues in other clinics.

You? You need to be very careful about your overall health. People don't pay enough attention disease symptoms and do not realize that these diseases can be life-threatening. There are many diseases that at first do not manifest themselves in our body, but in the end it turns out that, unfortunately, it is too late to treat them. Each disease has its own specific signs, characteristic external manifestations - the so-called disease symptoms. Identifying symptoms is the first step in diagnosing diseases in general. To do this, you just need to several times a year be examined by a doctor not only to prevent a terrible disease, but also to maintain a healthy spirit in the body and the body as a whole.

If you want to ask a doctor a question, use the online consultation section, perhaps you will find answers to your questions there and read self care tips. If you are interested in reviews about clinics and doctors, try to find the information you need in the section. Also register on the medical portal Eurolaboratory to be constantly up to date with the latest news and information updates on the site, which will be automatically sent to you by mail.

Other diseases from the group Diseases of the nervous system:

Absence epilepsy Kalp

brain abscess

Australian encephalitis

Angioneuroses

Arachnoiditis

Arterial aneurysms

Arteriovenous aneurysms

Arteriosinus fistulas

Bacterial meningitis

amyotrophic lateral sclerosis

Meniere's disease

Parkinson's disease

Friedreich's disease

Venezuelan equine encephalitis

vibration sickness

Viral meningitis

Exposure to microwave electromagnetic field

Effects of noise on the nervous system

Eastern equine encephalomyelitis

congenital myotonia

Secondary purulent meningitis

Hemorrhagic stroke

Generalized idiopathic epilepsy and epileptic syndromes

Hepatocerebral dystrophy

herpes zoster

Herpetic encephalitis

Hydrocephalus

Hyperkalemic form of paroxysmal myoplegia

Hypokalemic form of paroxysmal myoplegia

hypothalamic syndrome

Fungal meningitis

Influenza encephalitis

decompression sickness

Pediatric epilepsy with paroxysmal EEG activity in the occipital region

Cerebral palsy

Diabetic polyneuropathy

Dystrophic myotonia Rossolimo-Steinert-Kurshman

Benign childhood epilepsy with EEG peaks in the central temporal region

Benign familial idiopathic neonatal seizures

Benign recurrent serous meningitis Mollare

Closed injuries of the spine and spinal cord

Western equine encephalomyelitis (encephalitis)

Infectious exanthema (Boston exanthema)

Hysterical neurosis

Ischemic stroke

California encephalitis

candida meningitis

oxygen starvation

Tick-borne encephalitis

Coma

Mosquito viral encephalitis

Measles encephalitis

Cryptococcal meningitis

Lymphocytic choriomeningitis

Pseudomonas aeruginosa meningitis (pseudomonous meningitis)

Meningitis

meningococcal meningitis

myasthenia gravis

Migraine

Myelitis

Multifocal neuropathy

Violations of the venous circulation of the brain

Spinal circulatory disorders

Hereditary distal spinal amyotrophy

trigeminal neuralgia

Neurasthenia

obsessive-compulsive disorder

neuroses

Neuropathy of the femoral nerve

Neuropathy of the tibial and peroneal nerves

Neuropathy of the facial nerve

Ulnar nerve neuropathy

Radial nerve neuropathy

median nerve neuropathy

Spina bifida and spinal hernias

Neuroborreliosis

Neurobrucellosis

neuroAIDS

Normokalemic paralysis

General cooling

burn disease

Opportunistic diseases of the nervous system in HIV infection

Tumors of the skull bones

Tumors of the cerebral hemispheres

Acute lymphocytic choriomeningitis

Acute myelitis

Acute disseminated encephalomyelitis

cerebral edema

Primary reading epilepsy

Primary lesion of the nervous system in HIV infection

Skull fractures

Shoulder-facial form of Landouzy-Dejerine

Pneumococcal meningitis

Subacute sclerosing leukoencephalitis

Subacute sclerosing panencephalitis

Late neurosyphilis

Polio

Polio-like diseases

Malformations of the nervous system

Transient disorders of cerebral circulation

- This is an acute disease in which the membranes of the brain are affected by a tubercle bacillus and become inflamed. It is a complication of the pulmonary form of tuberculosis. This article will describe the causes and mechanisms of its occurrence, the main symptoms, the principles of diagnosis and treatment.

Causes and mechanisms of development

Tuberculous meningitis develops in people who already have pulmonary tuberculosis. The causative agent is Koch's tubercle bacillus.

Mycobacterium tuberculosis is an acid-fast bacterium. A person is infected with it by airborne droplets. The source of infection is a sick person. In our time, there is a significant increase in cases of tuberculosis. Doctors note that the incidence rates are approaching epidemic.

Bacteria enter the membranes of the brain through the bloodstream, hematogenously. First, they settle on the vessels of the brain, and then penetrate into its membranes, and cause acute inflammation there. Allocate groups of people who have an increased risk of developing this disease. These include:

• people who have tuberculosis, or those who have already completed a course of therapy;
• people with immunodeficiency - HIV, AIDS;
• people who have a weakened immune system;
• people who have recently been in contact with patients with an open form of tuberculosis.

Clinical picture

Unlike bacterial or viral inflammation of the membranes of the brain, tuberculous meningitis does not develop at lightning speed, but gradually. This form of meningitis is characterized by the presence of a pronormal period of the disease, in which the following symptoms can be observed:

• The appearance of a headache. First, the head hurts in the evening, or during sleep, and then it becomes almost constant. This headache is almost not relieved by pain medications.
• Weakness, apathy, increased drowsiness.
• A significant decrease in appetite, up to anorexia.
• Irritability and excessive nervousness.

All these symptoms develop due to gradually increasing intracranial pressure. Since the inflammatory process develops gradually, meningeal syndrome begins to appear only after 7-10 days, after the start of the pronormal period. The main symptoms of meningeal syndrome are presented in the table:

The main symptoms of tuberculous meningitis
Symptom Name	General characteristics of the symptom
Stiff neck and neck muscles	The muscles of the neck and occipital region become hard, not elastic. They have an increased tone. It is difficult for the patient to bend or straighten the neck. The doctor, trying to passively bend it, feels the resistance of the muscles.
Pointing Dog Pose	The patient lies on his side with his head thrown back, pressing his legs to his stomach. So he subconsciously slightly reduces intracranial pressure.
Headache	A headache of a bursting nature, may be more pronounced in the forehead or temples. Not reduced by painkillers.
Reaction to sound and light	Patients react very painfully to all sounds and bright lights, and ask to draw the curtains and not make noise.
Vomit	Vomiting happens at the top of the headache. There is no nausea in front of her. Such vomiting does not bring relief. Vomiting occurs due to increased intracranial pressure.
Kernig's sign	The patient lies on his back, the doctor bends one leg at the hip joint and knee. But he can't bend his knee. This is due to high tension in the posterior thigh muscles, which causes flexion contracture.
Symptom Brudzinsky	Upper - the doctor passively flexes the patient's neck, and his lower limbs reflexively bend in the joints. Medium - if you press the patient on the pubis, his knees will bend. Lower - if you bend one leg, the second will also bend.

Principles of diagnosis of the disease

Tuberculous meningitis - symptoms

First of all, the doctor examines the patient, collects an anamnesis, a medical history. Then he examines him, and checks for meningeal symptoms. Already at this stage of diagnosis, the doctor suspects the development of meningitis. But to prescribe treatment and make an accurate diagnosis, one cannot do without laboratory and instrumental diagnostics.

The main research method is lumbar puncture. With its help, cerebrospinal fluid, cerebrospinal fluid, is taken for analysis. The main characteristics of cerebrospinal fluid for tuberculous meningitis:

1. Increased CSF pressure during the puncture itself. With tuberculous meningitis, cerebrospinal fluid flows out in a stream, or in frequent drops.
2. If you put the liquor in the light, on the windowsill, for example, in an hour a film will fall out in it, which will glow under the rays of the sun.
3. An increased number of cells in the cerebrospinal fluid. Normally, out of 3-5 in the field of view, and with tuberculous meningitis 200-600.
4. The level of protein in the cerebrospinal fluid rises to 1.5-2 grams per liter. The norm is 0.1-0.2.
5. A decrease in the level of glucose in the cerebrospinal fluid is observed only in patients who are not additionally infected with the HIV virus.
6. In 10% of the cerebrospinal fluid, Koch's tubercle bacillus can be isolated.

In addition to lumbar puncture, the following examinations are carried out:

1. Plain radiography of the chest. It is needed to identify the primary tuberculosis focus.
2. General blood analysis. It is needed to assess the severity of the inflammatory process in the body, as well as to determine the blood cell composition. With a reduced color index, hemoglobin erythrocytes, the patient will have anemia.
3. Computed tomography of the brain is performed in acute forms of meningitis, it is needed to assess the volume of tissue affected by the inflammatory process.
4. Sputum microscopy - performed to detect acid-resistant tuberculosis bacteria in sputum.

Basic principles of treatment of tuberculous meningitis

Treatment of tuberculous meningitis is carried out in intensive care units at tuberculosis dispensaries. Treatment for tuberculous meningitis includes:

• Strict bed rest.
• Constant control over the level of arterial blood pressure, heart rate, oxygen and carbon dioxide levels in the blood.
• Oxygen support is provided through a mask.
• Taking anti-tuberculosis drugs. The scheme of these drugs is developed by the attending physician. The standard scheme includes Isoniazid, Rifampicin, Ethambutol, Pyrazinamide. Before prescribing these drugs, a sensitivity test to them is carried out. Recently, cases of resistance of tuberculosis bacteria to standard treatment regimens have become more frequent.
• Detoxification therapy. It includes intravenous administration to the patient of solutions such as Ringer's solution, Trisol, Disol, Rheosorbilact, Polyglukin. These drugs are administered together with diuretics (Furosemide, Lasix) to prevent the development of cerebral edema.
• Hepatoprotectors - are prescribed to protect the liver from the hepatotoxic effect of anti-tuberculosis drugs. These include Heptral, Milk Thistle, Karsil.
• Corticosteroids are prescribed for toxic shock.

Complications of tuberculous meningitis

The course of tuberculous meningitis can be complicated by such conditions:

• swelling of the brain;
• Infectious-toxic shock;
• Encephalitis - involvement in the inflammatory process of the tissues of the brain itself;
• Sepsis;
• Partial paralysis or paresis;
• herniation of the brain;
• Hearing, vision, speech impairment.

Tuberculous meningitis is a complication of primary meningitis. Unlike other types of inflammation of the meninges, the disease does not develop quickly, but gradually, over 1-2 weeks. Such patients are treated in tuberculosis dispensaries, in intensive care units, under the constant supervision of medical personnel.

Tuberculous meningitis is a predominantly secondary tuberculous lesion (inflammation) of the soft, arachnoid membranes and less of the hard one, which occurs in patients with various, more often active and widespread, forms of tuberculosis. Tuberculosis of this localization is the most difficult. In adults, tuberculous meningitis is often a manifestation of an exacerbation of tuberculosis and may be its only established localization.

Tuberculosis of the central nervous system, tuberculous meningitis - the most severe form of extrapulmonary tuberculosis, occurs at any age, but 8-10 times more often in young children. Most cases of this pathology are observed during the first 2 years of MBT infection.

Pathogenesis

In the pathogenesis of tuberculous meningitis, sensitization of the body plays an important role, leading to a violation of the blood-brain barrier under the influence of various non-specific factors that reduce protective reactions:

• injuries, especially to the head;
• hypothermia;
• hyperinsolation;
• viral diseases;
• neuroinfections.

In addition, it should be taken into account that the infection “breaks through” into the nervous system when the vascular barrier is violated in a certain hyperergic state of the vessels, when the necessary immunobiological conditions are created for this: contact with a patient with tuberculosis, difficult material and living conditions, severe intercurrent diseases; in children - early age, lack of BCG vaccination; in adults - alcoholism, drug addiction, HIV infection, etc.

There are several theories of the pathogenesis of tuberculous meningitis:

• hematogenous;
• liquorogenic;
• lymphogenous;
• contact.

Most scientists adhere hematogenous-liquorogenic theory occurrence of tuberculous meningitis. According to this theory, the development of meningitis occurs in two stages.

Stage one, hematogenous, occurs against the background of general bacteremia. MTB in conditions of hypersensitization and a decrease in the body's defenses in primary, disseminated tuberculosis penetrate the blood-brain barrier; at the same time, the choroid plexuses of the ventricles of the brain are affected.

The second stage, liquorogenic, accompanied by the penetration of MTB from the vascular plexuses into the cerebrospinal fluid; further along the cerebrospinal fluid to the base of the brain, where they settle in the area from the optic chiasm to the medulla oblongata and adjacent parts of the cerebellum. A specific inflammation of the soft meninges of the base of the brain develops - basilar meningitis.

MV Ishchenko (1969) proved the existence of a lymphogenous route of infection of the meninges, which he observed in 17.4% of patients. At the same time, MBT from the upper cervical fragment of the jugular chain of lymph nodes affected by tuberculosis through the perivascular and perineural lymphatic vessels enter the meninges.

In addition, with the localization of the tuberculous process in the spine, bones of the skull, the inner ear, the infection is transferred to the meninges by liquorogenic and contact routes. The meninges can also become infected from pre-existing tuberculous foci (tuberculoma) in the brain due to the activation of tuberculosis in them.

In the vast majority of cases, TM develops in patients with pulmonary or extrapulmonary tuberculosis of any form and at various phases of the process. . In young children, inflammation of the meninges can develop against the background of tuberculosis of the intrathoracic lymph nodes or a primary tuberculosis complex complicated by hematogenous generalization. However, in 15% of patients, meningitis may occur in the absence of visible tuberculous changes in the lungs and other organs ("isolated" primary meningitis). Early diagnosis of tuberculous meningitis determines the success of treatment.

Tuberculosis of the central nervous system manifests itself in damage to the brain and its membranes, which is a consequence of hematogenous dissemination in both primary and secondary tuberculosis. Tuberculous inflammation of the meninges is localized, as a rule, in the region of the base of the brain. The shells acquire a greenish-yellowish jelly-like appearance with separate grayish tubercles on the surface. Microscopic examination reveals inflammatory infiltrates in the walls of small vessels, consisting of leukocytes and lymphocytes. Thickening of the walls of blood vessels leads to narrowing of the lumen and the appearance of blood clots. Typical tuberculous granulomas and infiltrates of a specific nature may occur. Infiltrates may also undergo cheesy necrosis.

The spread of inflammation to adjacent tissues and the development of destructive vasculitis leads to the appearance of foci of softening of the brain substance. In later periods, adhesions of the meninges are found and, as a result, hydrocephalus.

Initially, the inflammatory process is localized at the base of the brain behind the optic chiasm, capturing the infundibulum, mastoid body, the region of the quadrigemina and the legs of the brain.

The pia mater becomes cloudy, gelatinous, translucent. Along the olfactory tracts, near the intersection of the optic nerves, on the lower surface of the frontal lobes of the brain and in the Sylvian furrows, rashes of small tuberculous tubercles are visible. The ventricles of the brain are filled with a clear or slightly cloudy fluid. With the defeat of the Sylvian sulcus, the middle cerebral artery passing through it is often involved in the process. Vessel wall necrosis or thrombosis may develop, leading to ischemia of a certain part of the brain and irreversible consequences. With tuberculous meningitis, changes are always found in the hypothalamic-pituitary region, and the bottom and the area of ​​\u200b\u200bthe third ventricle adjacent to it are affected. Such localization entails the defeat of the numerous vegetative centers located here. In the future, dysfunctions of the cranial nerves - optic, oculomotor, trochlear, abducent, trigeminal, facial - join. With the progression of the process, the pons and medulla are involved in the inflammatory process, disorders of the cranial nerves appear (IX, X, XII). Death occurs from paralysis of the vasomotor and respiratory centers, which are located in the medulla oblongata.

Clinical picture

There are three main forms:

• basal meningitis (damage to the pia mater of the base of the brain);
• meningoencephalitis;
• cerebrospinal leptopachimeningitis.

There are three periods during tuberculous meningitis:

• premonitory;
• period of irritation of the central nervous system;
• period of paresis and paralysis.

prodromal period lasts 1-3 weeks (usually 7 days in children). At this time, insufficiently typical and inconsistent symptoms occur that do not allow a timely diagnosis. The disease develops gradually. The period of the prodrome is characterized by intermittent headaches, apathy, lethargy, drowsiness during the daytime, interspersed with excitability (anxiety, whims), loss of appetite, low-grade body temperature. At the end of the prodromal period, vomiting is added, not associated with food intake, and a tendency to delay stool. In this period of the disease, bradycardia is noted.

During the period of stimulation of the central nervous system- 8-15th day of illness (irritation of the central nervous system) - all of the listed symptoms increase in intensity, especially headache, which becomes constant (in the forehead and occiput), and vomiting. Vomiting is a constant and very early symptom. Vomiting typical of tuberculous meningitis is characterized as fountain-like. Decreased appetite comes to complete anorexia, which leads to rapid and abrupt loss of body weight. Body temperature reaches high figures - 38-39 ° C. The symptoms of irritation of the meninges join - stiff neck, positive symptoms of Kernig, Brudzinsky, the intensity of which increases towards the end of the second week of the disease. As a result of irritation of the nervous system, hyperesthesia of the analyzers, photophobia, tactile hypersensitivity, and increased hearing irritation occur. Abdominal reflexes usually disappear, tendon reflexes may be reduced or increased. Vegetative disorders are expressed in tachycardia, increased blood pressure, increased sweating, red dermographism and Trousseau spots. At the same time, lesions of the cranial nerves are noted: most often - oculomotor, abducent, facial, which is detected in the form of eyelid drooping, strabismus, smoothing of the nasolabial fold, anisocoria. When examining the fundus, congestive disc nipples or optic neuritis, tuberculous tubercles on the choroid are found. Damage to the optic nerve can lead to total blindness. By the end of the second period, which lasts approximately one week, the patient is in a characteristic position - he lies on his side with his legs pulled up to his stomach and his head thrown back. There are signs of confusion, the patient is negative and sharply inhibited. Tuberculous meningitis is serous meningitis.

The composition of the cerebrospinal fluid is changed: its pressure is increased due to increasing hydrocephalus up to 300-500 mm of water. Art. (normally 50-150 mm water column), it is transparent, colorless, may be opalescent. The protein content increases to 0.8-1.5 g/l and higher (normally 0.15-0.33 g/l) mainly due to globulins (Pandy and Nonne-Apelt globulin reactions are sharply positive), drops out in the cerebrospinal fluid fibrin mesh in the form of an hourglass 12-24 hours after sampling. After centrifugation of the test tube, a smear is made from the sediment on the glass and stained according to Ziehl-Neelsen. This allows you to detect the MBT. Pleocytosis reaches 200-700 cells per 1 ml (normally 3-5-8, in young children - up to 15 per 1 μl), has a lymphocytic-neutrophilic character, less often - neutrophilic-lymphocytic in the early stages of diagnosis. As the duration of the disease increases, cytosis becomes persistently lymphocytic. It should be noted that the number of cells in the cerebrospinal fluid can periodically reach large numbers of 1000-2000, which can make differential diagnosis difficult. The glucose level is reduced to 1.5-1.6 mmol/l (normally 2.2-2.8 mmol/l), chlorides - up to 100 mmol/l (normally 120-130 mmol/l), Mycobacterium tuberculosis in cerebrospinal fluid are found in 10-20% of patients by simple bacterioscopy and culture. With meningoencephalitis and spinal meningitis, the composition of the cerebrospinal fluid changes even more.

Terminal period of paresis and paralysis also lasts about a week (15-24th day of illness) and is characterized by signs of meningoencephalitis: complete loss of consciousness, convulsions, central (spastic) paresis and paralysis of the limbs. Tachycardia, violation of the rhythm of breathing according to Cheyne-Stokes, thermoregulation is disturbed - hyperthermia up to 41 ° C or a sharp drop in temperature below normal. Cachexia develops, bedsores appear. Then death occurs as a result of paralysis of the respiratory and vasomotor centers.

spinal meningitis is relatively rare. In this process, there is a transition of inflammatory changes from the membranes of the brain to the membranes of the spinal cord, all this manifests itself against the background of meningoencephalitis. Radicular disorders, paraparesis, blockade of liquor pathways with protein-cell dissociation (a very high level of protein with moderately pronounced cytosis) join the meningeal symptoms. The course of the disease is long, an unfavorable outcome is possible.

In blood tests for tuberculous meningitis, a decrease in the level of hemoglobin and erythrocytes, an increase in ESR to 25-50 mm / h, moderate leukocytosis and a shift of the leukocyte formula to the left, lymphocytopenia, monocytosis, and the absence of eosinophils are observed. Tuberculin tests are usually negative.

The development of tuberculous meningitis in a child, according to the majority of domestic and foreign clinicians, occurs mainly in the first 3-9 months of MBT infection. The most difficult issues in diagnosing this form of tuberculosis arise when meningitis is the first clinical manifestation of tuberculosis and there is no information about contact with the patient, there is no tuberculin diagnostic data. The presence of a vaccination mark on the shoulder against BCG vaccination at birth does not allow doctors to think about the possibility of a tuberculosis nature of the disease. And this is a mistake. According to the City Children's Tuberculosis Hospital, in the last 10-12 years, 60% of children with tuberculous meningitis were vaccinated with the BCG vaccine.

Young children are characterized by a short (3 days) prodromal period, an acute onset of the disease, convulsions and focal symptoms of damage to the central nervous system occur in the first days of the disease, meningeal symptoms are mild, and there is no bradycardia. There is an increase in stool up to 3-5 times a day, which, in combination with vomiting, resembles dyspepsia. The fontanel is tense and bulging and there is no exsicosis. Hydrocephalus develops rapidly. Sometimes there is only a slight increase in body temperature, drowsiness and protrusion of the fontanel. The prognosis may be poor if a lumbar puncture is not performed and treatment is not started on time.

Differential Diagnosis with meningitis of another etiology

(bacterial, viral, fungal), encephalitis, poliomyelitis, abscess and brain tumor and other diseases that have similar clinical symptoms, should be based on the indicators of cerebrospinal fluid, the presence of MBT in it, the presence of other localizations of tuberculosis (X-rays of the lungs and tomograms of the mediastinum are required), contact with tuberculosis patients, acute or gradual onset of the disease, the nature of the course of the disease, the epidemic situation. Conducting tuberculin diagnostics and serological studies, PCR, blood and cerebrospinal fluid tests can confirm the fact of infection and the activity of tuberculosis infection.

Diagnosis of tuberculous meningitis should be very quick, no later than the 10th day of illness from the first vomiting, which appears already in the prodromal period. Timely treatment with anti-tuberculosis drugs is highly effective, without consequences.

In situations of difficult diagnosis of meningitis, when the tuberculous etiology of the disease cannot be proven, but is not removed in diagnostic searches, therapy with the three main anti-tuberculosis drugs (rifampicin, isoniazid, streptomycin) should be immediately started and differential diagnosis should be continued against this background.

Treatment

Chemotherapy. Treatment of patients with tuberculous meningitis must necessarily be comprehensive and carried out in specialized institutions. During the first 24-28 weeks, treatment should be carried out in a hospital, then, for 12 weeks, in a sanatorium. Use 4 chemotherapy drugs during 6 months, then - 2 tuberculostatics before the end of the main course on the background of pathogenetic therapy.

Dehydration therapy for tuberculosis of the meninges is more moderate than for other meningitis. Diuretics are prescribed: lasix, furosemide, diacarb, hypothiazide, in severe cases - mannitol (intravenously 15% solution at the rate of 1 g of dry matter per 1 kg of body weight), 25% solution of magnesium sulfate - intramuscularly 5 - 10 days; 20-40% glucose solution is injected intravenously 10-20 ml, after 1-2 days, only 6-8 injections; unloading lumbar punctures 2 times a week. Control lumbar punctures are performed in the 1st week of treatment 2 times, and then 1 time per week, from the 2nd month 1 time per month until the composition of the cerebrospinal fluid is normalized, after which - according to indications. Detoxification therapy is also shown - the introduction of rheopolyglucin, gelatinol, saline solutions under the control of diuresis.

The prognosis of tuberculous meningitis in children under 3 years of age is usually less favorable than in older age groups. The probability of complete recovery is the less, the later the diagnosis of this difficult process was before the start of specific treatment. One of the frequent and dangerous complications of tuberculous meningitis is hydrocephalus.

The death of such patients occurs in 20-100% of cases, depending on the stage of the process. In the absence of the effect of conservative therapy and persistent CSF circulation disorders, hydrocephalus can be corrected by CSF shunting operations, when, with the help of permanent implantation of special drainage systems, excess cerebrospinal fluid from the ventricles or subarachnoid spaces is removed into the extracranial serous cavities or into the bloodstream.

These operations provide stable correction of CSF circulation in 80-95% of cases. Under our supervision there were two children with tuberculous meningitis who underwent liquor shunting operations in the treatment of hydrocephalus with a favorable clinical effect. In some cases, this can save the life of the patient, but the use of these interventions should be limited due to the danger of generalization of the infection. Tuberculostatic therapy after surgery should continue for at least 18 months.

After recovery, the child is observed in the anti-tuberculosis dispensary until the age of 18 and is not subjected to any preventive vaccinations.

The content of the article

The pathogenesis of tuberculous meningitis

Modern ideas about the pathogenesis of tuberculous meningitis can be formulated in the following terms:
1) tuberculous meningitis - a pathogenetically secondary disease, i.e., for its occurrence, it is necessary to have an earlier tuberculous lesion in the body;
2) tuberculous meningitis, as a rule, is basilar meningitis, i.e., it is localized mainly on the pia mater of the base of the brain;
3) its development proceeds in two stages. At the first stage, the choroid plexuses of the ventricles of the brain are affected by the hematogenous way with the formation of a specific granuloma in them; choroid plexuses are the main source of formation of cerebrospinal fluid; along with the endothelium of the capillaries and meninges, they serve as an anatomical substrate for the blood-brain barrier. The second stage is liquorogenic, when tuberculous mycobacteria from the vascular plexuses, along the current of the cerebrospinal fluid, settle on the base of the brain, infect the meninges and, due to vascular changes, cause a sharp allergic reaction, which manifests itself clinically as an acute meningeal syndrome.
The introduction of effective anti-tuberculosis drugs into clinical practice has significantly changed the pathoanatomical picture of tuberculous meningitis compared to the past.

Pathological anatomical picture of tuberculous meningitis

The pathoanatomical picture of tuberculous meningitis treated with streptomycin is characterized by limited localization, a clear decrease in the exudative component of the inflammatory reaction on the pia mater, and a predominance of productive inflammatory changes with a tendency to form scars and adhesions.
After the introduction of isonicotinic acid hydrazide preparations into practice, a number of features are noted in comparison with what was observed during the period of treatment with streptomycin alone: ​​the proportion of fibroplastic processes over exudative and productive ones increased significantly; processes occurring with softening of the brain substance due to thrombosis of the cerebral vessels as a result of progressive endarteritis began to be observed much less frequently; degenerative changes in the region of the VIII pair of cranial nerves associated with the toxic effects of streptomycin began to occur less frequently.

Clinic, course, differential diagnosis of tuberculous meningitis

In the symptomatology of any meningitis, the following clinical signs come to the fore in the clinical picture:
1) meningeal syndrome, directly related to the pathological process in the pia mater;
2) paralysis of the spinal roots and cranial nerves;
3) symptoms of irritation and prolapse from the brain.
Meningeal syndrome, in turn, consists of two symptoms; headache and contractures. The headache is usually very intense, to the point of feeling intolerable. It intensifies under the influence of external influences (noise, light) or movement and is accompanied by vomiting without nausea, without tension, with a stream. Headache is caused by damage to the pia mater.
Two factors play the main role in the mechanism of its occurrence:
1) toxic irritation by the inflammatory process of the roots of the trigeminal and vagus nerves passing through the pia mater;
2) hydrocephalus usually associated with meningitis with increased intracranial pressure as a result of hypersecretion of cerebrospinal fluid, which is caused by an inflammatory process on the meninges and vascular bodies; increased intracranial pressure increases the headache, irritating the endings of the autonomic nerves of the pia mater.
Vomiting is caused by direct or reflex irritation of the vagus nerve and its nuclei located at the bottom of the IV ventricle or vomiting center in the reticular substance of the medulla oblongata.
The second constant symptom of meningitis - contractures - is caused by irritation of the roots by the inflammatory process and increased pressure of the cerebrospinal fluid, which overflows the subarachnoid space; contractures and are an expression of increased activity of the reflex apparatus of the spinal cord, which protects the roots from mechanical irritation.
Irritation of the roots of the spinal cord leads to an increase in the tone of the muscles of the occiput, trunk and abdomen, causing neck stiffness, opisthotonus and abdominal retraction.
Clinically, the presence of contractures is determined by two constant symptoms of meningitis: neck stiffness and Kernig's symptom. Stiffness of the occiput causes a characteristic tilting of the head; any attempt to change this fixed position and bend the head forward causes a sharp painful reaction. An important and early diagnostic symptom is Kernig's symptom: the patient, lying on his back, bend his leg at a right angle in the hip and knee joints and then try to straighten it in the knee joint. At the same time, increased resistance is felt: it depends on the reflex contraction of the lower leg flexors (stronger than the extensors); this contraction is due to tension and contraction of the nerve roots.
Brudzinsky's symptoms are less constant: upper (with a sharp bending of the head, the legs bend and pull them to the stomach) and lower (when one leg is bent at the knee and hip joints, the other also bends).
Meningeal syndrome is accompanied by a number of concomitant clinical disorders:
1) elevated temperature;
2) dissociation between pulse and temperature (bradycardia at elevated temperature and tachycardia at normal), arrhythmia: fluctuations in blood pressure;
3) disturbances in the rhythm of breathing (stopping breathing, discrepancy between chest and abdominal breathing, chain-stokes breathing);
4) vasomotor disorders (sharp dermographism - "Trousseau's meningeal feature"; frequent change of blanching and reddening of the face - "Trousseau's spots");
5) secretory disorders (increased perspiration and salivation);
6) general hyperesthesia (due to irritation of the posterior roots or cells of the intervertebral nodes).
7) disorders of the mental sphere: lethargy at the first stages with symptoms of retrograde amnesia (or, conversely, psychomotor agitation, mainly in those suffering from alcoholism), as the process progresses (approximately after 10 days from the onset of meningeal syndrome) - the onset of confused consciousness with the transition to coma condition, after 15-16 days - with symptoms of swallowing disorders and dysfunction of the pelvic organs and, as a rule, fatal
on the 19th-21st day from the onset of the disease (in the absence of treatment). Experience has shown that in the majority of patients with advanced processes, it is completely impossible to establish the etiology of meningeal syndrome on the basis of data from neurological status alone. This applies in particular to patients delivered in an unconscious state, when a neurological examination in all its details is not possible. Therefore, it is advisable to build a method for diagnosing tuberculous meningitis based on ideas about its pathogenesis.
If an active tuberculosis process, pulmonary or extrapulmonary, is detected in a patient with a meningeal symptom complex in the body, the doctor has the right to diagnose tuberculous meningitis and is obliged to start appropriate treatment. Tuberculous meningitis in adults is accompanied by an active tuberculous process in other organs in 90% (80% in the lungs).
When a patient is admitted, regardless of the severity of the condition, an x-ray of the lungs is necessary.
It is well known that tuberculous meningitis differs from meningitis of other etiologies in its gradual onset, sometimes in the form of a prodromal period. The latter is characterized by general changes in the mental state of the patient, standing on the verge of normal and pathological: the regulatory adaptations of the body are still preserved, which sometimes prevents others from suspecting the presence of a serious, dangerous disease, although there are obvious symptoms of it.
During the period of gradual development of the disease, the most frequent diagnostic errors occur: the doctor to whom the patient turns does not associate vague complaints with a formidable idea of ​​tuberculous meningitis. The patient is unsuccessfully referred from one doctor to another, precious time is lost, and the intensity of the symptoms is steadily increasing.
Initially, patients report headaches in the evenings, fever, and sometimes neck stiffness, very often these phenomena are accompanied by a catarrhal condition of the respiratory tract. Children develop drowsiness, lethargy, lack of interest in games and communication with friends, schoolchildren have a noticeable, for no apparent reason, decrease in academic performance.
The general condition of the patient is almost not disturbed, he does not even stop his professional activity and is treated with home remedies. But the increase in headache makes him see a doctor on the 3-4th day. The general practitioner usually diagnoses influenza or upper respiratory catarrh and prescribes appropriate home treatment. Due to the lack of effect, the sick person visits the same doctor again after a few days. The discrepancy between the intensity of headaches and a satisfactory general condition sometimes leads to the assumption of frontal sinusitis or sinusitis, and the patient is referred to an otolaryngologist. The therapy prescribed by the otolaryngologist also has no effect, headaches increase, the general condition worsens, the temperature rises to febrile, attempts to continue the active mode (walks) lead to fainting. The worsened condition of the patient forces him to invite a doctor to his house, and in some cases, the presence of a pronounced meningeal syndrome (headaches, vomiting, stiff neck, Kernig's symptom) and, which is especially characteristic, an associated lesion of the cranial nerves (oculomotor, abducent, facial, hyoid, optic ) lead to a correct diagnosis.
In rare cases (usually in young children), tuberculous meningitis occurs acutely; sometimes such a development is observed immediately after a severe trauma to the skull.
Tuberculous meningitis is characterized by seasonal confinement (mainly in spring).
Meningeal syndrome, in particular headache, is usually more pronounced in patients who have not been treated with modern anti-tuberculosis drugs in the past.
With regard to vomiting, there is a relationship that is inverse to age: the younger the patient, the more often he vomits. Kernig's symptom is positive in 80-90% of patients with tuberculous meningitis, more common in children than in adults. In the same way, the symptom of stiff neck is distinguished by a high constancy.
The meningeal symptom complex is a typical picture that serves as a starting point for the diagnosis of tuberculous meningitis.
Since the introduction of anti-tuberculosis drugs into medical practice, patients have appeared in whom tuberculous meningitis occurs against the background of long-term antibacterial treatment (inpatient or outpatient) and manifests itself with a mild clinical picture of the meningeal symptom complex - the so-called erased form of tuberculous meningitis. In recent years, such erased forms of tuberculous meningitis began to appear in patients who had not been treated with anti-tuberculosis drugs in the past.
In these cases, the decisive factors in the diagnosis of tuberculous meningitis are the presence of a tuberculous process in the body, against which a meningeal symptom complex has developed, and characteristic changes in the cerebrospinal fluid, which, in erased forms, do not differ from what is observed in a typical course of tuberculous meningitis.
In the first place in terms of the frequency of damage to the cranial nerves in tuberculous meningitis is the oculomotor nerve. With paralysis of the oculomotor nerve, symptoms such as ptosis, dilated pupil (mydriasis), diverging strabismus are observed; the eyeball on the healthy side looks straight, and on the affected side it is turned outward and slightly down. In addition, diplopia and paralysis of accommodation, and sometimes exophthalmos, are noted.
The second most common is paralysis of the VI pair - the abducens nerve. When it is damaged, converging strabismus occurs, the inability to turn this eyeball outward, double vision, especially when looking towards the affected muscle, sometimes dizziness and a forced position of the head.
The third most common is peripheral paralysis of the facial nerve, resulting in a sharp asymmetry of the face. The affected side is mask-like, the forehead and nasolabial folds are smoothed, the palpebral fissure is wider, the corner of the mouth is lowered. When wrinkling the forehead on the side of the paralysis, folds do not form, when squinting, the palpebral fissure does not close (lagophthalmos). More often there is a central paralysis of the facial muscles, which can be combined with hemiplegia. With central paralysis, the upper facial muscles do not suffer and only the lower branch is affected.
Finally, paralysis of the XII pair sometimes develops - the hypoglossal nerve, which is the motor nerve of the tongue. Peripheral paralysis or paresis of the corresponding half of the tongue develops with atrophy and thinning of the muscles. When protruding the tongue from the mouth, it deviates with its end towards the affected muscle.
Lesions of these four cranial nerves are easily diagnosed and form a picture of the so-called base syndrome, characteristic of the neurological picture of tuberculous meningitis. In addition, there are often lesions of the fundus (tuberculous choroidal tubercles, congestive nipples, optic neuritis or atrophy). Diagnosis of such lesions Put by an ophthalmologist; in each case of tuberculous meningitis, an appropriate special examination is necessary.
Along with damage to the cranial nerves in tuberculous meningitis, clinical disorders associated with focal lesions of the brain substance (aphasia, hemiparalysis or hemiparesis of central origin) naturally occur. These lesions are based on progressive endarteritis of the cerebral vessels with complete closure of its lumen, ischemia and subsequent softening of the corresponding area of ​​the brain tissue and damage to the pyramidal pathway.
At the same time, in the initial forms of tuberculous meningitis, one or another degree of damage to the pyramidal tract can be noted, which does not yet cause loss of focal function. A symptom of such a lesion is a change in the conduction of abdominal reflexes - their unevenness, decrease or absence. There may be various deviations from the norm of tendon reflexes (uneven revival, decrease and absence).
Along with this, for the diagnosis of tuberculous meningitis, data from the study of cerebrospinal fluid are of great importance.
Tuberculous meningitis is characterized by the following pathological changes in the cerebrospinal fluid: increased intracranial pressure in the range from 300 to 500 mm of water. Art., and sometimes higher (normally 100-200 mm of water. Art.); the protein content increases (from 0.6 to 1.5-2% o; normally 0.3% 0); cytosis from 100 to 600 cells per 1 mm3, predominantly lymphocytic (normal up to 3-5 lymphocytes per 1 mm3). Reduced compared with the norm, the level of sugar and chlorides; of these indicators, the level of sugar is of particular importance (normally 40-60 mg% of sugar, 600-700 mg% of chlorides). When the liquid is standing, a characteristic delicate cobweb-like film falls out in it; the Pandey and Nonne-Apelt protein reactions are positive, which indicate a change in the protein profile of the liquid, mainly the predominance of the globulin component in it compared to the albumin fractions. Finally, mycobacterium tuberculosis is found in the cerebrospinal fluid or film. But in practice, in the cerebrospinal fluid in 90-80% of cases of indisputable tuberculous meningitis, Mycobacterium tuberculosis is not found even when examining the most subtle methods, including the sowing method.
The presence of inflammatory changes in the cerebrospinal fluid is one of the indispensable conditions for the diagnosis of tuberculous meningitis. The significance of this indicator in diagnostics has especially grown recently, when the erased forms of tuberculous meningitis mentioned above appeared, in which the characteristic neurological features of meningitis are significantly obscured.
When interpreting data from a study of cerebrospinal fluid, a very large place is occupied by the protein-cell dissociation syndrome typical of tuberculous meningitis, i.e., such lesions in which congestion comes to the fore compared to inflammatory ones. They are characterized by a high protein content in the cerebrospinal fluid, reaching 30% o, and a relatively low cytosis, close to normal or slightly exceeding it. These data always indicate a significant violation of the circulation of cerebrospinal fluid or even the separation of the upper and lower parts of the subarachnoid space - the so-called block of the CSF tract. Diagnosis of the CSF tract block is also confirmed by the symptom of Quekkenshtedt: during endolumbar puncture, the manometer does not detect an increase in intracranial pressure when pressing the jugular veins; in the absence of a block, such pressure causes a clear increase in intracranial pressure.
Blood test data: tuberculous meningitis is characterized by a moderate increase in ESR, normal numbers of leukocyte count, stab shift and lymphopenia.
Diagnosis of tuberculous meningitis is determined by five main elements: 1) the presence in the body of an active pulmonary or extrapulmonary tuberculosis process (in addition to damage to the meninges); 2) a characteristic anamnesis with the gradual development of a meningeal symptom complex against a background of febrile temperature; 3) the presence of damage to the cranial nerves; 4) characteristic changes in the cerebrospinal fluid; 5) blood picture typical for tuberculosis. The combination of all these elements greatly facilitates the task of diagnosis, but in practice this combination is not always observed.

Classification of tuberculous meningitis

As for the issue of classification of tuberculous meningitis, it is rational to distinguish the following three main forms: basilar tuberculous meningitis (most common - up to 90%), tuberculous meningoencephalitis and spinal form of tuberculous meningitis. This grouping is simple and corresponds to the main forms that are found in practice in both adults and children.
With basilar meningitis, the meningeal syndrome and cranial nerve damage without any other complications come to the fore. This group also includes erased forms of meningitis, as well as those forms in which there is no damage to the cranial nerves.
The second form - meningoencephalitic, or meningovascular - is clinically characterized by a combination of meningeal syndrome with manifestations of focal lesions of the brain substance (aphasia, hemiparalysis and hemiparesis).
In the third - spinal - form of tuberculous meningitis, the clinical picture is dominated by phenomena that indicate damage to the substance, membranes or roots of the spinal cord, mainly the lower extremities, and dysfunction of the pelvic organs
With uncomplicated basilar meningitis, the cure can be complete, without residual effects or with residual functional effects associated with the drug-toxic effect of streptomycin with its subarachnoid administration.
With meningoencephalitic meningitis, severe lesions of the musculoskeletal system, which are restored over a long time, may come to the fore as residual effects. Residual effects in spinal meningitis require even longer periods of treatment and can cause irreversible or very difficult to reverse movement disorders such as paraplegia or paraparesis associated with adhesive processes in the region of the spinal cord roots.

Differential diagnosis of tuberculous meningitis

First of all, you need to keep in mind meningitis of a different etiology: purulent (pneumococcal, less often staphylo- or streptococcal, meningococcal) and non-purulent, serous (viral).
Purulent meningitis has the following differences from tuberculous:
1) acute, sometimes lightning-fast occurrence;
2) localization of the process mainly on the pia mater in the region of the cerebral hemispheres (convexive meningitis) with the corresponding clinical picture of psychomotor agitation, in contrast to basilar meningitis, which occurs more often with symptoms of general lethargy and damage to the cranial nerves;
3) acute inflammatory reaction of the cerebrospinal fluid, which is manifested by high pleocytosis (4000-8000 cells per 1 cm3), as a rule, neutrophilic, with the detection of the corresponding pathogen in the fluid (pneumococcus, meningococcus);
4) as a rule, high leukocytosis.
Non-purulent meningitis (serous, viral) is characterized by an acute onset, moderately severe meningeal syndrome, a slight tendency to involve cranial nerves in the process, less pronounced inflammatory changes in the cerebrospinal fluid (sometimes with a pattern of cell-protein dissociation, i.e., increased cytosis at a normal level protein) at normal sugar levels (which especially distinguishes these processes from tuberculous meningitis), abortive meningeal syndrome (within 3-5 days) and rapid sanitation of cerebrospinal fluid. Such a clinical picture in the absence of pulmonary or extrapulmonary tuberculosis gives grounds to exclude tuberculous meningitis.
It should also be noted the so-called meningisms - toxic-allergic, rapidly transient reactions of the membranes of the brain in patients with active, mainly fibrous-cavernous pulmonary tuberculosis, who had never previously suffered from lesions of the central nervous system. Much more often, such reactive states occur in people who have had tuberculous meningitis in the past; they arise under the influence of seasonal factors, regime errors and other provocative moments. Clinically, these conditions are manifested by attacks of headache with mild symptoms of neck stiffness and Kernig or their absence. They proceed, as a rule, without a temperature reaction and are eliminated within a few days without treatment, but sometimes they drag on for a longer time. There may be increased intracranial pressure, but the composition of the cerebrospinal fluid is normal, and this indicator is decisive for the diagnosis. The recent increase in the erased forms of tuberculous meningitis makes it necessary to treat the diagnosis of "meningism" or "reactive state" with extreme caution and require a control spinal puncture.
Differential diagnostic difficulties arise when recognizing tuberculomas of the brain (more characteristic of childhood), often against the background of hematogenous disseminated pulmonary tuberculosis. Neurological manifestations in brain tuberculomas are uncharacteristic: meningeal syndrome can be expressed unsharply and is caused by contact irritation of the meninges,
Mo may be completely absent; there may be damage to the cranial nerves, epileptiform seizures are sometimes observed; in other cases, focal lesions of the substance of the brain raise the suspicion of a neoplasm of the brain; changes in the cerebrospinal fluid are mild, there may be a decrease in sugar levels. In these difficult to diagnose situations, the presence of pulmonary or extrapulmonary tuberculosis, as well as the clinical effect of specific anti-tuberculosis therapy, decides.
More rare, but recently more and more common forms of limited tuberculous meningitis (synonym: tuberculous arachnoiditis). Anatomically, these forms are a limited tuberculous process in the phase of fibrous involution, most often localized in the area of ​​the pia mater of the convex part of the brain and soldered to the corresponding zone of the medulla. Their clinical manifestations are polymorphic; there are forms that occur under the guise of a tumor or with a clinical picture of Jacksonian epilepsy without signs of high blood pressure or with a cyclic course of a meningo-like syndrome in the form of headache attacks. The reference points for diagnosing these forms in the presence of the above-mentioned clinical symptoms are: a) their development against the background of tuberculous generalization; b) normal composition of cerebrospinal fluid; c) the effectiveness of specific anti-tuberculosis therapy.
In patients with tuberculosis, exacerbations of chronic sinusitis or otitis media can cause a meningeal syndrome. An appropriate laryngological examination, which is necessary for every patient with suspected tuberculous meningitis, and the normal composition of the cerebrospinal fluid make it possible to navigate the picture of the disease.
A twofold error can occur if the patient has a pregnancy: either pregnancy toxicosis is mistaken for tuberculous meningitis, or vice versa. In this difficult situation, only an analysis of the composition of the cerebrospinal fluid (normal in toxicosis of pregnancy) can make it possible to correctly diagnose.
Finally, attacks of uremia or diabetic coma in patients with widespread fibrous-cavernous pulmonary tuberculosis with a corresponding complication can be mistaken for tuberculous meningitis. And in these cases, the study of the composition of the cerebrospinal fluid is decisive for the diagnosis.
It is natural to send a patient with abscessing pneumonia or bronchiectasis and damage to the central nervous system, which is mistaken for tuberculous meningitis, to a tuberculosis hospital after a certain period of time, but in fact it turns out to be a secondary metastatic process with the development of a brain abscess. Typically, such patients are admitted in a far advanced stage of the disease, in a very serious condition, with such a confused neurological picture that in itself, without other auxiliary factors, it does not provide any strong points for differential diagnosis. The reason for diagnostic difficulties is the presence of a moderately severe meningeal syndrome in a brain abscess (a positive Kernig's symptom in brain abscesses was noted by the author of this symptom himself); difficulties are aggravated by the fact that the study of cerebrospinal fluid in brain abscesses reveals moderate inflammatory changes in the form of lymphocytic pleocytosis and an increase in protein levels; sugar levels are usually normal; often increased leukocytosis in the blood. In these cases, taking into account the underlying disease, as well as the lack of effect of anti-tuberculosis therapy, are decisive for clarifying the etiology of damage to the central nervous system. To the same extent, this applies to recurrent endocarditis, the course of which can be complicated by meningoencephalitis, and to primary neoplasms of the lungs with brain metastasis.
The greatest diagnostic difficulties arise in primary brain tumors. The strong points for differential diagnosis are: slower development of the disease in tumors (within a month) compared with tuberculous meningitis, localized nature of headaches, signs of focal lesions of the brain substance, early development of congestive nipples in the fundus and progression of this symptom, mild changes in the composition of the cerebrospinal fluid or normal data, in particular, on the part of the sugar level. Of practical importance may be the results of a study of brain biocurrents, which reveal asymmetry in the localization of the process.
Differential diagnostic difficulties can also arise with subarachnoid hemorrhages, since they are clinically characterized by the presence of a pronounced meningeal syndrome. The bloody nature of the cerebrospinal fluid with a normal or almost normal composition of other indicators, as well as a quick (within a few days) recovery of a satisfactory condition of the patient, make it possible to make a correct diagnosis.

Treatment of tuberculous meningitis

In the treatment of tuberculous meningitis in adults and children, if necessary, all known anti-tuberculosis drugs can be used. Due to their ability to easily penetrate into the subarachnoid space and create a high bacteriostatic concentration there, GINK preparations (tubazid, ftivazid, metazid) are the best treatment for tuberculous meningitis.
Treatment should begin with a combination of first-line drugs. GINK preparations are prescribed continuously in doses slightly higher than optimal, throughout the entire period of treatment. Streptomycin is administered intramuscularly for the first 2-3 months, then the issue is resolved depending on the course of tuberculous meningitis and the state of the underlying tuberculous process. PAS can be added later, after the headache, nausea and vomiting have stopped.
In case of difficulty in taking GINK preparations orally (unconsciousness, persistent vomiting, swallowing disorder), tubazide should be administered in suppositories into the rectum or a 5% saluzide solution, 10 ml 3 times a day, intramuscularly. In these cases, as well as in the late diagnosis of tuberculous meningitis, a limited number of subarachnoid injections of the calcium chloride complex of streptomycin or a 5% solution of saluzide is indicated.
With fatal intolerance to GINK preparations, ethionamide, prothionamide, cycloserine, ethambutol can be successfully used.
At the same time, dehydration therapy is indicated: intravenous infusions of a 40% glucose solution, calcium chloride, intramuscular injections of a 25% magnesium sulfate solution, drip intravenous infusions of dry plasma, diuretics, etc.
Restorative treatment consists of placing the patient in a well-ventilated quiet room, the appointment of good nutrition, vitamins. After the acute phenomena of meningitis subside, blood transfusion is indicated in small doses.
The patient is discharged from the hospital in a generally good condition, after the disappearance of the clinical manifestations of meningitis and normalization of the cerebrospinal fluid, but not earlier than after 6 months, even with the mildest, uncomplicated form of tuberculous meningitis.

Treatment of complications

With occlusive hydrocephalus, vigorous dehydration therapy is indicated: glucose intravenously, magnesium sulfate intramuscularly, plasma intravenously, etc. In case of central and peripheral paralysis, treatment is carried out according to general rules with the use of massage, therapeutic exercises, prozerin or dibazol as early as possible.
Treatment of pulmonary, osteoarticular and other localizations of tuberculosis carried out according to indications, determined by the nature of a particular lesion. With a stable clinical cure of meningitis, major surgical interventions can be performed no earlier than a year after the end of hospital treatment.
Sanatorium treatment carried out after the end of the stationary. In the sanatorium, specific therapy (GINK + PAS or ethionamide) is usually continued for 4-5 months.
After discharge from the sanatorium, specific therapy is continued at home, taking into account the total duration of continuous anti-tuberculosis therapy of 18-20 months. After stopping treatment in the next 2 years, it is necessary to carry out preventive seasonal courses of antibacterial treatment - in spring and autumn for 2-3 months.

Dispensary observation

Upon returning to the place of permanent residence, those who have had tuberculous meningitis are enrolled in group I of dispensary observation for 2-3 years, followed by transfer to groups II and III.
The question of working capacity or continuing education can be raised no earlier than one year after the end of treatment in a hospital. Professions associated with heavy physical exertion and the adverse effects of sudden changes in temperature are not recommended.
A new method for the treatment of tuberculous meningitis without subarachnoid injections of streptomycin caused a change in the regimen of patients during their stay in the hospital: strict bed rest lasts 1-2 months, sparing regimen (gradual transition to active behavior - eating while sitting, subsequent lengthening of the sitting position, walking on ward, use of the restroom - the next 2-4 months, then the training regimen (meals in the common dining room, walks, participation in labor processes).
Observation of cured from tuberculous meningitis in anti-tuberculosis dis-
Paiserakh. Those cured of tuberculous meningitis Upon discharge from a medical institution, they are sent for observation to an anti-tuberculosis dispensary at the place of residence, where they are enrolled in group I under the special heading “condition after tuberculous meningitis”. In the first year after treatment of tuberculous meningitis, a control study in a hospital is indicated once every 3-4 months, then, depending on the condition, once every six months or once a year.
In the intervals between control studies in the hospital, the dispensary must organize systematic monitoring of the cured. Within 1 year after treatment, observation is carried out by regular visits to patients by doctors and nurses at home. In this case, special attention should be paid to the elimination of factors of everyday life and regimen that can provoke an exacerbation of meningitis (overheating, hypothermia, alcohol abuse, heavy home physical work, too early start of professional activity). Likewise, special attention should be paid to clinical manifestations suspicious of relapse of tuberculous meningitis (while keeping in mind the possibility of an erased form of meningeal syndrome).
In the second year after the cure, with clinical well-being, the cured from tuberculous meningitis is left in the I group of observation and is called to the anti-tuberculosis dispensary at least once every 3 months (more frequent calls are determined by the presence of active tuberculosis in other organs).
During the examination, it is necessary to pay special attention to the conditions of life and regime and not to allow professional overload (for example, combining professional work and study).
At the end of treatment in a hospital, a convalescent after tuberculous meningitis is subjected to outpatient combined antibacterial treatment, carried out with the clinical well-being of the patient for 2 years according to the following scheme: in spring and autumn for 2-3 months - tubazid (0.6 g per day) and PAS ( 8-12 g per day).
Convalescents who continue to suffer from active pulmonary or extrapulmonary tuberculosis, and after the end of treatment for tuberculous meningitis, then continue to be treated according to indications due to this localization of tuberculosis.
In the event of exacerbations of tuberculous meningitis, therapy is carried out according to clinical indications.
Within 1 year after treatment for tuberculous meningitis and in the presence of pronounced residual effects, the cured is considered professionally disabled and in need of outside care (I group of disability), in the absence of residual effects and in general satisfactory condition - professionally disabled and not in need of outside care (Group II ). After this period, after the cure of tuberculous meningitis, subject to clinical well-being, the absence of residual effects and contraindications from other organs, it is necessary to raise the question of returning the cured person to professional activities or continuing their studies.
After a two-year observation of a person cured of tuberculous meningitis in group I, provided that he is clinically well and that there are no contraindications from other organs, a transfer to group II of the dispensary is indicated.
Data from a study of long-term results in convalescents after tuberculous meningitis suggest that 75-80% after treatment continue their studies or successfully work in a wide variety of professions.
The patient's ability to work is limited by the presence of active pulmonary (mainly fibrous-cavernous) or extrapulmonary tuberculosis or residual changes associated with the course of meningitis (paralysis, paresis).
Convalescents after tuberculous meningitis are contraindicated in professions associated with hard work (loaders), thermal factors (work in hot shops, field work), exposure to meteorological factors in the open air.

Tuberculosis can affect most organs and systems in the human body, and the central nervous system is no exception. And although in recent years the disease has been diagnosed at an earlier stage, methods of treatment have become more advanced, and mortality from it has been significantly reduced, tuberculous meningitis is still a great danger today.

What is tuberculous meningitis

Tuberculous meningitis is a predominantly secondary inflammation of the meninges, usually occurring in patients with various forms of tuberculosis. Among patients, children under 5 years of age, adolescents, the elderly, as well as patients with immunodeficiency are more likely to be. Outbursts of the disease are observed in the winter-spring period, although the risk of infection also remains throughout the calendar year.

Pathogenesis

Let's talk about how tuberculous meningitis is transmitted.
The causative agent of the disease is Mycobacterium tuberculosis (MBT). This means that the occurrence of tuberculosis of the meninges and its development occurs only if the body already has a tuberculous lesion of any organ or system. Only in 3% of patients it was not possible to establish the primary focus of the disease.

Infection occurs in 2 stages:

• through the blood: granuloma formation occurs, caused by damage to the choroid plexus of the ventricles;
• liquorogenic distribution: MBT reach the base of the brain, infecting the meninges and causing an allergy in the vessels, manifested by acute meningeal syndrome.

Causes

The main cause of the disease is the defeat of any organ of the patient by Mycobacterium tuberculosis. Tuberculosis bacillus enters the cerebrospinal fluid with blood, is placed on the pia mater and begins to multiply, which leads to the development of tuberculous meningitis.

The most susceptible to tuberculous meningitis are people with weakened immune systems (including AIDS and HIV patients, alcoholics, drug addicts), and those who have recently been in contact with a patient with tuberculosis (and in any form) or have suffered it themselves are also at risk.

Symptoms of the disease

The characteristic features of the symptoms of tuberculous meningitis is a gradual onset with a long prodromal period (up to 6 weeks), during which some change in the mental status of the patient can be noted.

Namely:

• apathy;
• increased irritability;
• fatigue;
• worsening sleep;
• lack of appetite;
• appearance daily (usually in the evenings).

At the same time, the general condition can be considered normal, at first the patient even continues his professional activities. However, the intensity of the headache increases (vomiting often appears), the body temperature rises, the general condition worsens significantly, the patient can no longer lead a normal life and consults a doctor.

If a doctor detects the presence of meningeal syndrome, the likelihood of making a correct diagnosis is high.

Meningeal syndrome is a stiff neck, severe (almost unbearable) headaches and Kernig's symptom.

Rigidity of the neck muscles refers to a fairly early symptom of the disease. It is manifested by throwing the patient's head back, and any change in this position is given by severe pain. This problem is observed throughout the entire period of the disease.

Kernig's symptom is characterized by the inability to extend the leg at the knee, provided that it is bent at the knee and hip joints. And when you try to bend the patient's leg in the hip joint with the knee extended, he will simultaneously bend it in the knee joint.

Disorders accompanying meningeal syndrome:

• secretory disorders (increased salivation and sweating);
• respiratory disorders;
• fluctuations in blood pressure;
• elevated temperature (up to 40 ° C);
• noise intolerance and photophobia. Patients lie with their eyes closed, do not talk, they try to answer questions in monosyllables;
• in the later stages - confusion and coma, body temperature can rise to 41-42 ° C or, conversely, decrease to 35 ° C, the pulse reaches 200 beats per minute, breathing is arrhythmic.

At the last stage, the cure is no longer possible and the patient dies (as a rule, as a result of paralysis of the vasomotor and respiratory centers)

Classification of tuberculous meningitis

Photo of tuberculous meningitis revealed by MRI

Depending on the prevalence and localization of the pathological process, 3 clinical types of tuberculous meningitis are distinguished:

• basal(basilar);
• cerebrospinal meningoencephalitis;
• serous tuberculous meningitis.

Basilar meningitis affects the cranial nerves. The meningeal symptom is expressed, at the same time, intellectual disorders are not noted. The course of the disease is quite severe, there is a possibility of exacerbations. The outcome of treatment is favorable.

Meningoencephalitis leads to hemorrhages and softening of the brain. The course of this form of the disease is severe, and the likelihood of relapse is also high. In 50% of cases, the outcome is unfavorable. Moreover, even half of those who have recovered still have movement disorders (paresis of the limbs), mental disorders and hydrocephalus phenomena.

With the serous type of tuberculous meningitis, there is an accumulation at the base of the brain of exudate (a clear liquid containing cells of the serous membranes). Meningeal syndrome is mild. The outcome is favorable, this form usually proceeds without complications and relapses.

Diagnostics

The analysis of cerebrospinal fluid is of great importance in the diagnosis. The likelihood of tuberculous meningitis is high if the puncture:

• cerebrospinal fluid is transparent, flows out in drops, its pressure is increased;
• the protein content is higher than normal;
• glucose content is lower.
• At the same time, the blood picture remains practically unchanged.

Mandatory for diagnosis:

• chest x-ray;
• tuberculin test.

Dispensary observation

After returning home, those who have had meningitis of the meninges are observed for another 2-3 years. The question of their ability to work is raised at least one year after the end of treatment in a hospital.

In the presence of residual effects (expressed), the cured is considered to be in need of constant care and professionally disabled, in the absence of such phenomena - disabled, but without the need for outside care.

In the absence of residual effects and other contraindications, the question of returning to professional activity can be raised.

Tuberculous meningitis is a very serious and dangerous disease.

And timely diagnosis is of great importance for successful treatment. Remember this and take care of yourself!

A video that talks about how meningitis is dangerous: