Tuberculous meningitis (TB) is the most severe form of extrapulmonary TB and the leading cause of death from TB. Due to the widespread BCG vaccination and TB prevention and control, its incidence has been significantly reduced, but in recent years there is a significant trend of increase, especially the increase of drug-resistant TB infection.
I. Clinical manifestations
(1) Prodromal phase (early): about 1 to 2 weeks, the prodromal symptoms include changes in mental status, in addition to low fever, loss of appetite, sleep disturbance, thinness, constipation or unexplained vomiting. Older children may complain of headache, which is initially mild or non-persistent. In infants and young children, the onset of the disease may be rapid, with a short or no prodromal period, and the onset of meningeal irritation.
(2) Meningeal irritation phase (middle phase): about 1 to 2 weeks, headache persists and worsens, vomiting increases and may become jet-like, vomiting is the most common symptom in all age groups. Gradually drowsiness appears, or drowsiness alternates with restlessness. There may be perceptual hypersensitivity and shouting due to pain when touched or examined. Convulsive episodes may occur, but the patient is still conscious after the episode.
Signs during this period may include a full or bulging fontanelle, a tense collar, a hip and knee flexion sign (Kernig′s sign), a flexed neck and leg movement sign (Brudzinski′s sign) and a positive pathological plantar reflex (Babinski′s sign), and a generally weak or absent superficial reflex, with a hyperactive tendon reflex. In addition, there are muscle tremors and red scratches on the skin.
Symptoms of cerebral nerve disorders are common, such as ptosis, exotropia, diplopia, pupillary dilation, spreading nerve and facial nerve palsy.
At this stage, many patients have obvious signs and symptoms of high cranial pressure and hydrocephalus, such as high fever, abnormal respiration, unequal pupil size, and optic disc edema in the fundus, etc. Finally, corneal arcus, hemiparesis or limb ankylosis may appear.
(3) Coma stage (late stage): about 1 to 3 weeks, the above symptoms gradually worsen, the consciousness from hazy, semi-coma and into a complete coma, mostly after the convulsions into coma. Clonic or tonic convulsions are frequent.
The phenomenon of increased cranial pressure and hydrocephalus is more obvious. Finally, the muscles of the extremities are relaxed and paralyzed, urinary retention occurs, all reflexes disappear, or the brain is deactivated; in critical cases, the body temperature may increase suddenly, the blood pressure drops, the pulse rate is fine and rapid, Chen-Schiller’s respiration occurs, and death eventually occurs due to respiratory and cardiovascular motor center paralysis.
Diagnosis
Clinical manifestations + auxiliary examinations
Laboratory tests.
1. Normal or mildly elevated peripheral blood leukocyte count.
2, cerebrospinal fluid pressure is elevated, the appearance can be hairy glass, placed for several hours can be seen in the formation of white fibrous film, the film antacid staining direct smear easier to find tuberculosis bacilli. There are tens to hundreds of leukocytes, mostly of mixed type, with monocytes predominating in about 85% of cases. The protein content is mildly to moderately elevated, and sodium chloride and glucose are mostly reduced.
3.The basis of pathogenesis
(1) CSF bacterial smear and bacterial culture detection rate is low, TB-SPOT test increases the positive rate.
(2) Skin tuberculin test.
(3) Early diagnosis: polymerase chain reaction (PCR) is mostly used to detect the DNA of tuberculosis bacteria in CSF.
In addition, the enzyme-linked immunosorbent assay (ELISA) can be used to detect tuberculosis antibodies in CSF. The use of the above two tests together can improve the reliability of the diagnosis. However, the possibility of false positives and false negatives should be noted.
Other ancillary tests.
1.X-ray examination Chest X-ray is particularly important to detect TB lesions.
2, CT, MRI examination about half of the brain CT shows abnormalities. Inflammatory exudate fills the basal pool and lateral fissure of the brain, and some patients show tuberculoma in the brain parenchyma, 0.5-125px in diameter, single or multiple, mostly located in the frontal, temporal and parietal lobes. Enhancement scans showed circumferential enhancement or increased density.
Brain MR with Gd-DTPA enhancement shows enhancement in the basal pool and other areas, and is more likely to detect tuberculomas and small infarct foci in the brain parenchyma.
III. Complications
1, Systemic tuberculosis manifestations.
2, whole brain or focal signs caused by brain lesions: limb movement and sensory disorders; secondary epilepsy; disorders of consciousness; various syndromes of the brainstem.
IV. Treatment
1.General treatment The following measures must be strictly implemented.
(1) Cut off contact with open tuberculosis patients.
(2) Strict bed rest, nutrition must be rich.
(3) Careful care: change the patient’s position, take care of the patient’s eyes, mucous membranes and skin, and prevent skin bedsores; apply nasal feeding to comatose patients.
(4) It is better to be hospitalized, and outpatient treatment should be considered only when the conditions do not allow, but follow-up visits should be strengthened and adherence to treatment should be urged.
2. Anti-tuberculosis drug therapy The principle of treatment is early and thorough (uninterrupted treatment and long-term treatment).
At present, the treatment of tuberculous meningitis is mostly combined with streptomycin (SM), isoniazid (INH), rifampicin (RFP) and pyrazinamide (PZA). Among them, isoniazid INH is the most dominant drug and is applied from the beginning to the end of the whole course of treatment. The duration of treatment is 1 to 1.5 years, or not less than six months after the cerebrospinal fluid is normal.
3. The principle of hormone therapy is that it must be applied simultaneously with effective anti-tuberculosis drugs, and the dose and duration of treatment should be moderate, and the earlier it is applied, the better.
IV. Prognosis
Early diagnosis and systematic treatment have a good prognosis, but delayed treatment or unsystematic treatment often leads to serious sequelae such as limb paralysis, convulsions and hydrocephalus. The recurrence rate is generally 5% to 10% after the cure of cerebral nodules.