The initial pathogenesis of CNS tuberculoma is identical to that of tuberculous (TB) meningitis. Instead of rupturing into subarachnoid space, however, tubercles continue to grow, walled off from brain parenchyma and meninges by a dense fibrous capsule. Grossly, the lesions are well-circumscribed masses varying in size from less than a centimeter up to several centimeters. A patient can have one or several, localized to any brain region. Tuberculomas occasionally develop during or after treatment for TB meningitis.
Clinical sequelae of CNS tuberculomas are those of single or multiple intracranial mass lesions, primarily seizures and correlates of increased intracranial pressure. The features of the seizures can strongly suggest lesion location. Neuroimaging, especially MRI, is diagnostically indispensable, although biopsy remains the gold standard.
One study examining the clinical course of cerebral tuberculoma in patients with and without HIV infection found that cerebral tuberculoma in HIV-negative patients was more likely to be characterized by seizures.78
Intracranial tuberculoma without evidence of systemic TB is relatively rare and difficult to diagnose. It is often clinically quiescent for a long time, and a seizure can be an important sentinel event in such cases. Tseng et al. reported a patient without any history of TB who presented with focal left-hand seizures. Neuroimaging revealed a leptomeningeal lesion in the left frontoparietal region. Subsequent histopathologic analysis of a biopsy sample was consistent with tuberculoma.74 Tosomeen et al. reported a similarly seizure-presenting case of multiple intracranial tuberculomas.75
If the caseous core of a tuberculoma liquefies, a TB abscess results. These patients tend to be clinically worse overall than those with correspondingly sized tuberculoma. Again, focal seizures can be an important initial clinical manifestation.76
Reviewed and revised March 2004 by Steven C. Schachter, MD, epilepsy.com Editorial Board.
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