RESUMO
This study reevaluates the conventional understanding of midbrain anatomy and neuroanatomical nomenclature in the context of recent genetic and anatomical discoveries. The authors assert that the midbrain should be viewed as an integral part of the forebrain due to shared genetic determinants and evolutionary lineage. The isthmo-mesencephalic boundary is recognized as a significant organizer for both the caudal midbrain and the isthmo-cerebellar area. The article adopts the prosomeric model, redefining the whole brain as neuromeres, offering a more precise depiction of brain development, including processes like proliferation, neurogenesis, cell migration, and differentiation. This shift in understanding challenges traditional definitions of the midbrain based on external brain morphology. The study also delves into the historical context of neuroanatomical models, including the columnar model proposed by Herrick in 1910, which has influenced our understanding of brain structure. Furthermore, the study has clinical implications, affecting neuroanatomy, neurodevelopmental studies, and the diagnosis and treatment of brain disorders. It emphasizes the need to integrate molecular research into human neuroanatomical studies and advocates for updating neuroanatomical terminology to reflect modern genetic and molecular insights. The authors propose two key revisions. First, we suggest reclassifying the isthmo-cerebellar prepontine region as part of the hindbrain, due to its role in cerebellar development and distinct location caudal to the genetically-defined midbrain. Second, we recommend redefining the anterior boundary of the genetically-defined midbrain to align with genetic markers. In conclusion, the authors highlight the importance of harmonizing neuroanatomical nomenclature with current scientific knowledge, promoting a more precise and informed understanding of brain structure, which is crucial for both research and clinical applications related to the human brain.
Assuntos
Neoplasias do Tronco Encefálico , Humanos , Neoplasias do Tronco Encefálico/genética , Neoplasias do Tronco Encefálico/patologia , Mesencéfalo , Tronco EncefálicoRESUMO
INTRODUCTION: Sarcoma spinal metastases (SSM) are particularly difficult to manage given their poor response rates to chemotherapy and inherent radioresistance. We evaluated outcomes in a cohort of patients with SSM uniformly treated using single-fraction simultaneous-integrated-boost (SIB) spine stereotactic radiosurgery (SSRS). MATERIALS AND METHODS: A retrospective review was conducted at a single tertiary institution treated with SSRS for SSM between April 2007-April 2023. 16-24 Gy was delivered to the GTV and 16 Gy uniformly to the CTV. Kaplan-Meier analysis was conducted to assess time to progression of disease (PD) with proportionate hazards modelling used to determine hazard ratios (HR) and respective 95 % confidence intervals (CI). RESULTS: 70 patients with 100 lesions underwent SSRS for SSM. Median follow-up was 19.3 months (IQR 7.7-27.8). Median age was 55 years (IQR42-63). Median GTV and CTVs were 14.5 cm3 (IQR 5-32) and 52.7 cm3 (IQR 29.5-87.5) respectively. Median GTV prescription dose and biologically equivalent dose (BED) [α/ß = 10] was 24 Gy and 81.6 Gy respectively. 85 lesions received 24 Gy to the GTV. 27 % of patients had Bilsky 1b or greater disease. 16 of 100 lesions recurred representing a crude local failure rate of 16 % with a median time to failure of 10.4 months (IQR 5.7-18) in cases which failed locally. 1-year actuarial local control (LC) was 89 %. Median overall survival (OS) was 15.3 months (IQR 7.7-25) from SSRS. Every 1 Gy increase in GTV absolute minimum dose (DMin) across the range (5.8-25 Gy) was associated with a reduced risk of local failure (HR = 0.871 [95 % CI 0.782-0.97], p = 0.009). 9 % of patients developed vertebral compression fractures at a median of 13 months post SSRS (IQR 7-25). CONCLUSION: This study represents one of the most homogenously treated and the largest cohorts of patients with SSM treated with single-fraction SSRS. Despite inherent radioresistance, SSRS confers durable and high rates of local control in SSM without unexpected long-term toxicity rates.
Assuntos
Fraturas por Compressão , Segunda Neoplasia Primária , Radiocirurgia , Sarcoma , Fraturas da Coluna Vertebral , Neoplasias da Coluna Vertebral , Humanos , Pessoa de Meia-Idade , Radiocirurgia/efeitos adversos , Fraturas da Coluna Vertebral/etiologia , Fraturas por Compressão/etiologia , Neoplasias da Coluna Vertebral/radioterapia , Neoplasias da Coluna Vertebral/secundário , Recidiva Local de Neoplasia/cirurgia , Sarcoma/radioterapia , Sarcoma/cirurgia , Estudos Retrospectivos , Segunda Neoplasia Primária/etiologiaRESUMO
Over the past 30 years, the treatment of deep and eloquent arteriovenous malformations (AVMs) has moved away from microneurosurgical resection and towards medical management and the so-called minimally invasive techniques, such as endovascular embolization and radiosurgery. The Spetzler-Martin grading system (and subsequent modifications) has done much to aid in risk stratification for surgical intervention; however, the system does not predict the risk of hemorrhage nor risk from other interventions. In more recent years, the ARUBA trial has suggested that unruptured AVMs should be medically managed. In our experience, although these eloquent regions of the brain should be discussed with patients in assessing the risks and benefits of intervention, we believe each AVM should be assessed based on the characteristics of the patient and the angio-architecture of the AVM, in particular venous hypertension, which may guide us to treat even high-grade AVMs when we believe we can (and need to) to benefit the patient. Advances in imaging and intraoperative adjuncts have helped us in decision making, preoperative planning, and ensuring good outcomes for our patients. Here, we present several cases to illustrate our primary points that treating low-grade AVMs can be more difficult than treating high-grade ones, mismanagement of deep and eloquent AVMs at the behest of dogma can harm patients, and the treatment of any AVM should be tailored to the individual patient and that patient's lesion.