• 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.
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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
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, Cladophialophorabantiana 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 Cladophialophorabantiana in a renal transplant patient: a case report and the literature review. Egypt J RadiolNucl Med. 2024;55:59. doi:10.1186/s43055-024-01229-8.
2. Rathod P, et al. Cerebral phaeohyphomycosis due to Cladophialophorabantiana in an immunocompetent individual: a case report and brief review of literature. Curr Med Mycol. 2020;6(2):52–57.
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.
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:
Feature
Angioinvasive Aspergillosis
CNS Leukemic Infiltrates
Progressive Multifocal Leukoencephalopathy
Pathophysiology
Angioinvasion causing vessel occlusion, infarction, and hemorrhage.
CNS relapse with proliferation of leukemic blasts.
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
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.
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.
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.
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
