Collaborative retrospective multicentre series of giant intracavernous carotid aneurysms

2015 
Abstract Giant intracavernous carotid aneurysms (GICCA) occur with very unusual clinical symptoms often resulting from a compressive mechanism that may possibly resolve although seldom from a rupture or haemorrhage. In fact, due to their clinical presentation their treatment is different from that of the intracranial subarachnoid aneurysms. The aim of this study was to analyze the clinical symptoms, therapeutic decisions, and the clinical state at 6 months follow up in a retrospective consecutive multicentre series of 27 GICCA between 2004 and 2008. All the patients in the series were female, mean age 65 years (21 to 82 years). A pseudo tumoural cavernous sinus syndrome revealed the disease in 25 patients (92.6%), an atypical headache in one patient, and in another patient an intraoperative haemorrhage led to the diagnosis. In most of the cases the aneurysms were sacciform in shape (89%), with a size between 25 and 30 millimeters (66.6%) and contained a blood clot due to intrasacular thrombosis (57.5%). An occlusion test of the internal carotid artery was performed during the diagnostic angiography in 24 cases (88.8%) and good tolerance of occlusion was observed in 16 of them. An endovascular procedure was performed in 21 patients (77.7%): selective coiling of the aneurysm facilitated by stenting or by remodeling techniques in 2 cases, whereas internal carotid artery occlusion was performed on the 19 other cases. Among these latter patients, 2 of them (10.5%) presented with a poor tolerance during the pre-therapeutic carotid occlusion test, necessitating a surgical intra-extra cranial by-pass prior to the carotid endovascular occlusion. In 1 other case of these 19, the internal carotid endovascular occlusion was carried-out in emergency because the aneurysm was revealed by a major haemorrhage during the surgical transsphenoidal approach of a hypophyseal tumour. No treatment was decided in the remaining 6 cases of the series (22.2%). At 6 months follow-up, 18 of the 21 treated patients experienced a clinical recovery of their symptoms and 10 of them (50%) had a complete clinical recovery. Among the 6 untreated patients, 4 had a partial recovery but no complete recovery of oculomotor deficits was observed in this group of patients. No clinical worsening was observed in the entire series, neither among the treated patients nor among the untreated patients. In conclusion, this study underlines the need of a treatment for symptomatic GICCA in order to achieve a complete clinical recovery of the symptoms due to intracavernous compression, although only partial recovery may be expected from spontaneous evolution.
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