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A 40-year-old female presented with sudden onset of severe headache and vomiting due to subarachnoid hemorrhage. Angiography demonstrated a saccular aneurysm on a dolichoectatic left middle cerebral artery (MCA) and delayed filling of the MCA. Magnetic resonance imaging showed a partially thrombosed giant aneurysm on the dolichoectatic MCA. An intentionally delayed operation was performed, during which the neck of the aneurysm was successfully clipped. The patient exhibited aphasia 48 hours after surgery. Single-photon emission computed tomography revealed hyperperfusion in the territory of the left MCA. The patient's blood pressure was maintained normotensively, and her symptoms gradually improved. She returned to work 1 month after surgery. The saccular aneurysm was formed on the dolichoectatic MCA, presumably due to an abnormal arterial wall and hemodynamic stress. The preoperative hypoperfusion might have been caused not only by the giant aneurysm, but also to some degree by the dolichoectatic MCA. After neck clipping, the increase in blood flow might have caused hyperperfusion., (Copyright © 2011 National Stroke Association. Published by Elsevier Inc. All rights reserved.)

Background: Although elevation of blood pressure in aneurysms induced by injection of contrast medium has been postulated as a major cause of rerupture of ruptured cerebral aneurysms during angiography, no study has proved the elevation of intra-aneurysmal pressure because of difficulty in measuring the intra-aneurysmal pressure during angiography. The present study demonstrated intra-aneurysmal pressure to be raised by injection of contrast medium, using a microcatheter introduced into aneurysms., Methods: To confirm the accuracy of pressure measurement through a microcatheter, we measured intra-aneurysmal pressure in a plastic model of an artery and an aneurysm during and after injection of contrast medium through a microcatheter and a needle inserted into the aneurysm. In a clinical study, intra-aneurysmal pressures were measured through the microcatheter in nine cerebral aneurysms of seven patients., Results: In the model experiment, changes in the pressure measured through the microcatheter correlated well with those observed through the needle. In the clinical study, intra-aneurysmal systolic pressures increased by 5-23 mm Hg immediately after injection of contrast medium for 1-3 s in four basilar tip, three internal carotid-ophthalmic, and one middle cerebral artery aneurysm, whereas no pressure change was observed in a posterior cerebral artery aneurysm. Systemic blood pressure during angiography remained unchanged in all cases., Conclusions: This abruptly elevated intra-aneurysmal pressure by injection of contrast medium might cause rerupture of an aneurysm soon after rupture of the aneurysm, especially when the rupture site is fragile.

This study was undertaken to elucidate comprehensively the serial changes occurring in hemostatic systems after aneurysmal subarachnoid hemorrhage (SAH) and thereby to ascertain whether the examination of the integrity of these systems is helpful in predicting delayed ischemic neurological deficits (DINDs). The authors examined 117 patients admitted to the hospital within 24 hours after onset of SAH. Blood samples were collected from each patient on Days 0 (at admission), 3, 6, 14, and 30. A number of hemostatic parameters were examined in these samples, and the relationships between their changes and DINDs were assessed. Eighteen (15.4%) of the patients exhibited DINDs, and their frequency increased as the severity of subarachnoid clotting increased. Also, the frequency of DINDs was significantly higher in the patients with hydrocephalus on initial computerized tomography (CT) scans than in those without hydrocephalus. Regarding the hemostatic parameters at admission, there was no significant difference between the patients with and without DINDs. On Day 3, however, the fibrinogen and D-dimer levels were higher in the patients with than in those without DINDs. The fibrinogen and thrombin-antithrombin complex levels on Day 6 and the D-dimer level on Day 14 in the patients with DINDs were higher than the corresponding levels in those without DINDs. Multivariate analyses revealed that the following variables (in order of importance) were independent predictors of DINDs: the levels of D-dimer on Day 3, fibrinogen on Day 6, and the presence of hydrocephalus on admission. These data indicate that the levels of hemostatic parameters in concert with the CT findings may enable us to predict the appearance of DINDs.

To comprehensively examine changes in the hemostatic systems early after spontaneous subarachnoid hemorrhage (SAH) and to assess the relationships between those changes and neurological findings, computed tomographic findings, and clinical outcomes, we reviewed 167 patients who were admitted within 24 hours of the onset of SAH. Blood was taken from all of the patients at admission for detailed examinations of the hemostatic systems. The following results were obtained: 1) the levels of the thrombin-antithrombin complex (elevation indicating the activation fo the blood coagulation system), plasmin-antiplasmin complex, and D-dimer (elevation indicating the activation of the fibrinolytic system) significantly increased with the neurological severity, amount of subarachnoid clot, and severity of clinical outcome; 2) the levels of the thrombin-antithrombin complexes and plasmin-antiplasmin complexes were significantly higher in patients with intracerebral or intraventricular hematomas than in patients without those hematomas; 3) in each of almost all the neurological and computed tomographic grades, the levels of the thrombin-antithrombin complexes were significantly higher in the patients with poor outcomes than in those with good outcomes; 4) the poor outcome rate significantly increased with neurological severity and the amount of subarachnoid clot. These data suggest that the activation of the blood coagulation system as well as of the fibrinolytic system occurred early in the course of SAH and that these systems were activated to a greater extent with the severity of neurological grades, computed tomographic findings, and clinical outcome.(ABSTRACT TRUNCATED AT 250 WORDS)

We report the long term results of the treatment of 23 intracranial ruptured aneurysms by coating. Twenty-three patients treated by coating were followed for a mean period of 11.2 years. The mean interval between the last hemorrhage and the operation was 22.4 days. Ten aneurysms underwent total coating, 9 with Biobond and 1 with Aron Alpha. Thirteen aneurysms underwent partial coating, 11 with Biobond and 2 with Aron Alpha. Six aneurysms were reinforced partially by other materials, but no aneurysm was wrapped totally with these materials. Rebleeding occurred in 6 patients, of whom 5 died. The mean interval between coating and rebleeding was 4 years. All patients suffering rebleeding had been treated with Biobond, and 3 patients had undergone total coating of aneurysms. The risk of recurrent hemorrhage after total coating with Biobond was 33%. One rebleeding patient underwent a second operation 10.5 years after total coating of the aneurysm. Biobond was found only at the tip of the aneurysmal sac. From these results, reinforcement of ruptured aneurysms with Biobond seems to be of little value, and a more reliable method must be developed for aneurysms that cannot be clipped.

Four cases of aneurysms associated with a fenestrated anterior cerebral artery are presented. The combination of aneurysms and fenestration of the anterior cerebral artery is rare, and nine cases including ours have been reported. In all cases fenestrations were found within the distal two-thirds of the horizontal portion of the anterior cerebral artery. It may be presumed that fenestration of the anterior cerebral artery is the remnant of the plexiform anastomosis in the fetal stage, especially between the anterior cerebral artery and the primitive olfactory artery.