The many faces of intracranial tuberculosis: atypical presentations on MRI—a descriptive observational cohort study
Egyptian Journal of Radiology and Nuclear Medicine volume 54, Article number: 116 (2023)
Atypical MRI findings of cranial tuberculosis can lead to prolonged delay in diagnosis resulting in high costs to evaluate for alternative diagnoses. The aim of this study was to describe a series of cranial tuberculosis patients with spectrum of MRI features, other than hydrocephalus, parenchymal tuberculomas, and leptomeningeal thickening. The final diagnosis was made based on CSF findings, clinical findings, and/or marked improvement after antitubercular treatment.
A total of 39 patients met the inclusion criteria and were diagnosed with vasculitis (n = 15), tubercular abscess (n = 5), miliary tuberculosis (n = 3), tubercular cerebritis (n = 9), sellar and parasellar tuberculosis (n = 7), mass forming tuberculosis (n = 1), choroid plexitis (n = 2), and intraventricular tuberculomas (n = 1).
A significant number of patients of cranial tuberculosis can have variable presentations and may be misdiagnosed. This analysis helps to reinvestigate the spectrum of MRI findings.
Central nervous system (CNS) involvement is one of the most disastrous manifestations of tuberculosis (TB), seen in 5–10% of extra-pulmonary TB cases . It carries a high mortality and neurological morbidity. Imaging, especially MRI, can frequently provide a considerable diagnostic clue for a definitive diagnosis of cranial tuberculosis. In conjunction with CSF analysis and clinical findings, imaging findings aid in the diagnosis of cranial tuberculosis without a biopsy.
Cranial tuberculosis in its typical form presents as tubercular meningitis (TBM), hydrocephalus, or focal tuberculoma on MRI . Meningeal thickening of basal subarachnoid cisterns and abnormal leptomeningeal enhancement along the cerebral hemispheres, sylvian fissures, or the tentorium are the most common findings suggestive of TBM . Hydrocephalus encountered in TBM is usually of the communicating type caused due to blockage of CSF resorption by inflammatory exudates in the basal subarachnoidal cisterns . Occasionally, the hydrocephalus can be of the obstructive type, secondary to narrowing of the aqueduct or a ventricle by a focal parenchymal lesion and mass effect or due to entrapment of a ventricle by granulomatous ependymitis . Tuberculomas are frequent manifestations of brain tuberculosis, presenting as either homogenously enhancing nodules (non-caseous granuloma) or ring-enhancing lesions (caseating granuloma) .
Although most cases of cranial tuberculosis can be confidently diagnosed based on the typical imaging findings, a small number of cases present a diagnostic challenge that can result in a delay in diagnosis or misdiagnosis. The purpose of this study is to evaluate and describe the constellation of atypical MRI features of cranial tuberculosis.
This was a prospective, observational, cohort study carried out for two years in a university-based tertiary care hospital. The study was approved by the Institute's ethical committee at the outset, and an informed consent was obtained from each patient/legal guardian.
We included the patients with a diagnosed case of TB based on one or more of following positive test results: (a) CSF culture, CSF ADA > 10 U/L, CSF PCR, CSF study (cellularity, protein, glucose, chloride) consistent with tubercular etiology, (b) patients showing definite clinical and radiological improvements after antitubercular treatment (ATT).
MR imaging and interpretation
MRI was done on a 1.5 T superconducting magnet (Magnetom Avanto, Siemens medical system, Erlangen-Germany). The routine sequences acquired were T1 axial, T2 axial, T2 sagittal and coronal, T2 FLAIR axial, diffusion-weighted images (DWI), T1 Post-Gadolinium Turbo Spin Echo sequences. Additional MR techniques were also obtained according to findings, as and when required. Magnetization transfer sequence was obtained in a suspected tubercular abscess which involved an addition of saturation pulse immediately before the 90-degree radiofrequency pulse to saturate the magnetization of protons with restricted motion. MR images were interpreted by two radiologists in tandem with 9 years and 17 years of experience, respectively. We excluded the patients who had only. hydrocephalus, leptomeningitis, basal-enhancing exudates, and parenchymal tuberculomas. In cases of vasculitis, the distribution of infarcts was analyzed in details and an attempt was made to classify the infarcts into “TB zone” and “ischemic zone” originally described by Hsieh et al. . The ischemic zone supplied by lateral striate, anterior choroidal, and thalamo-geniculate arteries consists of lentiform neucleus, posteriorlimb of internal capsule, and thalami, whereas TB zone supplied by medial striate and thalamo-perforating arteries consists of caudate and anterior limb of internal capsule. Lesions involving sellar and parasellar regions were evaluated based on the involvement of pituitary and other structures, enhancement pattern and mass effect. Ring-enhancing lesions were evaluated for the presence of diffusion restriction at the center of the lesion to identify tubercular abscess. MR spectroscopy carried out for distinguishing these lesions from pyogenic abscesses using image-guided, single-voxel, point-resolved MR spectroscopy (PRESS; repetition time [TR] 1500 ms and echo time [TE] 35 ms and 135 ms) was used. The presence of lipid/lactate peak at 1.3 ppm and the absence of an amino acid peak at 0.9 ppm were suggestive of the tubercular lesion.
A total of 39patients of cranial tuberculosis were included in the study with a mean age of 28 years. The most common age group in the present study was 21–30 years. Female predominance was noted with male: female ratio of 17:23. The clinical features, coexisting tubercular involvement of other sites, other coexisting illnesses, results of laboratory investigations are summarized in Table 1. CSF evaluation and sputum culture were done in all the patients while PCR was performed in 24 patients. The diagnosis was confirmed in 60% cases (n = 24) and was probable in the rest of the cases (n = 15). Fever was the most common presenting complaint, followed by headache and altered sensorium. Pulmonary tuberculosis was present in 43% of our patients and abdominal tuberculosis in 20% cases, whereas Potts's spine was coexistent in 25% cases. Seven out of 39 were positive for HIV. Based on the MRI appearances, our cohort presented with following findings: vasculitis (n = 15), tubercular abscess (n = 5), miliary tuberculosis (n = 3), tubercular cerebritis (n = 9), sellar and parasellar tuberculosis (n = 7), mass forming tuberculosis (n = 1), choroid plexitis (n = 2), and intraventricular tuberculomas (n = 1).
A total of 15 patients in our study showed evidence of vasculitis predominantly in the form of vasculitic infarcts. Basal ganglia, internal capsule, and thalamus were the most common sites of involvement (Fig. 1). All of the 15 patients with features of vasculitis showed involvement of either or all these three sites. 20% of the cases showed involvement confined exclusively to the ischemic zone, whereas the majority (80%) showed the involvement of both ischemic and TB zones. One of the patients showed hemorrhagic foci as well as infarct (Fig. 1). The infarcts mainly involved the lateral lenticulostriate arteries (7/15), medial lenticulostriate arteries (5/15), perforators from the posterior cerebral artery (5/15) & terminal perforators from basilar arteries (6/15) with 1 case each of involvement of superior cerebellar and anterior inferior cerebellar artery territories.
Sellar/Parasellar region tuberculosis
A total of 7 patients in the present study showed tuberculosis of the sellar & parasellar region in forms other than basal exudates found commonly in the related region. Of these 7 cases, 3 showed involvement of pituitary, whereas 4 were supra or intrasellar tuberculomas without the involvement of pituitary. Table 2 summarizes the sellar involvement of tuberculosis in our study (Figs. 2 and 3).
Five cases of the tubercular abscess were found in our study. Table 3 shows the imaging features found in 5 cases of tubercular abscess. Three cases presented as lesions showing T1 hypointensity and T2 hyperintensity with peripheral T2 hypointense rim showing ring enhancement (Figs. 4 and 5). Mass effect and perilesional vasogenic edema were present in all these cases. Two cases presented with multiple lesions. On conventional MR imaging, they were thin-walled showing peripheral ring enhancement. All the lesions showed central diffusion restriction with low ADC value and lipid, lactate peaks, and absence of amino acid peak characteristic of TB. Magnetization transfer pre-contrast T1-weighted sequences showed a strongly hyperintense rim in these lesions.
In our study, 9 cases were affected by tubercular cerebritis (Table 4). Out of these, 6 cases also showed adjacent meningeal thickening. We found an ill-defined area of T1 iso-hypointensity and T2 hyperintensity with patchy enhancement in 1 case, and a gyral enhancement pattern was seen in 8 out of 9 cases. These lesions also showed restriction on DWI in all of the cases. Two of the cases also showed a “tree in bud” appearance similar to that obtained in pulmonary tuberculosis (Figs. 6 and 7).
Choroid plexitis and intraventricular tuberculoma
Primary involvement of the choroid plexus was the sole finding in 2 cases without any obvious evidence of secondary involvement of ventricular system/choroid plexus from adjacent parenchymal tubercular focus. First case (28 years male) who presented with headache and mild fever had left-sided involvement while 2nd case who (27 years male) presented with fever, neck rigidity, altered sensorium, and vomiting showed right-sided choroid plexitis. In both cases, there was a strongly enhancing lesion involving the choroid plexus with sequestration of the temporal horn of the ipsilateral lateral ventricle and asymmetrical hydrocephalus (Fig. 8a–c).
One of our cases presented with intraventricular tuberculoma involving septum pellucidum (Fig. 8d). The lesion did not abut the ependymal lining and there was no associated evidence of ventriculitis.
Three patients in our study showed evidence of miliary tuberculosis. The lesions in the present study measured approximately 2–4 mm in diameter (Fig. 9). The lesions exhibited nodular enhancement on T1-weighted images after gadolinium injection. Most were located at the corticomedullary junction. Clinically two of the patients exhibited mild clinical manifestations without typical systemic signs of TB infection. Only one of our 3 patients showed a disturbance of consciousness who exhibited the nodules close to the meningeal surface and concomitant meningeal thickening.
One case of focal pachymeningeal mass-like thickening was included in this study who presented with a strongly enhancing meningeal mass in the left parietal region similar to meningioma (Fig. 10). Dural tail was present and there was secondary involvement and mild edema in the adjoining parietal lobe.
One of the 23-year-old male patients showed a strongly enhancing mass lesion in the right insular region with gross surrounding edema and mass effect (Fig. 11). The lesion showed restricted diffusion on DWI and MRS was inconclusive. The patient had coexisting miliary pulmonary tuberculosis as well as Pott’s spine.
Our study describes the extremely variable appearance of cranial tuberculosis on MRI with vasculitis, abscess, miliary tuberculosis, tubercular cerebritis, sellar and parasellar tuberculosis, tubercular encephalopathy, mass-forming tuberculosis, choroid plexitis and intraventricular tuberculomas. Although vasculitis is a known feature of tuberculosis, we have included vasculitis in our analysis to identify the pattern and distribution of involvement. The number of patients in our study suggests that these atypical forms are rare and are probably considerably under-reported. Despite their rarity, identification of clues to correctly diagnose them is critical, and based on our study we have developed a basic algorithm to diagnose atypical cases of cranial tuberculosis (Fig. 12).
The presence of vasculitic infarcts in association with tubercular meningitis is a major factor contributing to residual neurological deficits or death. Early identification of cerebral infarcts in TBM can lead to early administration of aspirin, corticosteroid, and reduced morbidity . It should be noted that even if there is no evidence of stroke on initial imaging, age > 25 years, cranial nerve involvement, sylvian fissure exudates, posterior fossa exudates, optic chiasmal exudates on the initial scan can act as predictors of subsequent stroke . Furthermore, serial brain scans to monitor for worsening or new infarcts or vasospasm are also recommended. Vasculitis in TBM is initiated by direct invasion of the vessel wall by mycobacteria or may result from secondary extension of adjacent arachnoiditis. Also, the exudates at the basal region surround the arteries, leading to arterial narrowing or reactive vasospasm and subsequently stroke [10, 11].
Similar to various previous studies, the most common sites of infarcts were in the basal ganglia, thalami, and internal capsules [8, 11, 12]. Distribution of the vasculitic infarcts in our study was not confined to “TB zone” described by Hsieh et al., and majority of strokes were distributed in combined ischemic (supplied by lateral striate, anterior choroidal, and thalamo-geniculate arteries) and TB zones (supplied by medial striate and thalamo-perforating arteries) . Infarcts from total occlusion of major intracranial arteries were not seen among our patients, and various combinations of involvement of perforators and the terminal cortical branches were demonstrated in all cases.
Sellar tuberculosis is extremely rare and when seen presents a diagnostic dilemma to the interpreting radiologists as it can mimic sellar neoplasms, especially pituitary macroadenoma, both radiologically and clinically. The correct diagnosis can be only obtained after surgical excision and histopathological evaluation which shows necrotizing granulomatous inflammation. Acid-fast bacilli (AFB) are rarely demonstrated which makes it difficult to distinguish from sarcoidosis or fungal infection . Variable involvement of pituitary gland, stalk, sellar-suprasellar cisternal space was noted in our series with headache being the only symptom in the majority. Sharma et al. who reported 18 cases have described the largest series of sellar tuberculosis . Rarely, tuberculoma in the pituitary gland can transform into pituitary abscess or can lead to pituitary apoplexy .
Tubercular abscesses are similar to tuberculomas on conventional T1W and T2W MR sequences presenting as ring-enhancing lesions. Unlike tuberculomas, the wall of abscesses lacks the granulomatous reaction and is visible as a low signal rim on T2-weighted images. The center contains semiliquid pus that is filled with tubercular bacilli which are visible as strongly T2 hyperintense contents that are not suppressed on FLAIR and show diffusion restriction. Tubercular granuloma contains only a few bacilli and majority show no diffusion restriction, although rarely tuberculomas can also restrict. Few studies suggest size > 2 cm to be suggestive of abscess; however, in our study we encountered smaller multiple abscesses. Recognition of abscess is important in the setting of cranial tuberculosis because it has a more accelerated clinical course than tuberculomas and may require surgical drainage along with antitubercular treatment. The differential diagnosis of a tubercular abscess is pyogenic and fungal abscesses. Important MR features that distinguish tubercular abscesses from pyogenic and fungal abscesses are listed in Table 5 [16,17,18,19]. Magnetization transfer T1 (MT-T1) images can also be used to distinguish tuberculoma from tubercular abscess. In tubercular abscess, the hypointense peripheral T2 rim shows hyperintensity on MT T1, whereas, in tuberculomas, the T2 hypointensity is surrounded by a hyperintense rim on MT-T1, and that layer is not otherwise visible on T2-weighted images as this layer merges with edema .
Tubercular cerebritis is a unique entity which is characterized by extensive inflammatory exudates, Langerhans’ giant cells, reactive parenchymal changes, and caseating and noncaseating microgranulomas in the cortex. On MR images, it is seen as an area of gyriform post-contrast enhancement and corresponding hyperintensity on T2WI/FLAIR. In our study, we got 9 cases affected by tuberculous cerebritis with gyriform enhancement similar to previous studies . Besides in two cases, both in the posterior fossa showed tree in bud pattern of enhancement with clusters of microgranulomas (buds) attached to the enhancing gyrus (tree). The location of cerebritis of tubercular etiology is predominantly cerebral and cerebellar cortex in contrast with pyogenic cerebritis which involves the white matter and fungal cerebritis which involves basal ganglia and centrum semiovale .
Disseminated miliary brain tuberculosis is characterized by numerous small (2–3 mm) nodules in the brain, which consists of caseating or non-caseating granulomas. On MRI, they show ring or nodular enhancement with a variable degree of adjacent edema. The imaging differentials are neurocysticercosis, metastasis, or fungal infection. Studies have shown that similar to miliary pulmonary TB, this imaging pattern results due to hematogenous spread from a preexisting primary focus [22, 23]. This type of brain tuberculosis exhibits a relatively mild clinical presentation without typical systemic signs of infection. Small lesions close to the ventricular ependymal wall or surface of the brain are prone to rupture causing severe TBM as seen in 1 of our patients .
Rarely meningeal tuberculosis present as a predominantly dural-based mass-like lesion with secondary pial or parenchymal involvement also termed as en-plaque tuberculoma . Both focal and diffuse forms exist. This entity is distinct from the inflammation in the dura mater adjacent to an intraparenchymal tuberculoma. These can present as isolated dural-based lesions or multiple lesions in which parenchymal involvement is caused by the dural inflammation. Isolated or focal lesions can mimic meningioma while diffuse pachymeningeal involvement can be similar to that in lymphoma, sarcoidosis, intracranial hypotension, Wegener's granulomatosis, or idiopathic hypertrophic pachymeningitis [23,24,25].
Tubercular choroid plexitis and intraventricular tuberculoma
The involvement of primarily choroid plexus was the sole finding in the present series of 2 cases who exhibited asymmetrically thickened enhancing choroid plexus with temporal lobe sequestration and dilatation similar to previously described cases [26, 27]. Choroid plexitis is thought to spread from the adjacent subependymal inflammatory focus of Rich, which eventually ruptures into the ventricle [26, 27]. The diagnostic differential may include choroid plexus papilloma; however, the hydrocephalus in papilloma is usually symmetrical on both sides with enlargement of the entire ventricular system.
Berthier et al. reported four cases of large intraventricular tuberculoma in children. Of these, three cases had tuberculoma in the frontal horn attached to the ependyma and the septum pellucidum and one had a thalamic tuberculoma extending into the ventricular body . Besides two cases of choroid plexitis, we also came across a case of intraventricular peripherally enhancing tuberculoma centered at septum pellucidum.
A study by Algahtani et al. described a series of 9 cases of intra-axial tuberculosis whose clinical features and MRI suggested intra-axial tumors . The study concluded that young age, history of tubercular contact, and presence of extracranial tuberculosis should suggest a non-neoplastic diagnosis in the space-occupying lesion. Ripamonti et al. reported 5 patients with a mass of tubercular origin in the brain . The masses were markedly hypointense on T2-weighted images and showed strong post-contrast enhancement with few cases also revealing adjacent meningeal thickening and enhancement similar to our case. Radiological differentials are metastatic or primary intraaxial tumors such as glial tumors or lymphoma. A recent study has assessed the utility of MR perfusion study to distinguish between intracranial tubercular lesions and neoplastic lesions  and reported that tuberculomas/conglomerated tubercular lesions showed hypoperfused centers (rCBV 0.42 ± 0.25) and hyperperfused walls (rCBV 2.04 ± 0.61) while the rCBV of metastasis was significantly higher (5.43 ± 2.1). A cutoff value of ≥ 3.745 for peripheral wall rCBV was suggested for differentiating ring-enhancing metastases from ring-enhancing tuberculomas.
Figure 11 summarizes the variable presentation and imaging manifestations of cranial tuberculosis according to the location. Within the parenchyma, tuberculoma and vasculitic infracts are the most common presentation while cerebritis (gyriform cortical enhancement), abscess (diffusion restriction), and mass-like conglomerated granuloma. Tubercular encephalopathy (TBE) is an extremely rare form of tuberculosis caused due to delayed type IV hypersensitivity due to cell-mediated immunity to tuberculin protein [32, 33]. Only few reported cases have showed pathological and radiological similarity to acute disseminated encephalomyelitis with bilateral white matter disease . Previous studies have identified a TBE in a 16-year-old girl with pulmonary TB who developed paraparesis and subsequent death 4 days after initiation of ATT for pulmonary tuberculosis, and post-mortem autopsy showed extensive demyelination of the brain . Another case reported in the literature was a 45 year-old man with HIV infection and miliary TB  who developed a rapidly fatal hemorrhagic white matter disease. Varied presentation of extraaxial tuberculosis can occur in form of leptomeningtis, focal or diffuse pachymeningitis, epidural or subdural empyema, or calvarial lesions. Our study also demonstrates the spectrum of sellar-suprasellar manifestations of TB. Ventricles can be affected in form of hydrocephalus, choroid plexitis, or intraventricular tuberculoma.
Our study has a few limitations. Firstly, this is a descriptive study and the findings may not be necessarily extrapolated to other populations. Secondly, the diagnosis in all cases could not be confirmed by the lab investigations and surgical biopsy in all cases and was presumptive in few cases based on the presence of evidence of coexisting cranial or extracranial tuberculosis. Thirdly, the number of cases included in our study is relatively small.
In conclusion, a significant number of patients of cranial tuberculosis can have atypical and misleading imaging manifestations. Our study highlights the variable and atypical imaging appearances of tubercular involvement of the brain. Familiarity with unusual presentations and their imaging findings is critical in ensuring prompt, accurate diagnosis, and treatment.
Availability of data and materials
The datasets analyzed during the current study are available with the corresponding author.
Magnetic resonance imaging
Acute disseminated encephalomyelitis
Human immunodeficiency virus
Magnetic resonance spectroscopy
Cherian A, Thomas SV (2011) Central nervous system tuberculosis. Afr Health Sci 11(1):116–127
Javaud N, CertalRda S, Stirnemann J et al (2011) Tuberculous cerebral vasculitis: retrospective study of 10 cases. Eur J Intern Med 22(6):e99-104
Gupta RK, Gupta S, Singh D et al (1994) MR imaging and angiography in tuberculous meningitis. Neuroradiology 36(2):87–92
Raut T, Garg RK, Jain A, Verma R, Singh MK, Malhotra HS, Kohli N, Parihar A (2013) Hydrocephalus in tuberculous meningitis: Incidence, its predictive factors and impact on the prognosis. J Infect 66(4):330–337
Dastur DK, Manghani DK, Udani PM (1995) Pathology and pathogenetic mechanisms in neurotuberculosis. Radiol Clin North Am 33(4):733–752
Khatri GD, Krishnan V, Antil N, Saigal G (2018) Magnetic resonance imaging spectrum of intracranial tubercular lesions: one disease, many faces. Pol J Radiol 83:e524–e535
Hsieh FY, Chia LG, Shen WC (1992) Locations of cerebral infarctions in tuberculous meningitis. Neuroradiology 34:197–199
Misra UK, Kalita J, Maurya PK (2011) Stroke in tuberculous meningitis. J Neurol Sci 303:22–30
Kalita J, Misra UK, Nair PP (2009) Predictors of stroke and its significance in the outcome of tuberculous meningitis. J Stroke Cerebrovasc Dis 18(4):251–258
Hosoğlu S, Ayaz C, Geyik MF, Kökoğlu OF, Ceviz A (1998) Tuberculous meningitis in adults: an eleven-year review. Int J Tuberc Lung Dis 2(7):553–557
Chan KH, Cheung RT, Lee R, Mak W, Ho SL (2005) Cerebral infarcts complicating tuberculous meningitis. Cerebrovasc Dis 19:391–395
Andronikou S, Wilmshurst J, Hatherill M, Vantoorn R (2006) Distribution of brain infarction in children with tuberculous meningitis and correlation with outcome score at 6 months. Pediatr Radiol 36:1289–1294
Majumdar K, Barnard M, Ramachandra S, Berovic M, Powell M (2014) Tuberculosis in the pituitary fossa: a common pathology in an uncommon site. Endocrinol Diabetes Metab Case Rep 2014:14–0091
Sharma MC, Arora R, Mahapatra AK, Sarat-Chandra P, Gaikwad SB, Sarkar C (2000) Intrasellar tuberculomas–an enigmatic pituitary infection: a series of 18 cases. Clin Neurol Neurosurg 2000(10):272–277
Arunkumar MJ, Rajshekhar V (2001) Intrasellar tuberculoma presenting as pituitary apoplexy. Neurol India 49:407
Whiteman M, Espinoza L, Post MJ, Bell MD, Falcone S (1995) Central nervous system tuberculosis in HIV-infected patients: clinical and radiographic findings. Am J Neuroradiol 16(6):1319–1327
Luthra G, Parihar A, Nath K et al (2007) Comparative evaluation of fungal, tubercular, and pyogenic brain abscesses with conventional and diffusion MR imaging and proton MR spectroscopy. AJNR Am J Neuroradiol 28(7):1332–1338
Parry AH, Wani AH, Shaheen FA, Wani AA, Feroz I, Ilyas M (2018) Evaluation of intracranial tuberculomas using diffusion-weighted imaging (DWI), magnetic resonance spectroscopy (MRS) and susceptibility weighted imaging (SWI). Br J Radiol 91(1091):20180342
Gupta RK, Vatsal DK, Husain N et al (2001) Differentiation of tuberculous from pyogenic brain abscesses with in vivo proton MR spectroscopy and magnetization transfer MR Imaging. AJNR Am J Neuroradiol 22:1503–1509
Jenkins JR (1988) Focal tuberculous cerebritis. AJNR Am J Neuroradiol 9:121–124
Whiteman M, Espinoza L, Post MJ, Bell MD, Falcone S (1995) Central nervous system tuberculosis in HIV-infected patients: clinical and radiographic findings. AJNR Am J Neuroradiol 16:1319–1327
Garg RK (1999) Tuberculosis of the central nervous system. Postgrad Med J 75(881):133–140
Donald PR, Schaaf HS, Schoeman JF (2005) Tuberculous meningitis and miliary tuberculosis: the rich focus revisited. J Infect 50(3):193–195
Goyal M, Sharma A, Mishra NK, Gaikwad SB, Sharma MC (1997) Imaging appearance of pachymeningeal tuberculosis. AJR Am J Roentgenol 169(5):1421–1424
Fonseka CL, Kanakkahewa TE, Singhapura SDAL et al (2018) Tuberculous pachymeningitis presenting as a diffused dural thickening in a patient with chronic headache and recurrent neurological abnormalities for more than a decade: a case report and a review of the literature. Case Rep Infect Dis 2018:3012034
Bhattacharyya A, Boruah DK, Handique A et al (2010) Involvement of the choroid plexus in neurotuberculosis: MR findings in six cases. Neuroradiol J 23(5):590–595
Sadashiva N, Nandeesh BN, Shukla D, Devi BI (2017) Choroid plexus tuberculoma. Diagnosis, management and role of endoscopy. Neurosciences (Riyadh) 22(3):216–219. https://doi.org/10.17712/nsj.2017.3.20160465
Berthier M, Sierra J, Leiguarda R (1987) Intraventricular tuberculoma: report of four cases in children. Neuroradiology 29:163–167
Algahtani HA et al (2013) Tumour-like presentation of central nervous system tuberculosis: a retrospective study in Kingdom of Saudi ArabiaQ1. J Taibah Univ Med Sci 9:143–150
Ripamonti D, Barbo R, Rizzi M et al (2004) New times for an old disease: intracranial mass lesions caused by Mycobacterium tuberculosis in 5 HIV-negative African immigrants. Clin Infect Dis 39(5):e35–e45
Sankhe S, Baheti A, Ihare A, Mathur S, Dabhade P, Sarode A (2013) Perfusion magnetic resonance imaging characteristics of intracerebral tuberculomas and its role in differentiating tuberculomas from metastases. Acta Radiol 54(3):307–312
Dastur DK, Udani PM (1966) The pathology and pathogenesis of tuberculous encephalopathy. Acta Neuropathol 6(4):311–326
Udani PM, Dastur DK (1970) Tuberculous encephalopathy with and without meningitis. Clinical features and pathological correlations. J Neurol Sci 10(6):541–561
Lammie GA, Hewlett RH, Schoeman JF, Donald PR (2007) Tuberculous encephalopathy: a reappraisal. Acta Neuropathol 113(3):227–234
Char G, Morgan OS (2000) Tuberculous encephalopathy. A rare complication of pulmonary tuberculosis. West Indian Med J 49(1):70–72
Chetty KG, Kim RC, Mhutte CK (1997) Acute hemorrhagic leukoencephalitis during treatment for disseminated tuberculosis in a patient with AIDS. Int J Tuberc Lung Dis 1:579–581
The authors wish to acknowledge the contribution of the MRI technologist, Mrs Raichel Luyees in this study.
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The study was approved by the Institutional ethical committee of Institute of Medical Sciences, Banaras Hindu University. Written informed consent to participate in the study was obtained from all the patients/legal guardians included in the study.
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Kumar, I., Shekhar, S., Yadav, T. et al. The many faces of intracranial tuberculosis: atypical presentations on MRI—a descriptive observational cohort study. Egypt J Radiol Nucl Med 54, 116 (2023). https://doi.org/10.1186/s43055-023-01061-6
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