PEER-REVIEW REPORTS Visual Complications After Stent-Assisted Endovascular Embolization of Paraophthalmic and Suprasellar Variant Superior Hypophyseal Aneurysms: The Duke Cerebrovascular Center Experience in 57 Patients Andrew S. Ferrell1, Mark L. Lessne1, Michael J. Alexander 2, Pratish Shah 3, Kiarash Golshani 3, Ali Zomorodi 3, Tony P. Smith1, Gavin W. Britz 3 Key words 䡲 Clipping 䡲 Embolization 䡲 Endovascular 䡲 Intracranial aneurysm 䡲 Ophthalmic artery 䡲 Outcomes 䡲 Visual complications Abbreviations and Acronyms ICA: Internal carotid artery SAH: Subarachnoid hemorrhage From the 1Department of Radiology, Duke University Medical Center, Durham, North Carolina; 2Department of Neurosurgery, Cedars-Sinai Medical Center, Los Angeles, California; and 3Department of Surgery, Division of Neurosurgery, Duke University Medical Center, Durham, North Carolina, USA To whom correspondence should be addressed: Gavin W. Britz, M.D. [E-mail: gavin.britz@duke.edu] Citation: World Neurosurg. (2012) 78, 3/4:289-294. DOI: 10.1016/j.wneu.2011.12.003 Journal homepage: www.WORLDNEUROSURGERY.org Available online: www.sciencedirect.com 1878-8750/$ - see front matter © 2012 Elsevier Inc. All rights reserved. 䡲 OBJECTIVE: To review retrospectively experience with stent-assisted coiling of ophthalmic segment internal carotid artery (ICA) aneurysms to report outcome data and identify the rate of associated visual complications. 䡲 METHODS: The Duke endovascular database was retrospectively reviewed to identify all ICA aneurysms treated with stent-assisted embolization between November 2002 and October 2009. Only aneurysms arising from the ophthalmic segment of the ICA and originating from the paraophthalmic or suprasellar variant superior hypophyseal artery were included. These aneurysms have the potential to create visual disturbances related to mass effect on the optic nerve or chiasm or to disrupt the ophthalmic artery. Chart review was performed to obtain clinical information, immediate incidence, and follow-up of aneurysm remnants and any visual complications. 䡲 RESULTS: There were 63 aneurysms (48 paraophthalmic and 15 suprasellar variant superior hypophyseal) identified in 57 patients. The ophthalmic artery was preserved in all but two (3.5%) cases, neither of which resulted in visual deficits. One (1.8%) patient experienced transient acute visual disturbances, and two (3.5%) patients had delayed, persistent deficits. 䡲 CONCLUSIONS: Stent-assisted embolization of ophthalmic segment ICA aneurysms is technically achievable and in our series did not appear to result in increased visual complications compared with coil embolization alone or surgical treatment. INTRODUCTION Aneurysms of the ophthalmic segment of the internal carotid artery (ICA) are diverse in their anatomic site of origin and spatial orientation with 20% of lesions having no named branch directly associated with the aneurysm neck (5, 23). This diversity has led to numerous terms and classification systems for surgical and angiographic purposes, creating significant confusion (5). The two dominant types of aneurysms that arise from this segment are named for their associated vessel: the ophthalmic or superior hypophyseal artery (23). The ophthalmic artery arises from the anterior or anteromedial aspect of the ICA immediately after it traverses the distal dural ring and enters the subarachnoid space (1, 3, 5, 8, 11, 14, 26). The optic nerve is intimately associated with the ophthalmic artery, coursing just superior and medial to the ophthalmic origin as it proceeds toward the optic canal. Paraophthalmic aneurysms typically arise at the distal aspect of the ophthalmic origin and point superior or superomedially, and with progressive enlargement, their anatomic proximity to the optic apparatus may lead to visual disturbances (5). Visual field loss may be seen from compressive or ischemic optic neuropathy, or diplopia may be evident from oculomotor nerve compression (21). Superior hypophyseal aneurysms arise along one of several perforating branches from the medial or inferomedial wall of the ICA. They may extend ventrally and burrow beneath the clinoid process (paraclinoid variant) or project medially beneath and elevate the optic chiasm (suprasellar variant) (5). The suprasellar variant may produce an ipsilateral or bitemporal visual field deficit similar to a pituitary tumor; however, the paraclinoid variant is unlikely to result in visual abnormalities even when the aneu- WORLD NEUROSURGERY 78 [3/4]: 289-294, SEPTEMBER/OCTOBER 2012 rysms become quite large. In a surgical series of 39 superior hypophyseal aneurysms reported by Day (5) in 1990, no paraclinoid variant superior hypophyseal aneurysm caused visual disturbances. The intimate relationship between the optic nerve and ophthalmic artery makes surgical exposure and clipping of paraophthalmic aneurysms challenging. Complete exposure often requires removal of the clinoid process and dissection of the dural ring to identify the aneurysm neck completely (5). During surgery, visual loss can be caused by direct vascular injury, manipulation of the optic nerve, thermogenic effects from high-speed drilling of the clinoid, or other unknown causes (9, 10, 12, 15, 18). Endovascular techniques for intracranial aneurysms, with their own unique but equally threatening list of possible compli- www.WORLDNEUROSURGERY.org 289 PEER-REVIEW REPORTS ANDREW S. FERRELL ET AL. cations, have been increasingly employed over the past 2 decades. With specific regard to paraclinoid aneurysms, coil embolization does not prevent possible visual complications. Acute and delayed visual deficits after endovascular treatment of paraophthalmic aneurysms have previously been described (21, 22, 25). In the acute setting, the deficit is typically related to mass effect on the optic apparatus or loss of the ophthalmic artery; delayed deficits are attributed to either progressive mass effect or perianeurysmal inflammation (25). Delayed effects have been reported 35 days after embolization (25). The use of stent assistance has increased further the number of aneurysms that can be treated endovascularly, and this is true for paraophthalmic aneurysms. Given the wide neck configuration of these aneurysms as the typical indication for stent placement, it is reasonable to assume that the neck of these aneurysms more often incorporates the origin of the ophthalmic artery, which could be impacted and occluded by the coil mass. In addition, the stent itself may cover the ophthalmic artery origin resulting in retinal ischemia or thromboembolic complications. It has been reported that stent-assisted coiling results in improved coil packing (2, 20). Hypothetically, this improved packing may result in increased mass affect on the optic apparatus in paraophthalmic aneurysms or the chiasm in suprasellar variant superior hypophyseal aneurysms. We investigated the outcome and visual complication rate of stentassisted coil embolization of paraophthalmic or suprasellar variant superior hypophyseal aneurysms. METHODS After obtaining institutional review board approval, a retrospective review of the Duke Cerebrovascular Center database was performed to identify all patients for whom the Neuroform Microdelivery Stent System (Boston Scientific Corp., Natick, Massachusetts, USA) was successfully deployed for stent-assisted embolization of aneurysms of the ICA from November 2002 until October 2009. Angiograms obtained before and after embolization were reviewed by two of the authors (A.S.F. and T.P.S.) to identify all aneurysms originating from paraophthalmic and suprasellar variant su- 290 www.SCIENCEDIRECT.com VISUAL COMPLICATIONS AFTER STENT-ASSISTED COILING perior hypophyseal arteries. For the purposes of our study, paraophthalmic aneurysms were defined as aneurysms arising from the anterior wall of the ICA above the roof of the cavernous sinus (intradural) and below the origin of the posterior communicating artery, at or just distal to the ophthalmic origin and with a superior or superomedial projection. Suprasellar variant superior hypophyseal aneurysms were defined as aneurysms arising from the inferior or inferomedial wall of the proximal intradural ICA, not in immediate association with the ophthalmic origin and projected medially toward the suprasellar cistern. We specifically excluded all aneurysms of the cavernous sinus, carotid cave, paraclinoid variant superior hypophyseal artery, posterior and lateral wall ophthalmic segment ICA, and supraclinoid ICA (anterior choroidal, posterior communicating, carotid terminus). An extensive retrospective chart review was performed to identify patient demographics and clinical history. Patients were categorized into patients with or without subarachnoid hemorrhage (SAH) at presentation. Among the patients without SAH, an attempt was made to define and categorize presenting symptoms as headache, transient ischemic attack, or other incidental and unrelated neurologic symptoms. Aneurysm size was classified as small (⬍ 5 mm), medium (5–10 mm), large (10 –25 mm), or giant (ⱖ 25 mm). Although stents are typically placed for assistance with coiling of wide-necked aneurysms (average neck size 5.4 mm, range 2.5–10 mm, average dome-to-neck ratio 1.4), the decision to use a stent-assisted coiling technique at our institution was left to the discretion of the attending physician as deemed appropriate for patient anatomy at the time of the procedure. Immediate aneurysm remnants were categorized as small neck (⬍ 2 mm), significant neck (⬎ 2 mm), or partial embolization (persistent contrast opacification of the aneurysm dome). Angiographic follow-up of remnants was reviewed to record interval healing, stability, or progressive enlargement. If the aneurysm required additional interventional or surgical therapy, this was noted. Hospital notes, discharge summaries, outpatient clinic and emergency department visits, and any additional hospital admissions were reviewed further to identify any immediate or delayed visual disturbances. Defi- cits were considered acute if noted within 24 hours of the intervention and delayed if seen later than this. Fisher exact test was used to determine whether there was a statistical association between preservation of the ophthalmic artery and occurrence of acute or delayed visual deficits. RESULTS Patients The database contained 112 patients with a stent placed in the ICA for embolization of at least one intracranial aneurysm. After review of the catheter angiograms, we identified 57 patients who harbored at least one paraophthalmic or superior hypophyseal aneurysm for which stent-assisted embolization was performed. Multiple aneurysms were identified in 20 (35%) patients; one patient had seven lesions. There was a striking female predominance, with 51 (89.5%) female patients and 6 (10.5%) male patients. The mean age was 61 years (range 28 – 83 years). Only five (8.8%) patients presented with SAH; three (5.3%) patients had visual symptoms attributable to mass effect from the aneurysm. Seven (12.3%) patients were being evaluated for recurrence of a lesion previously treated surgically (3) or endovascularly (4). One patient had undergone both coil embolization and surgical wrapping previously without complete occlusion. Lesions were identified during work-up for headache unrelated to SAH in 15 (26.3%) patients and for presumed transient ischemic attacks in 9 (17.5%) patients, although it is unlikely that the aneurysm contributed to these symptoms. The remaining 17 (29.8%) lesions were found incidentally during work-up for other neurologic deficits unrelated to the aneurysm (e.g., syncope, vertigo), trauma evaluations, or in one case screening evaluation of a high risk patient. Aneurysm Characteristics In 57 patients, 63 aneurysms were identified; 48 were paraophthalmic, and 15 were suprasellar variant superior hypophyseal. There were 36 lesions located on the left and 27 on the right. The average maximum dimension was 7.74 mm with the largest lesion measuring 20 mm and the smallest measuring 3 mm. There were 13 small (⬍ 5 WORLD NEUROSURGERY, DOI:10.1016/j.wneu.2011.12.003 PEER-REVIEW REPORTS ANDREW S. FERRELL ET AL. VISUAL COMPLICATIONS AFTER STENT-ASSISTED COILING Figure 3. Arterial phase angiogram shows late filling of the ophthalmic artery (arrow). Figure 1. Angiogram obtained immediately after embolization shows preservation of the ophthalmic artery (arrow). mm), 36 medium (5–10 mm), 14 large (10 –20 mm), and 0 giant (ⱖ 25 mm) aneurysms. The average neck size was 5.4 mm (range 2.5–10 mm) with an average dometo-neck ratio of 1.4. There were 60 stents placed to treat 63 aneurysms (three patients had two aneurysms each, which were both covered with one stent). Three stents were placed to stabilize coil loop herniation into the parent vessel during the procedure with the remainder placed for wide neck lesions. Angiographic Success of Embolization During the initial embolization, 43 (68.3%) lesions were completely occluded. Small immediate residual neck (⬍ 2 mm) was present in 13 (20.6%) lesions, and significant residual neck (⬎ 2 mm) was present in 3 (4.8%) lesions; 4 (6.3%) lesions were considered incomplete or partially treated. The ophthalmic artery was preserved in all but Figure 2. Angiogram obtained at 6-month follow-up shows no angiographic filling of the ophthalmic artery. two (3.5%) cases. In each of these two cases, the artery was patent at the completion of the procedure but was found to be occluded on follow-up angiogram, one case as a result of stent thrombosis and ICA occlusion and the other presumably related to thromboembolic occlusion (Figures 1 and 2). No visual deficits were present in either of these cases. ICA stent thrombosis occurred very early in the series and was associated with an earlier version of the Neuroform stent. In one patient, the ophthalmic artery showed sluggish flow at the completion of the initial procedure (Figures 3 and 4), and the patient was maintained on heparin infusion overnight. Magnetic resonance imaging and magnetic resonance angiography performed 2 days later showed vessel preservation (Figure 5). A second episode of acute ICA stent thrombosis occurred early in the series in which the ophthalmic artery continued to fill through external carotid collaterals, further showing the robust supply to this vessel (Figure 6). There was no significant association be- Figure 4. Late arterial phase image shows delayed clearing of the ophthalmic artery related to sluggish flow (arrow). WORLD NEUROSURGERY 78 [3/4]: 289-294, SEPTEMBER/OCTOBER 2012 Figure 5. Magnetic resonance angiography performed 2 days after the procedure shows ophthalmic patency (arrow). tween preservation of the ophthalmic artery and the occurrence of acute or delayed visual deficits (P ⫽ 1.0). Angiographic follow-up was available for 45 (71.4%) of 63 aneurysms in 44 (77.2%) of 57 patients (mean 12 months, median 6 months, standard deviation 17.3 months). Of the 20 aneurysms with immediate residual, 10 showed progressive healing or complete occlusion, 4 showed stability, 1 showed progressive enlargement, and 5 were lost to follow-up. Four (6.3%) aneurysms that initially appeared completely occluded showed evidence of recurrence. Five patients underwent subsequent embolization procedures in attempts to occlude the residual; successful obliteration occurred in three of five. At the time of completion of this study, 6 (13.6%) of the 44 patients for Figure 6. Despite internal carotid artery thrombosis, the ophthalmic artery continues to fill via external carotid collaterals (arrows). www.WORLDNEUROSURGERY.org 291 PEER-REVIEW REPORTS ANDREW S. FERRELL ET AL. VISUAL COMPLICATIONS AFTER STENT-ASSISTED COILING whom angiographic follow-up was available showed evidence of residual aneurysm (four ⬍ 5 mm and two ⬎ 5 mm). Visual Complications Mean length of clinical follow-up was 12.1 months (median 7 months, mode 1.0 month, standard deviation 16.2 months). Four patients were lost to follow-up. None of the four patients without long-term clinical follow-up showed any visual deficits at the time of discharge. Only three visual complications were identified— one acute and two delayed—for an overall visual complication rate of 5.3% with a permanent complication rate of 3.5%. The acute event was seen in a 44-year-old woman undergoing retreatment of a recurrent 5-mm paraophthalmic aneurysm that had been treated previously with embolization. The procedure was uneventful, and she experienced mild blurry vision ipsilateral to the side of the aneurysm, which completely and spontaneously resolved within 24 hours. No true visual field deficit could be elicited by clinical examination, and no formal visual fields were obtained. The patient had no subjective visual symptoms at 1-month follow-up examination. The first of two delayed deficits was seen in a 74-year-old woman undergoing additional embolization for a 3-mm recurrence of a previously treated 15-mm right superior hypophyseal aneurysm. She began to notice loss of peripheral vision on the contralateral side over the next 6 – 8 months, although the exact duration of onset from time of embolization was unclear. She was ultimately diagnosed with a left homonymous hemianopsia with some nonspecific depression in the right hemifields as well. The second delayed complication occurred in a 51-year-old woman undergoing treatment for an incidentally discovered 9.8-mm paraophthalmic aneurysm. The procedure went well, and she was discharged home the following day without any evidence of complication. During the month following the procedure, she developed mild intermittent superior nasal field deficits ipsilateral to the lesion, which were confirmed with formal visual field testing (Figure 7). Three patients in our series presented with visual disturbances that were possibly related to their aneurysms. One patient had a bitemporal hemianopsia thought to be related to a 20-mm superior hypophyseal an- 292 www.SCIENCEDIRECT.com Figure 7. Formal visual field testing shows superior nasal deficit attributable to left paraophthalmic aneurysm treatment. eurysm. This case occurred early in our series as we were learning which aneurysms were best dealt with surgically as opposed to endovascularly. Stable visual deficits were evident after the procedure with 11 months of available clinical follow-up. Another patient showed a nasal field deficit ipsilateral to a 20-mm paraophthalmic aneurysm. This patient was considered to be a poor candidate for surgical clipping because of neck calcification and underwent embolization with clinically stable visual deficit after the procedure with 18-month clinical follow-up. The third patient had intermittent double vision with an 8.3-mm paraophthalmic aneurysm. Given the small size of the aneurysm and the uncertainty of the relationship between the aneurysm and the intermittent, nonspecific double vision, the patient was offered surgical or endovascular treatment and chose endovascular therapy. No additional episodes of visual disturbance were evident after the procedure with 5-month clinical follow-up. DISCUSSION Paraophthalmic ICA aneurysms present unique challenges to both interventional and surgical therapies with respect to pos- WORLD NEUROSURGERY, DOI:10.1016/j.wneu.2011.12.003 PEER-REVIEW REPORTS ANDREW S. FERRELL ET AL. sible visual complications. In 1981, Ferguson and Drake (9) reported visual deficits in 32 of 100 surgical cases of carotid-ophthalmic aneurysms at the time of presentation. For the 29 patients for which follow-up visual results were available, improvement was seen in 12 patients, no change was seen in 11 patients, and worsening of symptoms was seen in 6 patients. In 1990, Day (5) reported new visual deficits in 6 (7.5%) of 80 cases of both paraophthalmic and superior hypophyseal aneurysms treated surgically. In 2009, Fulkerson et al. (10) reported a 4.8% incidence of new visual deficits in 126 paraophthalmic aneurysms treated surgically, which suggests that although microsurgical techniques have improved, visual complications remain a concern even in the most experienced hands. The ever-increasing employment of interventional therapies has done little to reduce these risks; regardless of the preferred choice of management, the incidence of visual complications is estimated to be approximately 5% (10, 25). In experienced hands, the choice between surgery and intervention for these lesions is equivocal if visual symptoms related to mass effect are not seen at the time of presentation. In a 2001 series of 180 surgically and 57 endovascularly treated paraclinoid aneurysms, an equal 3% incidence of new or worsened visual deficits was reported for both groups (13). Thromboembolic stroke is likely the most common and feared complication related to endovascular therapy (7). Visual deficits that are maximal at the time of onset and seen during or immediately after endovascular treatment of paraclinoid aneurysms likely are related to ophthalmic thromboemboli and subsequent retinal infarcts or emboli to the posterior circulation via the posterior communicating artery, resulting in cortical blindness (25). Recent reports with limited numbers of patients have shown evidence of more progressive and delayed visual deficits following and specific to endovascular therapy, which seem to be related to progressive mass effect from aneurysm thrombosis or perianeurysmal edema (21, 25). Several articles have suggested that the occurrence of this inflammatory response may be greater in patients treated with bioactive coils such as the HydroCoil Embolic System (MicroVention, Inc., Aliso Viejo, California, USA), although the number of patients in these VISUAL COMPLICATIONS AFTER STENT-ASSISTED COILING reports was small (17, 25). It is important to recognize the different pathophysiologic etiologies of these two impaired visual presentations because thromboembolic causes may require additional emergent intervention with thrombolysis to save vision, with the latter possibly responding to corticosteroid administration (25). In our series, we report another variable to the equation: stent-assisted embolization. We treat a significant number of wide neck paraclinoid aneurysms in our practice with stent-assisted embolization. From the time of our first cases, we have been concerned about mass effect during coil deployment resulting in visual complications given the proximity of the ophthalmic origin to the aneurysm neck. Despite this concern, we have treated 57 patients with this strategy and have seen a similar temporary visual complication rate of 5.3% and a permanent visual complication rate of 3.5%, which is comparable to surgery or standard coil embolization. None of the three patients in our series who presented with visual disturbances potentially related to their lesions experienced worsening of symptoms. Our concerns of mass occlusion of the ophthalmic artery origin related to the adjacent coil mass seem unsupported given that the ophthalmic artery was preserved angiographically in all but two cases, one of which was the result of stent thrombosis and complete ICA occlusion. In our practice, we typically manage large paraclinoid aneurysms that manifest with clinical evidence of optic nerve compression surgically to decompress the aneurysm dome, reduce mass effect, and prevent delayed visual deterioration. Patients with smaller aneurysms and aneurysms without visual disturbances at presentation are more likely to be offered endovascular treatment, although age and other risk factors are considered individually; this is an important point in that our series comprises only 14 large (10 –25 mm) and 0 giant (ⱖ 25 mm) aneurysms. Larger lesions may result in higher complication rates, although in our series only one of the lesions that were associated with visual complications was considered large. However, of the three patients who presented with visual disturbances, two had large aneurysms, and neither of the two patients had improvement in vision after embolization. These cases emphasize the necessity to relieve mass effect WORLD NEUROSURGERY 78 [3/4]: 289-294, SEPTEMBER/OCTOBER 2012 surgically if possible in attempts to restore vision. Our patient population is heterogeneous with preoperative mass effect present in some and absent in others. Because of this limitation, further studies are needed to delineate visual complication risk completely based on aneurysm size and dimensions. One limitation of our study other than its retrospective nature is that formal visual fields were not obtained before and after embolization on all patients. Simple clinical bedside examination of visual fields may miss subtle deficits detectable by formal examination, although if deficits were present, they would have been clinically silent, and it is questionable if this would have altered decisions about treatment strategy. The 12-month median follow-up period is also shorter than what would be considered optimal to ensure delayed visual deterioration is not occurring related to the procedure. Another limitation is that only five (8.8%) patients in our series presented with SAH related to their aneurysm, which is a smaller number than seen with other surgical or endovascular series of similar size. Hemorrhage can create additional mass effect on the optic nerve itself, even dissecting into the substance of the nerve, which would alter decision making because surgical decompression may be more desirable in these circumstances. We achieved primary aneurysm occlusion in 68.3% of patients with 7% having a significant residual neck (ⱖ 2 mm) or incomplete treatment. At the time of completion of this study, 6 (13.6%) of 44 patients for whom angiographic follow-up was available showed evidence of residual aneurysm. If one compares these rates with similar surgical series, the results are suboptimal; however, they seem in keeping with series results of coil embolization alone. De Jesus et al. (6) reported successful clipping of 32 of 35 clinoid and paraclinoid aneurysms, and Hoh et al. (13) reported a 94% complete occlusion rate in 180 surgically treated paraclinoid aneurysms. However, in this same study, complete endovascular occlusion was achieved only in 25 (44%) of 58 lesions with partial occlusion in 32 (56%) and a 26% rate of regrowth or coil compaction on follow-up (13). Thornton et al. (24) reported a 46% complete primary occlusion in 71 paraclinoid aneurysms that were endovascularly treated; Roy et al. (19) achieved www.WORLDNEUROSURGERY.org 293 PEER-REVIEW REPORTS ANDREW S. FERRELL ET AL. total occlusion in 50% of 28 patients who underwent attempted endovascular treatment of ophthalmic segment aneurysms. Park et al. (16) reported outcome data from the endovascular treatment of paraclinoid aneurysms in 73 patients. They reported complete occlusion in 53 (72.6%), nearcomplete occlusion in 6 (8.2%), and partial occlusion in 14 (19.2%). Final angiographic outcome was available for 49 of the 73 aneurysms and showed complete occlusion in 43 (87.8%), near-complete occlusion in 3 (6.1%), and partial occlusion in 3 (6.1%) (16). A significant drawback of endovascular therapy compared with surgery has always been a relatively high rate of initial incomplete treatment and long-term recurrence. The reason for the comparatively high rate of residual and recurrent lesions after coil embolization of paraclinoid aneurysms is unclear. One possible factor is shear hemodynamic stresses that occur at the region of the carotid siphon, which may hinder endothelialization and healing of the partially occluded aneurysm neck (4). In our limited series, the addition of stent assistance did not seem to result in improved rates of aneurysm obliteration compared with coil embolization alone, although this was not the specific aim of this study. Additional prospective series are needed to address this issue. CONCLUSIONS Stent-assisted embolization of paraophthalmic and superior hypophyseal aneurysms does not appear to result in increased risk of visual complications compared with surgical or standard endovascular embolization without stent placement. VISUAL COMPLICATIONS AFTER STENT-ASSISTED COILING 3. Benedetti A, Curri D: Direct attack on carotid ophthalmic and large internal carotid aneurysms. Surg Neurol 8:49-54, 1977. 4. Boet R, Wong GK, Poon WS, Lam JM, Yu SC: Aneurysm recurrence after treatment of paraclinoid/ophthalmic segment aneurysms—a treatment-modality assessment. Acta Neurochir (Wien) 147:611-616, 2005. 18. Rizzo JF 3rd: Visual loss after neurosurgical repair of paraclinoid aneurysms. Ophthalmology 102:905910, 1995. 5. Day AL: Aneurysms of the ophthalmic segment. A clinical and anatomical analysis. J Neurosurg 72: 677-691, 1990. 19. Roy D, Raymond J, Bouthillier A, Bojanowski MW, Moumdjian R, L’Esperance G: Endovascular treatment of ophthalmic segment aneurysms with Guglielmi detachable coils. AJNR Am J Neuroradiol 18: 1207-1215, 1997. 6. De Jesus O, Sekhar LN, Riedel CJ: Clinoid and paraclinoid aneurysms: surgical anatomy, operative techniques, and outcome. Surg Neurol 51:477-487, 1999. 7. Derdeyn CP, Cross DT 3rd, Moran CJ, Brown GW, Pilgram TK, Diringer MN, Grubb RL Jr, Rich KM, Chicoine MR, Dacey RG Jr: Postprocedure ischemic events after treatment of intracranial aneurysms with Guglielmi detachable coils. J Neurosurg 96: 837-843, 2002. 8. Drake CG, Vanderlinden RG, Amacher AL: Carotidophthalmic aneurysms. J Neurosurg 29:24-31, 1968. 9. Ferguson GG, Drake CG: Carotid-ophthalmic aneurysms: visual abnormalities in 32 patients and the results of treatment. Surg Neurol 16:1-8, 1981. 10. Fulkerson DH, Horner TG, Payner TD, Leipzig TJ, Scott JA, DeNardo AJ, Redelman K, Goodman JM: Results, outcomes, and follow-up of remnants in the treatment of ophthalmic aneurysms: a 16-year experience of a combined neurosurgical and endovascular team. Neurosurgery 64:218-229, 2009. 11. Guidetti B, La Torre E: Management of carotid-ophthalmic aneurysms. J Neurosurg 42:438-442, 1975. 12. Heros RC, Nelson PB, Ojemann RG, Crowell RM, DeBrun G: Large and giant paraclinoid aneurysms: surgical techniques, complications, and results. Neurosurgery 12:153-163, 1983. 13. Hoh BL, Carter BS, Budzik RF, Putman CM, Ogilvy CS: Results after surgical and endovascular treatment of paraclinoid aneurysms by a combined neurovascular team. Neurosurgery 48:78-89, 2001. 14. Kothandaram P, Dawson BH, Kruyt RC: Carotidophthalmic aneurysms. A study of 19 patients. J Neurosurg 34:544-548, 1971. REFERENCES 1. Almeida GM, Shibata MK, Bianco E: Carotid-ophthalmic aneurysms. Surg Neurol 5:41-45, 1976. 2. Bendok BR, Parkinson RJ, Hage ZA, Adel JG, Gounis MJ: The effect of vascular reconstruction deviceassisted coiling on packing density, effective neck coverage, and angiographic outcome: an in vitro study. Neurosurgery 61:835-840, 2007. 294 www.SCIENCEDIRECT.com 17. Pickett GE, Laitt RD, Herwadkar A, Hughes DG: Visual pathway compromise after hydrocoil treatment of large ophthalmic aneurysms. Neurosurgery 61:E873-874, 2007. 15. Kumon Y, Sakaki S, Kohno K, Ohta S, Ohue S, Oka Y: Asymptomatic, unruptured carotid-ophthalmic artery aneurysms: angiographical differentiation of each type, operative results, and indications. Surg Neurol 48:465-472, 1997. 20. Sadasivan C, Lieber BB: Numerical investigation of coil configurations that provide ultra-high packing density of saccular aneurysms. J Med Device 3:41005, 2009. 21. Schmidt GW, Oster SF, Golnik KC, Tumialan LM, Biousse V, Turbin R, Prestigiacomo CJ, Miller NR: Isolated progressive visual loss after coiling of paraclinoid aneurysms. AJNR Am J Neuroradiol 28:18821889, 2007. 22. Stracke CP, Krings T, Moller-Hartmann W, Mahdavi A, Klug N: Severe inflammatory reaction of the optic system after endovascular treatment of a supraophthalmic aneurysm with bioactive coils. AJNR Am J Neuroradiol 28:1401-1402, 2007. 23. Tanaka Y, Hongo K, Tada T, Nagashima H, Horiuchi T, Goto T, Koyama J, Kobayashi S: Radiometric analysis of paraclinoid carotid artery aneurysms. J Neurosurg 96:649-653, 2002. 24. Thornton J, Aletich VA, Debrun GM, Alazzaz A, Misra M, Charbel F, Ausman JI: Endovascular treatment of paraclinoid aneurysms. Surg Neurol 54: 288-299, 2000. 25. Turner RD, Byrne JV, Kelly ME, Mitsos AP, Gonugunta V, Lalloo S, Rasmussen PA, Fiorella D: Delayed visual deficits and monocular blindness after endovascular treatment of large and giant paraophthalmic aneurysms. Neurosurgery 63:469-474, 2008. 26. Yasargil MG, Gasser JC, Hodosh RM, Rankin TV: Carotid-ophthalmic aneurysms: direct microsurgical approach. Surg Neurol 8:155-165, 1977. Conflict of interest statement: M.J.A. is a device proctor and consultant for Boston Scientific Neurovascular. Received 10 March 2011; accepted 01 December 2011; published online 10 December 2011 Citation: World Neurosurg. (2012) 78, 3/4:289-294. DOI: 10.1016/j.wneu.2011.12.003 Journal homepage: www.WORLDNEUROSURGERY.org 16. Park HK, Horowitz M, Jungreis C, Kassam A, Koebbe C, Genevro J, Dutton K, Purdy P: Endovascular treatment of paraclinoid aneurysms: experience with 73 patients. Neurosurgery 53:14-23, 2003. Available online: www.sciencedirect.com 1878-8750/$ - see front matter © 2012 Elsevier Inc. All rights reserved. WORLD NEUROSURGERY, DOI:10.1016/j.wneu.2011.12.003