Tuberculous meningitis is inflammation of the membranes surrounding the brain and spinal cord caused by Mycobacterium tuberculosis. It typically develops secondary to a pulmonary tuberculosis infection. Symptoms progress through three stages - an initial prodromal stage with nonspecific symptoms, followed by signs of meningeal irritation and cranial nerve palsies, and finally a terminal stage with coma and death if untreated. Diagnosis involves lumbar puncture showing lymphocytic pleocytosis and decreased glucose. Treatment consists of a combination of antitubercular drugs for 12 months along with corticosteroids to reduce inflammation and complications. Prognosis depends on the stage of disease at treatment initiation, with mortality rates as high as 50%

1. BY
Dr. Sabahat
PGR Paeds Medicine

2. Definition:
It is inflammation of the
leptomenings (pia-arachnoid) by
Mycobacterium tuberculosis

4. Pathogenesis
 Tuberculous meningitis is always a secondary lesion
with primary usually in the lungs
 Meningitis results from formation of a metastatic
caseous lesion in the cerebral cortex, meninges and
choroid plexus during the process of initial occult
lympho-hematogenous spread of primary infection.

5.  Then Caseous foci form on the surface of brain (
Rich’s foci). They increase in the size and discharge
bacilli in CSF.
 A thick , gelatinous exudate may infiltrate the
cortical or meningeal blood vessel , producing
inflammation, obstruction , or infarction .
 Most commonly involved site is the brain stem
causing frequent involvement of 3rd , 6th and 7th
cranial nerves.
 Basal cisterns are obstructed causing
communicating hydrocephalus. Accompanying
inflammation may cause cerebral edema.

6. Clinical Features:
 In a classical case, onset is insidious but may be
fulminant in certain cases.
 A more rapid progression of the disease may occur
in young infants in whom symptoms develop for only
several days before the onset of acute hydrocephalus
brain infarction , or seizures.
 Classically , the onset is gradual (over several weeks).
 The clinical manifestations may be divided into 3
stages and each stage last approximately 1 week.

7. Stage 1(Prodromal stage):
 Lasts for 1-2 weeks
 The child becomes listless or irritable ,loss interest in
the play ,has fever, anorexia,vomiting , constipation
and weight loss.
 May complain of headaches and drowsiness.
 No focal neurologic signs.
 May be loss of or stagnation of the developmental
milestones.

8. Stage 2:
 Onset is more abrupt.
 Signs of meningeal irritation with increased CSF pressure.
 Positive Kerning and Brudziniski signs with increased
tendon jerks and extensor plantar responses.
 There may be generalized hypertonia.
 Headache is cardinal symptom in older children with
constant Fever.
 Vomiting and constipation may become severe.
 Abducent nerve paralysis is common . Oculomotor lesion
causes internal squint . Facial palsy is also common.
 May have disorientation , and speech and movement
disorders.

9.  In the infants anterior fontanelle may be bulging and
sutures become separated with “crackpot” sign.
 In older children papilledema develops. Head
circumference starts enlarging rapidly.
 Choroid tubercles may be seen on fundoscopy.
 Child is semiconscious and develops convulsions.

10. Stage 3:
 Rapidly become comatose .
 High grade irregular fever and convulsions.
 There may be hemiplegia or paraplegia.
 Extreme neck stiffness opisthotonus develops with the
decerebrate rigidity and pupil become dilated and
fixed.
 Deterioration of vital signs especially hypertension.
 Death may occur if treatment is started late during
this stage.

11. DIAGONSIS
1. Suspicion:
• A high index of clinical suspicion is important where
tuberculosis contact is positive.
• Tuberculin skin test is negative is 50% of the patients.
2. Blood:
• ESR is high
• Total and differential leukocyte count reveals normal count
with predominant lymphocytosis.
3. X-Rays Chest:
• Chest X-rays may be normal in 20-50% of the cases.
• Usually there is some evidence of tuberculosis in the lungs
, hilar adenopathy , and patch of pneumonia or miliary
tuberculosis

12. 4. LUMBER PUNCTURE (CSF examination):
• CSF pressure increased.
• Color is clear, hazy or straw colored.
• Cobweb is formed when left for over 12 hours.
• Protein is markedly raised( 400-5,000mg/dl) because of
hydrocephalus and spinal block.
• Glucose is decreased (below 40 mg/dl).
• Pleocytosis with predominant lymphocytes (10-
500/mm3).
• Smear and culture: Ziehl- Nelson stain may reveal
acid-fast bacilli .CSF culture confirms the diagnosis.
• Mycodot : Antigen detection by polymerase chain reaction.

13. 5. GASTRIC LAVAGE OR SPUTUM EXAMINATION for
tubercle bacilli.
6. LYMPH NODE BIOPSY in certain cases to confirm the
diagnosis.
7. FUNDOSCOPY (choroid tubercles , papilledema or optic
atrophy)
8. CT SCAN with contrast may help establish a diagnosis of
tuberculous meningitis. It also aids in evaluating the success of
therapy. There may be:
 Brain stem meningitis (Brain Enhancement ).
 Hydrocephalus,
 Focal infarcts
 Tuberculomas
 (CT scan may be normal during the early stages of the TBM).

14. MANAGEMENT:
Specific Treatment:
 Start treatment with 4 anti- tuberculous drugs and treatment should
be continued for 12 months.
1. Isoniazid (INH):
• It is the drug of first choice.
• It is rapidly absorbed and penetrates into the CSF.
• Isoniazid and rifampicin and highly bactericidal for
M.tuberculosis.
• Dose is 10-15 mg/kg/day.
• Main side effect are hepatotoxicity , peripheral
neuropathy ,optic neuritis, hypersensitivity and
fever. Neuritis is due to competitive inhibition of
pyridoxine.
• Transient elevation of amino-transferases may be seen
at 6-12 weeks, but therapy should continue.

15. 2. Rifampicin:
• It is also a first line drug, well absorbed and
penetrates CSF well.
• Dose is 10-20mg/kg/day one half an hour before
breakfast
• It causes orange discoloration of the urine and
tears , GIT disturbance and hepato-toxicity.
• Combined use of INH and rifampicin increases the
risk of hepatotoxicity , which can be decreases by
lowering the dose of INH (10 mg/kg/day)

16. 3. Pyrazinamide
• It is bactericidal in acid medium and enters CSF readily.
• It is used as a third drugs for 2-3 months initially
• Dose is 30 mg/kg/day.
• Main side effect are arthralgia ,arthritis ,hyper-uricemia
(gout)
4. Streptomycin:
• It is bactericidal for extracellular tubercle bacilli, but its
penetration into macrophages is poor.
• Its penetrance into CFS through inflamed meninges is
excellent but do not cross the un-inflamed meninges.
• Dose 20-40 mg/kg/day given 1/M for 2 months.
• Side effect are ototoxicity (vestibular or hearing loss)
nephrotoxicity and may cause hypersensitivity reactions.

17. 5. Ethambutol:
• It is not recommended below 6 years of age.
• Dose 15-25 mg/kg once daily.
• Side effects are Optic neuritis ,hypersensitivity and
GIT upsets.

18.  GENERAL MEASURES:
1. Corticosteroids:
• Decrease mortality rate and long term neurologic
sequelae.
• Reduce vasculitis ,inflammation , and intracranial
pressure.
• Dose of prednisolone is 1-2mg/kg/day for 6-8 weeks.
• Help to reduce cerebral edema and prevents
formation of adhesions .
2. Careful record of vital signs

19. 3. Daily monitoring of complications:
Main complications are to be monitored
• Raised intracranial pressure
• Drugs toxicity, etc.
4. Phenobarbitone:
Dose 5 mg/kg/day to control convulsions.
5. Antipyretics:
Paracetamol(10—15mg/kg/dose 4-6 hourly) and fresh water
sponging to control temperature.
6. Pyridoxine:
1 mg/kg/day daily to prevent polyneuritis.

20. 7. Feeding :
NG tubes feeding according to requirement .
Ideally 100 calories /kg/day are given . Iron and
multivitamins can be added too.
8. Bed Sores :
Change posture every two hours.
9. Care of comatose Patient.
10. Care of bowel and bladder .
11. Screening:
Important to screen the family members for tuberculosis
and treat infected persons.

21. COMPLICATIONS:
1. Mental retardation
2. Cranial nerve palsies (3rd , 6th and 7th )
3. Blindness (optic atrophy)
4. Deafness
5. Hydrocephalus
6. Hemiplegia, paraplegia
7. Epilepsy
8. Endocrine disturbances (diabetes insipidus).
9. Tuberculoma.

22. PROGNOSIS:
 It depends upon two factors:
1. Age of patient
2. Stage of disease at which treatment started.
 Without treatment it is fatal.
 In stage1, 100% cure rate is expected.
 Even with optimal therapy mortality ranges from 30-50%
and incidence of neurologic sequelae is 75-80%
especially in stage 3. There may be blindness, deafness
, paraplegia, mental retardation and diabetes insipidus.
 Infants and young children have poor prognosis as
compared to older children