# Indian Society of Neuroradiology (ISNR) The Official site of Indian Society of Neuroradiology - Site: https://isnr.in/ ## October 2026 - Link: https://isnr.in/october-2026/ - Published: 2026-10-10T11:15:12+05:30 - Author: ISNR **CASE HISTORY** • A 7-year-old girl was referred from IGICH with a 20-day history of headache, vomiting, and fever, followed by altered sensorium. Initial evaluation at a local hospital included lumbar puncture, which revealed hypoglycorrhachia (CSF glucose: 11 mg/dL) and elevated CSF protein (160 mg/dL). CSF culture grew Kocuria rosea, and antibiotic therapy was initiated. • Her past history was significant for chronic diarrhea of 3 years’ duration and esophageal candidiasis. Serum IgE levels were elevated, raising the suspicion of an underlying hyper-IgE syndrome. • Immunological profile: Markedly elevated serum IgE (~7,694 IU/mL), low serum IgM( <16 mg/dL), and absolute lymphocyte count of ~1,240 cells/µL, raising suspicion for an underlying immunodeficiency, including hyper-IgE syndrome. • On examination, the child was conscious and oriented (GCS: E4V5M6). Both pupils were equal and reactive to light. Motor examination revealed reduced power in the right upper limb (3/5) and right lower limb (4+/5), with power greater than 3/5 in the left upper and lower limbs. Head circumference was 91.5 cm and mid-upper arm circumference (MUAC) was 13.5 cm. There was no history of loss of consciousness, seizures, or limb weakness reported in the initial history. • Neuroimaging raised initial suspicion of an infective lesion. Antitubercular therapy( ATT) and dexamethasone were subsequently initiated. • She underwent left frontal craniotomy with ultrasound-guided aspiration of the suspected abscess on 23/08/2026, followed by re-exploration and resection on 27/ 08/2026. In view of neurological deterioration, worsening cerebral edema, and midline shift, she underwent extension of the craniotomy to a left frontotemporoparietal decompressive craniectomy with right frontal external ventricular drain (EVD) placement on 29/08/2026. ![](https://isnr.in/wp-content/uploads/2026/10/Picture-1-scaled.png) ![](https://isnr.in/wp-content/uploads/2026/10/Picture-2-scaled.png) ## What’s your diagnosis?⏎ Post your answer below.Stay tuned! ## September 2026 - Link: https://isnr.in/september-2026/ - Published: 2026-09-10T09:57:35+05:30 - Author: ISNR ## **CASE HISTORY** A 23 years old female underwent bilateral percutaneous nephrostomy (PCN) placement for nephrolithiasis. Following the procedure, the patient developed progressive right-sided hemiparesis, which subsequently worsened with the development of altered sensorium. ## Section Editors Dr. Arpita Sahu, Dr. Sarbesh Tiwari, Dr. Sabha Ahmed, Dr. Smily Sharma, Dr. Meena Nedunchelian ## Authors Dr. Genesis Giddo Koodaly — Fellow, Department of Neuroimaging and Interventional Radiology, NIMHANS, Bengaluru, India Dr. Adarsh Mohapatra — Fellow, Department of Neuroimaging and Interventional Radiology, NIMHANS, Bengaluru, India Dr. Meghana Kancharla, Fellow, Department of Neuroimaging and Interventional Radiology, NIMHANS, Bengaluru, India Dr. Vignavishal Nandakumar – DM resident, Department of Neuroimaging and Interventional Radiology, NIMHANS, Bengaluru, India Dr. Gauri Bhimrao Bornak — Senior Resident, Department of Neuroimaging and Interventional Radiology, NIMHANS, Bengaluru, India Dr. Jitender Saini — Professor and Head, Department of Neuroimaging and Interventional Radiology, NIMHANS, Bengaluru, India ![](https://isnr.in/wp-content/uploads/2026/09/Picture-1.png) ![](https://isnr.in/wp-content/uploads/2026/09/Picture-1-1.png) **A–B:** Axial T2; **C:** Axial T1; **D:** SWI; **E:** Coronal T2; **F:** DWI; ** G:** ADC; **H:** Axial post-contrast T1; **I:** Coronal post-contrast T1; **J:** Sagittal post-contrast T1. Multiple conglomerate and few discrete T2 hyperintense lesions are seen within the left thalamus and left medial temporal lobe, demonstrating a T2-intermediate signal intensity rim (orange arrows). The lesions show absent FLAIR suppression with both central and peripheral diffusion restriction (yellow arrows), resulting in expansion of the left thalamus. The lesion walls demonstrate intrinsic T1 hyperintensity ( blue arrow). Patchy susceptibility blooming is seen on SWI (green arrow). On post-contrast images, the lesions demonstrate peripheral enhancement with crenated margins (grey arrows). Few T2 hyperintense enhancing foci are seen in the right thalamic region (white arrows). Significant perifocal vasogenic edema is seen extending into the left cerebral peduncle and hypothalamus, with resultant partial effacement of the left crural cistern and atrium of the left lateral ventricle. Mild upstream dilatation of the bilateral lateral ventricles is noted. **HISTOPATHOLOGY** Sections show small fragments of neuroparenchyma with a cyst wall thrown into folds, demonstrating extensive suppurative necrosis. The necrotic areas contain numerous fungal hyphae, which are long, slender, septate and branching, and are highlighted by Periodic acid–Schiff (PAS) and Grocott’s methenamine silver (GMS) stains. The adjacent neuroparenchymal fragments show edema, along with chronic lymphocytic inflammation and scattered epithelioid histiocytes. Ziehl–Neelsen stain is negative for acid-fast bacilli. **Diagnosis:** Necrotizing fungal inflammation (cerebral phaeohyphomycosis), consistent with _Cladophialophora bantiana_. Cerebral phaeohyphomycosis is a rare but potentially fatal opportunistic fungal infection of the central nervous system caused by dematiaceous (melanized) fungi. Among these, _Cladophialophora__ __bantiana_ has a distinctive neurotropism and is an important cause of cerebral phaeohyphomycosis, particularly because infection may occur even in immunocompetent individuals. The route of CNS infection is predominantly hematogenous, with the lungs representing a potential portal of entry, although no primary extracranial focus may be demonstrable. The imaging appearance is variable and may mimic other intracranial mass-forming lesions. Brain abscess formation is the most characteristic presentation, typically appearing as solitary or multiple lesions with surrounding vasogenic edema and variable rim enhancement. On MRI, the lesions are generally T2 hyperintense with a relatively hypointense or intermediate-signal capsule. Central diffusion restriction may be seen due to the high cellularity and viscous necrotic contents within the abscess cavity. Intrinsic T1 hyperintensity of the lesion wall, as observed in our case, may reflect the presence of melanin, proteinaceous contents, blood products, or a combination of these factors. Susceptibility effects, however, are variable and may be absent. The presence of multiple conglomerate lesions with central diffusion restriction and a T2-intermediate rim suggested an infective abscess rather than a conventional neoplasm. The differential diagnosis of such lesions includes pyogenic abscess, tuberculoma, toxoplasmosis, metastases and high-grade glioma. Negative Ziehl–Neelsen staining in our case further argued against a mycobacterial etiology. Definitive diagnosis relies on histopathological examination and fungal identification. The prognosis of cerebral _C. __bantiana_ infection remains poor, with high mortality despite antifungal therapy and surgical intervention. Early diagnosis, prompt surgical drainage or excision when feasible, and prolonged targeted antifungal therapy are important components of management. Learning point: Cerebral phaeohyphomycosis should be considered in the differential diagnosis of rim-enhancing intracranial lesions with central diffusion restriction and disproportionate surrounding edema, even when the clinical history does not strongly suggest an invasive fungal infection. **References** 1. Patil PN, Chavan R, Borse SS. Imaging in a rare case of cerebral phaeohyphomycosis caused by _Cladophialophora__ __bantiana_ in a renal transplant patient: a case report and the literature review. _Egypt J __Radiol__ __Nucl__ Med._ 2024;55:59. doi:10.1186/s43055-024-01229-8. 2. Rathod P, et al. Cerebral phaeohyphomycosis due to _Cladophialophora__ __bantiana_ in an immunocompetent individual: a case report and brief review of literature. _Curr__ Med Mycol._ 2020;6(2):52–57. ## August 2026 - Link: https://isnr.in/august-2026/ - Published: 2026-08-11T10:07:20+05:30 - Author: ISNR ## **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. ![](https://isnr.in/wp-content/uploads/2026/08/isnr1.png) ![](https://isnr.in/wp-content/uploads/2026/08/isnr2.png) ![](https://isnr.in/wp-content/uploads/2026/08/isnr3.png) ![](https://isnr.in/wp-content/uploads/2026/08/isnr4.png) ## 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 ![](https://isnr.in/wp-content/uploads/2026/08/Picture-1.png) ## **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 Parameter** | **Tuberculoma** | **Metastasis** | | T2 signal | Often T2 hypointense (caseating granuloma) | Usually T2 hyperintense necrotic center | | Lesion morphology | Conglomerate lesions common | Discrete lesions common | | Meningeal enhancement | Relatively common | Uncommon | | DWI | Variable | Usually no central restriction | | Perfusion (rCBV) | Low | Increased | | MR spectroscopy | Prominent lipid-lactate peak; lower Cho/Cr compared to aggressive tumors | Markedly elevated choline; higher Cho/Cr | | 3.8 ppm peak on MRS | May be present | Rare | | PET uptake | Can be intensely avid | Often avid | | Ancillary findings | TB elsewhere, meningitis, tuberculomas | Known 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. ## July 2026 - Link: https://isnr.in/july-2026/ - Published: 2026-07-10T12:10:48+05:30 - Author: ISNR ## **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. ![](https://isnr.in/wp-content/uploads/2026/07/Picture-1.png) **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.** ![](https://isnr.in/wp-content/uploads/2026/07/Picture-11.png) **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) ![](https://isnr.in/wp-content/uploads/2026/07/Picture-21.png) **T2-weighted linear hypointense areas noted within the lesions.** ![](https://isnr.in/wp-content/uploads/2026/07/Picture-31.png) ![](https://isnr.in/wp-content/uploads/2026/07/Picture-41.png) **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.** ![](https://isnr.in/wp-content/uploads/2026/07/isnr.png) ## **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** ![](https://isnr.in/wp-content/uploads/2026/07/Picture-1-1.png) **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 ![](https://isnr.in/wp-content/uploads/2026/07/Picture-2.png) Interval increase in the patchy areas of diffusion restriction with peripheral SWI blooming are seen in left frontal lobe ![](https://isnr.in/wp-content/uploads/2026/07/Picture-3.png) 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.** ![](https://isnr.in/wp-content/uploads/2026/07/Picture-5.png) ## CONCLUSION: | **Feature** | **Angioinvasive Aspergillosis** | **CNS Leukemic Infiltrates** | **Progressive Multifocal Leukoencephalopathy** | | **Pathophysiology** | Angioinvasion causing vessel occlusion, infarction, and hemorrhage. | CNS relapse with proliferation of leukemic blasts. | JC virus opportunistic infection destroying oligodendrocytes (demyelination). | | **Primary Location** | Corticomedullary 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 Architecture** | **Linear/nodular hypointensities** (represents fungal elements and blood products). | Homogeneous. Lacks dark internal bands. | Homogeneous. Lacks dark internal bands. | | **Lab Diagnostics** | Elevated 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](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.** **‌** ## June 2026 - Link: https://isnr.in/june-2026/ - Published: 2026-06-10T09:49:23+05:30 - Author: ISNR ## **CASE HISTORY** 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. ## **INVESTIGATIONS** Hb- 13.0 g/dl (normal). TLC: 10.2 x 10^(9)/L (elevated). ESR: 73mm/ 1^(st) hour ( elevated). CRP: 9.2 mg/ L (elevated). LDH : 156 U/L (normal). ## **AUTHORS** Dr. Anusha Shree Thaneeru, Department of Radiology, Manipal Hospitals, Kanakapura Road, Bangalore. Dr. Sharath Kumar G G, Lead Consultant, Interventional Neuroradiology, Manipal Hospitals, Kanakapura Road, Bangalore. Dr. Veekshit Shetty, Consultant Neurosurgery, Manipal Hospitals, Kanakapura Road, Bangalore. Dr. Vidya. M. N., Lead Consultant Pathologist, Manipal hospitals, Old airport Road, Bangalore. ![](https://isnr.in/wp-content/uploads/2026/06/Picture-1-1.png) ## **DESCRIPTION** • A & B : Axial and sagittal STIR images showing hyperintense lesion involving the S2 vertebral body (blue arrow) with heterogenous soft tissue component (red arrow). Adjacent bone marrow edema seen. • C : Areas of diffusion restriction seen within the S2 vertebral body lesion and the presacral soft tissue component. • D : Axial T1 pre contrast image shows T1 hypointensity. • E & F : Axial and sagittal T1 post contrast images showing heterogenous enhancement of the lesion. • G : Sagittal CT images in bone window showing osteolysis involving the S2 vertebral body.         No foci of calcification seen within the lesion. • H : Histopathology slide -shows chronic granulation tissue. Proliferating capillaries are seen with extravasated RBC’s and chronic inflammation. ## **FINAL DIAGNOSIS** A Granulomatous masquerade – Central body type sacral tuberculosis mimicking neoplasm. ## **FURTHER MANAGEMENT:** • The patient underwent S1-S2 decompression laminectomy, lumbosacral- iliac fixation using L5.      Biopsy of S2 vertebral body lesion was obtained for histopathological evaluation. • Intraoperatively, there was destruction of S2 vertebral body, replaced by granulation tissue. • Mycobacteria were detected on Gene Xpert and acid-fast bacilli stain showed scanty bacilli. • Post surgery patient was started on antitubercular therapy. ## **DISCUSSION:** • Osteoarticular tuberculosis accounts of 2 to 5% of all tuberculosis cases. The lower thoracic and lumbar spine are the most involved sites. The sacrum and cervical spine are rarely involved^(1).   • Spinal tuberculosis is almost always due to hematogenous spread of mycobacteria from primary foci in the lungs and/or urogenital tract^(2). • The paravertebral venous plexus of Batson is generally thought to be the primary route of spread into the spine. The most common presenting symptoms include discharging sinuses and abscesses in young, sciatic pain and low back pain in adults. ## **IMAGING CHARACTERISTICS :** Four common imaging patterns of spinal tuberculosis are – paradiscal, central, anterior subligamentous and posterior types ^(4). • Paradiscal type is the most common pattern and involved the vertebral bodies adjacent to the intervertebral disc with early involvement of the disc. • Central type is characterized by involvement of the central vertebral body. It is considered atypical form as the disc is spared breaking the paradigm of paradiscal type where there is early involvement of the intervertebral disc.  • Subligamentous type is spread of infection beneath the anterior longitudinal ligament. • Posterior element involvement is rare. Plain radiograph: Very insensitive. May show nonspecific features like osteopenia, loss of definition of vertebral end plate. Cold abscesses may be visible as peri- vertebral soft tissue densities . CT: Computed tomography is better at delineating bone destruction. It can demonstrate paravertebral abscess and enhancing granulation tissue. MRI: It is the imaging modality of choice. It allows for early detection of disease before bony deformity occurs. Inflammatory marrow edema appears hypointense on T1- weighted imaging and hyperintense on STIR and T2-weighted imaging showing heterogenous enhancement. Disc involvement is seen as reduced disc space, high T2 signal and contrast enhancement. Phlegmon and cold abscess appear hyperintense on T2 weighted images and hypo-intensity on T1 weighted images. On post contrast T1 weighted images, phlegmon shows uniform enhancement and cold abscess show peripheral enhancement. **MANAGEMENT**: Includes primary therapy ATT. Surgical decompression. **DIFFERENTIAL DIAGNOSIS**: Primary sacral tumors like chordoma and giant cell tumor. **CONCLUSION: ** • Considering the significant overlap in imaging features between atypical central type of tuberculosis involving the sacrum and primary tumors, a high clinical suspicion for tuberculosis is important especially in endemic regions. • A definitive diagnosis requires histopathological confirmation through biopsy or fine needle aspiration cytology to identify Mycobacterium tuberculosis. • Initiating antitubercular chemotherapy on time is often effective in treatment and prevention of permanent neurological damage and hence extensive surgeries can be avoided. | | **TUBERCULOSIS** | **CHORDOMA** | ** GIANT CELL TUMOR** | | Etiology and epidemiology | Infective etiology, common in young adults. | Most common primary malignant tumor of sacrum. Peak incidence in the 5^(th) decade with male preponderance. (5) | Bening but locally aggressive tumor. Incidence between 20-40 years. | | Characteristics | Often paracentral with adjacent disc involvement. | Midline slow growing sacral mass. Lower sacral vertebrae are commonly involved. | Typically, eccentric lesion involving the upper sacral vertebrae. Fast local expansion to involve the sacroiliac joint. | | Imaging findings: | Mainly lytic lesion with marginal sclerosis. Calcification and hemorrhagic component – rare. | Purely lytic destructive lesion. Calcifications are common “rings and arcs”. | Expansile lytic lesion. No mineralized matrix. May show cystic changes, fluid-fluid level (ABC like changes). | | MRI findings: | Heterogenous lesion with cold abscess showing rim enhancement. Disc involvement common. | T2 hyperintense midline lobulated mass with soft tissue extension. | A solid heterogenous mass with extension into adjacent bones. Less T2 hyperintense than chordoma. | | Soft tissue component | Cold abscess – common. | Large soft tissue component. | Significant soft tissue extension with cortical breakthrough. | | Investigations | Elevated ESR, CRP. | Usually normal. | Usually normal. | ## **REFERENCES** 1. Shantanu K, Sharma V, Kumar S, Jain S. Tuberculosis of sacrum mimicking as malignancy. 2. Patankar T, Krishnan A, Patkar D, Kale H, Prasad S, Shah J, et al. Imaging in isolated sacral tuberculosis: a review of 15 cases. Skeletal Radiol. 2000;29:392– 6. doi:10.1007/s002560000229. 3. Pun WK, Chow SP, Luk KDK, Cheng CL, Hsu LCS, Leong JCY. Tuberculosis of the lumbosacral junction: long term follow-up of 26 cases. J Bone Joint Surg Br 1990; 72:675–678. 4. Vijay Kubihal, Raju Sharma, RG Krishna Kumar, SH Chandrashekara, Rakesh Garg. Imaging update in spinal tuberculosis. DOI: [10.1016/j.jcot.2021.101742](https://doi.org/10.1016/j.jcot.2021.101742) 5. Gerber S, Ollivier L, Leclère J, et al. Imaging of sacral tumours. Skeletal Radiol 2008;37:277–89 ## May 2026 - Link: https://isnr.in/may-2026/ - Published: 2026-05-10T01:00:00+05:30 - Author: ISNR ## **CASE HISTORY** A 5-year-old male child presented with complaints of recurrent generalized tonic– clonic seizures and right-sided weakness ,predominantly involving the lower limb along with anger outbursts and abnormal behaviour. No history of fever, head trauma, vision loss, sensory loss, or headache. No family history of seizure disorder or chronic neurological illness. Birth history: Full-term normal vaginal delivery, birth weight 2.8 kg, no NICU stay ## **CASE CONTRIBUTED BY-** **Dr Somya Gupta** – 3rd year Resident , Department of Radiodiagnosis, Kalinga Institute of Medical Sciences , Bhubaneswar , Odisa **Dr. Tapas kumar sahu** , Assistant Professor ,Department of Radiodiagnosis, Kalinga Institute of Medical Sciences , Bhubaneswar , Odisa **Dr. Basanta Manjari Swain** (HOD and Professor),Department of Radiodiagnosis, Kalinga Institute of Medical Sciences , Bhubaneswar , Odisa ![](https://isnr.in/wp-content/uploads/2026/05/Picture-1-1.png) ## **DESCRIPTION** A and B  :Axial section of T2 sequence and axial section of FLAIR sequence shows a diffuse, symmetrical  hyperintensity in  bilateral cerebral white matter including subcortical U-fiberss. The white matter appears swollen, without significant volume loss. Relative sparing of deep white matter C: Axial FLAIR sequence shows few well-defined subcortical cysts  in the anterior temporal lobes bilaterally D: Axial section of Diffusion weighted sequence shows no abnormality E: 3D Sagittal cube FLAIR FS  sequence shows relatively increased fronto-occipital dimension, consistent with macrocephaly . ## **Diagnosis:Megalencephalic Leukoencephalopathy with Subcortical Cysts (MLC), also known as Van der Knaap disease** **Background** Megalencephalic Leukoencephalopathy with Subcortical Cysts (MLC), also known as Van der Knaap disease, is a rare inherited leukodystrophy . It follows predominantly an autosomal recessive inheritance pattern **Pathophysiology** MLC is caused by mutations in: MLC1 (≈75% cases) HEPACAM (≈20% cases) These genes encode proteins involved in astrocytic membrane function and regulation of brain water and ion homeostasis. Defective astrocyte function leads to: Impaired ion and water regulation leading to white matter swelling ,vacuolation of myelin and Formation of subcortical cysts The disease produces intramyelinic vacuolation rather than primary demyelination. **Classical Features** Macrocephaly (at birth or infancy; earliest and most consistent sign) Delayed motor milestones Early-onset seizures Mild early cognitive impairment with progressive Ataxia ,Spasticity, Dysarthria **Key MRI Findings** Diffuse bilateral symmetric T2/FLAIR hyperintensity of subcortical and deep white matter with corresponding T1 hypointensity “Swollen white matter” appearance in early stage Relative sparing of deep grey nuclei and brainstem Subcortical cysts, predominantly in: Anterior temporal lobes (classical) and Frontoparietal regions Structures Typically Spared: Basal ganglia Thalami Brainstem Cerebellar white matter (early stage) Diffusion Imaging: Usually no true diffusion restriction **Differential Diagnosis-** Canavan disease Alexander disease metachromatic leukodystrophy others causes of megalencephaly other leukoencephalopathies **References** 1) Roy U, Joshi B, Ganguly G. Van der Knaap disease: a rare disease with atypical features. BMJ Case Rep. 2015 Jul 22;2015:bcr2015209831. doi:10.1136/bcr-2015-209831. 2) Jhancy M, Al Homsi A, Chowdhury F, Hossain S, Ahamed R. Van der Knaap Disease( Vanishing White Matter) – Unusual Presentation in a Neonate: A Case Report. Neurol India. 2020 May-Jun;68(3):669-672. doi:10.4103/0028-3886.289018. 3) Das S, Dhibar T. Van der Knaap Disease: A Case Series Highlighting Clinical and Radiological Features. Int J Anat Radiol Surg. 2025 Sep;14(5):RS01-RS03. doi:10.7860/ IJARS/2025/81128.3062 ## April 2026 - Link: https://isnr.in/april-2026/ - Published: 2026-04-14T15:13:26+05:30 - Author: ISNR ## CASE HISTORY **45 YEAR OLD MALE** **Presenting compaints:** Patient presented with lower back pain since 5 years;  right leg numbness and tingling since 6 months and acute onset urinary incontinence **Past history and comorbidities :** H/o pulmonary TB and TB meningitis 15 years ago, completed ATT; Hypertensive since 1 year , on medication. **Physical examination: **Unremarkable, with a full range of motion of the cervical and lumbar spine with no pain elicited on movement. Full strength in both legs with diminished sensation to touch in the right leg and foot in a non-dermatomal distribution. Reflexes were elevated at the lower extremities bilaterally, but no clonus or Babinski sign was detected. **Workup:** Patient was referred for a lumbar spine MR ## CASE CONTRIBUTED BY Dr. **MEGHANA KANCHARLA**, SENIOR RESIDENT, ST JOHNS MEDICAL COLLEGE AND HOSPITAL Dr. **STALLON SEBASTIAN**, ASSISTANT PROFESSOR, ST JOHNS MEDICAL COLLEGE AND HOSPITAL ##### **SAGITTAL T2** ![](https://isnr.in/wp-content/uploads/2026/04/Screenshot-2026-05-04-at-2.22.51- PM.png) ##### **AXIAL T2** ![](https://isnr.in/wp-content/uploads/2026/04/Screenshot-2026-05-04-at-2.23.15- PM.png) ##### **SAGITTAL T1** ![](https://isnr.in/wp-content/uploads/2026/04/Screenshot-2026-05-04-at-2.24.11- PM.png) ##### **CORONAL T2 STIR** ![](https://isnr.in/wp-content/uploads/2026/04/Screenshot-2026-05-04-at-2.24.25- PM.png) ##### **DWI** ![](https://isnr.in/wp-content/uploads/2026/04/Screenshot-2026-05-04-at-2.25.48- PM.png) ##### **ADC** ![](https://isnr.in/wp-content/uploads/2026/04/Screenshot-2026-05-04-at-2.26.03- PM.png) ##### **T1 PRE CON** ![](https://isnr.in/wp-content/uploads/2026/04/Screenshot-2026-05-04-at-2.27.11- PM.png) ##### **T1 POST CON** ![](https://isnr.in/wp-content/uploads/2026/04/Screenshot-2026-05-04-at-2.27.27- PM.png) ##### **FAT PHASE** ![](https://isnr.in/wp-content/uploads/2026/04/Screenshot-2026-05-04-at-2.28.20- PM-1.png) ##### **CT** ![](https://isnr.in/wp-content/uploads/2026/04/Screenshot-2026-05-04-at-3.22.17- PM-2.png) ##### **INPHASE** ![](https://isnr.in/wp-content/uploads/2026/04/Screenshot-2026-05-04-at-3.21.00- PM.png) ## Diagnosis: Atypical Spinal Epidermoid Cyst **Clinical diagnosis:** L2 L3 IDEM ? Lipoma **Gross Description:** Bottle contains 1 irregular piece of grey white soft tissue measures 4×1.8×0.5cm 2 bits embed all – A Bottle contains <0.25gms of grey white soft tissue <0.25gms embed all – B Grossed By – Dr. Deepthi Benny **Microscopy:** 1. Section shows portions of cyst lined by stratified squamous epithelium. Cyst wall is composed of fibrocollagenous tissue and lymphoplasmacytic infiltrate, admixed with pigment-laden macrophages. Also noted are areas of calcification and congested blood vessels. 2. Section shows lamilated keratin flakes **Impression:** Consistent with epidermoid cyst, L2L3 IDEM #### **DISCUSSION**: **Background** Spinal epidermoid cysts are rare, benign, slow-growing intradural lesions arising from ectodermal inclusions, either congenital or acquired following lumbar puncture, spinal surgery, or trauma. They account for <1% of spinal tumors and most commonly involve the lumbar and lumbosacral regions. Due to their indolent growth, patients typically present with long-standing symptoms, which may progress to radiculopathy and sphincter dysfunction. **Imaging** **MRI is the modality of choice** for evaluation of spinal epidermoid cysts. Although** classically described as T1 hypointense, T2 hyperintense lesions** with **diffusion restriction**, imaging appearances may be variable, particularly in **chronic or protein-rich lesions**. In the present case, the lesion demonstrates T1 hyperintensity and T2 hypointensity, an atypical appearance attributed to dense keratinaceous debris, cholesterol crystals, high protein concentration, and chronic desiccation, resulting in shortening of T1 and T2 relaxation times. Such lesions are described as** atypical or “white” epidermoid cysts.** While diffusion restriction is a characteristic feature, its absence does not exclude the diagnosis, especially in long-standing lesions with compact internal contents and in the setting of technical limitations of spinal diffusion imaging. Dixon fat-phase imaging demonstrates absence of fat signal, effectively excluding a dermoid cyst and supporting the diagnosis of an epidermoid cyst. Post-contrast imaging shows no significant internal enhancement, supporting a non- neoplastic cystic etiology. Associated scalloping of the lumbar vertebral bodies reflects chronic, slow-growing mass effect, further supporting the benign and indolent nature of the lesion. The **imaging differential diagnosis** includes dermoid cyst, arachnoid cyst, subacute hemorrhage, melanin-containing lesions, and cystic neoplasms, which were considered less likely based on signal characteristics, lack of fat suppression signal drop, minimal enhancement, chronicity, and histopathological confirmation. **Management** Surgical excision is the treatment of choice. Complete resection may be limited by capsular adherence to neural structures, particularly in chronic lesions, and subtotal excision may predispose to recurrence. Overall, clinical outcomes are favorable following adequate surgical decompression. **Conclusion** •In a patient with long-standing, slowly progressive neurological symptoms, including radiculopathy and sphincter involvement, a benign, indolent intradural pathology should be strongly considered. •Atypical MRI signal characteristics (T1 hyperintensity, T2 hypointensity) do not exclude spinal epidermoid cyst, particularly in chronic, protein-rich lesions. •Absence of diffusion restriction, lack of significant enhancement, and associated vertebral scalloping favor a long-standing benign cystic lesion over aggressive or neoplastic etiologies. •Awareness of imaging variability in chronic epidermoid cysts and correlation with clinical course and histopathology are essential to avoid misdiagnosis. ## March 2026 - Link: https://isnr.in/march-2026/ - Published: 2026-03-11T04:34:31+05:30 - Author: ISNR ## CASE HISTORY 60-year-old adult, chronic smoker with history of angioplasty, presented with recent onset hemoptysis, weight loss and generalized fatigue with mild fever. CECT Thorax revealed an irregular spiculated mass in the right lung upper lobe. Underwent CT guided lung biopsy for the same. Patient developed left sided hemiparesis immediately post procedure with a power of 4/5 in both left upper and lower limb. Patient was started on 100% O2, he regained full power in both upper and lower limb within 24hrs. ## CASE CONTRIBUTED BY Dr. **Jose Siju**, MD, Senior Resident, Department of Radiodiagnosis, Tata Memorial Hospital, Mumbai Dr. **Rajas Thaker**, MD DNB DM, Senior Resident, Department of Radiodiagnosis, Tata Memorial Hospital, Mumbai Dr. **Varun Yadav**, MD FIVR PDCC, Consultant, Department of Radiodiagnosis, Homi Bhabha Cancer Hospital & Research Center, Mullanpur ![](https://isnr.in/wp-content/uploads/2026/03/case-of-the-month-march-2026-7.jpg) #### **Day 1** ![](https://isnr.in/wp-content/uploads/2026/03/case-of-the-month-march-2026-8.jpg) **T2 FLAIR** ![](https://isnr.in/wp-content/uploads/2026/03/case-of-the-month-march-2026-9.jpg) **POST CONTRAST T1 FLAIR** ![](https://isnr.in/wp-content/uploads/2026/03/case-of-the-month-march-2026-10.jpg) **Follow Up** **Non-contrast Thorax:** Focus of air in the ascending aorta **Non-contrast CT Brain:** Focus of air in the superior sagittal sinus **MRI Brain (Day 1):** * FLAIR hyperintensities in the bilateral parietooccipital region. * Post contrast T1 FLAIR images showing leptomeningeal enhancement in the same areas. **MRI Brain (Follow Up):** Resolution of previously seen FLAIR hyperintensities and leptomeningeal enhancement in bilateral parietooccipital region. ## **Diagnosis: Cerebral Air Embolism** #### **Discussion** **Background:** * Systemic air embolism (SAE) is an extremely rare complication of a CT-guided PTNB, but one that is potentially fatal. * Reported Incidence: 0.02 to 0.07% (likely underdiagnosed). * This case highlights the CT and MRI findings of cerebral air embolism post CT guided lung biopsy. **Pathology:** Cerebral air embolism occurs when intravascular air, introduced during procedures such as CT-guided lung biopsy, reaches the cerebral circulation, mechanically obstructs small vessels, triggers endothelial injury and inflammation, and results in acute cerebral ischemia and infarction. **Clinical Presentation:** * Patient can present with sudden neurological deficit (hemiparesis, aphasia, visual loss, or altered sensorium) within minutes. * They can also present with seizures or cardiopulmonary symptoms (chest pain, dyspnea, arrhythmia, or hypotension) * The symptoms can be transient or fluctuating and deficits may improve as air redistributes or dissolves. **Diagnosis:** Air embolism is diagnosed by correlating sudden clinical deterioration after procedures such as CT-guided lung biopsy with imaging evidence of intravascular air on CT or MRI, often supported by diffusion-restricted ischemic lesions in the brain. #### **Neuro-imaging Features:** **CT Brain:** * Linear or punctate air foci within cortical sulci or cerebral vessels. * Air outlining cortical arteries or dural venous sinuses. * Early scans may be normal if air has dissolved. * Delayed hypodensity in affected territories due to infarction. **MRI Brain:** * DWI shows acute diffusion restriction in cortical or subcortical regions. * Lesions often do not follow a single vascular territory. * SWI or GRE may show blooming from residual intravascular air. * FLAIR shows cortical sulcal hyperintensity and edema. * Post-contrast images may show leptomeningeal enhancement. **Treatment:** * It is crucial for radiologists to diagnose cerebral air embolism both during and after lung biopsy, since the patient is usually in the radiology department at the time of symptom onset, and may even still be on the CT table. * Starting 100 % oxygen immediately can help reduce air bubble size and improves tissue oxygenation. * Placing the patient supine or in left lateral decubitus position limits further cerebral air migration. * Starting hyperbaric oxygen therapy as early as possible, this is the definitive treatment and improves neurological outcome. * Maintain hemodynamic stability, use IV fluids and vasopressors if needed. * Avoid further air entry, secure lines and stop the procedure at once. **In our case we were able to save the patient due to prompt diagnosis and timely intervention.** #### **References** * Vincent M. Timpone, Andrew L Callen. Characteristic MR Imaging Findings of Cerebral Air Embolism Infarcts: A Case Series American Journal of Neuroradiology May 2024, ajnr.A8349; DOI: 10.3174/ajnr.A8349 * Brown AE, Rabinstein AA, Braksick SA. Clinical Characteristics, Imaging Findings, and Outcomes of Cerebral Air Embolism. Neurocrit Care 2023;38:158- 164 * Kuo HL, Cheng L, Chung TJ. Systemic air embolism detected during percutaneous transthoracic needle biopsy: report of two cases and a proposal for a rountine postprocedure computed tomography scan of the aorto-cardiac region. Clin imaging 2010;34:53-6. ## February 2026 - Link: https://isnr.in/february-2026/ - Published: 2026-02-11T01:50:29+05:30 - Author: ISNR ## CASE HISTORY A term, appropriate-for-gestational-age neonate with **normal APGAR scores** and** no history of perinatal hypoxia** presented with **seizures on day 2 of life**. There were no antenatal or perinatal complications. Initial consideration was hypoxic– ischemic encephalopathy (HIE); however, the clinical history was discordant with this diagnosis. ## CASE CONTRIBUTED BY Dr **Thapasya**, DNB resident, KMCH, Coimbatore ![](https://isnr.in/wp-content/uploads/2026/02/case-of-the-month-february-2026-1. jpg) **DWI**: **Diffuse, symmetric cortical thickening with widespread diffusion restriction**, involving bilateral cortical and subcortical regions, **basal ganglia**, **thalami**, and **cerebral peduncles**. **SWI**: Susceptibility-weighted imaging shows no hemorrhage #### **MRI Spectrum** **Acute:** Diffuse white matter and caudate T2 hyperintensity with widespread diffusion restriction; MRS shows **elevated lactate and reduced NAA**. **Subacute:** **T1/ T2 shortening of basal ganglia**, mimicking HIE, with relative thalamic sparing.** Chronic:** **Severe volume loss** of basal ganglia and white matter with **cystic degeneration**. #### **Imaging Differentials:** HIE-like metabolic disorders (MoCD/ISOD) Epileptic encephalopathyMitochondrial cytopathy. ## **Diagnosis**: Targeted metabolic evaluation followed by **genetic testing confirmed molybdenum cofactor deficiency**. LIKELY COMPOUND HETEROZYGOUS VARIANTS TO BE CAUSATIVE OF THE REPORTED PHENOTYPE WERE IDENTIFIED | **Gene (Transcript)** | **Location** | **Variant** | **Zygosity** | **Disease (OMIM)** | **Inheritance** | **Classification** | | MOCSI (-) (ENST00000373186.4) | Exon 7 | c.955C>T(p.Arg319Ter) | Heterozygous | Molybdenumcolactor deficiencyofcomplementationgroup A | Autosomalrecessive | Pathogenic | | | Exon 1 | c.217C>T(p.Arg73Trp) | Heterozygous | | | Likely Pathogenic | **“Reclassification of these variants could be considered based on parental testing.”** #### **Discussion**: Hypoxic–ischemic encephalopathy (HIE) is the most common cause of neonatal encephalopathy. MoCD leads to toxic sulfite accumulation, resulting in severe excitotoxic neuronal injury and HIE-like imaging patterns, often in the absence of a hypoxic insult. #### **Conclusion:** MoCD is a HIE-like imaging patterns that are discordant with clinical history, thucritical metabolic mimic of HIE. Imaging plays a pivotal role in identifying molybdenum cofactor deficiency by recognizing s guiding timely metabolic and genetic testing, preventing misdiagnosis. | **Feature** | **HIE** | **MOCD** | | **Perinatal hypoxia** | Present | Absent | | **DWI pattern** | Watershed/deep nuclei | Diffuse, non-vascular | | **Brainstem (cerebral peduncles)** | Spared | Involved (hallmark) | | **SWI microbleeds** | Rare | Absent | | **Evolution** | Cystic encephalomalacia | Rapid atrophy, no cysts | | **MRS** | ↑Lactate | ↓↓NAA, ↑Lactate, ↑Glutamine | ## January 2026 - Link: https://isnr.in/january-2026/ - Published: 2026-01-10T00:32:14+05:30 - Author: ISNR ## CASE HISTORY * 35 yr old male c/o headache, quadriparesis and blurring of vision. * H/o GTCS 7 months ago and difficulty in gripping the objects. * No history of fever or weight loss. * Was diagnosed as CNS TB on imaging and treated with ATT and VP shunt for hydrocephalus at other hospital. ## CASE CONTRIBUTED BY Dr. **Mohd Asif**, Consultant Neuroradiologist, Department of Radiology, Glenfield Mallareddy Hospital, Nampally, Hyderabad. Dr. **Syed Abdul Jaleel Kirmani**, Consultant Neurosurgeon, Department of Neurosurgery, Glenfield Mallareddy Hospital, Nampally, Hyderabad. ![](https://isnr.in/wp-content/uploads/2026/01/case-of-the-month-january-2026-1- 1.jpg) ![](https://isnr.in/wp-content/uploads/2026/01/case-of-the-month-january-2026-2- 1.jpg) ## **Diagnosis: Synchronous Pineal and Sellar-suprasellar Diffuse Midline Glioma, H3 K27 M Mutant CNS WHO Grade 4 with leptomeningeal and drop metastases.** #### **MRI:** * Heterogeneous, multiloculated solid-cystic lesion with calcifications and haemorrhage in **pineal region **causing mass effect of brainstem, the solid component shows intense enhancement and the cystic areas show peripheral enhancement. * Similar solid lesion seen in **sellar****-suprasellar region, **shows intense contrast enhancement. * Multifocal areas of nodular and smooth leptomeningeal enhancement predominantly along the cerebral hemispheres (L>R). * There is leptomeningeal enhancement along the visualised cervical cord – leptomeningeal drop metastasis. **Incidental finding: **multiple flow voids seen along the cervical and thoracic cord, no nidus and oedematous cord signal changes secondary to venous congestion– dural AV fistula. #### **Differential diagnoses:** * Germ cell tumor * Intracranial metastasis * AT/RT and ETMR in pediatric age group #### **Microscopic Description:** Sections studied show a hypercellular lesion in a fibrillary background. The lesional cells are polygonal to spindle shaped with marked pleomorphism. They have vesicular nuclei, prominentnucleoli and moderate eosinophilic cytoplasm. Frequent mitosis is seen, including atypical mitosis. There is no necrosis / microvascular proliferation in the sections studied. **Report on IHC:** **H3 K27 Me3** – **Loss of expression****H3 K27 M** – **Positive**** ATRX** – **Retained****P53** – **Diffuse strong positive****SALL4** – **Negative**** Ki67** – **36%** #### **Diagnosis: Diffuse Midline Glioma, H3 K27M Altered, H3 K27 M Mutant, CNS WHO Grade 4.**