To investigate pathophysiology of moyamoya disease, we analyzed brain single photon emission tomography (SPECT) images of patients with this disease by using interface software for a 3-dimensional (3D) data extraction format. Presenting symptoms were TIA in 21 patients and hemorrhage in 6 patients. All the patients underwent brain SPECT scan of ¹²³I-IMP at rest and after acetazolamide challenge (17 mg/kg iv, 2-day method). Cerebral blood flow (CBF) was quantitatively measured using arterial blood sampling and an autoradiography model.
The group of the patients who presented with TIAs showed decreased CBF in the frontal lobe at rest compared to that of patients with hemorrhage, but Z-score ((mean—patient data)/SD) did not reach statistical significance. Significant CBF decrease after acetazolamide challenge was observed in a wider cerebral cortical area in the TIA group than in the hemorrhagic group. The brain region of hemodynamic ischemia (stage II) correlated well with the responsible cortical area for clinical symptoms of TIA. A hemodynamic ischemia stage image clearly represented recovery of reserve capacity after bypass surgery.
Statistical evaluation of SPECT may be useful to understand and clarify the pathophysiology of this disease.

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Obtaining detailed anatomical information is crucial before aneurysm microsurgery. The anterior cerebral communicating artery complex (AcoC) is particularly complicated compared to other parts. The anatomical structure of the AcoC is sometimes difficult to understand using conventional angiography. We evaluated the advantages of 3-dimensional digital angiography (3D-DA) for aneurysm microsurgery on the anterior cerebral communicating artery.
Subjects comprised 10 men and 5 women (mean age, 61 years; range, 33-79 years) who underwent surgery in our hospital between November 2002 and October 2005. Twelve aneurysms were ruptured, and 3 aneurysms were unruptured. We compared 3D-DA images and surgical findings to assess aneurysmal morphology and relationships to neighboring vessels. We also examined both the presence and visualization of variations on AcoC. In all cases, surgical findings corresponded well to 3D-DA images. Variations on AcoC included fenestration (n=3), azygos (n=1) and aplasia or hypoplasia of the A1 segment of a unilateral anterior cerebral artery (n=9), and these were all well-visualized in 3D-DA. In addition, 3D-DA was also useful for aneurysms with 2 domes for selection of surgical approach, and provided assessment of not only aneurysmal morphology, but also variations of AcoC.
This tool provided useful information for the selection of operation approach and intraoperative manipulations by using it together with 2-dimensional digital substraction angiography.

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Carotid artery stenosis should be discussed in relation to its frequency or after NASCET, ECST and ACAS surveys. We normally examine a patient's stenotic frequency through the narrow directions of angiography. It is possible that such evaluation is insufficient.
The importance of the futures of a carotid artery wall, which is largely studied through ultrasound sonography, is well understood. The presence of ulceration, the surface condition and sonographic intensity of the plaque are routinely examined, but we focused on the existence of neovascularization in plaques, one of the pathological factors leading to plaque hemorrhage and rupture. This pathological process appears to be responsible for carotid artery stenosis, occlusion and artery-to-artery embolisms.
Harmonic image is a contrast specific imaging modality that males use of the nonlinear properties of ultrasound contrast agents by transmitting at the fundamental frequency and receiving at multiples of these frequencies. Pulse inversion harmonic image (PIHI), using pulse inversion to eliminate and strengthen the harmonic frequency, is more effective than conventional harmonic imaging. We can detect a tissue perfusion by contrast sonographic imaging with PIHI. This method has already been reported on the clinical fields, e.g. in imaging cardiac infarction, liver tumors, brain tumors and cerebrovascular diseases.
There are 2 routes of vascular wall feeding: diffusion through the endothelium, and diffusion through the vasa vasorum from the adventitious to the outer part of the medium. There is no neovascularization at the inner side of the carotid artery, but some plaques are associated with neovascularization in themselves, so an attempt was made to detect such plaques by the intermittent and real time contrast sonographic imaging method with PIHI. The evaluation of neovascularization by the intermittent method and its classification as Type I to IV, according to the distribution of neovascular vessels in the plaque, have already been reported.
The real time contrast sonographic imaging method with PIHI has revealed some characteristics of neovascularization:
1. The newly formed vessels from the advantitia are larger than the ones from the endothelium.
2. There is some anastomosis between the neovasculatures.
3. The distribution of neovascular vessels is concentrated in an inner part of plaque. In addition, these vessels run in a spiral pattern.
4. Neovascular circulation is related to the pulsation of the carotid artery.
5. It seems that many newly formed vessels sprout from the endothelium.

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We investigated the effect of sustained administration of intrathecal nicardipine, calcium antagonist, in 16 cases to prevent post-subarachnoid hemorrhage (SAH) vasospasm. Patients with SAH of Fisher CT Group 3 (15 cases) or Group 4 (1 case) underwent direct clipping surgery and the placement of the cisternal catheter. From 1-4 days after SAH onset, the nicardipine solution (0.09 mg/ml) was continuously injected through the cisternal catheter at the rate of 2 ml/h for 4-16 days. The vasospasm was evaluated from postoperative angiography performed 1 week after SAH onset.
The ratios of diameter at internal carotid arteries (ICA) C1 portion, middle cerebral arteries (MCA) M1 portion and anterior cerebral arteries A1 portion were obtained from preoperative and post-operative angiograms. Mild localized vasospasm was observed in 5 cases. The ratios of diameter at C1, M1 and A1 were 1.15±0.19, 1.13±0.23 and 1.17±0.26, respectively. No symptomatic vasospasm was observed in any of the cases.
These findings demonstrated that the vaso-dilative effect of nicardipine prevented the post SAH vasospasm of intracranial arteries at C1, M1 and A1. The mild angiographical vasospasm in the 5 cases was probably due to the insufficient delivery of nicardipine solution. Following the operative manipulation of the exposure of ICA and MCA with radical clot removal, administration of nicardipine solution through the catheter in the contralateral carotid cistern and draining from the catheter in ipsilateral sylvian cistern brought the widespread nicardipine delivery to peripheral arteries.
Though further improvement of this method is required, sustained intrathecal administration of nicardipine effectively prevents vasospasm following SAH.

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Reduction of complications of carotid endarterectomy (CEA) for carotid artery stenosis is essential for keeping the superiority of CEA over the medical treatment. Therefore, we must recognize the specific features of the asymptomatic carotid artery stenosis (AS-ICAS) to avoid operative complications.
Of 290 CEAs performed on patients with carotid artery stenosis, 109 CEAs were done for the AS-ICAS. Our indications of CEA for AS-ICAS were stenosis over 60%, hypoechoic or heterogeneous echogenesity and ulceration detected by B-mode ultrasonography and progression of the stenosis. We routinely use the T-shaped shunt tube and intraoperative monitoring such as somatosensory evoked potential (SEP). To obtain specific features of AS-ICAS, we analyzed cerebral blood flow, intraoperative monitoring and frequencies of associated systemic diseases in the patients with AS-ICAS.
Perioperative mortality and morbidity of CEA for the patients with AS-ICAS were 0 and 1.8%, respectively. Cerebral blood flow of the territory of the middle cerebral artery (rCBF) and cerebrovascular reactivity (rCVR) were not lower than those on the contralateral side. Compared with those of symptomatic carotid artery stenosis (S-ICAS), there was no significant difference in rCBF or rCVR, although rCVR of S-ICAS was relatively lower than that of AS-ICAS. There was no significant difference in the intraoperative monitoring between AS-ICAS and S-ICAS. Hyperperfusion after CEA of AS-ICAS occurred in 2.0% which was not significantly lower than the 6.5% of S-ICAS. Specific features of CEA for AS-ICAS were not obtained from this study.
According to the mortality and morbidity of our CEAs, CEA for AS-ICAS was acceptable.

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EC-IC bypass surgery to prevent cerebral ischemia must be performed carefully and safely. We apply several techniques and devices to reduce the operative risk as much as possible by: preoperatively planning for redistribution of cerebral blood supply as selection of the recipient and the supplied part, arranging the operative field to ensuring the working space and control of epidural bleeding or cerebral spinal fluid (CSF) and avoiding postoperative skin trouble by preserving blood flow in the subcutaneous layer just under skin incision. Recently we tried a new retractor by firmly attaching an extremely small tube to control CSF easily in the operative field.
These techniques and devices very effectively reduce complications.

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Although antiplatelet therapy is usually continued throughout the perioperative period of carotid endarterectomy to reduce the risk of recurrent stroke and other cardiovascular events, individualization still has not been standardized. To evaluate the relationship between preoperative antiplatelet agents and platelet aggregability, we analyzed 42 patients who underwent carotid endarterectomy from August 2005 to May 2006 in our institute.
Among the 42, 19 were treated with aspirin alone, 5 with ticlopidine alone, 2 with cilostazol alone, 12 with aspirin and ticlopidine, 3 with aspirin and cilostazol and 1 with aspirin, ticlopidine, and cilostazol. Platelet aggregation in response to platelet agonist was measured in platelet-rich plasma obtained from the brachial vein 2 days prior to surgery. 1 μM and 10 μM ADP, or 2 μg/ml and 5 μg/ml collagen were used as agonists. Aggregation in response to appropriate agonist was inhibited in 73% of the aspirin group and 80% of ticlopidine group. None of the cilostazol group showed effects on aggregability. Patients were divided into 2 groups according to their preoperative platelet aggregability: inhibited (n=3) or non-inhibited (n=39). Intraoperative blood loss was 169.0±23.3 g (144-190 g) or 45.5±31.2 g (9-164 g), respectively. Operation time was 221.7±53.5 min (160-255 min) or 147.3±20.6 min (115-205 min), respectively. The main reason for blood loss and prolonged operation time was oozing from connective tissue.
Aggregability in older patients who received multiple antiplatelet agents tended to be inhibited excessively. Taken together, preoperative analysis of platelet aggregability could be useful to reduce the risk of perioperative complication.

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Internal carotid artery (ICA) trapping+radial artery graft could be performed for ICA cavernous, paraclinoid portion aneurysms. Direct clipping procedures are not always possible to carry out in these cases, because there are a lot of neurostructures surrounding aneurysms. These nerve structures could be easily damaged during the direct clipping procedure. Compared with direct clipping procedure, ICA trapping+radial artery graft could be a safe and easy method to achieve intra-aneurysm thrombosis and neurological improvement.
However, treatment strategy may differ among nonbleeding and bleeding cases. Endovascular proximal occlusion is the first choice for nonbleeding cases who mainly suffered from ophthalmoparesis. But it is important to estimate ischemic tolerance before permanent proximal occlusion by balloon occlusion test (BOT).
ICA trapping+radial artery graft should be selected in cases without ischemic tolerance for BOT. On the other hand, ICA trapping+radial artery graft should be primarily performed for patients with ruptured anterior wall ICA aneurysms without the BOT procedure, because re-bleeding may occur during the BOT procedure.

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Preoperative angiography is basically essential for a patient of intracerebral hematoma, so as to check any underlying vascular anomaly such as a ruptured aneurysm or an arteriovenous malformation (AVM). When the hematoma causes impending herniation, however, we omit preoperative angiography to save time and perform emergency surgery even if a ruptured aneurysm or an AVM is highly suspected. We experienced 8 such cases during 2.5 years: 6 cases of ruptured aneurysm and 2 of AVM. Three of them achieved good recovery and none died.
Some special considerations and tactics are required before and during surgery to ensure safety. When a ruptured aneurysm is suspected, a microscope, a self-retractor and clips should be ready prior to surgery. The superficial temporal artery should be preserved just in case. After the craniotomy, the hematoma is evacuated partially for decompression away from the suspected aneurysm. Then, in case of premature rupture, the dissection is performed directly toward the bleeding site; otherwise sylvian fissure is dissected for aneurysm exploration. When an AVM is suspected, care must be taken not to injure the draining veins. It is safer to finish the emergency surgery after evacuating the hematoma and to go on to cerebral angiography. The resection of an AVM should then be performed in the chronic period.
In our experiences, we were able to perform emergency surgery safely for a ruptured aneurysm or an AVM, even when we had to omit preoperative angiography because of impending herniation.

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We report the case of 41-year-old woman with a de novo aneurysm originating at the antero-lateral wall of the contralateral internal carotid artery (ICA) 31 days after the cerebral infarction due to the dissection of the ipsilateral cervical ICA. She developed right hemiparesis and aphasia. Head CT showed fresh cerebral infarction in the left ICA territory, and head MRA showed a stenosis in the left cervical ICA. Carotid ultrasonography indicated an intramural hematoma at the origin of the left ICA, and staccato flow was observed on the Doppler examination, suggesting the dissection of the ICA.
Although neuroprotective and anticoagulant therapies were carried out, she developed a sudden severe headache and generalized convulsion on Day 31 since cerebral infarction. Head CT revealed subarachnoid hemorrhage, and a following 3D-CT angiogram showed a saccular de novo aneurysm at the anterolateral and non-branching wall of the supraclinoid ICA on the right. We performed right fronto-temporal craniotomy and neck clipping of the aneurysm. Since no aneurysms had been observed at the affected site on the initial MRA, which was conducted at the onset of cerebral infarction, it was surmised that a de novo aneurysm developed over a short period of time as a result of the hemodynamic stress after the occlusion of the left ICA.
This case study may be of importance for clarifying the pathogenesis of aneurysms.

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