Tuberculosis of the nervous system, cerebral tuberculosis

Meningitis is an inflammation of the membranes of the brain and spinal cord. Leptomeningitis is an inflammation of the soft and arachnoid meninges. Arachnoiditis – inflammation of the arachnoid membrane. Pachymeningitis is an inflammation of the dura mater. In practice, the term “meningitis” is understood primarily as leptomeningitis. In case of severe intoxication syndrome, irritation of the meninges may occur without affecting them by the inflammatory process. This condition is called meningism. Mycobacterium tuberculosis was first isolated from cerebrospinal fluid in 1893.


Tuberculosis of the nervous system and the meninges occurs by hematogenous, lymphogenous or perineural ways with the spread of MBT from lesions in the lungs, affected hilar lymph nodes or extrapulmonary lesions. The first stage in the development of tuberculous meningitis is hematogenous, which ends with a breakthrough in the blood-brain barrier and infection of the vascular plexuses. The second stage is liquorogenic. Mycobacterium tuberculosis from the choroid plexus enters the cerebrospinal fluid, is deposited on the base of the brain, which leads to the defeat of the pia mater by a specific process.


The inflammatory effusion accumulates in the area of ​​the junction of the optic nerves, on the lower side of the pons, on the surface of the cerebellum and the medulla oblongata, that is, in the area of ​​cistern localization. In addition, the accumulation of exudate can be observed in the fronto-parietal and temporal lobes, that is, on the convex surface of the brain. The exudate may be in the subarachnoid space of the brain and spinal cord, and also fills the ventricles of the brain. In the pia mater, miliary or large tubercles are noticeable. The pia mater may be impregnated with serous fibrinous effusion and undergo caseous necrosis. The pia mater, epindhema and choroid plexus are hyperemic, edematous, with the presence of hemorrhages.

Subacute and chronic tuberculous meningitis is characterized by the formation of predominantly epithelioid cell granulomas, often with caseous necrosis in the center. Similar granulomas are also observed in the vascular wall, where caseous necrosis with thrombosis can occur. Damage to the blood vessels can cause softening and local swelling of the brain tissue. A specific inflammatory process often affects the substance of the brain, as a result of which encephalitis develops.

After suffering tuberculous meningitis in the subarachnoid space, adhesions can form in the brain and spinal cord. The vessels in this area are obliterated, which leads to severe violations of the circulation of the cerebrospinal fluid and hemodynamic disorders.

Classification of tuberculosis of the nervous system and meninges depending on the location of the lesion:

  • basal;
  • convexital;
  • meningoencephalitis;
  • meningoencephalomyelitis (ascending, descending).

Basal meningitis – the inflammatory process is localized in the region of the base of the brain; characterized by a combination of meningeal symptoms with symptoms of lesions of the cranial nerves. Among tuberculous meningitis occurs in 85-90%.

Convexital meningitis – begins acutely with a headache, disturbances of consciousness are growing rapidly. The clinical picture is dominated by phenomena of irritation of the cortex with psychomotor agitation and various impairments of consciousness.

Meningoencephalitis – symptoms of focal lesions of the nervous system join to the meningeal syndrome and predominate.

Meningoencephalomyelitis. Ascending – there are symptoms of meningoradiculoneuritis: dysfunction of the pelvic organs, later meningeal symptoms join. Descending – the pathological process from the base of the brain spreads to the membranes and the spinal cord.


Clinical manifestations of tuberculous meningoencephalitis in adults and children can be divided into three periods:

  • Prodromal, or the period of precursors, lasting from 3-5 to 21-26 days.
  • The period of clinical manifestations of irritation of the meninges and cranial nerves.
  • The period of clinical manifestations of brain tissue damage.

Difficulties in diagnosis at the onset of the disease are due to the fact that meningoencephalitis can develop against the background of acute respiratory disease, influenza, etc.

In the prodromal period, intoxication symptoms come to the fore:

  • general weakness,
  • headache,
  • malaise,
  • increased fatigue,
  • lethargy,
  • reduced performance,
  • sweating,
  • loss of appetite,
  • sleep disturbance,
  • irritability,
  • periodically low-grade fever,
  • indefinite lethargy,
  • apathy.

The prodromal period is changed by pronounced clinical manifestations of irritation of the meninges and cranial nerves. There are 4 syndromes characteristic of this period:

  • general infectious,
  • meningeal,
  • symptoms of damage to the cranial nerves and spinal roots,
  • changes in the cerebrospinal fluid.
  1. General infection syndrome – there is a constantly elevated temperature from subfebrile to hectic, preceding headache, or occurs with it.
  2. Meningeal syndrome – its gradual development is characteristic of tuberculous meningitis, but there is also an acute onset. Meningeal syndrome includes:
    • headache,
    • nausea,
    • vomiting,
    • hyperesthesia,
    • characteristic meningeal position,
    • stiff neck,
    • symptoms of Kernig, Brudzinsky, zygomatic symptom Bechterew and others.

    Headache – may be diffuse or localized (mainly in the forehead and occiput). Its occurrence is associated with the irritation of sensitive endings of the third pair of cranial nerves, as well as the parasympathetic (X pair) and sympathetic fibers, as they innervate the meninges.

    Vomiting accompanies a headache, has a “fountain-like” character, does not bring relief, does not depend on food intake. It has a central character, due to irritation of the receptors of the vagus nerve or its nuclei (located at the bottom of the IV ventricle) or the vomiting center in the medulla. General hyperesthesia and hypersensitivity due to irritation of the posterior roots.

    The “chicken” position is characteristic – the patient lies with his head thrown back, the body is stretched, the stomach is retracted (scaphoid), the legs are bent at the knees and pulled to the stomach. Taks position is a consequence of tonic muscle contraction. Tilted head due to stiff neck (increased tonus of the extensor muscles of the neck).

    The main clinical symptoms of tonic muscle tension are:

    • Symptom stiff neck – muscle tension of the neck, sharp white
    when trying to tilt the patient’s head forward and get his chin to his chest.

    • Kernig’s symptom is the inability to straighten the leg at the knee joint, which was previously bent (at a right angle) at the knee and hip joints.

    • Symptoms of Brudzinsky (there are four):

    – First (upper) – when trying to bring the head to the chest, the lower extremities involuntarily bend at the knee joint
    – Second (zygomatic) – with the percussion of the zygomatic arch, the same reaction is observed;
    – Third (middle or pubic) – pressing in the region of the pubic joint causes involuntary bending of the legs at the knee joints;
    – Fourth (lower) – when trying to bend one leg at the knee joint (examination of Kernig’s symptom), the other leg reflexively bends at the knee joint and pulls up to the abdomen.

    • Symptom Bekhtereva – with the percussion of the zygomatic arch increases headache and involuntarily a grimace of pain on the corresponding side of the face.

  3. Symptoms of damage to the cranial nerves and spinal roots. More often, III, VI, VII, IX, X, XII pairs of cranial nerves are affected due to compression of their exudate, as well as direct damage by the inflammatory process. With the defeat of the third pair, ptosis, mydriasis (dilated pupil), strabismus, diplopia occurs; VI pairs – convergent squint, diplopia; VII pairs – face asymmetry due to peripheral paralysis of the facial muscles (wrinkles on the forehead and face are smoothed, the eye slit becomes wider, the mouth angle is lowered); XII pairs – squint, paresis or paralysis of the corresponding half of the tongue, its atrophy. When you try to stick out his tongue, he deviates towards defeat.There are also chorioretinitis, as well as fundus lesions: swelling of the optic nerve papillae, optic neuritis.Chorioretinitis is an inflammation of the posterior choroid and retina. There are nodules on them – lymphoid infiltration with giant epithelioid cells or tuberculous granulomas with caseosis. With the localization of chorioretinal changes at the edge of the optic nerve head, neuroretinitis develops.
  4. Changes in cerebrospinal fluid – cerebrospinal fluid is transparent or opalescent, colorless, its pressure is increased. In patients with tuberculous meningitis, during the puncture, the cerebrospinal fluid flows under pressure more often in drops or a stream (normally 20-40 drops per minute). It is forbidden to release the CSF jet, because an instantaneous death of the patient may occur due to the medulla oblongata entering the occipital foramen (wedging results from a sharp decrease in pressure in the subarachnoid space of the spinal cord while maintaining increased fluid pressure in the subarachnoid space of the brain).

For tuberculous meningitis, such changes in the cerebrospinal fluid are characteristic:

  • increase in protein content – 1-2 g / l and more, therefore, the reactions of Pandy and Nonne – Appell are positive;
  • pleocytosis – an increase in the number of cells in the cerebrospinal fluid (average 100-300 in I mm3), lymphocytes (T-lymphocytes) prevail; normally 1 mm3 contains 10 leukocytes;
  • for tuberculous meningitis typical protein-cell dissociation, which occurs due to the prevalence of stagnation over inflammatory. It is characterized by a high content of protein in the cerebrospinal fluid and a relatively small cytosis and indicates a significant impairment of the circulation of the cerebrospinal fluid. Less common is cell-protein dissociation, which is not inherent in active tuberculous meningitis
  • a decrease in the concentration of glucose (less than half the glucose content in the blood) and chloride (up to 110 mmol / l or less);
  • a day later, in the cerebrospinal fluid, a soft fibrin film falls out, in which mycobacteria are found only in 10-20% of patients.

The third period of clinical manifestations of brain tissue damage is characterized by symptoms of irritation and loss of function of the brain substance. Symptoms of the brain substance damage – aphasia, hemiparesis, hemiplegia, paralysis. The basis of these processes is the progressive endarteritis of the cerebral vessels with the complete closure of their lumen, ischemia, softening of the corresponding portion of the brain tissue.

Differential diagnosis of tuberculosis of the meninges and the central nervous system should be carried out with meningitis of a different etiology: viral, meningococcal, staphylococcal. Clinical manifestations of meningoencephalitis are the same. They differ only in the composition of the cerebrospinal fluid.

The use of anti-tuberculosis drugs in the treatment of patients with tuberculous meningitis significantly changed the clinical course and consequences of this serious disease. In the antibacterial period, patients with tuberculous meningitis were doomed. Now the majority of patients with tuberculous meningitis can be cured. The success of treatment depends entirely on early diagnosis. The prognosis is favorable when a diagnosis is made and treatment is started before the 10th day after the onset of the headache. In cases of late diagnosis, the prognosis becomes unfavorable, since irreversible morphological changes are already occurring in the meninges and brain substance.


Treatment of patients with tuberculous meningitis is carried out in special departments and above all in the appointment of isoniazid. If the patient is unconscious, isoniazid is administered intramuscularly or intravenously. Isoniazid for tuberculous meningitis is the main drug. It penetrates well through the blood-brain barrier and is contained in the cerebrospinal fluid in sufficient concentration for a therapeutic effect. In addition to isoniazid, prescribe rifampicin, ethambutol, streptomycin. A spinal puncture for a control study of cerebrospinal fluid is done in a month.

If the patient is unconscious, or his condition worsens, then, in addition to the described treatment, a spinal puncture is performed daily and the calcium calcium chloride of streptomycin is administered subarachnoidally 0.1 g (100,000 IU) or 0.2 g (200,000 IU) of the calcium chloride streptomycin dissolve ex tempore in 2 ml of double-distilled water or an isotonic solution of sodium chloride and inject endolyumbally once a day for 10–20 days. Along with this, carry out non-specific treatment.

Patients with tuberculous meningitis require careful care. Bed rest is prescribed for 2-3 months, and the hospital stay lasts 5-7 months, after which sanatorium treatment is indicated. Getting out of bed should be preceded by physical therapy in bed. In cases of sluggish tuberculous meningitis, treatment with prednisone is recommended (0.005-0.01 g 3 times a day), as well as injections of thiamine and prescription of ascorbic acid.

To reduce headache, chloral hydrate is prescribed in enemas (0.5 g per 20 l of water) or analgin (0.3 g) and paracetamol (0.4 g). The headache is caused by an increase in intracranial pressure, which is why it decreases after unsupervaginal punctures, as well as a decrease in the secretion of cerebrospinal fluid, which can be achieved through dehydration therapy (25% magnesium sulfate intramuscularly or 40% glucose solution intravenously). In cases of motor disorders (paresis: paralysis), after the acute period of meningitis subsides, Dibazol (0.005-0.01 g 1 time per day per os), prozerin (0.005-0.015 g 2 times per day per os) is prescribed. When antibacterial treatment is carried out, the clinical symptoms of tuberculous meningitis subside after 1-2 months, the cerebrospinal fluid is normalized only in the 3-4th month of treatment.

Of the complications of tuberculous meningitis is the development of hydrocephalus. In addition, there may be movement disorders, impaired vision and hearing, as well as a decrease in mental abilities. A favorable prognosis is observed in cases of serous and diffuse basilar forms of tuberculous meningitis. With the timely treatment of patients with such forms can achieve a complete cure.

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