De novo aneurysm formation on internal carotid artery at origin of thick posterior communicating artery: 7 years after transient occlusion of contralateral internal carotid artery

Masato Takeda; Kazutaka Shirokane; Eiichi Baba; Atsushi Tsuchiya; Motohiro Nomura

doi:10.4103/ajns.AJNS_261_18

Asian Journal of Neurosurgery, Inhaltsverzeichnis

CC BY-NC-ND 4.0 · Asian J Neurosurg 2019; 14(02): 571-574
DOI: 10.4103/ajns.AJNS_261_18

Case Report

De novo aneurysm formation on internal carotid artery at origin of thick posterior communicating artery: 7 years after transient occlusion of contralateral internal carotid artery

Autoren

Masato Takeda

Department of Neurosurgery, Kanto Rosai Hospital, Kawasaki
Kazutaka Shirokane

Department of Neurosurgery, Kanto Rosai Hospital, Kawasaki
Eiichi Baba

Department of Neurosurgery, Kanto Rosai Hospital, Kawasaki
Atsushi Tsuchiya

¹Department of Neurology, Kanto Rosai Hospital, Kawasaki
Motohiro Nomura

Department of Neurosurgery, Kanto Rosai Hospital, Kawasaki

Abstract

The incidence of de novo intracranial aneurysm formation has been reported to be 0.84% per year. It is rare for de novo aneurysm formation to be observed on serial radiological examinations. A 64-year-old male with a history of right internal carotid artery (ICA) occlusion 7 years ago had subarachnoid hemorrhage (SAH) due to a ruptured left ICA aneurysm at the bifurcation of the posterior communicating artery (PComA). At the time of ICA occlusion, the left PComA was thick, about 3.0 mm in diameter, and no aneurysm was detected on radiological examinations. Thirty-eight months later, a small aneurysm was detected on the left ICA on magnetic resonance angiography (MRA). At the onset of SAH, the aneurysm was larger than that observed on the previous MRA. Left frontotemporal craniotomy was performed, and the aneurysm was clipped. A thick PComA might contribute to the development of an aneurysm at its origin due to hemodynamic stress. Persistent hemodynamic stress may cause enlargement of an aneurysm in 4 years and its subsequent rupture. In patient with a thick PComA, close observation is necessary to screen for de novo formation of a cerebral aneurysm.

Key-words:

Cerebral aneurysm - de novo - internal carotid artery - posterior communicating artery - thick

Volltext

Referenzen

References
1 Juvela S, Poussa K, Porras M. Factors affecting formation and growth of intracranial aneurysms: A long-term follow-up study. Stroke 2001;32:485-91.
2 Okazaki T, Nishi T, Yamashiro S, Koga K, Nagahiro S, Fujioka S, et al. De novo formation and rupture of an intracranial aneurysm 10 months after normal findings on conventional magnetic resonance angiography in a patient with no history of intracranial lesions: Case report. Neurol Med Chir (Tokyo) 2010;50:309-12.
3 Arambepola PK, McEvoy SD, Bulsara KR. De novo aneurysm formation after carotid artery occlusion for cerebral aneurysms. Skull Base 2010;20:405-8.
4 Briganti F, Cirillo S, Caranci F, Esposito F, Maiuri F. Development of “de novo” aneurysms following endovascular procedures. Neuroradiology 2002;44:604-9.
5 Lebland R. De novo formation of familial cerebral aneurysms: Case report. Neurosurgery 1999;44:871-6.
6 Tonn J, Hoffmann O, Hofmann E, Schlake HP, Sörensen N, Roosen K, et al. “De novo” formation of intracranial aneurysms: Who is at risk? Neuroradiology 1999;41:674-9.
7 Yang K, Park W, Koo HW, Suh DC. A tiny bleb at junctional dilatation of the posterior communicating artery as a predisposing factor for development of a de novo aneurysm. Neurointervention 2016;11:59-63.
8 Karekezi C, Boutarbouch M, Djoubairou BO, Melhaoui A, Arkha Y, El Ouahabi A, et al. Are infundibular dilatations at risk of further transformation? Ten-year progression of a prior documented infundibulum into a saccular aneurysm and rupture: Case report and a review of the literature. Neurochirurgie 2014;60:307-11.
9 Sámano A, Ishikawa T, Moroi J, Yamashita S, Suzuki A, Yasui N, et al. Ruptured de novo posterior communicating artery aneurysm associated with arteriosclerotic stenosis of the internal carotid artery at the supraclinoid portion. Surg Neurol Int 2011;2:35.
10 Jou LD, Lee DH, Morsi H, Mawad ME. Wall shear stress on ruptured and unruptured intracranial aneurysms at the internal carotid artery. AJNR Am J Neuroradiol 2008;29:1761-7.
11 Nixon AM, Gunel M, Sumpio BE. The critical role of hemodynamics in the development of cerebral vascular disease. J Neurosurg 2010;112:1240-53.
12 Avci E, Bademci G, Oztürk A. Posterior communicating artery: From microsurgical, endoscopic and radiological perspective. Minim Invasive Neurosurg 2005;48:218-23.
13 Can A, Ho AL, Emmer BJ, Dammers R, Dirven CM, Du R, et al. Association between vascular anatomy and posterior communicating artery aneurysms. World Neurosurg 2015;84:1251-5.
14 van der Schaaf IC, Velthuis BK, Wermer MJ, Majoie C, Witkamp T, de Kort G, et al. New detected aneurysms on follow-up screening in patients with previously clipped intracranial aneurysms: Comparison with DSA or CTA at the time of SAH. Stroke 2005;36:1753-8.