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|NI FEATURE: NORMATIVE DATA-ORIGINAL ARTICLE
|Year : 2019 | Volume
| Issue : 3 | Page : 823-828
Intraoperative microsurgical anatomy of the anterior communicating artery complex harbouring an anterior cerebral territory aneurysm
Atul Agrawal, Anita Jagetia, Shaam Bodeliwala, Daljit Singh, Gautam Dutta, Ankit Shah
Department of Neurosurgery, Govind Ballav Pant Institute of Postgraduate Medical Education and Research (GIPMER), New Delhi, India
|Date of Web Publication||23-Jul-2019|
Dr. Atul Agrawal
Department of Neurosurgery, Govind Ballabh Pant Institute of Postgraduate Medical Education and Research (GIPMER), New Delhi - 110 002
Source of Support: None, Conflict of Interest: None
Background: The vascular anatomy of the anterior communicating artery complex (ACAC), the most frequent site of occurrence of aneurysms, is complex and associated with many anatomical and morphological variations.
Aims: The aim of this study was to determine the anatomical variations of ACAC in the Indian population. Setting and Design: This was an observational study.
Materials and Methods: Sixty-two patients of ACAC aneurysms were subjected to clipping, and intraoperative microsurgical details were analyzed.
Results: Twenty-two (35.48%) patients had anatomical and morphological variations that were more common on the right side. Right A1 was hypoplastic in 5 (8.06%), aplastic in 2 (3.22%), and tortuous in 1 (1.61%) patient. Left A1 was aplastic in 3 (4.83%), hypoplastic in 1 (1.61%) and prominent in 2 (3.22%) patients. One patient (1.61%) had a prominent left A2 segment and 2 (3.22%) had a prominent right A1 and A2 segment. Two patients (3.22%) had fenestration of the ACAC and 3 (4.83%) had the median artery of corpus callosum. The recurrent artery of Heubner was identified in only 44 (70.96%) patients, and in these patients, distinct anatomical variations were noted. Eleven patients were found to present with a parent vessel anomaly, having a total of 23 (mean, 2.09) perforators arising from ACAC, whereas those without a parent vessel anomaly had a total of 57 (mean, 1.11) perforators. This difference was statistically significant.
Conclusion: The ACAC region is the area of highest anatomical and morphological variability. This variability is even more exhaustive when associated with aneurysmal formation. A sound anatomical knowledge of the perforators and their preservation during the surgical management of the ACAC is of paramount importance for ensuring a good clinical outcome of patients.
Keywords: Anterior communicating arterial complex, aplasia, fenestration, hypoplasia, perforators, recurrent artery of Heubner
Key Message: The anterior communicating artery complex is anatomically a highly variable region and the most common site for an intracranial aneurysm formation. A good clinical recovery in the postoperative period depends upon a sound knowledge of the normal anatomy and associated variations of this particular region. Through this article, we sincerely attempt to throw some light upon the anatomy and variations found in this region and review the available literature.
|How to cite this article:|
Agrawal A, Jagetia A, Bodeliwala S, Singh D, Dutta G, Shah A. Intraoperative microsurgical anatomy of the anterior communicating artery complex harbouring an anterior cerebral territory aneurysm. Neurol India 2019;67:823-8
|How to cite this URL:|
Agrawal A, Jagetia A, Bodeliwala S, Singh D, Dutta G, Shah A. Intraoperative microsurgical anatomy of the anterior communicating artery complex harbouring an anterior cerebral territory aneurysm. Neurol India [serial online] 2019 [cited 2019 Aug 17];67:823-8. Available from: http://www.neurologyindia.com/text.asp?2019/67/3/823/263174
The anterior communicating artery (AcomA), the paired A1 and A2 segments of anterior cerebral artery (ACA), and the recurrent artery of Heubner (RAH), combined with their perforators and other branches, are referred to as the anterior communicating artery complex (ACAC). The presence of such a large number of vessels and the plexiform development of AcomA, perhaps, results in the development of many anatomical variations and concomitantly aneurysmal formation. Significant anatomical variations in the anterior cerebral circulation may promote aneurysm formation due to stronger hemodynamic changes, arterial wall sheer, and activation of various molecular mechanisms.,,,
Most of the studies reported in the literature are focused on the radiologic images and cadaveric dissection; however, both cannot provide the finer details of this region that are obtainable utilizing an intraoperative high-definition microscopic picture in the actual cases harbouring an aneurysm in these vessels. It is also true that in the modern changing trend of treating ACAC aneurysms by the endovascular means, especially the pipeline devices, it may not be possible to appreciate the variations as well as that seen under the high definition and high magnification views of an operating microscope. This study was done to analyze the intraoperative microsurgical anatomy along with the associated variations of ACAC in an Indian population and to review their relevance to surgery.
| » Materials and Methods|| |
This observational study included 62 patients of ACAC treated by pterional craniotomy and clipping of aneurysm under intraoperative indocyanine green (ICG) videoangiography over a period of 20 months. Intraoperative microsurgical details were recorded and analyzed by the same team. Patients were excluded if the intraoperative microsurgical anatomy (particularly the contralateral vessels) was not clear. Ethical clearance was taken from the institutional review board for the study.
The collected data were analyzed using the IBM Statistical Package for the Social Sciences (SPSS) software version 22.0. Data was tabulated in the form of percentage and mean value. Qualitative and quantitative data were analyzed to assess the statistical significance with unpaired and paired t-test and chi-square test to calculate the P–value.
| » Results|| |
The patients were in the age group of 24–72 years, with an average age of 49.33 years. Twenty-nine (46.7%) patients were males and 33 (53.22%) were females. Most patients had a ruptured ACAC aneurysm, except three, who presented with only headache. Twenty-two (35.48%) of the 62 patients had anatomical and morphological variations, and they were more common on the right side when compared to the left [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5] and [Table 1], [Table 2].
|Figure 5: Aplastic left A1 artery with median artery of corpus callosum with multiple perforators arising from the anteroinferior surface of anterior communicating artery|
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We chose an arbitrary criterion to classify ACA on the basis of the diameter: prominent – larger than opposite ACA diameter; hypoplastic – less than half of the opposite ACA diameter; aplastic – absent or very thin (strand like) ACA, or no flow in the vessel on ICG videoangiography.
Five (8.06%) patients had a right A1 segment hypoplasia, 2 (3.22%) patients had an aplastic right A1 segment, and 1 (1.61%) patient had a tortuous right A1 segment. Left A1 was aplastic in 3 (4.83%) patients and hypoplastic in 1 (1.61%) patient. A prominent left A1 was seen in 2 (3.22%) patients, and a prominent left A2 segment in 1 (1.61%) patient. Two (3.22%) patients had prominent right A1 and A2 segments. Two (3.22%) patients had fenestration of AcomA and 3 (4.83%) had a median artery of the corpus callosum [Table 2].
Out of the 62 patients, the RAH could be identified in only 44 (70.96%) patients, of which in 31 (70.45%), the artery had an origin from the proximal A2; in 3 (6.81%) patients, it had an origin from the A1-A2 junction, and in 5 (11.36%) patients, it had an origin from the distal A1 segment. 2 (4.54%) patients had very proximal origin of RAH from the A1 segment, and 1 (2.27%) had its origin from the distal A2 segment. In 2 (5.54%) patients, the RAH had an asymmetrical site of origin [Table 3] and [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5].
Acom A had a number of perforators varying from 0 to 5, with an average of 1.29. Two patients had >4 perforators arising from AcomA. Out of the 62 patients, 11 had a parent vessel anomaly. These patients had a total of 23 (mean, 2.09) perforators arising from the AcomA, whereas the remaining patients who were not having parent vessel anomaly had a total of 57 (mean, 1.11) perforators. Unpaired t-test was applied to assess the differences in the mean number of perforators between the AcomAs with or without anomalies. The P value was 0.00036, which was statistically highly significant [Table 4] and [Figure 6].
|Table 4: Anterior communicating artery perforators with and without parent vessel anomaly|
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|Figure 6: Average number of perforators arising from anterior communicating artery with and without parent vessel hypoplasia/aplasia|
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The number of perforators arising from the A1 segment of the anterior cerebral artery ranged from 0 to 9 with an average of 3.11 on the left side; and, 0 to 8 with an average of 2.69 on the right side. Out of the 62 patients, 7 on the right side and 4 on the left side had A1 segment being hypoplastic and/or aplastic. On comparison, the number of perforators were more on the contralateral mirror vessels in these patients. Paired t-test was applied to assess the difference between the number of perforators in mirror vessels when one of them was hypoplastic or aplastic. The P value was 0.000635 suggesting a statistically significant difference [Table 5] and [Figure 7].
|Table 5: Comparison between mean number of perforators on both sides with the variation present ipsilateraly|
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|Figure 7: Average number of perforators from ipsilateral hypo/aplastic A1 segment as well as from the normal contralateral mirror vessel|
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| » Discussion|| |
The incidence of vascular anatomical and morphological variations was quite high in the cases of ACAC harbouring an aneurysm, i.e., 35.48% in this study. Most of the available literature on anatomical variations has been based on the preoperative angiographic study or cadaveric dissection. According to the cadaveric and autopsy study by Swetha et al., and Kapoor et al., the incidence of anatomical variations is 21.4% and 54.8%, respectively. Many studies described the A1-ACA segment anomalies as variants most commonly accompanying the AcomA aneurysm, in the range of 41.33%–50%.,, Bazowski et al., determined that the frequency of anomalies in the anterior communicating artery complex harbouring an aneurysm occurred in 37.7% of patients [Table 6].
|Table 6: Comparison between available literature and our study over anatomical variations of anterior cerebral artery (ACA)|
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In our study, aneurysm formation and anatomical variations were more common in females compared to males (1.14:1, 1.44:1) although this was not statistically significant. This is contrary to the study done by Aarhus et al., who demonstrated that AcomA aneurysms had a higher rupture risk, and that ruptured AcomA aneurysms are over-represented among men.
Right-sided vessels were more commonly involved than the left-sided ones (Right: Left, 1.71:1). The A1 segment had more anatomical and morphological variations compared to the AcomA and A2 segment of the anterior cerebral artery. The most commonly found variations were hypoplasia and aplasia of the vessels, as well as variations in the site of origin, and the size and number of perforators. This perhaps can correlate with the association of aneurysm on the dominant side, as reported by Charbel et al.
In this study, patients had variations in the form of aplasia in 8.1% (on the right side in 3.22% cases and on the left side in 4.83% cases), hypoplasia in 9.67% (8.06% of cases on the right side and 1.61% of cases on the left side), tortuosity of vessels in 1.61%, asymmetric site of origin in 6.81% and origin of vessels at aberrant sites in 4.54%. More than one anatomical variation was seen in 9.6% patients. Existing literature suggests hypoplasia in 10% and aplasia in 1–2% of postmortem series, whereas angio-MR demonstrated an hypoplasia of the A1 segment in 3% and of the A2 segment in 2% of the cases. In such cases, the contralateral A1 segment of ACA is dilated. The reason for some difference in percentages from the existing literature is attributed to the live microscopic study where the variations were best appreciated under magnification and flowing blood. These variations in blood vessel anatomy may increase the risk of ischemia during temporary clip placement or may explain the unexplained neurological deficit that may develop during clipping or coiling.
The incidence of median artery of the corpus callosum (MACC), also called the transitional anterior communicating artery, in our study was 4.83%, whereas in the literature, it is reported to be in the range of 2–13%.,, A careful dissection around the aneurysm is important to avoid an inadvertent clip placement on the said artery.
In the present study, the incidence of AcomA fenestration was 3.62% and both the patients had associated AcomA aneurysm, which are findings that are concordant with the study by De Gast et al., who reported the incidence of AcomA aneurysm formation with fenestration of 4.4%, based on rotational digital subtraction angiography. The incidence of aneurysms based on CT angiography is approximately 10%. Their prevalence in the A1 region is 0–4%, as described in anatomical studies, and 0.058%, as described in angiographic studies., The discrepancy in the occurrence of an aneurysms in various studies is perhaps due to the very small diameter of this artery so that it is rarely visualized unless a high magnification, high-resolution focused angiographic study is done. This variation is associated with a high incidence of aneurysm formation, as seen in our study, where both the cases had an aneurysm at the same location. The importance of knowing about such a variant lies in the fact that these patients can have new aneurysms and recurrence of aneurysm formation at this site. An intraoperative inadvertent clip application should be avoided on this artery.
RAH injury or occlusion can cause significant hemiparesis predominantly faciobrachial, and aphasia (if occlusion of RAH is on the dominant side). Understanding the anatomy and its variations around the ACAC area is essential for the safe and effective dissection and clipping of the aneurysm. According to Perlmutter and Rhoton, 95% of the RAHs can be identified within 4 mm proximal or distal from the AcomA. In our study, we could identify the origin of RAH in 70.96% of the patients, of which 93.18% had origin of RAH in the vicinity of AcomA region, 70.45% had origin of RAH from proximal A2, 11.36% patients had origin of RAH from the distal A1 segment, 6.81% had origin of RAH from the A1-A2 junction, and 11.36% had aberrant origins, in which 2.27% patients had origin of RAH from the distal A2 segment, 4.54% patients had very proximal origin of RAH, and, 4.54% patients had asymmetrical origin of RAH. Our results are in concordance with the results of Perlmutter and Rhoton [Table 7].,,,,,
|Table 7: Comparison between available literature and our study on origin of recurrent artery of Heubner (RAH)|
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According to the available literature, A1 segment of the anterior cerebral artery has an average of 8 (2–15) perforators, 2/3 of which arise from the proximal half of A1 segment whereas 1/3 arises from the distal half, and most arise from the superior (54%) and posterior (32%) surface. In the present study, an average of 2.69 (0–8) perforators from A1 segment of the right ACA and 3.11 (0–9) from the left ACA were seen. This number is lesser than the average number of perforators reported in literature. This discrepancy may be seen because of many associated factors. Most studies are based on cadaveric studies with formalin-fixed brain. In those studies, it was impossible to conclude that the perforators which the authors had counted were actually physiologically patent. In our study, we used ICG video angiography in 74.19% patients to assess the anatomically functioning perforators. In patients in whom we did not use the ICG, the operating surgeon judicially assessed the viability of perforators, based upon their clinical experiences. The second important factor, which played a major role is the presence of aneurysmal sac in the vicinity, especially in the case of the large aneurysms. They can cause adhesions, which can result in perforator damage during the skeletonization of the vascular territory. Patients having A1 segment hypoplasia or aplasia had lesser number of perforators compared to the opposite site normal A1 segment. In hypoplastic A1, the number of perforators arising from the right side was 10 (mean, 1.4) while from the contralateral A1 segment, the number was 30 (mean, 4.2). Similarly, the number of perforators arising from hypoplastic and aplastic left A1 segments were 2 (mean, 0.5), whereas in the same patients, the number of perforators arising from the contralateral right A1 segment were 18 (4.2), which is statistically significant (paired t-test, P value 0.000635). This could perhaps be due to associated anatomical variations, in the form of hypoplasia or aplasia of proximal anterior cerebral artery; there is an increased number of perforators from the contralateral normal side to perfuse the opposite side territory, which is normally perfused by ipsilateral perforators. Its clinical significance lies in the fact that when we attempt surgical clipping of the anterior cerebral territory aneurysm from the dominant side for achieving a good proximal control, we have to be cautious regarding these perforators arising from the dominant A1. These perforators might be the major source of perfusion and their injury may result in a poor surgical outcome. Knowing the perforator anatomy is also important to avoid the overuse of cautery, as an iatrogenic injury to the perforators in this area may result in an adverse clinical outcome.
The Acom A may have 1–4 perforators arising mainly from the posterior and superior surface (in 90% of the cases), based on the data reported by Perlmutter and Rhoton. In our study, we found 0–5 perforators (mean, 1.29) mainly arising from the inferior wall of AcomA. A comparative analysis of the number of perforators arising from the AcomA, and the number of patients having a parent vessel hypoplasia or aplasia with those who do not have parent vessel aplasia or hypoplasia showed a statistically significant variation (P value = 0.00396). Patients who had parent vessel aplasia or hypoplasia have more number of perforators (mean, 2.09 vs 1.11, P value <.05) which are bigger in diameter as well. In 2 cases, we found multiple, very large perforators arising from the anteroinferior wall of AcomA. Such large perforators originating from the AComA have never been reported in literature and were perhaps a replacement for the aplastic or hypoplastic A1 of the other side. Such cases are not suitable for flow diverter placement to treat aneurysms.
| » Conclusion|| |
To perform a safe surgery and obtain a fruitful recovery in patients harbouring an anterior cerebral territory aneurysm, a sound knowledge of the microsurgical anatomy is of paramount importance. The number of perforators in the region of AcomA artery could be several and may arise even from the anteroinferior wall of AcomA. Patients of anterior cerebral territory aneurysms along with parent vessel anomaly have altered distribution of perforators. These patients are prone to developing perforator injury during clipping as well as coiling of aneurysms. These variations may cause local alterations of intravascular dynamics, which might provide the mechanical basis for the development of these aneurysms.
Limitation of study
This was an intraoperative study, and frequently, it may not be possible to see the entire course of the vessel, particularly when the aneurysm sac is large and the vessels are adherent to or hidden by the sac. The presence of vasospasm or vasculitis may falsely give an impression of vascular anomaly such as hypoplasia of the vessels. Patients having a giant aneurysmal sac are prone to developing perforator injury. These patients may also erroneously show a low count of perforators in the region.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| » References|| |
Castro MA, Putman CM, Cebral JR. Patient-specific computational fluid dynamics modeling of anterior communicating artery aneurysms: A study of the sensitivity of intra-aneurysmal flow patterns to flow conditions in the carotid arteries. AJNR Am J Neuroradiol 2006;27:2061-8.
Castro MA, Putman CM, Sheridan MJ, Cebral JR. Hemodynamic patterns of anterior communicating artery aneurysms: A possible association with rupture. AJNR Am J Neuroradiol 2009;30:297-302.
Hashimoto N, Handa H, Hazama F. Experimentally induced cerebral aneurysms in rats: Part II. Surg Neurol 1979;11:243-6.
Penn DL, Komotar RJ, Sander Connolly E. Hemodynamic mechanisms underlying cerebral aneurysm pathogenesis. J Clin Neurosci 2011;18:1435-8.
Swetha B, Dakshayani K. Variable anterior cerebral artery in human cadavers. Anatomica Karnataka 2011;5:8-11.
Kapoor K, Singh B, Dewan L. Variations in the configuration of the circle of Willis. Anatomical Sci Int 2008;83:96-106.
Catteruza M, Dimigen C, Ehrenreich H, Hecker M. Strech-induced endothelial B receptor-mediated aptosis in vascular smooth muscle cells. FASEB J 2000;14:991-8.
Ağayev K, Önal B, Yavuz K, Ziyal MI. The association of A1 segment hypoplasia/aplasia with anterior communicating artery aneurysm: A radiological study. Turk Neurosurg 2005;15:196-9.
Karazincir S, Ada E, Sarsilmaz A, Yalcin O, Vidinili B, Sahin E. Frequency of vascular variations and anomalies accompanying intracranial aneurysm. Tani Girisim Radyol 2004;10:103-9.
Bazowski P, Ladziński P, Gamrot J, Rudnik A, Baron J. Aneurysms of the anterior communicating artery and anomalies of the anterior part of the circle of Willis. Neurol Neurochir Pol 1991;25:485-90.
Aarhus M, Helland CA, Wester K. Differences in anatomical distribution, gender, and sidedness between ruptured and unruptured intracranial aneurysms in a defined patient population. Acta Neurochir (Wien) 2009;151:1569-74.
Charbel FT, Seyfried D, Metha B, Dujovny M, Ausman JI. Dominant A1: Angiographic and clinical correlations with anterior communicating artery aneurysms. Neurol Res 1991;13:253-6.
Dimmick SJ, Faulder KC. Normal variants of the cerebral circulation at multidetector CT angiography. Radiographics 2009;29:1027-43.
Given C, Morris P. Recognition and importance of an infraoptic anterior cerebral artery: Case report. Am J Neuroradiol 2002;23:452-4.
Nathal E, Yasui N, Sampei T, Suzuki A. Intraoperative anatomical studies in patients with aneurysms of the anterior communicating artery complex. J Neurosurg 1992;76:629-34.
Ogawa A, Suzuki M, Sakurai Y. Vascular anomalies associated with aneurysms of the anterior communicating artery: Microsurgical observation. J Neurosurg 1990;72:706-9.
De Gast A, Van Rooij W, Sluzewski M. Fenestrations of the anterior communicating artery: Incidence on 3D angiography and relationship to aneurysms. Am J Neuroradiol 2008;29:296-8.
Bożek P, Pilch-Kowalczyk J, Kluczewska E, Zymon-Zagórska A. Detection of cerebral artery fenestrations by computed tomography angiography. J Neurol Neurochir Polska 2012;46:239-44.
Zhao H, Fu J, Lu ZL, Lu HJ. Fenestration of the anterior cerebral artery detected by magnetic resonance angiography. Chin Med J 2009;122:1139-42.
Perlmutter D, Rhoton AL Jr. Microsurgical anatomy of the anterior cerebral-anterior communicating -recurrent artery complex. J Neurosurg 1976;45:259-72.
Gomes F, Dujovny M, Umansky F, Ausman JI, Diaz FG, Ray WJ, et al
. Microsurgical anatomy of the recurrent artery of Heubner. J Neurosurg 1984;60:130-9.
Loukas M, Louis R, Childs R. Anatomical examination of the recurrent artery of Heubner. Clin Anat 2005;19:25-31.
Tao X, Yu XJ, Bhattarai B. Microsurgical anatomy of the anterior communicating artery complex in adult Chinese heads. Surg Neurol 2006;65:155-61.
Uzun I, Gurdal E, Cakmak YO. A reminder of the anatomy of the recurrent artery of Heubner,” Central Eur Neurosurg 2009;70:36-8.
Aydin I, Onder A, Takci E, Kadioglu H, Kayaoglu C, Tuzun Y. Heubner's artery variations in anterior communicating artery aneurysms. Acta Neurochir 1994;127:17-20.
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7]
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7]