Masaru Yamada

Rerupture of cerebral aneurysms during angiography – a retrospective study of 13 patients with subarachnoid hemorrhage

SummaryObjective, background. Cerebral angiography, performed within 24 hr of aneurysmal rupture, carries an increased risk of rebleeding. We have investigated the rerupture rate during angiography procedures under deep general anesthesia and the factors that contribute to rebleeding.Methods. We divided 69 patients who had experienced aneurysmal rerupture into 2 groups. Group I (n = 13) suffered rebleeding during cerebral angiography and group II (n = 56) who rebled at a different time. We assessed the effects on rebleeding of the (1) time between the first insult and angiography, (2) WFNS clinical grade on admission, (3) blood pressure during angiography, (4) age and sex, (5) Fisher classification on admission, (6) aneurysmal site, and (7) Glasgow outcome score (GOS).Results. Factors that had a statistically relevant effect on rebleeding during cerebral angiography (Group I) were the performance of angiography within 3 hr of the initial insult, the admission grade, and the aneurysmal site. Especially, the rerupture events during cerebral angiography were concentrated within 3 hr of the initial insult; the rate was 23.9% when angiograms were obtained within 3 hr of onset. Group I patients manifested a worse clinical grade and middle cerebral artery (MCA) aneurysms were prevalent in this group. However, there was no significant difference between the 2 groups with respect to blood pressure, age, sex, Fisher classification, and GOS.Conclusions. Cerebral angiography at ultra-early timing (within 3 hr of the insult) carries a high risk of aneurysmal rerupture, even if the procedure is performed under deep anesthesia and normotensive blood pressure. Cerebral angiography during that period should be avoided.

Significance of the Hemorrhagic Site for Recurrent Bleeding: Prespecified Analysis in the Japan Adult Moyamoya Trial

Background and Purpose— The primary results of the Japan Adult Moyamoya Trial revealed the statistically marginal superiority of bypass surgery over medical treatment alone in preventing rebleeding in moyamoya disease. The purpose of this analysis is to test the prespecified subgroup hypothesis that the natural course and surgical effects vary depending on the hemorrhagic site at onset. Methods— The hemorrhagic site, classified as either anterior or posterior, was the only stratifying variable for randomization. Statistical analyses were focused on the assessment of effect modification according to the hemorrhagic site and were based on tests of interaction. Results— Of 42 surgically treated patients, 24 were classified as anterior hemorrhage and 18 as posterior hemorrhage; of 38 medically treated patients, 21 were classified as anterior and 17 as posterior. The hazard ratio of the primary end points (all adverse events) for the surgical group relative to the nonsurgical group was 0.07 (95% confidence interval, 0.01–0.55) for the posterior group, as compared with 1.62 (95% confidence interval, 0.39–6.79) for the anterior group (P=0.013 for interaction). Analysis within the nonsurgical group revealed that the incidence of the primary end point was significantly higher in the posterior group than in the anterior group (17.1% per year versus 3.0% per year; hazard ratio, 5.83; 95% confidence interval, 1.60–21.27). Conclusions— Careful interpretation of the results suggests that patients with posterior hemorrhage are at higher risk of rebleeding and accrue greater benefit from surgery, subject to verification in further studies. Clinical Trial Registration— URL: http://www.umin.ac.jp/ctr/index.htm. Unique identifier: C000000166.

The effect of encephalo-myo-synangiosis on abnormal collateral vessels in childhood Moyamoya disease

Abstract Child patients with Moyamoya disease initially present with ischemic symptoms. However, the long-term risk of intracranial hemorrhage for childhood Moyamoya disease is unknown. Hemodynamic overload to the fragile collateral vessels has been considered to cause hemorrhage. We reviewed angiograms to evaluate the effect of encephalo-myo-synangiosis (EMS) on abnormally dilated collateral vessels in 13 child patients with Moyamoya disease. EMS was performed on 24 sides in 13 patients ranging from 5 to 14 years of age. Post-operative angiography (6-88 months after surgery) revealed good revascularizations through EMS (larger than one-third of the middle cerebral artery (MCA) distribution) in 18 sides (75%) and smaller revascularizations in 6 sides (25%). In cases with a good revascularization through EMS, reduction of the abnormal collateral vessels was observed not only in the basal Moyamoya vessels (94% of sides) but also in the medullary arteries derived from the choroidal arteries (62% of sides), which are considered to cause intraventricular hemorrhages in adult patients. It is suggested that EMS may reduce the hemodynamic load on dilated collateral vessels and, subsequently, the long-term risk of intracranial hemorrhage in childhood Moyamoya disease. [Neurol Res 2000; 22: 341-346]

Impaired Autoregulation in an Experimental Model of Chronic Cerebral Hypoperfusion in Rats

BACKGROUND AND PURPOSE To verify the hypothesis that impaired autoregulation may contribute to cerebral swelling or hemorrhage after a sudden recovery of perfusion pressure, we studied the chronic effects of cerebral hypoperfusion on the autoregulatory responses of the pial arterioles in situ. METHODS Eight to 12 weeks after a carotid-jugular fistula was created in rats, experiments were performed under alpha-chloralose and urethane anesthesia. Regional cerebral blood flow (rCBF) was determined by the hydrogen clearance method, and carotid pressure was measured. Using a closed cranial window, we determined the autoregulatory responses of the arterioles (30 to 50 microns) to both hypertension induced by norepinephrine and sudden fistula closure at various mean arterial pressures (MAPs). RESULTS rCBF on the fistula side was reduced by 27%. Carotid pressure was significantly lower than normal but was immediately increased by fistula closure. The pial arterioles showed marked elongation and enlargement. During induced hypertension, the arterioles in the fistula group started to dilate at an MAP lower than that of the control group (130 versus 180 mm Hg, respectively). The arterioles constricted when the fistula was occluded at normal MAP. However, when the fistula was occluded at an MAP higher than 130 mm Hg, the vessels dilated. CONCLUSIONS It was demonstrated that (1) chronic hypoperfusion induced impairment of the upper limit of autoregulation and (2) sudden fistula closure under hypertensive conditions caused vasodilation of the arterioles. These findings suggest that rapid restoration of perfusion pressure is possibly followed by a pressure breakthrough phenomenon in a chronically hypoperfused cerebrovasculature.

Mass effect caused by clinically unruptured cerebral arteriovenous malformations.

OBJECTIVE It is generally considered that mass effect caused by arteriovenous malformations (AVMs) is evidence of ruptures. In the present study, the incidence of mass effect in clinically unruptured AVMs was evaluated, and the underlying causative factors and pathophysiological mechanisms were studied. METHODS Twenty-seven patients with clinically unruptured supratentorial pial AVMs were examined. The majority were suffering from epilepsy, and frontal lobe involvement was revealed in approximately half of the patients. Angiographic studies, computed tomographic scans, and magnetic resonance images were obtained for all patients. Twenty-one patients underwent removal of AVMs. In 10 of the surgically treated patients, intraoperative vascular pressure measurements were obtained before removal of the AVMs. RESULTS Mass effect was detected in 12 (44%) of the 27 patients. Cortical sulci obliteration (eight patients) and lateral ventricle displacement (seven patients) were frequently noted. The volume of AVMs was significantly larger in patients with mass effect than in those without mass effect (P < 0.001). Large dilated venous sacs or ectatic veins were observed to be associated with mass effect (P < 0.001). In only one patient was gross displacement related to a surrounding massive brain edema. Draining vein pressure in patients with mass effect was significantly elevated as compared to the average value in patients without mass effect (22 +/- 5 versus 12 +/- 3 mm Hg) (P < 0.01). CONCLUSION The present study suggests that mass effect is not infrequent in clinically unruptured AVMs. Furthermore, multiple causative factors were detected, including the large size of AVMs, marked draining vein dilatation, and brain edema around the AVMs. Findings also indicated that a pathophysiologically high pressure in the venous drainage system may contribute to mass effect.

Outcomes analysis of ruptured distal anterior cerebral artery aneurysms treated by endosaccular embolization and surgical clipping.

Although endovascular surgery is now widely used to treat intracranial aneurysms, no comparative studies of clipping versus endovascular surgery to address distal ACA aneurysms at the same institution are available. We compared the results of these treatment modalities to address distal ACA aneurysms at our institution. We treated 68 patients with ruptured distal ACA aneurysms (endovascular surgery, n=13; clipping surgery, n=55). We performed a retrospective comparison of the treatment outcomes. To study the efficacy of endovascular surgery we classified all our cases into three types: type A were small-necked aneurysms, type B were wide-necked aneurysms on the parent artery, and type C were aneurysms in which the A3 portion of the ACA arose from the aneurysmal dome near the neck. Intraoperative hemorrhage occurred in 7.7% of aneurysms treated by endovascular surgery and in 34.5% treated by clipping surgery. In 7.7% of the endovascularly-treated aneurysms we noted coil migration during embolization surgery; venous infarction due to cortical vein injury occurred in 7.3% of clipped aneurysms. Of the endovascularly-treated aneurysms, 7.7% manifested post-embolization hemorrhage; 23.1% manifested coil compaction. In clipping surgery, postoperative rerupture occurred in 1.8% of the aneurysms; one patient presented with postoperative acute epidural hematoma. Clip dislocation was noted in 1.8% of aneurysms. Angiography was indicative of post-treatment vasospasm in 7.7% of aneurysms treated endovascularly and in 50.9% of the clipped aneurysms. The clinical outcome showed no significant difference between endovascular surgery and clipping surgery.

Direct-puncture approach to the extraconal portion of the superior ophthalmic vein for carotid cavernous fistulae

IntroductionThe transvenous approach via the superior ophthalmic vein (SOV) is an available approach for carotid cavernous fistula (CCF), especially in the event that there is no other suitable approach route to the fistula. Surgical exposure of the peripheral roots of the SOV is commonly used; however, often, the SOV is often not accessible because of anatomical problems and/or complications. In this paper, we present and discuss our original direct-puncture approach to the extraconal portion of the SOV.MethodsAn attempt on three patients with traumatic CCF failed with the transarterial approach and the conventional venous approach via the inferior petrosal sinus; therefore, the patients were treated with the direct-puncture approach to the extraconal portion of the SOV using two-dimensional digital subtraction angiography with local anesthesia.ResultsAll cases that had tortuous and partially stenotic division of the SOV were treated successfully with this approach and without complications.ConclusionThis approach will become an alternate approach, especially when the peripheral roots of the SOV are focally narrowed and tortuous, making it impossible to insert a catheter.

Impact of Platelet Transfusion on Survival of Patients with Intracerebral Hemorrhage after Administration of Anti-Platelet Agents at a Tertiary Emergency Center

This study examined the impact of platelet transfusion (PLT) on the survival of intracerebral hemorrhage (ICH) patients who had been administered anti-platelet agents (APA). This retrospective cohort analysis investigated 432 patients (259 men, 60%) who were newly diagnosed with ICH between January 2006 and June 2011 at the tertiary emergency center of Kitasato University Hospital. Median age on arrival was 67.0 years (range, 40–95 years). ICH was subcortical in 72 patients (16.7%), supratentorial in 233 (53.9%), and infratentorial in 133 (30.8%). PLT was performed in 16 patients (3.7%). Within 90 days after admission to the center, 178 patients (41.2%) had died due to ICH. Before the onset of ICH, 66 patients had been prescribed APA because of atherosclerotic diseases. Multivariate regression analysis indicated APA administration was an independent risk factor for death within 7 days (odds ratio, 5.12; P = 0.006) and within 90 days (hazard ratio, 1.87; P = 0.006) after arrival. Regarding the effect of a PLT in ICH patients with APA, no patient with PLT died. PLT had a survival benefit on patients with ICH, according to our analysis. Further prospective analysis is necessary to confirm the effects of PLT on survival in ICH with APA.

An Oral Administration of Cilostazol Before Focal Ischemia Reduces the Infarct Volume with Delayed Cerebral Blood Flow Increase in Rats

We studied the acute brain protection provided by an antiplatelet agent, cilostazol, in rat experimental focal ischemia model. We administered 30 mg/kg of cilostazol or vehicle orally 2 hours before transient middle cerebral artery (MCA) occlusion (MCAO) by the intraluminal thread method. We measured the absolute cerebral blood flow (CBF) 2 hours after cilostazol administration, the regional CBF (rCBF) of MCA territory during MCAO, and neurologic deficits and the infarct volume at 22 hours after reperfusion. We found that cilostazol did not increase absolute CBF just before MCAO. rCBF in the MCA territory was reduced to the same degree in both groups up to 60 minutes post-MCAO. A significant increase of rCBF was observed in cilostazol-treated rats at 90 minutes and maintained until reperfusion compared with the controls (P = .031 and P = .047). The average neurologic score and the infarct volume, determined by 2,3,5-triphenyltetrazolium chloride monohydrate staining, were significantly lower in cilostazol-treated rats (P = .010). The single oral administration of cilostazol before transient ischemia in healthy adult rats induced a delayed penumbral CBF increase and resulted in a significant reduction of stroke damage.

Dissecting aneurysm of the intracranial vertebral artery associated with proximal focal degeneration of the elastica: a comparative pathological study of the vertebral artery in patients with and without aneurysms.

BACKGROUND The pathogenesis underlying intracranial dissecting aneurysms remains unclear. We performed a detailed study using vertebral artery specimens obtained at autopsy from patients with and without aneurysms to identify the primary abnormality resulting in weakness of the elastica. We compared our observations with those made in specimens manifesting the normal atherosclerotic process. METHODS Using histologic methods, we examined intracranial vertebral artery specimens from two autopsied aneurysm patients and 13 autopsied control cases to compare the state of atherosclerosis and the weakness of the elastica at this aneurysm predilection site. RESULTS Case 1: A 54-year-old woman with 2 dissecting aneurysms of the bilateral vertebral arteries (VA) who died from recurrent subarachnoid hemorrhage (SAH). Case 2: A 53-year-old woman who died from SAH. Microscopically, all 3 vertebral aneurysms were typical transmural dissecting aneurysms. They manifested areas of focal, severe degeneration of the elastic lamina and calcification at VA sites proximal to the aneurysms. These lesions could be differentiated from secondary changes attributable to the aneurysms because of their separate location only proximal to the site of aneurysmal rupture. Atherosclerotic changes were minimal in both cases. In the controls, the degenerative state of the elastic lamina of the VA reflected an atherosclerotic process. CONCLUSIONS We postulate that focal degeneration of elastic tissue not involved in the atherosclerotic process was the vasculopathy resulting in aneurysm formation in our SAH cases.