2_2019_. F. Cr. J j. .

Pathology

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. 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:
1)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 (1000-8000 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 14
th

day, 1 month, 6
th
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.