KEY WORDS aneurysm mass effect embolization Guglielmi detachable coil coil. J. Neurosurg. / Volume 89 / December, J Neurosurg 89: , 1998

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1 J Neurosurg 89: , 1998 Unruptured aneurysms presenting with mass effect sypmtoms: response to endosaccular treatment with Guglielmi detachable coils. Part I. Symptoms of cranial nerve dysfunction TIM W. MALISCH, M.D., GUIDO GUGLIELMI, M.D., FERNANDO VIÑUELA, M.D., GARY DUCKWILER, M.D., Y. PIERRE GOBIN, M.D., NEIL A. MARTIN, M.D., JOHN G. FRAZEE, M.D., AND JOAN S. CHMIEL, PH.D. Division of Interventional Neuroradiology and Department of Neurosurgery, University of California Medical Center, Los Angeles, California; and Departments of Radiology and Preventive Medicine, Northwestern University Medical School, Chicago, Illinois Object. Embolization of intracranial aneurysms by using Guglielmi detachable coils (GDCs) is proving to be a safe method of protecting aneurysms from rupture. Occasionally, patients with unruptured intracranial aneurysms present with symptoms related to the aneurysm s mass effect on either the brain parenchyma or cranial nerves. In the present study, the authors conducted a retrospective review to evaluate the response to GDC embolization in a series of 19 patients presenting with cranial nerve dysfunction due to mass effect. Methods. Aneurysms were classified by size, shape, wall calcification, and amount of intraluminal thrombus. Patients were classified by duration of symptoms prior to GDC treatment (range 1 month to 10 years). Clinical assessment was performed within days of the GDC procedure and at later follow-up appointments (range 1 70 months, mean 24 months). In the immediate post GDC period, four patients experienced worsening of cranial nerve deficits. Two of the four patients had transient worsening of visual acuity, which later improved to better than baseline status. Another patient who had presented with headache and seventh and eighth cranial nerve deficits from a vertebrobasilar junction aneurysm had improvement in these symptoms, but developed a new diplopia. The fourth patient had worsening of her visual acuity, which had not resolved at the 1-month follow-up examination; this patient later underwent surgical decompression. Conclusions. On late follow-up review, the response was classified as complete resolution of symptoms in six patients (32%), improvement in eight patients (42%), no significant change in four patients (21%), and symptom worsening in one patient (5%). Patients with smaller aneurysms and those with shorter pretreatment duration of symptoms were more likely to experience an improvement in their symptoms following GDC treatment, although statistical significance was not reached in this series (p = and p = 0.111, respectively). The presence of aneurysmal wall calcification (six patients) or intraluminal thrombus (12 patients) showed no correlation with the response of mass effect symptoms in these patients. KEY WORDS aneurysm mass effect embolization Guglielmi detachable coil coil E NDOVASCULAR treatment of intracranial aneurysms by using the Guglielmi detachable coil (GDC) is proving to be a safe method of preventing aneurysm rupture ,24,25,39 Patients with unruptured intracranial aneurysms may present with symptoms related to the aneurysm s mass effect on either the brain parenchyma or cranial nerves. Previous reports have suggested that such symptoms can be affected by GDC embolization of the aneurysm. 11,17,18,22,24,25,38 This study was undertaken to evaluate the response of patients with cranial nerve deficits to endosaccular GDC treatment of unruptured intracranial aneurysms. 956 Clinical Material and Methods Between May 1990 and April 1997, 360 patients underwent GDC embolization of intracranial aneurysms at our institution. Thirty (8%) of these patients presented with symptoms of mass effect from an unruptured aneurysm. Eleven patients had symptoms of parenchymal compression and 19 patients presented with cranial nerve dysfunction. All 19 of the latter patients fulfilled the five criteria for inclusion in this series: 1) they had a cranial nerve deficit that could be objectively appreciated on examination; 2) the deficit could be explained by the location of

2 Endosaccular treatment of unruptured aneurysms with GDCs TABLE 1 Clinical presentation and aneurysm characteristics in 19 patients treated by GDC embolization* Case Age (yrs), Aneurysm Aneurysm Shape Degree of Wall Cal- Duration of No. Sex Aneurysm Location Size (mm) & Neck Size Thrombosis cification Presenting Clinical Signs Symptoms 1 38, M VB junction 45 fusiform majority CN VII & VIII palsies , F cavernous ICA 25 fusiform majority + CN III & VI palsies , F COA 38 saccular, W majority decreased visual acuity , F COA 43 saccular, W majority + binocular blindness , F PCoA 25 saccular, W minimal CN III palsy , F cavernous ICA 20 saccular, W majority CN VI palsy , F SCA 19 saccular, S majority CN VII palsy , F COA 7 saccular, S minimal CN III palsy , F COA 26 saccular, W majority monocular blindness , F P 1 /PCoA 10 bilobed saccular, S minimal visual field deficit , F SHA 24 saccular, W majority + visual field deficit , F cavernous ICA 10 saccular, W minimal CN III, IV, & VI palsies , F ACoA 22 saccular, W minimal decreased visual acuity , F PCoA 21 saccular, S majority + CN III palsy , F PCoA 23 saccular, S majority + CN III palsy , F COA 18 saccular, W minimal visual field deficit & decreased acuity , F trigeminal artery 14 saccular, W minimal CN III & VI palsies , F SCA 30 saccular, W majority CN III & IV palsies , F paraophthalmic ICA 35 saccular, W majority + decreased visual acuity 9 * ACoA = anterior communicating artery; CN = cranial nerve; P 1 = segment of posterior cerebral artery; S = small; W = wide; + = present; = absent. Duration of symptoms in months before GDC treatment. This patient presented with decreased visual acuity in 1987, which resolved after Selverstone clamping of the common carotid artery. Symptoms recurred in 1996 and had persisted for 9 months before GDC treatment. the aneurysm; 3) the aneurysm was unruptured; 4) the aneurysm was treated by endosaccular packing with GDCs; and 5) there was reliable clinical follow-up review after GDC treatment. Follow-up evaluation ranged from 1 to 70 months, with an average of 24 months and consisted of a review of medical records, telephone interviews with patients, and correspondence with the primary clinicians. All surviving patients were successfully contacted between April and July 1997; no patient was lost to follow-up review in this series. On follow-up examination, cranial nerve deficits were classified as resolved, improved, unchanged, or worsened. Symptom improvement was defined as objective improvement with increased functionality reported by the patient. In patients reaching follow-up endpoints of death or subsequent non-gdc intervention (aneurysm clipping or trapping or parent artery sacrifice), deficits were classified on the basis of function immediately before the endpoint. The patient population consisted of one man and 18 women (Table 1), whose ages ranged from 38 to 79 years (average age 62 years). Oculomotor nerve palsies and visual deficits (decreased acuity and/or field cuts) were the most frequent deficits and were present in eight patients. Other clinical presentations included diplopia due to dysfunction of the abducent (four patients) or trochlear (two patients) cranial nerves, and combined facial/vestibular nerve dysfunction (one patient). Five patients had multiple cranial nerve deficits. Headache was a common coexisting symptom that was present in six patients. Duration of symptoms before GDC treatment ranged from less than 1 month to longer than 10 years. Seventeen patients were considered by referring physicians to be at high risk because of aneurysm location (nine cases) or size (five cases), unsuccessful previous surgical attempt (four cases), poor patient medical condition (three cases), or calcification of the neck of the aneurysm (one case). Five of these patients had two risk factors for surgical treatment. Two patients had no obvious contraindications for surgery, but chose to be treated by GDC embolization. On the basis of angiographic data obtained at the time of embolization, the aneurysms were classified by size and shape. The method used for such measurements has been published previously. 9 Four aneurysms were small ( 15 mm in diameter), seven were large (15 25 mm), and eight were giant ( 25 mm in diameter). Computerized tomography scanning, magnetic resonance imaging, and angiographic data were also used to classify the degree of thrombus within the aneurysm lumen. Five aneurysms were saccular with small necks ( 4 mm), 12 were saccular with wide necks ( 4 mm), and two aneurysms were fusiform. Four aneurysms were located in the posterior circulation and 15 arose from the anterior circulation. Specifically, the most common location was the carotid ophthalmic artery ([COA] five aneurysms), followed in descending order by the cavernous internal carotid artery ([ICA] three aneurysms), the posterior communicating artery ([PCoA] three aneurysms), the superior cerebellar artery ([SCA] two aneurysms), the anterior communicating artery (one aneurysm), the vertebrobasilar (VB) junction (one aneurysm), the superior hypophyseal artery ([SHA] one aneurysm), the paraophthalmic ICA (one aneurysm), the junction of the PCoA with the P 1 segment of the posterior cerebral artery (one aneurysm), and one persistent trigeminal artery aneurysm. None of the patients was taking steroid medications to decrease cranial nerve inflammation before GDC embolization. Dexamethasone (4 mg every 6 hours) was admin- 957

3 T. W. Malisch, et al. TABLE 2 Response of mass effect symptoms following GDC treatment and current clinical status in 19 patients Preservation of Response of Follow Case Parent Mass Effect Up No. Artery Symptoms (mos) Definition of Endpoint 1 yes improvement 70 living 2 yes* improvement 2 balloon sacrifice at 2 mos for incomplete aneurysm thrombosis 3 yes worsening 1 surgical trapping & decompression at 1 mo for worsened mass effect 4 yes unchanged 51 living 5 yes resolution 16 death at 16 mos, cause of death unknown 6 yes resolution 58 living 7 yes resolution 57 living 8 yes resolution 33 living 9 yes unchanged 10 surgical clipping at 10 mos for incomplete aneurysm thrombosis 10 yes improvement 41 living 11 yes improvement 39 living 12 yes improvement 38 living 13 yes unchanged 2 death at 2 mos, cause of death unknown 14 yes resolution 14 living 15 yes unchanged 14 living 16 yes improvement 15 living 17 yes improvement 1 living 18 yes resolution 4 living 19 no improvement 2 living * Guglielmi detachable coil treatment was initially performed with preservation of the parent artery. At the 2-month follow-up angiographic examination, aneurysm thrombosis was observed to be incomplete and balloon sacrifice was performed. The parent artery was intentionally occluded in this patient who had previously undergone surgical sacrifice of the common carotid artery. The GDC treatment consisted of endosaccular packing of the aneurysm followed by GDC sacrifice of the distal ICA at the aneurysm orifice. istered intravenously to one patient who developed worsened mass effect after the GDC procedure. Statistical Analysis Comparisons of cranial nerve responses between the clinicoradiographic groups were analyzed using a twotailed Fisher s exact test. For these analyses, the response variable was collapsed to create a simplified dichotomous outcome variable (resolved or improved symptoms compared with unchanged or worsened symptoms); aneurysm size and symptom duration were similarly collapsed (giant compared with large or small aneurysm and 12 months compared with 12 months symptom duration). Results It was possible to achieve endosaccular packing of the aneurysm with preservation of the parent artery in 18 of 19 cases (Table 2). In the single case of GDC occlusion of the parent artery (Case 19), the patient had previously undergone surgical sacrifice of the common carotid artery during treatment of a paraophthalmic aneurysm that recurred. Although preservation of the distal ICA would have been technically simple, we elected to sacrifice it with GDCs in addition to endosaccular packing of the aneurysm. In the immediate post-gdc period, four patients displayed symptoms indicating worsening of the mass effect. The first of these patients (Case 16) presented with a 2- year history of decreased visual acuity from a large COA aneurysm. Four hours after the GDC procedure, the patient was noted to have worsening of her visual impairment. This improved spontaneously and had resolved to baseline status 4 months after the procedure. The 15- month follow-up ophthalmological examination in this patient documented continued improvement in vision to better than pre-gdc status. A second patient (Case 19) also had transient monocular worsening of a visual acuity deficit, which began 2 days after the GDC procedure and improved spontaneously approximately 2 weeks later. Formal ophthalmological evaluation performed 6 weeks after the GDC procedure showed near resolution of the visual acuity deficit. A third patient (Case 1) who presented with headache and seventh and eighth cranial nerve deficits due to a giant VB junction fusiform aneurysm had improvement of these symptoms, but experienced new diplopia immediately after the GDC procedure. The improvements in the presenting symptoms and the new diplopia both persisted at 70-month clinical follow-up evaluation. The fourth patient (Case 3) presented with a 5- month history of decreased visual acuity and a nasal field cut from a giant COA aneurysm. After GDC treatment she experienced worsening of her visual acuity, which persisted 1 month after treatment. She underwent surgical trapping and decompressive resection of the dome of the aneurysm and had improvements in both visual acuity and visual fields at her 6-month follow-up evaluation. On late follow-up examination, the response was classified as complete resolution of symptoms in six patients (32%), improvement in eight patients (42%), unchanged in four patients (21%), and symptom worsening in one patient (5%). The patient with the marked improvements in headache, ataxia, and hearing, who developed a new diplopia following the GDC procedure (Case 1), is classified as improved here, based on his perception of an improved quality of life. Patients with smaller aneurysms and those with shorter pretreatment duration of symptoms were more likely to experience an improvement in their symptoms following GDC treatment, although statistical significance was not reached in this series (p = and p = 0.111, respectively; Table 3). The presence of aneurysm wall calcification (six patients) or intraluminal thrombus (12 patients) showed no correlation with mass effect response to GDC treatment. Three of the nineteen patients in this series underwent subsequent procedures after GDC treatment of their aneurysms. One patient (Case 2) with a giant aneurysm underwent balloon sacrifice of the parent vessel after her 2- month follow-up angiographic examination documented incomplete aneurysm thrombosis. The second patient (Case 3) underwent trapping and decompressive resection of the aneurysm dome 1 month after the GDC procedure for worsened symptoms of mass effect. The mass symptoms improved following the surgery and this case was 958

4 Endosaccular treatment of unruptured aneurysms with GDC TABLE 3 Response of patients with cranial nerve mass effect symptoms after endosaccular GDC treatment: effect of aneurysm size and symptom duration No. of Patients Factor Resolved Improved Unchanged Worsened Total aneurysm size small large giant total duration of symptoms before GDC treatment 3 mos mos mos total published as a case report. 22 The third patient (Case 9) underwent clipping of the aneurysm for incomplete thrombosis 10 months following GDC treatment. The patient s monocular blindness remained stable. TABLE 4 Summary of seven surgical series specifying the response to direct or indirect surgical treatment of cranial nerve dysfunction caused by unruptured aneurysms Mass Effect Response (no. of patients) No. of Resolved Worsened Aneu- or or Com- Un- Authors & Year rysms* Improved Stable plication known Drake, Peiris & Ross Russell, Ferguson & Drake, Heros, et al., Symon & Vajda, Whittle, et al., Rice, et al., total no. of patients percent * Number of unruptured aneurysms in patients presenting with cranial nerve deficits. Discussion The treatment of intracranial aneurysms by using electrically detachable electrothrombolytic coils was developed by Guglielmi in 1989 and the first patient was treated in ,16 Over the past 8 years many medical centers have published their experiences with this treatment modality and these data show the procedure to be both safe and effective in protecting most intracranial aneurysms from rupture ,24,25,39 The exception to this generally favorable outcome is seen in patients with giant aneurysms measuring 2.5 cm or larger. It was shown in early GDC series that although post-gdc aneurysm rupture was exceedingly uncommon in all aneurysms smaller than 2.5 cm in diameter, a significant percentage of giant aneurysms bled after GDC treatment. 24 It must be stressed that protection of the aneurysm from hemorrhage is the primary and most vital goal of any treatment. It is clear that most aneurysms presenting with mass effect symptoms are larger aneurysms and differ from smaller aneurysms in patient demographics, pathophysiological characteristics, mechanism of growth, natural history, and response to surgical and nonsurgical interventions. 1,2,10,32 34 The incidence with which intracranial aneurysms present with mass effect symptoms and no history of hemorrhage was reported to be 46 of 602 patients, or 8%, by Solomon, et al. 35 Ferguson and Drake 8 reviewed 100 cases of COA aneurysms and found that 25 presented with mass effect symptoms and no history of hemorrhage. In giant aneurysm series, the number of giant aneurysms presenting unruptured and with symptoms of mass effect ranges from 19 to 79%. 3,4,21,27,28,36 These reports exclude aneurysms 2.4 cm or smaller in diameter, although in the present series such smaller aneurysms were responsible for 11 of the 19 cases of mass effect. Michael 26 documented the grim natural history of large and giant aneurysms presenting in patients with symptoms of mass effect. In that series of seven patients, all died within 1 year of diagnosis. Other authors 23,27,29,30,38 have reported outcomes of untreated patients with giant aneurysms, with generally poor outcomes. It is now recognized that the presence of mural thrombus or wall calcification is not protective against hemorrhage from these lesions. Previous Reports of the Response of Cranial Nerve Dysfunction to Direct and Indirect Surgical and Endovascular Approaches A summary of seven large surgical series providing information on the responses of patients with cranial nerve dysfunction to surgical treatment of the responsible unruptured aneurysm is given in Table 4. This overview of surgical results is compromised by four factors: 1) although two of the series included aneurysms of all sizes, four series included only aneurysms larger than 2.5 cm in diameter and one series included only aneurysms smaller than 2.5 cm; 2) the 1981 series by Ferguson and Drake 8 and the 1979 series by Drake 6 may have some patient overlap; 3) the response of patients with cranial nerve deficits to surgery was not documented in 10% of the cases in these series; and 4) the duration of symptoms before surgery was not specified in many cases. Still, this survey of patients with cranial nerve mass effect responses to direct or indirect surgical procedures illustrates the difficulty of achieving complete restoration of cranial nerve function. Deconstructive endovascular techniques (trapping the aneurysm with detachable balloons or coils) have led to improved cranial nerve mass effect symptoms according to several reports. 5,7,20,38 Constructive endovascular series have also been reported. Halbach and associates 18 reported the efficacy of endosaccular aneurysm occlusion in alleviating mass symptoms in 26 patients, 23 of whom were treated with hydroxyethyl methacrylate filled detachable silicone balloons, two with fibered platinum coils, and one with GDCs. The outcomes in these 26 patients were classified as resolved in 13 patients (50%), improved in 11 (42%), and unchanged in two (8%). Vargas, et al., 38 and Martin, et al., 25 also described improvements in mass effect symptoms following GDC treatment. 959

5 T. W. Malisch, et al. To the authors knowledge, the current series represents the largest series to date of patients with unruptured intracranial aneurysms presenting with cranial nerve deficits and treated with GDCs. In this series, the response of mass effect symptoms to GDC treatment was favorable (improved or completely resolved) in 74% of cases, with symptoms remaining unchanged in 21% and worsening in 5%. Endosaccular GDC treatment is a constructive intervention that alleviates cranial nerve mass effect in the majority of cases, without subjecting the patient to the risks of cerebral hypoperfusion or the risks of de novo aneurysm formation, which are inherent to deconstructive strategies. Conclusions Three major points should be made about this series. 1) Patients with cranial nerve deficits generally respond favorably to endosaccular GDC treatment of the responsible aneurysm. In this series 32% of patients had complete resolution of their symptoms, 42% had significant improvement of their symptoms, 21% had no significant change, and 5% (one case) had worsened symptoms. Transient worsening of symptoms was seen in two (11%) of the patients, but resolved spontaneously and was probably related to the acute stage of aneurysm thrombosis. 2) Aneurysm size and preoperative duration of mass effect symptoms may affect the likelihood of symptoms improving after GDC treatment, although statistical significance was not reached in this series. Aneurysm wall calcification and the presence of intraluminal thrombus before GDC treatment were not predictive of mass effect response. 3) It is emphasized that the primary goal of any method of treating intracranial aneurysms is to prevent aneurysm rupture. Considerations of mass effect response are secondary to considerations of the safety, efficacy, and durability of aneurysm obliteration. In this series, two patients (Cases 5 and 13) died at 16 months and 2 months, respectively, after GDC treatment. Although the circumstances of both deaths are uncertain (neither death was witnessed and no autopsy was performed), the possibility of aneurysm rupture is certainly present. In those cases in which giant aneurysms can be surgically obliterated with acceptable risks of morbidity and mortality, that approach remains the treatment of choice because GDC treatment of giant aneurysms does not appear to offer the same durability of protection from rupture. In those cases in which patients presenting with mass effect symptoms on cranial nerves cannot be surgically treated with acceptable risks of morbidity and mortality, GDC treatment offers an alternative. In this series, most mass effect symptoms either improved or resolved entirely. References 1. Artmann H, Vonofakos D, Muller H, et al: Neuroradiologic and neuropathologic findings with growing giant intracranial aneurysm. 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6 Endosaccular treatment of unruptured aneurysms with GDCs 24. Malisch TW, Guglielmi G, Viñuela F, et al: Intracranial aneurysms treated with the Guglielmi detachable coil: midterm clinical results in a consecutive series of 100 patients. J Neurosurg 87: , Martin D, Rodesch G, Alvarez H, et al: Preliminary results of embolisation of nonsurgical intracranial aneurysms with GD coils: the 1st year of their use. Neuroradiology 38 (Suppl 1): S142 S150, Michael WF: Posterior fossa aneurysms simulating tumours. J Neurol Neurosurg Psychiatry 37: , Morley TP, Barr HWK: Giant intracranial aneurysms: diagnosis, course, and management. Clin Neurosurg 16:73 94, Onuma T, Suzuki J: Surgical treatment of giant intracranial aneurysms. J Neurosurg 51:33 36, Peerless SJ, Wallace MD, Drake CG: Giant intracranial aneurysms, in Youmans JR (ed): Neurological Surgery, ed 3. Philadelphia: WB Saunders, 1990, Vol 3, pp Peiris JB, Ross Russell RW: Giant aneurysms of the carotid system presenting as visual field defect. J Neurol Neurosurg Psychiatry 43: , Rice BJ, Peerless SJ, Drake CG: Surgical treatment of unruptured aneurysms of the posterior circulation. J Neurosurg 73: , Rosta L, Battaglia R, Pasqualin A, et al: Italian cooperative study on giant aneurysms: 2. Radiological data. Acta Neurochir Suppl 42:53 59, Sarwar M, Batnitzky S, Schechter MM: Tumorous aneurysms. Neuroradiology 12:79 97, Schubiger O, Valavanis A, Wichmann W: Growth-mechanism of giant intracranial aneurysms: demonstration by CT and MR imaging. Neuroradiology 29: , Solomon RA, Fink ME, Pile-Spellman J: Surgical management of unruptured intracranial aneurysms. J Neurosurg 80: , Sonntag VKH, Yuan RH, Stein BM: Giant intracranial aneurysms: a review of 13 cases. Surg Neurol 8:81 84, Symon L, Vajda J: Surgical experiences with giant intracranial aneurysms. J Neurosurg 61: , Vargas ME, Kupersmith MJ, Setton A, et al: Endovascular treatment of giant aneurysms which cause visual loss. Ophthalmology 101: , Viñuela F, Duckwiler G, Mawad M: Guglielmi detachable coil embolization of acute intracranial aneurysm: perioperative anatomical and clinical outcome in 403 patients. J Neurosurg 86: , Whittle IR, Dorsch NW, Besser M: Giant intracranial aneurysms: diagnosis, management and outcome. Surg Neurol 21: , 1984 Manuscript received September 15, Accepted in final form July 20, Address reprint requests to: Tim W. Malisch, M.D., Interventional Neuroradiology, Northwestern Memorial Hospital, Olson Pavilion, 710 North Fairbanks Court, Chicago, Illinois