Meningitis is a disease in which the mild cerebral cortex of the brain is affected.
Meningitis of tuberculous etiology is found in any age group. The risk group consists of children with immature immune system and people with immunodeficiency states (AIDS, alcoholism, drug addiction).
At the heart of tuberculous meningitis is the defeat of the meninges with a tubercle bacillus. The source of the tubercle bacillus (Koch's stick) is the primary foci of infection (lymph nodes, lungs, bones and other organs). From the focus, bacteria spread through the body, causing a disseminated form of tuberculosis. In the brain, the infection penetrates hematogenously, i.e. with the help of blood vessels.
Hematogenous bacteria reach the vascular plexus of the ventricles of the brain, where they settle with the formation of granulomas. From the vascular plexuses, the infection with the flow of cerebrospinal fluid reaches the base of the brain, where it affects the soft medulla. The histological picture of lesions of the brain envelopes has a specific manifestation. The tubercle bacillus, affecting the membranes of the brain, forms formations in the form of miliary tubercles (resemble a millet grain), especially a large cluster of them on the basis of the brain. Miliary tubercles cause perifocal (around tubercles) inflammatory-allergic changes, which are aimed at limiting foci of infection and clinically manifesting meningeal syndrome. Inflammatory changes are accompanied by the appearance of a large amount of serous exudate (serous fluid), lead to a clouding of the shells, a change in the permeability of the vessels. Changes in the initial stages, as well as with adequate treatment from the first days of the disease, can completely disappear. If the treatment is not effective, it is started late, the inflammatory changes in combination with tuberculous infiltration lead to organic changes in the membranes of the brain, brain substance and blood vessels. Adhesive processes appear, cerebrospinal fluid is disturbed, which leads to the development of hydrocephalus.
The peculiarity of tuberculous meningitis is most often gradual development. The first symptoms are nonspecific. A person may be troubled by weakness, general malaise, drowsiness during the day and insomnia at night, decreased appetite, apathy. Subfebrile body temperature may appear (up to 37.5 C), especially in the evening. Gradually a person begins to lose weight, in some cases there is vomiting, behavior changes, interest to the surrounding world disappears.
As the disease progresses, the headache increases, insomnia becomes worse, nightmarish dreams appear. Drastically deteriorating memory, attention.
This period is called prodromal and lasts from 2 to 8 weeks. Then comes the period of the height of infection.
During the height of the clinical picture is composed of symptoms of brain damage and symptoms of defeat certain parts of the brain, cranial nerves, and may differ slightly in different patients.
When a neurological examination reveals specific symptoms of damage to the meninges (rigidity of the occipital muscles, Kernig symptom, a symptom of Brudzinsky). Body temperature reaches febrile digits (38.5-39C). In older people, an increase in body temperature may be absent. The headache is of an intense nature, exhausting the person and does not bring him relief when changing the position of the body. These symptoms form a clinical picture of the meningeal syndrome.
In childhood, generalized epileptic seizures often occur, which represent a loss of consciousness and the occurrence of seizures throughout the body. Any impact on a person (stroking, touching) causes discomfort. Damage to the cranial nerves. When involved in the process of 3, 4, 6 pairs of cranial nerves (CMN), there is a squint, double vision. Dizziness, hearing loss occurs when 8 pairs of CMN are affected. A terrible complication of meningitis is the irreversible loss of vision in the development of atrophy of the optic nerves (2 pairs of CMN).
If the clinical picture consists only of meningeal syndrome and / or lesions of the cranial nerves, then talk about the basilar form of tuberculous meningitis.
In the midst of the heat, blood supply to the brain is disturbed, which leads to the development of focal symptoms: paresis (weakness) in the hands or feet, a violation of understanding and reproduction of speech (aphasia), a violation of sensitivity.
Meningovascular form is characterized by a combination of meningeal syndrome and focal symptomatology.
The appearance of symptoms from the side of the spinal cord injury indicates the development of the spinal form of tuberculous meningitis. With this form, first of all, the function of the pelvic organs is affected by the type of incontinence of urine and feces, weakness in the legs.
The defeat of the hypothalamus is manifested by the confusion of consciousness, the appearance of convulsions, in which the patient throws back his head, leads the legs to the stomach, draws the stomach.
The course of tuberculous meningitis can be lightning fast, which leads to a lethal outcome within 4-8 weeks without treatment, or is slowly progressive. Slowly progressing course can pass into a chronic form with the development of dementia, pelvic disorders (incontinence of urine and feces), hydrocephalus.
Diagnostic measures are complex in the course of which a differential diagnosis is performed with other brain lesions with a similar clinical and laboratory picture.
- Investigation of cerebrospinal fluid.
In the cerebrospinal fluid, the protein content, neutrophils, is increased, which changes after a week by increasing lymphocytes. An important marker of tuberculosis infection is a decrease in glucose in the cerebrospinal fluid. When sowing, mycobacterium tuberculosis is detected.
- CT, MRI reveal focal lesions of the brain, tuberculomas, cerebral infarcts.
- The Mantoux reaction and the Diaskin test are not always informative.
Therapeutic measures are aimed primarily at fighting the mycobacterium tuberculosis. Treatment of neurological disorders is secondary, since it does not make sense in the presence of active foci of infection.
- Anti-tuberculosis therapy.
Antibacterial therapy is used with 5 anti-tuberculosis drugs: isoniazid, rifampicin, pyrazinamide, ethambutol, streptomycin. After assessing the effectiveness of treatment at 2 and 4 months of the patient, with a positive dynamics, they translate into triple antibiotic therapy with isoniazid, rifampicin, pyrazinamide and / or ethambutol. The supporting course continues for another 8 months. Another treatment regimen includes 5 months of receiving 5 anti-TB drugs, after 7 months, three anti-tuberculosis drugs.
Anti-TB drugs cause the development of hepatitis, allergic reactions, polyneuropathies, hearing loss, therefore, maintenance therapy is prescribed with vitamins, hepatoprotectors, antiallergic agents.
- Vitamin B6 is prescribed for prevention of isoniazid polyneuropathy.
- Hepatoprotectors (Essentiale-N, Karsil, etc.) protect the liver from the toxic effects of antibacterial drugs.
- Glucocorticosteroids (Dexamethasone, Prednisolone) are prescribed in severe cases: with confused consciousness, development of hydrocephalus and infectious-toxic shock.
- Maintaining water-salt metabolism (Glucose, Mannitol, Ringer's solution, etc.).
- Neuroprotectants (Cerebrolysin, Pyracetam, etc.) improve cerebral circulation and energy supply of nerve cells.
- Anticonvulsant therapy (magnesium sulphate, diazepam, etc.) is prescribed in generalized attacks.
Symptomatic therapy is assigned to the clinic in each case individually, since not all patients may have seizures or foci of a heart attack in the brain, for example.
Treatment of tuberculous meningitis, like tuberculosis of any other localization, takes many months (in some cases up to 18 months, and maybe longer).
Each antituberculosis drug has toxicity to various organs and tissues to varying degrees, therefore, therapy is performed with a regular assessment of biochemical indicators blood, cerebrospinal fluid, neurological status, and in the first months of treatment is carried out in the intensive care unit with a subsequent transfer to a specialized department.
Among all cases of tuberculous meningitis, about 10% result in a fatal outcome. In other cases, 20% of patients have persistent neurologic abnormalities when treatment is started in the 2 stages of the process: paresis, deafness, strabismus, double vision, gait disturbance, headaches, delayed psychomotor development, and others.
The prognosis of the disease depends on several factors:
- Timely detection of tuberculous meningitis at early stages;
- Lack of resistance of mycobacteria to anti-tuberculosis drugs;
- Individual tolerance of antibacterial agents and long absence of adverse reactions from organs and systems;
- A person's focus on the complete course of therapy.
Practically always there comes complete recovery of the person at the treatment, begun at an early stage of the disease.
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