Objective: Several clinical studies have explored the feasibility and efficacy of radiosurgical treatment for mesial temporal lobe epilepsy, but the long-term safety of this treatment has not been fully characterized. This study aims to report and describe radiation-induced cavernous malformation as a delayed complication of radiosurgery in epilepsy patients.
Methods: The series includes 20 patients with mesial temporal lobe epilepsy who underwent Gamma Knife radiosurgery (GKRS). The majority received a prescribed isodose of 24 Gy as an adjuvant treatment after anterior temporal lobectomy.
Results: In this series, we identified radiation-induced cavernous malformation in three patients, resulting in a cumulative incidence of 18.4% (95% confidence interval, 6.3% to 47.0%) at an 8-year follow-up. These late sequelae of vascular malformation occurred between 6.9 and 7.6 years after GKRS, manifesting later than other delayed radiation-induced changes, such as radiation necrosis. Neurological symptoms attributed to intracranial hypertension were present in those three cases involving cavernous malformation. Of these, two cases, which initially exhibited an insufficient response to radiosurgery, ultimately demonstrated seizure remission following the successful microsurgical resection of the cavernous malformation.
Conclusion: All things considered, the development of radiation-induced cavernous malformation is not uncommon in this population and should be acknowledged as a potential long-term complication. Microsurgical resection of cavernous malformation can be preferentially considered in cases where the initial seizure outcome after GKRS is unsatisfactory.
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http://dx.doi.org/10.3340/jkns.2023.0203 | DOI Listing |
J Cereb Blood Flow Metab
January 2025
Neurovascular Surgery Program, Department of Neurological Surgery, University of Chicago Medicine and Biological Sciences, Chicago, IL, USA.
Increases in mean lesional iron content by quantitative susceptibility mapping (QSM) by ≥6% and/or vascular permeability by dynamic contrast enhanced quantitative perfusion (DCEQP) by ≥40% on MRI have been associated with new symptomatic hemorrhage (SH) in cerebral cavernous malformations (CCMs). It is not known if plasma biomarkers can reflect these changes within the lesion proper. This cohort study enrolled 46 CCM patients with SH in the prior year.
View Article and Find Full Text PDFNeurosurg Rev
January 2025
Department of Neurology and Neurosurgery, Universidade Federal de São Paulo, São Paulo, SP, Brazil.
To evaluate the incidence of mortality, hemorrhage, and neurological deficits in treating intracranial arteriovenous malformations (AVMs) in patients over 18 through a comparative analysis of surgical approaches and other therapeutic modalities. A systematic review was conducted using MEDLINE, Embase, CENTRAL, and LILACS databases in November 2023. Inclusion criteria included clinical trials, cohorts studies, case-controls studies, and case series comparing patients over 18 undergoing surgery or microsurgery versus other treatments (radiosurgery, isolated embolization, and conservative treatment).
View Article and Find Full Text PDFEpilepsia
January 2025
Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.
Objective: To evaluate iron deposition patterns in patients with cerebral cavernous malformation-related epilepsy (CRE) using quantitative susceptibility mapping (QSM) for detailed analysis of iron distribution associated with a history of epilepsy and severity.
Methods: This study is part of the Quantitative Susceptibility Biomarker and Brain Structural Property for Cerebral Cavernous Malformation Related Epilepsy (CRESS) cohort, a prospective multicenter study. QSM was used to quantify iron deposition in patients with sporadic cerebral cavernous malformation (CCMs).
Cell Commun Signal
January 2025
School of Medicine, Nanjing University of Chinese Medicine, Nanjing, 210023, China.
Endothelial-mesenchymal transition (EndMT) is defined as an important process of cellular differentiation by which endothelial cells (ECs) are prone to lose their characteristics and transform into mesenchymal cells. During EndMT, reduced expression of endothelial adhesion molecules disrupts intercellular adhesion, triggering cytoskeletal reorganization and mesenchymal transition. Numerous studies have proved that EndMT is a multifaceted biological event driven primarily by cytokines such as TGF-β, TNF-α, and IL-1β, alongside signaling pathways like WNT, Smad, MEK-ERK, and Notch.
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