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  • Author or Editor: Yoshihisa Nishiyama x
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Yoshihisa Nishiyama, Hiroyuki Kinouchi, Nobuo Senbokuya, Tatsuya Kato, Kazuya Kanemaru, Hideyuki Yoshioka and Toru Horikoshi

Recently, intraoperative fluorescence video angiography using indocyanine green (ICG) has been widely used in aneurysm surgery. This is a simple and useful method to confirm complete occlusion of the aneurysm lumen and preservation of blood flow in the arteries around the aneurysm. However, the observation field of ICG video angiography is limited under a microscope, making it difficult to confirm the flow in the arteries behind the parent arteries or aneurysm. The authors developed a new technique of intraoperative endoscopic ICG video angiography to assess the blood flow in perforating arteries hidden by the parent arteries or aneurysm. The endoscope emits excitation light with a wavelength of approximately 800 nm, and video images were obtained through a cut filter. The authors used this ICG fluorescence endoscope in treating 3 patients with unruptured cerebral aneurysms. During clip placement, the endoscope was inserted to confirm aneurysm occlusion. Then, ICG was intravenously administered, and the fluorescence in the vessels was observed via the endoscope as well as under the microscope. The blood flow in the perforating arteries was clearly identified, and no procedural complication occurred. The authors conclude that the technique is very useful and facilitates intraoperative real-time assessment of the patency of perforating arteries behind parent arteries or aneurysms.

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Kazuya Kanemaru, Hiroyuki Kinouchi, Hideyuki Yoshioka, Takashi Yagi, Takuma Wakai, Koji Hashimoto, Yuichiro Fukumoto, Takako Umeda, Hiroshi Onishi, Yoshihisa Nishiyama and Toru Horikoshi


The severity of cerebral hemodynamic disturbance caused by retrograde leptomeningeal venous drainage (RLVD) of a dural arteriovenous fistula (dAVF) is related to neurological morbidity and unfavorable outcome. However, the cerebral hemodynamics of this disorder have not been elucidated well. The aim of this study was to assess the relationship between the cerebral venous congestive encephalopathy represented as a high-intensity area (HIA) on T2-weighted MR images and the cerebral hemodynamics examined by 123I-iodoamphetamine (IMP) single photon emission computed tomography (SPECT), as well as the predictive value of 123I-IMP SPECT for the development and reversibility of venous congestion encephalopathy.


Based on the pre- and posttreatment T2 HIAs associated with venous congestion encephalopathy, patients were divided into 3 groups: a normal group, an edema group, and an infarction group. The regional cerebral blood flow (rCBF) at the region with RLVD was analyzed by 123I-IMP SPECT, and the results were compared among the groups.


There were 11, 6, and 3 patients in the normal, edema, and infarction groups, respectively. No patients in the normal group showed any symptoms related to venous congestion. In contrast, all patients in the edema and infarction groups developed neurological symptoms. The rCBF in the edema group was significantly lower than that in the normal group, and significantly higher than that in the infarction group. The cerebral vascular reactivity (CVR) of the infarction group was significantly lower than that of the normal and edema groups. After treatment, the neurological signs disappeared in the edema group, but only partial improvement was seen in the infarction group. The rCBF also significantly increased in the normal and edema groups, but not in the infarction group.


Quantitative rCBF measurement is useful for evaluating hemodynamic disturbance in dAVF with RLVD. The reduction of rCBF was strongly correlated with the severity of venous congestive encephalopathy, and loss of CVR is a reliable indicator of irreversible venous infarction caused by RLVD.

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Nobuo Senbokuya, Hiroyuki Kinouchi, Kazuya Kanemaru, Yasuhiro Ohashi, Akira Fukamachi, Shinichi Yagi, Tsuneo Shimizu, Koro Furuya, Mikito Uchida, Nobuyasu Takeuchi, Shin Nakano, Hidehito Koizumi, Chikashi Kobayashi, Isao Fukasawa, Teruo Takahashi, Katsuhiro Kuroda, Yoshihisa Nishiyama, Hideyuki Yoshioka and Toru Horikoshi


Cerebral vasospasm following aneurysmal subarachnoid hemorrhage (SAH) is a major cause of subsequent morbidity and mortality. Cilostazol, a selective inhibitor of phosphodiesterase 3, may attenuate cerebral vasospasm because of its antiplatelet and vasodilatory effects. A multicenter prospective randomized trial was conducted to investigate the effect of cilostazol on cerebral vasospasm.


Patients admitted with SAH caused by a ruptured anterior circulation aneurysm who were in Hunt and Kosnik Grades I to IV and were treated by clipping within 72 hours of SAH onset were enrolled at 7 neurosurgical sites in Japan. These patients were assigned to one of 2 groups: the usual therapy group (control group) or the add-on 100 mg cilostazol twice daily group (cilostazol group). The group assignments were done by a computer-generated randomization sequence. The primary study end point was the onset of symptomatic vasospasm. Secondary end points were the onset of angiographic vasospasm and new cerebral infarctions related to cerebral vasospasm, clinical outcome as assessed by the modified Rankin scale, and length of hospitalization. All end points were assessed for the intention-to-treat population.


Between November 2009 and December 2010, 114 patients with SAH were treated by clipping within 72 hours from the onset of SAH and were screened. Five patients were excluded because no consent was given. Thus, 109 patients were randomly assigned to the cilostazol group (n = 54) or the control group (n = 55). Symptomatic vasospasm occurred in 13% (n = 7) of the cilostazol group and in 40% (n = 22) of the control group (p = 0.0021, Fisher exact test). The incidence of angiographic vasospasm was significantly lower in the cilostazol group than in the control group (50% vs 77%; p = 0.0055, Fisher exact test). Multiple logistic analyses demonstrated that nonuse of cilostazol is an independent factor for symptomatic and angiographic vasospasm. The incidence of new cerebral infarctions was also significantly lower in the cilostazol group than in the control group (11% vs 29%; p = 0.0304, Fisher exact test). Clinical outcomes at 1, 3, and 6 months after SAH in the cilostazol group were better than those in the control group, although a significant difference was not shown. There was also no significant difference in the length of hospitalization between the groups. No severe adverse event occurred during the study period.


Oral administration of cilostazol is effective in preventing cerebral vasospasm with a low risk of severe adverse events. Clinical trial registration no. UMIN000004347, University Hospital Medical Information Network Clinical Trials Registry.