August 2026

CASE HISTORY

• 53 year old female came with complaints of imbalance while standing and walking since 2 months. Patient was anaemic. No other co-morbidities. No significant past history.

• Patient underwent MRI brain imaging followed by whole body FDG PET-CT study.

Authors

1. Dr Shilali M S, Department of Radiology, Manipal Hospitals, Kanakapura Road, Bangalore.

2. Dr Lakshmikanth G N , Consultant, Department of Radiology, Manipal hospitals, Kanakapura Road, Bangalore.

3. Dr Chaitra P Adiga, Consultant, Department of Radiology, Manipal hospitals, Kanakapura Road, Bangalore.

4. Dr Yashwanth A N, Consultant, Department of Radiology, Manipal hospitals, Kanakapura Road, Bangalore.

5. Dr Sharath Kumar GG, HOD and Senior Consultant, Department of Radiology, Manipal Hospitals, Kanakapura Road, Bangalore.

DESCRIPTION

A & B – T2 and FLAIR axial images showing a well defined intra-axial heterogeneous and iso-hypointense lesion in the right high frontal lobe( mid cingulate gyrus ) with adjacent vasogenic edema.

C & D –  DWI and ADC images showing no restricted diffusion.

E – Post contrast T1 images showing irregular rind of peripheral enhancement with central non enhancing necrotic areas.  Mild enhancement of adjacent falx cerebri was also noted.

F : SWI images showing no areas of blooming.

G : Arterial spin labelling study showing no areas of hyper perfusion in the lesion or surrounding brain parenchyma

H : MR spectroscopy showing raised choline peak with raised choline to creatinine ratio. Lipid –lactate peak noted.

DESCRIPTION : 18F FDG PET-CT study

I – A tracer avid peripherally enhancing centrally necrotic mass lesion in the right high frontal lobe (mid cingulate gyrus) and adjacent vasogenic edema.

J – Tracer avid irregular enhancing circumferential wall thickening seen involving the hepatic flexure and proximal transverse colon.

K – Low grade tracer avid lesion in spleen. 

L – Tracer avid lesion in the anterior cortex of the interpolar region of the left kidney.

M : Multiple tracer avid enlarged bilateral common iliac lymph nodes.

Final diagnosis: Disseminated Tuberculosis with cerebral tuberculoma

TUBERCULOMA –THE GREAT MASQUERADER

Discussion:  

Background: Cerebral tuberculomas are granulomatous mass lesions resulting from hematogenous dissemination of Mycobacterium tuberculosis. On neuroimaging, tuberculomas can closely mimic primary or secondary intracranial neoplasms, particularly when presenting as solitary ring-enhancing lesions with surrounding vasogenic edema. Disseminated tuberculosis involving multiple organ systems may further complicate diagnosis by simulating metastatic malignancy on cross-sectional and metabolic imaging.

Key differentiating features

Imaging ParameterTuberculomaMetastasis
T2 signalOften T2 hypointense (caseating granuloma)Usually T2 hyperintense necrotic center
Lesion morphologyConglomerate lesions commonDiscrete lesions common
Meningeal enhancementRelatively commonUncommon
DWIVariableUsually no central restriction
Perfusion (rCBV)LowIncreased
MR spectroscopyProminent lipid-lactate peak; lower Cho/Cr compared to aggressive tumorsMarkedly elevated choline; higher Cho/Cr
3.8 ppm peak on MRSMay be presentRare
PET uptakeCan be intensely avidOften avid
Ancillary findingsTB elsewhere, meningitis, tuberculomasKnown systemic malignancy

In our case, the combination of a solitary necrotic ring-enhancing cerebral lesion with extensive perilesional edema and multiple FDG-avid extracranial lesions initially suggested metastatic disease. However, several features favoured tuberculosis, including absence of hyperperfusion on ASL, a prominent lipid–lactate peak on MR spectroscopy, lack of intralesional haemorrhage, mild adjacent falcine enhancement, and multisystem FDG-avid involvement compatible with disseminated tuberculosis. Histopathology ultimately confirmed the diagnosis.

Teaching point :

In endemic regions, a ring-enhancing lesion demonstrating low perfusion, T2 hypointense caseating components, and a dominant lipid-lactate peak should strongly raise suspicion for cerebral tuberculoma, even in the presence of multifocal FDG-avid systemic lesions suggestive of metastatic disease.

REFERENCES

• Koesbandono, Muljadi R, Sutanto R, et al. Intracranial tuberculomas: review of MRI findings and clinical features. Clinical Radiology. 2024;79(5):354-362. A recent comprehensive review of MRI characteristics of intracranial tuberculomas.

• Sankhe S, Baheti A, Ihare A, et al. Perfusion Magnetic Resonance Imaging Characteristics of Intracerebral Tuberculomas and Its Role in Differentiating Tuberculomas from Metastases. Acta Radiologica. 2013;54:307-312. Demonstrated significantly lower perfusion parameters in tuberculomas compared with metastases.

• Morales H, Alfaro D, Martinot C, et al. MR spectroscopy of intracranial tuberculomas: A singlet peak at 3.8 ppm as potential marker to differentiate them from malignant tumors. Neuroradiology Journal. 2015;28:294-302. Showed lower Cho/Cr ratios and a characteristic 3.8-ppm peak in tuberculomas compared with malignant tumors.

• Kumar V, Chawla S, Shah J, et al. Differentiation of tubercular infection and metastasis presenting as ring-enhancing lesions by diffusion and perfusion MRI. Journal of Neuroradiology. 2010;37:167-171. Demonstrated the value of combining diffusion and perfusion imaging in differentiating tuberculomas from metastases.

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