Tuberculous meningitis is an inflammation of the meninges caused by Mycobacterium tuberculosis. At the Yusupov Hospital, treatment of the disease is carried out comprehensively, always in a hospital setting. Such measures allow you to cope with the disease and prevent the development of severe complications.
Tuberculous meningitis is manifested by headaches, general deterioration of health, nausea, vomiting, disturbances in the functioning of the cranial nerves, disturbance of consciousness, etc.
Tuberculous meningitis is diagnosed based on clinical data in combination with the results of a study of cerebrospinal fluid. Treatment of this disease always has an integrated approach. The treatment program is long and includes anti-tuberculosis, detoxification, dehydration, vitamin and symptomatic therapy.
Symptoms
The main symptoms of tuberculous meningitis are similar to those of meningitis of other etiologies. A sick person develops general weakness, malaise, may have headaches, muscle pain - these are common symptoms. The fever gradually increases, however, with the tuberculous nature of the process, the increase occurs slowly, over 1-2 weeks.
At the height of the fever, a person develops meningeal symptoms: tension (stiffness) of the neck muscles, severe headaches that are not relieved by painkillers, and vomiting may develop at the height of the headache.
Gradually, all cognitive functions of a person are impaired, consciousness becomes clouded, and sensitivity to light and sound develops. Severe tuberculous meningitis can quickly lead to death. An untreated process leads to death in almost 100% of cases within a month from the onset of the disease.
Treatment of pathology
When tuberculosis pathology is diagnosed, immediate targeted treatment begins with antibacterial agents that inhibit the activity and viability of the pathogen. The earlier the disease is identified, the higher the chance of suppressing the anomaly. During the first two months, complex drug therapy is carried out. At the initial stage, drugs are administered intravenously, then orally. If positive dynamics are obtained, the dosage is reduced and potent drugs are discontinued. On average, the duration of antibacterial treatment ranges from 9 months to a year.
Neurological recovery is aimed at reducing cerebrospinal fluid pressure, detoxification measures are taken, and vitamin courses are prescribed that have a positive effect on the patient’s own immunity. For the first two months, bed rest and complete rest are prescribed; physical activity is allowed to increase only at the end of the third month. Constant monitoring of the course of the disease is carried out using laboratory tests of cerebrospinal solution. To restore muscle functionality, courses of physical therapy and massage are conducted (4-5 months). After complete completion of therapeutic treatment, systemic monitoring is necessary to prevent the risk of relapse.
Diagnostics
Diagnosis of the disease is quite difficult; it is carried out mainly on the basis of a neurological examination and analysis of cerebrospinal fluid. The neurological status reveals symptoms of inflammation of the meninges (Kernig's, Brudzinski's symptoms of various levels, stiffness of the neck muscles, etc.). If a person has tuberculous meningitis, his cerebrospinal fluid acquires characteristic properties:
- Increased cerebrospinal fluid pressure.
- Protein-cell dissociation with an increase in protein levels (mainly fibrin up to 5-10 grams per liter, and cells up to several hundred). It is noteworthy that in the first few days the basis of the cells is represented by neutrophils, and only then by lymphocytes (a characteristic sign of the tuberculous nature of the process).
- Reduced glucose levels by 40-50%, reduced chloride and sodium levels in small quantities.
- Often, a day after the collection of cerebrospinal fluid, a fibrin mesh forms in the test tube. Often the amount of protein is so large that the cerebrospinal fluid immediately coagulates.
- When inoculating the cerebrospinal fluid with special cultures, colonies of tubercle bacilli are obtained.
There is a point of view in which any meningitis with fever of moderate intensity, an unclear picture of the cerebrospinal fluid, should be considered tuberculous and treated as this particular pathology. This opinion is justified, because in 30% of cases the rod is not sown, and accurate diagnosis leads to a delay in the process and increases the risk of complications.
Composition of cerebrospinal fluid for various nosologies
MENINGITIS
Cerebrospinal fluid testing is the only method that can quickly diagnose meningitis. The absence of inflammatory changes in the cerebrospinal fluid always allows one to exclude the diagnosis of meningitis. The etiological diagnosis of meningitis is established using bacterioscopic and bacteriological methods, virological and serological studies.
Pleocytosis is the most characteristic feature of CSF changes. Based on the number of cells, serous and purulent meningitis are distinguished. With serous meningitis, cytosis is 500-600 in 1 μl, with purulent meningitis - more than 600 in 1 μl. The study must be carried out no later than 1 hour after receiving it.
According to the etiological structure, 80-90% of bacteriologically confirmed cases are Neisseria meningitides, Streptococcus pneumoniae and Haemophilus. Bacterioscopy of CSF, due to the characteristic morphology of meningococci and pneumococci, gives a positive result at the first lumbar puncture 1.5 times more often than culture growth.
CSF with purulent meningitis ranges from slightly cloudy, as if whitened with milk, to densely green, purulent, sometimes xanthochromic. In the initial stage of development of meningococcal meningitis, there is an increase in intracranial pressure, then mild neutrophilic cytosis is noted in the cerebrospinal fluid, and in 24.7% of patients the CSF is normal in the first hours of the disease. Then, in many patients, already on the first day of the disease, cytosis reaches 12,000-30,000 in 1 μl, neutrophils predominate. A favorable course of the disease is accompanied by a decrease in the relative number of neutrophils and an increase in lymphocytes. Occurring cases of purulent meningitis with a typical clinical picture and relatively little cytosis can probably be explained by a partial blockade of the subarachnoid space. There may not be a clear correlation between the severity of pleocytosis and the severity of the disease.
The protein content in the CSF during purulent meningitis is usually increased to 0.6-10 g/l and decreases as the cerebrospinal fluid is sanitized. The amount of protein and cytosis are usually parallel, but in some cases with high cytosis the protein level remains normal. A high protein content in the CSF is more common in severe forms with ependymitis syndrome, and its presence in high concentrations during the recovery period indicates an intracranial complication (block of the cerebrospinal fluid tract, dural effusion, brain abscess). The combination of low pleocytosis with high protein content is a particularly unfavorable prognostic sign.
In most patients with purulent meningitis, from the first days of illness there is a decrease in glucose levels (below 3 mmol/l); in case of death, the glucose level was in the form of traces. In 60% of patients, the glucose level is below 2.2 mmol/l, and the ratio of glucose level to that in the blood in 70% is less than 0.31. An increase in glucose level is almost always a prognostically favorable sign.
In tuberculous meningitis, bacterioscopic examination of the CSF often gives a negative result. Mycobacteria are more often found in fresh cases of the disease (in 80% of patients with tuberculous meningitis). The absence of mycobacteria in lumbar punctate is often noted when they are detected in the cisternal CSF. In case of negative or questionable bacterioscopic examination, tuberculosis is diagnosed by culture or biological test. In tuberculous meningitis, the CSF is clear, colorless, or slightly opalescent. Pleocytosis ranges from 50 to 3000 in 1 μl, depending on the stage of the disease, amounting to 100-300 in 1 μl by the 5-7th day of illness. In the absence of etiotropic treatment, the number of cells increases from the beginning to the end of the disease. There may be a sudden drop in cytosis with a repeat lumbar puncture performed 24 hours after the first. The cells are predominantly lymphocytes, but often at the onset of the disease mixed lymphocytic-neutrophilic pleocytosis occurs, which is considered typical for milliary tuberculosis with seeding of the meninges. Characteristic of tuberculous meningitis is the diversity of the cellular composition, when, along with the predominance of lymphocytes, there are neutrophils, monocytes, macrophages and giant lymphocytes. Later, pleocytosis acquires a lymphoplasmacytic or phagocytic character. A large number of monocytes and macrophages indicates an unfavorable course of the disease.
Total protein in tuberculous meningitis is always increased to 2-3 g/l, and earlier researchers noted that protein increases before the onset of pleocytosis and disappears after its significant decrease, i.e., in the first days of the disease, protein-cell dissociation takes place. Modern atypical forms of tuberculous meningitis are characterized by the absence of typical protein-cell dissociation.
With tuberculous meningitis, an early decrease in glucose concentration is observed to 0.83-1.67 mmol/l and below. In some patients, a decrease in chloride levels is detected. In viral meningitis, about 2/3 of cases are caused by the mumps virus and a group of enteroviruses.
In serous meningitis of viral etiology, the CSF is transparent or slightly opalescent. Pleocytosis is small (rarely up to 1000) with a predominance of lymphocytes. In some patients, neutrophils may predominate at the onset of the disease, which is typical for a more severe course and a less favorable prognosis. Total protein is within 0.6-1.6 g/l or normal. In some patients, a decrease in protein concentration is detected due to overproduction of cerebrospinal fluid.
CLOSED CRANIO BRAIN INJURY
The permeability of cerebral vessels in the acute period of traumatic brain injury is several times higher than the permeability of peripheral vessels and is directly dependent on the severity of the injury. To determine the severity of the lesion in the acute period, a number of liquorological and hematological tests can be used. These include: the severity and duration of the presence of hyperproteinorachia as a test characterizing the depth of dysgemic disorders in the brain and the permeability of the blood-cerebrospinal fluid barrier; the presence and severity of erythroarchia as a test that reliably characterizes ongoing intracerebral bleeding; the presence of pronounced neutrophilic pleocytosis within 9-12 days after the injury, which serves as an indication of the unresponsiveness of the tissues limiting the cerebrospinal fluid spaces and the inhibition of the sanitizing properties of the arachnoid cells or the addition of an infection.
— Concussion: CSF is usually colorless, clear, and contains little or no red blood cells. On days 1-2 after injury, cytosis is normal; on days 3-4, moderately pronounced pleocytosis appears (up to 100 in 1 μl), which decreases to normal numbers on days 5-7. In the liquorogram, lymphocytes with the presence of a small number of neutrophils and monocytes, macrophages, as a rule, are absent. The protein level on days 1-2 after injury is normal, on days 3-4 it rises to 0.36-0.8 g/l and returns to normal by days 5-7.
— Brain contusion: the number of red blood cells ranges from 100 to 35,000 and with massive subarachnoid hemorrhage reaches 1-3 million. Depending on this, the color of the CSF can be from grayish to red. Due to irritation of the meninges, reactive pleocytosis develops. For bruises of mild and moderate severity, pleocytosis on days 1-2 is on average 160 in 1 μl, and in severe cases it reaches several thousand. On days 5-10, pleocytosis significantly decreases, but does not reach normal in the next 11-20 days. In the cerebrospinal fluid there are lymphocytes, often macrophages with hemosiderin. If the nature of pleocytosis changes to neutrophilic (70-100% neutrophils), purulent meningitis develops as a complication. The protein content in mild to moderate cases is on average 1 g/l and does not return to normal by 11-20 days. With severe brain damage, protein levels can reach 3-10 g/l (often fatal).
With traumatic brain injury, the energy metabolism of the brain switches to the path of anaerobic glycolysis, which leads to the accumulation of lactic acid in it, and, ultimately, to brain acidosis.
The study of parameters reflecting the state of brain energy metabolism allows one to judge the severity of the pathological process. A decrease in the arteriovenous difference in pO2 and pCO2, an increase in glucose consumption by the brain, an increase in the venoarterial difference in lactic acid and an increase in it in the cerebrospinal fluid. The observed changes are the result of disruption of the activity of a number of enzyme systems and cannot be compensated by the blood supply. It is necessary to stimulate the nervous activity of patients.
HEMORRHAGIC STROKE
The color of the cerebrospinal fluid depends on the admixture of blood. In 80-95% of patients, during the first 24-36 hours the CSF contains an obvious admixture of blood, and later it is either bloody or xanthochromic. However, in 20-25% of patients with small lesions located in the deep parts of the hemispheres, or in the case of blockage of the cerebrospinal fluid pathways due to rapidly developing cerebral edema, red blood cells are not detected in the CSF. In addition, red blood cells may be absent during lumbar puncture in the very first hours after the onset of hemorrhage, while the blood reaches the spinal level. Such situations are a reason for diagnostic errors - the diagnosis of “ischemic stroke”. The largest amount of blood is found when blood breaks through into the ventricular system. The removal of blood from the cerebrospinal fluid tract begins from the very first day of the disease and continues for 14-20 days in case of traumatic brain injury and stroke, and in case of cerebral aneurysms up to 1-1.5 months and does not depend on the massiveness of the hemorrhage, but on the etiology process.
The second important sign of CSF changes in hemorrhagic stroke is xanthochromia, detected in 70-75% of patients. It appears on the 2nd day and disappears 2 weeks after the stroke. With a very large number of red blood cells, xanthochromia may appear within 2-7 hours.
An increase in protein concentration is observed in 93.9% of patients and its amount ranges from 0.34 to 10 g/l and higher. Hyperproteinorachia and increased bilirubin levels can persist for a long time and, along with liquorodynamic disorders, can cause meningeal symptoms, in particular headaches, even 0.5–1 year after subarachnoid hemorrhage.
Pleocytosis is detected in almost 2/3 of patients, it is increasing over 4-6 days, the number of cells ranges from 13 to 3000 in 1 μl. Pleocytosis is associated not only with the breakthrough of blood into the cerebrospinal fluid pathways, but also with the reaction of the meninges to the shed blood. It seems important to determine the true cytosis of the cerebrospinal fluid in such cases. Sometimes, with hemorrhages in the brain, the cytosis remains normal, which is associated with limited hematomas without a breakthrough into the cerebrospinal fluid space, or with the unresponsiveness of the meninges.
With subarachnoid hemorrhages, the admixture of blood can be so large that the cerebrospinal fluid is visually almost indistinguishable from pure blood. On the 1st day, the number of red blood cells, as a rule, does not exceed 200-500 x 109/l, later their number increases to 700-2000 x 109/l. In the very first hours after the development of small-volume subarachnoid hemorrhages, a lumbar puncture can produce clear cerebrospinal fluid, but by the end of the 1st day an admixture of blood appears in it. The reasons for the absence of blood in the CSF may be the same as for a hemorrhagic stroke. Pleocytosis, mainly neutrophilic, over 400-800x109/l, is replaced by lymphocytic by the fifth day. Within a few hours after hemorrhage, macrophages may appear, which can be considered markers of subarachnoid hemorrhage. An increase in total protein usually corresponds to the degree of hemorrhage and can reach 7-11 g/l and higher.
ISCHEMIC STROKE
CSF is colorless and transparent, in 66% the cytosis remains within the normal range, in the rest it increases to 15-50x109/l, in these cases characteristic cerebral infarctions are detected, located close to the cerebrospinal fluid pathways. Pleocytosis, predominantly lymphoid-neutrophilic, is caused by reactive changes around extensive ischemic foci. In half of the patients, the protein content is determined within the range of 0.34-0.82 g/l, less often up to 1 g/l. The increase in protein concentration is due to necrosis of brain tissue and increased permeability of the blood-brain barrier. Protein content can increase by the end of the first week after a stroke and last for over 1.5 months. Quite characteristic of ischemic stroke is protein-cell (increase in protein content with normal cytosis) or cell-protein dissociation.
BRAIN ABSCESS
The initial phase of abscess formation is characterized by neutrophilic pleocytosis and a slight increase in protein. As the capsule develops, pleocytosis decreases and its neutrophilic character is replaced by lymphoid, and the greater the development of the capsule, the less pronounced the pleocytosis. Against this background, the sudden appearance of pronounced neutrophilic pleocytosis indicates a breakthrough of the abscess. If the abscess is located near the ventricular system or the surface of the brain, the cytosis will be from 100 to 400 in 3 μl. Minor pleocytosis or normal cytosis may occur when the abscess was delimited from the surrounding brain tissue by a dense fibrous or hyalinized capsule. The zone of inflammatory infiltration around the abscess in this case is absent or weakly expressed.
CNS TUMORS
Along with protein-cell dissociation, which is considered characteristic of tumors, pleocytosis may occur with normal protein content in the cerebrospinal fluid. With gliomas of the cerebral hemispheres, regardless of their histology and location, an increase in protein in the cerebrospinal fluid is observed in 70.3% of cases, and in immature forms - in 88%. A normal or even hydrocephalic composition of the ventricular and spinal fluid can occur both with deep-seated and with gliomas growing into the ventricles. This is mainly observed in mature diffusely growing tumors (astrocytomas, oligodendrogliomas), without obvious foci of necrosis and cyst formation and without gross displacement of the ventricular system. At the same time, the same tumors, but with gross displacement of the ventricles, are usually accompanied by an increase in the amount of protein in the cerebrospinal fluid. Hyperproteinorachia (from 1 g/l and above) is observed in tumors located at the base of the brain. With pituitary tumors, the protein content ranges from 0.33 to 2.0 g/l. The degree of shift in the proteinogram is directly dependent on the histological nature of the tumor: the more malignant the tumor, the more severe the changes in the protein formula of the cerebrospinal fluid. Beta lipoproteins appear that are not normally detected, and the content of alpha lipoproteins decreases.
In patients with brain tumors, regardless of their histological nature and location, polymorphic pleocytosis quite often occurs. The cellular reaction is determined by the peculiarities of the biological processes occurring in the tumor at certain stages of its development (necrosis, hemorrhage), which determine the reaction. The brain tissue and membranes surrounding the tumor. Tumor cells of the cerebral hemispheres in the fluid from the ventricles can be detected in 34.4%, and in the spinal cerebrospinal fluid - from 5.8 to 15% of all observations. The main factor determining the entry of tumor cells into the cerebrospinal fluid is the nature of the structure of the tumor tissue (poor connective stroma), the absence of a capsule, and the location of the tumor near the cerebrospinal fluid spaces.
CHRONIC INFLAMMATORY DISEASES (arachnoiditis, arachnoencephalitis, periventricular encephalitis)
The protein content in the cerebrospinal fluid in most patients remains within normal limits or is slightly increased (up to 0.5 g/l). An increase in protein up to 1 g/l is observed extremely rarely and more often with meningoencephalitis than with arachnoiditis.
Treatment
Therapy for the disease should begin in the first days of the onset of the disease. It should be noted that treatment of tuberculous meningitis must begin with anti-tuberculosis drugs, and not with antibiotics. For the first two weeks, 4 drugs should be combined, gradually, when the symptoms are relieved, the inflammatory process is relieved, switch to 3 drugs, continuing therapy for up to 2-3 months.
Symptomatic treatment methods are the fight against meningeal edema (mannitol), neuroprotective therapy, and restorative treatment. In severe cases and early development of convulsive syndrome, anticonvulsant drugs should be used in addition to treatment.
Treatment of tuberculous meningitis
Without appropriate treatment, meningitis leads to death. The patient should be immediately hospitalized in a specialized clinic and prescribed special anti-tuberculosis drugs. Often, glucocorticoids are prescribed along with them - drugs of the adrenal cortex that suppress inflammation.
Treatment lasts a long time, usually 12 months. After this, the patient should be monitored by a doctor, as there is a risk of relapse.
Meningitis caused by Mycobacterium tuberculosis cannot always be accurately diagnosed immediately, even by an experienced doctor. In this case, the disease is life-threatening. By self-diagnosis and self-medication, the patient loses time that could be spent on effective therapy. If you experience symptoms of the disease, immediately consult a neurologist. Call our clinic
The material was prepared by an infectious disease specialist at the international clinic Medica24, Doctor of Medical Sciences Margarita Vasilievna Nagibina.
Consequences and prognosis
Tuberculous meningitis, the consequences of which can be expressed in convulsive syndrome, intracranial hypertension, disturbances in the functioning of the sensory organs, proceeds favorably only with timely treatment. The prognosis of tuberculous meningitis is generally positive and usually ends without any significant consequences.
However, the very fact of meningitis indicates a low level of immunity, the probable presence of HIV in the AIDS stage, as well as the extensiveness of the tuberculosis process, which in itself very often leads to death.
The annual diagnostic measures for tuberculosis infection (fluorography) should be taken as seriously as possible, and the identified process should be treated comprehensively and fully. Indeed, unfortunately, very often patients with this insidious infection come from low strata of society and, as a rule, do not undergo full treatment, which takes months or even years, and ultimately remain a source of infection for other people.
Signs of the disease
Symptoms have clearly demarcated stages:
- Initial form. Lasts for 7-14 days. The primary manifestations are evening headaches, weakness, deterioration in general well-being, irritability or a complete lack of interest in what is happening around. Symptoms increase, aversion to food appears, nausea ends with vomiting. It is difficult to diagnose TM at this stage, since the signs are nonspecific.
- Irritation stage. The temperature rises sharply to 39-40 degrees. Pain in the head does not decrease when taking conventional analgesics, increased light sensitivity appears in the eyes, a painful reaction to loud sounds and light touches. The patient feels the need to constantly sleep, spots appear on the skin, which also suddenly disappear, which is associated with a violation of vascular functionality. The muscles of the back of the head are in constant tension. By the end of the second period, the person is inhibited, consciousness is unclear, a typical lying position is on the side with legs pulled up and the head tilted back.
- Paralytic stage. Consciousness is completely lost, attacks of paralysis often occur, sensitivity is completely impaired. Breathing and heart rhythm change from a sharp slowdown to an increase in speed, the temperature is either very elevated or noticeably drops below normal. If medical measures are not taken at this stage, death is inevitable, since the respiratory and cardiac centers of the brain structure are completely stopped.
In addition to brain pathology, spinal tuberculous meningitis also occurs. It develops when pathogens enter the spinal canal from affected bone fibers of the spinal column. In addition to the symptoms described above, there are severe girdling pains in the body, which are not relieved even by powerful analgesics. At the end of the last period, pelvic disorders characterized by incontinence appear.
