Search

Fifty cases of verified intracranial ruptured saccular aneurysm were analyzed to investigate the relationship of the development of a delayed cerebral ischemic deficit to the presence of cerebral vasospasm visualized on angiography. Twenty-five patients developed a delayed ischemic deficit (DID), and all showed Grade 3+ or 4+ vasospasm. Nineteen patients had Grade 0, 1+, or 2+ vasospasm, and none developed a DID. It was concluded that in this study vasospasm accounted for all DID's and that in the absence of vasospasm DID did not occur. The DID occurred most often on Day 8 (7 of 25 cases).

EEG was monitored at bilateral scalp sites outside the operative field during hypotensive aneurysm surgery in 21 patients. Mean arterial blood pressure at axillary level was 50-60 mm Hg (average 55 mm) for 1.9-5.3 hours (average 3.6). Four new deficits were noted immediately post-operatively, all related to the operated site: these were attributable to intra-operative rupture with forced vascular clipping, vasospasm, or edema. In no instance was hypotension solely responsible for a new deficit. EEG showed persistent slowing in relation to surgery in only 1 patient, where aneurysmal rupture led to severe hypotension, forced clipping of 1 posterior cerebral artery, and subsequent brain stem infarction. In the 3 other patients with fresh focal postoperative deficits, no persistent intraoperative EEG changes were observed. EEG monitoring did not detect ischemia in these 3 patients because 1) hypotension was moderate and did not per se cause new deficit, and 2) EEG electrodes did not survey the area at maximal risk, namely the operative field. EEG scalp electrodes near but outside the operative site do not seem useful for monitoring cerebral function in the region of aneurysm surgery. Epidural or cortical electrodes in the operative field may prove to be more useful.

Angiography in patients with subarachnoid hemorrhage secondary to aneurysm gives precise information on the location and size of the aneurysm and the aneurysm and the presence of spasm but gives incomplete information on ventricular size, size and location of hematoma, and extent of infarction. CT demonstrates precisely brain or intraventricular hematoma and, at times, subarachnoid hemorrhage, indicates the extent of infarction; and rapidly documents the degree of hydrocephalus. Infarction secondary to spasm, hematoma, and hydrocephalus are readily differentiated. The CT examination may be repeated as often as necessary without patient discomfort or morbidity. Serial scans allow rapid assessment of change in ventricular size, development and persistence of infarction, and change in size of hematoma.

Twenty-five patients with giant (greater than 25 mm in diameter) and 9 patients with large (15 to 25 mm in diameter) aneurysms of the internal carotid artery in the ophthalmic or paraophthalmic region are reviewed. In 23 of these patients the aneurysm was clipped directly. There was 1 death in this group, and none of the survivors had disabling neurological complications outside the visual system. The other 11 patients were treated by a trapping procedure or by either common carotid ligation or internal carotid ligation in the neck. Of the 5 patients treated by internal carotid ligation preceded by an extracranial to intracranial bypass graft, 3 developed embolic complications, which in 1 patient resulted in death. One of the 4 patients treated by ligation of the common carotid artery died 1 year later from a recurrent subarachnoid hemorrhage. Of the total group, 18 patients had visual loss preoperatively as a result of aneurysmal compression; in 10 the vision was improved by operation, in 3 it was made worse, and in 2 it was unchanged. In another patient the vision continued to deteriorate slowly after common carotid occlusion, and the other 2 patients died postoperatively before vision could be assessed. The complications in the patients are described and analyzed in detail. Maneuvers found to be of value in the direct approach to these lesions are described. Of these, exposure of the internal carotid artery in the neck for temporary occlusion during clipping and thorough drilling of the anterior clinoid process and unroofing of the optic canal were particularly helpful. The literature on indirect methods of treatment by carotid occlusion with and without bypass graft is reviewed with special reference to the complications and effectiveness of each alternative. Based on this review of the literature and our experience, a treatment scheme is suggested for these aneurysms depending on their mode of presentation.

Aneurysms of the bifurcation of the middle cerebral artery (MCA) can be approached through a small incision in the anterior portion of the superior temporal gyrus. The pterion and the lateral aspect of the lesser wing of the sphenoid bone are removed. The aneurysm is approached, using microsurgical techniques, by following the main divisions of the MCA to the parent trunk and the base of the aneurysm. Once the parent vessel and the origin of the major divisions are clearly identified, it is usually preferable to dissect and mobilize the entire aneurysmal complex to elucidate the anatomy and prepare the neck for clipping. This approach offers the advantages of minimal brain retraction and minimal manipulation of the main trunk and perforators of the MCA. In addition, it allows a more complete exposure of the aneurysmal complex and facilitates dissection behind the aneurysm, which is more difficult when the aneurysm is approached from the front by opening the sylvian fissure medially to laterally. A potential disadvantage of this method is that proximal control is not obtained until the base of the aneurysm is reached, but this has not been a problem in our experience. Other disadvantages are the need for a slightly larger bone flap and the potentially increased risk of epilepsy. This approach is not suitable when the main trunk of the MCA is short and the aneurysm is in front of the insula. It is also not recommended for the rare cases in which the aneurysm points back over the insula. During a 6-year period, this approach was used in 49 of 58 cases of MCA aneurysm. The only deaths in this group occurred in patients who were in deep coma before operation. Two patients were made worse by operative complications, and 2 more worsened as a result of postoperative vasospasm. There was a significant incidence of thrombophlebitis and pulmonary embolism in this series.

In a case of subarachnoid hemorrhage, the arteries of the circle of Willis were left undisturbed and undissected at postmortem examination. A block of frontal lobe tissue with the attached vessels was serially sectioned disclosing in its entirety a saccular aneurysm that had ruptured at the base rather than the dome. The histology of the hemostatic process was clearly depicted.