Management of giant intracranial aneurysms of the posterior circulation
Michael Besser MBBS, FRACS, FRCS(Canada), Vini G. Khurana MBBS, BSc(Med) Department of Neurosurgery, Royal Prince Alfred Hospital, Sydney, Australia
Between 1980 and 1995, 14 patients underwent treatment at Royal Prince Alfred Hospital for giant posterior circulation aneurysms. Two (14%) patients presented with subarachnoid haemorrhage (SAH). Eight (57%) of the 14 giant aneurysms were located at the basilar caput. A total of 7 (50%) contained significant intraluminal thrombus. Surgery was undertaken in 10 (72%) patients and endovascular embolization in the remaining 4 (28%). Of the patients treated surgically, 3 underwent clipping and a further 4 underwent Hunterian ligation. Of the 4 patients in whom embolization was carried out, 2 were coil treated and 2 balloon treated. Six (60%) patients undergoing surgery experienced significant complications, but in only 4 (40%) surgically treated patients was the complication directly attributable to the surgical procedure. All 4 (100%) patients treated interventionally suffered major complications, and in 3 (75%) of these the complication was directly attributable to the endovascular procedure. The clinical outcome at a median of 12 months follow-up was favourable in 8 (62%) of the 13 patients for whom follow-up information was available. We conclude that radiological techniques are not satisfactory for direct treatment of giant posterior circulation aneurysms and surgical exploration is advisable. In addition, timely referral to, and well planned management at, an experienced centre will undoubtedly contribute significantly towards securing a more favourable overall outcome.
Journal of ClinicalNeuroscience 1998, 5 (2): 161-168
© Harcourt Brace & Co. Ltd 1998
Keywords: giant aneurysm; posterior circulation; surgical treatment; endovascular embolization
Introduction Giant intracranial aneurysms, measuring 25 m m or greater, comprise approximately 5% of all aneurysms 1 and typically present with symptoms and signs related to mass effect rather than subarachnoid h a e m o r r h a g e (SAIl) ?,~ The natural history of giant aneurysms is associated with rates of morbidity and mortality that are significantly higher than those of their smaller counterparts. >1° It is well known that u n r u p t u r e d giant and n e a r giant aneurysms have a higher probability of subsequent rupture than smaller ones u,12 and that aneurysmal t h r o m b o sis, even if extensive, does not preclude a n e u r y s m growth ~3 o r r u p t u r e . 4,14,~5 F u r t h e r m o r e , a recent study of 105 r u p t u r e d giant aneurysms ~ indicates that the rate of rebleeding a m o n g s t such lesions may be equal to or greater than that for smaller a n e u r y s m s ) 6,17 The most satisfactory treatment of giant aneurysms is t h r o m b e c t o m y followed by p l a c e m e n t of a clip across the neck of the lesion) 8,19 However, for a variety of reasons m a n y giant aneurysms, particularly those of the posterior circulation, are not readily amenable to clipping. ~8,2° For example, the large size of the aneurysm is often associated with a wide neck and there is frequently close proximity of the lesion to diencephalic or brain stem structures. F u r t h e r m o r e , perforating vessels may be
f o u n d incorporated into the wall of the aneurysmal neck. Occasionally, the p a r e n t vessel itself is found included withing the sac and the aneurysmal wall may have undergone atherosclerotic change, making a clip p l a c e m e n t significantly m o r e difficult. As a result, giant aneurysmal surgery often requires t e m p o r a r y (sometimes prolonged) arterial occlusion intraoperatively, 2~,22 and perhaps perm a n e n t proximal vessel occlusion. 23,24 It is no surprise, therefore, that the risk of ischaemic complications related to m a n a g e m e n t of giant aneurysms is significant. 7 Several studies have indicated a p o o r e r overall outc o m e for aneurysms, particularly the giant ones, of the posterior circulation c o m p a r e d to those located anteriorly. 19,21,24-26 In two large series including b o t h u n r u p tured and r u p t u r e d giant intracranial aneurysms, a favourable o u t c o m e for surgically treated anterior circulation aneurysms was r e p o r t e d in 84% by Drake 25 and in 79% by Sundt. 21 For posterior aneurysms such an outc o m e was r e p o r t e d in 65% by Drake and 74% by Sundt. A m o n g 80 surgically treated giant aneurysms, Sundt and Piepgras I9 n o t e d an overall rate of morbidity of 14%, although the rate was as high as 50% for lesions located in the posterior circulation. Finally, Drake's series 24 of 201 patients who u n d e r w e n t proximal occlusion of their posterior circulation aneurysms, 87% of which were
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Clinical studies giant, indicated an unfavourable outcome in over 25%. This is compared with an unfavourable outcome of approximately 15 % among patients with giant aneurysms of the anterior circulation treated in a similar m a n n e r Y Neuroradiological techniques are gaining increasing acceptance as an effective alternative to surgery in the treatment of eerebrovascular lesions, including aneurysms, in selected patients. 27-34However, indications for direct endovascular aneurysm treatment are still controversial. Medical instability precluding the use of a general anaesthetic and failed surgical repair are the most obvious? 4 On the other hand, fusiform and broad-based aneurysms without well defined surgical necks remain difficult m a n a g e m e n t problems for either surgical or endovascular therapy. Endovascular treatment is not without significant risks; 33-37these include balloon deflation causing aneurysmal refilling and regrowth, balloon rupture leading to cerebral ischaemia, cerebral abscess formation, transient ischaemic attacks from herniation of the intra-aneurysmal embolization apparatus into the carotid or vertebrobasilar circulation, completed stroke from occlusion of distal vasculature from dislodgement or frank migration of the apparatus, arterial or aneurysmal rupture from trauma during endovascular navigation, incomplete intra-aneurysmal occlusion, with or without recanalization of the thrombus, leading to further progression of the lesion, and increased risk of intracranial haemorrhage from the concomitant use of systemic anticogulants. Further, a recent histopathological study ss has demonstrated the presence of unorganized, friable blood clot within the aneurysm and a r o u n d the intra-aneurysmal embolization system even at 6 months after its insertion. The issue of efficacy of endovascular treatment of aneurysms has been addressed by several groups? 2-36,3941 In a multicentre study of 120 aneurysm patients undergoing coiling carried out by Guglilmi et al, 39 the overall morbidity among 42 patients with posterior circulation aneurysms treated in this m a n n e r was found to be 4.8% and the overall mortality 2.4%. A generally favourable outcome was found for the subgroup of 10 patients with exclusively giant aneurysms, although the average follow-up for these patients was only 4 weeks. Furthermore, the authors reported that among 26 patients in the series with wide aneurysmal necks, complete occlusion was possible in only 4 (15%)? 9 Casasco and colleagues 4° have reported that platinum coil treatment of 71 aneurysms, 59% of which were vertebrobasilar and 53% of which were large or giant, resulted in a good overall outcome in 84.5% of cases in 12 months. However, they noted that among the subgroup of patients with exclusively giant aneurysms, the result at 6 months was 70% good, 10% poor and 20% dead, with only 60% of giant aneurysms achieving total occlusion. 4° Given the high rates of morbidity and mortality associated with giant intracranial aneurysms of the posterior circulation, the aim of the present study was to describe the experience of a tertiary referral institution in the treatment of patients with these lesions. The various complications associated with the different treatment modalities and the overall clinical outcome have also been
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Giant posterior circulationaneurysms addressed. The considerable technical difficulties posed by posterior circulation giant aneurysms obviate the n e e d for timely referral to, and careful planning at, experienced neurosurgical centres.
Clinical m a t e r i a l s and m e t h o d s This study represents a retrospective analysis of all patients admitted to Royal Prince Alfred Hospital between 1980 and 1995 with a diagnosis of giant posterior circulation aneurysm.
Demographic data T h e r e was a total of 14 patients, ranging in age from 17 to 76 years, with a median age of 49 years. O f the 14 patients, 8 were male and 6 female. A history of hypertension was present in half of the patients, whilst 2 (14%) of the patients had a family history of aneurysmal SAH.
Diagnostic details Irrespective of clinical presentation, all patients were investigated by c o m p u t e d tomography (CT) a n d / o r magnetic resonance imaging (MRI). Magnetic resonance angiography (MRA) was used to aid diagnosis in two patients and a diagnostic lumbar puncture was carried out in one other. All 14 patients u n d e r w e n t cerebral angiography with an aneurysmal lesion demonstrated in each case. In one patient u n d e r g o i n g diagnostic angiography, concomitant cerebrovascular spasm was noted. It is also of interest that hydrocephalus was demonstrated radiologically in 4 (30%) of the 12 patients with unruptured lesions, while SAH was diagnosed in 2 others.
Aneurysm specifications All aneurysms were giant lesions, that is, greater than or equal to 25 m m in size. All were located in the posterior circulation, the most c o m m o n site being the basilar caput (n = 8). O t h e r aneurysm sites and characteristics are summarized in Table 1. Some degree of intraaneurysmal thrombosis was noted in 7 of 11 cases in which the presence or absence of thrombus was specified. Single aneurysms were f o u n d in all but one patient, the exception having both a giant basilar caput aneurysm and a 10 m m aneurysm of the left middle cerebral artery.
Clinical characteristics O f the 14 patients, 2 (14%) presented SAH; the remaining 12 patients (86%) had u n r u p t u r e d lesions. Nine patients presented with evidence of raised ICP, eight with cranial nerve palsy and eight with a focal neurological deficit. Among the 12 patients who presented with mass effect due to an enlarging u n r u p t u r e d lesion, the median length of history of progressive symptoms and signs was 6 months (range 1-12 months). Assessment of the patient's neurological grade on admission, preoperatively and at the time of discharge from hospital was made according to three grades: 'excellent' or no significant neurological deficit; 'good'
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Giant posterior circulation aneurysms Table 1
Clinical studies
Specifications of 14 giant posterior circulation aneurysms
Variable
Cases Number
Neurological state
Percent
(Size range in mm) Distribution Basilar caput Posterior cerebral Vertebral trunk Basilar trunk PICA* (Total)
8 2 2 1 1 (14)
57 14 14 7 7 (100)
Extent of aneurysmal thrombosis None Partial Extensive Not specified (Total)
4 6 1 3 (14)
29 43 7 21 (100)
(25-30)
Excellent Good Poor (Total)
Admission n
Preop n
Discharge n
4 9* 1 (14)
4 8 2* (14)
8 4 2 (14)
*Preoperative neurological deterioration in one patient due to cerebral vasospasm. Table 3 Surgical and interventional treatment of 13" giant posterior circulation aneurysms Procedure
*PICA = posterior cerebellar artery.
or m i n o r neurological deficit; and ' p o o r ' or major deficit; this is given in Table 2. O n e patient who was admitted in g o o d neurological grade following SAIl f r o m a r u p t u r e d aneurysm deteriorated preoperatively, the cause attributed to radiologically demonstrable cerebrovascular spasm. Both patients who presented following SAtI were admitted in modified Botterell Grade 2. 7 Aneurysm
Table 2 Neurological status on admission, preoperative and at discharge
Number
Surgery Direct Clipping Indirect Hunterian ligation Simple trapping Ventriculoperitoneal shunt (Total)
4 1 1 (9)
Embolization Coil Balloon (Total)
2 2 (4)
3
*One patient lost to follow-up.
Surgery
treatment
All aneurysms were treated by either surgery or endovascular embolization. Surgery was either direct (clipping) or indirect ( H u n t e r i a n ligation, simple trapping, or ventriculoperitoneal (VP) shunt insertion), while endovascular embolization involved the use of either a detachable coil or balloon.
Morbidity and mortality A m o n g patients in w h o m surgery was carried out, 'surgical', as o p p o s e d to 'medical', complications were those directly attributable to the operative procedure. Similarly, a m o n g patients treated by endovascular means, 'interventional', as o p p o s e d to 'medical', complications were those directly the result of the interventional procedure.
Outcome M a n a g e m e n t results were assessed at the time of last medical follow-up, which o c c u r r e d between 4 m o n t h s and 13 years (median 12 months) after the definitive procedure. Five categories of assessment were used (excellent, good, poor, dead and lost to follow-up) as defined by Sundt and Whisnant. s W h e r e specified, a favourable o u t c o m e refers to one that was either excellent or good.
RESULTS Treatment All aneurysms were treated by either surgical or endovascular m e a n s as s u m m a r i z e d in Table 3.
Direct surgery was carried o u t in three patients with u n r u p t u r e d lesions (Fig. 1). In one of these, clipping was carried out after previous H u n t e r i a n ligation of a trilobed giant basilar c a p u t aneurysm failed to prevent an increase in the size of the lesion, which subsequently manifested as progressive bulbar palsy and quadriparesis. This patient also had an u n r u p t u r e d 10 m m left middle cerebral artery aneurysm which was also clipped at the time of re-operation. Indirect surgery was carried out in 6 patients. In 4 of these, the lesion was treated by H u n t e r i a n ligation (Fig. 2). O f the remaining 2, simple trapping of the aneurysm was carried out in one (Fig. 3), while sole p l a c e m e n t of a VP shunt was done in the other. In the case of the latter patient, a 76-year-old w o m a n with an u n r u p t u r e d giant basilar caput a n e u r y s m who h a d presented with a clinical and radiological picture of obstructive hydrocephalus, p l a c e m e n t of a VP shunt was associated with excellent short- and intermediate-term clinical outcome. However, late r u p t u r e of the original lesion resulted in a fatal SAEI 2 years postoperatively.
Embolization Four patients were treated by embolization, 2 via a detachable balloon and 2 via a coil (Fig. 4). In three of the four patients embolization was u n d e r t a k e n after failure of surgical means such as a t t e m p t e d clipping a n d / o r H u n t e r i a n ligation. In the r e m a i n i n g patient, coil embolization of the u n r u p t u r e d giant posterior inferior cerebellar artery (PICA) aneurysm was carried out as the p r i m a r y definitive procedure.
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Giant posterior circulation aneurysms
Fig, 2 Hunterian ligation of a giant basilar caput aneurysm. (A) Anteroposterior (AP) angiogram. (B) Postoperative AP angiogram (vertebral injection). (C) Postoperative angiogram (carotid injection) demonstrating filling of upper basilar vessels via posterior communicating artery,
Morbidity and mortality
Fig. 1 Clipping of giant vertebral artery aneurysm. (A) Axial T1 MRI scan. (B) Lateral vertebral angiogram. (C) Postoperative lateral vertebral angiogram.
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Of the 10 patients treated by surgery, 6 suffered a significant complication. In 4 of these, the event was directly attributable to surgery (Table 4). Postoperative complications in the other 2 patients were perforated duodenal ulcer in one, and pneumonia plus general sepsis in the other. All 4 patients with aneurysms treated by embolization suffered a major complication, 3 being directly attributable to the interventional procedure (Table 4).
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Fig, 3 Trapping of giant posterior cerebral artery aneurysm. (A) Coronal T1 MRI scan. (B) Lateral vertebral angiogram. (C) Anteroposterior (AP) vertebral angiogram. (D) Postoperative AP vertebral angiogram.
Fig~ 4 Surgicaland endovascular treatment of an aneurysm complex including a giant left basilar-superior cerebellar artery aneurysm. (A) Anteroposterior (AP) angiogram. (B) Postoperative AP angiogram following direct surgery and Guglielmi Detachable Coil (GDC) embolization (note some residual neck).
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Clinical studies
Giant posterior circulation aneurysms Table 4
Non-medical complications of surgical and interventional management
Procedure
Site of aneurysm
Complication
Surgical 1 Hunterian ligation 2 Hunterian ligation 3 VP Shunt 4 Attempted clipping
VA BC BC PCA
Brain stem ischaemia Cerebral ischaemia Shunt blockage; latent fatal SAH Intraoperative haemorrhage
Interventional 1 Coil 2 Balloon 3 Coil
PICA BC BC
Acute brain stem compression Brain stem infarct (balloon shift) SAH Aneurysmal neck enlargement
VP = ventriculoperitoneal; VA = vertebral artery; BC = basilar caput; PCA = posterior cerebral artery; PICA = posterior inferior cerebellar artery; SAH = subarachnoid haemorrhage.
Table 5
Overall outcome according to treatment m o d a l i t y *
Outcome Excellent Good Poor Dead LTFU+ (Total)
Surgery n
Embolization n
Total n
5 1 2 1 1 (10)
2 0 0 2 0 (4)
7 1 2 3 1 (14)
* A t last medical f o l l o w - u p (median 12 months). +LTFU = lost to follow-up.
The remaining patient suffered a massive p u l m o n a r y embolus post embolization.
Surgical complications One patient who u n d e r w e n t Hunterian ligation of a 30 m m right vertebral artery aneurysm suffered from a partial right lateral medullary syndrome postoperatively, the deficit attributed to ligature-induced ischaemia. Another patient in whom Hunterian ligation of a giant basilar caput aneurysm was carried out subsequently developed right occipital and thalamic ischaemia resulting in aphasia, hemiparesis and hemianopia (all gradually resolved). In a third patient, described above, early favourable outcome from placement of a VP shunt was followed by shunt blockage (with successful revision) at 12 months and fatal SAH at 2 years following the initial surgery. In the fourth patient, massive intraoperative haemorrhage from inadvertent laceration of the left lateral sinus occurred, without significant postoperative neurological sequelae. This patient was planned for subsequent surgery but was lost to follow-up.
Interventional complications Of the three patients in whom major interventional complications occurred, one suffered acute brain stem compression and obstructive hydrocephalus due to rapid thrombosis within the left PICA aneurysmal sac induced by coiling. This necessitated emergency posterior fossa craniectomy with insertion of a VP shunt. Another patient with a giant basilar caput aneurysm in which a detachable balloon was inserted suffered a large brain stem and left PC& territory ischaemic stroke to inadvertent balloon shift 3 days after insertion. The patient eventually died of
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fatal SAH from latent rupture of the lesion. Finally, progressive enlargement of the aneurysmal neck was demonstrated by serial follow-up cerebral angiography of a third patient who had u n d e r g o n e coiling of a ruptured giant basilar caput aneurysm complex (see Fig. 4).
Outcome At a median of 12 months' follow-up, a favourable outcome (7 excellent, 1 good) was obtained in 8 (62%) of the 13 patients for whom follow-up information was available. The outcome for 2 other patients was poor, 1 patient suffering persistent bulbar palsy and quadriparesis, the other suffering from ongoing major preoperative illnesses (hepatic cirrhosis and congestive cardiac failure) in addition to postoperative seizures and lateral medullary syndrome. T h r e e patients were dead at last follow-up. In one, death was attributable to latent aneurysmal SAH from failed balloon embolization of the lesion. In another, a massive p u l m o n a r y embolization within days of balloon embolization occurred. Late rupture of an aneurysm whose effects had been treated by VP shunt only caused the third fatality. One of the 14 patients was lost to follow-up. The clinical outcome according to treatm e n t modality for patients in our series is shown in (Table 5).
Discussion Aneurysm treatment Surgery versus embolization Although surgery is not possible in all instances, it is widely regarded that direct surgical obliteration of an aneurysm constitutes the best definitive treatment. 18,19,91 Particular technical difficulties arise in the subgroup of patients h a r b o u r i n g ' g i a n t posterior circulation aneurysms, namely the proximity of brain stem structures and the close presence or incorporation of perforation vessels. Despite these factors, however, the highly unfavourable natural history associated with such lesions makes definitive treatment m a n d a t o r y whenever possible, although the choice between surgical and endovascular therapy remains a matter of controversy?7'38'4°'41In the present study, as in other series, ~9-36,39 radiological embolization was typically carried out for patients in
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Clinical studies
whom failure (or acknowledgement of the likelihood of failure) of surgical means such as clipping a n d / o r Hunterian ligation had occurred. The biophysical basis of interventional embolization techniques, detailed descriptions of which may be f o u n d elsewhere ~1,~4,42 is the induction of thrombosis by mechanical a n d / o r electrochemical means within the aneurysmal sac, the basic premise being that stable intraaneurysmal thrombosis will confer a significant degree of protection against further progression of the lesion. However, several studies have f o u n d that intra-aneurysreal thrombosis, even if extensive, does not preclude rupture of the lesion, 4,14'I5 n o r does it preclude further growth 13 or rerupture of the aneurysm, processes probably linked to the development of intrathrombotic capillary channels} 3 In addition, a recent histopathological study 3s demonstrating the presence of unorganized, friable blood clot within and a r o u n d the intra-aneurysmal coil system, even after 6 months in vivo, suggests that patients undergoing such a procedure may be at a heightened risk of distal thromboembolism from, or frank rupture of, the aneurysm. T h e r e is no doubt that such a risk is greatly magnified in larger aneurysms, in which the volumes of clotting are much greater and the process of resolution correspondingly prolonged. 3s Furthermore, the difficulty of interventional treatment in achieving p e r m a n e n t total occlusion of aneurysms, particularly those with wide necks, has been widely documented. 3-9'34'~7-4°Reports of the p r o p o r t i o n of subtotally occluded interventionally treated aneurysms vary from 8% reported by Moret et a143 in a series of patients with predominantly smaller u n r u p t u r e d aneurysms, up to 40% r e p o r t e d by Casasco et al. 4° among a subpopulation of patients with giant lesions. The significance of subtotal occlusion, the likelihood of which increases with aneurysm size, 4° is the c o m p o u n d e d predisposition towards aneurysmal regrowth and rupture. One important role that endovascular techniques play in the treatment of giant posterior circulation aneurysms is to assist in the demonstration of the definitive neck of a giant aneurysm (otherwise obscured by thrombus or jetstream distortion) through microcatheterization procedures. In addition, trial balloon occlusion can yield important preoperative information with regard to tolerance of a trapping p r o c e d u r e or proximal Hunterian ligation if indirect surgical obliteration, in particular clipping, of an aneurysm constitutes the best definitive treatment and that, whenever possible, surgical exploration is advisable.
procedures being 30% and 75%, respectively. Despite the relatively low numbers of patients in both treatment groups, these complication rates serve to highlight the fact that, in our experience, although surgery for giant posterior circulation aneurysms carries a significant rate of morbidity and mortality, radiological techniques for such lesions are even less satisfactory. It is of interest to note that, in keeping with the dismal natural history of this condition, one patient in whom a VP shunt was placed as the only form of treatment and another in whom a detachable balloon subsequently shifted out of the aneurysm, both suffered fatal SAIt from latent aneurysmal rupture. Outcome
Several studies have indicated a p o o r e r overall outcome for giant aneurysms compared to smaller ones, with the prognosis worsening for lesions arising from the posterior circulation. 19,21,23,2~ Among patients with posterior circulation giant aneurysms treated surgically, the series of Drake 25 reports a 35% unfavourable outcome, whilst that of Sundt 21 reports a similar outcome in 26%. In our series an unfavourable overall outcome at a median of 12 mouths was obtained in 38% of patients for whom adequate follow-up information was available. Similar to the findings of Drake and Sundt, this proportion was 33% for the subpopulation of patients in our study treated surgically. In a subgroup of giant aneurysms treated interventionally by Casasco et al 4° the overall poor outcome at 6 months was 30%. Among patients in our series treated interventionally, at a median of 7 months, 50% had an overall unfavourable outcome, but again the significance of our data is limited by the relatively small n u m b e r of patients in our treatment group.
Conclusion Giant posterior circulation aneurysms pose particular management difficulties and are associated with high rates of morbidity and mortality. Surgical exploration is advisable and endovascular embolization techniques are generally not satisfactory in the direct treatment of such lesions. Although total wall excision is not indicated, aneurysmorrhaphy and thrombectomy are usually required. Careful planning at experienced referral centres is desirable in order to effect a more favourable overall outcome. Received 26 February 1996 ; Accepted 15 March 1996
Correspondence and offprint requests: Dr Michael Besser, RPAH Medical Centre, 100 Carillon Avenue, Newtown 2042, Australia, Tel: 61 2 9519 9669, Fax: 61 2 9517 2503
Morbidity and m o r t a l i t y The high rates of morbidity and mortality associated with intracranial aneurysms are well recognized. 3 The greater the proportion of procedural complications associated with larger aneurysms, in particular those of the posterior circulation, are also widely known. 19,21,23-26In the present study, 60% of patients treated surgically and 100% of patients treated interventionally experienced significant complications, the rates directly attributable to definitive
References 1. Peerless SJ, Wallace MC, Drake CG. Giant intracranial aneurysms. In: YoumansJR (ed). Neurological Surgery, Vol 7. Philadelphia: WB Saunders, 1990. 2. Sengupta RP. Management of large and giant aneurysms. Neurosurg Rev 1982; 5: 173-178. 3. Weir B. Aneurysms Affecting The Nervous System. Baltimore: Williams and Wilkins, 1987.
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Clinical studies 4. Drake CG. Giant intracranial aneurysms. Experience with surgical treatment in 174 patients. Clin Neurosurg 1979; 26: 12-95. 5. Kassell NF, TornerJC, Clarke Haley E Jr et al. The International Cooperative Study on the timing of aneurysm surgery.J Neurosurg 1990; 73: 18-47. 6. Onuma T, SuzukiJ. Surgical treatment of giant intracranial aneurysms. J Neurosurg 1979; 51: 33-36. 7. Sundt TMJr, WhisnantJR Subarachnoid haemorrhage form intracranial aneurysms: surgical management and natural history of disease. N EnglJ Med 1978; 299: 116-122. 8. Symon L. Surgical experiences with giant intracranial aneurysms. Acta Neurochir 1992; 118: 53-58. 9. Whittle IR, Dorsch NW, Besser M. Giant intracranial aneurysms: diagnosis, management and outcome. Surg Neurol 1984; 21: 218-230. 10. RosenornJ, Eskesen V. Patients with ruptured intracranial saccular aneurysms: clinical features and outcome according to the size. BrJ Neurosurg 1994; 8: 73-78. 11. Wiebers DO, WhisnantJP, Sundt TMJr et al. The significance of unruptured intracranial saccular aneurysms.J Neurosurg 1987; 66: 23-29. 12. Juvela S, Porras M, Heiskanen O. Natural history of unruptured aneurysms: a long-term follow-up study. J Neurosurg 1993; 79: 174-182. 13. Nagahiro S, Takada A, Goto S, Kai Y, Ushio Y. Thrombosed growing giant aneurysms of the vertebral artery: growth mechanism and management. J Neurosurg 1995; 82: 796-801. 14. Swearingen B, Heros RC. Fatal rupture of a thrombosed giant basilar artery aneurysm. Surg Neurol 1985; 23: 299-302. 15. Whittle IR, Dorsch NW, Besser M. Spontaneous thrombosis in giant intracranial aneurysms. J Neurol Neurosurg Psychiatry 1982; 45: 1040-1047. 16. Kassell NF, TornerJC. Aneurysmal rebleeding: a preliminary report from the Cooperative Aneurysm Study. Neurosurgery 1983; 13: 479-481. 17. TornerJC, Kassell NF, Wallace RB et al. Preoperative prognostic factors for rebleeding and survival in aneurysm patients receiving antifibrinolytic therapy: report of the Cooperative Aneurysm Study. Neurosurgery 1981; 9: 506-513. 18. Symon L, VajdaJ. Surgical experiences with giant intracranial aneurysms. J Neurosurg 1984; 61: 1009-1028. 19. Sundt TMJr, Piepgras DG. Surgical approach to giant intracranial aneurysms: operative experience with 80 cases.J Neurosurg 1979; 51: 731-742. 20. Hosobuchi Y. Direct surgical treatment of giant intracranial aneurysms.J Neurosurg 1979; 51: 743-756. 21. Sundt TMJr. Giant aneurysms. Neurosurgeons 1989; 8: 230-243. 22. Sundt TMJr. Surgical techniques for saccular and giant intracranial aneurysms. Baltimore: Williams and Wilkins, 1990. 23. Drake CG, Peerless SJ, Ferguson GC. Hunterian proximal arterial occlusion for giant aneurysms of the carotid circulation.J Neurosurg 1994; 81: 656-665. 24. Steinberg GK, Drake CG, Peerless SJ. Deliberate basilar or vertebral artery occlusion in the treatment of intracranial aneurysms: immediate results and long-term outcome in 201 patients.J Neurosurg 1993; 79: 161-173. 25. Drake CG. The treatment of aneurysms of the posterior circulation. Clin Neurosurg 1979; 26: 96-144. 26. Schievink Wl, Wijdicks EFM, Piepgras DG, Chu C-P, O'Fallon M, WhisnantJR The poor prognosis of ruptured
168
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27. 28. 29. 30.
31.
32.
33.
34.
35.
36.
37. 38.
39.
40. 41.
42.
43.
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intracranial aneurysms of the posterior circulation. J Neurosurg 1995; 82: 791-795. Luessenhop AJ, Velasquez AC. Observation on the tolerance of the intracranial arteries to eatheterisation. J Neurosurg 1964; 21: 85-91. Serbinenko FA. Catheterization and occlusion of cerebral major vessels and prospects for the development of vascular neurosurgery. Vopr Neirokhir 1971; 35: 17-27. Serbinenko FA. Balloon catheterization and occlusion of major cerebral vessels. J Neurosurg 1974; 41: 125-145. Hilal SK. Synthetic coated platinum coils successfully used for the endovascular treatment of arteriovenous malformations, aneurysms and direct arteriovenous fistulae of the central nervous system. Radiology 1988; 169 [Suppl] : 28-29. Guglielmi G, Vinuela F, Sepetka I, Macellari V. Electrothrombosis of saccular aneurysms via endovascular approach. Part 1: electrochemical basic technique, and experimental results.J Neurosurg 1991; 75: 1-7. Gugliemi G, Viiauela F, DionJ, Duckwiler G. Electrothrombosis of saccular aneurysms via endovascular approach. Part 2: preliminary clinical experience. J Neurosurg 1991; 75: 8-14. Higashida RT, Halbach W, Dowd CF, Barnwell SL, Hieshima GB. Interventional neurovascular treatment of a giant intracranial aneurysm using platinum microcoils. Surg Neurol 1991; 35: 64-68. Higashida RT, Halbach VV, Dowd CF, Barnwell SL, Hieshima GB. Intracranial aneurysms: interventional neurovascular treatment with detachable balloons. Radiology 1991; 178: 663-670. Fox AJ, Vinuela F, Pelz DM et al. Use of detachable balloons for proximal artery occlusion in the treatment of unclippable cerebral aneurysms. J Neurosurg 1987; 66: 40-46. HodesJE, Aymard A, Gobin Pet al. Endovascular occlusion of intracranial vessels for curative treatment of unclippable aneurysms: report of 16 cases. J Neurosurg 1991; 75: 694-701. Nichols DA. Endovascular treatment of acutely ruptured intracranial aneurysm.J Neurosurg 1993; 79: 1-2. Molyneux AJ, Ellison DW, Morris J, ByrneJV. Histological findings in giant aneurysms treated with Gugliemi detachable coils: report of two cases with autopsy correlation.J Neurosurg 1995; 83: 129-132. Gugliemi G, Vinuela F, Duckwiler Get al. Endovascular treatment of posterior circulation aneurysms by electrothrombosis using electrically detachable coils. J Neurosurg 1992; 77: 515-524. Casasco AE, Aymard A, Gobin Pet al. Selective endovascular treatment of 71 intracranial aneurysms with platinum coils. J Neurosurg 1993; 79: 3-10. Halbach VV, Higashida RT, Dowd CF et al. The efficacy of endosaccular aneurysm occlusion in alleviating neurological deficits produced by mass effect. J Neurosurg 1994; 80: 659-666. Higashida RT, Halbach VV, Dormandy B et al. Endovascular treatment of intracranial aneurysms with a new silicone microballoon device: technical considerations and indications for therapy. Radiology 1990; 174: 687-691. MoretJ, Picard L, Mawad M et al. A critical study on endosaccular treatment of berry aneurysrns based on 60 cases. Presented at the 28th Annual Meeting of the American Society of Neuroradiology, Los Angeles, March 19-23, 1990.