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ORIGINAL ARTICLE
Year : 2014  |  Volume : 62  |  Issue : 4  |  Page : 410-416

A1-segment aneurysms: Management protocol based on a new classification


Department of Neurosurgery, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India

Date of Submission06-Apr-2014
Date of Decision01-Jun-2014
Date of Acceptance24-Aug-2014
Date of Web Publication19-Sep-2014

Correspondence Address:
Sanjay Behari
Department of Neurosurgery, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow - 226 014, Uttar Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.141284

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 » Abstract 

Background: Aneurysms of proximal (A1)-segment of anterior cerebral artery (ACA) constitute <1% of all intracranial aneurysms. Aim: Management dilemmas of A1-segment aneurysms were studied utilizing a new classification based upon their location on the longitudinal and circumferential axis of A1-segment. Setting and Design: Tertiary care referral center. Materials and Methods: This is a retrospective analysis of 14 patients (0.98%; mean age: 38.02 ± 15.74 years) with A1-segment aneurysms. The data collected included clinical features, computed tomography (CT) scan and CT-angiography (CTA)/digital subtraction angiography (DSA) findings, modified Hunt and Hess (H and H) grade, surgical steps and difficulties encountered. Results: The modified Hunt and Hess (H and H) grades in the 14 patients were: grade I in two, grade II in two, grade III in four, grade IV in five and grade V in 1. The mean ictus-admission duration was 5.07 ± 2.30 days (range: 1-10 days). Multiple aneurysms were two. Thirteen patients underwent clipping and one, wrapping. Bilateral lateral ventricle hemorrhage occurred in 8 (66%) patients and frontal intracerebral hematoma in 2 (16.66%) patients. In one patient, the aneurysm could only be detected following the third angiogram. A1-aneurysms were classified as proximal (n = 6), distal (n = 7), and mid-segment (n = 1); and, anterior (n = 2), posterior-inferior (n = 7) and posterior-superior (n = 5). Follow-up (range: 6 months-10 years, mean: 2.9 years) recovery (assessed using Modified Rankin's score or mRS) correlated with preoperative status. The preoperative H and H grade and follow-up mRS status were as follows: H and H I (n = 2): mRS 0 (asymptomatic, n = 2); H and H II (n = 2): mRS 1 (minor symptoms without disability, n = 2); H and H III (n = 4):mRS 1 (n = 2) and mRS 2 (slight disability but performing unassisted activities of daily living, n = 1); H and H IV (n = 5): mRS 3 (moderate disability, requiring help for daily living but unassisted walking, n = 2) and mRS 4 (moderately severe disability, requiring help for daily living and walking, n = 2). One patient each from H and H grade III, IV and V died (mRS 6) during treatment due to severe vasospasm, pneumonitis and septicemia. Conclusions: A1-segment aneurysms have unique properties: rupturing of small-sized aneurysms; multiplicity; undetectable on initial imaging; frontal lobar/intraventricular bleeding; origin from main trunk and not bifurcating points; neck obscuration by A1-trunk; close proximity to perforators; and, associated A1-segment and ACA anomalies. A new classification identifies surgical difficulties inherent in different sites of origin of A1-aneurysms.


Keywords: Anterior cerebral artery, A1 segment aneurysms, A1 segment vascular anomalies, classification, clipping, subarachnoid hemorrhage, surgery


How to cite this article:
Bhaisora KS, Behari S, Prasadh G, Srivastava AK, Mehrotra A, Sahu RN, Jaiswal AK. A1-segment aneurysms: Management protocol based on a new classification. Neurol India 2014;62:410-6

How to cite this URL:
Bhaisora KS, Behari S, Prasadh G, Srivastava AK, Mehrotra A, Sahu RN, Jaiswal AK. A1-segment aneurysms: Management protocol based on a new classification. Neurol India [serial online] 2014 [cited 2020 Oct 24];62:410-6. Available from: https://www.neurologyindia.com/text.asp?2014/62/4/410/141284



 » Introduction Top


Aneurysms of the proximal segment of anterior cerebral artery (ACA; also known as A1-segment aneurysm) account for 1% of all intracranial aneurysms. [1] Their unique properties include: Rupturing even when small in size, frequent re-rupture, presenting with sessile neck or as blister aneurysms, being enmeshed by perforator vessels, being one amongst multiple intracranial aneurysms, being adherent to the frontal lobe precipitating a consequent frontal lobar rather than a subarachnoid hemorrhage (SAH) and often not being detectible on the immediate post-hemorrhage angiograms. [2] Moreover, the A1-segment is prone to numerous vascular anomalies. [2],[3] This study discusses the dilemmas encountered in the management of these aneurysms. We also propose a new classification based upon the location of aneurysmal neck relative to the longitudinal axis and circumference of A1-segment of ACA that considerably helps in anticipating challenges encountered during their surgical management.


 » Materials and Methods Top


Of the 1420 consecutive patients presenting with aneurysmal SAH who underwent clipping between January 2001-May 2013, 14 patients (0.98%; eight male and six female patients; age range of 5-68 years; mean age 38.02 ± 15.74 years) had an A1-segment aneurysm. The data collected included: Clinical features, computed tomographic (CT) scan and CT angiography (CTA)/digital subtraction angiography (DSA) findings, modified Hunt and Hess (H and H) grade [4] at presentation, surgical steps and difficulties encountered. On CTA/DSA, the A1-segment was divided into three equal segments. The A1-segment aneurysms were classified as proximal (those near internal carotid artery or ICA bifurcation); distal (those in close proximity to anterior communicating artery or AcomA; and, mid segment aneurysms (those present between the proximal and distal segments). They were also classified as anterior, posterior-inferior, and posterior-superior based on the location of their neck along the circumference of A1-segment. Radiological vasospasm was diagnosed on the basis of focal arterial narrowing on CTA/DSA images.

A standard pterional craniotomy, wide opening of sylvan fissure and standard exposure of anterior circle of Willis was performed for clipping the aneurysm. Oral nimodipine (60 mg 4 hourly) and triple H therapy were started at the onset of "clinical vasospasm,". The outcomes were assessed using modified Rankin scale [5] at 6 monthly to yearly intervals.


 » Results Top


The H and H grade in the 14 patients were: Grade I in two, grade II in two, grade III in four, grade IV in five and grade V in one patients. The mean ictus-admission interval was 5.07 ± 2.30 days (range: 1-10 days) [Table 1]. Non-contrast CT scan at admission revealed, in addition to hemorrhage in suprasellar cisterns, an intra-third ventricular bleed and blood in occipital horn of bilateral lateral ventricles in 8 (66%) patients; and, intracerebral hematoma in 2 (16.66%) patients. Both of the latter patients had an aneurysm pointing in the posterior-superior direction. In one of these patients (with a frontal hematoma), the initial CTA and DSA were negative; the subsequent DSA done after 6 weeks revealed an aneurysm.
Table 1: Clinical spectrum and outcome of the patients with an A1-segment aneurysm

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The size of the aneurysms varied between 3-15 mm [Table 2]. Of the 14 (7 left-sided and 7 right-sided) A1-segment aneurysms, 13 had ruptured and one was unrupture. The latter was incidentally detected following a CTA for diagnosing a ruptured paraclinoid aneurysm. One other patient among the group with a ruptured A1-segment aneurysm had an additional unruptured paraclinoid aneurysm.
Table 2: Radiological features of the patients

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These aneurysms could be classified into various groups based upon their location on the A1 artery [Table 3] and [Figure 1],[Figure 2] and [Figure 3]. Aneurysms located on the proximal A1 segment close to ICA bifurcation were classified as proximal A1 segment aneurysms; those at the distal end near the anterior communicating artery were classified as distal aneurysms; and, aneurysms in the segment in between were classified as mid-segment aneurysms. In addition, 6 (42.85%) patients had an anomalous A1 or A2 segment and anterior communicating complex including a fenestrated A1-segment (n = 2), an azygous A2 (n = 2), a fenestrated anterior communicating artery (ACommA; n = 1) and contralateral hypoplastic A1-artery [n = 2; Table 2].
Figure 1: (a) CT head obtained at admission showing bleed in anterior interhemispheric fissure, basal cisterns and medial temporal lobe on right side; (b): CT angiogram showing a distal A1-segment aneurysm directed postero-inferiorly

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Figure 2: CTA revealing a blister proximal A1-segment aneurysm directed postero-inferiorly. The ipsilateral main A1-segment trunk often obscures the visualization of such aneurysms

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Figure 3: Trilobed fusiform aneurysm on the left A1-proximal segment. Opposite A1 is hypoplastic

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Table 3: The classification based on the site of origin of the aneurysm situated on the longitudinal and circumferential
axes of the A1 segment


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Thirteen patients underwent clipping of the A1-segment aneurysm [Figure 4] and [Figure 5]. One patient, who underwent clipping of the ruptured paraclinoid aneurysm, was incidentally found to be having a posterior-inferiorly directed, small (3 mm) A1-segment aneurysm enmeshed within A1-artery perforators. This aneurysm had to be wrapped rather than clipped. There were 13 patients with a saccular aneurysm [Figure 1], [Figure 2] and [Figure 4]; two being blister aneurysms with a sessile neck] and one, a fusiform aneurysm arising from the superior fenestration of a fenestrated A1-segment [Figure 3]. This fusiform aneurysm had ruptured due to its location within the confines of the narrow space between the two A1-segment fenestrations resulting in a high intraluminal pressure. Temporary clips were applied for 3 minutes during dissection of the A1 aneurysm in only one patient. Papavarine was instilled in the surgical cavity following clip application in all patients. Triple-H therapy was instituted following surgery and was continued for 7-14 days in 6 patients in the series.

At follow-up (range 6 months-10 years, mean follow up: 2.9 years), recovery correlated with the preoperative modified H and H status. Thus, 2 patients in H and H grade I had an mRS 0 (were asymptomatic); two patients in H and H grade II were discharged with minor symptoms with no disability (mRS 1). Among four patients with H and H grade III, 2 patients improved to mRS 1 and 1 patient had a slight disability but was able to independently carry out activities of daily living (mRS 2). Five patients were in H and H grade IV. Among these, two patients persisted with moderate disability requiring some help, but were able to walk without assistance (mRS 3) and 2 had a moderately severe disability, that is, unable to walk without assistance and also unable to attend to own bodily needs without assistance (mRS 4). 1 patient each from H and H grade III, IV and V died (m RS 6) during treatment. Two of them (in H and H grade IV and V) did not show improvement from the poor neurological grade they arrived in and developed pneumonitis and septicemia. The third patient (in H and H grade III), who underwent clipping of the paraclinoid aneurysm and wrapping of A1-segment aneurysm developed infarction in the right middle cerebral artery and anterior cerebral artery territory due to vasospasm despite being on triple-H therapy and oral nimodipine (60 mg 4 hourly).
Figure 4: (A) A large mid-segment A1 aneurysm directed antero-superiorly (B) Operative steps: (a) wide opening of sylvian fissure reveals internal carotid artery (ICA) and optic nerve (II); (b) Excision of orbitofrontal cortex reveals the large aneurysm (*) arising from the mid-segment A1 artery (arrow); (c) The proximal A1-segment (arrow) control; (d) The distal A1-segment control (arrow); (e) A clip applied to the neck of the aneurysm (*). The entire length of A1-segment visualized (arrow); and (f) Reinforcing clips applied to neck of aneurysm (*)

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Figure 5: (a) Axial CECT; (b) CTA showing proximal posteroinferior A1 large aneurysm (*); (c) Aneurysm exposed by excising gyrus rectus; (d) Aneurysm exposure shows a wide neck; and, (e) its clipping using fenestrated clips with A1 segment reconstruction

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 » Discussion Top


The incidence of A1-segment aneurysms in this study was 0.9% that was similar to the average incidence of <1% (range 08-3.4%) reported in the literature. [1],[2],[3],[6] A proximal A1-segment aneurysm may closely resemble an ICA bifurcation aneurysm and a distal one an ACommA aneurysm. On preoperative DSA/CTA images, for the diagnosis, it is imperative to visualize the A1-segment both proximal and distal to it. [3] Its often elusive presence (as seen in one of our patients where ipsilateral frontal lobe and suprasellar hemorrhage were characteristic but the aneurysm was not visualized on repeated angiograms) may be due to several factors. The aneurysms are usually much smaller when they rupture. The fundus is often covered by the ipsilateral frontal lobe. This localizes the hemorrhage around its fundus causing temporary obliteration of its lumen due to the pressure of the surrounding clot and the edematous fronto-orbital cortex. The overlapping main A1-segment often hides the posteriorly directed aneurysm. The high incidence of multiple aneurysms associated with an A1-segment aneurysm may divert the attention to the ruptured aneurysm located elsewhere. The presence of the often associated duplication and fenestration of A1-segment; temporary vasospasm of the parent vessel with an intact A1-segment on the opposite side supplying both A2 arteries (that creates the erroneous impression of a hypoplastic A1-segment on the side of the aneurysm); and, a frontal lobar hemorrhage rather than a predominantly subarachnoid hemorrhage (that may direct attention towards detecting a vascular anomaly such as an arteriovenous malformation, a cavernous angioma or vasculitis) may also lead to its non-visualization. The diagnosis of A1-segment aneurysm, therefore, requires high a degree of suspicion with performance of multiple views and angles on angiograms.

There are four important differences between A1-segment aneurysms and the other frequently encountered aneurysms in that location namely the ICA bifurcation and the ACommA aneurysms. Firstly, the latter aneurysms have a predominantly cisternal location of their fundus while the A1-segment aneurysms often have their fundus buried deep into the orbitofrontal cortex. Thus, splitting the sylvian fissure (in the case of an ICA bifurcation aneurysm); and, either splitting the interhemispheric fissure or resecting a small part of the gyrus rectus (in the case of an ACommA aneurysm) often provides proximal control and an easy access for clipping the aneurysm. Retraction of the frontal lobe during sylvian fissure dissection may cause rupture of the A1-segment aneurysm before proximal control of the A1 artery is obtained.

The second difference is related to the A1-segment aneurysms (especially the posteriorly directed ones) often being enmeshed within perforators (supplying the optic chiasm, anterior third ventricle, hypothalamus, anterior commissure, caudate nucleus, globus pallidus, anterior limb of the internal capsule and superior thalamus). [1],[3] The number of perforating arteries of the A1-segment varies from 2-15 (average: 8). [3] These perforating arteries usually arise from the proximal half of A1-segment and are usually directed postero-inferiorly. [1],[2],[3] Thus, the perforators hugging the aneurysm need to be dissected free before the latter is clipped. Deep-seated ischemia due to perforator spasm may be the consequence of aneurysmal subarachnoid hemorrhage in close proximity to the perforating end-arteries. In our study, a patient had multiple perforators adherent to the dome of the aneurysm and in 2 patients, the recurrent artery of Huebner was inferior to the A1 trunk and in close proximity to the aneurysm. Three of our patients exhibited hypodensities in the basal ganglia and internal capsular region perhaps due to vasospasm or occlusion of some small perforating arteries.

The third issue relates to the A1-segment aneurysms often being sessile (or presenting as blister aneurysms) and arising from the longitudinal axis of the A1 artery where there are no bifurcating vessels (unless the aneurysm is located at the apex of an A1-segment fenestration). Their neck is located perpendicular to the long axis of the parent vessel. In contrast, all the other saccular aneurysms usually have a well-defined neck and originate from bifurcating points of the medium-to-large sized vessels of the circle of Willis. Thus, their neck is located in line with the parent vessel. During endovascular embolization of A1-segment aneurysms, its often sessile nature with a relative wide neck poses the danger of the coils slipping into the parent vessel, an incomplete embolization and an intra-procedural rupture due to fragility of its wall. [7],[8]

The final point relates to A1-segment aneurysms being associated with a much higher incidence of multiple aneurysms (25-70%). [2],[3],[8] Park et al., [3] reported the incidence of multiple aneurysms to be around 40% while Suzuki et al., [6] reported an incidence of around 44.7%. Hino et al., [2] reported a much higher incidence of multiple aneurysms of approximately 73%. In our series, 2 (18%) patients had an additional paraclinoid aneurysm.

Vascular anomalies often occur concurrently with A1-segment aneurysms. Suzuki et al., [6] reported vascular anomalies in 20.5% of patients with A1-segment fenestration being the commonest. In our series, 6 (42.85%) patients had vascular anomalies including a fenestrated A1 (n = 2), an azygous A2 (n = 2), hypoplasia of the contralateral A1 (n = 2) and a fenestrated ACommA (n = 1). These vascular anomalies may induce hemodynamic perturbations in the A1-segment predisposing to aneurysm formation. A fenestration of A1-segment may be due to partial duplication, incomplete fusion or persistence of a remnant plexiform anastomosis between the primitive olfactory artery and the ACA. [9],[10],[11],[12] Aneurysms usually arise from the proximal end of the fenestration although their origin from the distal end has also been reported. A defect in the tunica media associated with the hemodynamic stress of the direct impact of the turbulent blood flow on the vessel wall may give rise to an aneurysm formation. [9],[12] A tortuosity of the A1-segment and focal defects in the tunica media may also result in an asymmetrical impact of this turbulence on focal areas of the vessel wall. This may explain the development of a small-sized and wide-necked A1-segment aneurysm without any major branching points even when not associated with a vascular anomaly. [12] The etiopathogenesis of the single patient in our study with a trilobulated, fusiform (rather than a saccular) aneurysm associated with an A1-segment fenestration was perhaps different. It may have occurred due to the expansion of a wide area of vessel wall vulnerability due to the development of arterial fenestration or at the point of origin of the multiple perforators. A wide angulation of the bifurcating point of the A1 fenestration may have led to a direct impact of the turbulent blood flow over a larger area of the wall of the fenestrated segment leading to its fusiform dilatation.

The classification of A1 segment aneurysms into proximal, middle and distal groups has significant surgical implications. The proximal and distal subgroup A1 aneurysms are approached similar to the approach adopted for ICA bifurcation and ACommA aneurysms, respectively, with the added precaution that the frontal lobe retraction should be minimized. Maximum perforator vessels are situated in the proximal A1-segment. [1],[2],[3] In the presence of fenestrations or duplications of the A1-segment, the direct hemodynamic stress at the bifurcation of the proximal and distal ends of the fenestration may result in a saccular aneurysm in line with the long segment of the A1 artery. [9],[11] An aneurysm of the middle A1-segment may be fusiform if it is due to a long segmental defect in the tunica media or saccular if it is related to the turbulence or a small vessel wall weakness at the junction of a perforator with the main trunk.

A further subdivision into anterior, postero-superior and postero-inferior groups based on the relationship of the origin of the aneurysm on the circumference of the A1 segment also has an important bearing on management. An anteriorly directed aneurysm is relatively easier to clip but may be in intimate relation with the recurrent artery of Huebner. An antero-inferior inclination may cause its burrowing into the optic chiasma. Blood may penetrate through the lamina terminalis into the ventricular system. A posterior-superiorly directed aneurysm is often embedded into the orbito-frontal cortex where frontal lobe retraction during sylvian opening may cause it to rupture before proximal control is obtained; and, a postero-inferior one may be completely enmeshed within perforators. [2],[3] As is already mentioned, the A1-segment trunk may obscure the visualization of small, posteriorly directed aneurysms. Thus, the present classification is extremely useful for surgical planning and for anticipating the risks involved in the surgical clipping of these aneurysms.

A wide and deep opening up of the sylvian fissure so that its edges spontaneously fall apart without frontal retraction facilitating proximal control of the A1-segment; excising a small portion of the orbito-frontal cortex to gain access to the lamina terminalis and carotid cisterns; minimum manipulation of the posteriorly directed perforators; opening up of the carotico-optic space, the membrane of Lilliquest and the lamina terminalis to release cerebrospinal fluid and facilitate brain retraction; and, obtaining distal control over the distal A1-segment, ACommA or both A2 arteries (based upon the location of the aneurysm on the A1 segment) by opening the interhemispheric fissure or excising the gyrus rectus, are some of the technical steps that may be undertaken to facilitate a proper clipping of these aneurysms. The posteriorly directed blister and sessile aneurysms are the ones most difficult to manage as the aneurysm may avulse from the vessel wall during clipping with the main A1 trunk preventing its direct visualization. The bleeding edges retract and may make it impossible to control the ensuing hemorrhage without causing luminal compromise. Reinforced wrapping of such aneurysms prior to their clipping as well as the use of fenestrated clips and clips in tandem facilitate a safe obliteration of these lesions. The temptation to aggressively evacuate a cisternal hematoma surrounding the perforators around the aneurysm has to be resisted in order to prevent injury and vasospasm of these vital end arteries by excessive manipulation. The A1-segment harboring the aneurysm is often dominant and may be supplying both A2-segments through the ACommA. In addition, the A2 arteries may be in vasospasm. In this situation, temporary clipping should be judiciously avoided to prevent even a transient distal ischemia in the ACA territory that has the potential to precipitate a catastrophic paraplegia or even a locked-in syndrome. The morbidity/mortality in the series was mainly influenced by the preoperative H and H grade of the patients. We deferred surgery in grade V patients (with decerebration or no response) until they improved to a better grade. The patient in grade V included in the study was actually in grade IV with superadded diabetes mellitus and hypertension that downgraded him to a poorer grade.

Our study has drawbacks. The data was retrospectively analyzed. A larger number of patients in each category would have permitted a meaningful statistical analysis. The surgeons analyzing outcome were participating in the care of the patients. A longer follow up would perhaps have led to further recovery of our patients and perhaps better results. The patients were operated as early as possible to prevent rebleeding and no effort was made to wait for their spontaneous recovery to a better H and H grade before performing surgery. Inability to perform postoperative angiograms at follow-up was also a limitation.

In conclusion A1-segment aneurysms are unique due to their often-elusive character, their sessile shape, their intimate relationship to vital perforators and their tendency to occur in the main vessel trunk and not at its bifurcating points. Multiple A1-segment anomalies also increase the degree of complexity. A new classification is proposed that preoperatively identifies the problems inherent in different locations of the aneurysm on the A1-segment and considerably helps in the surgical planning.

 
 » References Top

1.Dashti R, Hernesniemi J, Lehto H, Niemelä M, Lehecka M, Rinne J, et al. Microneurosurgical management of proximal anterior cerebral artery aneurysms. Surg Neurol 2007;68:366-77.  Back to cited text no. 1
    
2.Hino A, Fujimoto M, Iwamoto Y, Oka H, Echigo T. Surgery of proximal anterior cerebral artery aneurysms. Acta Neurochir (Wein) 2002;144:1291-6.  Back to cited text no. 2
    
3.Park HS, Choi JH, Kang M, Huh JT. Management of aneurysms of the proximal (A1) segment of the anterior cerebral artery. J Cerebrovasc Endovasc Neurosurg 2013;15:13-9.  Back to cited text no. 3
    
4.Hunt WE, Hess RM. Surgical risk as related to the time of intervention in repair of intracranial aneurysm. J Neurosurg 1968;28:14-20.  Back to cited text no. 4
    
5.Singh RK, Behari S, Kumar V, Jaiswal AK, Jain VK. Posterior inferior cerebellar artery aneurysms: Anatomical variations and surgical strategies. Asian J Neurosurg 2012;7:2-11.  Back to cited text no. 5
[PUBMED]  Medknow Journal  
6.Suzuki M, Onuma T, Sakurai Y, Mizoi K, Ogawa A, Yoshimoto T. Aneurysms arising from the proximal (A1) segment of the anterior cerebral artery: A study of 38 cases. J Neurosurg 1992;76:455-8.  Back to cited text no. 6
    
7.Chang HW, Youn SW, Jung C, Kang HS, Sohn CH, Kwon BJ, et al. Technical strategy in endovascular treatment of proximal anterior cerebral artery aneurysms. Acta Neurochir (Wien) 2011;153:279-85.  Back to cited text no. 7
    
8.Yu B, Wu Z, Lv X, Liu Y, Sang M. Endovascular treatment of A1 segment aneurysms of the anterior cerebral artery. Neurol India. 2010;58:446-8.  Back to cited text no. 8
    
9.Kachhara R, Nair S, Gupta AK. Fenestration of the proximal anterior cerebral artery (A1) with aneurysm manifesting as subarachnoid hemorrhage: Case report. Neurol Med Chir (Tokyo) 1998;38:409-12.  Back to cited text no. 9
    
10.Teal JS, Rumbaugh CL, Bergeron RT, Segall HD. Angiographic demonstration of fenestrations of the intradural intracranial arteries. Radiology 1973;106:123-6.  Back to cited text no. 10
    
11.Friedlander RM, Oglivy CS. Aneurysmal subarachnoid hemorrhage in a patient with bilateral A1 fenestrations associated with an azygos anterior cerebral artery. Case report and literature review. J Neurosurg 1996;84:681-4.  Back to cited text no. 11
    
12.Kumar R, Behari S, Singh K, Sahu RN, Jaiswal AK. Trilobulated fusiform aneurysm from proximal fenestrated segment of dominant A1 causing subarachnoid haemorrhage. Neurol India 2013;61:315-7.  Back to cited text no. 12
[PUBMED]  Medknow Journal  


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]
 
 
    Tables

  [Table 1], [Table 2], [Table 3]

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