Aesthetics must be considered in surgery for unruptured cerebral aneurysms, since it is a prophylactic treatment and a good-quality postoperative life should be maintained. We introduce several of our attempts to this end.
To prevent postoperative alopecia, scalp clips are not used, and a skin incision is made perpendicular to the hairline and parallel to the hair-growing angle. Prevention of postoperative atrophy of the temporal muscle is attempted by not using keyholes, not using incision in the anterior part of the muscle, and preserving deep temporal arteries and veins. Any craniotomy lines and burr holes should be covered by artificial devices or autologous bone powder obtained during craniotomy and tightly covered by subgaleal connective tissue or temporal muscle with periosteum.
In bald-headed patients, keyhole surgery is effective to make the scar ambiguous. Otherwise, a craniotomy under a skin incision on a wrinkle of the forehead, which can offer a larger operative field than keyhole surgery, effectively obscures the skin incision postoperatively.
These attempts have resulted in satisfactory aesthetic effects both subjectively and statistically.

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We report surgical techniques for gaining a wide operative view without brain retractors in a pterional approach to an unruptured aneurysm. In Summary, the techniques involve:
1) Head positioning with the chin slightly up (vertex down), allowing the frontal lobe to fall away from the orbital roof. 2) Wide arachnoidal dissection using a long strip of Bemsheets serving as brain retractors. 3) Further epidural removal of bone from the sphenoid ridge and the flattening of the orbital roof after gaining the appropriate subdural space. 4) Optic canal unroofing and anterior clinoidectomy resulting in mobilizing the internal carotid artery.
A wide operative view without brain retractors contributes to the safe dissection and clipping of an unruptured aneurysm, preserving the parent arteries and their perforators.

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We developed a tailor-made method based on surgical simulation using three-dimensional (3D) imaging of individual patients to allow safe performance of aneurysm clipping surgery via keyhole mini-craniotomy. 3D images were reconstructed of the skin, skull, cerebral arteries and veins, and the aneurysm. The size, shape, and location of the scheduled keyhole and the patient’s head position were determined by virtual osteostomy technique. The site of opening of the sylvian fissure was also determined according to the spatial relationships between the aneurysm and sylvian veins. A total of 170 tailor-made clipping surgeries have been performed in 160 patients. Good recovery was seen in 98.8% of the patients, and the morbidity rate was low at 1.6%.
Detailed preoperative simulation allows the performance of safe keyhole clipping surgery.

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We examined the relation between carotid stenosis rate and arm-to-retina circulation time (A-R time) and retinal circulation time (RC time) in patients with carotid artery stenosis and evaluated changes before and after carotid artery stenting (CAS). Twenty-six patients, 22 men and 4 women ranging in age from 56 to 86 years (mean 72 years), with carotid artery stenosis were examined. A-R time and RC time were demonstrated by fluorescein angiography. Twenty patients out of 26 were also examined after CAS. The side of carotid artery stenosis consisted of right in 11 and left in 15 of 26 patients. Seventeen patients were symptomatic (amaurousis fugax in 4), 9 patients were asymptomatic. The ratio of carotid stenosis was 62% to 95% (NASCET), mean 79±7.6%. A-R time was 12.8 seconds (sec) to 32.2 sec, mean 24.6±5.6 sec. Twenty-four of 26 (92.3%) patients presented delayed A-R time. RC time was 6.4 sec to 42.1 sec, and the mean was 19.3±8.9 sec. Twenty-three of 26 (88.5%) patients presented delayed RC time. In comparison of before and after CAS, RC time was significantly reduced after CAS (p＜0.05, paired t-test).
The measurement of retinal circulation by fluorescein angiography was useful to evaluate carotid artery stenosis.

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We examined improvement of ocular ischemia in patients with carotid endarterectomy (CEA) with chorioretinal blood flow measurements using laser speckle flowgraphy (LSFG). LSFG allowed the quantitative measurement of chorioretinal blood flow.
Five CEA patients, 4 men and 1 women ranging in age from 59 to 79 years, with carotid stenosis were examined. Three patients were symptomatic, and 2 patients were asymptomatic. The ratio of carotid stenosis was 68% to 98%. None of the patients presented delayed arm-to-retina circulation by fluorescein angiography. Four of 5 patients presented a mean increase in chorioretinal blood flow. The mean increase ratio of blood flow was 7.84%.
LSFG was useful to evaluate peripheral blood flow in CEA patients and revealed that CEA may improve ocular ischemia.

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Surgical treatment for the cerebral aneurysms of the proximal (M1) segment of the middle cerebral artery, especially those that project superiorly, carries a high risk of infarct caused by damage of perforating arteries.
Between January 2004 and November 2009, of 114 patients with MCA aneurysms treated surgically in our hospital, 11 patients with aneurysms of the proximal MCA were diagnosed on the basis of angiographic or surgical findings. Among them, 8 patients had aneurysms projected superiorly. All patients underwent surgery via fronto-temporal craniotomy and trans-sylvian approach. Four patients with ruptured aneurysms underwent emergency surgery within 72 hours of the insult. Motor evoked potential (MEP) was monitored during surgery in the latest 2 patients. We reviewed retrospectively 8 patients with such aneurysms treated by direct surgery.
The average age in our patient population was 64.3 years (range, 56-81 yr). There were 2 men and 6 women. The average size of aneurysms was 8.1 mm (range, 3-25 mm). Four patients had ruptured aneurysms. Intracerebral hematoma was recognized on computer tomographic (CT) scan in 2 patients with ruptured aneurysms. Neck clipping was performed in 7 patients and wrapping in 1 patient. STA-MCA bypass was performed for the patient with giant aneurysm. Temporary occlusion of the M1 segment was required in 2 patients, including the patient with giant aneurysm. CT scans after surgery revealed cerebral infarction in the territories of the perforating artery from the M1 segment in 3 patients, and aphasia remains in 1 of the 3 patients. At 3 months after surgery, 5 patients made a good recovery (GR), 2 had a moderate disability (MD), and 1 a severe disability (SD), according to Glasgow Outcome Scale (GOS). All of the unruptured aneurysms made GR, though 1 patient presented with cerebral infarction.
The aneurysms of the M1, which project superiorly, represent one of the most complicated aneurysms. Understanding the relationship between the perforating arteries arising from the M1 segment and the aneurysm neck should allow surgeons to avoid many postoperative ischemic complications.

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In this paper, we retrospectively analyze the factors related to infarction of the medulla oblongata causing Wallenberg syndrome after endovascular trapping for dissecting aneurysm of the vertebral artery (VA).
Seven cases of dissecting aneurysm of the VA including 5 ruptured cases were treated with endovascular coil embolization between 2003 and 2009 in our hospital. The posterior inferior cerebellar arteries (PICA) originated proximal to the aneurysm in 1 case, at the site of the aneurysm in 1 case, distal in 2 cases, and from the basilar artery (BA) in 3 cases.
Complete obliteration of the dissecting aneurysms preserving blood flow of the PICA and opposite VA could be obtained in all cases except 1 case in which the aneurysm involved the PICA. No rebleeding was experienced, but infarction of the lateral medulla occurred in all 3 cases in which the PICA originated from the BA.
Though the outcome of the 3 cases was favorable (mRS 0-2; 100%), surgeons should be aware of the risk of the trapping of the VA if the PICA originate from the BA.

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We report the usefulness of a routine aspiration method, in which aspirations of blood column in the proximal internal carotid artery (ICA) to the filter are always performed regardless of the flow state on digital subtraction angiography immediately before the filter retrieval to prevent ischemic complications in filter protected carotid artery stenting (CAS). The purposes of the present study were to summarize the clinical results of patients undergoing CAS using the routine aspiration method and Angioguard XP, and to investigate limitations of this method and countermeasures to prevent ischemic complications.
The routine aspiration method was performed in 71 consecutive CAS procedures using Angioguard XP between November 2008 and June 2010. Two patients suffered from stroke within 30 days of the procedures (2.8%). Cerebral infarction occurred during CAS in 1 patient, and cerebral hemorrhage by hyperperfusion syndrome occurred 2 days after CAS in another. In the cerebral infarction case, the ICA was kinking just distal to the stenosis, and the kink was extended by the CAS procedure. A large amount of debris was found in both the retrieved filter and the aspirated blood columns.
Even in the routine aspiration method, ischemic complications can occur in a few cases. In cases of a kink in the ICA just distal to the stenosis, avoidance of the kink extension during CAS is recommended to prevent ischemic complications.

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We report a new computed tomographic (CT) finding of hyperacute ischemic stroke. We examined the CT findings of patients with acute ischemic stroke within 3 h of onset by using a very narrow CT window width. The CT number (Hounsfield unit, HU) of the ischemic area was decreased by only 1 or 2 units. The areas of decreased CT number were larger than the hyperintense areas observed in magnetic resonance imaging diffusion-weighted images (MRI-DWI). These areas were not detected as so called “early CT signs” of acute ischemia on conventional CT.
We examined 3 patients of hyperacute stroke, and treated them with tissue-plasminogen activator within 3 h of onset. Their narrow-window CT examination revealed low-density areas that were not detected in the conventional study. After arterial recanalization and resolution of ischemic symptoms, these low-density areas reduced and the CT number was normalized. When recanalization did not occur, these areas showed signs of infarction.
A low-density area in a narrow-window CT study may be a hypo-perfused area and include reversible ischemic area (or penumbra).

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A 66-year-old male patient suffered a lacunar infarction 7 years previously and was treated with 100 mg/day of cilostazol. The fluid attenuated inversion recovery (FLAIR) image of a follow-up magnetic resonance imaging (MRI) scan revealed dolichoectasia of the basilar artery with a small luminal thrombus.
Thirteen months later, a left cerebellar infarction occurred. The size of the aneurysm and luminal thrombus had increased. The dosage of cilostazol was increased to 200 mg/day. Three weeks later, he suffered a left pontine infarction and 100 mg/day of aspirin was added to the treatment regimen.
Seventeen months after the cerebellar infarction, the aneurysm enlarged further. Surgical treatment was performed using a flow reduction method. After anastomoses of the right superficial temporal artery-superior cerebellar artery and left superficial temporal artery-posterior cerebral artery were performed, the bilateral vertebral arteries were embolized using a coil.
The patient became comatose 12 hours after the last procedure. Three-dimensional computed tomography angiography revealed the complete occlusion of the basilar artery. Four days later, recanalization of the basilar artery was achieved by using an intravenous urokinase infusion. Nevertheless, marked infarction occurred in the bilateral cerebellar hemispheres and brain stem. He died and an autopsy was performed.
The aneurysm was found embedded in the brain stem at autopsy. A microscopic examination showed fragmentation of the internal elastic lamina with atrophy of the muscle layer and adventitia. Neoangiogenesis within the thickened intima may have caused intramural hemorrhage and thrombus formation. Furthermore, a new sickle-shaped clot located between the arterial wall and the old thrombus may have caused the hemodynamic expansion of the aneurysm.
Antiplatelet drugs were used to treat ischemic events caused by perforator or branch occlusion. However, use of these drugs should be carefully considered with regards to the risk of potentiating the compression of the brain stem due to aneurysmal enlargement.

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We report a case of posterior reversible encephalopathy syndrome (PRES) with subarachnoid hemorrhage in eclampsia. A 31-year-old female presented with a sudden severe headache and generalized convulsive seizure 6 days after delivery. Initial blood pressure was 198/100 (mean 133). Moderate disturbance of consciousness was observed. A brain CT scan was performed by her gynecologist and revealed subarachnoid hemorrhage. Therefore she was referred to our neurosurgery department. A 3D-CTA and MRA were performed on the day of admission, and no ruptured aneurysm and only very mild segmental vasoconstrictions at the vertebral artery and posterior cerebral artery were shown. A FLAIR image revealed multiple vasogenic edema in the cerebellar hemisphere, cerebral cortices and basal ganglia bilaterally. PRES was the most likely diagnosis. The sedative Propofol was administered for 3 days, and the patient recovered clinically. A follow-up MRI and MRA were performed 3, 10, and 21 days and 1 and 2 months after admission. Although a continuous reduction of the vasogenic edemas was shown by a follow-up FLAIR image, the severest diffuse vasoconstrictions in multiple cerebral arteries appeared 3 days after admission. Vasoconstrictions gradually improved during 2 months of follow-up.
Concerning the clinical cause of vasogenic edema in PRES, Bertynski mentioned 2 theories in his review. One theory is “Injury of the endothelium caused by altered autoregulation of cerebral arteries following excessive hypertension results in vasogenic edema,” and the other is “Vasogenic edema caused by the cerebral infarction after vasoconstriction.” In the present case, an elevated initial blood pressure was shown, but the mean arterial pressure did not seem high enough to injure the endothelium. Besides, the severest vasoconstriction of cerebral arteries did not occur until 3 days after the peak of the vasogenic edema. This means vasoconstriction did not precede vasogenic edema. Both theories are still controversial, and our case does not correspond to either theory.
We conclude that the present case shows a new theory for the clinical cause of vasogenic edema in PRES should be considered.

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