Symptoms and treatment of tuberculous meningitis. Tuberculous meningitis - when tuberculosis infection hits the bull's eye Brain tuberculosis symptoms first signs

Tuberculous meningitis- a pathology that is characterized by the development of inflammation in the lining of the brain. The source of the disease is mycobacterium.

Features of the disease

Tuberculosis of the brain is another name of this disease. The disease appears suddenly. In adults and children, the state of health sharply deteriorates, hyperthermia, headache, feeling of nausea, urge to vomit occur, the functioning of the cranial nerves is disrupted, a disorder of consciousness and a meningeal symptom complex appear.

An accurate diagnosis is made based on a comparison of clinical data and the results of cerebrospinal fluid examination. The patient awaits a long and complex therapy, which includes anti-tuberculosis, dehydration, and detoxification treatments. In addition, it is carried out symptomatic treatment.

The risk group mainly includes people whose immunity is weakened by HIV, malnutrition, alcoholism, and drug addiction.

Elderly people are susceptible to the disease. In 9 out of 10 cases, meningeal tuberculosis is a secondary disease. It occurs against the background of the development of the disease in other human organs. In more than 75% of cases, the pathology is initially localized in the lungs.

If the location of the original source of the disease cannot be determined, tuberculous meningitis is called isolated.

How the disease is transmitted: cerebral tuberculosis develops as a result of penetration of the Koch bacillus into the meninges. In some cases there is a possibility of infection by contact. In case of tuberculosis infection of the skull bones, the causative agent of the disease enters the cerebral membranes. In spinal tuberculosis, the bacterium penetrates the lining of the spinal cord. According to statistics, about 15% of cases of tuberculous meningitis occur due to lymphogenous infection.

The main route of spread of Koch's bacillus to the meninges is hematogenous. This is the route by which pathogenic microorganisms are spread circulatory system throughout the body. The penetration of harmful bacteria into the cerebral membrane is due to an increase in the permeability of the blood-brain barrier.

Initially there is a defeat vascular network soft membrane, after which pathogenic microorganisms enter the cerebrospinal fluid, which provokes the development of inflammation of the arachnoid and soft membranes.

The membranes at the base of the brain are predominantly damaged, which leads to the development of basilar meningitis. Inflammation gradually spreads to the membranes of the hemispheres. Further inflammatory process affects the substance of the brain, a disease known as tuberculous meningoencephalitis occurs.

Morphologically, a serous-fibrous inflammatory process of the membrane occurs with the presence of characteristic tubercles. Pathological change blood vessels (fibrosis or thrombosis) can lead to circulatory disorders of a certain area of the medulla. After completing a course of treatment, the inflammatory process can be localized, resulting in the formation of adhesions and scars. Hydrocephalus often occurs in sick children.

Periods of occurrence

There are several periods of tuberculous meningitis:

premonitory;
irritation:
paresis and paralysis.

The prodromal period lasts from one to two weeks. It is the presence of this phase of the disease that distinguishes the tuberculous form of meningitis from the usual one. The prodromal stage of the disease is characterized by the appearance of headaches in the evening or at night. The patient's general well-being worsens. He becomes irritable or apathetic. Gradually, the headache intensifies, and the patient begins to feel nauseous. There is a steady increase in body temperature. Due to such specific symptoms, put accurate diagnosis at this stage it is very difficult.

The period of irritation begins with an exacerbation of symptoms with sharp increase body temperature up to 39°C. Headaches become more intense, excessive sensitivity to light (photophobia), sound occurs, and worsen tactile sensations. The patient experiences constant lethargy and a feeling of drowsiness. On the skin in different areas red spots appear and disappear on the body. The last symptom can be explained by a violation of vascular innervation.

At this stage, the symptoms of tuberculous meningitis become meningeal in nature. Tension of the neck muscles occurs, and manifestations of Brudzinski and Kernig symptoms are observed. At first these signs are not clearly expressed, but over time they intensify. At the end of this period (1-2 weeks after its start), the patient experiences lethargy, confusion, and the person involuntarily assumes a characteristic meningeal posture.

During the period of paresis and paralysis, the patient completely loses consciousness, central paralysis and sensory disorders occur. Respiratory and heart rhythm disturbances occur. Limb cramps may appear, body temperature rises up to 41°C or, conversely, drops to abnormally low levels. If a person is not given effective treatment, he will die within a week.

The cause of death is most often paralysis of the part of the brain responsible for regulating breathing and heartbeat.

There are several clinical forms of this pathology.

Tuberculous basilar meningitis

Tuberculous basilar meningitis develops gradually in more than 2/3 of cases and has a prodromal period lasting up to 1 month. During the irritation stage, an increasing headache appears, signs of anorexia are observed, the patient constantly feels sick, severe drowsiness and lethargy occurs.

The manifestation of meningeal syndrome occurs together with disorders of the cranial nerves. For this reason, the patient may develop strabismus, blurred vision, hearing loss, anisocoria, and drooping of the upper eyelid. In less than half of cases, ophthalmoscopy detects disc congestion optic nerve. Upset may occur facial nerve, which will cause facial asymmetry.

As the disease progresses, dysarthria, dysphonia, and choking appear. These symptoms indicate further damage to the cranial nerves. In case of absence effective treatment the disease progresses to a period of paresis and paralysis.

Tuberculous meningoencephalitis

The occurrence of tuberculous meningoencephalitis most often occurs in the third period of meningitis. The symptoms are similar to those of encephalitis. Paresis and spastic paralysis appear, unilateral or bilateral hyperkinesis develops. In this state, the patient is completely unconscious.

At the same time, arrhythmia, tachycardia, respiratory distress can be detected, and in some cases Cheyne-Stokes breathing is noted. With further progression, the disease leads to the death of the patient.

Spinal meningitis

Tuberculous spinal meningitis is observed infrequently. The manifestation of this form of the disease begins with symptoms of damage cerebral membranes. Next, girdling pain appears, which is caused by the spread of inflammation to the spinal roots.

In some cases pain syndrome can be so strong that even narcotic analgesics cannot relieve it. As the disease progresses, problems with stool and urination begin. The appearance of peripheral flaccid paralysis, para- or monoparesis is observed.

Diagnosis and treatment

Diagnostic measures are carried out jointly by phthisiatricians and neurologists. Main stage in the diagnostic process - examination of spinal cord fluid, a sample of which is obtained using lumbar puncture.

Liqueur in tuberculous meningitis is released from high blood pressure up to 500 mm water. Art. There is the presence of cytosis, which in the first stages of the pathology has a neutrophilic-lymphocytic character, but later tends more towards lymphocytic. The quantitative indicators of chlorides and glucose decrease.

The lower the glucose concentration, the more difficult the upcoming treatment. Based on this, doctors choose the appropriate treatment method. Differential diagnosis of tuberculous meningitis is carried out using CT and MRI of the brain.

At the slightest suspicion of a tuberculous origin of meningitis, doctors resort to prescribing specific anti-tuberculosis therapy.

Treatment of tuberculous meningitis is carried out with the use of Isoniazid, Rifampicin, Ethambutol and Pyrazinamide. If therapy gives positive results, the dosage of the drugs is gradually reduced. If treatment is successful, Ethambutol and Pyrazinamide are abandoned after 3 months. Taking other drugs in reduced doses should last for at least 9 months.

In parallel with anti-tuberculosis drugs, treatment is carried out with dehydration and detoxification drugs. Glutamic acid, vitamin C, B1 and B6 are prescribed. In some cases, treatment with glucocorticosteroids is resorted to. If there are seizures, treatment will include Neostigmine. In case of optic nerve atrophy, nicotinic acid, Papaverine and Pyrogenal are prescribed.

Tuberculoma of the brain is a form of tuberculosis that affects the nervous system. Essentially, it is a tumor that has clear boundaries. It develops in people who have tuberculosis of the lungs, lymph nodes of the chest or other organs. The infection enters the brain through lymph or blood, which continuously circulates in the body.

Most often, this form of tuberculoma affects children aged 5 to 10 years, and this formation is twice as likely to be detected in male patients. The symptoms of the disease are in many ways similar to those of a regular brain tumor. But, of course, there are some differences.

Causes of the disease

As already indicated, cerebral tuberculoma is provoked by tuberculosis, which has developed in some organ. Through lymph or blood dangerous infection enters the brain and begins to have a destructive effect on some part of it. As the disease progresses and swelling appears, symptoms begin to appear. True, in rare cases, brain tuberculoma can develop independently, even if there is no source of infection in some other organ.

Although tuberculoma can develop in any part of the brain, it most often forms in the posterior parts of the brain.

Symptoms

Almost always the disease manifests itself acutely, like a common infectious disease. The first thing that appears is temperature. It can reach 38ºС and higher. Along with a feverish state, headaches appear, nausea is felt, and vomiting may occur. General weakness is often accompanied by unsteadiness when walking, cramps in the legs or arms. Gradually the symptoms become more pronounced. Periodically, a state of relief sets in, after which the disease makes itself known again.

So, the most common symptoms of brain tuberculoma can be considered the following manifestations:

Most often, the patient experiences general weakness. It manifests itself as fatigue and tiredness. It is very difficult for a person to do even simple and familiar work.
Also, the patient almost always begins to sweat profusely. And this happens even when a person does not experience serious physical or psycho-emotional stress.
Fever occurs in approximately 70% of cases of the disease.
Unsteadiness when walking is also quite common.
In approximately half of the cases, the patient suffers from nausea, headache (spreads to the entire head), and seizures. Loss of consciousness may even occur, sometimes accompanied by convulsions.
A little less often (in approximately 40% of all cases of incidence), severe vomiting occurs and a strange weakness is felt in one half of the body.
Sometimes memory impairment may occur. A person begins to forget some facts and moments from life.

The symptoms of the disease may differ depending on in which part of the brain the tuberculoma formed and at what stage of development it is. For example, if the cerebellum is affected, then motor disorders will appear, if the central gyri are affected, sensitivity disorders and convulsions will appear. If tuberculoma has formed in the frontal lobe of the brain, then serious problems with coordination and mental health may occur.

The illness can last from several days to several months. If at first the patient’s symptoms are pronounced, then gradually they subside and become vague. A low temperature increase persists for a long time. As the disease progresses, after 4-6 months, work disturbances begin to appear seriously. nervous system. For example, children become lethargic, lethargic, and show all the symptoms of intoxication (poisoning) of the body.

Treatment

A number of tests help diagnose tuberculoma. A blood and cerebrospinal fluid test is performed. A chest x-ray is also taken, since pulmonary tuberculosis is often the cause of brain infection. You may also need an electroencephalography, which examines brain activity, and an x-ray of the skull, which can reveal deposits of calcium salts in it. Doctors may prescribe magnetic resonance imaging or CT scan, with which you can study each part of the brain in detail.

If brain tuberculoma has been identified and its exact location has been determined, then there can be only one treatment - surgery to remove the tumor. But for the result to be successful, the patient needs to take medications as part of anti-tuberculosis therapy. It is definitely worth repeating the examinations to know how effective the treatment is.

If earlier the mortality rate as a result of surgery to remove cerebral tuberculoma reached 96%, today the situation is more encouraging - 75%. And all this thanks to the fact that it is possible to use more modern drugs against tuberculosis, which are much more effective than those that preceded them.

Prevention

There are combinations of factors that can provoke this disease: severe infections, poor living conditions, poor nutrition, drug or alcohol use. Because of this, a person’s immune strength is greatly reduced, as a result of which he may develop tuberculosis. Knowing this, you need to try to avoid these provoking factors. You should also avoid contact with people with tuberculosis and undergo preventive examinations from doctors in a timely manner.

Extrapulmonary tuberculosis.

Extrapulmonary tuberculosis is a conditional concept that unites forms of tuberculosis of any localization, except for the lungs and other respiratory organs. In accordance with clinical classification tuberculosis, adopted in our country, to T. century. include tuberculosis of the meninges and central nervous system, intestines, peritoneum and mesenteric lymph nodes; bones and joints; urinary and genital organs; skin; peripheral lymph nodes, eyes. Other organs are affected extremely rarely. Tuberculosis of the ear, thyroid gland, adrenal glands, spleen, endocardium, pericardium, and esophagus is practically not observed. The localization of tuberculosis lesions determines the characteristics of the clinical course. Separate forms of T. v. can be combined with each other and with damage to the respiratory system.

Tuberculosis of the meninges and central nervous system

There are tuberculosis of the meninges - tuberculosis, which, as a rule, is accompanied by damage to the substance of the brain and spinal cord (meningoencephalitis, meningoencephalomyelitis); cerebral tuberculoma; damage to the spinal cord due to tuberculosis (see below Tuberculosis of bones and joints).

Tuberculosis of the meninges. Pathogenesis and pathological anatomy. Tuberculosis of the meninges in the vast majority of cases develops as a result of hematogenous dissemination of Mycobacterium tuberculosis from the primary focus in the lungs, lymph nodes or kidneys. In more than 50% of patients, damage to the meninges is the first clinical manifestation of tuberculosis. In 1/3 of patients, tuberculosis of the meninges occurs against the background of disseminated pulmonary tuberculosis, which, as a rule, is detected simultaneously with damage to the meninges. The importance of fibrous-cavernous pulmonary tuberculosis as a source of meningeal tuberculosis has decreased.

Morphologically, the process is characterized by acute serous-fibrinous inflammation of the meninges. In the subarachnoid (subarachnoid) space of the brain and spinal cord, a grayish-yellow effusion is found, in the soft membrane and ependyma - miliary and larger tuberculous granulomas, incl. with symptoms of caseous necrosis. Lymphocytes predominate in foci of tuberculous inflammation. The inflammatory process usually involves the substance of the brain and spinal cord. The ventricles of the brain dilate and fill with cloudy fluid (hydrocephalus). More often (in 85-90% of cases), the meninges and brain are affected in the area of its base, at the level of the interpeduncular cistern (basal).

Clinical picture and diagnosis. Basal meningoencephalitis develops gradually in most cases. A prodromal period is often observed, characterized by malaise, lethargy, decreased performance, appetite, sleep disturbance, irritability, and low-grade body temperature. The prodromal period is replaced by a detailed picture of the disease. However, it is possible acute development illnesses, especially in young children. Constant symptom is a fever (low-grade, remitting, hectic or irregular), which often precedes the onset of headache or occurs simultaneously with it. Headache It has different intensities and is gradually increasing. Some patients also report pain in the chest or lumbar regions spine, indicating damage to the membranes and roots of the spinal cord. On the 5th-8th day of illness, vomiting appears, subsequently it becomes more intense. In the first days of the disease, meningeal symptoms are mild, the patient continues to walk, and often even work. On the 5-7th day of illness, these symptoms become clear and their intensity increases.

Characterized by mental disorders and various focal symptoms. In the 1st week of illness, along with headache, increasing lethargy, apathy, and decreased motor activity are noted. In the 2nd week of the disease, general hyperesthesia appears, apathy and stupor intensify, and delirious or oneiric states develop (see. Delirious syndrome, Oneiric syndrome ). Memory weakens current events, orientation in space and time is gradually lost. Damage to the cranial nerves is detected at the end of the 1st - beginning of the 2nd week of illness. The most characteristic are the III, IV and VII cranial nerves. Damage to the diencephalic region causes symptoms such as bradycardia, red dermographism, Trousseau spots, sleep disturbances. Signs of congestive optic nerves appear and increase (see. Congestive nipple ). Development of pain and paralysis (see. Paralysis ) often precede paresthesia of the corresponding limbs. At the 2nd week of illness, disturbances in tendon reflexes and muscle tone, pathological reflexes of Babinsky, Rossolimo, Oppenheim, etc. Pronounced pain in the extremities in patients who have not received specific therapy usually occurs in the 3rd week. Aphasia with ah, it is observed in 25% of patients. Along with them (less often in their absence) arise hyperkinesis. In young children and the elderly, hemiparesis develops more often, sometimes in the first days of the disease. In some cases they are combined with seizures. At the end of the 2nd week of illness, functions are impaired pelvic organs. During the 3rd week, the patients' condition continued to deteriorate progressively. Stupefaction progresses to precoma, and then to coma. Tendon and pupillary reflexes fade, sometimes developing decerebrate rigidity.

Rarer variants of the disease include diffuse and limited convexital tuberculosis (damage to the convexital, i.e., surface of the brain facing the vault of the skull) and tuberculous meningoencephalomyelitis (cerebrospinal form of tuberculous a). The features of diffuse convexital a are a more acute onset than with basal e (headache and increased body temperature), rapid impairment of consciousness. With limited convexital meningoencephalitis (the process is localized in the area central gyri cerebrum), the initial symptoms of the disease are paresthesia, hemiparesis, aphasia, epileptic seizures against a background of increasing fever and headache. With this localization, the disease can take long course with remissions and exacerbations. After some (more or less long) time, basal meningoencephalitis occurs.

Tuberculous meningoencephalomyelitis can be ascending or descending. Ascending is manifested primarily by symptoms of meningoradiculoneuritis with dysfunction of the pelvic organs: meningeal symptoms join later (sometimes after a few weeks). Descending is characterized by the rapid spread of the process from the base of the brain to the spinal cord and the predominance in the clinical picture of the disease of symptoms of damage to the membranes and substance of the spinal cord.

The diagnosis is made based on clinical picture, medical history (contact with a patient with tuberculosis, pulmonary tuberculosis), laboratory test results.

It is important to identify Mycobacterium tuberculosis in the cerebrospinal fluid (using microscopic, cultural examination, biological tests) or the pathogen antigen (by enzyme immunoassay).

There are two types of disease. The first type is characterized by an acute onset with a rise in body temperature, rapid development of symptoms of brain damage, depending on the localization of the process, a subsequent wave-like course and prolonged low-grade fever. In this case, meningoencephalitis is often mistakenly diagnosed. The second type of disease is characterized by slow development: at first, intermittent headaches and unstable low-grade fever may be noted; subsequently focal neurological symptoms, which periodically weaken due to a temporary stop in the growth of tuberculoma.

Diagnosis of brain tuberculomas is difficult. In this case, the anamnesis, clinical manifestations and results of a neurological examination are taken into account. X-ray data (including computer scan) are of great importance tomography, angiography ), electroencephalography, echoencephalography, allowing to establish the location and size of tuberculoma. Differential diagnosis should be made with brain tumors, syphilitic gummas of the brain (see. Syphilis ), neuroinfections of non-tuberculous etiology. For timely diagnosis disease, patients with cerebral, meningeal or focal symptoms should be urgently consulted by a neurologist.

For brain tuberculoma, surgery is indicated - enucleation of the tuberculoma within healthy tissue. Antituberculosis, diuretics and restoratives are prescribed. The prognosis is serious. When the process is far advanced, changes in the nervous system are irreversible. The principles of dispensary observation of patients with cerebral tuberculoma are the same as for tuberculosis of the meninges.

Like other types of the disease, these types are caused by the tuberculosis bacillus, which has entered the body in one way or another. Mycobacterium tuberculosis was first identified from cerebrospinal specimens in 1893.

Morphology and pathogenesis

Tuberculosis of the brain and nervous system has three ways of occurrence and spread:

Mycobacterium tuberculosis spreads throughout the body from foci of infection, which may be in the lungs, lymph nodes, or other areas outside the lungs.

At the first stage, tuberculous meningitis develops through the hematogenous route, eventually breaking through the blood-brain barrier. As a result, infection of the choroid plexuses occurs. Further development the disease occurs in the cerebrospinal fluid. Once in the spinal cord fluid, mycobacterium tuberculosis is deposited on the brain base, affecting the soft membrane and gradually destroying it.

As a result of inflammation, a specific exudate is formed. It accumulates in the area where the intersection of the optic nerves is located on the surface of the cerebellum, where the cisterns are localized.
In addition to the optic fascicles, inflammatory discharge can accumulate on the convexities of the brain, in its temporal lobes, as well as in the frontoparietal.
Exudate can penetrate into the subarachnoid space and cerebral ventricles.
During the pathological process, the pia mater of the brain is often saturated with serous-fibrinous contents, causing tissue necrosis.
The choroid plexuses and the membrane itself have an edematous appearance, with an abundance of hemorrhages.
In addition, miliary bulges are visible on the tissues of the shell.

The chronic and subacute course of meningitis of tuberculous origin is characterized by the formation of granulomas in the tissues, in the center of which caseous necrosis is observed. Granulomas are visible not only in the tissues themselves, but also on the walls of blood vessels; this phenomenon can be accompanied by thrombosis. Damage to blood vessels most likely leads to swelling of certain areas of brain tissue and their softening. Since an inflammatory process also occurs in the background, it can also affect the brain matter, causing encephalitis.

Even if tuberculous meningitis is successfully transferred and the patient recovers, adhesions will likely remain in the spinal cord, brain, and subarachnoid region. In their zones blood vessels are damaged, this leads to disturbances in blood circulation and cerebrospinal fluid, often with adverse consequences.

Symptoms

Signs of brain tuberculosis are usually divided into several groups, according to the time of manifestation:

prodromal symptoms preceding the main symptoms. The period itself can last from 3 days to a month;
symptoms of irritation of the cranial nerves and soft membranes of the brain;
symptoms of brain tissue damage.

The main symptoms at this stage are associated with poisoning of the body by the products of mycobacteria:

headaches, migraines;
lethargy;
weakness;
high level of fatigue, poor endurance;
general ailments;
poor performance;
poor appetite or its complete absence;
sweating;
nightmares, bad and disturbing sleep;
anxiety and irritability;
inhibition of thinking and action;
apathy;
from time to time – an increase in temperature to subfebrile levels.

At the end of the prodromal period, the time comes for the manifestation of symptoms of pathologies of the cranial nerves and lining of the brain.

The following are distinguished: characteristic syndromes for this period:

meningeal;
general infectious;
cerebrospinal fluid lesions;
damage to the spinal roots and fibers of the cranial nerves.

vomiting and nausea;
headache;
hyperesthesia;
neck muscle tension;
specific body posture and characteristic phenomena: zygomatic ankylosing spondylitis symptom and others.

Headache can be felt both “everywhere” and in certain areas (mainly in the frontal and occipital zones; this is due to the effect of inflammation on certain cranial nerves. The pain is often accompanied by vomiting, which does not lead to relief, and it occurs regardless of whether the patient has taken food.The emetic effect is also caused by irritation of the nerve endings and the corresponding center.

The so-called chicken pose is very characteristic of meningeal syndrome - the patient lies with his head thrown back and his torso extended, his stomach retracted. The legs are bent and pressed towards the stomach. The pose is caused by irritation of the nerves and the contraction of certain muscle groups stimulated by them.

General infectious syndrome - as the name suggests, demonstrates a picture of infection. The temperature is elevated and can range from low-grade to very high. An increase in temperature may begin before the headache or occur simultaneously.

Changes in cerebrospinal fluid are determined by tests. The liquid taken for analysis has an opalescent or transparent appearance; when a sample is taken, it flows out with increased pressure and can flow in a stream. Found in liquid high content protein and lymphocytes, and mass fraction glucose, on the contrary, is reduced.

This phenomenon is characterized by specific external symptoms, depending on which nerves are affected:

strabismus may develop;
partial or complete paralysis of facial muscles, tongue;
dilated pupils and other manifestations.
Inflammation of the retina and the posterior part of the choroid may develop.

In the third stage, brain tissue is directly affected. Symptoms of this are deterioration or complete loss of functions for which the affected areas are responsible. These phenomena develop as a result pathological processes brain vessels, as a result of which their lumen closes completely. Ischemia and softening of brain tissue develops in the affected area with loss of the functions they perform.

Diagnosis and treatment

Symptoms of damage to the brain and central nervous system by tuberculous mycobacteria are similar to those of meningitis of other origins (caused by meningococci, viruses, staphylococci). Their main difference from each other is different composition fluid taken during spinal cord puncture. Therefore, to determine tuberculosis as the cause of the lesion, differential diagnosis is necessary to exclude non-tuberculosis infection and prescribe the correct treatment.

For effective treatment Patients with tuberculous meningitis must be placed in hospitals specially equipped for this; keeping them at home is strictly unacceptable! The main drug for the treatment of all forms of tuberculosis is isoniazid. It can be prescribed in the form of tablets, if the patient is unconscious, then as injections into the muscles or intravenously. Isoniazid is considered the basic treatment for tuberculosis. The active substance passes the blood-brain barrier well and accumulates in the cerebrospinal fluid, quickly reaching an effective concentration.

In addition to Isoniazid, auxiliary medications are also prescribed:

For unconscious patients and those whose condition is getting worse, puncture is done daily, and calcium chloride streptomycin is also injected into the subarachnoid space daily, doing this for up to 10 days.

Patients require careful and constant care. Strict bed rest is prescribed for up to 3 months, and inpatient treatment can last more than six months. After the patient is discharged from the hospital, treatment does not stop; for a complete recovery, the person is prescribed sanatorium treatment, for which there are special sanatoriums. Before the patient begins to get up, he is supposed to undergo physical therapy exercises right in bed.

During treatment, doctors may encounter complications, one of the most severe of which is the likelihood that the patient will develop hydrocephalus. Other complications include motor activity disorders, decreased hearing and vision, and in some cases the patient’s intelligence decreases.

In general, timely treatment of tuberculosis of the brain and central nervous system has favorable forecasts. Today, complete healing can be achieved in a large number of cases. This is largely due to modern anti-tuberculosis drugs. Until a certain point, doctors tried to use conventional antibacterial agents, and, unfortunately, the patients were doomed because the drugs were ineffective. But these days, the means developed by medicine provide healing for the majority of patients with tuberculosis, including those with lesions of the brain, spinal cord and central nervous system.

How does brain tuberculosis manifest and is it contagious?

When entering the human body, Mycobacterium tuberculosis can affect not only the lungs. One of the most dangerous forms manifestations of the disease is cerebral tuberculosis. Typically this is secondary manifestation diseases, infection of the membranes of the brain occurs from foci of tuberculosis already existing in the body. Treatment of such a disease is fraught with great difficulties and takes a long time, but despite this it does not always lead to a complete recovery; the disease is often accompanied by serious complications. The decisive factor for a favorable outcome of the disease is timely initiation of correct treatment.

Causes of the disease, forms of the disease

Tuberculosis is a serious and dangerous disease, which, despite all the preventive measures taken, remains very common. And although it is believed that this disease threatens only people of low social status, statistics indicate the opposite. Regardless of standard of living, age and area of activity, everyone is at risk of contracting tuberculosis. After all, patients with an open form of tuberculosis often do not know about their diagnosis and continue to remain in society, actively spreading the infectious agent - Koch's bacillus - around them.

The reason for the development of tuberculosis damage to the brain is the entry of mycobacterium tuberculosis from the lesion located in the body (most often in the lungs) into the blood and penetration into the brain.

Infection of the brain with Koch's bacillus can occur in three ways:

Hematogenous (through blood);

Lymphogenic (via lymph);

Mycobacterium tuberculosis, entering the blood, first infects the spinal cord, and then, through the flow of cerebrospinal fluid, penetrates the lining of the brain.

The process of infection spreading occurs very quickly, and it is extremely difficult to resist it.

Brain tuberculosis manifests itself in two forms:

Tuberculous meningitis - mycobacteria act in the meninges and destroy them. Often the progression of meningeal tuberculosis is accompanied by damage to other organs.
Solitary tuberculoma - characterized by a localized focus of tuberculous inflammation in the cerebellum or brain stem. As tuberculoma grows, it gives rise to purulent processes and leads to an abscess. Tuberculous spondylitis is a lesion of the central nervous system.

In addition, brain tuberculosis is classified depending on the area of damage, and the following forms are distinguished:

Basal - damage to parts of the brain occurs at the base of the skull.
Convexital - the convex surfaces of the brain are affected; this form is characterized by impaired consciousness.
Meningoencephalitis - inflammation of the brain in acute miliary tuberculosis; severe form of the disease, often ending in death.
Meningoencephalomyelitis is a simultaneous inflammation of the brain and spinal cord.

As a result destructive processes on the membranes of the brain, the walls of blood vessels thicken, as a result of which blood circulation is disrupted, hypoxia (lack of oxygen) occurs, which gives rise to ischemic disease, brain tissue softens.

Most often, the development of brain tuberculosis occurs in people with weakened immune systems, patients with AIDS and HIV. Knowing the first signs and symptoms of this disease, a person has a better chance of seeking help from a TB specialist in a timely manner and receiving the necessary treatment, thereby minimizing the risk of complications.

Symptoms

Depending on the form of the disease, its stage and the location of the lesions, the symptoms of the disease can manifest themselves in different ways:

In the prodromal period - headaches of a short duration (up to minutes), occurring at a certain time of the day. As the disease progresses, the pain becomes longer and longer, eventually becoming permanent. Sleep is disturbed, the person becomes nervous and irritable. There is general malaise, increased fatigue, decreased concentration and performance. The lymph nodes become inflamed and painful. The duration of such a period can last up to 2 months.
During the period of irritation - weakness, loss of strength, low-grade fever 37.0-37.5 0 C. Headaches intensify, bright light and sharp sounds cause severe discomfort. The gastrointestinal tract manifests itself as nausea and vomiting, and lack of appetite. This stage is accompanied by sudden weight loss up to anorexia. Vision problems may occur - decreased sharpness, squint, distorted color perception.
Terminal period - occurs when the disease is advanced without necessary treatment. Characterized by high temperature, signs of central paralysis most often appear, the patient is in unconscious. At this stage, it is almost impossible to achieve a complete cure; in addition, the likelihood of death is high. If the person can be saved, the accompanying complications will not allow him to return to life. full life.

Solitary tuberculoma is characterized by nausea and vomiting, the temperature can rise to 39.0 0 C.

It has been noted that this manifestation of cerebral tuberculosis is more common in children and can provoke the development of hydrocephalus. An increase in temperature is accompanied by convulsions progressing to paralysis. It is assumed that a child can inherit tuberculosis at the genetic level.

In general, in children with brain tuberculosis, the symptoms of the disease manifest themselves clearly and progress quickly. Against the backdrop of a constantly rising temperature, the child has weakness, various kinds of manifestations of visual impairment and impaired motor activity are possible.

Special attention When diagnosing, the doctor looks for meningeal syndrome, which most likely indicates tuberculosis damage to the brain. A characteristic sign of this syndrome is the patient’s special posture, when the head is thrown back and the stomach is retracted. Any attempts to change position result in a severe headache. This happens due to the stiffness of the neck muscles. There are also interruptions in breathing, pressure surges, and an increase in body temperature to critical levels.

Diagnostics

Since the symptoms of tuberculosis of the meninges are similar to the manifestations of other infectious lesions body, for an accurate diagnosis, the doctor must conduct a comprehensive examination.

Diagnosis is also complicated by the fact that often the patient himself does not see the first signs of the disease and is in no hurry to associate them with tuberculosis, since this form of the disease usually manifests itself against the background of an existing infectious disease - ARVI or influenza, which are accompanied by similar symptoms.

examination of biomaterials (blood, urine, feces, sputum) for the presence of Koch’s bacillus, including the PCR (polymerase chain reaction) method;
X-rays, computed tomography, MRI diagnostics will help identify foci of infection and assess the extent of damage to the body, and with the help of a magnetic resonance imaging scanner, a specialist can obtain photos of not only the superficial membranes of the brain, but also its internal layers;
spinal cord puncture is crucial in establishing the diagnosis. A number of indicators of this sample are assessed, focusing special attention on the glucose level: the more serious the stage of the disease, the lower this indicator will be.

In addition to the above studies, special attention is paid to the study of the patient’s medical history, predisposition to infectious diseases, presence of contacts with tuberculosis patients.

Treatment

Complex treatment of tuberculosis brain damage is carried out exclusively in a hospital setting and takes quite a long time. Firstly, the person at this time is contagious to others, and secondly, due to the severity of the disease, the patient must be constantly under the supervision of doctors.

The patient is prescribed complex drug therapy:

A complex of anti-tuberculosis drugs, the duration of which is at least six months. These include Isoniazid, Pyrazinamide, Rifampicin, Ethambutol - these are drugs with increased anti-tuberculosis effectiveness.
Analgesics - for relief pain patient, migraine relief.
Antipyretics - the disease is accompanied by an increase in body temperature.
Dehydration and detoxification drugs are prescribed by a neurologist.
Vitamins C, group B, glutamic acid.

In severe cases of the disease, treatment may be prescribed hormonal drugs, as well as symptomatic treatment aimed at restoring the functions of the optic nerve, paralyzed muscles and other consequences of the disease.

Medicines are produced in different forms, which allows them to be taken either orally (in tablet form) or bypassing the gastrointestinal tract in cases where the patient is unconscious.

If drug treatment turns out to be ineffective, the feasibility of surgical intervention is considered. Mainly to surgical care are used for solitary tuberculoma, removing the focus of tuberculous inflammation.

After hospitalization, patients are shown restorative rehabilitation in an anti-tuberculosis sanatorium, the program of which includes physical therapy and physiotherapy.

In addition, persons who have had cerebral tuberculosis need to undergo a course of maintenance therapy several times a year aimed at preventing possible relapses of the disease.

For several years after treatment, the patient will be registered at the tuberculosis dispensary. This measure is necessary for systematic monitoring of the body’s condition in order to prevent re-infection and the development of complications.

Complications and consequences

If for some reason timely diagnosis of tuberculosis brain damage and adequate treatment are not carried out, the risk of developing severe complications.

There is a high probability of developing the following pathologies:

development of hydrocephalus (water on the brain);
epilepsy;
loss of vision up to complete blindness;
decreased hearing acuity;
impaired motor activity - a person may remain paralyzed for life;
various types of mental disorders and disruptions in the central nervous system;
relapses of the disease.

If there is no treatment at all, irreversible consequences develop in the body, and an adult dies 3-4 weeks after the onset of infection.

If complications occur, it is almost impossible to completely restore all functions of the body, and the chances of returning a person to a full life are negligible.

However, at the current level of development of medicine, in general, the prognosis for the treatment of tuberculosis brain lesions is quite favorable. At timely application Seeing a doctor and correct treatment helps to avoid complications and achieve complete healing of the patient.

Prevention

And people who have suffered this serious illness, in order to avoid possible relapses, should especially carefully monitor their health, if possible, eliminate the impact of negative factors, healthy image life.

Refusal bad habits, regular physical exercise, proper nutrition, enriched with vitamins and microelements, will strengthen the body’s protective functions and reduce the risk of relapse to a minimum. Food rich in animal proteins and fats, as well as high in iodine, is recommended.

Life after tuberculosis

Depending on how effective the treatment turned out to be, and whether a person managed to fully recover from the illness, his quality of life and the ability to continue working depend.

The scope of activity will have to be changed if the professional activity before the illness was related to:

production providing harmful effects on the body;

With increased risk injuries.

To maintain health and prevent relapses of the disease, a person needs the most comfortable conditions for living and working.

If the disease was accompanied by complications, then the issue of a person’s ability to work will be decided individually in each specific case. After all, the consequences of such complications can be varying degrees severity, sometimes a person remains disabled for life.

Meningeal tuberculosis

Tuberculosis of the meninges is divided into:

tuberculous meningitis, which is often accompanied by damage to the substance of the brain and spinal cord (meningoencephalitis, meningoencephalomyelitis);
cerebral tuberculoma;
spinal cord damage due to tuberculous spondylitis.

Tuberculosis of the meninges in most cases develops as a result of hematogenous dissemination of Mycobacterium tuberculosis from the primary focus in the lungs, lymph nodes or kidneys. In more than 50% of patients, damage to the meninges is the first clinical manifestation of tuberculosis. In 1/3 of those infected, tuberculosis of the meninges occurs against the background of disseminated pulmonary tuberculosis, which is detected simultaneously with damage to the meninges. The importance of fibrous-cavernous pulmonary tuberculosis as a source of meningeal tuberculosis has become significantly lower.

Morphologically, the process is characterized by acute serous-fibrinous inflammation of the meninges. In the subarachnoid (subarachnoid) space of the brain and spinal cord, a grayish-yellow effusion is found, in the soft membrane and ependyma - miliary and larger tuberculous granulomas, incl. with symptoms of caseous necrosis. Lymphocytes predominate in foci of tuberculous inflammation. The ventricles of the brain dilate and fill with cloudy fluid (hydrocephalus). The inflammatory process often involves the substance of the brain and spinal cord. In 85-90% of cases, tuberculosis attacks the meninges and the brain at its base, at the level of the interpeduncular cistern (basal meningoencephalitis).

Basal meningoencephalitis develops gradually in most cases. A prodromal period is often observed, which is accompanied by:

low-grade body temperature;
general malaise and weakness;
decreased performance and appetite;
sleep disturbance;
irritability.

The prodromal period for tuberculosis of the meninges is replaced by a detailed picture of the disease. However, acute development of the disease is possible, especially in young children. A constant symptom is fever (low-grade, remitting, hectic or irregular), which often precedes the onset of headache or occurs simultaneously with it. The headache varies in intensity and gradually increases. Some patients also note pain in the thoracic or lumbar spine, indicating damage to the membranes and roots of the spinal cord. On the 5th-8th day of illness, vomiting appears, subsequently it becomes more intense. In the first days of the disease, meningeal symptoms are mild, the patient continues to walk, often even work. On the 5-7th day of illness, these symptoms become clear and their intensity increases.

There are mental disorders and various focal symptoms.

In the 1st week of illness, along with headache, increasing lethargy, apathy, and decreased motor activity are noted.

In the 2nd week of the disease, general hyperesthesia appears, apathy and partial hearing loss intensify, and delirious or oneiric states develop. Memory for current events weakens, orientation in space and time is gradually lost.

Damage to the cranial nerves can be detected at the end of the 1st - beginning of the 2nd week of illness. The most typical are paresis of the III, IV and VII cranial nerves. Due to damage to the diencephalic region, symptoms such as bradycardia, red dermographism, Trousseau spots, and sleep disturbances are observed. Signs of congestive optic nerves appear and increase. The development of paresis and paralysis is often preceded by paresthesia of the corresponding limbs.

In the 2nd week of the disease, disturbances in tendon reflexes and muscle tone, pathological reflexes of Babinsky, Rossolimo, Oppenheim, etc. appear. Severe paresis and paralysis of the limbs in patients who have not received specific therapy usually occur in the 3rd week. Aphasia with paralysis is observed in 25% of infected people. In most cases, hyperkinesis occurs along with paralysis. Hemiparesis is observed much more often in young children and the elderly, sometimes in the first days of illness. In some cases they are combined with seizures. At the end of the 2nd week of the disease, the functions of the pelvic organs are disrupted. During the 3rd week, the patients' condition continued to rapidly deteriorate. Stupefaction progresses to precoma, and then to coma. Tendon and pupillary reflexes fade, and decerebrate rigidity sometimes develops.

Rarer varieties of the disease include diffuse and limited convexital tuberculous meningoencephalitis(damage to the convexital, i.e., surface of the brain facing the vault of the skull) and tuberculous meningoencephalomyelitis (cerebrospinal form of tuberculous meningitis). Features of diffuse convexital meningoencephalitis are a more acute onset than with basal meningoencephalitis (headache and fever), rapid impairment of consciousness.

With limited convexital meningoencephalitis (the process is localized in the central convolutions of the cerebrum), the initial symptoms of the disease are paresthesia, hemiparesis, aphasia, epileptic seizures against a background of increasing fever and headache. With such localization, the disease can take a long course with remissions and exacerbations. After some time, basal meningoencephalitis occurs.

Tuberculous meningoencephalomyelitis can be ascending or descending.

Ascending is manifested primarily by symptoms of meningoradiculoneuritis with dysfunction of the pelvic organs: meningeal symptoms join later (sometimes after a few weeks).

Descending is expressed by the rapid spread of the process from the base of the brain to the spinal cord and the predominance in the clinical picture of the disease of symptoms of damage to the membranes and substance of the spinal cord.

The diagnosis is established on the basis of the clinical picture, medical history, including contact with a patient with tuberculosis, pulmonary tuberculosis, and laboratory test results. Important has the detection of Mycobacterium tuberculosis in the cerebrospinal fluid (using microscopic, cultural examination, biological tests) or the pathogen antigen.

Cerebrospinal fluid, as a rule, is transparent or opalescent, colorless (in case of damage to the membranes of the spinal cord with a block of the cerebrospinal fluid tract - xanthochromic), its pressure is increased (more than 300-500 mm of water column). The content of total protein is increased to an average of 1-3, 3 g/l, with damage to the spinal cord membranes it is 30-60 g/l or more.

Moderate pleocytosis is observed (on average 100-500 cells in 1 μl), in most cases - lymphocytic, less often - mixed. In some cases, neutrophils predominate in the cerebrospinal fluid. The sugar content in the cerebrospinal fluid progressively decreases as the disease progresses. The amount of chlorides decreases to 141-169 mmol/l. When cerebrospinal fluid stands in a test tube for 24 hours, a thin fibrin film forms in it. Changes in the blood are mild.

Differential diagnosis in the early stages of meningeal tuberculosis is carried out with influenza, typhoid fever; when neurological symptoms appear - with viral, bacterial and fungal meningitis (meningoencephalitis), abscess and brain tumor.

Treatment of meningeal tuberculosis

Treatment of patients with meningeal tuberculosis is complex. Combinations of three or four anti-tuberculosis drugs are used. Isonicotinic acid hydrazide derivatives (isoniazid, ftivazid, metazide), which penetrate the blood-brain barrier in bacteriostatic concentrations, rifampicin, ethambutol, streptomycin (intramuscular) and pyrazinamide, are used.

Duration antibacterial therapy must be at least 6 months from the date of sanitation of the spinal fluid. With late diagnosis of tuberculous meningitis and in serious condition The patient is indicated for the use of glucocorticosteroid hormones. Tuberculostatic therapy should be combined with the administration of vitamins B1, B6, ascorbic and glutamic acids. Dehydration and detoxification therapy is also necessary. For paresis and paralysis, after mitigation of the meningeal syndrome (after 3-4 weeks), proserin is prescribed, massage and exercise therapy are indicated.

Patients with meningeal tuberculosis in the acute period of the disease should be on strict bed rest for 1-2 months. Subsequently, as you improve general condition the regime is being expanded. Discharge from the hospital can be carried out after disappearance clinical manifestations illness and rehabilitation of cerebrospinal fluid, but not earlier than 6 months from the start of treatment. From the hospital, patients are sent to an anti-tuberculosis sanatorium.

Prognosis for early diagnosis of meningeal tuberculosis and adequate treatment, often favorable - recovery occurs. Late start specific treatment Epilepsy and compensated hydrocephalus may develop, paresis persists, and death is possible. Severe hydrocephalus, cerebrospinal fluid block, and cholesteatomas are rare.

Dispensary observation.

Adults who have had tuberculosis of the meninges are observed by a phthisiatrician at an anti-tuberculosis dispensary for 2 years in subgroup A of group I dispensary registration in the presence of pulmonary tuberculosis or in subgroup A of group V in its absence.

Subsequently, they are registered for an average of 1 year in subgroups B and C of group V. Children are observed by a phthisiatrician for 1 year in subgroup A of group V, then 2 years in subgroup B of group V and the next 7 years in subgroup B of group V.

At residual effects problems with the nervous system or eyes also require observation and treatment by a neurologist, psychiatrist, or ophthalmologist. For 2-3 years after discharge from the hospital, three-month preventive courses of treatment with isoniazid in combination with ethambutol or pyrazinamide are carried out annually.

The issue of the ability to work or disability of patients who have had tuberculosis of the meninges is decided by the VKK individually, taking into account changes in the neurological status and profession of the patient. In most cases, patients return to their professional activities. Persons engaged in heavy physical labor before illness or working in hazardous industries need to be transferred to a more light work. The question of continuing studies is decided individually. During the first year after inpatient treatment Increased mental stress and traumatic operations are not recommended.

Brain tuberculosis

Extrapulmonary tuberculosis is a fairly common phenomenon. In this pathological process, Mycobacterium tuberculosis lives in the tissues of many human organs (tuberculosis of the eyes, bones, and gastrointestinal tract is known). When Koch's bacillus affects the nervous system, brain tuberculosis develops. According to medical statistics, cerebral tuberculosis currently accounts for about 3% of all tumors affecting the brain.

Brain tuberculosis: types

Doctors distinguish two main forms of cerebral tuberculosis:

Tuberculous meningitis is a specific inflammation of the meninges. Most often, this disease occurs after tuberculosis of some other localization or is combined with existing tuberculosis of other organs.
Solitary tubercle is a specific brain tumor. As a rule, tubercles consist of tuberculous tissue, where, over some time, purulent decay forms with the formation of a tuberculous abscess. The size of the tubercles ranges from grain to large chicken egg. The main locations of the pathological process are the brain stem and cerebellum.

Brain tuberculosis: symptoms

Symptoms and signs of the disease depend on the form of the disease.

With tuberculous meningitis, symptoms will appear depending on the period of development of the disease.

Prodromal period – average duration from 1 week to 2 months. At this time, headache, nausea, vomiting, and fever appear. Body temperature is most often subfebrile (37 - 37.5 0 C), urinary retention may be observed.
The period of irritation occurs 1-2 weeks after the cessation of the previous period. The main symptoms are fever, headache localized mainly in the frontal and occipital lobes, scaphoid abdomen, depression, lethargy. Photophobia and noise intolerance gradually appear. Large red spots periodically appear on the face and chest. By the beginning of the second week of the period, characteristic meningeal symptoms (stiff neck, Kerning and Brudzinki symptoms) are observed. Quite often there are disorders of the visual organs - strabismus, deterioration in focusing, paralysis of the eyelid.
The terminal period is 2-3 weeks of illness. This period is characterized by lack of consciousness, paralysis, paresis, and high fever.

With solitary tuberculus, the symptoms will be as follows: with an increase intracranial pressure nausea and vomiting are observed. Young children are characterized by an increase in the size of the skull. The disease begins with the appearance of convulsions, and paralysis gradually develops.

Brain tuberculosis: treatment

Treatment of cerebral tuberculosis is carried out in inpatient conditions, chemotherapy (Streptomycin, Ftivazid) is indicated; for solitary tubercle, surgical intervention is performed followed by removal of the tubercle. In the absence of treatment, death occurs in 100% of cases.

Tuberculous meningitis is a specific inflammation of the meninges. Most often, this disease occurs after tuberculosis of some other localization or is combined with existing tuberculosis of other organs.
Solitary tubercle - specific brain tumors. As a rule, tubercles consist of tuberculous tissue, where, over some time, purulent decay forms with the formation of a tuberculous abscess. The size of tubercles ranges from a grain to a large chicken egg. The main places of localization of the pathological process are the brain stem and cerebellum.

Brain tuberculosis: symptoms

Symptoms and signs of the disease depend on the form of the disease.

With tuberculous meningitis, symptoms will appear depending on the period of development of the disease.

Prodromal period - average duration from 1 week to 2 months. At this time, headache, nausea, vomiting, and fever appear. Body temperature is most often subfebrile (37 - 37.50C), and urinary retention may occur.
The period of irritation occurs 1-2 weeks after the cessation of the previous period. The main symptoms are fever, headache localized mainly in the frontal and occipital lobes, scaphoid abdomen, depression, lethargy. Photophobia and noise intolerance gradually appear. Large red spots periodically appear on the face and chest. By the beginning of the second week of the period, characteristic meningeal symptoms (stiff neck, Kerning and Brudzinki symptoms) are observed. Quite often there are disorders of the visual organs - strabismus, poor focusing, paralysis of the eyelid.
The terminal period is 2-3 weeks of illness. This period is characterized by lack of consciousness, paralysis, paresis, and high fever.

With solitary tuberculosis, the symptoms will be as follows: with increased intracranial pressure, nausea and vomiting are observed. Young children are characterized by an increase in the size of the skull. The disease begins with the appearance of convulsions, and paralysis gradually develops.

Classification

Pathology can take two forms:

tuberculous meningitis;
solitary tubercle.

With tuberculous meningitis, the inflammatory process of any of the meninges progresses. Most often, this disease develops as a secondary disease or together with tissue damage to other organs.

Solitary tubercle is a focus of inflammation in the form of a neoplasm (tuberculoma) in the brain. After some time, tuberculoma turns into purulent stage with the formation of an abscess. The pathology is mainly localized in the cerebellum or brain stem tissues.

Based on the route of spread, cerebral tuberculosis is divided into:

hematogenous;
lymphatic;
perineural.

By area of damage there are:

basal form;
convexital form;
meningoencephalitis;
meningoencephalomyelitis.

Symptoms and periods

The clinical picture of brain tuberculosis depends on which area of the organ is affected, which brain centers are affected by the mechanical action of inflammation or tuberculoma of the brain, as well as on the period (stage) of the disease.

Signs of brain tuberculosis will depend on the form.

With tuberculous meningitis, there are three periods of illness:

prodromal period
period of irritation
terminal period.

Signs of prodromal or initial stage tuberculous meningitis are as follows:

periodic, occurring at the same time, increasing headache, migraine;
nausea;
fever;
slight increase in temperature;
general malaise;
apathy;
lack of appetite;
decreased vitality and performance.

These manifestations of the disease are caused by the active activity of pathogenic mycobacteria and intoxication of the body by the products they secrete.

The prodormal period lasts from several days to 2 months.

The period of irritation begins 7-14 days after the initial cessation. From a physiological point of view, it is characterized by irritation of the meninges and nerve endings.

Symptoms of the period of irritation:

headaches of a general and local nature (associated with the area of localization of tuberculosis lesions);
gag reflex, nausea;
increased sensitivity to external irritants, photophobia;
hyperemia of the skin (large red spots on the chest and face);
temperature increase;
tension in the back of the head.

In the terminal period, the patient experiences symptoms caused by damage to certain brain centers:

thickening of the walls of blood vessels occurs, which causes a narrowing of the lumen, and, as a result, insufficient supply of oxygen to some parts of the brain;
development of muscle paresis, complete paralysis is possible;
disturbances in the functioning of the ocular and auditory nerves;
dysfunction of the visual organs (uneven dilation of the pupils with lack of reaction to light, strabismus).

Changes in brain tissue also cause mental disorders. The patient may experience symptoms such as partial or complete loss of memory, disturbances in behavior, thinking and perception. It also happens that patients lose consciousness during this time.

If the disease has reached terminal stage, then it will no longer be possible to restore brain tissue and damaged brain centers. The patient most often remains disabled for life, and death is also not uncommon.

The following symptoms are typical for solitary tubercle:

increase in intracranial pressure;
Against this background, nausea and vomiting are possible.

In children in early age with this form of the disease the size of the skull increases. With the development of tuberculoma in the brain, seizures and eventually paralysis are common.

Diagnostics

Due to the similarity of symptoms with brain lesions of other origins, careful differentiated diagnosis is required. First, the patient’s medical history is carefully studied and the causes of tuberculosis are determined. Conducted lab tests blood, urine, sputum and other discharged fluids for the detection of mycobacteria. To accurately identify brain damage caused by mycobacteria, a cerebrospinal fluid puncture is taken.

To establish the stage of the disease, the area and extent of the lesion, radiography and ultrasound examinations are performed. To eliminate doubts about the diagnosis, if they arise for some reason, studies such as CT or MRI may be prescribed.

During treatment, diagnostics are also required to determine whether the treatment regimen has been chosen correctly and to assess the dynamics of the disease. Analyzes and studies of the patient are carried out at each stage of treatment, as well as after its completion, to monitor the development of complications and dangerous consequences.

Treatment

Treatment of tuberculosis brain disease is carried out exclusively in a hospital setting under constant medical supervision. Today, therapy for all forms of tuberculosis is based on the administration of the drug Isoniazid. The patient can receive the medicine either in the form of tablets or intramuscular or intravenous injections.

The active substance isoniazid accumulates quite quickly in the body and successfully fights the blood-brain barrier of the brain.

If the patient is in a coma, and with negative dynamics of the disease, potassium chloride streptomycin is injected into the space between the meninges. If therapy with Isoniazid is not effective, or the patient develops an allergy to the active substance, other drugs are used, most often Ethambutol or Rimfapicin.

Simultaneously with treatment aimed at eliminating the cause of the disease, the patient is prescribed symptomatic treatment. To reduce the intensity of headaches, analgesic drugs that do not cause drug dependence are used.

In the first two or three months, the patient is given strict bed rest and complete rest. In the future, the doctor may prescribe physical therapy and exercise therapy to shorten the recovery period.

Forecast and consequences

Without treatment, 100% of cases result in death. If therapy is started in a timely manner, the outcome depends on the stage and speed of progression of the disease. Medicine has a fairly wide range of methods and means for treating tuberculosis, and their use is the key to a favorable prognosis.

One of the most severe complications of cerebral tuberculosis is the development of hydrocephalus, provoked by vasculitis and softening of tissue in the affected area, which leads to the formation of adhesions in the meninges.

Morphology and pathogenesis

Tuberculosis of the brain and nervous system has three ways of occurrence and spread:

Hematogenous;
Lymphogenic;
Perineural.

Mycobacterium tuberculosis spreads throughout the body from foci of infection, which may be in the lungs, lymph nodes, or other areas outside the lungs.

At the first stage, tuberculous meningitis develops through the hematogenous route, eventually breaking through the blood-brain barrier. As a result, infection of the choroid plexuses occurs. Further development of the disease occurs in the cerebrospinal fluid. Once in the spinal cord fluid, mycobacterium tuberculosis is deposited on the brain base, affecting the soft membrane and gradually destroying it.

Features of the disease:

As a result of inflammation, a specific exudate is formed. It accumulates in the area where the intersection of the optic nerves is located on the surface of the cerebellum, where the cisterns are localized.
In addition to the optic fascicles, inflammatory discharge can accumulate on the convexities of the brain, in its temporal lobes, as well as in the frontoparietal.
Exudate can penetrate into the subarachnoid space and cerebral ventricles.
During the pathological process, the pia mater of the brain is often saturated with serous-fibrinous contents, causing tissue necrosis.
The choroid plexuses and the membrane itself have an edematous appearance, with an abundance of hemorrhages.
In addition, miliary bulges are visible on the tissues of the shell.

Even if tuberculous meningitis is successfully transferred and the patient recovers, adhesions will likely remain in the spinal cord, brain, and subarachnoid region. In their zones, blood vessels are damaged, this leads to disturbances in blood circulation and cerebrospinal fluid, often with adverse consequences.

Symptoms

Signs of brain tuberculosis are usually divided into several groups, according to the time of manifestation:

SENSATION! Follow the link: Tuberculous granuloma

prodromal symptoms preceding the main symptoms. The period itself can last from 3 days to a month;
symptoms of irritation of the cranial nerves and soft membranes of the brain;
symptoms of brain tissue damage.

Diagnostics on initial stage may be difficult, since meningitis caused by mycobacteria often develops against the background of existing influenza and other acute respiratory infections.

The main symptoms at this stage are associated with poisoning of the body by the products of mycobacteria:

headaches, migraines;
lethargy;
weakness;
high level of fatigue, poor endurance;
general ailments;
poor performance;
poor appetite or its complete absence;
sweating;
nightmares, bad and disturbing sleep;
anxiety and irritability;
inhibition of thinking and action;
apathy;
from time to time – an increase in temperature to subfebrile levels.

At the end of the prodromal period, the time comes for the manifestation of symptoms of pathologies of the cranial nerves and lining of the brain.

The following characteristic syndromes for this period are distinguished:

meningeal;
general infectious;
cerebrospinal fluid lesions;
damage to the spinal roots and fibers of the cranial nerves.

Meningeal syndrome usually develops gradually, although sometimes there is a very acute course from the very beginning.

This includes:

vomiting and nausea;
headache;
hyperesthesia;
neck muscle tension;
specific body posture and characteristic phenomena: zygomatic ankylosing spondylitis symptom and others.

Changes in cerebrospinal fluid are determined by tests. The liquid taken for analysis has an opalescent or transparent appearance; when a sample is taken, it flows out with increased pressure and can flow in a stream. The liquid contains a high content of protein and lymphocytes, and the mass fraction of glucose, on the contrary, is reduced.

SENSATION! Follow the link: Where does tuberculosis come from? Pathology of the cranial nerves occurs due to compression of them by inflammatory exudate, and due to the spread of inflammation to the nerve fibers themselves.

This phenomenon is characterized by specific external symptoms, depending on which nerves are affected:

strabismus may develop;
partial or complete paralysis of facial muscles, tongue;
dilated pupils and other manifestations.
Inflammation of the retina and the posterior part of the choroid may develop.

In the third stage, brain tissue is directly affected. Symptoms of this are deterioration or complete loss of functions for which the affected areas are responsible. These phenomena develop as a result of pathological processes in the blood vessels of the brain, as a result of which their lumen closes completely. Ischemia and softening of brain tissue develops in the affected area with loss of the functions they perform.

Tuberculous meningitis

Tuberculous meningitis as a separate nosology has existed since 1893, when Mycobacterium tuberculosis was first identified in the cerebrospinal fluid of patients with meningitis. At the end of the twentieth century, tuberculous meningitis was considered a disease primarily of children and adolescence. However Lately the difference between the incidence of children and adults has decreased significantly. The most susceptible to meningitis of tuberculous etiology were patients with reduced immunity due to HIV, malnutrition, alcoholism, drug addiction, and old age. In 90% of cases, tuberculous meningitis is secondary, that is, it develops against the background of active tuberculosis in other organs or signs of previous tuberculosis. In 80% of cases, the primary tuberculosis focus is localized in the lungs. If the primary focus cannot be identified, then such tuberculous meningitis is designated as isolated.

Causes of tuberculous meningitis

Tuberculous meningitis develops when Mycobacterium tuberculosis penetrates the meninges. The source of tuberculosis infection can be disseminated pulmonary tuberculosis, genital tuberculosis, bone tuberculosis, breast tuberculosis, kidney tuberculosis, laryngeal tuberculosis, etc. In rare cases, infection occurs by contact: in the presence of tuberculosis of the skull bones, the pathogen enters the cerebral membranes, in case of spinal tuberculosis - into the membranes of the spinal cord. According to some data, in approximately 17% of cases, tuberculous meningitis is caused by lymphogenous infection.

The main method of infection of the meninges is hematogenous, in which mycobacteria are spread through the bloodstream. Moreover, their penetration into the cerebral membranes is associated with an increase in the permeability of the blood-brain barrier. Initially affected choroid plexuses soft membrane, then mycobacteria penetrate the cerebrospinal fluid and initiate inflammation in the arachnoid and soft membranes - leptomeningitis. In most cases, the membranes at the base of the brain are affected, causing so-called basilar meningitis. Specific inflammation can spread further to the membranes of the hemispheres, and from them to the substance of the brain with the development of tuberculous meningoencephalitis.

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

Symptoms of tuberculous meningitis

Periods of flow

The prodromal period lasts on average 1-2 weeks. Its presence distinguishes tuberculous meningitis from other meningitis. It is characterized by the appearance of cephalalgia (headache) in the evenings, subjective deterioration of well-being, irritability or apathy. Then the cephalalgia intensifies, nausea occurs, and vomiting may occur. Low-grade fever is often noted. When visiting a doctor during this period, it is not possible to suspect tuberculous meningitis due to the nonspecificity of these symptoms.

The period of irritation is manifested by a sharp increase in symptoms with a rise in body temperature to 39 °C. The headache is intense and is accompanied by hypersensitivity to light (photophobia), sounds (hyperacusis), touch (cutaneous hyperesthesia). Lethargy and drowsiness worsen. The appearance and disappearance of red spots in various areas skin, which is associated with a disorder of autonomic vascular innervation. Meningeal symptoms occur: rigidity (tension) of the neck muscles, Brudzinski and Kernig symptoms. Initially they are vague in nature, then gradually intensify. By the end of the second period (after 8-14 days), the patient is lethargic, consciousness is confused, and the typical meningeal “pointing dog” posture is characteristic.

The period of paresis and paralysis (terminal) is accompanied by a complete loss of consciousness, the appearance of central paralysis and sensory disorders. Respiratory and heartbeat, possible convulsions, hyperthermia up to 41 ° C or low temperature bodies. If untreated during this period, tuberculous meningitis within a week leads to fatal outcome, the cause of which is paralysis of the vascular and respiratory centers of the brain stem.

Clinical forms

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

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

Spinal tuberculous meningitis is rare. As a rule, it manifests with signs of damage to the cerebral membranes. Then, in 2-3 periods, shingles pain occurs, caused by the spread of tuberculosis to the spinal roots. When the cerebrospinal fluid pathways are blocked, the radicular pain is so intense that it cannot be relieved even with the help of narcotic analgesics. Further progression is accompanied by pelvic disorders: first, retention, and then urinary and fecal incontinence. Peripheral flaccid paralysis, mono- and paraparesis are observed.

Diagnosis of tuberculous meningitis

Tuberculous meningitis is diagnosed by a phthisiatrician together with specialists in the field of neurology. Of primary importance in diagnosis is the study of cerebrospinal fluid taken by lumbar puncture. Changes can be detected already in the prodrome. Colorless, transparent cerebrospinal fluid flows out with increased pressure of 300-500 mmH2O. Art., sometimes in a stream. Cytosis is noted - an increase in cellular elements to 600 per 1 mm3 (at normal - 3-5 per 1 mm3). At the beginning of the disease it is neutrophilic-lymphocytic in nature, then becomes lymphocytic. The concentration of chlorides and glucose decreases. Particular attention is paid to the glucose level: the lower it is, the more serious the prognosis.

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

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

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

Treatment of tuberculous meningitis

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

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

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

Sources

http://bez-posrednukov.com/mediczinskij-spravochnik/katalog-boleznej/tuberkulez/golovnogo-mozga/
http://tbdoc.ru/class/golovnogo-mozga.html
http://tuberkulez03.ru/vidy/tuberkulez-mozga.html
http://www.krasotaimedicina.ru/diseases/zabolevanija_neurology/tuberculous-meningitis