The clinical and postembolization outcomes in patients treated with the GDC system have improved in the past 5 years. Aneurysm recanalization, however, is still a major limitation of current GDC therapy. Follow-up angiography is mandatory after GDC embolization of cerebral aneurysms. Further technical and device improvements are mandatory to overcome current GDC limitations.

Diffusion magnetic resonance imaging provides an early marker of acute cerebral ischemic injury. Thrombolytic reversal of diffusion abnormalities has not previously been demonstrated in humans. Serial diffusion and perfusion imaging studies were acquired in patients experiencing acute hemispheric cerebral ischemia treated with intra-arterial thrombolytic therapy within 6 hours of symptom onset. Seven patients met inclusion criteria of prethrombolysis and postthrombolysis magnetic resonance studies, presence of large artery anterior circulation occlusion at angiography, and achievement of vessel recanalization. Mean diffusion-weighted imaging lesion volume at baseline was 23 cm3 (95% confidence interval [95% CI], 8-38 cm3) and decreased to 10 cm3 (95% CI, 3-17 cm3) 2.5 to 9.5 hours after thrombolysis. Mean apparent diffusion coefficient lesion volume decreased from 9 cm3 (95% CI, 2-16 cm3) at baseline to 1 cm3 (95% CI, 0.4-2 cm3) early after thrombolysis. A secondary increase in diffusion volumes was seen in 3 of 6 patients at day 7. In all 4 patients in whom perfusion imaging was obtained before and after treatment, complete resolution of the perfusion deficit was shown. Diffusion magnetic resonance signatures of early tissue ischemic injury can be reversed in humans by prompt thrombolytic vessel recanalization. The ischemic penumbra includes not only the region of diffusion/perfusion mismatch, but also portions of the region of initial diffusion abnormality.

Eleven experimental saccular aneurysms were created on the common carotid artery of swine. Between 3 and 15 days after creation of these aneurysms, they were thrombosed via an endovascular approach, using a very soft detachable platinum coil delivered through a microcatheter positioned within the aneurysm. This detachable platinum coil was soldered to a stainless steel delivery guidewire. Intra-aneurysmal thrombosis was then initiated by applying a low positive direct electric current to the delivery guidewire. Thrombosis occurred because of the attraction of negatively charged white blood cells, red blood cells, platelets, and fibrinogen to the positively charged platinum coil positioned within the aneurysm. The passage of electric current detached the platinum coil within the clotted aneurysm in 4 to 12 minutes. This detachment was elicited by electrolysis of the stainless steel wire nearest to the thrombus-covered platinum coil. Control angiograms obtained 2 to 6 months postembolization confirmed permanent aneurysm occlusion as well as patency of the parent artery in all cases. No angiographic manifestation of untoward distal embolization was noted. Due to the encouraging results of this research, this technique has been applied in selected clinical cases which are described in Part 2 of this study.

In a multicenter study, 120 patients with intracranial aneurysms presenting a high surgical risk were treated using electrolytically detachable coils and electrothrombosis via an endovascular approach. The results of treatment in patients with posterior fossa aneurysms (42 patients with 43 aneurysms) are presented. The most frequent clinical presentation was subarachnoid hemorrhage (24 cases). The clinical follow-up periods ranged from 1 week to 18 months. Complete aneurysm occlusion was obtained in 13 of 16 aneurysms with a small neck and in four of 26 wide-necked aneurysms. A 70% to 98% thrombosis of the aneurysm was achieved in 22 of 26 aneurysms with a wide neck and in three of 16 small-necked aneurysms. One aneurysm could not be treated due to a technical complication. Two cases required postprocedural surgical clipping of a residual aneurysm. One patient (originally in Hunt and Hess Grade V) experienced procedural rupture of the aneurysm requiring an emergency parent artery occlusion. He eventually died 5 days later. Another patient (originally in Grade IV) had coil migration and posterior cerebral artery territory ischemia. A third patient developed a permanent neurological deficit (hemianopsia) after complete occlusion of a wide-necked basilar bifurcation aneurysm. One patient, harboring an inoperable giant basilar bifurcation aneurysm, died from aneurysm bleeding 18 months after partial occlusion. Overall morbidity and mortality rates related to treatment were 4.8% (two cases) and 2.4% (one case), respectively (2.6% and 0% if considering only patients in Hunt and Hess Grades I, II, and III). It is suggested that this technique is a viable alternative in the management of patients with posterior fossa aneurysms associated with high surgical risk. Longer angiographic and clinical follow-up study is necessary to determine the long-term efficacy of this recently developed endovascular occlusion technique. Close postoperative angiographic and clinical monitoring of patients with wide-necked subtotally occluded aneurysms is mandatory to check for potential aneurysmal recanalization, regrowth, and rupture.