Recent some reports recommended endovascular coil embolization as the first treatment option rather than surgical clipping [24–26, 35]. However, we decided to consider surgical clipping as a first line of treatment because long-term follow-up data demonstrated that the risk of rebleeding was lower in patients treated by surgical clipping than by endovascular coiling even the patients with ruptured posterior circulation aneurysms were treated by surgical clipping when the aneurysm was assessed as being relative easy to access by craniotomy.

In this study, our combined EN and PN with cilostazol administration significantly reduced the frequency of symptomatic VS and the incidence of cerebral infarction related to VS, which significantly improved the clinical outcomes. Based on the multiple logistic analyses, introduction of combined EN and PN with cilostazol administration reduced angiographic VS to 42 % and symptomatic VS to 19 %. Combined EN and PN with cilostazol administration was the only factor that reduced angiographic VS and symptomatic VS.

The effects of cilostazol are basically mediated by inhibition of phosphodiesterase 3 in smooth muscle cells and platelets, leading to relaxation of intact smooth muscle cells and inhibition of platelet aggregation. Previous studies reported the effectiveness of cilostazol administration for cerebral VS [32, 36, 40]. Yoshimoto et al. reported the efficacy of cilostazol for cerebral VS in their series of patients who were treated by cilostazol administration in the same way as in our study. In their series, symptomatic VS occurred in 5 of the 26 (19.2 %) patients in the cilostazol group and 9 of the 24 (37.5 %) patients in the control group, showing a reduction in symptomatic VS by cilostazol, but not significantly. They also reported that new lesions caused by VS on CT or MR scans were detected in 3 of the 26 patients in the cilostazol group and 7 of the 24 patients in the control group, showing no significant difference [40]. In 2011, Suzuki et al. reported on a series of patients treated in the same way, in which the frequency of symptomatic VS was occurred in 11 of 49 patients (22.4 %) in the cilostazol group and 19 of 51 patients in the control group (37.3 %) in the control group, with findings of new cerebral infarction caused by VS detected in 5 of the 49 patients (10.2 %) in the cilostazol group and 14 of the 51 patients (27.5 %) in the control group, showing no significant difference. However, they showed an improvement in clinical outcomes [36]. In 2013, Senbokuya et al. performed a multicenter prospective, randomized, open-label, blinded endpoint trial under the same treatment protocol as used in our study. In their series, the frequency of symptomatic VS was 7 of 54 patients (13.0 %) in the cilostazol group, 22 of 55 patients (40 %) in the control group; and cerebral infarction was detected in 6 of 54 patients (11.1 %) and 16 of 55 patients (29.1 %), respectively. There were significant differences between two groups. However, they failed to prove significant improvement of clinical outcomes. Comparing with these data, the occurrence of symptomatic VS was 19.2, 22.4, 13.0 % in the cilostazol groups previously reported and 12.0 % in our series and the findings of cerebral infarction was detected in 11.5, 10.2, 11.1 % in the cilostazol group, and no more than 6.9 % in our series. Comparing our data with the previous studies, the incidence of symptomatic VS may be slightly lower and the incidence of cerebral infarction may be slightly suppressed with the aid of the combined nutrition.