Neuro tuberculosis

Moderator-Dr. Rajender sir

Presentor- Chandresh Rai
Introduction

• Causative organism: Mycobacterium tuberculosis.

• Most severe form of tuberculosis.

• Predisposing factors:
• Young age

• House hold contact

• Recent measles infection

• Protein energy malnutrition.

• About 1% of total TB cases and 5-10% of extra- pulmonary TB cases
develop CNS tuberculosis.

• The majority of the cases (75-85 %) are below the age five years.

• The peak incidence - 3-5 years age group.

Classification of CNS Tuberculosis
Intracranial TBM Spinal TB

• Tubercular Meningitis • Pott’s spine and paraplegia

• Space occupying lesions (tuberculomas,

• Tubercular arachnoiditis
tubercular abscess)
• osseous spinal tuberculoma
• Tubercular encephalopathy
• Spinal meningitis
• Tubercular vasculopathy
Pathophysiology
Primary Infection & dissemination- (occurs within the first 3-6 months after the primary infection)

Lymphohematogenous dissemination of bacilli

Formation of caseous lesions in meninges/ cerebral cortex

Discharge bacilli in subarachnoid space -> Produce Exudates

Infiltrates cortical and meningeal blood vessel

Inflammation , obstruction and formation of INFARCTS

Hinder normal flow of CSF in ventricular system -> cause HYDROCEPHALUS

Stages of TBM
Stage 1:- Stage 2-
• Lasts 1 to 2 weeks. Begins abruptly
• Nonspecific Stage 3-
symptoms • Increased intracranial Coma,hemiplegia
- Fever, headache pressure, paraplegia, decerebrate
- irritability/ • Signs of meningeal posturing, deterioration
drowsiness irritation in vital signs
- malaise, anorexia • vasculitis without
- inadequate weight marked changes in
gain or significant sensorium.
weight loss • Seizures
- stagnation / • cranial nerve palsies
regression of with basal meningitis
developmental and other focal
milestones. neurological deficits.
APPROACH TO A CASE OF SUSPECTED TBM
Diagnosis of Tubercular Meningitis

A. Tuberculin Skin Test (TST) is an intradermal injection of Purified

Protein Derivative (PPD).

• It may not be reactive in 50% of cases.

• Intradermal injection of 0.1 ml of PPD containing 5 TU PPD.

• Raises a wheal 6 to 10 mm (7 to 8 mm is sufficient).

• Not to be repeated at the same site where previous test has been done.
B. Chest Xray- Radiological findings (may show abnormality in 20-50% of
cases)
 miliary shadows

 intrathoracic lymphadenopathy

 Chronic fibro-cavitary shadows

C. Ultrasound abdomen- revealing retroperitoneal

lymphadenopathy or matted bowel loops.
D. CSF Smear for AFB
• Definitive diagnosis of TBM can be made only if acid-fast bacilli are
isolated.

• A recent study established that both CSF volume and duration of the
microscopic evaluation are independently associated with bacteriological
confirmation of CNS tuberculosis.

• Minimum of 6 ml of CSF fluid should be examined microscopically for a

period of 30 minutes.
E. CSF culture for M. tuberculosis-
• It is not usually positive.

• Rates of positivity range from 25-70%.

• Isolation of M. tuberculosis on solid media often takes 3 to 6 weeks,

followed by another 2 to 4 weeks for drug susceptibility testing.

• Solid (Middlebrook and LJ), Liquid (BACTEC and MGIT) culture media.
F. CSF Cyto/bio-
• Clear/straw colored, CSF leukocyte count- 10 to 500 cells/mm3
(occasionally higher) with lymphocytic predominance. CSF glucose -
<40mg/dl, protein is elevated ( >100 mg/dl).

• Cobweb is formed when left over 12 hours.

G. Rapid NAAT-
• Nucleic acid amplification tests (NAATs) are very sensitive and detect as few as
10 bacilli/ml.

• Sensitivity of PCR for the diagnosis of TBM ranges from 33 to 90.5%.

• Sensitivity is improved when multiple samples are tested, because not all
samples necessarily contain detectable nucleic acid.
H. ADA (adenosine deaminase) –
• ADA is produced by lymphocytes and monocytes.

• The adenosine deaminase (ADA) activity test is a rapid test, that has been used
for the diagnosis of the pleural, peritoneal and pericardial forms of tuberculosis.

• The usefulness of ADA in TBM is uncertain.

• ADA is also increased in pyogenic meningitis and it cannot be used to

discriminate between TBM and bacterial meningitis.
Specific Radiological Test:
CECT head
It may have one or more of the following:
• basal meningeal enhancement
• Hydrocephalus
• Tuberculoma
• Infarcts in different areas, the basal ganglia and precontrast basal

hyperdensity.

• MRI has higher sensitivity than CECT for abnormalities such as

meningeal enhancements, infarcts, and tuberculoma, especially of brain

stem lesions.
CNS tuberculosis other than TBM - Tuberculoma

• Tuberculoma in the brain presents an intracranial space-occupying

lesion (ICSOL).

• Its location, size and perilesional oedema predisposes the manifestations

like seizures, headache and focal neurological deficits.
Tuberculoma NCC

• Age of presentation- at any age • Rare below 3 years

• Appearance - >2 cm, irregular thick • ≤ 2cm, regular, thin, rounded outline with
outline, marked perilesional edema. variable edema

• Location Infratentorial or supratentorial • Predominantly supratentorial

• Midline shift More likely. • Less likely.

• On MRS, lipid peaks are present. • On MRS, amino acid peaks are present
Spinal TB
• Spinal TB can involve the bones of vertebral column
(Pott’sdisease), the cord (myelitis, abscess, or granuloma), and
its dura (arachnoiditis or extradural abscess)

• Back pain (spinal or radicular) is the earliest and most common

symptom. pain may worsen with activity.

• Most common site of Pott’s Spine is thoracic, followed by lumbar/ cervical areas.
• Plain X-Ray of the spine is less sensitive in early disease as it does not reveal any
abnormality till about 30- 50% of bone loss has occurred.

• The typical findings are -

• endplate erosion

• decreased vertebra height,

• collapse and narrowing of discal space and paravertebral soft tissue shadow.
MRI - most sensitive (nearly 100%).

• Features in MRI –

• marrow oedema

• destruction of adjacent vertebral bodies and opposing endplates.

• destruction of the intervening disc.

• occurrence of prevertebral, paravertebral, and epidural abscesses.

CT-guided biopsy of the paravertebral soft tissue/ vertebral body for

histopathological examination (HPE), culture, or NAAT.
Complications of Tuberculous Meningitis

Acute Complications-

• Features of raised intracranial tension.

• Seizures - may also occur due to various electrolyte abnormalities like

hyponatremia (repeated vomiting, SIADH or cerebral salt wasting),
hypernatremia (secondary to diabetes insipidus to diffuse cerebral damage),
hypoglycemia or hypocalcemia.
Hydrocephalus

Communicating hydrocephalus is the commonest type.

• Progressive hydrocephalus if not appropriately treated may have

devastating consequences of irreversible optic atrophy and loss of vision.

• Patient with TBM with altered sensorium should immediately be

evaluated for hydrocephalus.

• Hydrocephalus is also likely to be present in patients who are alert and

who complain of increasing headache with or without vomiting and
blurring of vision.
Tubercular Cerebrovascular Disease-

• On angiographic studies in TBM, irregular beaded narrowing in supra-clinoid

portion of internal carotid artery, widely sweeping pericallosal artery, and
thalamostriate vein and delayed circulation of middle cerebral vein with
scanty collateral circulation is seen.

• In CT scan studies show infarctions in 17 to 63% of patients.

• Infarct has been reported as a poor prognostic predictor in children with TBM.
Ocular Lesions-
• The common ocular lesions in order of frequency are papillitis, optic atrophy
and papilledema.

• Choroidal tubercles may be associated with miliary tuberculosis.

Spinal Tuberculous Arachnoiditis -

• It is a rare complication of CNS tuberculosis.

• It is an inflammatory condition that involves the arachnoid lining along the

spinal tract.
Treatment
1. Supportive treatment :

• Maintenance of airway , breathing and circulation.

• Intravenous fluid therapy.

• Maintenance of acid-base and electrolyte balance.

• Anti-epileptic drugs for control of seizures.

• Treatment of raised ICP.

• Prevention of other complications (exposure keratitis, aspiration pneumonia,

bed sores).
Specific treatment

Anti-tubercular therapy along with corticosteroid therapy.

Intensive phase HRZE- 2months

Continuation phase- HRE- 10months

• Corticosteroids usually prednisolone at 2mg/kg/day daily for 4 weeks

and than gradually tapered over 4 weeks. Alternatively dexamethasone
0.4mg/kg/day followed by oral prednisolone
ATT Doses
Range Average Maximum dose(mg)
mg/kg/day mg/kg/day

Rifampicin (R) 10-20 15 600

Isoniazid (H) 7-15 10 300

Pyrazinamide (Z) 30-40 35 2000

Ethambutol (E) 15-25 20 1500

Streptomycin (S) 15-20 20 1000

• 4 Drug ATT with Weight band and Brand
Brand R H Z E Company

Forcox (22kg) 225 300 750 400 Mcleod

Forcox 150 (15kg) 150 100 500 275 Mcleod

AKT-4 Kit (45kg) 450 300 750 800 Lupin

Akurit-4 (15kg) 150 75 400 275 Lupin

• 3 Drug ATT with weight band and Brand

Brand R H Z E Company
Macox ZH (22kg) 225 150 750 Mcleod
Macox ZH kid (10kg) 100 50 300 Mcleod

R`cinex Z (22kg) 225 150 750 Lupin

Akurit-3 (15kg) 150 75 275 Lupin
AKT-3 kit (45kg) 450 300 800
• 2 Drug ATT with Weight band and Brand

Brand R H Company

Macox Plus kid (10kg) 100 50 Mcleod

R`cinex 50 (5kg) 50 100 Lupin

R`cinex kid (10kg) 100 100 Lupin

Rifa 16 kid fort (15mg) 200 150 Concept

Rifa 16 kid (10kg) 100 100 Concept

Single Drug
Isoniazid Tab/Cap Syp/5ml
Isonex 100mg Pfizer
Solonex 100mg Themis

Rifampicin
Macox 100 Mcleod
Rcin 150 100 Lupin
Pyrazinamide
Pzina kid 300 Lupin
Pza ciba 250 Novartis
Ethambutol

Combutol 200/400/800 Lupin

3. Surgical treatment –

• VP shunt or endoscopic third ventriculotomy for hydrocephalus if indicated.

• Surgical decompression in cases of Pott’s paraplegia.

• In cases of large tuberculoma causing mass effect and tuberculous brain abscess.

• In case of Non-communicating hydrocephalus, which carries the risk of

herniation, is treated by immediate ventriculoperitoneal shunt.
Thank You!