Morphology and hemodynamics have been revealed to play important roles in the generation and rupture of intracranial aneurysms [14]. As reported, the fPCA is a common variant of Willis circulation in the whole population [1, 2, 15, 16]. Generally speaking, fPCA contributes to a particular architecture of Willis circle and is more likely to gestate aneurysms due to disturbed hemodynamics distribution [17, 18]. In a comparative analysis about PComA, Thiarawat et al. revealed that ipsilateral fPCAs get a higher possibility to harbor aneurysms than other hemodynamics types (42% vs 14%, P < 0.001) [19]. Similarly, in this series, we found the fPCA aneurysm patients accounted for 19.1% (74 out of 388) of the population with PComA aneurysms.
The ipsilateral fPCA feeds the whole territory, which is formerly supplied by conventional posterior cerebral artery, and exposes to more violent impact of blood flow. In this case, aneurysms grow more easily. In case of blocking or injury of fPCA, infarction develops and patients tend to suffer from poor outcomes because of the lack of compensatory from posterior cerebral circulation [20]. Cerebral infarction is strongly correlated with angiographic vasospasm for ruptured aneurysms. The constituent and accompanying inflammatory could cause a strong constriction of the blood vessels. But in some cases, angiographic vasospasm was not detected. It is because that there were still other reasons, such as small-vessel spasm and micro-thromboembolism, cortical spreading ischemia, intraoperative hypotension, coagulopathy, perforator occlusion attributable to the aneurysm-securing procedure, or a complication of catheter angiography. Therefore, in order to prevent the occurrence of postoperative cerebral infarction, blood pressure should be controlled steadily throughout the perioperative period to ensure effective cerebral perfusion pressure, careful handling should be recommended to protect perforating blood vessels during operation, and hemostatic agents should be used cautiously.
In this study, we described clinical data of 74 aneurysms in the origin site of posterior cerebral artery firstly (Table 1). We noticed some common features as aneurysms of other types, such as a female preponderance (56 vs 18) [21, 22], high prevalence of hypertension (62.2%) [23], and high rupture rate, which are in accordance with the previous reports.
The architecture of fPCA is easier to cause hemodynamic aberrance. Due to the autocephalous architecture, injury or occlusion of the fPCA may bring about severe occipital infarcts and subsequent clinical complications, such as homonymous hemianopsia, alexia, aphasia, and hemiachromatopsia [16]. As suggested by the previous study, endovascular occlusion of an aneurysm and its parent artery is of high risk for patients with fetal-type PCA aneurysms [24]. In this surgical series of 74 cases, 19 (25.7%) patients presented postoperative radiological infarction. Of them, 14 are from the perforator PComA, 2 have distal PCA infarct, and 3 share both. There are 4 that refer to MCA or ACA territory infarcts in this series. The univariate analysis (χ2 = 5.873, P = 0.027) and binary logistic regression (OR = 0.264, 95% CI (0.066–1.056), P = 0.060) demonstrated that full type of fPCA tend to be a predictive factor for postoperative radiological infarction.
Endovascular embolization of the PComA aneurysms has been widely accepted as an effective treatment modality. But endovascular treatment of fetal PComA faces some challenges, specifically for the ruptured ones. Roy et al. reported an independent association between incomplete occlusion and fPCA configuration [25]. Wallace et al. reported a complication rate of 14% and overall complete occlusion rate of 33% [26]. In this series, all aneurysms were completely clipped and 11 (15.0%) suffered complications.
The follow-up data at 3 months after surgery showed that 63 patients (85.1%) got favorable prognosis with the GOS of 4 and 5. The regression analysis showed that postoperative radiological infarction, rupture, and hypertension tend to be the independent predictive factor for poor prognosis at 3 months after discharge.
Our study has some limitations. First, this study is a retrospective study and the number of patients is small, thus leading to bias. Prospective and a larger number of patients are needed to confirm the results. Second, the patients are screened in one institution and selection bias may have affected the veracity of outcome.