1. TB Meningitis - consist of 5 % meningitis.
- common in developing countries.
- In 1985: increased mostly among young males (25-44) years old due to AIDS.
- Younger children < 5 years are 2nd risk group.
- in < 20 years, male to female ratio is 1:1
- In > 20 years : the male-to-female ratio is approximately 2:1.

2. Cause: Mycobacterium tuberculosis Risk factors
-Human migration: during wars and famines.
-HIV co-infection is the strongest risk factor.
-Neglected peoples.
Predisposing factors
malnutrition, alcoholism, substance abuse, diabetes mellitus, corticosteroid use, malignancy, head trauma.

3. Pathophysiology: The development of TBM is a 2-step process:
1.Mycobacterium tuberculosis bacilli enter the lung by droplet inhalation.
During stage of lung invasion, a short but significant bacterial seeding, via blood, is present, which can seed tubercle bacilli to other organs in the body.
In those who develop TBM, bacilli seed to the meninges or brain parenchyma, resulting in the formation of small subpial or subependymal foci of metastatic caseous lesions termed Rich foci (also known as tubercles). Dissemination to the CNS is more likely if miliary TB develops.

4. 2. increase in size of a Rich foci
2. increase in size of a Rich foci. The location of the expanding Rich foci determines the type of CNS involvement. Rich foci near subarachnoid space will rupturing into this space cause meningitis. Those deeper in the brain coalesce with one another forming tuberculomas or (less commonly) abscesses.

5. Markers on clinical features:
Usually chronic infection affect immunocompromized patient.
However occasionally affect immunocompetent individual & here take form of acute or subacute process.
Approximately two-thirds of patients with tuberculous meningitis there is evidence of active tuberculosis elsewhere, usually in the lungs and occasionally in the other organs.
Fever, headache & signs of meningeal irritation can be absent in 25% of patients.
Malaise can be absent in up to 60% of cases.

6. Opthalmological findings:
papilledema in 20%
a small grayish-white choroidal nodule, highly suggestive of TB. It is rare.
primary optic atrophy in children.
Examination may elicit visual impairment.

7. Other Neurologic findings:
Focal neurological deficits may include monoplegia, hemiplegia, aphasia, and tetraparesis. These are uncommon & result from long tract affection due to 2ndary vasculitis. More commonly focal signs being in the form of extraxial cranial neuropathy due to vasculitis or basal adhesion.
Cranial neuropathies are frequent & most often involving CN VI & next in frequency CN III, IV, VII ; but any cranial nerve could be involved.

8. Investigations:
Cerebrospinal fluid
Typically, the pressure is higher than normal.
Color is clear or slightly turbid. If the CSF is left to stand, a fine clot resembling a pellicle or cobweb may form. This faintly visible "spider's web clot" is due to the very high level of protein in the CSF ( mg/dL) typical of this condition.
CSF contains between 10 and 500 white cells per cubic millimeter, rarely more. Early in the disease the neutrophils may be predominate; but after several days, lymphocytes predominate in the majority of cases.
The protein content of the CSF is always elevated, between 100 to 500 mg/dL in most cases, but much higher if the flow of CSF is blocked around the spinal cord.
Glucose is reduced to levels below 40 mg/dL and rarely lower. It can be normal in certain cases.
Acid-fast stain (positive in 25%).
Culture for M tuberculosis (positive in 50-80%), requires 3-6 weeks.
Polymerase chain reaction (PCR): it can provide a rapid and reliable diagnosis of TBM, (100% specifity , 80% sensitivity)

9. 2) Chest radiography: 50 % +ve
3) CT scan and MRI of the brain reveal hydrocephalus, basilar meningeal thickening, infarcts, edema, and tuberculomas.

10. Treatment: 1) Anti-TB drugs:
Duration of anti-TB course in TBM is12 months.
For the first 2 months, four drugs are recommended: Isoniazid, Rifadin, Pyrazinamide, and Streptomycin or Ethambutol. Then reduce the regimen to 2drugs (INH+R) for remianing 10 months.
Doses are the same for Lung TB with exception of maximum dose of Rifadin which can be increased to 900 mg/day.
Within a few days after starting anti-TB therapy, the initial mononuclear pleocytosis may change briefly in some patients to polymorphonuclear predominance, This has been regarded by some authors as virtually pathognomonic of TBM
2) Steroid:
Prednisolone is given in a dose of 60 mg/day, or dexamethasone, 0.15 mg/kg/day in 4 divided doses i.v is given. Steroid is continued for 4 weeks.

11. Follow-up: Repeated LPs are performed at 14th day, 1 month, 6th month, 1 year and 2 years after beginning therapy if the patient is clinically stable.
Relapses: The main reason for relapse is noncompliance with treatment. Inadequate therapy has caused an alarmingly high incidence of organisms resistant to multiple drugs which associated with bad prognosis.

12. Complications:
The syndrome of inappropriate antidiuretic hormone secretion (SIADH) is a common complication and is linked to a poor prognosis.
Tuberculomas: The larger ones may produce symptoms of a space-occupying lesion, and periventricular ones may cause obstructive hydrocephalus, but many are asymptomatic. In developing countries they constitute from 5 to 30 percent of all intracranial mass lesions.
Dementia,
Obstructive Hydrocephalus: due to obstruction of basilar cisterns by adhesion caused by basal meningitis. It associated with bad prognosis
Hypothermia: Also linked to bad prognosis.
Visual impairment

13. Prognosis:
The overall mortality of patients with CNS tuberculosis is still significant (about 30 percent). If untreated it will kill the patient within few weeks.The highest mortality rate occur in HIV-infected patients.