Deliberate occlusion of the basilar or vertebral arteries was performed in 201 patients with intracranial aneurysms, where the aneurysmal neck could not be clipped directly. The aneurysms arose from the basilar apex in 83 cases, the basilar trunk in 46, the vertebrobasilar junction in 35, and the vertebral artery in 37; 87% of the aneurysms were classified as giant lesions (> 2.5 cm). There were 85 upper basilar occlusions, 41 lower basilar occlusions, 29 bilateral vertebral occlusions, and 48 unilateral vertebral artery occlusions. The clinical follow-up period varied from 1 to 23 years, with a mean of 9.5 years. Overall long-term results were excellent in 68% of the patients, good in 5%, and poor in 3%; 24% died. Clinical outcome varied according to aneurysm site; excellent or good results were achieved in 64% of the patients with basilar apex, 76% with basilar trunk, 74% with vertebrobasilar junction, and 87% with vertebral artery aneurysms. Clinical outcome also varied depending on preoperative grade: 86% of the patients with an excellent presenting grade achieved excellent results. The size of the posterior communicating arteries was a good predictor of tolerance to basilar artery occlusion (p < 0.05). Successful aneurysm thrombosis was achieved in 78% of the patients. The neurological status in 26 patients (13%) deteriorated due to vertebrobasilar ischemia occurring within the 1st postoperative week, and thrombosis or embolism was implicated much more frequently than hemodynamic insufficiency. Subarachnoid hemorrhage (SAH) in 14 patients, vasospasm in five patients, and surgical trauma in seven patients accounted for additional morbidity in the 1st month following operation; however, many of these patients ultimately made an excellent recovery. Late vertebrobasilar ischemic complications or neurological deterioration from persistent mass effect occurred in 4% of patients with successful aneurysm thrombosis 6 weeks to 18 months after arterial ligation. Among the 43 patients with incompletely thrombosed aneurysms, 67% developed early or late neurological deterioration from SAH, progressive brain-stem compression, or brain-stem stroke, with 86% of the complications proving fatal.

The paucity of information about giant fusiform intracranial aneurysms prompted this review of 120 surgically treated patients. Twenty-five aneurysms were located in the anterior and 95 in the posterior circulation. Six patients suffered from atherosclerosis and only three others had a known arteriopathy. The remaining 111 patients presented with aneurysms resulting from an unknown arterial disorder; these patients were much younger than those harboring atherosclerotic aneurysms. Mass effect occurred in only 50% of cases and hemorrhage in 20%. Eight aneurysms caused transient ischemic attacks. Hunterian proximal occlusion or trapping were dominant among the treatment methods. In contrast to the management of giant saccular aneurysms, the usual thrombotic occlusion of a giant fusiform aneurysm after proximal parent artery occlusion requires the presence of two collateral circulations to prevent infarction, one for the end vessels and another for the perforating vessels that arise from the aneurysm. Although there was some reliance on the circle of Willis and on collateral vessels manufactured at surgery, the extent of natural leptomeningeal and perforating collateral, thalamic, lenticulostriate, and brainstem vessels was astonishing and formerly unknown to the authors. Good outcome occurred in 76% of patients with aneurysms in the anterior circulation; two of the six cases with poor results included patients who were already hemiplegic. Ninety percent of patients with posterior cerebral aneurysms fared well. Only 67% of patients with basilar or vertebral aneurysms had good outcomes, although more (17%) of these patients were in poor condition preoperatively because of brainstem compression.

In 58 patients with progressive neurological deterioration from angiographically confirmed cerebral vasospasm after spontaneous subarachnoid hemorrhage, arterial hypertension was induced in an attempt to improve their deficits. The most effective regimen consisted of intravascular volume expansion, blockade of the vagal depressor response, and the administration of antidiuretics and vasopressor agents. With this protocol, arterial blood pressure could be sustained at high levels for prolonged periods. Neurological deterioration was reversed in 47 patients, transiently in 4; permanent improvement occurred in 43. Complications experienced during therapy included pulmonary edema, dilutional hyponatremia, aneurysmal rebleeding, coagulopathy, hemothorax, and myocardial infarction. Elevating systemic arterial pressure in states of cerebrovascular insufficiency resulting from vasospasm is safe if meticulous attention is paid to physiological, biochemical, and hematological parameters, with the exception that it may be hazardous in the presence of an untreated ruptured or intact aneurysm. Intravascular volume expansion and induced hypertension are effective in reversing ischemic deficits from vasospasm provided that treatment commences before cerebral infarction and that adequate pressures are maintained for a sufficient period. The production of a hypervolemic state by the use of colloid and crystalloid infusion accompanied by atropine blockade of the vagal depressor response and blunting of the diuresis with vasopressin enables arterial pressure to be elevated for longer than 1 week.

Sixty-five carotid-cavernous fistulas were studied at University Hospital, London, Canada, from 1978 to 1982, 20 of which fulfilled the clinical and angiographic criteria of a spontaneous carotid-cavernous fistula. Of these 20 fistulas, 17 were unilateral, and three were bilateral. In 18 cases the angiographic findings were typical of an arteriovenous malformation (AVM), and in two a ruptured giant intracavernous aneurysm was found. These patients were treated according to whether they had a nonresolving or progressive cavernous sinus syndrome or deterioration of vision. The cavernous dural AVM's were treated with polyvinyl-alcohol and/or isobutyl-2-cyanoacrylate (IBCA) embolization of the external carotid artery blood supply. Two patients underwent postembolization surgical procedures. The detachable balloon technique was used to occlude the fistulas associated with the two giant ruptured intracavernous aneurysms and a small dural intracavernous AVM. Eight patients received no therapy; in two, spontaneous obliteration of the fistula occurred. Of the nine cavernous AVM's embolized with particles and/or IBCA, successful transvascular embolization was achieved in seven cases, and partial embolization followed by surgery in two cases. Successful balloon obliteration of the giant intracavernous ruptured aneurysm was obtained in two cases. In one patient, right hemiplegia with aphasia resulted from reflux of IBCA emboli through the artery of the foramen rotundum into the left middle cerebral artery.

Hunterian proximal artery occlusion was used in the treatment of 160 of 335 patients harboring giant aneurysms of the anterior circulation. One hundred and thirty-three of these aneurysms arose from the internal carotid arteries, 20 from the middle cerebral arteries, and seven from the anterior cerebral arteries. Ninety percent of the patients had satisfactory outcomes. The safety of internal carotid artery occlusion has been greatly enhanced by preoperative flow studies and by test occlusion with an intracarotid balloon to identify those patients who require preliminary extracranial-to-intracranial bypass, which was used in all of the middle cerebral occlusions. The anterior cerebral artery had magnificent leptomeningeal collateral flow that prevented infarction even without cross flow. Obliteration of the aneurysm by thrombosis was complete, or nearly so, in all but four patients whose treatment was completed. Analysis of poor outcome in 16 patients revealed that hemodynamic ischemic infarction was known to occur after only two of the carotid occlusions.