Citations 2
Surgical treatment of brainstem cavernous malformations: an international Delphi consensus
Dammann, Philipp , Abla, Adib A. , Salman, Rustam Al‐Shahi , Cenzato, Marco , Connolly, E. Sander , Cornelius, Jan F. , Hauck, Erik F. , Hernesniemi, Juha , Kivelev, Juri , MacDonald, Ryan , Ogilvy, Christopher S. , Steiger, Hans‐Jakob , Steinberg, Gary K. , Rauschenbach, Laurèl , Schmidt, Börge , Spetzler, Robert F., Schaller, Karl , Lawton, Michael T. , Abla, Adib , Ogilvy, Christopher S , Al-Shahi Salman, Rustam , Steinberg, Gary K , Rauschenbach, Laurèl , Andrade-Barazarte, Hugo , Beneš, Vladimír , Couldwell, William T. , Sola, Rafael García de , Gomez‐Paz, Santiago , Lanzino, Giuseppe , Macdonald, R. Loch, Morcos, Jacques J. , Santos, Alejandro N. , Oppong, Marvin Darkwah , Sure, Ulrich
Journal of Neurosurgery | October 1, 2021 | Volume: 136 | Issue: 5 | Pages: 1220-1230
OBJECTIVE Indication for surgery in brainstem cavernous malformations (BSCMs) is based on many case series, few comparative studies, and no randomized controlled trials. The objective of this study was to seek consensus about surgical management aspects of BSCM. METHODS A total of 29 experts were invited to participate in a multistep Delphi consensus process on the surgical treatment of BSCM. RESULTS Twenty-two (76%) of 29 experts participated in the consensus. Qualitative analysis (content analysis) of an initial open-ended question survey resulted in 99 statements regarding surgical treatment of BSCM. By using a multistep survey with 100% participation in each round, consensus was reached on 52 (53%) of 99 statements. These were grouped into 4 categories: 1) definitions and reporting standards (7/14, 50%); 2) general and patient-related aspects (11/16, 69%); 3) anatomical-, timing of surgery–, and BSCM-related aspects (22/37, 59%); and 4) clinical situation–based decision-making (12/32, 38%). Among other things, a consensus was reached for surgical timing, handling of associated developmental venous anomalies, handling of postoperative BSCM remnants, assessment of specific anatomical BSCM localizations, and treatment decisions in typical clinical BSCM scenarios. CONCLUSIONS A summary of typical clinical scenarios and a catalog of various BSCM- and patient-related aspects that influence the surgical treatment decision have been defined, rated, and interpreted.
Shared Genetic Risk Factors of Intracranial, Abdominal, and Thoracic Aneurysms
Hof, Femke N. G. van ’t, Ruigrok, Ynte M. , Lee, Cue Hyunkyu , Ripke, Stephan , Anderson, Graig, Baas, Annette F., Blankensteijn, Jan D. , Böttinger, Erwin P. , Bown, Matthew J. , Broderick, Joseph P., Bijlenga, Philippe , Crosslin, David R. , Ebeling, Christian , Eriksson, Johan G. , Fornage, Myriam , Foroud, Tatiana, Fraunberg, Mikael von und zu , Friedrich, Christoph M. , Gaál, Emília Ilona, Gottesman, Omri, Guo, Dongchuan , Harrison, Seamus C. , Hernesniemi, Juha , Hofman, Albert , Inoue, Ituro , Jääskeläinen, Juha E. , Kiemeney, Lambertus A. , Kivisaari, Riku , Ko, Nerissa , Koskinen, Seppo, Kubo, Michiaki , Kuivaniemi, Helena , Laakso, Aki , Lehto, Hanna, LeMaire, Scott A. , Malinowski, Jennifer , McCarty, Catherine A. , Mosley, Thomas H., Nakaoka, Hirofumi , Peissig, Peggy , Pera, Joanna , Rasmussen‐Torvik, Laura J. , Ritchie, Marylyn D. , Rivadeneira, Fernando , Rij, André M. van , Santos‐Cortez, Regie Lyn P., Saratzis, Athanasios , Słowik, Agnieszka , Tromp, Gerard , Uitterlinden, André G. , Vermeulen, Sita H. , Wang, Gao T., Han, Buhm , Bakker, Paul I. W. de , Verissimo, Ana Raquel, Wright, Benjamin J., Bumpstead, Suzannah, Grétarsdóttir, Sólveig , Badger, Stephen A., Child, Anne H. , Cockerill, Gillian, Hafez, Hany , Futers, Simon , Sohrabi, Soroush, Smith, Alberto, Thompson, Matthew M., Bockxmeer, Frank M. van, Matthíasson, Stefán E., Þorsteinsdóttir, Unnur , Graaf, Jacqueline de , Palmen, Jutta, Lindholt, Jes S. , Bradley, Declan , Waltham, Matthew, Gwilliam, Rhian, Golledge, Jonathan , Eriksson, Per , Stefánsson, Kāri , Thompson, John R., Humphries, Steve E. , Sayers, Robert D., Deloukas, Panos , Samani, Nilesh J. , Phillip, L. Victoria, Hill, Geraldine B., Williams, Michael , Thomson, Ian , Krysa, Jo, Wilkins, Gerard , Vasudevan, Thodor M., Lewis, David R. , Blair, Ross D., Hill, Andrew A., de Andrade, Mariza, Ripke, Stephan , Andrade, Mariza de , Broderick, Joseph, Carrell, David , Crawford, Dana C. , Jones, Gregory T. , Kullo, Iftikhar J. , Kurki, Mitja , Lai, Dongbing , Leal, Suzanne M. , Low, Siew‐Kee , Milewicz, Dianna M. , Nakamura, Yusuke , Niemela, Mika R. , Pacheco, Jennifer A. , Takahashi, Atsushi , Verma, Shefali S. , Rinkel, Gabriël J.E. , Clough, Rachel E. , Scott, D. Julian A., Þorleifsson, Guðmar , Teijink, Joep A.W. , Wijmenga, Cisca , Smith, Andrew J P , Edkins, Sarah , Hunt, Sarah E , Potter, Simon , Norman, Paul E , Powell, Janet T. , Merriman, Tony Raymond , Kiemeney, Lambertus A , Bijlenga, Philippe , Lindholt, Jes Sanddal , Malinowski, Jennnifer , Rasmussen-Torvik, Laura J , Eriksson, Per
Journal of the American Heart Association | July 15, 2016 | Volume: 5 | Issue: 7 | Pages: No page available
Background Intracranial aneurysms ( IAs ), abdominal aortic aneurysms ( AAAs ), and thoracic aortic aneurysms ( TAAs ) all have a familial predisposition. Given that aneurysm types are known to co‐occur, we hypothesized that there may be shared genetic risk factors for IAs , AAAs, and TAAs . Methods and Results We performed a mega‐analysis of 1000 Genomes Project‐imputed genome‐wide association study ( GWAS ) data of 4 previously published aneurysm cohorts: 2 IA cohorts (in total 1516 cases, 4305 controls), 1 AAA cohort (818 cases, 3004 controls), and 1 TAA cohort (760 cases, 2212 controls), and observed associations of 4 known IA , AAA , and/or TAA risk loci (9p21, 18q11, 15q21, and 2q33) with consistent effect directions in all 4 cohorts. We calculated polygenic scores based on IA ‐, AAA ‐, and TAA ‐associated SNP s and tested these scores for association to case‐control status in the other aneurysm cohorts; this revealed no shared polygenic effects. Similarly, linkage disequilibrium–score regression analyses did not show significant correlations between any pair of aneurysm subtypes. Last, we evaluated the evidence for 14 previously published aneurysm risk single‐nucleotide polymorphisms through collaboration in extended aneurysm cohorts, with a total of 6548 cases and 16 843 controls ( IA ) and 4391 cases and 37 904 controls ( AAA ), and found nominally significant associations for IA risk locus 18q11 near RBBP 8 to AAA (odds ratio [ OR ]=1.11; P =4.1×10 −5 ) and for TAA risk locus 15q21 near FBN 1 to AAA ( OR =1.07; P =1.1×10 −3 ). Conclusions Although there was no evidence for polygenic overlap between IAs , AAAs , and TAAs , we found nominally significant effects of two established risk loci for IAs and TAAs in AAAs . These two loci will require further replication.