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Comprehensive Endovascular and Open Surgical Management of Cerebral Arteriovenous Malformations
Published on: October 20, 2017
Cerebral Arteriovenous Malformations and Epilepsy, Part 1: Predictors of Seizure Presentation
Dale Ding1, Robert M Starke1, Mark Quigg2
1Department of Neurological Surgery, University of Virginia, Charlottesville, VA, USA.
Objective:
Seizures are relatively common in patients harboring cerebral arteriovenous malformations (AVMs). Because the pathogenesis of AVM-associated epilepsy is not well-defined, we aim to determine the factors associated with seizure presentation in AVM patients.
Methods:
We evaluated our institutional AVM radiosurgery database, from 1989-2013, to select patients in whom pertinent clinical information at presentation and adequate clinical and radiologic follow-up was available. Baseline patient demographics and AVM angioarchitectural features were compared between patients with and without seizure presentation. In addition to standard descriptive statistics, logistic regression analyses were performed to identify predictors of seizure presentation.
Results:
Of the 1007 AVM patients included for analysis, 229 patients presented with seizures (22.7%). The incidence of seizure presentation was significantly higher in cortical than noncortical AVMs (33.1% vs. 6.6%, P < 0.0001). Among the cortical locations, occipital AVMs had the lowest rate of seizure presentation (21.5%, P = 0.0012), whereas the rates of seizure presentation in frontal (37.3%), temporal (37.7%), and parietal (34.0%) AVMs were similar. The lack of prior AVM hemorrhage (P < 0.0001), larger nidus diameter (P < 0.0001), and cortical location (P < 0.0001) were independent predictors of seizure presentation in the multivariate analysis. The strongest independent predictors of seizure presentation were lack of prior AVM hemorrhage (OR 16.8) and cortical location (OR 4.2).
Conclusions:
Large, unruptured, cortical nidi are most prone to seizure presentation in patients referred for radiosurgery. Further investigations of the molecular biology, neuronal and glial physiology, and natural history of AVM-associated epilepsy appear warranted.
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