Meningioma

Paraspinal Intramuscular Hemangioma at L5-S1 With Concurrent Disc Herniation

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In a case report Hamza Mahdi et al. from the Windsor Regional Hospital, Windsor published in the Journal of medical cases to describe a rare case of intramuscular hemangioma in the lumbar paraspinal region with coexisting L5-S1 disc herniation, and to discuss diagnostic complexities and management strategies. This case underscores the diagnostic challenge of distinguishing benign vascular tumors from other soft tissue lesions in the context of coexisting spinal pathologies. The lesion was misidentified preoperatively despite advanced imaging and biopsy, requiring definitive surgical excision for diagnosis. The authors advocate for the inclusion of vascular tumors in the differential diagnosis of persistent lumbar pain, especially when imaging reveals atypical soft tissue masses 1).

Critical Review

This is the seventh documented adult case of lumbar paraspinal intramuscular hemangioma, lending marginal novelty to the case. The radiologic and histologic evaluation is competently detailed, yet the lack of advanced imaging modalities such as contrast-enhanced MRI or MR angiography limits preoperative characterization. Furthermore, the diagnostic sequence—proceeding to surgery after an inconclusive CT-guided biopsy—reflects a pragmatic yet debatable strategy in light of possible biopsy sampling errors.

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Pain Relief, Disability, and Hospital Costs After Intradiscal Ozone Treatment or Microdiscectomy for Lumbar Disc Herniation: A 24-Month Real-World Prospective Study

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In a prospective real-world comparative study Sara Bisshopp et al. from Dr. Negrín University Hospital, Las Palmas published in the Journal of Clinical Medicine to compare clinical outcomes, hospital stay, and direct costs between initial intradiscal ozone treatment and standard microdiscectomy/discectomy in patients with lumbar disc herniation over a 24-month follow-up. Both groups experienced significant improvements in pain and disability scores. The ozone group had similar clinical outcomes to surgery but with significantly fewer surgical interventions (47% vs. 100%), shorter hospital stays, and reduced costs at 12 months 1).

Critical Appraisal

This study taps into a timely and pragmatic clinical question: Can minimally invasive ozone therapy reduce the surgical burden and costs while maintaining efficacy for lumbar disc herniation? While the 24-month prospective design and real-world context strengthen external validity, several methodological shortcomings temper enthusiasm.

First, the non-randomized design introduces considerable selection bias. The criteria for choosing ozone therapy vs. surgery, though labeled as “offered,” are not rigorously controlled. This self-selection can strongly influence outcomes. Second, sample size is modest (n=70), particularly when divided into two groups (32 ozone, 38 surgery), limiting statistical power.

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What drives clinic follow-up after traumatic spinal injury? An observational cohort study from Tanzania

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In a Retrospective Observational Cohort Study Ikwuegbuenyi et al. From Muhimbili Orthopaedic Institute, Dar es Salaam; Weill Cornell Medicine, New York publisher in the journal BMJ Open to identify demographic, injury-related, and healthcare system factors associated with clinic follow-up adherence after traumatic spinal injury (TSI) in Tanzania. Fewer than 13% of patients remained in follow-up at 12 months post-TSI. Key predictors of clinic return included private insurance, injury mechanism, shorter hospital stay, neurological improvement, and female sex. The authors call for targeted strategies to enhance long-term follow-up in LMICs 7).

Content and Scientific Merit

The study attempts to quantify and elucidate predictors of follow-up adherence among patients with traumatic spinal injuries in a low-resource setting. While the topic is relevant, particularly given global disparities in neurosurgical care, the analysis remains superficial. The selection of variables lacks depth—omitting psychological, transportation, or caregiver support factors. The authors rely heavily on retrospective registry data, yet provide minimal discussion of data quality or loss to follow-up bias beyond basic exclusions.

There is also insufficient interrogation of systemic barriers endemic to Tanzanian healthcare—such as infrastructure deficits or cultural mistrust of allopathic medicine—that could more meaningfully contextualize the findings. The regression analysis is underutilized; while odds ratios are presented, there’s no effort to model interaction effects or assess multicollinearity. Additionally, the use of ASIA Impairment Scale categories in logistic regression, without discussion of baseline functional capacity or socioeconomic stratification, undermines interpretability.

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Molecular insights into glioblastoma progression: role of CHCHD2P9 in tumor heterogeneity and prognosis

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In a translational research integrating single-cell RNA sequencing, flow cytometry, and in vitro functional assays. Ding et al. from the Anhui Medical University, Hefei; Shanghai Ninth People’s Hospital, Shanghai; University of Science and Technology of China, Hefei. published in Frontiers in Immunology to elucidate the role of the pseudogene CHCHD2P9 in glioblastoma progression and tumor heterogeneity by leveraging single-cell RNA sequencing and functional assays. CHCHD2P9 is overexpressed in glioma and correlates with worse prognosis. It may influence glioma proliferation and migration and serve as a novel prognostic biomarker or therapeutic target 1).

Critical Review: This study attempts a multidimensional exploration of glioblastoma heterogeneity by integrating advanced single-cell transcriptomics with basic cellular assays. The identification of CHCHD2P9 as a putative prognostic marker is intriguing, but the study lacks depth in mechanistic validation. While the correlation between CHCHD2P9 expression and clinical outcome is statistically supported, causality remains speculative. The study’s reliance on a pseudogene raises biological plausibility concerns, especially without sufficient evidence for its protein-coding function or epigenetic regulation. The model’s translational utility is also not directly tested in patient-derived xenografts or organoids. The work is hypothesis-generating rather than definitive, with significant promise for future mechanistic follow-up.

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LINC01783 Promotes Glioma Tumorigenesis by Enhancing GATA3 Expression Through CBP-Mediated H3K27 Acetylation to Suppress PTEN Expression

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LINC01783

In vitro and in vivo molecular mechanistic investigations

Study Summary

Type of Study: In vitro and in vivo molecular mechanistic investigation First Author: Shaocai Hao et al. Author Affiliations:

  • Department of Neurosurgery, General Hospital of Ningxia Medical University, Yinchuan, Ningxia, China

Journal: Biofactors DOI: 10.1002/biof.70029 PMID: 40546096 Publication Date: May–June 2025 Title: LINC01783 Promotes Glioma Tumorigenesis by Enhancing GATA3 Expression Through CBP-Mediated H3K27 Acetylation to Suppress PTEN Expression

Purpose

To elucidate the oncogenic function of the long intergenic non-coding RNA LINC01783 in glioma progression, focusing on its effect on GATA3 expression and PTEN suppression via CBP-mediated H3K27 acetylation.

Conclusions

LINC01783 is significantly upregulated in glioma tissues and enhances glioma progression by promoting GATA3 expression through CBP-mediated H3K27 acetylation. This, in turn, transcriptionally represses PTEN, contributing to increased tumor cell proliferation and stemness.

Critical Review

Methodological Weaknesses

  • Sample opacity: No clear details on glioma sample number, subtype stratification, or clinical metadata; undermines reproducibility and clinical significance.
  • In vivo data insufficiently controlled: No information on animal randomization, group sizes, or blinding procedures. Xenograft conclusions are weakly supported.
  • Epigenetic mechanistic oversimplification: Attribution of GATA3 regulation solely to CBP-H3K27ac is unconvincing; alternative pathways and compensatory mechanisms are unexamined.
  • Lack of causal proof: The PTEN axis is emphasized, but whether GATA3 mediates all observed phenotypes is not demonstrated.
  • No translational bridge: No therapeutic agent, inhibitor, or antisense strategy explored. The leap to “potential therapeutic target” is scientifically unfounded.

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Oncolytic virus‑mediated immunomodulation in glioblastoma: Insights from clinical trials and challenges

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In a Review Raziye Piranlioglu *et al.* from

Affiliations Harvey Cushing Neuro‑oncology Laboratories, Dept. Neurosurgery, Brigham and Women’s Hospital, Boston, MA, USA; Dana‑Farber Cancer Institute, Boston, MA, USA

published in *Seminars in Immunology* with the Purpose to synthesize data from clinical trials of oncolytic viruses (OVs) in glioblastoma, evaluating immunomodulatory effects, delivery strategies, and challenges in assessing immune responses. They concluded that Oncolytic virus therapy is well tolerated in GBM trials and can convert the immunosuppressive microenvironment into an immunologically active state. However, limitations in post‑treatment sampling and delivery methods impede full understanding of biological mechanisms.

This review is a rehash of well‑known take‑home messages, offering little in the way of novel synthesis or incisive critique. The authors lean heavily on canonical trials (e.g., oHSV, adenovirus) but fail to integrate preclinical correlates from myeloid-targeting strategies, such as macrophage polarization dynamics or MDSC modulation. There’s no fresh mechanism, no meta‑analysis of response rates, and no exploration of why most trials remain phase I with limited impact. Sample‑scarcity is once again highlighted as a blocker—but no alternative trial designs (e.g., neoadjuvant window cohorts, liquid biopsy) are proposed. In short, the review scratches the surface of challenges without pushing the field forward.

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A national study of neurosurgical residency competency development

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In a retrospective observational cohort study Using national milestone data from 2478 neurosurgery residents across 120 U.S. programs (2018–2022), with descriptive statistical analysis Khalid et al.evaluate the progression of neurosurgical residents across the 6 ACGME core competencies and 20 subcompetencies, specifically: Assessing how many residents reach level 4 proficiency by the final year (PGY-7). Identifying patterns of co-occurring deficiencies in competencies. They conclude that neurosurgery residents demonstrate substantial milestone progression throughout training, but gaps remain—particularly in specialized clinical skills and self-assessment (Reflective Practice). Nearly 45% fail to reach level 4 in at least one subcompetency by PGY-7. These deficiencies are concentrated in areas often covered during fellowship training (e.g., epilepsy, pain, peripheral nerve). Therefore, residency programs may need to enhance exposure to these areas or redefine competency expectations. The authors recommend: Targeted educational interventions

Specialized procedural training To ensure that all residents achieve the necessary competencies for independent practice 1)

🧠 1. Conceptual Overreach: Competency as a Bureaucratic Fantasy

This study mistakes numerical progression in a checklist for actual neurosurgical maturity. “Milestones” are treated as objective truths, when in reality they are administrative fictions imposed top-down by ACGME to simulate accountability. The implicit assumption—that every resident must hit an arbitrary “level 4” to be considered competent—is never questioned. The authors do not interrogate what level 4 means, who defines it, or whether it maps to meaningful clinical outcomes. Instead, they deliver descriptive statistics masquerading as insights.

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Post-traumatic hydrocephalus after decompressive craniectomy: a multidimensional analysis of clinical, radiological, and surgical risk factors

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In a retrospective observational cohort study Romualdo et al. from the Department of Neurosurgery Faculty of Medicine, Technische Universität Dresden University Hospital Carl Gustav Carus published in the Neurosurgical Review to identify clinical, radiological, and surgical risk factors associated with the development of shunt-dependent posttraumatic hydrocephalus (PTH) in patients who underwent decompressive craniectomy following severe traumatic brain injury (TBI). Shunt-dependent post-traumatic hydrocephalus (PTH) occurred in 27% of patients after decompressive craniectomy for severe TBI. Independent risk factors included older age, basal cistern subarachnoid hemorrhage, post-traumatic ischemic infarcts, transcalvarial herniation, subdural hygroma, and progressive contusion hemorrhages. Surgical parameters were not predictive. Patients requiring shunt placement had significantly worse neurological outcomes 5).

🚨 The Illusion of Multidimensionality Despite claiming a “multidimensional” analysis, the study delivers a monotonous list of obvious associations—many of which have been reported in the literature for over a decade. Subarachnoid hemorrhage, infarction, hygroma, contusion progression… yes, thank you, we knew that. What’s new? Almost nothing.

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Outcomes of CT-Guided Targeted Epidural Patching for Lateral Dural Tears in Spontaneous Intracranial Hypotension: A Multicenter Retrospective Cohort Study

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In a multicenter retrospective cohort study, Callen et al. — from the University of Colorado Anschutz, Kaiser Permanente Santa Clara, University of Freiburg, Cambridge University Hospitals, Newcastle upon Tyne Hospitals, Guy’s & St Thomas’s / King’s College Hospitals, and King’s College London — published in the American Journal of Neuroradiology, the clinical and radiologic outcomes of CT-guided epidural patching in patients with lateral dural tear causing spontaneous intracranial hypotension (SIH). The study also aimed to determine whether anatomic factors (e.g., herniated arachnoid pouch) or procedural variables (e.g., patch volume, material, approach) predict treatment success.

CT-guided patching led to complete symptom resolution in approximately one-third of patients. The presence of a herniated arachnoid pouch was associated with lower radiologic resolution of CSF collections. Procedural variables — such as patch type, approach, and volume — were not associated with outcomes. Notably, some patients experienced clinical improvement despite persistent CSF collections, highlighting the need for long-term follow-up and cautious reliance on imaging alone.

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🧠 Takeaway Message for Neurosurgeons

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Long-Term Mortality of Patients With Head Injuries—A 10-Year Follow-up Study With Population Controls

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In a retrospective, population-based cohort study with matched controls and longitudinal follow-up, Heinonen et al. from Tampere University Hospital, Helsinki University Hospital, and Harvard Medical School in the Neurosurgery Journal compared 10-year survival rates and causes of death between patients with traumatic head injuries treated at a university hospital and matched population controls. They aimed to identify factors associated with long-term mortality after TBI.

Patients with head injuries exhibited significantly reduced long-term survival compared to matched controls, even after excluding early mortality. However, patient-related characteristics (e.g., comorbidities, lifestyle factors) — more than injury severity itself — appeared to drive this increased mortality risk.

Notably, even patients without documented TBI (likely mild or undiagnosed) showed decreased survival, suggesting an under-recognized long-term impact of head injury across all severity levels 2).

In this population-based cohort study, the authors track 10-year mortality in over 1,900 patients with head injuries versus 9,600 matched controls. Unsurprisingly, trauma patients die more — especially from alcohol, accidents, and “patient characteristics.” The conclusion? It’s not the injury; it’s the person. This study doesn’t just underdeliver — it underthinks.

🧠 1. Conceptual Cowardice: “Patient Characteristics” as a Black Box

The study’s main conclusion — that patient-related factors, not injury severity, explain increased mortality — is not only reductive but evasive. The term “patient characteristics” serves as a statistical landfill for all the unmeasured, uncontrolled, and misunderstood variables: mental health, addiction, social deprivation, neurobehavioral sequelae… all dumped under one lazy label.

Rather than confront the neuropsychiatric aftermath of head trauma, the authors retreat behind correlational shields.

❝They died because of who they were, not what happened to them.❞ — That’s not science. That’s resignation.

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