Background Cavernous carotid artery aneurysms (CCAs) represent a unique subset of intracranial aneurysms due to their distinct natural history and the anatomy of the cavernous sinus. Enlarging CCAs can cause elastic compression of the parent internal carotid artery (ICA). We suggest defining aneurysms that cause luminal stenosis of their parent vessels as ‘matricidal aneurysms.’
Though many patients are asymptomatic, presenting symptoms of CCAs include ophthalmoplegia with resulting diplopia, vision changes, pain, ptosis, facial numbness, and cavernous-carotid fistula. Less commonly, patients with CCAs can present with epistaxis, subarachnoid hemorrhage, and—in cases of matricidal aneurysms—ischemia due to stenosis. The proper management of stenosis caused by a matricidal CCA is not well established and may not be intuitive.
Methods We present a multicenter retrospective case series of patients with matricidal CCAs.
Results Forty patients with matricidal aneurysms presented with both asymptomatic and symptomatic stenosis. These patients were either treated with conservative medical management, coiling, flow diversion, or endovascular sacrifice of the parent artery. Planned treatment modalities were not executed in 11 cases (28% treatment failure rate). Presenting symptoms, patient outcomes, and follow-up data are presented for all cases.
Conclusion Matricidal aneurysms require careful consideration and planning. The restricted anatomy of the cavernous sinus can make successful execution of endovascular interventions more difficult. Direct elastic compression of the parent artery does not respond to angioplasty and stenting in the same way atherosclerotic stenosis does. Because of this, planning for the possibility of parent vessel sacrifice is important.
- flow diverter
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Contributors All authors of this work met ICMJE criteria for authorship and made substantial contributions to the conception and design, acquisition of data, analysis and interpretation of data, drafting, critical revising, and final approval of this manuscript.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial, or not-for-profit sectors.
Competing interests CN is a consultant for Leica and has received research support from Microvention. BGW is a consultant for Stryker Neurovascular, serves as a proctor for Medtronic, and receives royalties from Peter Lazic, Inc. AJR is a consultant for Microvention. LJK serves as a consultant for Medtronic, receives grant support from the National Institutes of Health and the National Institute of Neurological Disorders and Stroke, and is a shareholder of Spi Surgical, Inc. MRL serves as a consultant for Medtronic and Minnetronix, Inc., receives unrestricted educational grants from Medtronic and Stryker, and is a shareholder of eLoupes, Inc. PK is a consultant for Medtronic and Stryker. ASA is a consultant for Leica, Medtronic, Microvention, Penumbra, Siemens, and Stryker; received research support from Microvention, Penumbra, and Siemens; received personal fees from Sequent; and is a shareholder in Cerebrotech and Synchron.
Ethics approval The University of Tennessee Health Science Center IRB, Memphis, TN # 18-05813-XM.
Provenance and peer review Not commissioned; externally peer reviewed.
Data sharing statement No other data are available for sharing.
Collaborators Adam Arthur, Bernard Bendock, Mandy Jo Binning, Alan S. Boulos, Richard Fessler, Lee Guterman, Ricardo Hanel, Daniel Hoit, L.Nelson Hopkins, III, Jay Howington, Robert James, Peter Kan, Alex A Khalessi, Louis Kim, David Langer, Giuseppe Lanzino, Elad Levy, Demetrius Lopes, William Mack, Robert Mericle, J Mocco, Aditya Pandey, Robert Replogle, Howard Riina, Andrew J Ringer, Rafael Rodriguez, Eric Saugaveau, Clemens Schirmer, Adnan Siddiqui, Rabih Tawk, Raymond Turner, Erol Veznedaroglu, Babu Welch, Jonathan White.
Patient consent for publication Not required.
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