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Outcome for Tuberculosis of the Central Nervous System in Children

This page was last updated on April 8th, 2024

  • Outcome for TB meningitis stage dependent: If treatment is started in stage I, the mortality and morbidity rates are very low; whereas if treatment is started in stage III, almost 50% of patients will die and those who recover may have some form of neurological deficit (62).
  • Outcome for tuberculomas: The radiological investigation of choice is CT scanning with contrast enhancement, and the presence of a target lesion is considered to be pathognomonic of a tuberculoma. Most tuberculomas of the brain can be treated medically with antituberculous chemotherapy. However, a definitive histological diagnosis with CT-guided stereotactic techniques prior to commencing anti-TB therapy is recommended. Surgical excision is necessary in patients with raised ICP secondary to the lesion and not responding to medical therapy (63).
  • Outcome for TB abscess: Appropriate treatment options for TB abscesses include simple puncture, continuous drainage, fractional drainage, repeated aspiration through a bur hole, stereotactic aspiration, and total excision of the abscess. An early surgical procedure can improve the efficacy of anti-TB therapy, promote a better clinical response after reduction of bacillary load, and reduce mortality risk (43).
  • 20–30% have neurological sequelae: Mental retardation, psychiatric disorders, seizures, blindness, deafness, ophthalmoplegia, and hemiparesis are among the sequelae that occur. Endocrinopathies due to progressive damage of either the hypothalamus itself or adjacent basal cisterns can occur, as can obesity, hypogonadism, Frolich syndrome, sexual precocity, diabetes insipidus, and growth retardation. Intracranial calcification develops in 20– 48% of patients with TB meningitis, with these usually becoming detectable 2–3 years after the onset of the disease (51).
  • Accurate prognosis for TB meningitis difficult: Accurate prognosis for TB meningitis is difficult because of the protracted course, diversity of underlying pathological mechanisms, variation of host immunity, and virulence of M. tuberculosis (64). Age, stage of disease, focal weakness, CN palsy, and hydrocephalus are the most significant predictors. Children with advanced disease with neurological complications and those with SIADH have poor outcomes. Sinha et al. reported visual impairment resulting from optochiasmatic arachnoiditis or optochiasmal tuberculoma as a prelude to severe disability or death (65). Coexisting HIV encephalopathy and diminished immune competence undoubtedly contributed to the more severe clinical and neuroradiological features. EEG and MEP can be useful in assessing the severity of lesions and help in predicting outcome (66). Misra et al. found that focal weakness, GCS score, and somatosensory evoked potential findings were the best predictors of 6-month outcome in patients with TB meningitis (67).
  • BCG vaccine: Kumar et al. reported that children with TB meningitis and prior BCG vaccination maintained better mentation and had superior outcomes (68). This finding is due to the better immune response to infection, as is reflected in the higher CSF cell counts in this patient group, compared to those who were unvaccinated.
  • New tuberculomas while on treatment: CNS tuberculoma is a controllable condition with a good prognosis and effective therapy options. The development of new lesions while on treatment has been reported. But if the diagnostic certainty is high, it does not warrant any alteration in the treatment strategy in most cases, with the possible exception of prolonging the use of steroids in the regimen, which may mitigate these unwanted sequelae. Enhanced brain and spine MRI should be performed to ensure the diagnosis is not missed. Early surgical decompression is recommended for intramedullary tuberculoma. Craniotomy is indicated for patients with intracranial hypertension, while more conservative therapy is appropriate for patients who have intracranial tuberculomas without intracranial hypertension (17).