Right Temporal Lobe Tuberculoma Presenting as Seizures in a Patient With Pulmonary Tuberculosis

Introduction

Despite considerable efforts to eliminate TB, it remains one of the most widespread neglected diseases, affecting roughly one-quarter of the global population [1]. Extrapulmonary manifestations arise through hematogenous spread of Mycobacterium tuberculosis and can affect nearly every organ system, with CNS involvement being one of the most severe forms of disease. Diagnosis of TB relies on a combination of clinical assessment, microbiologic testing, and imaging, while management consists of prolonged multidrug anti-tuberculous therapy, with surgical intervention reserved for select complications [1]

Within the central nervous system, tuberculosis can manifest as meningitis, tuberculomas, or spinal arachnoiditis, each varying in presentation and prognosis [2]. A tuberculoma is a granulomatous lesion of the CNS, which more commonly presents in immunocompromised individuals, although occurrence in immunocompetent patients has also been reported [3].

A tuberculoma classically appears as a ring-enhancing calcified lesion on computed tomography (CT), while its appearance on magnetic resonance imaging (MRI) varies based on the lesion’s stage of maturation [3]. However, a tuberculous lesion can mimic other pathological processes in its radiographic features, including abscesses and brain tumors, creating uncertainty and delaying therapy. Similar diagnostic challenges have been described in prior case reports [4,5].

Management of tuberculomas is primarily with anti-tuberculous medications, with the exact duration of treatment not universally established. Various studies suggest a treatment course ranging from 6 to 30 months [1,3]. Surgical intervention is appropriate for cases with mass effect, diagnostic uncertainty, or failure of medical therapy.

This report describes the case of a 30-year-old woman with a history of alcohol use disorder, polysubstance abuse, and pulmonary TB previously treated with RIPE, who presented following a seizure and was diagnosed with a right temporal lobe tuberculoma.

Case Report

A 30-year-old Hispanic woman with a past medical history of alcohol use disorder, cocaine use, non-epileptic seizures, and pulmonary TB presented to the ED after a witnessed seizure lasting 5 min.

She had undergone a prior complicated treatment course for pulmonary TB earlier in the year. She was hospitalized for 8 weeks on RIPE therapy due to persistently positive sputum cultures. Drug susceptibility testing from that admission demonstrated fully drug-sensitive M. tuberculosis, with no evidence of antimicrobial resistance. She was ultimately approved for discharge by the Department of Health after a stable residence was confirmed and the patient agreed to outpatient directly observed therapy (DOT). In the interval between discharge and her current ED presentation, she developed hepatotoxicity from the standard 4-drug regimen of rifampin, isoniazid, pyrazinamide, and ethambutol (RIPE), with alcohol use contributing to her liver injury. As a result, anti-tuberculous medications had been held for several months.

In the ED, she reported heavy daily alcohol consumption, averaging 2 to 3 pints of vodka per day, and admitted to recent frequent falls related to intoxication. She also endorsed nonadherence to all her prescribed medication, including levetiracetam and RIPE therapy. Over the prior several months, she had experienced an unintentional 18 kg weight loss, which she attributed to decreased appetite in the setting of heavy alcohol intake.

On admission, the patient was intoxicated, but alert and able to converse appropriately. Her blood alcohol concentration was 446 mg/dL. Laboratory evaluation revealed transaminitis, hypokalemia, and elevated creatine kinase. Lactic acidosis was elevated to 4.2 mmol/L. Sputum AFB smears were repeated and were negative. Although her pulmonary TB showed radiographic improvement on CT compared with earlier imaging, she now presented with neurologic findings.

Head CT revealed a rim-enhancing lesion in the right temporal lobe, measuring 1.6×1.4 cm, with new surrounding vasogenic edema compared with her prior imaging. Seven months prior to the current admission, MRI revealed an 8×6 mm rim-enhancing mass with mild vasogenic edema, raising concern for a neoplasm. A repeat MRI from 5 months prior to the current admission showed the same lesion, but smaller at 0.5×0.4×0.5 cm, with minimal edema, which was interpreted as a slight interval improvement. Subsequent brain MRI in this admission confirmed interval enlargement, now with a bilobed and septated appearance, peripherally enhanced, and increased vasogenic edema (Figure 1). These findings were radiographically interpreted as most concerning for cerebral abscess rather than neoplasm or granulomatous disease.

Considering the radiographic concern for abscess and the patient’s seizure presentation, Neurosurgery recommended operative intervention. The patient underwent right temporal craniotomy with resection of the lesion. Intraoperative cultures, including aerobic, anaerobic, and fungal, demonstrated no growth. Histopathology revealed caseating granulomas and no liquified cavity. The tissue was positive for rare acid-fast organisms on Ziehl-Neelsen staining (Figure 2). Thus, based on histopathologic findings of caseating granuloma with AFB on Ziehl-Neelsen staining, the patient was definitively diagnosed with a right temporal lobe intracranial tuberculoma due to M. tuberculosis.

Management consisted of surgical resection for diagnostic confirmation and seizure control, followed by resumption of anti-tuberculous therapy. Postoperatively, the patient was restarted on isoniazid and rifampin with pyridoxine supplementation, while pyrazinamide and ethambutol were discontinued due to recurrent transaminitis. She also continued to be treated with levetiracetam for seizure prophylaxis. She remained stable throughout her hospitalization, with no recurrent seizures or new neurologic deficits. On postoperative day 10, she was discharged home with close follow-up arranged through the local TB clinic. A chronological summary of the patient’s imaging and management course is presented in Figure 3.

Discussion

Our case demonstrates the persistent difficulty in diagnosis of intracranial tuberculoma, as it can closely mimic pyogenic abscess or neoplasm on imaging, and underscores the importance of early tissue diagnosis when clinical response or treatment adherence is uncertain.

Our patient’s presentation and diagnostic course parallel several previously reported cases of intracranial tuberculoma mimicking alternative intracranial pathologies. In the case reported by McMahon et al, a 10-year-old boy presented with recurrent generalized seizures and a solitary cortical lesion radiographically interpreted as a primary brain tumor, ultimately requiring craniotomy for diagnosis. Similarly, Suslu et al described a 30-year-old woman presenting with new-onset epilepsy and a ring-enhancing occipital lesion strongly suspicious for high-grade glioma, with definitive diagnosis only achieved after surgical excision. In all 3 cases, seizure was the initial manifestation and neuroimaging favored neoplasm or abscess rather than granulomatous disease, underscoring the nonspecific radiographic appearance of tuberculomas in low-incidence settings.

Notably, our case differs in that the patient had known pulmonary tuberculosis with documented interruption of anti-tuberculous therapy due to hepatotoxicity and alcohol use, whereas prior reports involved patients without active systemic TB at presentation. Despite this, diagnostic uncertainty persisted, and imaging progression favored pyogenic abscess, prompting neurosurgical intervention. As in the prior cases, operative cultures were non-diagnostic, and histopathology was required for definitive diagnosis. Our patient’s course highlights the added complexity introduced by treatment nonadherence and functional immunosuppression, reinforcing the importance of maintaining a low threshold for early biopsy when radiographic progression occurs or adherence is questionable, even in patients already diagnosed with tuberculosis.

In low-incidence settings, CNS tuberculosis is uncommon yet diagnostically challenging. Intracranial tuberculomas are rare but often mimic bacterial abscesses and neoplasms on presentation and imaging, delaying diagnosis [6,7]. Although our patient lacked traditional immunocompromising conditions such as human immunodeficiency virus (HIV) or corticosteroid use, her chronic alcohol consumption leading to malnutrition and hepatic dysfunction likely produced functional immune impairment. Chronic alcohol use is known to impair macrophage and T-cell-mediated immunity. These factors together with interruption of RIPE therapy may have facilitated the hematogenous spread of M. tuberculosis to the central nervous system, aligning with prior reports describing CNS involvement in functionally immunocompromised but HIV-negative individuals [8].

This combination of impaired host defense and atypical clinical presentation contributed to the diagnostic uncertainty in our case. Advanced imaging modalities such as diffusion-weighted imaging (DWI) and magnetic resonance spectroscopy (MRS) can aid in differentiating intracranial ring-enhancing lesions. On DWI, pyogenic abscesses typically show marked central restriction whereas tuberculous abscesses and solid tuberculomas exhibit variable or absent restriction. MRS complements this by showing lipid-lactate peaks in tuberculoma, amino acid resonances in abscesses, and high choline with low N-acetylaspartate in neoplasms [9,10].

Her temporal lobe MRI initially resembled an abscess, underscoring how CNS TB can mimic alternative etiologies even in low-burden regions. Negative sputum AFB smears and sterile operative cultures are well-described pitfalls, and reliance on these alone can lead to misclassification [8,11] as was the case in our patient, whose microbiology was negative. The underlying pathogenesis involves hematogenous dissemination of M. tuberculosis to the CNS with subsequent granulomatous inflammation and caseous necrosis, which explains both the mass effect and the radiologic similarity to other intracranial lesions [12]. Advanced MRI techniques, including MR spectroscopy and diffusion-weighted imaging, can provide additional supportive clues but remain insufficient for a definitive diagnosis [13]. Thus, histopathology continues to serve as the diagnostic cornerstone, particularly in cases with inconclusive microbiology [8,11].

Treatment principles are equally nuanced. The standard 4-drug regimen, RIPE, is effective but requires prolonged administration, often for 9–12 months to ensure adequate CNS penetration [14,15]. Corticosteroids are frequently added when significant perilesional edema or mass effect is present, reducing morbidity from inflammation [14]. In patients with hepatotoxicity or alcohol abuse, treatment modification may be required, as illustrated in our patient with alcohol use disorder in whom RIPE therapy had to be held, highlighting the need for individualized management [15]. In patients who do not respond to medical therapy, whether due to drug resistance or nonadherence, surgical intervention to resect the lesion should be considered. It is especially important to maintain a low threshold for deciding to perform a biopsy early in the course when suspicion for tuberculoma is high, particularly in settings of treatment nonadherence, worsening radiologic findings, or lack of clinical improvement, so that resistance, alternative diagnoses, or need for surgery can be identified without delay [6,16].

This case reinforces several lessons. First, CNS tuberculomas can mimic bacterial brain abscesses even in patients without classical immunocompromising conditions in low-incidence settings [7]. Second, negative sputum acid-fast bacilli (AFB) smears and negative cerebrospinal fluid (CSF) or operative cultures do not exclude CNS TB; tissue diagnosis remains decisive [8,11]. Third, when clinical or radiographic response is equivocal, an early biopsy with histopathology should be considered to avoid delays in definitive management [17]. Finally, optimal outcomes depend on prolonged, individualized multidrug therapy and coordinated care among infectious disease, neurosurgery, and public health teams [17].

Conclusions

This case underscores the persistent diagnostic difficulty of CNS tuberculosis. Imaging favored pyogenic abscess and operative cultures were sterile; only histopathology established tuberculoma. Alcohol-related malnutrition, chronic illness, and treatment interruption likely produced functional immune impairment, permitting intracranial progression. In practice, tuberculoma should remain on the differential for ring-enhancing lesions in low-incidence settings. If the clinical or radiographic course is equivocal and treatment interruption cannot be distinguished from resistance, early biopsy (with histopathology, mycobacterial culture, and drug susceptibility testing) should be considered. Management should be individualized with prolonged multidrug therapy, adjunctive corticosteroids for edema when indicated, and surgery for mass effect or diagnostic uncertainty, coordinated among infectious diseases, neurosurgery, and public health teams.