Tuberculous meningitis. What is tuberculous meningitis? What is Tuberculous meningitis

Tuberculosis can affect more than just the lungs. The causative agent of the disease (Koch bacillus) penetrates into different systems human body. One of the most severe manifestations of this infection is tuberculous meningitis. In this disease, bacteria cause damage to the brain. Modern diagnostics allows us to identify this disease early stages. In this case, the disease can be cured. However, the tuberculosis process in the central nervous system remains extremely dangerous pathology. An advanced disease can lead to the death of the patient.

What kind of disease is this

Tuberculous meningitis- This It is of a secondary nature. All patients either suffer from an active form of tuberculosis or have had this disease in the past. Determining the primary source of infection can sometimes be very difficult.

Outbreaks of tuberculous meningitis of the brain most often occur in winter or spring. However, a person can get sick at any time of the year. Children, elderly people and patients with severely reduced immunity are especially susceptible to this disease.

Causative agent and pathogenesis of the disease

The causative agent of the disease is Koch's bacillus. It is also called Mycobacterium tuberculosis (MBT). This microorganism enters the brain in two stages:

  1. First, the bacterium enters the blood from the primary lesion. From there it enters the brain, overcoming the barrier between the circulatory and central nervous systems. Koch's bacillus causes damage to the vessels of the lining of the brain. This leads to the appearance of granulomas in the organ.
  2. Together with the cerebrospinal fluid, bacteria enter the base of the brain. Infection of the meninges occurs, accompanied by inflammation.

In this case, tubercles form in the brain. They are microscopic nodules or bumps in the lesion. Inflammation affects not only the tissues of the membranes, but also the blood vessels. There is a narrowing of the cerebral arteries, which leads to disruption of local blood circulation. Pathological changes also occur in the tissue of the organ, but they are less pronounced than in the membrane. A gray mass appears at the base of the brain, the consistency of which resembles jelly.

Who is at risk

In addition to patients with tuberculosis, people who have been in contact with the patient are also at risk. This pathology is often observed in persons suffering from alcoholism and drug addiction. Bad habits extremely negatively affect the immune system. Tuberculous meningitis in HIV infection occurs quite often and is severe. Also increased risk The disease occurs in people who have suffered a traumatic brain injury.

Classification of the disease

In medicine, it is customary to distinguish several forms of tuberculous meningitis, depending on the location of the affected areas:

  1. Basilar meningitis. In this type of disease, the damage affects the cranial nerves. Signs of irritation of the meninges are pronounced, but there are no intellectual impairments. The disease is severe and can recur, but with timely treatment it ends in complete recovery.
  2. Cerebrospinal meningoencephalitis. This is the most severe form of tuberculous meningitis. It occurs with damage not only to the membranes, but also to the substance of the brain. In 30% of cases, the pathology ends in death. After recovery there are often severe complications: paralysis of limbs and mental disorders.
  3. Serous meningitis. Fluid (exudate) accumulates at the base of the brain. There are no signs of irritation of the meninges. This form is mild and usually ends with complete recovery. Complications and relapses are not observed.

Stages of the disease

In the clinic of tuberculous meningitis, several stages of the disease can be distinguished:

  • prodromal;
  • stage of irritation (meningeal syndrome);
  • terminal.

The pathology is characterized by gradual development. The prodromal stage can last up to 6-8 weeks. Then signs of irritation of the meninges appear, they are observed within 15-24 days. If left untreated, the disease enters the terminal stage. Patients experience signs of encephalitis, paralysis, and the disease often ends in death. Next, we will consider in detail the symptoms and consequences of tuberculous meningitis at each stage.

Symptoms

The disease begins with a long period of time. At an early stage, the signs of the disease are nonspecific. Patients complain of headache in the evening, malaise, dizziness, nausea, loss of appetite. irritability. Body temperature may be slightly elevated, but there are cases of the onset of the disease without fever. There is a delay in urination and defecation. Such a slow development of pathology is characteristic feature tuberculous meningitis.

Then comes the stage of irritation. The patient's headache, it becomes painful and is localized in the forehead and back of the head. The temperature rises sharply to 38-39 degrees. The patient becomes lethargic, apathetic and drowsy. His mind is confused. Red spots appear on the skin of the chest and face. which then quickly disappear.

At this stage there is severe irritation receptors of the meninges, which is called meningeal syndrome. Along with an unbearable headache, other specific symptoms of tuberculous meningitis arise:

  1. Stiff neck. The patient's neck muscle tone sharply increases, making it difficult for him to tilt his head.
  2. Kernig's sign. The patient lies on his back. His leg is bent at the hip and knee joint. The patient cannot independently straighten the limb due to increased tone of the lower leg muscles.
  3. Respiratory disorders. The patient is breathing heavily and intermittently. He has a feeling of lack of air.
  4. Fear of light and sounds. The patient constantly lies with his eyes closed and talks little.
  5. Increased secretion of saliva and sweat.
  6. Blood pressure surges.

In the absence of therapy or insufficient treatment, terminal stage diseases. Body temperature either rises to +41 degrees or drops to +35. Severe tachycardia is noted, the pulse rate reaches 200 beats per minute. The patient falls into a coma. At a late stage of the disease, death occurs due to respiratory paralysis.

Features of the disease in children

Tuberculous meningitis is more common in children than in adults. Children under 5 years of age or teenagers are usually affected. The disease is accompanied by the same symptoms as in adults. However, children are more likely to experience Negative consequences pathologies such as hydrocephalus. Sometimes signs of the disease in the prodromal period resemble the clinical picture acute poisoning. Severe vomiting, weight loss, heat. Babies are already initial stage swelling and tension of the fontanelle occurs.

Complications

Tuberculous meningitis is dangerous because it can cause severe complications from the central nervous system. The most common condition is water on the brain (hydrocephalus). This pathology occurs due to adhesions in the meninges.

Approximately 30% of patients remain paralyzed after the illness cranial nerves and paresis of the limbs. In more rare cases, it is noted sharp deterioration sight and hearing. Some patients experience epileptic seizures.

Diagnostics

It is necessary to carry out a differential diagnosis of tuberculous meningitis with bacterial and viral forms of inflammation of the meninges, since the signs of these pathologies are similar. However, if the disease is caused by meningococcal bacteria or viruses, it always begins acutely. A gradual onset is characteristic only of tuberculous lesions of the meninges.

Important diagnostic study is to conduct spinal tap. With tuberculous meningitis, the following pathological changes are noted in the cerebrospinal fluid:

  1. Cerebrospinal fluid pressure increases.
  2. Noted increased content squirrel.
  3. The number of cellular elements is many times higher than normal.
  4. The presence of Koch's bacillus is detected.
  5. Sugar content is reduced.

It is also necessary to establish the localization of the primary focus of mycobacteria. For this purpose they use additional methods diagnosis of tuberculous meningitis:

  • chest x-ray;
  • fundus examination;
  • examination of lymph nodes, spleen and liver;
  • test with tuberculin (Mantoux reaction).

To assess the patient's neurological condition, CT and MRI of the brain are prescribed.

A phthisiatrician or neurologist makes a diagnosis based on comprehensive examination.

Treatment methods

The intensive stage of treatment of this pathology is carried out only in a hospital setting. Patients are prescribed combination treatment with several anti-tuberculosis drugs:

  • "Streptomycin."
  • "Isoniazid".
  • "Rifampicin".
  • "Pyrazinamide".
  • "Ethambutol."

Prescribe 4-5 drugs at the same time various combinations. This scheme is followed for the first 2-3 months. Then only two types of medicine are left: Isoniazid and Rifampicin. The general course of treatment for the disease is quite long, it takes about 12-18 months.

To prevent the development of complications, glucocorticoid hormones are prescribed: Dexamethasone or Prednisolone. Also, to prevent neurological disorders, B vitamins, glutamic acid, and Papaverine are administered.

During illness, patients have decreased production antidiuretic hormone. This leads to swelling of the brain. To relieve this symptom, angiotensin receptor antagonists are prescribed: Lorista, Diovan, Teveten, Micardis.

The patient must remain in bed for 30 to 60 days. Only in the third month of illness do doctors allow a person to get up and walk. The patient undergoes periodic spinal taps. Based on their results, the effectiveness of the prescribed treatment is assessed.

IN severe cases hydrocephalus, surgical intervention is indicated - ventriculoperitoneal shunting. During this operation, a catheter is inserted into the ventricle of the brain and excess fluid is drained. This helps reduce intracranial pressure and reduce brain swelling.

Forecast

The prognosis for life directly depends on the degree of pathology. If treatment is started in the early stages, the disease is completely cured. Advanced forms of the pathology are fatal in 50% of cases.

After recovery, approximately one third of patients remain neurological consequences: paresis of limbs, cranial nerve palsy. They can be stored for 6 months.

With timely treatment, the patient can return to his normal lifestyle after some time. Disease in childhood may have a negative impact on mental development.

Dispensary observation

After discharge from the hospital, the patient must be registered at an anti-tuberculosis dispensary for 2 - 3 years, regularly visit a doctor and undergo tests. During this time, he needs to take the drugs "Tubazid" and "Pask" according to a special regimen. A year after the course of therapy, the hospital decides on the patient’s continued ability to work.

If the patient has significant consequences of the disease, he is recognized as disabled and in need of care. If the patient still has moderate residual effects, then he is considered unfit for work, but without the need for care.

If the patient has fully recovered and does not experience any consequences of the illness, then the person returns to his regular work. However, heavy physical labor and exposure to cold are contraindicated for him.

Prevention

Prevention of the disease is to prevent infection with tuberculosis. People suffering from an active form of the pathology are given a separate living space, if they live in a dormitory or communal apartment. This is necessary in order to avoid infection of others.

Identifying tuberculosis in the early stages plays an important role in prevention. For this purpose, tuberculin tests and fluorography are used. regular medical examinations. Infants in the first month of life must be given BCG vaccine. This will help avoid dangerous disease and complications in the future.

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

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

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. There are groups of people whose risk of developing this disease is increased. These include:

  • people who have tuberculosis or those who have already completed a course of therapy;
  • people with immunodeficiency - HIV, AIDS;
  • people who are weakened the immune system;
  • people who have recently been in contact with patients with open 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 pro-normal period of the disease, in which the following symptoms may be observed:

  • The appearance of a headache. First, the headache hurts in the evening, or during sleep, and then it becomes almost constant. This headache is hardly relieved by painkillers.
  • Weakness, apathy, increased drowsiness.
  • Significant loss of appetite, up to anorexia.
  • Irritability and excessive nervousness.

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

Main symptoms of tuberculous meningitis
Symptom name general characteristics symptom
Stiffness of the neck and neck muscles The muscles of the neck and occipital region become hard and inelastic. They have increased tone. The patient has difficulty bending or straightening his neck. The doctor, trying to bend it passively, feels resistance from the muscles.
Pointing dog pose The patient lies on his side with his head thrown back, pressing his legs to his stomach. So it subconsciously slightly reduces intracranial pressure.
Headache A headache of a bursting nature, which may be more pronounced in the forehead or temples. It is not reduced by painkillers.
Reaction to sound and light Patients react very painfully to all sounds and bright lights, and are asked to close the curtains and not make noise.
Vomit Vomiting occurs at the top of the headache. There is no nausea before her. This kind of 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 and knee. But he cannot straighten his knee. This occurs due to high tension in the posterior femoral muscles, which causes flexion contracture.
Brudzinski's sign
  • Upper – the doctor passively bends the patient’s neck, and his joints reflexively bend lower limbs.
  • Medium – if you press on the patient’s pubis, his knees will bend.
  • Bottom - if you bend one leg, the other will also bend.

Principles of disease diagnosis

Tuberculous meningitis - symptoms

First of all, the doctor examines the patient, collects anamnesis and medical history. Then he inspects it and checks meningeal symptoms. Already at this stage of diagnosis, the doctor suspects the development of meningitis. But for prescribing treatment and staging accurate diagnosis It is impossible to do without laboratory and instrumental diagnostics.

The main research method is lumbar puncture. With its help, cerebrospinal fluid and cerebrospinal fluid are collected for analysis. Main characteristics of cerebrospinal fluid in tuberculous meningitis:

  1. Increased cerebrospinal fluid 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, after an hour a film will fall out of it, which will glow under the rays of the sun.
  3. Increased quantity 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 glucose levels in the cerebrospinal fluid is observed only in patients who are not additionally infected with the HIV virus.
  6. Koch's tuberculosis bacillus can be isolated in 10% of the liquor.

In addition to lumbar puncture, the following examinations are performed:

  1. General radiography of organs chest. It is needed to identify the primary tuberculosis focus.
  2. General analysis blood. 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, erythrocyte hemoglobin, the patient will have anemia.
  3. CT scan brain examination is carried out in acute forms of meningitis, it is needed to assess the volume of tissue affected by the inflammatory process.
  4. Sputum microscopy is used to detect acid-fast tuberculosis bacteria in sputum.

Basic principles of treatment of tuberculous meningitis

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

  • Strict bed rest.
  • Constant control over arterial blood levels blood pressure, heart rate, oxygen levels and carbon dioxide in blood.
  • Oxygen support is provided through a mask.
  • Taking anti-tuberculosis drugs. The regimen for these medications is developed by the attending physician. The standard regimen includes Isoniazid, Rifampicin, Ethambutol, Pyrazinamide. Before prescribing these drugs, a sensitivity test is carried out. IN Lately Cases of resistance of tuberculosis bacteria to standard treatment regimens have become more frequent.
  • Detoxification therapy. Includes intravenous administration to the patient of such solutions as Ringer's solution, Trisol, Disol, Reosorbilact, Polyglucin. 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 effects of anti-tuberculosis drugs. These include Heptral, Milk Thistle, Karsil.
  • Corticosteroids are prescribed for infectious-toxic shock.

Complications of tuberculous meningitis

The course of tuberculous meningitis can be complicated by the following conditions:

  • Brain swelling;
  • Infectious-toxic shock;
  • Encephalitis - involvement of the tissues of the brain itself in the inflammatory process;
  • Sepsis;
  • Partial paralysis or paresis;
  • Herniation of the brain;
  • Impaired hearing, vision, speech.

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 constant supervision medical personnel.

Tuberculosis of the meninges, or tuberculous meningitis, - predominantly secondary tuberculosis lesion (inflammation) of the membranes (soft, arachnoid and less hard), occurring in patients with various, often active and widespread, forms of tuberculosis. Tuberculosis in this localization is the most severe. In adults, tuberculous meningitis often serves as a manifestation of exacerbation of tuberculosis and may be its only established localization. The localization and nature of the main tuberculosis process influence the pathogenesis of tuberculous meningitis. In primary disseminated pulmonary tuberculosis, Mycobacterium tuberculosis penetrates the central nervous system through the lymphohematogenous route, since lymphatic system associated with the bloodstream. Tuberculous inflammation of the meninges occurs when mycobacteria directly penetrate the nervous system due to a violation of the vascular barrier. This occurs when there is a hyperergic state of the brain vessels, membranes, and choroid plexuses, caused by nonspecific and specific (mycobacteria) sensitization. Morphologically, this is expressed by fibrinoid necrosis of the vascular wall, as well as their increased permeability. The resolving factor is tuberculous mycobacteria, which, existing in the lesion, cause increased sensitivity of the body to tuberculosis infection and, penetrating through the altered vessels of the choroid plexuses of the ventricles of the brain, lead to their specific damage. Mostly soft tissues are infected meninges the base of the brain where tuberculous inflammation develops. From here, the process through the Sylvian cistern spreads to the membranes of the cerebral hemispheres, the membranes of the medulla oblongata and spinal cord.

When the tuberculosis process is localized in the spine, skull bones, or internal node, the infection is transferred to the meninges by liquorogenous and contact routes. The meninges can also become infected from pre-existing tuberculosis foci (tuberculomas) in the brain due to the activation of tuberculosis in them.

In the pathogenesis of tuberculous meningitis, climatic and meteorological factors, time of year, transmitted infections, physical and mental trauma, insolation, close and prolonged contact with a patient with tuberculosis are important. These factors cause sensitization of the body and decreased immunity.

Basal tuberculous meningitis- the most common form of tuberculous meningitis (about 60%). The inflammatory process is localized mainly on the membranes of the base of the brain. Clinical picture characterized by pronounced cerebral meningeal symptoms, disturbances of cranial innervation and tendon reflexes, moderately pronounced phenomena of hydrocephalus and changes in the composition of cerebrospinal fluid: protein level increased to 0.5-0.6% o, pleocytosis of 100-150 cells in 1 ml, sugar content , chlorides slightly reduced or normal. Mycobacteria are found in 5-10% of patients.

Pathological anatomy

For pathological anatomy tuberculous meningitis is characterized by differences in the nature and prevalence of the inflammatory reaction and originality, expressed in the occurrence of diffuse serous-fibrous inflammation of the pia mater, mainly the base of the brain: the orbital surface of the frontal lobes, the area of ​​the optic chiasm, the anterior and posterior hypothalamus (hypothalamus), the fundus III ventricle and its lateral walls with vegetative centers, the lateral (Sylvian) fissure, the membranes of the cerebral bridge (pons), the medulla oblongata with adjacent parts of the cerebellum. The substance of the brain and spinal cord, its membranes, and the ependyma of the ventricles of the brain are also involved in the hospital process. Characteristic signs diseases - rash of tuberculous tubercles on the membranes, ependyma and alterative damage to blood vessels, mainly the arteries of the soft meninges and choroid plexuses, such as periarteritis and endarteritis. Tuberculous meningitis is characterized by severe hydrocephalus, which occurs as a result of damage to the choroid plexuses and ependyma, impaired absorption of cerebrospinal fluid and occlusion of its circulation pathways. The transition of the process to the Sylvian fissure and the cerebral artery located in it leads to the formation of foci of softening of the cerebral cortex, subcortical ganglia and internal capsule.

Polymorphism pathological changes and the prevalence of the process determine the variety of clinical manifestations of tuberculous meningitis; in addition to meningeal symptoms, vital disorders are observed important functions and autonomic disorders, disorders of cranial innervation and motor functions with changes in tone in the form of decerebrate rigidity and disturbances of consciousness.
In cases of late diagnosis of tuberculous meningitis and ineffective treatment due to the progression of the process and its transfer to the vessels and substance of the brain, pathological changes occur in the cerebral hemispheres, bulbar centers, spinal cord, its roots, membranes of the trunk and spinal cord (diffuse leptopachymeningitis). If the treatment is effective, the prevalence of the inflammatory process is limited, the exudative and alterative components of inflammation are reduced, the productive reaction and reparative processes predominate, expressed in the almost complete disappearance of pathological changes, especially with early treatment.

Symptoms of tuberculous meningitis

The disease begins with a prodromal period, the duration of which is 1-3 weeks. During this period, patients experience general malaise, intermittent, mild headache, periodically occurring increase in body temperature (up to low-grade fever), worsening mood in children, decreased interest in the environment. Later (during the first 7-10 days of illness), lethargy appears, the temperature is increased, appetite is decreased, and the headache is more constant. Subsequently (from the 10th to the 15th day of illness), the headache becomes more intense, vomiting appears, lethargy increases, increased excitability, anxiety, anorexia, and stool retention are noted. Patients lose weight quickly. Body temperature rises to 38-39 °C, meningeal symptoms appear, tendon reflexes are increased, pathological reflexes and disorders of cranial innervation, paresis of the facial, oculomotor and abducens nerves are detected (smoothness of the nasolabial fold, narrowing of the palpebral fissure, ptosis, strabismus, anisocoria) and vegetative-vascular disorders: red dermographism, bradycardia, arrhythmia, as well as hyperesthesia, photophobia. When examining the fundus, congestive disc nipples or optic neuritis, tuberculous tubercles on the choroid are detected.

If treatment is not started in the 3rd week (days 15-21), the disease progresses. Body temperature rises to 39-40 °C, headache and meningeal symptoms become pronounced; forced posture and decerebrate rigidity appear, consciousness is darkened, and at the end of the 3rd week it is absent. Disorders of cranial innervation intensify and appear focal symptoms- paresis, paralysis of the limbs, hyperkinesis, automatic movements, convulsions, trophic and autonomic disorders intensify, sudden sweating or dry skin, Trousseau spots, tachycardia are noted, cachexia develops. Before death, which occurs 3-5 weeks from the onset of the disease, body temperature reaches 41-42 ° C or drops to 35 ° C, the pulse quickens to 160-200 per minute, breathing becomes arrhythmic, such as Cheyne-Stokes breathing. Patients die as a result of paralysis of the respiratory and vasomotor centers.

Acute onset of the disease is more common in children early age, in which the most persistent and early symptoms are headache, vomiting and an increase in body temperature to 38-39 ° C, appearing in the first days of the disease. Subsequently, the body temperature becomes higher, the headache intensifies, lethargy, drowsiness, anorexia, meningeal symptoms and disorders of cranial innervation appear. At the end of the 2nd week, some patients experience disturbances of consciousness, movement disorders and disorders of vital functions - breathing and circulation.

Treatment of tuberculous meningitis

The clinical picture of tuberculous meningitis when treated with anti-tuberculosis drugs depends to the greatest extent on the period of time that elapses from the onset of the disease to treatment. Depending on the predominant localization of the pathological process and its prevalence, the three most typical clinical forms of tuberculosis of the meninges are distinguished: basal (basilar) tuberculous meningitis, tuberculous meningoencephalitis and tuberculous cerebrospinal leptopachymeningitis (tuberculous meningoencephalomyelitis). As the process progresses, a transition from one form to another is possible - basal to meningoencephalitic or cerebrospinal. Some authors distinguish the convexital form, in which the process is localized primarily on the membranes of the convex part of the brain and is most pronounced in the area of ​​the central gyri. More rare ones have been described atypical forms tuberculous meningitis.

The course of the disease (with treatment) is predominantly smooth, without exacerbations, occasionally protracted, the outcome is favorable - full recovery without complications. Improvement general condition and disappearance of brain symptoms, a decrease in body temperature is observed within 3-4 weeks. Meningeal symptoms disappear after 2-3 months, and sanitation of cerebrospinal fluid occurs after 4-5 months. Necessary long-term treatment(10-12 months), since clinical recovery is significantly ahead of anatomical recovery, and also due to the fact that meningitis is usually combined with active tuberculosis of internal organs.

Tuberculous meningitis is predominantly a secondary tuberculous lesion (inflammation) of the soft, arachnoid membranes and less of the hard membrane, occurring in patients with various, often active and widespread, forms of tuberculosis. Tuberculosis in this localization is the most severe. In adults, tuberculous meningitis often serves as a manifestation of 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 disruption of the blood-brain barrier under the influence of various nonspecific factors, reducing defensive 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 disrupted 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 about 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.

First stage, hematogenous, occurs against the background of general bacteremia. MTB, in conditions of hypersensitization and decreased body defenses in primary, disseminated tuberculosis, penetrates the blood-brain barrier; in this case, the choroid plexuses of the ventricles of the brain are affected.

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

M. V. Ishchenko (1969) proved the existence of a lymphogenous route of infection of the meninges, which he observed in 17.4% of patients. In this case, MBT from the upper cervical fragment of the jugular chain affected by tuberculosis lymph nodes along perivascular and perineural lymphatic vessels reach the meninges.

In addition, when the tuberculosis process is localized in the spine, skull bones, inner ear transfer of infection to the meninges occurs via liquorogenous and contact routes. The meninges can also become infected from pre-existing tuberculosis foci (tuberculomas) 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 primary tuberculosis complex, complicated by hematogenous generalization. However, in 15% of patients, meningitis can occur in the absence of visible tuberculous changes in the lungs and other organs (“isolated” primary meningitis). Early diagnosis of tuberculous meningitis determines success in 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, at the base of the brain. The shells take on a greenish-yellowish jelly-like appearance with individual grayish tubercles on the surface. Microscopic examination detects inflammatory infiltrates in the walls 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 more later periods adhesions of the meninges are detected and, as a result, hydrocephalus.

Initially, the inflammatory process is localized at the base of the brain behind the optic chiasm, involving the infundibulum, mastoid body, quadrigeminal region and cerebral peduncles.

The pia mater becomes cloudy, gelatinous, and translucent. Along the olfactory tracts, near the optic chiasm, on the lower surface of the frontal lobes of the brain and in the Sylvian fissures, rashes of small tuberculous tubercles are visible. The ventricles of the brain are filled with clear or slightly cloudy fluid. When the Sylvian fissure is affected, the process often involves the middle cerebral artery. Necrosis of the vessel wall or thrombosis may develop, which leads to ischemia of a certain area of ​​the brain and irreversible consequences. With tuberculous meningitis, changes are always found in the hypothalamic-pituitary region, and the fundus and the adjacent region of the third ventricle are affected. This localization entails damage to the numerous vegetative centers located here. Subsequently, dysfunctions of the cranial nerves - optic, oculomotor, trochlear, abducens, trigeminal, facial - are added. As the process progresses, the pons and medulla oblongata are involved in the inflammatory process, and disorders of the cranial nerves (IX, X, XII) appear. Death occurs from vasomotor paralysis and respiratory centers, which are located in the medulla oblongata.

Clinical picture

There are three main forms:

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

During tuberculous meningitis there are three periods:

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

Prodromal period lasts 1-3 weeks (in children usually 7 days). At this time, insufficiently typical and inconsistent symptoms arise that do not allow a timely diagnosis. The disease develops gradually. The prodrome period is characterized by intermittent headaches, apathy, lethargy, drowsiness in daytime days, alternating with excitability (restlessness, moodiness), loss of appetite, low-grade fever bodies. At the end of the prodromal period, vomiting not associated with food intake and a tendency to retain stool occur. During this period of the disease, bradycardia is noted.

During the period of irritation 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 back of the head), and vomiting. Vomiting is a constant and very early symptom. Vomiting typical for tuberculous meningitis is characterized as fountain-like. Decreased appetite leads to complete anorexia, which leads to rapid and dramatic loss of body weight. Body temperature reaches high numbers - 38-39 °C. Symptoms of irritation of the meninges are added - stiff neck, positive Kernig, Brudzinsky symptoms, the intensity of which increases towards the end of the second week of the disease. As a consequence of irritation of the nervous system, hyperesthesia of the analyzers, photophobia, tactile hypersensitivity, and increased irritation of hearing occur. Abdominal reflexes usually disappear, tendon reflexes may be decreased or increased. Autonomic 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, abducens, facial, which is revealed in the form of drooping eyelids, strabismus, smoothing of the nasolabial fold, anisocoria. When examining the fundus, congestive disc nipples or optic neuritis, tuberculous tubercles on the choroid are detected. Damage to the optic nerve can lead to complete blindness. By the end of the second period, which lasts approximately one week, the patient is in a characteristic position - lying on his side with his legs pulled up to his stomach and his head thrown back. Signs of confusion appear, the patient is negative and severely inhibited. Tuberculous meningitis is serous meningitis.

The composition of the cerebrospinal fluid is changed: its pressure is increased due to increasing hydrocephalus to 300-500 mm of water. Art. (normally 50-150 mm water column), it is transparent, colorless, and can 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 (Pandey and Nonne-Apelt globulin reactions are sharply positive), and falls out in the cerebrospinal fluid fibrin mesh in the form hourglass 12-24 hours after collecting the material. After centrifuging the test tube, a smear is made from the sediment on the glass and stained with Ziehl-Neelsen. This makes it possible to detect 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, the 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 complicate differential diagnosis. The glucose level was reduced to 1.5-1.6 mmol/l (normally 2.2-2.8 mmol/l), chlorides - to 100 mmol/l (normally 120-130 mmol/l), mycobacterium tuberculosis in cerebrospinal fluid are detected in 10-20% of patients using 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, disturbance of the Cheyne-Stokes breathing rhythm, thermoregulation is disrupted - hyperthermia up to 41 ° C or a sharp drop in temperature below normal. Cachexia develops and bedsores appear. Next comes death as a result of paralysis of the respiratory and vasomotor centers.

Spinal form of meningitis is relatively rare. During this process, inflammatory changes occur from the membranes of the brain to the membranes of the spinal cord, all of which manifests itself against the background of meningoencephalitis. Meningeal symptoms are accompanied by radicular disorders, paraparesis, blockage of the cerebrospinal fluid pathways with protein-cell dissociation (very high protein levels with moderate cytosis). The course of the disease is long and an unfavorable outcome is possible.

In blood tests for tuberculous meningitis, a decrease in the level of hemoglobin and red blood cells, an increase in ESR to 25-50 mm/h, moderate leukocytosis and shift are observed leukocyte formula to the left, lymphocytopenia, monocytosis, absence of eosinophils. 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 MTB infection. The most difficult questions diagnoses of this form of tuberculosis occur when meningitis is the first clinical manifestation 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 from BCG vaccination at birth does not allow doctors to think about the possibility of the tuberculous nature of the disease. And this is a mistake. According to the city children's tuberculosis hospital, in the last 10-12 years, among those sick with tuberculous meningitis, 60% of children were vaccinated with the BCG vaccine.

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

Differential diagnosis with meningitis of other etiology

(bacterial, viral, fungal), encephalitis, poliomyelitis, abscess and brain tumor and other diseases that have similar clinical symptoms, should be based on indicators of the cerebrospinal fluid, the presence of MBT in it, the presence of other localizations of tuberculosis (radiographs 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, and 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 anti-tuberculosis drugs are highly effective, without side effects.

In situations where the diagnosis of meningitis is difficult, 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 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 month, then - 2 tuberculostatics until the end of the main course against the background of pathogenetic therapy.

Dehydration therapy for meningeal tuberculosis is more moderate than for other meningitis. Diuretics are prescribed: lasix, furosemide, diacarb, hypothiazide, in severe cases - mannitol (intravenous 15% solution at the rate of 1 g of dry matter per 1 kg of body weight), 25% solution of magnesium sulfate - intramuscularly for 5 - 10 days; a 20-40% glucose solution is administered intravenously, 10-20 ml, after 1-2 days, a total of 6-8 injections; unloading lumbar punctures 2 times per 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 indicated - the introduction of rheopolyglucin, gelatinol, saline solutions under the control of diuresis.

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

Death of such patients occurs in 20-100% of cases, depending on the stage of the process. If there is no effect from conservative therapy and persistent disorders of the cerebrospinal fluid circulation, the correction of hydrocephalus can be carried out through cerebrospinal fluid shunt 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 the cerebrospinal fluid circulation in 80-95% of cases. Under our supervision there were two children with tuberculous meningitis who underwent CSF shunt surgery in the treatment of hydrocephalus with a favorable clinical effect. In some cases, this can save the patient’s life, but the use of these interventions should be limited due to the risk of generalization of infection. Tuberculostatic therapy after surgery should continue for at least 18 months.

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

Meningitis in children and adults is very serious illness, often having a poor prognosis. Its symptoms are caused by a viral or bacterial infection, and the inflammatory process is localized in the tissues of the meninges. But if meningitis is caused by a specific infection, it is easily transmitted from a sick person, may respond poorly to treatment, and therefore is even more dangerous.

Tuberculous meningitis in adults and children is an inflammation of the membranes of the brain, occurring as a secondary disease against the background of existing tuberculosis of the lungs or other organs. The overwhelming majority of patients have had tuberculosis previously or currently have active tuberculosis. infectious process. The causative agent of the disease enters the cerebrospinal fluid, and from there into the soft, arachnoid, or even the dura mater, causing their inflammation.

Tuberculous meningitis can be called a complication of primary tuberculosis. Initially, infectious particles cause sensitization nerve cells to their toxins, as a result the blood-brain barrier will be disrupted, and the vessels of the meninges will become infected. After the infection spreads from the vessels into the cerebrospinal fluid, the tissues of the meninges themselves become inflamed. In addition, the disease leads to the formation of small tubercles in the brain and membranes, which can grow into the bones of the skull and spread through the cerebrospinal fluid to the spine. In patients, diagnostics often also show the presence of a gray, jelly-like mass at the base of the brain, narrowing and blockage of the arteries, and a variety of other serious problems.

Causes and routes of transmission of the disease

The causative agent of the pathology is Mycobacterium tuberculosis. These bacteria are very pathogenic, but not every person if they enter the body will cause infection. Their virulence—their ability to infect—depends greatly on conditions external environment, as well as on immunity and general human health. Initially, the patient develops tuberculosis of the following localizations:

  • Lungs
  • Lymph nodes
  • Kidney
  • Bones
  • Intestines

Over time, in children or adults, specific inflammation occurs, which boils down to the appearance of accumulations of mycobacteria in the form of granules that are prone to decay and penetration of infection into distant organs. In a patient, tuberculous meningitis can occur at any time during the course of tuberculosis or after ineffective treatment has been carried out.

Symptoms of this pathology can appear if a healthy person becomes infected from a sick person open form tuberculosis by airborne droplets, through food, kisses. IN rural areas The nutritional route of transmission of tuberculosis is common. Risk factors for the development of the disease include all types of immunodeficiencies. Meningitis develops especially often in children with somatic diseases, in those who have had rickets and have undergone surgery. In adults, the disease is more often observed with HIV infection and drug addiction, malnutrition, alcoholism, after a traumatic brain injury, with general exhaustion, and in old age. In some cases, it is not possible to establish the source of infection, the cause of the disease and the location of the primary focus.

How does tuberculous meningitis manifest?

All types of meningitis are more common in children than in adults. If the mother has tuberculosis, the child infancy can also suffer from this disease, and with serious consequences for life and health. Symptoms of a pathology such as tuberculous meningitis begin to appear after infection enters the cerebrospinal fluid. They develop in stages, according to three periods (prodromal, period of irritation, terminal).

In most cases, the disease in both children and adults begins slowly and develops up to 6-7 weeks, but in severely weakened people a sharp, acute onset is possible. Signs of the first period of meningitis are:

  • Apathy, Bad mood, lethargy
  • Tearfulness, breast refusal (in young children)
  • Low-grade body temperature
  • Dizziness
  • Nausea, vomiting
  • Constipation
  • Urinary retention

Symptoms next stage tuberculosis is due to the fact that the cerebrospinal fluid carries the infection directly to the meninges (around the end of the 2nd week).

They are like this:

  • Further increase in temperature (up to 39-40 degrees)
  • Sharp pain in the back of the head or forehead
  • , dizziness
  • Photophobia
  • Depression of consciousness, fainting
  • Stopping the passage of feces
  • Increased skin sensitivity
  • The appearance of bright red spots on the chest and face
  • Neck muscle tension
  • Deafness, decreased vision, squint, etc.

The end stage is caused by the inflammatory process damaging areas of the brain. Edema occurs - hydrocephalus, as cerebrospinal fluid and inflammatory transudate accumulate in the tissues and do not drain. Spinal cord blockade, paresis and paralysis, tachycardia, disturbances of consciousness and breathing often occur. By 15-24 days, tuberculous meningitis in children and adults, if not treated, leads to death from central paralysis - damage to the vascular and respiratory centers.

Diagnostics

In order for treatment to save a person, it is important early diagnosis this pathology. It is believed that the period is relatively safe condition is no more than 7-8 days. The presence of an underlying disease, tuberculosis, as well as existing symptoms should suggest the development of meningitis.

Diagnosis of the disease in children and adults should include a number of physical, laboratory, and instrumental examinations:

  1. Inspection, palpation of lymph nodes;
  2. X-ray of the lungs;
  3. Ultrasound of the liver and spleen;
  4. Tuberculin tests;
  5. General blood analysis;
  6. Blood test using ELISA for tuberculosis;

The main source for finding infection when diagnosed with tuberculous meningitis is cerebrospinal fluid. The patient's cerebrospinal fluid is taken for analysis during a spinal puncture. As a rule, the pressure of the cerebrospinal fluid during meningitis is high, so it may flow out in a trickle. The diagnosis is confirmed by cerebrospinal fluid, in which the concentration of protein, lymphocytes, high cellular composition, too much low rate glucose.

Unfortunately, the cerebrospinal fluid does not always contain Mycobacterium tuberculosis, which could be detected after bacterial culture, but during analysis by flotation they are usually detected and the diagnosis is confirmed. Differential diagnosis for a pathology such as tuberculous meningitis should be carried out with viral meningitis and bacterial meningitis.

How to treat tuberculous meningitis

This disease requires urgent hospitalization and inpatient treatment. Children and adults are placed in a specialized department or initially in an intensive care unit (depending on the condition). The duration of therapy is most often at least 6-12 months. For the most part, treatment comes down to the use of special drugs - Pyrazinamide, Rifampicin, Isoniazid and other drugs from the phthisiology section.

Additionally, treatment includes drugs to improve blood microcirculation and normalize cerebral circulation, antioxidants, drugs against hypoxia of brain tissue.

To prevent cerebral edema, treatment of a disease such as tuberculous meningitis is often based on taking decongestants and diuretics. To reduce the effects of intoxication, the patient is infused saline, glucose. It must be remembered that with tuberculosis, even after successful recovery, a person is weakened and needs rehabilitation activities. Most people are recommended to visit specialized sanatoriums, perform exercise therapy and massage at home. Very important proper nutrition- a diet with an abundance of protein foods, vegetable and animal fats.

Prevention of tuberculosis is very important, because this disease is one of the most serious among infectious pathologies and is fraught with death or disability. Everything must be done to protect children and all loved ones from infection, vaccinate on time and prevent the weakening of the immune system.

In contact with

Loading...Loading...