The efficacy of endosaccular aneurysm occlusion in alleviating neurological deficits produced by mass effect

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✓ Endovascular obliteration of intracranial aneurysms with preservation of the parent artery (endosaccular occlusion) has been advocated for patients who fail or are excluded from surgical clipping and cannot undergo Hunterian ligation therapy. To clarify the effect that endosaccular occlusion has on the presenting neurological signs, 26 patients with aneurysms and symptoms related to mass effect who underwent this therapy were followed for a mean of 60 months. Only patients with objective neurological deficits who had not suffered a hemorrhage were included in this series. Response to therapy was classified into one of three groups: “resolved,” if the patient had complete resolution of presenting signs; “improved,” if significant and sustained improvement was recorded in the neurological examinations, and “unchanged,” if no change was observed.

Thirteen patients (50%) were classified as resolved, 11 (42.3%) as improved, and two (7.7%) as unchanged. A comparison of patients classified as resolved with those who were improved revealed that the former group had less wall calcification (30% vs. 60%) and a shorter duration of symptoms. Patients with neurological sign resolution (62%) were more likely to have totally occluded aneurysms on late follow-up arteriograms than those who had improvement (28%) or were unchanged (0%). This study suggests that endosaccular embolization therapy can improve or alleviate presenting neurological signs unrelated to hemorrhage or distal embolization in the majority of cases.

Article Information

Address reprint requests to: Van V. Halbach, M.D., UCSF Medical Center, 505 Parnassus Avenue, Room L352, San Francisco, California 94143–0628.

© AANS, except where prohibited by US copyright law.

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Figures

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    Case 7. a: Proton-density spin-echo magnetic resonance (MR) image (TR 2000 msec, TE 35 msec), axial view, adjacent to the basilar tip demonstrating a signal-void area extending into the upper midbrain with adjacent intermediate signal consistent with chronic thrombus. b: T2-weighted MR image (TR 2000 msec, TE 70 msec), axial view, demonstrating increased signal within the posterior limb of the internal capsule, c: Right vertebral arteriogram, Towne's projection, demonstrating a bilobed aneurysm arising from the basilar tip and incorporating the left posterior cerebral artery. d: Arteriogram, same injection and projection status as c, obtained following embolization with two detachable silicone balloons demonstrating complete occlusion of the aneurysm. c: Contrast-enhanced computerized tomography (CT) scan obtained 2 months after balloon embolization demonstrating two high-density balloons in unchanged position within the neck of the aneurysm. A low-density thrombosed portion is noted extending laterally to the left. f: Contrast-enhanced CT scan at the same level as e obtained 6 months following balloon embolization demonstrating markedly diminished size within the thrombosed portion of the aneurysm. Sections through the internal capsule demonstrated complete resolution of the low-density process. g: Left vertebral arteriogram obtained at 1-year follow-up review demonstrating persistent occlusion of the basilar tip aneurysm.

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    Case 12. Left internal carotid angiograms, lateral projection. a: Pre-embolization angiogram revealing a giant aneurysm arising from the internal carotid artery bifurcation. There is occlusion of the middle cerebral artery, the territory of which fills via leptomeningeal collateral vessels from the anterior and posterior cerebral arteries. b: Follow-up angiogram obtained 13 months after initial balloon embolization demonstrating complete obliteration of the aneurysm.

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    Case 16. a: Noncontrast-enhanced computerized tomography scan demonstrating a giant aneurysm with heavy calcification within the wall and adjacent edema. b: T2-weighted magnetic resonance (MR) image (TR 2000 msec, TE 70 msec) showing a predominantly thrombosed aneurysm with extensive surrounding edema. The phase-encoding artifact extending horizontally corresponds to the residual lumen of the aneurysm. c: One-year follow-up MR image, same pulse sequence and location as b, demonstrating complete resolution of the frontal lobe edema.

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    Case 16. Left: Left internal carotid arteriogram, lateral anteroposterior projection, demonstrating an aneurysm arising from the anterior communicating artery and marked elevation in mass effect on the proximal anterior cerebral artery. Right: Arteriogram, same injection and projection, obtained after balloon embolization demonstrating complete obliteration of the aneurysm.

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