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Masato Tomii, Hisashi Onoue, Masaharu Yasue, Shogo Tokudome and Toshiaki Abe

Object. The authors have attempted to define the exact borders of the root exit zone (RExZ) of the facial nerve, measure the distribution of myelin histologically, and examine the relationship between contact vessels and the RExZ.

Methods. Seventy-five facial nerves were obtained from brainstems excised from 44 adult patients at autopsy. The arteries and veins associated with the facial nerve were counted and measured. The facial nerves, associated vasculature, and adjoining portions of the brainstem were then removed en bloc. These tissues were serially sectioned and stained, and a photomicrograph of each section was obtained. The distribution of myelin on each section was measured from the upper edge of the supraolivary fossette, and the relationship between contact vessels and the RExZ was examined.

The lateral transitional zone of the facial nerve began 8 mm distal to the upper edge of the supraolivary fossette (root exit point [RExP]) and had a mean length of 1.9 mm. The root detachment point (RDP) of the facial nerve at the medial side was located very close to the beginning of the medial transitional zone. In more than 80% of the nerves that were examined, vascular structures compressed the central glial myelin of the nerve.

Conclusions. The authors propose the use of the terms “RExP,” “RDP,” and “transitional zone,” instead of RExZ, which cannot be well defined. The RDP appears to be a good landmark for use during microvascular decompression.

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Hisashi Onoue, Nobuyoshi Kaito, Masahiko Akiyama, Masato Tomii, Shogo Tokudome and Toshiaki Abe

✓ To investigate the effects of subarachnoid hemorrhage (SAH) on the responsiveness of human cerebral arteries to vasoactive substances, the authors measured the isometric tension generated in helical strips of basilar and middle cerebral arteries isolated from human cadavers Contractions caused by KCl, prostaglandin F, noradrenaline, and serotonin were reduced in arteries obtained from cadavers with aneurysmal SAH damage and compared to those obtained from cadavers with no indication of intracranial diseases. Endothelium-dependent relaxation elicited by substance P and bradykinin, and endothelium-independent relaxation induced by prostaglandin I2 and nitroglycerin were also markedly decreased in arteries affected by SAH. However, the reduction in relaxation response to prostaglandin I2 was significantly less than that to the other vasodilator agents. These results indicate that human cerebral artery functions are severely impaired after SAH and that poor responses to vasoactive agents may result primarily from dysfunction of smooth-muscle cells.

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Sumito Okuyama, Shinjitsu Nishimura, Yoshiharu Takahashi, Keiichi Kubota, Takayuki Hirano, Ken Kazama, Masato Tomii, Junko Matsuyama, Junichi Mizuno, Tadao Matsushima, Masataka Sato and Kazuo Watanabe


Hypoperfusion during carotid artery cross-clamping (CC) for carotid endarterectomy (CEA) may result in the major complication of perioperative stroke. Median nerve somatosensory evoked potential (MNSSEP) monitoring, which is an established method for the prediction of cerebral ischemia, has low sensitivity in detecting such hypoperfusion. In this study the authors sought to explore the limitations of MNSSEP monitoring compared to tibial nerve somatosensory evoked potential (TNSSEP) monitoring for the detection of CC-related hypoperfusion.


The authors retrospectively analyzed data from patients who underwent unilateral CEA with routine shunt use. All patients underwent preoperative magnetic resonance angiography and were monitored for intraoperative cerebral ischemia by using MNSSEP, TNSSEP, and carotid stump pressure during CC. First, the frequency of MNSSEP and TNSSEP changes during CC were analyzed. Subsequently, variables related to stump pressure were determined by using linear analysis and those related to each of the somatosensory evoked potential (SSEP) changes were determined by using logistic regression analysis.


A total of 94 patients (mean age 74 years) were included in the study. TNSSEP identified a greater number of SSEP changes during CC than MNSSEP (20.2% vs 11.7%; p < 0.05). Linear regression analysis demonstrated that hypoplasia of the contralateral proximal segment of the anterior cerebral artery (A1 hypoplasia) (p < 0.01) and hypoplasia of the ipsilateral precommunicating segment of the posterior cerebral artery (P1 hypoplasia) (p = 0.02) independently and negatively correlated with stump pressure. Both contralateral A1 hypoplasia (OR 26.25, 95% CI 4.52–152.51) and ipsilateral P1 hypoplasia (OR 8.75, 95% CI 1.83–41.94) were independently related to the TNSSEP changes. However, only ipsilateral P1 hypoplasia (OR 8.76, 95% CI 1.61–47.67) was independently related to MNSSEP changes.


TNSSEP monitoring appears to be superior to MNSSEP in detecting CC-related hypoperfusion. Correlation with stump pressure and SSEP changes indicates that TNSSEP, and not MNSSEP monitoring, is a reliable indicator of cerebral ischemia in the territory of the anterior cerebral artery.