isnr1

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.

Picture 1

July 2026

CASE HISTORY

Patient of relapsed Early T cell precursor Acute lymphoblastic leukemia ( BM + testis) . He underwent Matched unrelated donor hematopoietic stem cell transplantation. He relapsed in CNS 3 months post transplant and is on weekly triple IT for CNS relapse. Now presented with altered sensorium and slurring of speach.

Section Editors

Dr. Arpita Sahu, Dr. Sarbesh Tiwari, Dr. Sabha Ahmed,

Dr. Smily Sharma, Dr. Meena Nedunchelian

Authors

Dr Prakhyath Gmabhira D

DNB resident, KMCH, Coimbatore.

Dr Kannan G,

Consultant, KMCH, Coimbatore

Evaluation

Sepsis workup, cerebrospinal fluid analysis, and serum electrolytes were normal, prompting evaluation for structural cause.

CT BRAIN:

Bilateral confluent subcortical white matter hypodensities (left > right), involving fronto-parietal and temporal regions, with extension into the corpus callosum, associated with mild mass effect.

Diffuse infiltrative FLAIR hyperintense signal abnormalities involving:
 o Bilateral fronto-parietal subcortical white matter (L > R)
 o Anterior temporal subcortical white matter (L > R)
 o Left lentiform nucleus and external capsule
 o Periventricular white matter (trigone region)
 o Bilateral basifrontal regions (L > R)

T2-weighted linear hypointense areas noted within the lesions.

Patchy areas of diffusion restriction with associated blooming on SWI in the left frontal white matter.

Heterogeneous post-contrast enhancement involving the affected area are seen.

Significant reducedin cerebral blood volume (CBV) on perfusion imaging.

Imaging Differentials:

Angioinvasive fungal infection, likely invasive cerebral aspergillosis.

Other differentials- 1.leukemic infiltrates  2. PML

Diagnosis

High levels of Glactomannan in Bronchoalveolar lavage confirms Angio invasive cerebral aspergilosis

TREATMENT STARTED- INJECTION VARICONOZOLE.

After 1 week- SENSORIUM AND SPEECH IMPROVED.

ADVISE- CONTINUE ANTIFUNGAL.

Continued on voriconazole for 2 weeks and came for follow-up

Interval increase in the patchy areas of diffusion restriction with peripheral SWI blooming are seen in left frontal lobe

Peripheral  enhancement are seen in left frontal lobe corresponding to areas of involvement, – likley evolving abscess.  MRS shows a prominent lipid-lactate peak.

FURTHER TREATMENT

Left frontotemporal craniotomy & excision biopsy done. Antifungal treatment continued.

CONCLUSION:

FeatureAngioinvasive AspergillosisCNS Leukemic InfiltratesProgressive Multifocal Leukoencephalopathy
PathophysiologyAngioinvasion causing vessel occlusion, infarction, and hemorrhage.CNS relapse with proliferation of leukemic blasts.JC virus opportunistic infection destroying oligodendrocytes (demyelination).
Primary LocationCorticomedullary junction, basal ganglia, thalami.Leptomeninges, cranial nerves, parenchyma.Asymmetric subcortical white matter (involves U-fibers).
Hemorrhage (SWI/T2)*Prominent. Blooming artifact due to micro/macro-hemorrhages.Typically absent.Absent.
Diffusion (DWI/ADC)Central restriction (due to ischemic/necrotic core).Variable restriction (due to hypercellularity of blasts).Usually absent (faint restriction possible at active advancing edge).
Enhancement (T1 C+)Ring or heterogeneous enhancement.Leptomeningeal or solid parenchymal enhancement.Non-enhancing (unless IRIS develops).
T2/FLAIR Signal“Target sign” (hyperintense core, dark rim, hyperintense edema).Homogeneous hyperintensity.Confluent, asymmetric hyperintensity.
T2 Internal ArchitectureLinear/nodular hypointensities (represents fungal elements and blood products).Homogeneous. Lacks dark internal bands.Homogeneous. Lacks dark internal bands.
Lab DiagnosticsElevated Galactomannan / Beta-D-glucan.Positive CSF cytology / Flow cytometry for ALL blasts.Positive JC Virus PCR in CSF.

Discussion

Post-HSCT/Immunocompromised status.

T2-Weighted Clues: Linear hypointense areas noted within the infiltrative lesions—a classic sign of fungal hyphae or angioinvasive architecture.

SWI (Susceptibility): Patchy areas of “blooming” in the left frontal white matter, indicating micro-hemorrhages.

DWI (Diffusion): Patchy areas of restricted diffusion, suggesting acute infarction or high cellularity.

Heterogeneous enhancement with mass effect.

Perfusion Imaging: No significant increase in Cerebral Blood Volume (CBV), helping to differentiate from high-grade neoplastic processes.

REFERENCE:

1.Matis GK, Voultsinou D, Chrysou O, Birbilis T, Geroukis T. Cerebral aspergillosis and acute myeloid leukemia. J Neurosci Rural Pract. 2013 Aug;4(Suppl 1):S134-5. doi: 10.4103/0976-3147.116459. PMID: 24174784; PMCID: PMC3808046.

2.1.Machaj W, Korbecki A, Bińczyk W, Siudek B, Ussowicz M, Zimny A. Atypical radiological presentation of fatal invasive cerebral aspergillosis in a patient with acute lymphoblastic leukemia after allogeneic bone marrow transplant: A case report. Radiology Case Reports [Internet]. 2025 Jun 26;20(9):4590–3. Available from: https://www.sciencedirect.com/science/article/pii/S1930043325005266

3.Chantelot, L., Sitterlé, E., Poirée, S. et al. Cerebral Aspergillosis: Diagnostic Challenges, Therapeutic Strategies, and Future Research. CNS Drugs 40, 43–58 (2026). https://doi.org/10.1007/s40263-025-01241-0.

Picture 1

June 2026

A 41-year-old male came with complaints of back pain radiating to both lower limbs which was gradually progressive, worsened on walking. Paresthesia in both lower limbs for 3 months. He developed urinary incontinence and constipation for 2 months.

There was no history of fever, cough, weight loss or loss of appetite. There was no history of trauma. On examination there was absent ankle jerk bilaterally and S1-S5 hypoaesthesia with perianal sensory loss.

Chest radiograph and abdominal screening showed no abnormality.

A plain CT and CE-MRI of the sacral spine were performed.