“True” Aneurysm of the Posterior Communicating Artery as a Possible Effect of Collateral Circulation in a Patient with Occlusion of the Internal Carotid Artery. A Case Study and Literature Review

Abstract

"True" posterior communicating artery (PCoA) aneurysms are extremely rare. A case of a 63-year-old patient with a ruptured "true" aneurysm of the right PCoA associated with the occlusion of the right internal carotid artery is presented. For nine years before he suffered from subarachnoid hemorrhage, the patient had developed symptoms of transient ischemic attack (TIA) due to the occlusion of the right internal carotid artery. The left vertebral angiogram demonstrated a "true" right PCoA aneurysm and collateral flow from the right posterior communicating artery to the right internal carotid artery. The right internal carotid system was also fed by collateral circulation from the left carotid artery through the anterior communicating artery. Transcranial colour-coded real-time sonography (TCCS) demonstrated increased velocity and turbulent blood flow in both communicating arteries. The patient was operated on and the aneurysm was clipped successfully. This case report suggests that the blood flow disturbances resulting from the collateral circulation through the PCoA could be a conductive factor in the formation and development of the aneurysm. This is the first described case of a "true" aneurysm of the PCoA coexistent with the occlusion of the internal carotid artery.

Posterior cerebral artery-posterior communicating artery (PCA-PComA) aneurysms: Report of five cases and literature review

“…Increased blood velocity and existed turbulence may lead to degeneration of the endothelial basement membrane and subendothelial connective tissue in the blood vessel wall, leading to the occurrence of PCA-PComA aneurysms. [2] In all of our patients, retrograde blood fl ow from posterior circulation to anterior circulation via PComA artery was noticed. The hypertrophied PComAs indicate increased blood fl ow and added hemodynamic stress.…”

“…[1] Usually, "PComA aneurysm" refers to internal carotid artery (ICA)-PComA aneurysms originating from the ICA-PComA junction and less frequently refers to the aneurysms of the PComA itself. [1,2] However, PComA aneurysm may also occur at the other junction of posterior cerebral artery (PCA) and PComA, which is extremely rare and not well documented. [3][4][5][6] To the best of our knowledge, only four cases have been reported earlier and this report presents fi ve additional cases.…”

Co-existence of Three Types of Fibromuscular Dysplasia associated with True Posterior Communicating Artery Aneurysm

“…Although the mechanisms of aneurysm growth and rupture remain controversial, it has been generally considered that hemodynamic factors play a significant role in the initial formation, the growth and the rupture of cerebral aneurysm. Kaspera et al reported a"true" PCoA aneurysm coexisting with the internal carotid occlusion and demonstrated increased velocity and turbulent blood flow in both communicating arteries, which suggested that the blood flow disturbances might be conducive to the formation and development of the aneurysm [9]. Ogasawara et al reported a case of ruptured true PCoA aneurysm 13 years after surgical occlusion of the ipsilateral cervical ICA with superficial temporal artery-middle cerebral artery anastomosis for ruptured right ICA aneurysm and suggested that hemodynamic factors were the reason for aneurysm formation [10].…”

Development of 'De novo' Aneurysm after Therapeutic Carotid Occlusion

“…The incidence of de novo aneurysm formation following carotid occlusion varies from 0% to 20 % with a mean around 4-11% 1,5,13) . There are more than 30 reports of de novo aneurysm formation after carotid occlusion [1][2][3][4]9,10,16,19,20) . The majority of these aneurysms were situated in the anterior circulation, in the anterior communicating artery, the contralateral posterior communicating artery, and the contralateral ICA; these vessels were the sites of the main hemodynamic changes associated with the increased blood flow necessary to supply the contralateral carotid circulation.…”