The occurrence of mesenchymal tumor, FET::CREB fusion-positive in the spinal compartment is exceptionally rare, with only a few previously documented cases. Here, we present a unique case of a 43-year-old man who developed a mesenchymal tumor, FET::CREB fusion-positive at the T1 spinal level. Clinically, the patient reported chronic posterior neck and shoulder pain accompanied by the intermittent paresthesia of the right arm. Magnetic resonance imaging demonstrated an intradural extramedullary mass, initially suggestive of a schwannoma. The patient underwent near-total surgical removal via a right C7-T1 hemilaminectomy. Histological examination revealed epithelioid and cord-like cellular arrangements within a mixed sclerotic and myxochondroid stroma. Immunohistochemistry revealed partial positivity for epithelial membrane antigen (EMA), smooth muscle actin (SMA), and CD99. Molecular analysis confirmed the presence of EWSR1::CREM fusion, establishing the diagnosis of a mesenchymal tumor, FET::CREB fusion-positive. To date, all reported spinal mesenchymal tumors within this molecular category have exclusively featured CREM as an FET gene family fusion partner, thereby highlighting a potential site-specific molecular signature. In this case report, we discuss the potential diagnostic challenges, characteristic pathological spectra, and clinical considerations associated with this rare entity of the spine.

Paraneoplastic neurological syndromes (PNS) are rare immune-mediated disorders typically associated with systemic malignancies, while their occurrence in primary brain tumors is exceptionally uncommon. We report a 59-year-old man who presented with acute-onset epileptic seizures and transient serum CASPR2 antibody positivity, initially suggestive of autoimmune encephalitis. Early magnetic resonance imaging (MRI) showed T2-FLAIR hyperintensity in the right temporoparietal region without mass effect; however, follow-up imaging revealed a space-occupying lesion consistent with glioblastoma (GBM). The patient experienced transient improvement following immunoglobulin and corticosteroid therapy but achieved definitive recovery only after surgical tumor resection. Histopathology confirmed IDH1 wild-type GBM (CNS WHO Grade IV), and postoperative antibody seroconversion supported a diagnosis of pseudoparaneoplastic syndrome rather than true PNS. This case underscores that primary intracranial tumors such as GBM can transiently mimic autoimmune encephalitis through tumor-associated immune activation without direct antibody pathogenicity. Clinicians should maintain a high index of suspicion for tumor-related processes in patients with neuronal antibody positivity-particularly when antibodies are low-titer, serum-restricted, and clinically discordant-and prioritize dynamic imaging surveillance alongside serial antibody monitoring to avoid diagnostic delay. Further research is warranted to elucidate the mechanisms of GBM-induced immune dysregulation and its implications for neuroimmunological disease.

Background and Objectives: Prognostic assessments in grade 4 diffuse astrocytic tumors primarily depend on clinical and molecular characteristics, with radiological attributes frequently assessed in isolation. In this study, we explored whether an integrated radiological approach combining tumor burden, anatomical spread, and mass effect could contribute to survival prediction. Materials and Methods: A total of 310 adult patients with histopathologically confirmed grade 4 diffuse astrocytic tumors, diagnosed between January 2022 and January 2025, were included in this retrospective single-center cohort. Preoperative MRI was used to assess contrast-enhancing tumor volume, edema volume, and brain volume, combined with anatomical spread and midline shift as a marker of mass effect. Tumor burden was defined as the ratio of enhancing tumor volume to brain volume (ETV/BV). Overall survival was analyzed using Kaplan-Meier and Cox regression methods. Model performance was evaluated with the C-index, bootstrap internal validation, and 12-month calibration. Results: Tumor burden was higher in IDH-wildtype tumors, which also showed higher midline shift and more frequent deep structure involvement and contralateral extension. In multivariable analysis, IDH status, age, tumor burden, midline shift, and deep structure involvement were independently associated with overall survival. A greater tumor burden was associated with reduced survival. The addition of molecular and imaging-derived variables improved discrimination, increasing the C-index from 0.69 to 0.76. Following bootstrap validation, the corrected value was 0.73. Calibration at 12 months demonstrated acceptable agreement between predicted and observed outcomes. Conclusions: An integrated radiological approach that combines tumor burden, anatomical spread, and mass effect may support prognostic assessment in addition to established clinical and molecular variables.

Background: Parents of children with cancer often experience significant stressors that can heighten distress and impact overall well-being. Despite recommendations supporting distress screening for adult and pediatric patients with cancer, systematic assessment of parent or caregiver distress in pediatric oncology settings remains limited. This Quality Improvement initiative aimed to implement routine distress screening for adult caregivers of pediatric patients with brain and solid tumors at our institution. Methods: Using the 18-item CancerSupportSource™-Caregiver (CSS-CG) instrument, our social work team invited eligible caregivers to complete monthly electronic distress screeners while their child was receiving treatment. Automated reports with tailored psychoeducational resources were sent to caregivers upon completion, and social workers received alerts when participants scored at-risk for anxiety, depression, or financial strain. The feasibility of the CSS-CG implementation was assessed via caregiver enrollment and completion rates, and clinician acceptability was evaluated through a post-implementation survey. Results: Of 122 eligible patients, 64 of their caregivers enrolled in the CSS-CG screening platform (52.45%), and 44 (36.06%) completed at least one screener. Of the 44 caregivers who completed the CSS-CG assessment, 59.09% (n = 26) screened positive at least once for risk of anxiety, 54.54% (n = 24) for risk of financial strain, and 59.09% (n = 26) for risk of depression. Among participating social workers, 83% reported that the screener improved their clinical practice, making their sessions more focused and helpful. They also noted that it improved their ability to identify a caregiver's overall needs. Conclusions: Implementing caregiver distress screening positively impacted social work practice at our institution. Despite variable caregiver enrollment and a few implementation challenges, the findings support the importance and potential benefit of screening for caregiver distress in a pediatric oncology setting.

Peritumoral edema (PTE) occurs with nearly all intracranial tumors and their treatments. PTE increases mass effect and intracranial pressure. This often causes neurologic decline, worsens function, and complicates treatment planning. At times, emergency care is needed. This review examines current PTE findings and their relevance to neuroimaging and neuro-oncology management. Blood-brain barrier failure results from tumor-induced mechanisms, including angiogenesis, changes in inflammation, alterations in aquaporin-mediated water transport, tight junction failure, pericyte loss, and vesicle signaling. These factors produce various edema types and outcomes. Conventional MRI usually cannot distinguish between these or tell if vasogenic edema is from tumor infiltration or treatment. Thus, this review highlights combined diffusion and perfusion modeling, thermodynamic approaches, AI, radiomics, and anesthetic agents for tracking temporal changes. Corticosteroid treatment for vasogenic edema has risks, such as tapering problems and rebound edema, which offset its benefits. Despite this, corticosteroids remain a first-line therapy. New options, vascular stabilization, changing the microenvironment and edema pathways, and anti-VEGF therapy, are being tested to limit steroid use. This review also covers pre-, intra-, and postoperative care for glioblastoma, meningioma, and brain metastases. Data algorithms now match symptom severity, imaging, and treatment context. Future research should seek biomarker validation, long-term safety, and standard imaging protocols.

A 3-year-old intact female Pit Bull Terrier mix-breed dog was examined because of acute vision loss. Ophthalmologic examination was consistent with bilateral optic neuritis. Abnormalities were not detected on the remainder of the neurological examination. Brain MRI identified multifocal lesions involving the optic nerves and cortical gray matter, while cerebrospinal fluid analysis demonstrated mixed pleocytosis. Abdominal ultrasonography revealed a cystic ovarian mass. Ovariohysterectomy was performed and histopathologic examination was consistent with an ovarian teratoma. Neural tissue within the teratoma featured extensive perivascular cuffing and immunohistochemistry confirmed mixed lymphocytic infiltration. After tumor resection, the dog was treated with corticosteroid for 40 days, leading to resolution of pleocytosis. Vision was preserved in the left eye but there was persistent vision loss in the right eye. Three years after initial presentation, good quality of life with no behavioral evidence of neurological disease or relapse was reported. This case highlights a suspected paraneoplastic neurological syndrome associated with an ovarian teratoma.

A working group of cIMPACT-NOW evaluated the literature on IDH-mutant gliomas for opportunities to improve pathology-based risk stratification and grading, especially at the interface of CNS WHO grade 2 and 3, since therapeutic decisions depend on risk assessment for clinical management. The group also evaluated newly described IDH-mutant glioma subgroups and considered multidisciplinary aspects of therapeutic decision-making. PDGFRA amplification was associated with highly aggressive clinical behavior of IDH-mutant astrocytomas, consistent with CNS WHO grade 4. Other genetic alterations associated with intermediate risk and most consistent with CNS WHO grade 3 included PIK3 mutations, EGFR amplification, MYCN amplification and specific RB pathway alterations, including CDK4, CDK6 and CCND2 amplification, RB1 homozygous deletion or mutation, and mutation of CDKN2A. DNA methylation signatures of G-CIMP-low or A_IDH_HG were consistent with CNS WHO grade 3 or 4, depending upon other grading criteria. We suggest a mitotic count of ≥ 3 per 2.4 mm2 could be considered as a CNS WHO grade 3 criterion. Our review did not uncover features to improve grading of oligodendroglioma, IDH-mutant and 1p/19q-codeleted, although CNS WHO grade 3 tumors with elevated mitotic rates, yet lacking necrosis, microvascular proliferation, CDKN2A/B homozygous deletion and MRI contrast enhancement, may be associated with extended survival. Implementing evidence-based criteria for risk stratification and grading will improve guidance for clinical decision-making.