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Case Report
Parent artery occlusion for ruptured ‘‘true’’ posterior communicating artery aneurysm
Interventional Neuroradiology 0(00) 1–4 ! The Author(s) 2015 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/1591019915583000 ine.sagepub.com
Takashi Mitsuhashi1,2, Nobuaki Takeda2,3, Hidenori Oishi4 and Hajime Arai2
Abstract A case of a patient with a ruptured true posterior communicating artery (PCoA) aneurysm is reported, who had been managed by early endovascular parent artery occlusion with coils. The small blister aneurysm was located at the proximal PCoA itself and directed superiorly. Postoperative course was uneventful. During 1-month follow-up, the patient recovered well and could care for herself. Aneurysms of the PCoA itself are very rare. As reported to date, surgical procedures would favor microsurgical clipping over endovascular coil embolization. Endovascular treatment may be a good alternative to surgical trapping for true PCoA blister aneurysm.
Keywords Intracranial aneurysm, posterior communicating artery aneurysm, endovascular procedure
Introduction Aneurysms that arise from the posterior communicating artery (PCoA) are extremely rare, with an incidence of 1.3% of all intracranial aneurysms and 6.8% of all PCoA aneurysms in a systematic review.1 Two types of aneurysm described by Pia et al. include the fusiform type without a definable neck and a saccular type.2 In addition, it is believed that ‘‘true’’ PCoA aneurysms have a higher risk of rupture at small sizes compared with more traditional PCoA aneurysms.3 We report a case of ruptured a ‘‘true’’ PCoA blister aneurysm successfully treated by endovascular parent artery occlusion.
Case report A 71-year-old female was admitted to our institute complaining of altered mental status followed by loss of consciousness. On admission she was hypertensive and drowsy but responded to commands. She had no focal neurological deficit. There was no relevant past medical history. Her consciousness recovered on arrival at our site. Computed tomography (CT) demonstrated diffuse thick subarachnoid hemorrhage (Figure 1a). Computed tomography angiography revealed a small aneurysm-like deformity, suspected as arising from the left internal carotid and PCoA junction. However, the complete four-vessel angiography revealed a small blister aneurysm arising from the left PCoA (Figure 1c). The left carotid angiography showed a small aneurysm, apparently arising from the region of the origin of
the left PCoA and passing directly backwards. There was good filling of the left posterior cerebral artery from the left internal carotid artery, via the left PCoA (Figure 1d). We selected endovascular parent artery occlusion rather than direct clipping or trapping. On the day of admission (day 0), the patient was placed under general anesthesia in the angiography suite. Thereafter, the patient had a lumbar drain placed. The bilateral femoral artery was punctured using the Seldinger technique to introduce a vascular sheath. Heparin was used to achieve an activated clotting time of more than 250 s. Vertebral angiography with carotid compression was performed before vascular embolization so as to observe the blood supply to the posterior circulation of the PCoA. The result showed that blood flow reversed into the internal carotid artery through the PCoA. Initially, a Medikit 7Fr VT(C) catheter (Medikit, Tokyo, Japan) was placed in the left internal carotid artery. A 5-French Shuttle guiding sheath (Cook Medical, Bloomington, IN, USA) was placed in the 1
Department of Neurosurgery, Tamananbu Chiiki Hospital, Tokyo, Japan Department of Neurosurgery, Juntendo University, Faculty of Medicine, Tokyo, Japan 3 Department of Neurosurgery, Kichijojiminami Hospital, Tokyo, Japan 4 Department of Neurosurgery and Neuroendovasular Therapy, Juntendo University, Faculty of Medicine, Tokyo, Japan 2
Corresponding author: Takashi Mitsuhashi, Department of Neurosurgery, Tamananbu chiiki Hospital, Nakazawa2-1-2, Tama-city, Tokyo 206-0036, Japan. Email: [email protected]
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Figure 1. Ruptured true blister posterior communicating artery aneurysm. Axial non contrast cranial computed tomography (a) shows diffuse thick subarachnoid hemorrhage. The left internal carotid angiograms lateral view (b) and left anterior oblique view (c), showing a true blister posterior communicating artery (PCoA) aneurysm. Left vertebral angiography with carotid compression showing an aneurysm via fetal-type posterior communicating artery (d). First, the microcatheter was placed into the PCoA via the posterior communicating artery (e). The coil was deployed in the aneurysm while the balloon was inflated into the PCoA branch (f).
left vertebral artery with its distal tip at the third segments (V2–V3), and after a suitable working angle was selected, a Headway 17 STR 2 M microcatheter (Terumo, Tokyo, Japan) was placed into the PCoA using a ASAHI CHIKAI 0.014 microguidewire (Asahi Intecc, Aichi, Japan) via the PCoA (Figure 1e). Thereafter, a Hyperform occlusion balloon catheter (eV3 Covidien, Irvine, CA, USA) was introduced into the left internal carotid artery (ICA), and was placed at the branching the PCoA to preserve the coil migration to the distal ICA (Figure 1f). Coil parent artery occlusion started with the creation of a coil basket at the fundus of the blister aneurysm and occlusion of a short segment of PCoA using a 3 mm 6 cm Cerecyte Cashmere 14 coil (Codman & Shurtleff, Johnson & Johnson, Raynham, MA,USA). Furthermore, Target 360 Ultra Coil 2 mm 4 cm (Stryker, Kalamazoo, MI, USA) and Target Helical Nano Coil 1.5 mm 3 cm (Stryker) were sequentially released to fill the PCoA branch and ‘‘true’’ PCoA aneurysm. The coil was deployed in the aneurysm while the balloon was inflated into the PCoA branch. The inflated Hyperform occlusion balloon was partially herniated into the neck of the aneurysm (Figure 2a). Finally, an Excelsior SL-10 2 M microcatheter (Stryker) was placed into the scattered coil mass using a GT wire 0.012-inch double angle (Terumo Clinical Supply, Gifu, Japan) from the guiding catheter placed in the ICA. Next, a Target Helical Nano Coil 1.5 mm 2 cm (Stryker) was released to the coil mass.
No enhancement of the ‘‘true’’ PCoA aneurysm and proximal PCoA was shown in the angiography of anterior or posterior circulation, and leakage of the contrast agent did not occur (Figure 2b–f). Following catheter and sheath removal, the procedure was completed. Postoperative course was uneventful. The patient was treated with aspirin and cilostazol. During 1-month follow-up, the patient recovered well and could care for herself. Follow-up digital subtraction angiography showed no signs of PCoA aneurysm.
Discussion Posterior communicating artery aneurysms are one of the most frequent forms of intracranial aneurysms, accounting for approximately 25% of all intracranial aneurysms.4 These PCoA aneurysms are actually ICA aneurysms that arise from the junction of the ICA and the PCoA. In 1951, Poppen first reported two surgically ‘‘true’’ PCoA aneurysms.5 In 1979, Yoshida et al. first defined a ‘‘true’’ PCoA aneurysm as an aneurysm 2–3 mm away from the ICA–PCoA junction.6 He et al. reviewed a total of 70 reported cases in the literature of ‘‘true’’ PCoA aneurysms. Among these reported cases, 42.9% occurred in men and 57.1% occurred in women.1 They suggest that there were no significant differences in complication rates between rupture status and treatment modalities.1 Furthermore, they pointed out that the appearance of a complication was positively correlated with the rupture status of the ‘‘true’’ PCoA aneurysm.1
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Figure 2. The microcatheter was placed into the scattered coil mass from internal carotid artery with balloon catheter (a). Postoperative angiography showing a good obliteration of the short segment PCoA at left anterior oblique view (b,c), anteroposterior view (d) and lateral view (e). No enhancement of the true PCoA aneurysm and proximal PCoA were shown in the left vertebral angiography (f).
In the surgical procedures in these published cases, most cases favored microsurgical clipping over endovascular coil embolization. Tamargo described that true PCoA aneurysms are best treated using microsurgery because the aneurysm neck can be clipped a small distance from the fragile PCoA, avoiding compromise of this vessel.7 The PCoA provides many important branches supplying the optic chiasm, oculomotor nerve, mammillary body, tuber cinereum, cerebral crura, ventral thalamus, and rostral portion of the caudate nucleus; interruption of flow through these vessels may result in ischemic damage to the diencephalon with significant morbidity even after an apparently uneventful surgical procedure. Kuzmik and Bulsara8 and Cho et al.9 described that in the case of ‘‘true’’ PCoA aneurysm, thalamoperforating arteries can arise from the PCoA both proximal and distal to the aneurysm, and these branches must be preserved. Some authors have suggested that it is desirable to spare the PCoA whenever possible to preserve these vessels, even if it is hypoplastic,10–12 whereas in some cases of a fusiform type of aneurysm, some authors have suggested that the only method of obliteration would be trapping, and it may not be possible to preserve perforating branches to avoid ischemic complications.13,14 In our case, angiography revealed the blood blister aneurysm, which made necessary parent artery occlusion by microsurgical trapping or endovascular coiling. We performed short segment parent artery occlusion with coils using the combined approach of anterior and posterior circulation in this case. Some authors have described that the endovascular treatment of these aneurysms often results in incomplete coiling of the base to preserve the PCoA origin
and may result in a recurrence of the aneurysm.7 Some have pointed out that as most ‘‘true’’ PCoA lesions occur within 2–3 mm of the PCoA origin, successful, safe cannulation of the aneurysm with a microcatheter might prove challenging, and the acuity of the approach angle may be too sharp to establish a stable microcatheter position, increasing the risk of possible coil extrusion into the parent vessel or intraprocedural rupture.1 A ‘‘true’’ PCoA aneurysm has two access routes, from the anterior and posterior circulation, in endovascular treatment. We successfully occluded the parent artery using this combined approach of anterior and posterior circulation without premature re-bleed. In this case, the distance from the internal carotid and blister aneurysm was very small. We used a Hyperform occlusion balloon to prevent coil migration to the distal ICA. The balloon conformed easily to the PCoA structure. When the balloon was deflated, the coil did not protrude into the ICA, and was stable in the aneurysm and PCoA. The Hyperform occlusion balloon is very compliant and supple, so it easily changes from its cylindrical shape when inflated to expand into the origin of the arterial branches. Endovascular treatment may be a good alternative to surgical trapping for true PCoA blister aneurysm.
Conclusions A case of ruptured ‘‘true’’ PCoA aneurysm treated by parent artery occlusion was reported. Endovascular treatment using the combined approach of anterior and posterior circulation was effective for this ‘‘true’’ PCoA blister aneurysm.
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[1–4] [INVALID Stage]
4 Funding This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.
Conflict of interest None declared.
References 1. He W, Gandhi CD, Quinn J, et al. True aneurysms of the posterior communicating artery: A systematic review and meta-analysis of individual patient data. World Neurosurg 2011; 75: 64–72. discussion 49. 2. Pia HW, Langmaid C and Zierski J (eds). Cerebral aneurysms. Advances in diagnosis and therapy. Berlin: SpringerVerlag, 1979, pp. 93–95. 3. He W, Hauptman J, Pasupuleti L, et al. True posterior communicating artery aneurysms: Are they more prone to rupture? A biomorphometric analysis. J Neurosurg 2010; 112: 611–615. 4. Golshani K, Ferrell A, Zomorodi A, et al. A review of the management of posterior communicating artery aneurysms in the modern era. Surg Neurol Int 2010; 1: 88. 5. Poppen JL. Specific treatment of intracranial aneurysms: Experiences with 143 surgically treatment patients. J Neurosurg 1951; 8: 75–102.
Interventional Neuroradiology 0(00) 6. Yoshida M, Watanabe M and Kuramoto S. ‘‘True’’ posterior communicating artery aneurysm. Surg Neurol 1979; 11: 379–381. 7. Tamargo RJ. True posterior communicating artery aneurysms. World Neurosurg 2011; 75: 64–72; discussion 49. 8. Kuzumik GA and Bulsara KR. Microsurgical clipping of true posterior communicating artery aneurysms. Acta Neurochir 2012; 154: 1707–1710. 9. Cho SM, Cho SM, Cho YJ, et al. True posterior communicating artery aneurysm – case report. Kor J Cerebrovascular Surg 2003; 5: 71–73. 10. Akimura T, Abiko S and Ito H. True posterior communicating artery aneurysm. Acta Neurol Scand 1991; 84: 207–209. 11. Gibo H, Lenkey C and Rhoton AL Jr. Microsurgical anatomy of the supraclinoid portion of the internal carotid artery. J Neurosurg 1981; 55: 560–574. 12. Peerless SJ. The surgical approach to middle cerebral and posterior communicating aneurysm. Clin Neurosurg 1974; 21: 151–165. 13. Timothy J, Sharr M and Doshi B. Perils of a ‘true’ posterior communicating artery aneurysm. Br J Neurosurg 1995; 9: 789–791. 14. Nakatsuka H, Ohta S, Kuroda J, et al. Ruptured true posterior communicating artery fusiform aneurysm: Case report. No Shinkei Geka 2007; 35: 691–696.
(INE)
[1–4] [INVALID Stage]
Case Report
Parent artery occlusion for ruptured ‘‘true’’ posterior communicating artery aneurysm
Interventional Neuroradiology 0(00) 1–4 ! The Author(s) 2015 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/1591019915583000 ine.sagepub.com
Takashi Mitsuhashi1,2, Nobuaki Takeda2,3, Hidenori Oishi4 and Hajime Arai2
Abstract A case of a patient with a ruptured true posterior communicating artery (PCoA) aneurysm is reported, who had been managed by early endovascular parent artery occlusion with coils. The small blister aneurysm was located at the proximal PCoA itself and directed superiorly. Postoperative course was uneventful. During 1-month follow-up, the patient recovered well and could care for herself. Aneurysms of the PCoA itself are very rare. As reported to date, surgical procedures would favor microsurgical clipping over endovascular coil embolization. Endovascular treatment may be a good alternative to surgical trapping for true PCoA blister aneurysm.
Keywords Intracranial aneurysm, posterior communicating artery aneurysm, endovascular procedure
Introduction Aneurysms that arise from the posterior communicating artery (PCoA) are extremely rare, with an incidence of 1.3% of all intracranial aneurysms and 6.8% of all PCoA aneurysms in a systematic review.1 Two types of aneurysm described by Pia et al. include the fusiform type without a definable neck and a saccular type.2 In addition, it is believed that ‘‘true’’ PCoA aneurysms have a higher risk of rupture at small sizes compared with more traditional PCoA aneurysms.3 We report a case of ruptured a ‘‘true’’ PCoA blister aneurysm successfully treated by endovascular parent artery occlusion.
Case report A 71-year-old female was admitted to our institute complaining of altered mental status followed by loss of consciousness. On admission she was hypertensive and drowsy but responded to commands. She had no focal neurological deficit. There was no relevant past medical history. Her consciousness recovered on arrival at our site. Computed tomography (CT) demonstrated diffuse thick subarachnoid hemorrhage (Figure 1a). Computed tomography angiography revealed a small aneurysm-like deformity, suspected as arising from the left internal carotid and PCoA junction. However, the complete four-vessel angiography revealed a small blister aneurysm arising from the left PCoA (Figure 1c). The left carotid angiography showed a small aneurysm, apparently arising from the region of the origin of
the left PCoA and passing directly backwards. There was good filling of the left posterior cerebral artery from the left internal carotid artery, via the left PCoA (Figure 1d). We selected endovascular parent artery occlusion rather than direct clipping or trapping. On the day of admission (day 0), the patient was placed under general anesthesia in the angiography suite. Thereafter, the patient had a lumbar drain placed. The bilateral femoral artery was punctured using the Seldinger technique to introduce a vascular sheath. Heparin was used to achieve an activated clotting time of more than 250 s. Vertebral angiography with carotid compression was performed before vascular embolization so as to observe the blood supply to the posterior circulation of the PCoA. The result showed that blood flow reversed into the internal carotid artery through the PCoA. Initially, a Medikit 7Fr VT(C) catheter (Medikit, Tokyo, Japan) was placed in the left internal carotid artery. A 5-French Shuttle guiding sheath (Cook Medical, Bloomington, IN, USA) was placed in the 1
Department of Neurosurgery, Tamananbu Chiiki Hospital, Tokyo, Japan Department of Neurosurgery, Juntendo University, Faculty of Medicine, Tokyo, Japan 3 Department of Neurosurgery, Kichijojiminami Hospital, Tokyo, Japan 4 Department of Neurosurgery and Neuroendovasular Therapy, Juntendo University, Faculty of Medicine, Tokyo, Japan 2
Corresponding author: Takashi Mitsuhashi, Department of Neurosurgery, Tamananbu chiiki Hospital, Nakazawa2-1-2, Tama-city, Tokyo 206-0036, Japan. Email: [email protected]
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Figure 1. Ruptured true blister posterior communicating artery aneurysm. Axial non contrast cranial computed tomography (a) shows diffuse thick subarachnoid hemorrhage. The left internal carotid angiograms lateral view (b) and left anterior oblique view (c), showing a true blister posterior communicating artery (PCoA) aneurysm. Left vertebral angiography with carotid compression showing an aneurysm via fetal-type posterior communicating artery (d). First, the microcatheter was placed into the PCoA via the posterior communicating artery (e). The coil was deployed in the aneurysm while the balloon was inflated into the PCoA branch (f).
left vertebral artery with its distal tip at the third segments (V2–V3), and after a suitable working angle was selected, a Headway 17 STR 2 M microcatheter (Terumo, Tokyo, Japan) was placed into the PCoA using a ASAHI CHIKAI 0.014 microguidewire (Asahi Intecc, Aichi, Japan) via the PCoA (Figure 1e). Thereafter, a Hyperform occlusion balloon catheter (eV3 Covidien, Irvine, CA, USA) was introduced into the left internal carotid artery (ICA), and was placed at the branching the PCoA to preserve the coil migration to the distal ICA (Figure 1f). Coil parent artery occlusion started with the creation of a coil basket at the fundus of the blister aneurysm and occlusion of a short segment of PCoA using a 3 mm 6 cm Cerecyte Cashmere 14 coil (Codman & Shurtleff, Johnson & Johnson, Raynham, MA,USA). Furthermore, Target 360 Ultra Coil 2 mm 4 cm (Stryker, Kalamazoo, MI, USA) and Target Helical Nano Coil 1.5 mm 3 cm (Stryker) were sequentially released to fill the PCoA branch and ‘‘true’’ PCoA aneurysm. The coil was deployed in the aneurysm while the balloon was inflated into the PCoA branch. The inflated Hyperform occlusion balloon was partially herniated into the neck of the aneurysm (Figure 2a). Finally, an Excelsior SL-10 2 M microcatheter (Stryker) was placed into the scattered coil mass using a GT wire 0.012-inch double angle (Terumo Clinical Supply, Gifu, Japan) from the guiding catheter placed in the ICA. Next, a Target Helical Nano Coil 1.5 mm 2 cm (Stryker) was released to the coil mass.
No enhancement of the ‘‘true’’ PCoA aneurysm and proximal PCoA was shown in the angiography of anterior or posterior circulation, and leakage of the contrast agent did not occur (Figure 2b–f). Following catheter and sheath removal, the procedure was completed. Postoperative course was uneventful. The patient was treated with aspirin and cilostazol. During 1-month follow-up, the patient recovered well and could care for herself. Follow-up digital subtraction angiography showed no signs of PCoA aneurysm.
Discussion Posterior communicating artery aneurysms are one of the most frequent forms of intracranial aneurysms, accounting for approximately 25% of all intracranial aneurysms.4 These PCoA aneurysms are actually ICA aneurysms that arise from the junction of the ICA and the PCoA. In 1951, Poppen first reported two surgically ‘‘true’’ PCoA aneurysms.5 In 1979, Yoshida et al. first defined a ‘‘true’’ PCoA aneurysm as an aneurysm 2–3 mm away from the ICA–PCoA junction.6 He et al. reviewed a total of 70 reported cases in the literature of ‘‘true’’ PCoA aneurysms. Among these reported cases, 42.9% occurred in men and 57.1% occurred in women.1 They suggest that there were no significant differences in complication rates between rupture status and treatment modalities.1 Furthermore, they pointed out that the appearance of a complication was positively correlated with the rupture status of the ‘‘true’’ PCoA aneurysm.1
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Figure 2. The microcatheter was placed into the scattered coil mass from internal carotid artery with balloon catheter (a). Postoperative angiography showing a good obliteration of the short segment PCoA at left anterior oblique view (b,c), anteroposterior view (d) and lateral view (e). No enhancement of the true PCoA aneurysm and proximal PCoA were shown in the left vertebral angiography (f).
In the surgical procedures in these published cases, most cases favored microsurgical clipping over endovascular coil embolization. Tamargo described that true PCoA aneurysms are best treated using microsurgery because the aneurysm neck can be clipped a small distance from the fragile PCoA, avoiding compromise of this vessel.7 The PCoA provides many important branches supplying the optic chiasm, oculomotor nerve, mammillary body, tuber cinereum, cerebral crura, ventral thalamus, and rostral portion of the caudate nucleus; interruption of flow through these vessels may result in ischemic damage to the diencephalon with significant morbidity even after an apparently uneventful surgical procedure. Kuzmik and Bulsara8 and Cho et al.9 described that in the case of ‘‘true’’ PCoA aneurysm, thalamoperforating arteries can arise from the PCoA both proximal and distal to the aneurysm, and these branches must be preserved. Some authors have suggested that it is desirable to spare the PCoA whenever possible to preserve these vessels, even if it is hypoplastic,10–12 whereas in some cases of a fusiform type of aneurysm, some authors have suggested that the only method of obliteration would be trapping, and it may not be possible to preserve perforating branches to avoid ischemic complications.13,14 In our case, angiography revealed the blood blister aneurysm, which made necessary parent artery occlusion by microsurgical trapping or endovascular coiling. We performed short segment parent artery occlusion with coils using the combined approach of anterior and posterior circulation in this case. Some authors have described that the endovascular treatment of these aneurysms often results in incomplete coiling of the base to preserve the PCoA origin
and may result in a recurrence of the aneurysm.7 Some have pointed out that as most ‘‘true’’ PCoA lesions occur within 2–3 mm of the PCoA origin, successful, safe cannulation of the aneurysm with a microcatheter might prove challenging, and the acuity of the approach angle may be too sharp to establish a stable microcatheter position, increasing the risk of possible coil extrusion into the parent vessel or intraprocedural rupture.1 A ‘‘true’’ PCoA aneurysm has two access routes, from the anterior and posterior circulation, in endovascular treatment. We successfully occluded the parent artery using this combined approach of anterior and posterior circulation without premature re-bleed. In this case, the distance from the internal carotid and blister aneurysm was very small. We used a Hyperform occlusion balloon to prevent coil migration to the distal ICA. The balloon conformed easily to the PCoA structure. When the balloon was deflated, the coil did not protrude into the ICA, and was stable in the aneurysm and PCoA. The Hyperform occlusion balloon is very compliant and supple, so it easily changes from its cylindrical shape when inflated to expand into the origin of the arterial branches. Endovascular treatment may be a good alternative to surgical trapping for true PCoA blister aneurysm.
Conclusions A case of ruptured ‘‘true’’ PCoA aneurysm treated by parent artery occlusion was reported. Endovascular treatment using the combined approach of anterior and posterior circulation was effective for this ‘‘true’’ PCoA blister aneurysm.
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(INE)
[1–4] [INVALID Stage]
4 Funding This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.
Conflict of interest None declared.
References 1. He W, Gandhi CD, Quinn J, et al. True aneurysms of the posterior communicating artery: A systematic review and meta-analysis of individual patient data. World Neurosurg 2011; 75: 64–72. discussion 49. 2. Pia HW, Langmaid C and Zierski J (eds). Cerebral aneurysms. Advances in diagnosis and therapy. Berlin: SpringerVerlag, 1979, pp. 93–95. 3. He W, Hauptman J, Pasupuleti L, et al. True posterior communicating artery aneurysms: Are they more prone to rupture? A biomorphometric analysis. J Neurosurg 2010; 112: 611–615. 4. Golshani K, Ferrell A, Zomorodi A, et al. A review of the management of posterior communicating artery aneurysms in the modern era. Surg Neurol Int 2010; 1: 88. 5. Poppen JL. Specific treatment of intracranial aneurysms: Experiences with 143 surgically treatment patients. J Neurosurg 1951; 8: 75–102.
Interventional Neuroradiology 0(00) 6. Yoshida M, Watanabe M and Kuramoto S. ‘‘True’’ posterior communicating artery aneurysm. Surg Neurol 1979; 11: 379–381. 7. Tamargo RJ. True posterior communicating artery aneurysms. World Neurosurg 2011; 75: 64–72; discussion 49. 8. Kuzumik GA and Bulsara KR. Microsurgical clipping of true posterior communicating artery aneurysms. Acta Neurochir 2012; 154: 1707–1710. 9. Cho SM, Cho SM, Cho YJ, et al. True posterior communicating artery aneurysm – case report. Kor J Cerebrovascular Surg 2003; 5: 71–73. 10. Akimura T, Abiko S and Ito H. True posterior communicating artery aneurysm. Acta Neurol Scand 1991; 84: 207–209. 11. Gibo H, Lenkey C and Rhoton AL Jr. Microsurgical anatomy of the supraclinoid portion of the internal carotid artery. J Neurosurg 1981; 55: 560–574. 12. Peerless SJ. The surgical approach to middle cerebral and posterior communicating aneurysm. Clin Neurosurg 1974; 21: 151–165. 13. Timothy J, Sharr M and Doshi B. Perils of a ‘true’ posterior communicating artery aneurysm. Br J Neurosurg 1995; 9: 789–791. 14. Nakatsuka H, Ohta S, Kuroda J, et al. Ruptured true posterior communicating artery fusiform aneurysm: Case report. No Shinkei Geka 2007; 35: 691–696.
