When Tuberculosis Strikes Twice: Cerebral Tuberculoma as a paradoxical reaction during antituberculous therapy in an immunocompetent patient: A case report

Cerebral tuberculoma is an uncommon manifestation of central nervous system tuberculosis (CNS-TB) and may develop as a paradoxical reaction during antituberculous therapy, even in immunocompetent individuals. Its clinical and radiological presentation poses a significant diagnostic challenge because it closely mimics other intracranial space-occupying lesions. We report the case of a 36-year-old immunocompetent man with pulmonary tuberculosis confirmed by Xpert MTB/RIF, demonstrating rifampicin susceptibility. Human immunodeficiency virus (HIV) infection and diabetes mellitus were excluded. Two months after initiating standard first-line antituberculous therapy with isoniazid, rifampicin, pyrazinamide, and ethambutol (HRZE), he developed progressive headache and left-sided hemiparesis. Brain computed tomography revealed two ring-enhancing lesions in the right frontoparietal region associated with marked vasogenic edema, consistent with cerebral tuberculomas. Cerebrospinal fluid analysis, including Xpert MTB/RIF testing, was negative for tuberculous meningitis. Toxoplasmosis, primary central nervous system lymphoma, and other infectious and neoplastic etiologies were excluded through comprehensive clinical, microbiological, and radiological evaluation. Given the high suspicion of a paradoxical inflammatory reaction, antituberculous therapy was continued without modification, and adjunctive dexamethasone was initiated, resulting in progressive neurological recovery without the need for neurosurgical intervention. This case highlights the importance of recognizing paradoxical reactions as a cause of newly developed intracranial lesions during otherwise effective antituberculous treatment. The integration of clinical, microbiological, and neuroimaging findings, together with the systematic exclusion of alternative diagnoses, allowed an accurate diagnosis and prevented unnecessary modifications to antimicrobial therapy. Early recognition of this entity may improve neurological outcomes and optimize the management of patients with central nervous system tuberculosis.