Giant Intracranial Aneurysms by Naci Kocer

Author:Naci Kocer
Language: eng
Format: epub
Publisher: Springer International Publishing, Cham

© Springer International Publishing Switzerland 2016

Naci KocerGiant Intracranial Aneurysms10.1007/978-3-319-41788-2_15

15. Case 15

Naci Kocer1

(1)Department of Neuroradiology, Istanbul University Cerrahpasa Medical School, Istanbul, Turkey

GIAs Causing Compression Syndromes

Keywords: Giant aneurysms, Compression syndrome, Mass effect

Introduction: Role of Coiling, Clipping, and Flow Diversion

Giant aneurysms are associated with increased morbidity due to their high incidence of rupture and neurological deficits caused by compression of the adjacent neural structures [1]. Large and giant aneurysms of the cavernous, ophthalmic, and supraclinoid segments of ICA frequently present with compression syndrome on adjacent cranial nerves. Compression of the optic nerve results in decreased visual acuity and visual field deficits and is commonly associated with carotico-ophthalmic or hypophyseal (supraclinoid) aneurysms [2]. The treatment of giant aneurysms that present with compression syndrome is limited by high surgical morbidity and limited efficacy of endovascular techniques due to high rate of incomplete aneurysmal occlusion and recurrence [1]. Patients treated by clipping are at risk of cranial nerve injury during manipulation or temporary clipping or total arterial occlusion. Patients treated by endovascular coiling are at risk of subsequent recanalization [3]. Parent vessel occlusion is an effective strategy to decrease aneurysmal compression syndrome but is restricted to aneurysms with sufficient collateral circulation. The addition of “surgical bypass” compensates the lack of collaterals but increases the overall morbidity of therapy. Flow diversion has been shown to reduce intra-aneurysmal circulation and cause aneurysmal thrombosis. Furthermore, collapse of large and GIAs has also been observed following flow diversion [1].

Etiology of Compression Syndrome

The underlying etiology includes a direct “compressive mass” effect, the pulsatile aneurysmal “water-hammer effect,” and the “irritant” effect of the adherent aneurysm/subarachnoid hemorrhage [3, 4]. The initial injury is in the form of neuropraxis and axonolysis (potentially reversible changes). However, with long-standing injury, there is axonal degeneration (irreversible change). The consensus is that the total duration and the initial degree of paresis affects cranial nerve recovery. Studies have demonstrated that the chances of complete recovery after cranial nerve palsy diminish in patients with persistent palsy for one month and those with a complete palsy at presentation [4].

Giant Aneurysmal Therapy in Compression Syndrome

It has also been claimed that neurosurgical clipping of aneurysms is better at reducing the mass effect on the cranial nerves compared to coiling [5]. Studies have also shown improvement in cranial nerve palsy following endovascular coiling. This has been attributed to the immediate cessation of the “pulsatile water-hammer effect” on the surrounding tissue after coiling [5–7]. However, this goal can be achieved only if the neck of the aneurysm can be completely sealed. Since the majority of aneurysms presenting with compression syndrome have wide necks, this sealing is difficult to achieve by coiling alone, and it decreases the efficacy of coiling in relieving compression syndromes. This also increases the tendency of coil compaction with increased chances of subsequent worsening of compression syndrome. Aneurysmal occlusion by liquid embolic agents may provide better stability by converting a soft aneurysmal mass into a hard mass that transmits arterial pulsation to adjacent cerebral parenchyma. Flow diversion has achieved a very high

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