Shigeki Nagai

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.

The value of long-term clinical follow-up for cases of spontaneous carotid cavernous fistula.

Summary To clarify the value of clinical long-term follow-up with radiological examination, ranging from 12 to 63 months (average: 35 months), 18 consecutive patients suffering from spontaneous carotid cavernous fistula (CCF), were studied prospectively.Five aged patients without aggressive symptoms were treated conservatively, and the other 13 underwent transarterial embolization. The radiological follow-up was primarily by magnetic resonance angiography (MRA), performed from 2 to 6 times (average: 4.1 times) during the follow-up period.In three cases, CCFs persisted, but the other fifteen (83%) demonstrated complete cure as defined by long-term follow-up MRA. The three patients with persistent CCFs were comparatively young, less than 60 years old, had no atherosclerotic factors and demonstrated multiple venous drainage routes with cortical venous drainage on angiography. In two of them, the symptoms completely disappeared, and the other had only mild chemosis. However, surprisingly, in two, MRA revealed residual CCF with drainage into only cortical veins through the sphenoparietal sinus, this radiological finding being well known to signify danger. During the follow-up period, central retinal vein thrombosis occurred in two cases. The common point in these cases was that the superior ophthalmic vein was the only venous drainage route. This is also a point requiring care. We therefore emphasize the importance of careful long-term radiological follow-up for spontaneous CCF patients even when their symptoms improve or disappear. MRA is particularly suitable for this purpose and applicable in the out-patient clinic because of its non-invasive nature.

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.

A CANINE MODEL OF INTRACRANIAL ARTERIOVENOUS SHUNT WITH ACUTE CEREBRAL VENOUS HYPERTENSION

Increased pressure of draining veins in intracranial arteriovenous fistula is considered an important cause of clinical symptoms. To investigate hemodynamic changes in intracranial arteriovenous fistula with cerebral venous hypertension, we developed a new canine model of this condition. A lingual artery-superior sagittal sinus (SSS) shunt was constructed using a section of the femoral artery as an interposed graft; immediately after which, monitoring of SSS pressure (SSSP) and regional cerebral blood flow (rCBF) was started. The baseline SSSP was 4.1 +/- 3.7 mmHg. After shunt opening, it increased slightly but not significantly. When the SSS was occluded with a clip with the shunt closed, SSSP rose to 20.3 +/- 9.0 mmHg (p < 0.01). Finally, on shunt opening, with the SSS caudal (downstream) to it occluded, the SSSP increased to 59.5 +/- 22.9 mmHg (p < 0.01, multiple analysis of variance, contrast). The frontal lobe rCBF decreased as the cerebral perfusion pressure (CPP) (mean blood pressure minus SSSP) fell. However, cerebral vascular resistance decreased significantly and proportionately to the reduced CPP (r = 0.66, p < 0.0001). In conclusion, when an intracranial arteriovenous shunt was present, venous outflow obstruction was shown to be necessary for cerebral venous hypertension to occur. In acute venous hypertension, decreases in rCBF occurred, but the autoregulatory vasodilating response was also active.