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Brain Tuberculosis (Intracranial Tuberculomas)

Key Points

  • Most common form of CNS TB after meningitis in children
  • Represents 5-30% of intracranial masses in children in endemic areas
  • Peak incidence: 2-12 years age group
  • Higher prevalence in immunocompromised children
  • Can occur with or without evidence of TB elsewhere

Epidemiology

  • More common in developing countries
  • Male:Female ratio = 2:1
  • Risk factors:
    • Malnutrition
    • HIV infection
    • Recent TB contact
    • Low socioeconomic status
    • Immunosuppressive therapy

Detailed Pathophysiology

Formation Mechanism

  • Rich Focus Formation:
    • Hematogenous spread from primary focus
    • Formation of microscopic tubercles
    • Coalescence into tuberculomas
  • Growth Stages:
    • Early non-caseating granuloma
    • Caseating granuloma with solid center
    • Caseating granuloma with liquid center

Common Locations

  • Frontal lobe (30%)
  • Parietal lobe (25%)
  • Cerebellum (20%)
  • Brainstem (15%)
  • Basal ganglia (10%)

Immunological Response

  • Cell-mediated immunity activation
  • Cytokine cascade:
    • TNF-α production
    • IFN-γ release
    • IL-12 mediated response
  • Formation of granulomatous inflammation

Clinical Manifestations

General Symptoms

  • Fever (80-90% cases)
  • Weight loss
  • Night sweats
  • Failure to thrive
  • Behavioral changes

Neurological Symptoms

  • Focal Neurological Signs:
    • Hemiparesis
    • Cranial nerve palsies
    • Visual disturbances
    • Speech disorders
    • Ataxia (in cerebellar lesions)
  • Features of Raised ICP:
    • Headache (progressive)
    • Vomiting
    • Papilledema
    • Altered consciousness
    • Sixth nerve palsy
  • Seizures:
    • Focal seizures (60%)
    • Generalized seizures (40%)

Age-Specific Presentations

  • Infants:
    • Irritability
    • Poor feeding
    • Developmental regression
    • Bulging fontanelle
  • Older Children:
    • Academic decline
    • Personality changes
    • Focal neurological deficits

Diagnostic Approach

Neuroimaging

  • MRI Findings:
    • T1: Iso/hypointense with peripheral rim
    • T2: Central hyperintensity with hypointense rim
    • Contrast: Ring enhancement
    • 'Target sign' - pathognomonic
    • Perilesional edema
  • CT Findings:
    • Irregular hyperdense lesions
    • Ring enhancement with contrast
    • Calcification in chronic cases
  • MR Spectroscopy:
    • Elevated lipid peak
    • Decreased N-acetylaspartate
    • Elevated choline/creatine ratio

Laboratory Investigations

  • CSF Analysis:
    • Opening pressure
    • Protein and glucose levels
    • Cell count and differential
    • AFB smear
    • Gene Xpert MTB/RIF
    • Culture
  • Blood Tests:
    • Complete blood count
    • ESR and CRP
    • HIV testing
    • Liver function tests
  • Immunological Tests:
    • Mantoux test
    • Interferon-gamma release assays

Treatment Protocol

Anti-tubercular Therapy

  • Initial Phase (2-3 months):
    • Isoniazid (H): 10-15 mg/kg/day
    • Rifampicin (R): 10-20 mg/kg/day
    • Pyrazinamide (Z): 30-35 mg/kg/day
    • Ethambutol (E): 15-20 mg/kg/day
  • Continuation Phase (9-12 months):
    • Isoniazid + Rifampicin
    • Total duration: 12-18 months

Adjunctive Therapy

  • Corticosteroids:
    • Prednisolone 2-4 mg/kg/day
    • Duration: 4-8 weeks with tapering
    • Indications:
      • Significant edema
      • Mass effect
      • Paradoxical reactions
  • Anti-epileptic Drugs:
    • For seizure control
    • Drug interactions with ATT considered
  • Management of Raised ICP:
    • Mannitol/hypertonic saline
    • Head elevation
    • Hyperventilation if needed

Surgical Intervention

  • Indications:
    • Large lesions with mass effect
    • Hydrocephalus
    • Failed medical management
    • Diagnostic uncertainty
  • Procedures:
    • Stereotactic biopsy
    • Excision of accessible lesions
    • CSF diversion procedures

Complications and Monitoring

Disease-related Complications

  • Neurological:
    • Permanent neurological deficits
    • Cognitive impairment
    • Epilepsy
    • Hydrocephalus
  • Paradoxical Reactions:
    • Development of new lesions
    • Enlargement of existing lesions
    • Usually occurs 2-3 months after ATT

Treatment-related Complications

  • Drug-induced hepatitis
  • Visual impairment (Ethambutol)
  • Peripheral neuropathy (Isoniazid)

Monitoring Protocol

  • Clinical Monitoring:
    • Neurological examination every 2 weeks
    • Visual acuity and fields monthly
    • Growth and development monitoring
  • Laboratory Monitoring:
    • Liver function tests monthly
    • Complete blood count
    • Renal function tests
  • Radiological Monitoring:
    • MRI at 3, 6, and 12 months
    • Earlier if clinical deterioration

Special Considerations

In HIV Co-infection

  • Higher risk of dissemination
  • Atypical presentations common
  • Longer duration of therapy needed
  • Drug interactions with ART

Prognostic Factors

  • Good Prognosis:
    • Early diagnosis
    • Single lesion
    • No hydrocephalus
    • Good treatment compliance
  • Poor Prognosis:
    • Multiple lesions
    • Brainstem involvement
    • Associated meningitis
    • HIV co-infection


Disclaimer

The notes provided on Pediatime are generated from online resources and AI sources and have been carefully checked for accuracy. However, these notes are not intended to replace standard textbooks. They are designed to serve as a quick review and revision tool for medical students and professionals, and to aid in theory exam preparation. For comprehensive learning, please refer to recommended textbooks and guidelines.





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