Neurosurgery最新文献

Background and objectives: Meningiomas are the most common primary intracranial tumors, with over 450 000 new cases each year. Although surgical resection remains the standard of care, recurrence occurs in up to 40% of cases. Reoperation poses additional risks due to anatomic changes and scar tissue. Elderly and frail patients experience increased rates of surgical morbidity, limiting treatment options. This study evaluates the potential of embolization, a technique traditionally used preoperatively to reduce intraoperative blood loss, as a definitive or palliative standalone treatment in select cases.

Methods: A systematic review was conducted following Preferred Reporting Items for System reviews and Meta-Analyses guidelines. PubMed/MEDLINE and EMBASE were searched for studies reporting standalone meningioma embolization, defined as embolization without resection or radiotherapy for at least 2 months postprocedure. Two blinded reviewers screened articles using Covidence and conducted standardized data extraction. Variables collected included patient demographics, tumor characteristics, embolic agents, outcomes, and complications.

Results: This review identified 121 patients across 34 studies treated with standalone embolization. Of these, 67 patients had long-term follow-up. Symptomatic improvement was reported in 77 ± 6% of symptomatic patients, with radiographic tumor shrinkage observed in 84 ± 6%, and complete resolution seen in 5%. The major complication rate (5%) was comparable with that of preoperative embolization (3%-6%) and lower than that of surgical resection (7%-31%).

Conclusion: Standalone embolization potentially represents a lower-risk alternative for meningioma patients unsuitable for surgery or refractory to standard treatments. Although current evidence is limited and largely retrospective, reported outcomes support further prospective investigation. Mechanistically, ischemia-induced necrosis may be the underlying cause of tumor and symptom regression. Larger studies are needed to establish standalone embolization as a safe and effective meningioma treatment.

Background and objectives: Brain invasion (BINV) and peritumoral edema (PTBE) have repeatedly been implicated as major contributors to meningioma-related seizures (MRS). By contrast, the influence of the precise tumor location on seizure risk is still insufficiently characterized. In this study, we systematically investigated clinical and imaging-derived predictors of MRS, integrating them with spatial analyses using voxel-based lesion symptom mapping (VLSM).

Methods: We reviewed clinical variables-including seizure history, histopathological subtype, World Health Organization (WHO) grade, BINV, and extent of resection-alongside MRI features such as PTBE, tumor dimensions, and anatomic location in a cohort of 532 meningioma patients. Significant predictors of MRS were identified using multivariate stepwise regression. These predictors were subsequently entered into a multivariate VLSM framework to determine their anatomic distribution.

Results: A total of 93 of 532 patients (17%) experienced seizures prior to surgery. BINV, PTBE, and tumor location emerged as independent predictors of preoperative MRS. VLSM revealed the frontoparietal transition zone (FPTZ) as the region most strongly associated with seizures linked to BINV, whereas PTBE predominantly predicted MRS in frontal convexity and sphenoid wing tumors. Although WHO grade and histological classification displayed distinct spatial patterns, neither was directly related to MRS. Postoperatively, persistent seizure activity occurred in 6% of patients, again implicating the FPTZ as a major risk region. Seizures associated with PTBE were more likely to resolve following tumor removal.

Conclusion: Tumor-intrinsic characteristics such as histology, WHO grade, and lesion size play only a limited role in the development of MRS. Instead, BINV, PTBE, and the anatomic location of the meningioma are the principal determinants of seizure risk. Our findings underscore the FPTZ as a critical region linking tumor invasiveness, seizure generation, and postoperative seizure control.

Background and objectives: Vagus nerve stimulation (VNS) is a United States Food and Drug Administration-approved treatment for refractory epilepsy, stroke rehabilitation, chronic or recurrent depression as adjunctive therapy, and rheumatoid arthritis. It is also being explored as a potential treatment modality for heart failure and relapsing-remitting multiple sclerosis among other disease states. The current mode of stimulation delivery employed widely is the use of nerve cuffs mounted directly on the nerve via an invasive cervical cutdown procedure. Furthermore, the feedback from the nerve upon stimulation delivery is not monitored. It has also been reported that the internal fascicular organization along the vagus nerve is highly variable and therefore different groups of fascicles can be selectively activated based on electrode position. However, it is not possible to change the position of the nerve cuff without additional surgery if placed in a suboptimal location.

Methods: In this work, we propose the development of a device for closed-loop endovascular VNS that helps mitigate the challenges highlighted earlier and demonstrate this in a preclinical model on 4 subjects. In this minimally invasive procedure, a resheathable stent form factor is deployed within the jugular vein, providing an opportunity for intraprocedural trialing.

Results: We demonstrate accurate detection of nerve activation via endovascular evoked compound action potential along with an indication of the specific fibers being activated. Furthermore, this procedure also offers an opportunity to reduce side effects including muscle activation that is seen in current VNS procedures by tuning the applied stimulation.

Conclusion: This closed-loop endovascular VNS stimulation platform technology opens up a new paradigm for ongoing research in peripheral nerve stimulation, affecting several disease states.

Background and objectives: Despite its clinical utility and consistent procedural volume, Medicare reimbursement for anterior cervical discectomy and fusion (ACDF) has undergone policy-driven changes over the past decade. This study investigated longitudinal Medicare reimbursement trends for ACDF among orthopedic and neurological spine surgeons from 2013 to 2023.

Methods: A retrospective analysis was performed using publicly available Centers for Medicare and Medicaid Services databases. Surgeons who billed ≥10 ACDF procedures (current procedural terminology 22551) per year were included. Provider demographics, procedural volumes, average Medicare standardized amount (AMSA), inflation-adjusted AMSA, and average annual procedural income (API) were analyzed. Comparisons were made by surgical subspecialty by year.

Results: A total of 10 311 spine surgeons performed 187 062 ACDF procedures between 2013 and 2023. Neurosurgeons comprised 65% of providers and procedures, while orthopedic surgeons comprised 35%. Average annual case volumes were similar across specialties. Between 2013 and 2023, inflation-adjusted AMSA declined 23% and API declined 27%, despite stable procedural volumes. These declines were consistent across neurosurgeons (-23% AMSA, -27% API) and orthopedic surgeons (-22% AMSA, -27% API). The number of neurosurgeons performing ACDF decreased over the study period (17% decrease), while the number of orthopedic surgeons increased (31% increase). Both specialties saw a reduction in average procedures per provider.

Conclusion: While unadjusted Medicare reimbursement for ACDF remained stable from 2013 to 2023, inflation-adjusted reimbursement declined substantially, reflecting an erosion in surgeon compensation. These findings raise concerns about the financial sustainability of providing ACDF services in the Medicare population and underscore the need for policy strategies that protect access to surgical care for an aging population.

Background and objectives: Racial/ethnic disparities in health literacy, self-perception of health status, and barriers to care access have been described for many disease processes. However, few studies have characterized these factors in patients with Chiari malformation type I (CM-1).

Methods: We performed a cross-sectional analysis of data from the National Institutes of Health All of Us Research Program. Adults with CM-1 were identified through International Classification of Diseases, ninth revision and 10th revision diagnostic codes and stratified by race/ethnicity: non-Hispanic White (NHW), non-Hispanic Black or African American, and Hispanic or Latino (HL). Patient demographics and socioeconomic status were examined. Group-level differences in survey-reported baseline health status, health perceptions, health literacy, and perceived barriers to care were evaluated.

Results: Of the 966 patients identified, 552 (57.1%) were NHW, 225 (23.3%) were non-Hispanic Black, and 189 (19.6%) were HL. Socioeconomic status varied between strata, with the highest education level, income level, employment, retirement, marital status, and home ownership reported by NHW patients (P < .001 for all). Average pain was highest among HL patients, as well as proportions of best and worst general health status (all P < .001). The NHW cohort was able to accomplish more of their everyday activities than the other cohorts (P = .003). The worst general mental health (P = .015), general physical health (P = .004), and general quality of life (P < .001) were reported by HL patients. The HL cohort had the highest rates of difficulty in understanding information, required health material assistance, and had low medical form confidence (P < .001 for all). Furthermore, difficulties affording follow-up care (P = .041), concerns about payment (P = .033), and transportation-related delays in care (P = .002) were most common in the HL cohort.

Conclusion: The results of our study indicate racial/ethnic disparities in CM-1 patients' perception of their health, health literacy, and access to care.

Background and objectives: Dual-energy x-ray absorptiometry (DXA) is the standard for assessing bone mineral density (BMD); however, its accuracy is limited by bone architecture, acquisition quality, and clinical context. Hounsfield units (HUs) offer an alternative for osteoporosis risk stratification. Machine learning (ML) models can segment computed tomography (CT) anatomy and integrate HU data to generate BMD metrics previously unavailable. This study elucidates the capabilities of an automated CT segmentation platform and investigates the relationship between vertebral HUs and DXA stratifications of BMD.

Methods: A retrospective analysis of 229 patients with lumbar CT and DXA scans within 1 year was performed. The TotalSegmentator ML model obtained segmentations of the lumbar spine which were integrated with CT radiographic data to compute volume (cm3) and HU density of vertebral bodies, trabecular bone, and cortical bone. Vertebral body HU means were compared against lumbar, hip, and femoral neck DXA T scores in healthy individuals (T-score > -1.0), patients with osteopenia (-1.0 ≥ T-score ≥ -2.5), and patients with osteoporosis (T-score < -2.5) .

Results: Patients (85.2% female) had a mean age of 71.02 ± 13.62 years and body mass index of 28.04 ± 7.51 kg/m2. Mean HUs from L1-L5 correlated with femoral neck (r = 0.54, P < .001), lumbar (r = 0.54, P < .001), and hip (r = 0.46, P < .001) DXA T-scores. Compared with osteopenic individuals, healthy individuals had higher L1-L5 total HU (265.0 vs 226.4, P < .001), trabecular HU (179.3 vs 136.5, P < .001), and cortical HU (312.0 vs 274.8, P < .001). The L1-L5 total, trabecular, and cortical bone were predictive for low BMD (area under the curve [AUC] = 0.77, AUC = 0.80, and AUC = 0.75) and osteoporosis (AUC = 0.79, AUC = 0.75, and AUC = 0.80), respectively. Youden Index analysis identified optimal trabecular and cortical bone threshold values of 141.3 HU and 254.2 HU for low BMD as well as 132.3 HU and 249.0 HU for osteoporosis, respectively.

Conclusion: ML-driven CT segmentation correlates with DXA BMD stratifications and can provide a robust, consistent, and efficient assessment of HU density of critical vertebral structures.

Background and objectives: Identification of the symptomatic aneurysm in patients with multiple intracranial aneurysms (MIAs) represents a challenge. Aneurysm wall enhancement is a potential imaging biomarker to assess symptomatic status among intracranial aneurysms. We aimed to use aneurysm wall enhancement in the identification of symptomatic aneurysms in patients with MIAs.

Methods: Patients who underwent high-resolution 3 Tesla magnetic resonance imaging between 2018 and 2024 at 3 institutions-one in the United States and 2 in China-were included in the analysis. Eligible patients had MIAs, with at least 1 aneurysm classified as symptomatic. Morphological measurements were obtained from angiography studies. Three-dimensional circumferential aneurysm wall enhancement (3D-CAWE) was assessed for all aneurysms. Multivariate logistic regression was used to identify variables independently associated with symptomatic status.

Results: Thirty patients with 82 MIAs were included, 30/82 (36.6%) were symptomatic and 52/82 (63.3%) were asymptomatic. Aneurysmal size (adjusted odds ratio [aOR]: 1.5, 95% CI: 0.95-2.8, P = .1) and size ratio (aOR: 2.2, 95% CI: 0.8-3.2, P = .2) were not associated with symptomatic presentation. Symptomatic aneurysms were more likely to have a higher 3D-CAWE (aOR: 1.15, 95% CI: 1.05-1.24, P = .01) when compared with asymptomatic aneurysms. Receiver operating characteristic analysis revealed that a 3D-CAWE cutoff point of 1.02 has a specificity of 88% and negative predictive value of 79% in detecting symptomatic aneurysms among patients with MIAs.

Conclusion: 3D-CAWE can be used in the identification of symptomatic aneurysms in patients with MIAs.

Since its introduction into medical terminology by Lord Henry Cohen in 1941, the term "neurapraxia" has become established in the neurological and neurosurgical lexicon, although it is often misused or misspelled. It denotes a transient dysfunction of a peripheral nerve, as distinct from axonotmesis and neurotmesis, which describe more significant structural injuries to a peripheral nerve. To expand our understanding of neurapraxia, it is necessary to examine the phenomenon in both temporal and spatial contexts. This study examines neurapraxia in: (A) Time-(1) the origins of the term neurapraxia and (2) the time-course of a neurapraxic injury and its recovery, and (B) Space-(3) the microstructure of a neurapraxic injury and (4) the locations of neurapraxic injuries within the peripheral nervous system. We demonstrate that the term neurapraxia encompasses both a temporal and a spatial definition. In time, it applies to transient peripheral nerve palsy, from which recovery occurs before there is sufficient time for axonal regeneration, typically within a few weeks. In space, there is a histopathological change limited to localized demyelination in nerves lined by epineurium and myelinated by Schwann cells. Nerves distal to the spine qualify as nerves to which the term neurapraxia can apply; however, cranial nerves and spinal nerve roots (including cauda equina) are inconsistent with this owing to the variability in myelinating cells along their course (oligodendroglia proximally, i.e., central glial segment), the absence of an epineurial covering, and exposure to cerebrospinal fluid.