Sunday, July 29, 2007


MR Morphology of Intracranial Tuberculomas

Dr. H. S. Das, Dr. N. Medhi, Dr. B. Saharia, Dr. S. K. Handique


Tuberculomas represent a common neurological disorder in developing countries, forming 12-30% of all intracranial masses – (1,2). Furthermore the incidence of intracranial TB in patients with AIDS is also increasing, the highest incidence recorded being 2.3% - (3,4) in one study to 18% in another – (5). Prompt diagnosis is mandatory since any delay in increased morbidity and mortality. Unfortunately the diagnosis is not always possible on the basis of clinical and epidemiological data, since clinical manifestations are nonspecific – (7,8) and objective evidence of systemic tuberculosis or exposure to the disease may be absent in upto 70% of the cases – (9). The role of CT in diagnosis of CNS tuberculomas in well established, nevertheless CT findings should be interpreted with caution since neoplastic, fungal or parasitic diseases may cause similar changes on CT – (10). Recently Magnetic Resonance (MR) Imaging has shown advantage over CT in the detection of intracranial pathology – (11) and its value in the diagnosis of infections diseases of the central nervous system (CNS) has been reported – (12,13). Although tubercular meningitis can not be differentiated from other meningitides on the basis of MR findings; but intraparenchymal tuberculomas show characteristic T2 shortening not found in most other space occupying lesions – (14). Thus in the appropiate clinical setting tuberculomas should be considered. Here, we report our experience in using MR for the evaluation of patients with intracranial tuberculoma.

Patients and Methods:

10 Patients with intracranial tuberculomas were evaluated with MR in our institution between August ’95 to August’ 99. 8 males and 2 females between 5-45 years (Mean 22.9 years) were included in this study. MRI was performed on a 1-tesla super conductive magnet. Standard spin echo techniques were used to obtain multiplanar T1 and T2 weighted images. Contrast was used in 6 patients. The diagnosis of CNS tuberculosis was made after proper integration of data from the surgical and medical findings. Data included positive biopsy in 2 patients; analysis of blood and CSF (elevation in 2 cases); positive response to anti tubercular drugs in 6 patients and MR findings. Initial CT was done upon admission to the hospital in all ten cases. MR was done to visualize the full extent of the lesion, to differentiate these lesions from other diseases affecting the brain and to delineate the contents (necrotic centre, capsule and surrounding edema). None of the patients tested positive for HIV.


Tuberculomas were supratentorial in 9 patients and infratentorial in 1. All but one patient had single lesions, which were located at the cortico-subcortical junction of the cerebral hemispheres and in the brainstem in 2 patients. 1 patient had a cerebellar tuberculoma. On MR intracranial tuberculoma caused prolongation of the T1 relaxation time which was most marked at the centre of the lesion. 5 patients had lesions hypointense to normal brain; 4 patients had lesions isointense and 1 patient had a mixed signal with hypointensity predominating on T1 weighted images. On the T2 weighted sequences the MR appearance varied. In six patients the centre of the lesion gave hypointense (dark) signal while the periphery gave a hyperintense (bright) signal relative to the brain parenchyma due to surrounding oedema. In 2 patients the centre of the lesion was hyperintense with a hypointense rim surrounded again by diffuse hyperintensity due to edema.

Follow up CT in 6 patients during the course of antituberculous drugs showed reduction in the six of the lesion as well as the oedema as a result of therapy. 2 patients positive biopsy while 2 patients were lost to follow up. Following contrast infusion in 6 patients ring enhancing lesions were observed in 4 patients, disc enhancing lesion size of less than 1 cm, 3 patients had lesion size of more then 2 cms while the lesion size varied between 1-2 cms in the rest of the 6 patients. 2 out of the 10 patients presented with meningitis, which shows diffuse thick meningeal contrast enhancement presumably due to granulation tissue. These 2 patients also had different degrees of hydrocephalus.


Tuberculomas develop in the brain when the initial Rich’s focus does not rupture into the meninges but expands locally within the parenchyma due to greater resistance of host tissues to the infecting organism (5). Meningitis can cause borderline encephalitis resulting in direct infiltration of the brain parenchyma and multiple small tuberculomas which coalesce to form mature tuberculomas – (16).

Tuberculomas have different appearances on T2 weighted images depending on their stage of evolution. At an early stage of formation of tuberculomas, an inflammatory reaction occurs; the mass has an abundance of giant cells and a capsule poor in collagen. At this stage the mass is isointense on T1 and T2 weighted images. At a later stage, the capsule becomes rich in collagen. When small tuberculomas coalesce to become larger lesions they give low signal on T2 weighted images because of fibrosis, scar tissue and free radicals produced by macrophages during active phagocytosis – (17).

22 of the 27 cases (84%) of NCS tuberculoma in the literature clearly showed low signal on T2 weighted images – (8, 18, 19, 20). 5 (16%) had lesions with central high signal thought to represent caseating pathologic examination revealed tuberculoma with dense reactive fibrosis.

In another study out of 97 patients presumed to harbour cerebral tuberculomas (of which 11 were confirmed by biopsy and 73 showed a therapeutic response to AKT) the lesions were either homogenously hypointense or revealed a central hyperintense nidus within the hypointense lesion on T2 weighted images (21).

Based on a histopathological grading of 7 proven tuberculomas, Gupta et al (22) concluded that the signal intensity on T2 weighted images is variable and dependant on the relative proportion of macrophages, cellular infiltrates and fibrosis. Granulomas, which were frankly hyperintense on T2 weighted images, exhibited increased cellular infiltrates, scantly macrophages and little fibrosis; while the hypointense lesions showed grater numbers of macrophages; more fibrosis and gliosis – (22). Large amounts of lipids were reported to contribute to the T2 shortening in 2 of the granulomas analysed by localized proton spectroscopy – (22). MR is of value to visualize the full extent of the lesion, in differentiation of the lesion with other diseases of the CNS (e.g. fungal granuloma, haemorrhagic metastases and “granulo-nodular” stage of neurocysticercosis) and to delineate the different components of the lesion (necrotic center, capsule and surrounding oedema), which is not always possible with CT.

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