Case Presentation: A 76-year-old Hispanic man with poorly-controlled diabetes mellitus complicated by nephropathy presented to a hospital with 2 weeks of nausea, vomiting, and progressive lethargy. During the initial evaluation, he developed a focal right-sided seizure advancing to a generalized tonic-clonic seizure lasting 30 seconds. He was afebrile, hypertensive, and non-tachycardic with normal saturation on room air. He was persistently lethargic and confused. The neurologic exam was non-focal without meningeal signs, and the remainder of the exam was unremarkable. Laboratory studies revealed 11.5 WBC/mm3 without left shift or bands, sodium 129mEq/L, creatinine 2.50mg/dL, lactate 28mg/dL, and negative HIV antibodies. Head CT reported focal superior left frontal lobe hyperdense sulcal effacement. A brain MRI confirmed a leptomeningeal enhancing lesion with abnormal FLAIR but no gyral edema or restricted diffusion. CT chest, abdomen and pelvis did not reveal miliary lesions in lung parenchyma or soft tissue. Initial lumbar puncture (LP) showed 2 WBCs, 1750 RBCs, protein 195mg/dL, and glucose 126mg/dL (serum glucose 230mg/dL). A subsequent LP on hospital day 3 revealed similar results. Cerebrospinal fluid studies were negative for organisms on bacterial culture, AFB, West Nile Virus, HSV, India ink, and cryptococcal antigen. Two tuberculin skin tests, blood cultures and serum bacterial antigens were negative. On hospital day 6, he underwent an intra-dural biopsy, which revealed caseating granulomas with acid-fast bacilli. Anti-tuberculous therapy of isoniazid, rifampin, pyrazinamide, and levofloxacin was promptly initiated. His course was complicated by post-operative respiratory failure and acute cerebrovascular accident resulting in residual left facial droop with contralateral hemiparesis. He was subsequently extubated and discharged to an acute rehabilitation facility with plans to complete 2 months of quadruple therapy followed by 16 months of isoniazid and rifampin.

Discussion: This case illustrates the diagnostic challenges of tuberculosis (TB) meningitis and tuberculomas. Presenting with stage 2 to 3 TB meningitis, he had multiple risk factors including childhood in Mexico, diabetes, and renal disease. Accounting for 1% of TB cases, TB meningitis rarely presents without active TB outside the central nervous system, making this presentation particularly unique. Tuberculomas, generally incidental findings in TB meningitis, rarely cause systemic illness or meningeal signs, advancing to later stages before detection. Due to brainstem herniation risk, LPs must be carefully considered and may yield non-diagnostic results. Therefore, invasive measures including needle biopsy may be required, as was necessary for diagnosis in this case.

Conclusions: TB meningitis is a rare and highly fatal manifestation of TB despite effective treatments. Clinical suspicion is crucial for early identification and therapy, which directly correlate with outcomes.