Journal of Neuro-Ophthalmology, March 2004, Volume 24, Issue 1

Delayed Execerbation of Third Nerve Palsy Due to Aneurysmal Regrowth After Endovascular Coil Embolization

A 72-year-old woman with a painful left third cranial nerve palsy due to a basilar artery aneurysm situated between the superior cerebellar and posterior cerebral arteries was treated with Guglielmi detachable coils (GDCs). Despite a good initial angiographic result with a small residual neck and improvement in the ocular motility and pain, the patient experienced worsening of the third cranial nerve palsy 15 months later. Cerebral angiography confirmed coil compaction with aneurysmal regrowth. A second endovascular coil embolization resulted in complete obliteration of the aneurysm. The patient experienced complete resolution of the pain and partial resolution of the third cranial nerve palsy. In some patients, a small residual aneurysm neck after endovascular embolization therapy with GDCs can result in delayed aneurysmal regrowth due to coil compaction. Clinical manifestations may herald this dangerous regrowth.

ORIGINAL CONTRIBUTION Delayed Exacerbation of Third Nerve Palsy Due To Aneurysmal Regrowth After Endovascular Coil Embolization M. Tariq Bhatti, MD, Keith R. Peters, MD, Christopher Firment, MD, and Robert A. Mericle, MD Abstract: A 72- year- old woman with a painful left third cranial nerve palsy due to a basilar artery aneurysm situated between the superior cerebellar and posterior cerebral arter­ies was treated with Guglielmi detachable coils ( GDCs). Despite a good initial angiographic result with a small re­sidual neck and improvement in the ocular motility and pain, the patient experienced worsening of the third cranial nerve palsy 15 months later. Cerebral angiography confirmed coil compaction with aneurysmal regrowth. A second endovascular coil embolization resulted in complete obliteration of the aneurysm. The patient experienced com­plete resolution of the pain and partial resolution of the third cranial nerve palsy. In some patients, a small residual aneu­rysm neck after endovascular embolization therapy with GDCs can result in delayed aneurysmal regrowth due to coil compaction. Clinical manifestations may herald this dangerous regrowth. (/ Neuro- Ophthalmol 2004; 24: 3- 10) An estimated 1 % to 6% of the general population harbors an intracranial aneurysm ( 1). The annual rupture rate of aneurysms has been estimated to range from 0.05% to 2%, with a higher rate associated with a previous history of subarachnoid hemorrhage, symptomatic clinical presen­tation ( mass effect or cranial neuropathy), large aneurysm size (> 10mm) or posterior circulation location ( 2). From 10% to 20% of patients presenting with aneurysmal SAH will die immediately prior to seeking medical attention ( 1). Treatment is recommended for all symptomatic aneurysms to avoid rupture and improve upon the grave prognosis associated with aneurysmal SAH ( 3). The treatment goal of intracranial aneurysms is their isolation from the parent From the Departments of Ophthalmology ( MTB), Neurology ( MTB), Neurological Surgery ( MTB, KRP, RAM), and Radiology ( KRP, CF), University of Florida College of Medicine, Gainesville, Florida. Address correspondence to M. Tariq Bhatti, MD, Box 100284, Depart­ment of Ophthalmology, Gainesville, Florida 32610- 0284. E- mail: tbhatti@ eye 1 . eye. ufl. edu Supported in part by an unrestricted departmental grant from Research to Prevent Blindness, Inc. ( New York, NY) vessel while maintaining normal cerebral circulation. Surgical clipping has traditionally been considered the mainstay of treatment. Recent advances in microcatheter technology, endovascular techniques, and embolization materials have increased the popularity of neurointerven-tional therapy in patients with intracranial aneurysms ( 4). A recent prospective comparison study found that patients who underwent endovascular coiling had a 6.9% absolute risk reduction in dependency ( modified Rankin score of 3- 5) or death at 1 year compared with those who underwent surgical clipping ( 5). Because of the intimate anatomic relationship be­tween the intracranial vasculature and the afferent and efferent visual pathways, neuro- ophthalmic signs and symptoms may often be the presenting manifestations of intracranial aneurysms ( 6). As more patients undergo endo­vascular embolization, a new set of post procedure situa­tions may emerge that are unfamiliar to ophthalmologists. We present a case of recurrent third nerve palsy, ocular pain and headache as the clinical manifestations of aneurysmal regrowth that occurred more than 1 year after endovascular treatment with Guglielmi detachable coils ( GDCs) ( Target Therapeutics/ Boston Scientific Corporation, Fremont, CA). CASE REPORT A previously healthy 72- year- old woman experi­enced OS pain in April 2001, which worsened to involve the left cranium and face. In May 2001, she experienced left upper lid ptosis. In June 2001, she noted diplopia and was diagnosed with a left third cranial nerve palsy. Almost 3 months after the onset of symptoms, magnetic resonance imaging ( MRI) and angiography ( MRA) suggested a pos­terior communicating artery aneurysm. A cerebral angio­gram showed that the aneurysm arose on the basilar artery between the left superior cerebellar and posterior cerebral arteries ( Fig. 1A). Endovascular embolization with GDCs was per­formed through a percutaneous right femoral artery punc­ture on the same day. A Prowler- 14 ( 0.014 inch diameter) microcatheter ( Cordis Neurovascular, Miami Lakes, FL) J Neuro- Ophthalmol, Vol. 24, No. 1, 2004 3 Bhatti et al. FIGURE 1. Cerebral angiogram. An­teroposterior ( left) and lateral ( right) views of left vertebral artery injection. A. A basilar apex aneurysm projects to the left between the left posterior cerebral artery and left superior cerebellar artery ( arrows). B. After embolization treat­ment with GDCs, a small aneurysm neck is outlined with contrast ( arrow). C. Fif­teen months after GDC treatment, con­trast fills a regrown aneurysm ( curved arrow). The coils have become com­pacted in the dome of the aneurysm ( arrowheads). There is a zone of throm­bosis ( arrow). D. Following the second endovascular coil embolization treat­ment, the aneurysm is obliterated. © 2004 Lippincott Williams & Wilkins Delayed Exacerbation of Third Nerve Palsy JNeuro- Ophthalmol, Vol. 24, No. 1, 2004 with two distal tip markers was advanced into the lumen of the aneurysm in a coaxial fashion. Seven coils were sequen­tially placed into the aneurysm without complications or parent vessel compromise. After delivery of the seventh coil, angiography confirmed the position and configuration of the coils and occlusion of the aneurysmal sac with a small residual neck ( Figs. IB and 2A). Further placement of coils was not performed due to concern for coil migration into the basilar artery. The patient tolerated the procedure well and was discharged home the next day. One week later, she was examined for the first time in the Neuro- Ophthalmology Clinic. She reported that the dip­lopia, ptosis, eye pain, and headache had improved. The left pupil measured 2 mm larger than the right with absence of a direct and consensual light response. There was 6 mm of left upper eyelid ptosis. Ocular motility of the OD was nor­mal. In the OS, there was 40% supraduction, 95% infraduc-tion, and 95% adduction ( Fig. 3 A). In primary gaze, there was a 6 prism diopter ( PD) right hypertropia and 4 PD left exotropia. Six months after embolization, the third nerve palsy was unchanged and the OS pain and headache continued. A skull radiograph demonstrated no change in the configu­ration of the coils. In August 2002, 13 months after the initial proce­dure, the patient continued to complain of left ocular pain and headaches. The ocular motility examination was FIGURE 2. Unsubtracted skull films. Anteroposterior ( left) and lateral ( right) views. Compare the compaction of the GDCs immediately after first embolization procedure ( A) to their dispersion 15 months after the second embolization treatment ( B). unchanged. Follow- up skull radiographs demonstrated al­teration in the configuration of the coil mass ( not shown). The patient was lost to follow- up until October 2002, when she developed worsening of the left upper eyelid ptosis. On examination, there was complete left upper eyelid ptosis. The left pupil continued to be 2 mm larger than the right pupil and unreactive to light. Ocular motility examination revealed 5% supraduction, 5% infraduction, and 5% adduc­tion of the OS. In primary gaze there was a 50 PD left ex­otropia ( Fig. 3B). The unsubtracted skull films and cerebral angiogram demonstrated a change in the configuration of the coils and regrowth of the aneurysm ( Figs. 1C and 2B). With a transcatheter endovascular technique, 5 Tru-fill DCS coils ( Cordis/ Johnson & Johnson, Miami Lakes, FL) were placed into the aneurysm. Sequential temporary inflation of a non- detachable balloon in the basilar artery during coil placement prevented the coils from protruding into the parent vessel. A post- procedure angiogram showed complete obliteration of the aneurysm with patency of the parent vessel ( Fig. ID). After awakening from general an­esthesia, the patient was disoriented and aphasic. Computed tomography of the head demonstrated a left thalamic and left cerebral hemispheric infarction. Cerebral angiography demonstrated normal filling of the intracranial vessels with a stable coil mass and complete obliteration of the aneu­rysm. Over the following week, the patient became more alert and language improved. She was discharged from the hospital with improvement of the OS pain and headaches. Three months later, the third cranial nerve palsy had im­proved and the patient was free of headaches and eye pain. There was 4 mm of left upper eyelid ptosis. The OS had 5% supraduction, 10% infraduction, and 70% adduction. In pri­mary gaze there was a 14 PD right hypertropia and a 40 PD left exotropia. DISCUSSION Our patient presented with a painful left third cranial nerve palsy due to compression by a basilar aneurysm situ­ated between the superior cerebellar and posterior cerebral arteries. Initial treatment with endovascular coil emboliza­tion resulted in partial improvement of the palsy. An imme­diate post- embolization angiogram showed occlusion of the aneurysm with a small residual neck. Fifteen months later, the palsy had worsened and a repeat angiogram demon­strated regrowth of the aneurysm with coil compaction. A second endovascular coil embolization treatment success­fully obliterated the aneurysm, relieved the head pain, and improved the third cranial nerve palsy. The first successful placement of an aneurysm clip was performed by Walter Dandy in 1937 ( 7). Since then, improvements in microsurgical technique and aneurysm clip design have made surgical clipping the gold standard in treatment of intracranial aneurysms. An alternative to 5 JNeuro- Ophthalmol, Vol. 24, No. 1, 2004 Bhatti et al. FIGURE 3. Ocular motility photographed in the nine positions of gaze. A. One week after the first GDC treatment. There is mild limitation of supraduction, infraduction, and adduction of the OS. B. Fifteen months after the first GDC treatment. The ductional deficits ( especially adduction) have increased. surgical treatment was first undertaken by neurosurgeons efficacy, and unpredictable outcomes, thrombogenic en-unsuccessfullyin 1964, with an attempt at endovascularoc- dosaccular platinum coils were developed ( 8,9). Subse-clusion by means of a silicon balloon ( 8). Once refined, en- quent work on platinum coils led to the development of the dovascular balloon embolization became a viable option, most widely used system currently, the Guglielmi detach-but because of the concern for complications, long term able coil ( GDC). 6 © 2004 Lippincott Williams & Wilkins Delayed Exacerbation of Third Nerve Palsy JNeuro- Ophthalmol, Vol. 24, No. 1, 2004 The GDC coil is made of a malleable platinum/ tung­sten alloy wire attached to a stainless steel delivery wire. A small electrical current ( default setting: 1mA) dissolves a portion of the delivery wire and detaches the coil into the aneurysm. The GDC system allows the operator to retrieve and reposition the coil prior to deployment if endosaccular placement is not deemed satisfactory. Once detached, each coil conforms to the shape of the aneurysm, filling the aneurysm pouch while maintaining the integrity of the an­eurysm wall ( 10). Aneurysm obliteration is generally ac­complished by filling approximately 30% of the aneurysm volume with coils ( 11). The placement of coils into the an­eurysm results in a complex and incompletely understood cascade of events, which include hemodynamic changes, thrombosis formation, and fibrocellular proliferation ( 8, 12- 15). Surgical clipping of unruptured intracranial aneu­rysms is associated with an approximately 10.9% morbidity and 2.6% mortality ( 16). Several studies have shown com­parable safety and efficacy with endovascular coil embo­lization ( 4,17,18). Furthermore, endovascular therapy is more effective in reducing health care costs, including the length of hospitalization ( 17). However, the long term effi­cacy and rupture rate of treated aneurysms following endo­vascular embolization therapy is not well known ( 18). Aneurysm regrowth after surgical clipping can occur from an inadequately placed or displaced clip with postop­erative angiography demonstrating a residual neck in 5% of patients ( 19,20). After endovascular coil embolization, 60% of patients may have a residual aneurysm neck ( 21- 24). The outcome of these aneurysm neck remnants after endovascular coil embolization is variable and may result in neck enlargement, stabilization, or occlusion ( 23,24). Hayakawa et al. ( 24) reviewed their experience with the natural history of residual neck remnants after GDC treatment. Twenty- five percent of aneurysms with post-embolization residual aneurysm necks had progressive thrombosis, 26% remained unchanged, and 49% demon­strated recanalization. The mean angiographic follow- up time was 17.3 months. Thorton et al. ( 23) found that 46% of aneurysms with post- embolization residual necks had progressive thrombosis, 26% remained stable, and 28% demonstrated enlargement of the residual neck with a mean angiographic follow- up time of 16.7 months. Several factors appear to be involved in aneurysm re-growth following endovascular coil embolization treat­ment. Because of their size, non- spherical shape, and wide neck, aneurysms can be difficult to pack and obliterate ( 25). Inadequate coil embolization volume or a change in coil reconfiguration may result in the reestablishment of blood flow within the spaces of the coils and cause aneurysmal regrowth ( recanalization) ( 11,26). If the aneurysm is not tightly packed with coils and a residual aneurysm neck is present, the constant pulsation of arterial blood flow from the parent vessel against the coils and into the residual neck (" water hammer effect") can cause the coils to change con­figuration, cluster together, and move toward the dome of the aneurysm ( coil compaction) ( 27- 30). We believe that the latter mechanism explains our patient's aneurysm re­growth ( Fig. 4). The effect of surgical clipping on aneurysmal third cranial nerve palsies has been well documented ( 31- 38). Leivo et al. ( 39) analyzed 283 published cases and found that complete recovery occurred in 41 %, partial recovery in 52%, and no change in 7%. Among patients surgically treated within 14 days of onset of symptoms, 64% had com­plete third cranial nerve recovery, whereas among those treated more than 30 days after onset of symptoms, only 14% had complete recovery. Among the authors' personal series of 28 patients with third cranial nerve palsy due to posterior communicating artery aneurysms, 57% of patients had complete recovery after surgery with 75% of these pa­tients having been treated within 1 week of the onset of symptoms ( 39). The recovery rate of aneurysmal third nerve palsy fol­lowing endovascular embolization treatment with detach­able platinum coils has been less well documented ( Table 1). Two reports with a total of four patients presenting less than 3 weeks from the onset of symptoms and treated with GDC embolization of posterior communicating artery an­eurysms have described complete recovery within 3 weeks of treatment ( 40,41). Yanaka et al. ( 38) treated one patient with endovascular embolization for a posterior communi­cating artery aneurysm 50 days after the onset of the initial symptoms and documented no recovery of the third cranial nerve palsy. Although no details were provided, Gruber et al. ( 25) and Uda et al. ( 42) identified two patients each with complete resolution of third cranial nerve dysfunc­tion after GDC treatment. Eskridge et al. ( 43) noted that 12.4% of patients had persistent third cranial nerve palsy after endovascular treatment of basilar tip aneurysms with GDCs, as compared with 20.8% with a palsy prior to treatment. The mechanism of recovery in third cranial nerve palsy following endovascular coil embolization is not clear. Unlike surgical clipping, in which the surgeon often de­flates the aneurysm after clip placement, endovascular coiling does not alter the volume of the aneurysm dome. A major factor in resolution appears to be a decrease in the transmission of arterial pulsation; other possible factors in­clude aneurysm shrinkage, aneurysm size stabilization, and reduced cerebral edema ( 44,45). Our patient's persistent ocular pain after emboliza­tion may have been based on irritation of third cranial nerve trigeminal pain fibers by the coiled aneurysm mass as it 7 JNeuro- Ophthalmol, Vol. 24, No. 1, 2004 Bhatti et al. Posterior cerebral artery Aneurysm cerebellar artery B V Thrombus H Compacted coils Aneurysm regrowth FIGURE 4. Artist's drawing of the mechanism of coil compaction and aneurysmal regrowth. ( Medical Illustrator: Dave Peace) A. Vascular anatomy of superior cerebellar- posterior cerebral artery aneurysm. B. Cross sectional view of the aneurysm. C- D. Endosaccular delivery of detachable coils. E. Small residual aneurysm neck ( arrow) after endovascular coil embolization. F- H. Persistent pulsation of the parent vessel blood flow through the small residual neck ( small arrows) results in a change in the position and configuration of the coils with enlargement of the aneurysmal neck. I. Regrowth of the aneurysm due to coil compaction. continued to pulsate from the arterial flow through the re­sidual neck ( 46). Endovascular embolization therapy with detachable platinum coils is an effective and safe treatment of intracranial aneurysms. Aneurysm neck remnant after endovascular coil embolization therapy may result in aneurysm regrowth months to years after treatment and present with neuro- ophthalmic manifestations. Therefore, patients with TABLE 1. Reported outcomes of isolated aneurysmal third cranial nerve palsy treated with endovascular coil embolization Author ( No.) Number ofcases Location of aneurysm Diameter of aneurysm Time interval from symptoms to treatment Outcome of third cranial nerve palsy Birchall et al. ( 40) Gruber et al. ( 25) Uda et al. ( 42) Inamasuet al. ( 41) Yanaka et al. ( 38) 3 2 2 1 1 PComA PComA PComA PComA SCA BA- SCA BA- SCA PComA PComA 6 mm 4 mm 5 mm > 25 mm 20- 25 mm > 25 mm < 11 mm NR 6 x 4mm 10 days 5 days 21 days NR NR NR NR 1 day 50 days Resolved Resolved Resolved Resolved Resolved Resolved Resolved Resolved No change PComA, posterior communicating artery; SCA, superior cerebellar artery; BA- SCA, basilar artery- superior cerebellar artery; NR, not reported. 8 © 2004 Lippincott Williams & Wilkins Delayed Exacerbation of Third Nerve Palsy JNeuro- Ophthalmol, Vol. 24, No. 1, 2004 intracranial aneurysms who undergo endovascular coil oc­clusion should be carefully monitored. REFERENCES 1. Weir B. Unruptured intracranial aneurysms: A review. JNeurosurg. 2002; 96: 3- 42. 2. Brennan JW, Schwartz ML. Unruptured intracranial aneurysms: ap­praisal of the literature and suggested recommendations for surgery, using evidence- based medicine criteria. Neurosurgery. 2000; 47: 1359- 71; discussion 71- 2. 3. Bederson JB, Awad I A, Wiebers DO, et al. Recommendations for the management of patients with unruptured intracranial aneu­rysms: A statement for health care professionals from the Stroke Council of the American Heart Association. Circulation. 2000; 102: 2300- 8. 4. Brilstra EH, Rinkel GJ, van der Graaf Y, et al. Treatment of intra­cranial aneurysms by embolization with coils: a systematic review. Stroke. 1999; 30: 470- 6. 5. Molyneux A, Kerr R, Stratton I, et al. International Subarachnoid Aneurysm Trial ( ISAT) of neurosurgical clipping versus endovas­cular coiling in 2143 patients with ruptured intracranial aneurysms: A randomised trial. Lancet. 2002; 360: 1267- 74. 6. Kasner SE, Liu GT, Galetta SL. Neuro- ophfhalmologic aspects of aneurysms. Neuroimaging Clin NAm. 1997; 7: 679- 92. 7. Louw DF, Asfora WT, Sutherland GR. A brief history of aneurysm clips. Neurosurg Focus. 2001; 11: Article 4. 8. Horowitz MB, Levy E, Kassam A, Purdy PD. Endovascular therapy for intracranial aneurysms: A historical and present status review. Surg Neurol. 2002; 57: 147- 58; discussion 158- 9. 9. Byrne J. Review article: Endovascular treatments for intracranial aneurysms. Br J Radiol. 1996; 69: 891- 9. 10. Pruvo JP, Leclerc X, Ares GS, et al. Endovascular treatment of rup­tured intracranial aneurysms. J Neurol. 1999; 246: 244- 9. 11. Tamatani S, Ito Y, Abe H, et al. Evaluation of the stability of aneu­rysms after embolization using detachable coils: correlation be­tween stability of aneurysms and embolized volume of aneurysms. AJNR Am JNeuroradiol. 2002; 23: 762- 7. 12. Sorteberg A, Sorteberg W, Rappe A, Strother CM. Effect of Guglielmi detachable coils on intraaneurysmal flow: experimental study in canines. AJNR Am J Neuroradiol. 2002; 23: 288- 94. 13. Padolecchia R, Guglielmi G, Puglioli M, et al. Role of electrofhrom-bosis in aneurysm treatment with Guglielmi detachable coils: An in vitro scanning electron microscopic study. AJNR Am J Neuroradiol 2001; 22: 1757- 60. 14. Stiver SI, Porter PJ, Willinsky RA, Wallace MC. Acute human his-topathology of an intracranial aneurysm treated using Guglielmi de­tachable coils: case report and review of the literature. Neurosur­gery. 1998; 43: 1203- 8. 15. Horowitz MB, Purdy PD, Burns D, Bellotto D. Scanning electron microscopic findings in a basilar tip aneurysm embolized with Guglielmi detachable coils. AJNR Am J Neuroradiol. 1997; 18: 688- 90. 16. Raaymakers TW, Rinkel GJ, Limburg M, Algra A. Mortality and morbidity of surgery for unruptured intracranial aneurysms: A meta- analysis. Stroke. 1998; 29: 1531- 8. 17. Johnston SC, Dudley RA, Gress DR, Ono L. Surgical and endovas­cular treatment of unruptured cerebral aneurysms at university hos­pitals. Neurology. 1999; 52: 1799- 805. 18. Johnston SC, Wilson CB, Halbach VV, et al. Endovascular and sur­gical treatment of unruptured cerebral aneurysms: comparison of risks. Ann Neurol. 2000; 48: 11- 9. 19. Thornton J, Bashir Q, Aletich VA, et al. What percentage of surgi­cally clipped intracranial aneurysms have residual necks? Neuro­surgery. 2000; 46: 1294- 8; discussion 1298- 300. 20. Forsting M, Albert FK, Jansen O, et al. Coil placement after clip­ping: endovascular treatment of incompletely clipped cerebral an­eurysms. Report of two cases,. J Neurosurg. 1996; 85: 966- 9. 21. Kuether TA, Nesbit GM, Barnwell SL. Clinical and angiographic outcomes, with treatment data, for patients with cerebral aneurysms treated with Guglielmi detachable coils: A single- center experience. Neurosurgery. 1998; 43: 1016- 25. 22. Vinuela F, Duckwiler G, Mawad M. Guglielmi detachable coil embolization of acute intracranial aneurysm: Perioperative ana­tomic and clinical outcome in 403 patients. J Neurosurg. 1997; 86: 475- 82. 23. Thornton J, Debrun GM, Aletich VA, et al. Follow- up angiography of intracranial aneurysms treated with endovascular placement of Guglielmi detachable coils. Neurosurgery. 2002; 50: 239- 49; discus­sion 249- 50. 24. Hayakawa M, Murayama Y, Duckwiler GR, et al. Natural history of the neck remnant of a cerebral aneurysm treated with the Guglielmi detachable coil system. J Neurosurg. 2000; 93: 561- 8. 25. Gruber A, Killer M, Bavinzski G, Richling B. Clinical and angio­graphic results of endosaccular coiling treatment of giant and very large intracranial aneurysms: A 7- year, single- center experience. Neurosurgery. 1999; 45: 793- 803; discussion 803- 4. 26. Mericle RA, Wakhloo AK, Lopes DK, et al. Delayed aneurysm re-growth and recanalization after Guglielmi detachable coil treat­ment. Case report. J Neurosurg. 1998; 89: 142- 5. 27. Piotin M, Mandai S, Murphy KJ, et al. Dense packing of cerebral aneurysms: An in vitro study with detachable platinum coils. AJNR Am J Neuroradiol. 2000; 21: 757- 60. 28. Turjman F, Massoud TF, Sayre J, Vinuela F. Predictors of aneurys­mal occlusion in the period immediately after endovascular treat­ment with detachable coils: A multivariate analysis. AJNR Am J Neuroradiol. 1998; 19: 1645- 51. 29. Fernandez Zubillaga A, Guglielmi G, Vinuela F, Duckwiler GR. Endovascular occlusion of intracranial aneurysms with electrically detachable coils: correlation of aneurysm neck size and treatment results. AJNR Am J Neuroradiol. 1994; 15: 815- 20. 30. Kawanabe Y, Sadato A, Taki W, Hashimoto N. Endovascular oc­clusion of intracranial aneurysms with Guglielmi detachable coils: Correlation between coil packing density and coil compaction. Acta Neurochir. 2001; 143: 451- 5. 31. Feely M, Kapoor S. Third nerve palsy due to posterior communi­cating artery aneurysm: the importance of early surgery. J Neurol Neurosurg Psychiatry. 1987; 50: 1051- 2. 32. Fujiwara S, Fujii K, Nishio S, et al. Oculomotor nerve palsy in patients with cerebral aneurysms. Neurosurg Rev. 1989; 12: 123- 32. 33. Giombini S, Ferraresi S, Pluchino F. Reversal of oculomotor disor­ders after intracranial aneurysm surgery. Acta Neurochir. 1991 ; 112: 19- 24. 34. Grayson MC, Soni SR, Spooner VA. Analysis of the recovery of third nerve function after direct surgical intervention for pos­terior communicating aneurysms. Br J Ophthalmol. 1974; 58: 118- 25. 35. Hamer J. Prognosis of oculomotor palsy in patients with aneurysms of the posterior communicating artery. Acta Neurochir. 1982; 66: 173- 85. 36. Kyriakides T, Aziz TZ, Torrens MJ. Postoperative recovery of third nerve palsy due to posterior communicating aneurysms. Br J Neu­rosurg. 1989; 3: 109- 11. 37. Soni SR. Aneurysms of the posterior communicating artery and oculomotor paresis. J Neurol Neurosurg Psychiatry. 1974; 37: 475- 84. 38. Yanaka K, Matsumaru Y, Mashiko R, et al. Small unruptured cere­bral aneurysms presenting with oculomotor nerve palsy. Neurosur­gery. 2003; 52: 553- 7; discussion 556- 7. 39. Leivo S, Hernesniemi J, Luukkonen M, Vapalahti M. Early surgery improves the cure of aneurysm- induced oculomotor palsy. Surg Neurol. 1996; 45: 430- 4. 40. Birchall D, Khangure MS, McAuliffe W. Resolution of third nerve paresis after endovascular management of aneurysms of the poste­rior communicating artery. AJNR Am J Neuroradiol. 1999; 20: 411- 3. 9 JNeuro- Ophthalmol, Vol. 24, No. 1, 2004 Bhatti et al. 41. Inamasu J, Nakamura Y, Saito R, et al. Early resolution of third nerve palsy following endovascular treatment of a posterior com­municating artery aneurysm. JNeuroophthalmol. 2002; 22: 12^ 1. 42. Uda K, Murayama Y, Gobin YP, et al. Endovascular treatment of basilar artery trunk aneurysms with Guglielmi detachable coils: clinical experience with 41 aneurysms in 39 patients. JNeurosurg. 2001; 95: 624- 32. 43. Eskridge JM, Song JK. Endovascular embolization of 150 basilar tip aneurysms with Guglielmi detachable coils: results of the Food and Drug Administration multicenter clinical trial. J Neurosurg. 1998; 89: 81- 6. 44. Halbach VV, Higashida RT, Dowd CF, et al. The efficacy of en-dosaccular aneurysm occlusion in alleviating neurologic deficits produced by mass effect. J Neurosurg. 1994; 80: 659- 66. 45. Malisch TW, Guglielmi G, Vinuela F, et al. Unruptured aneurysms presenting with mass effect symptoms: Response to endosaccular treatment with Guglielmi detachable coils. Part I. Symptoms of cra­nial nerve dysfunction. J Neurosurg. 1998; 89: 956- 61. 46. Lanzino G, Andreoli A, Tognetti F, et al. Orbital pain and unrup­tured carotid- posterior communicating artery aneurysms: The role of sensory fibers of the third cranial nerve. Acta Neurochir. 1993: 120: 7- 11. 10 © 2004 Lippincott Williams & Wilkins