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Mathias Kunz, Philipp Karschnia, Ingo Borggraefe, Soheyl Noachtar, Joerg-Christian Tonn, and Christian Vollmar


Reoperation may be an option for select patients with unsatisfactory seizure control after their first epilepsy surgery. The aim of this study was to describe the seizure-free outcome and safety of repeated epilepsy surgery in our tertiary referral center.


Thirty-eight patients with focal refractory epilepsy, who underwent repeated epilepsy surgeries and had a minimum follow-up time of 12 months after reoperation, were included. Systematic reevaluation, including comprehensive neuroimaging and noninvasive (n = 38) and invasive (n = 25, 66%) video-electroencephalography monitoring, was performed. Multimodal 3D resection maps were created for individual patients to allow personalized reoperation.


The median time between the first operation and reoperation was 74 months (range 5–324 months). The median age at reoperation was 34 years (range 1–74 years), and the median follow-up was 38 months (range 13–142 months). Repeat MRI after the first epilepsy surgery showed an epileptogenic lesion in 24 patients (63%). The reoperation was temporal in 18 patients (47%), extratemporal in 9 (24%), and multilobar in 11 (29%). The reoperation was left hemispheric in 24 patients (63%), close to eloquent cortex in 19 (50%), and distant from the initial resection in 8 (21%). Following reoperation, 27 patients (71%) became seizure free (Engel class I), while 11 (29%) continued to have seizures. There were trends toward better outcome in temporal lobe epilepsy and for unilobar resections adjacent to the initial surgery, but there was no difference between MRI lesional and nonlesional patients. In all subgroups, Engel class I outcome was at least 50%. Perioperative complications occurred in 4 patients (11%), with no fatalities.


Reoperation for refractory focal epilepsy is an effective and safe option in patients with persistent or recurrent seizures after initial epilepsy surgery. A thorough presurgical reevaluation is essential for favorable outcome.

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Daniel Duran, Philipp Karschnia, Jonathan R. Gaillard, Jason K. Karimy, Mark W. Youngblood, Michael L. DiLuna, Charles C. Matouk, Beverly Aagaard-Kienitz, Edward R. Smith, Darren B. Orbach, Georges Rodesch, Alejandro Berenstein, Murat Gunel, and Kristopher T. Kahle

Vein of Galen malformations (VOGMs) are rare developmental cerebrovascular lesions characterized by fistulas between the choroidal circulation and the median prosencephalic vein. Although the treatment of VOGMs has greatly benefited from advances in endovascular therapy, including technical innovation in interventional neuroradiology, many patients are recalcitrant to procedural intervention or lack accessibility to specialized care centers, highlighting the need for improved screening, diagnostics, and therapeutics. A fundamental obstacle to identifying novel targets is the limited understanding of VOGM molecular pathophysiology, including its human genetics, and the lack of an adequate VOGM animal model. Herein, the known human mutations associated with VOGMs are reviewed to provide a framework for future gene discovery. Gene mutations have been identified in 2 Mendelian syndromes of which VOGM is an infrequent but associated phenotype: capillary malformation–arteriovenous malformation syndrome (RASA1) and hereditary hemorrhagic telangiectasia (ENG and ACVRL1). However, these mutations probably represent only a small fraction of all VOGM cases. Traditional genetic approaches have been limited in their ability to identify additional causative genes for VOGM because kindreds are rare, limited in patient number, and/or seem to have sporadic inheritance patterns, attributable in part to incomplete penetrance and phenotypic variability. The authors hypothesize that the apparent sporadic occurrence of VOGM may frequently be attributable to de novo mutation or incomplete penetrance of rare transmitted variants. Collaboration among treating physicians, patients’ families, and investigators using next-generation sequencing could lead to the discovery of novel genes for VOGM. This could improve the understanding of normal vascular biology, elucidate the pathogenesis of VOGM and possibly other more common arteriovenous malformation subtypes, and pave the way for advances in the diagnosis and treatment of patients with VOGM.