Katsumi Irikura

The efficacy of bypass surgery for the patients with hemorrhagic Moyamoya disease

The efficacy of bypass surgery for the patients with hemorrhagic Moyamoya disease were studied by multi-center retrospective questionnaire study. The rebleeding rate was 28.3% (39/138 patients) in conservative treatment group and 19.1% (29/152 patients) in bypass surgery group with no significant statistical difference. It is still difficult to clarify the efficacy of bypass surgery for prevention of hemorrhagic attack.

A source of haemorrhage in adult patients with moyamoya disease: The significance of tributaries from the choroidal artery

SummaryThis study concerns 19 patients over 16 years of age with Moyamoya disease. Ten cases of intracranial haemorrhage, as the initial haemorrhagic event in patients aged from 21 to 55 (haemorrhagic group) and 9 cases of ischaemic events in 18- to 53-year-old patients (ischaemic group) were included. All haemorrhages were associated with intraventricular haemorrhages (IVH); and all but one case of thalamic haemorrhage were thought to be primary IVH (2 cases of small paraventricular haemorrhage; 2 of small haemorrhages in the splenium; 5 with no intracerebral haematoma). In the 9 patients of the ischaemic group, there were 2 cases of transient ischaemic attacks and 7 of cerebral infarction. Angiographic evaluations demonstrated that the abnormal basal vessel formation and the collateral supplies from the external carotid arteries were poorly developed in both groups. In contrast, the collateral circulation via the choroidal and posterior pericallosal arteries was well demonstrated. Furthermore, marked enlargement of the choroidal arteries and the medullary arteries derived from them was seen more frequently in the haemorrhagic group. These findings suggested that the haemodynamic load in the vessels supplying the walls of the posterior parts of the ventricles and the periventricular region was increased, especially in the haemorrhagic group. Those vessels were considered to be important sites of IVH in adult patients with Moyamoya disase.

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]

Correlation between intravascular pressure and risk of hemorrhage due to arteriovenous malformations

The correlation between intraoperative pressure levels measured in the feeding arteries and in the draining veins, and the risk of hemorrhage from arteriovenous malformations (AVMs) is discussed. Feeding artery pressure (FAP) was significantly higher in AVMs with hemorrhage (57 +/- 11 mmHg) than in AVMs without hemorrhage (38 +/- 4), and draining vein pressure (DVP) in the former (24 +/- 5) was significantly higher than that in the latter (13 +/- 5). FAP and DVP were inversely related to the number of draining veins and size of the AVMs. The present study suggests that a high FAP and a high DVP may contribute to the development of hemorrhage from AVMs, and supports previous reports that small AVMs and AVMs with only one draining vein are susceptible to hemorrhage.

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.

The Influence of Vascular Pressure and Angiographic Characteristics on Haemorrhage from Arteriovenous Malformations

Summary¶ Background. The present study was designed to determine whether there is a physiological explanation for the predisposition of patients with certain angiographic characteristics to haemorrhage from cerebral arteriovenous malformations (AVMs). Methods. Intra-operative measurement of feeding artery pressure (FAP) and intravascular pressures in the draining venous system [draining vein pressure (DVP) and cranial sinus pressure (SP)] were performed for 30 AVM cases using direct puncture of the vessels. The correlation between pressures and previously described angiographic characteristics predisposing to haemorrhage were evaluated. Findings. Small nidus size and only one draining vein increased the risk of haemorrhage. FAP and DVP are both inversely related to the number of draining veins and the size of the AVMs. DVP was significantly higher in AVMs with haemorrhage (23.1±8.7 mmHg) than in those without (13.5±4.4), as was FAP (58.6±12.8 as opposed to 38.7±4.7) (p<0.05). Moreover, the difference between systemic blood pressure and the FAP with haemorrhagic AVMs (17.0±9.5 mmHg) was significantly lower than that in nonhaemorrhagic cases (33.7±5.5) (p<0.05). The pressure difference between the feeding artery and draining vein was not significant between the haemorrhagic and nonhaemorrhagic groups. There was no significant difference of SP between haemorrhagic and nonhaemorrhagic patients. Interpretation. The present study suggests that a high DVP probably induced by high resistance in the venous drainage system, as well as a high FAP, may contribute to the development of haemorrhage from AVMs, and physiologically supports previous reports that small AVMs and AVMs with only one draining vein are susceptible to haemorrhage.

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.

Moderate Hypothermia Reduces Hypotensive, But Not Hypercapnic Vasodilation of Pial Arterioles in Rats

Two types of acid—base strategies are available for the blood gas management of patients during hypothermia: alpha-stat and pH-stat management However, the more suitable strategy for therapeutic hypothermia is unclear. We studied the effects of hypothermia (30°C) and acid—base management on reactivity to hypercapnia and hypotension in rat pial arterioles, using a closed cranial window, The baseline diameter during hypothermia decreased in the alpha-stat (Paco2 was maintained at 35 mm Hg when measured at 37°C, n = 8), but not in the pH-stat (Paco2 was maintained at 35 mm Hg when corrected to the animals actual temperature, n = 7), Vasodilation induced by hypotension was significantly reduced in hypothermic groups compared with the normothermic group (n = 7), whereas responses to hypercapnia were preserved, Moreover, hypotensive vasodilation was more attenuated in the pH-stat, than the alpha-stat, management These findings show that moderate hypothermia and acid-base management alter cerebrovascular autoregulation.

Spontaneous carotid cavernous fistulas with special reference to the influence of estradiol decrease

The etiology of the dural arteriovenous fistula (AVF) involving the cavernous sinus is still unknown. However, it is of interest that this condition usually occurs in post-menopausal women. The purpose of the present study was therefore to clarify the relationship between sex hormone blood levels and the occurrence of dural AVFs in the cavernous sinus. Serum sex hormone levels and factors associated with atherosclerosis were examined in 26 consecutive patients with dural AVF involving the cavernous sinus presenting at our institute during the last eight years and compared with those of a post-menopause control group. Of the present patient series, 21 (81%) were women. All except five had passed menopause. Five (24%) of the women patients presented with symptoms consistent with cessation of menstruation, namely, a blood level of estradiol significantly lower than the control value. Hypertension was recognized in 10 (71%) of 14 females who had experienced menopause 10 or more years previously and in all male patients. A sudden abnormal decrease of blood estradiol levels in female patients demonstrating symptoms consistent with menopause may thus be an important precipitating factor in the occurrence of dural AVFs involving the cavernous sinus. Hypertension, in older female and male patients, with or without longstanding low blood estradiol levels, may cause atherosclerosis of the feeding vessels in the dura mater, resulting in the opening of a normal AV shunt to provide collateral circulation.

The significance of hypothermic acid-base management induced before ischemia in a rat model of transient middle cerebral artery occlusion.

We investigated the effects of acid-base management during pre- and intra-ischemic hypothermia on regional cerebral blood flow (rCBF) and infarct volume using a transient focal cerebral ischemia model. Normal temperature was maintained in a group of 7 anesthetized rats, and hypothermia (30 degrees C) was maintained in two other groups of 7 anesthetized rats, in which alpha-stat (PaCO2 measured at 37 degrees C was maintained at 36 mmHg) and pH-stat (PaCO2 corrected for body temperature was maintained at 36 mmHg) conditions, respectively, were established. rCBF was monitored by laser-Doppler flowmetry in the ischemic penumbra. The middle cerebral artery (MCA) was occluded for 2 h and then reperfused. Infarct volume was measured after 24 h and expressed as a percentage of hemisphere volume. Pre-ischemic hypothermia reduced rCBF in the alpha-stat group and the pH-stat group to 52 +/- 2% and 86 +/- 7%, respectively (p < 0.01). After MCA occlusion, rCBF dropped in the control group, alpha-stat group, and pH-stat group to 57 +/- 11%, 31 +/- 9%, 27 +/- 10%, respectively. Infarct volume in the alpha-stat group, and pH-stat group was significantly smaller (10 +/- 1% and 7 +/- 2%) than in the control group (42 +/- 7%, p < 0.01), but no differences were found between the hypothermic groups. Differences in acid-base management in the present study did not affect infarct volume, but pre-ischemic rCBF in the alpha-stat group was significantly lower than in the pH-stat group. The steeper fall in rCBF after MCA occlusion in the pH-stat group suggested that the autoregulatory response of the collateral pathways may have been reduced in this group.