CASE REPORTNagoya J. Med. Sci. 85. 350–356, 2023
doi:10.18999/nagjms.85.2.350

Complex aneurysm formation in the proximal segment ofthe posterior cerebral artery: a report of two cases
Hiroo Sasaki1, Syuntaro Takasu2 and Yukio Seki2
1
Department of Neurosurgery, Nagoya University Graduate School of Medicine, Nagoya, Japan
Department of Neurosurgery, Japanese Red Cross Aichi Medical Center Nagoya Daini Hospital,Nagoya, Japan

2ABSTRACTPosterior cerebral artery (PCA) aneurysms are rare and often fusiform. We describe two cases ofcomplex proximal PCA aneurysm in two women in their 60’s, which probably resulted from segmental
arterial degeneration. Both presented with subarachnoid hemorrhage and had common angiographic andintraoperative findings: tortuous configuration of the affected P1 segment, whitish or yellowish appearanceof a portion of the lesion, lesion calcification, and multiple aneurysms in the segment. Interestingly, nosignificant atherosclerotic changes were noted in other cerebral arteries. The ruptured aneurysm could be
successfully trapped, with superficial temporal artery (STA)-PCA bypass in one and without bypass inthe other, and both patients recovered well. As complex aneurysm formation in the cases described here
are probably related to proximal PCA segmental degeneration, we recommend trapping the lesion, withor without STA-PCA bypass, depending on the size and patency of the posterior communicating artery.
Keywords: complex, bypass, posterior cerebral artery aneurysm, subarachnoid hemorrhage, trapping
Abbreviations:
PCA: posterior cerebral artery
PCoA: posterior communicating artery
STA: superficial temporal artery
This is an Open Access article distributed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
License. To view the details of this license, please visit (http://creativecommons.org/licenses/by-nc-nd/4.0/).

INTRODUCTION
Posterior cerebral artery (PCA) aneurysms are rare and account for 0.7%–2.3% of all intracranial aneurysms.1 Most are located in the precommunicating segment of the posterior cerebral
artery (P1) or at the junction of P1 and the posterior communicating artery (PCoA).2 About 24%of all PCA aneurysms are fusiform and are often present as multiple intracranial aneurysms.2,3Here, we describe two cases with complex proximal PCA aneurysms that were successfully
treated with microsurgery. Intraoperative and angiographic findings suggest that complex aneurysm
formation was probably due to proximal PCA segmental degeneration.
Received: March 24, 2022; accepted: April 26, 2022
Corresponding Author: Hiroo Sasaki, MD
Department of Neurosurgery, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku,
Nagoya 466-8550, Japan
Tel: +81-52-744-2353, Fax: +81-52-744-2360, E-mail: h-sasaki@med.nagoya-u.ac.jp350

Posterior cerebral artery aneurysm

CASE REPORTS
Case 1
A 66-year-old female with a past medical history of cardiac arrhythmia was transferred to ourhospital with a diagnosis of subarachnoid hemorrhage. On admission, her pupils were unequaland her Hunt and Kosnik grade was 2. Computed tomography (CT) of the head showed a small
amount of clot in the basal cisterns, a modest calcification in the left prepontine cistern, andhydrocephalus (Figure 1A). Digital subtraction angiography (DSA) revealed an irregularly shaped
P1 associated with multiple aneurysms (Figure 1B). On the day after admission, she underwent
surgical trapping of the lesion (Endovascular treatment had not been commonly performed atthat time).
Specifically, under general anesthesia, the patient’s head was fixed to a head holder and a left
frontotemporal craniotomy was performed. A left ventricular drain was inserted, and then underan operating microscope, the Sylvian fissure was widely opened to reveal the carotid cistern. Theabnormal P1 segment harboring multiple aneurysms was exposed by posterolaterally retracting thetemporal lobe (Figure 2). The arterial wall appeared yellowish in color and was associated withmultiple blister-like aneurysms and was visible a partially thrombosed aneurysm at the junction of
the P1 and P2 segments. Aneurysms were also seen behind the PCoA. As the abnormal arterial
segment had adhered to the oculomotor nerve, complete dissection was abandoned and trappingof the P1 segment was performed without disturbing blood flow to the left thalamoperforatingartery. No involvement of other cerebral arteries was apparent.
Postoperatively the patient experienced transient aphasia and disorientation, which graduallyresolved. Postoperative DSA showed disappearance of the aneurysms, preservation of the leftthalamoperforating artery, and opacification of the distal left PCA through the PCoA (Figure3). She received inpatient rehabilitation and was discharged home four weeks after admission

Fig. 1 Preoperative images in case 1
CT scan of case 1 on admission shows a small amount of subarachnoid hemorrhage in the basilar cisterns anda calcification of the left prepontine cistern (A). An anteroposterior view of the right vertebral angiogram showscomplex aneurysms of the precommunicating segment of the left posterior cerebral artery (B).
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Fig. 2 Intraoperative illustration for case 1
A drawing of the intraoperative view in case 1 shows multiple aneurysms including blood blister-like aneurysms
on the tortuous precommunicating segment of the left posterior cerebral artery associated with the degenerative
appearance of the arterial wall.
*Partially thrombosed aneurysm
PCoA: posterior communicating artery

Fig. 3 Postoperative angiographies in case 1Postoperative right vertebral angiogram (A) and left carotid angiogram (B) show complete occlusion of the lesionin the precommunicating segment of the left posterior cerebral artery (PCA) and opacification of the distal left
PCA through the posterior communicating artery. The left thalamoperforating artery is preserved (arrows).

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without neurological deficits. Three months later, she developed symptomatic normal pressurehydrocephalus and underwent ventriculoperitoneal shunt placement, which resolved her symptoms.
Case 2
A 63-year-old woman with a past medical history of hypertension was referred to our hospitalfor severe headache. Her initial Glasgow Coma Scale score was 13 (E3 V4 M6). No limb weakness was detected on neurological examination. A head CT scan showed diffuse subarachnoid
hemorrhage (Figure 4A), and a DSA acquired the next day showed complex fusiform andsaccular aneurysms in a tortuous right P1 segment (Figure 4 B, C). The right PCoA could not
be visualized and was thought to be hypoplastic. As stenosis was present within the lesion, anendovascular approach was ruled out. As a superficial temporal artery (STA)-PCA bypass wasrequired, right frontotemporal craniotomy and subtemporal approach were performed.
Intraoperative inspection revealed a thin-walled aneurysm with a daughter sac located at thePCoA-P2 junction, the latter was thought to be the ruptured aneurysm (Figure 5A), and thejunction appeared whitish or yellowish. STA-P2 bypass followed by trapping was performed asclipping the aneurysm neck was considered difficult because of its shape (Figure 5B). As thethalamoperforating arteries arose from the P1 fusiform aneurysm and the walls of the P1 aneurysms were not reddish, the anatomical connection between P1 and the PCoA was intentionally
maintained to avoid thrombosis at the origin of the perforators. Surgery was uneventful but rightoculomotor nerve palsy was observed after the procedure. Postoperative DSA showed obliterationof the aneurysm at the PCoA-P2 junction and patency of the STA-P2 bypass (Figure 6 A, B).

Fig. 4 Preoperative images of case 2
CT scan at admission shows diffuse subarachnoid hemorrhage and a calcification of the prepontine cistern (A).
Preoperative left vertebral angiograms, antero-posterior view (B) and lateral view (C), show a tortuous precommunicating segment of the right posterior cerebral artery that is associated with multiple complex aneurysms
and an intralesional stenosis (arrow).
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Hiroo Sasaki et alFig. 5 Intraoperative images of case 2
Intraoperative view (right subtemporal approach) shows the whitish appearance of the P1 segment and multiple
aneurysms (A). The thin-walled aneurysm (arrow) located just distal to the PCoA-P2 junction had ruptured, andthe point of rupture was located behind the tentorium cerebelli (*). Following STA-P2 bypass, the aneurysm
was trapped and collapsed (B).
CN III: oculomotor nerve
PCoA: posterior communicating artery
STA: superficial temporal artery

Fig. 6 Postoperative images of case 2
Postoperative anteroposterior views of the left vertebral angiogram (A) and right carotid angiogram (B) show
obliteration of the ruptured aneurysm and opacification of the right posterior cerebral artery through the bypass(arrow). Postoperative fluid-attenuated inversion recovery magnetic resonance imaging (C) shows no infarctionin the posterior cerebral artery distribution.

The right P1 segment had not opacified but thalamic infarction was not visualized on magnetic
resonance imaging, suggesting the presence of patent perforators (Figure 6C). The patient wasdischarged home one month after surgery with modified Rankin Scale score of 2, and her
oculomotor nerve palsy improved three months after discharge.

DISCUSSIONMultiple aneurysms are found in 53% of patients who harbor a PCA aneurysm; among these,
another aneurysm is located on the PCA in 12%.4 However, the multiple PCA aneurysms of thepatients in this report clearly differ from those previously reported. Based on angiographic andNagoya J. Med. Sci. 85. 350–356, 2023

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intraoperative findings, proximal PCA segmental degeneration seemed to be a background ofcomplex aneurysm formation. Common characteristics of this disorder included tortuous configuration of the affected P1 segment, whitish or yellowish appearance of a portion of the lesion, lesion
calcification, and multiple aneurysms of the segment; in addition, no significant atheroscleroticchanges of other cerebral arteries were noted. In case 2, significant stenosis was also noted within
the affected P1 segment. The similar age of presentation (7th decade), intraoperative findings,and presence of calcification in these cases suggest that the lesion is focal, degenerative, andprogressive. The presence of multiple aneurysms, including the blood blister-like aneurysms ofcase 1, also suggests a predisposing structural failure in the affected arterial segment.
The cause and pathological mechanisms leading to focal degeneration limited to the P1 segment are unclear. Considering the focality, it is likely that the initiating change occurred during
the stage of embryologic development of the vertebrobasilar system when the newly formed P1
segments complete the circle of Willis.5 This change then might have been promoted to form
multiple aneurysms by systemic factors such as hypertension and aging.
However, this report is limited by a lack of pathological findings of the lesion that could
elucidate the mechanism of degeneration.
Surgical trapping and bypass of fusiform PCA aneurysms has been previously reported.6-8
The optimal surgical management of complex aneurysms formed on the degenerated proximal
segment of PCA is also trapping of the affected segment that involves the ruptured aneurysm
while preserving the thalamoperforating arteries. STA-P2 bypass is necessary if the PCoA ishypoplastic or the PCoA-P2 junction is within the trapped segment. Endovascular trapping ofthe lesion would be another option if cannulation of the tortuous P1 segment is possible.

CONCLUSION
Two cases of a unique form of cerebrovascular disorder, complex aneurysm formation on theproximal PCA segment associated with the segmental parent artery degeneration, are presented.
It should be managed by trapping of the lesion with or without STA-P2 bypass, depending on
the size and patency of the PCoA.

CONFLICTS OF INTEREST DISCLOSURE
The authors declare they have no conflicts of interest and no commercial relationships andreceived no support from pharmaceutical or other companies.

INFORMED CONSENT
We received consent from all patients for the publication of this case report.

REFERENCES
123

Wang J, Sun Z, Bao J, Zhang B, Jiang Y, Lan W. Characteristics and endovascular treatment of aneurysmsof posterior cerebral artery. Neurol India. 2011;59(1):6–11. doi:10.4103/0028-3886.76849.
Goehre F, Jahromi BR, Lehecka M, et al. Posterior Cerebral Artery Aneurysms: Treatment and Outcome
Analysis in 121 Patients. World Neurosurg. 2016;92:521–532. doi:10.1016/j.wneu.2016.03.063.
Goehre F, Kamiyama H, Noda K, et al. Technical Description of the Medial and Lateral Anterior Temporal

Nagoya J. Med. Sci. 85. 350–356, 2023

355

doi:10.18999/nagjms.85.2.350

Hiroo Sasaki et al45678

Approach for the Treatment of Complex Proximal Posterior Cerebral Artery Aneurysms. World Neurosurg.
2016;86:490–496. doi:10.1016/j.wneu.2015.09.068.
Goehre F, Jahromi BR, Hernesniemi J, et al. Characteristics of posterior cerebral artery aneurysms: anangiographic analysis of 93 aneurysms in 81 patients. Neurosurgery. 2014;75(2):134–144. doi:10.1227/
neu.0000000000000363.
Padget DH. The Development of the Cranial Arteries in the Human Embryo. Contrib Embryol.
1948:32(212):205–261.
Zador Z, Lu DC, Arnold CM, Lawton MT. Deep bypasses to the distal posterior circulation: anatomical andclinical comparison of pretemporal and subtemporal approaches. Neurosurgery. 2010;66(1):92–100;discussion100-101. doi:10.1227/01.neu.0000362034.81037.FC.
Takeuchi S, Tanikawa R, Tsuboi T, et al. Superficial temporal artery to proximal posterior cerebral artery
bypass through the anterior temporal approach. Surg Neurol Int. 2015;6:95. doi:10.4103/2152-7806.157949.
Ota N, Goehre F, Miyazaki T, et al. Bypass Revascularization Applied to the Posterior Cerebral Artery.
World Neurosurg. 2016;96:460–472. doi:10.1016/j.wneu.2016.09.031.

References End

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