Versatility
Award-Winning Technology
by MicroVention
Trevo Retriever TRUSTED: Used Worldwide • Winner of the Prix Galien Award for Best Medical Technology • The only stent retriever with full-length visibility
Scepter C Scepter XC ®
®
Redefining deliveRability, veRsatility and ContRol Microvention has developed two occlusion balloon catheters. Scepter C® compliant balloon is designed for reliable vessel occlusion yet conforms to vessel anatomy. Scepter XC® x-tra compliant balloon conforms to extremely complex anatomies where neck coverage is more challenging.
Copyright © 2015 Stryker NV00014777.AA
Stroke: Our Only Focus. Our Ongoing Promise.
• Used with
MR CLEAN
1
PROVEN: Level 1 evidence • First Trial to show benefit of intra-arterial therapy + IV-tPA over IV-tPA alone • Largest of the randomized AIS trials, with over 500 patients enrolled For more information or a product demonstration, contact your local MicroVention representative: MICROVENTION, Scepter C, Scepter XC and Headway are registered trademarks of MicroVention, Inc. Scientific and clinical data related to this document are on file at MicroVention, Inc. Refer to Instructions for Use for additional information. Federal (USA) law restricts this device for sale by or on the order of a physician. © 2014 MicroVention, Inc. 11/14
MicroVention, Inc. Worldwide Headquarters 1311 Valencia Avenue Tustin, California 92780, USA MicroVention UK Limited MicroVention Europe, S.A.R.L. MicroVention Deutschland GmbH Web
PH +1.714.247.8000
PH +44 (0) 191 258 6777 PH +33 (1) 39 21 77 46 PH +49 211 210 798-0 microvention.com
• 2x higher chance for a mRS 0-2 and 7x more likely to recanalize* * Adjusted value odds ratio (95% CI) for “no intracranial occlusion on follow-up CT angiography” in the intervention group versus the control group was 6.88 (4.34 to 10.94). Values were adjusted for age, NIHSS at baseline, time from onset to randomization, status with respect to previous stroke, atrial fibrillation, diabetes mellitus and occlusion of the ICAT. Data for follow-up CT angiography were not available for 106 patients. 1
O.A. Berkhemer et al. A Randomized Trial for Intraarterial Treatment for Acute Ischemic Stroke. N Eng J Med December 2014.
Copyright © 2015 Stryker NV00014776.AA
Stroke: Our Only Focus. Our Ongoing Promise.
Case Report
Sufficient collateral blood supply from accessory middle cerebral artery in a patient with acute ischemic stroke
Interventional Neuroradiology 2015, Vol. 21(2) 215–217 ! The Author(s) 2015 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/1591019915583230 ine.sagepub.com
Zhen-Sheng Liu, Long-Jiang Zhou, Yong Sun, Xiong-Wei Kuang, Wei Wang and Cheng Li
Abstract We reported a case of acute embolic occlusion of the middle cerebral artery with a patent accessory middle cerebral artery. Because of the presence of sufficient collateral blood supply from the accessory middle cerebral artery, the patient only underwent transient ischemic attack and did not need endovascular treatment. There was mild infarction in the basal ganglia and temporal lobe, NIHSS score of the patient at discharge seven days after stroke onset was 0, and modified Rankin scale score at 90 days was 0.
Keywords Accessory middle cerebral artery, collateral, ischemic stroke
Introduction The accessory middle cerebral artery (AMCA) is a rare anomalous vessel arising from the anterior cerebral artery (ACA) and running through the sylvian fissure along with the middle cerebral artery (MCA).1,2 Several reports have described cerebral aneurysm and ischemic stroke associated with AMCA.3–5 We report one case of acute embolic occlusion of the MCA in association with an AMCA, in which the AMCA provided sufficient collateral blood supply to the MCA territory to avoid massive cerebral infarction.
Case report A 77-year-old woman was admitted to a primary stroke centre 1 hour after the onset of disturbance of consciousness and left-sided hemiparesis. Physical examination disclosed sensory loss of the left face, arm, and leg, left facial paralysis, and hemiplegia. The National Institutes of Health Stroke Scale (NIHSS) score was 12. The patient had a history of atrial fibrillation for 40 years, which suggested that the cause of the stroke was cardioembolism. A computed tomography (CT) scan showed a hyperdensity of the right MCA without associated ischemic parenchymal changes (Figure 1a). Because of the implantation of an artificial heart pacemaker, a magnetic resonance imaging examination was not performed on the patient. A total dose of 90 mg of rt-PA was administered intravenously without any change in neurological score at the end of the infusion, 2.5 hours after symptoms onset. Therefore, mechanical
thrombectomy was recommended for emergent neurovascular rescue and the patient was transferred to an interventional center for endovascular treatment. When femoral artery puncture was performed 3 hours after symptoms onset, the disturbance of consciousness and left-sided hemiplegia of the patient gradually recovered. The emergency cerebral angiography revealed right MCA occlusion (Figure 1b) and AMCA, which provided sufficient collateral blood supply to the MCA territory through leptomeningeal anastomoses (Figure 1c and d). Furthermore, neurological symptoms of the patient dramatically improved from an NIHSS score of 12 to 2 within 30 min of arrival at the interventional center, and she therefore did not undergo mechanical thrombectomy with the Solitaire device. The patient was discharged to the primary stroke center 24 hours later. A control CT three days after symptoms onset showed small area of infarction within the basal ganglia and temporal lobe (Figure 1e). NIHSS score at discharge seven days after stroke onset was 0 and modified Rankin scale score at 90 days was 0.
Department of Radiology, People’s Hospital, Affiliated Hospital of Southeast University, Yangzhou, China Corresponding author: Zhen-Sheng Liu, Department of Radiology, Yangzhou No.1 People’s Hospital, Affiliated Hospital of Southeast University, 45 Taizhou Road, Yangzhou, Jiangsu 225001, China. Email: [email protected]
216
Interventional Neuroradiology 21(2)
Figure 1. CT scan and emergency cerebral angiography of a 77-year-old female with acute ischemic stroke. (a) CT scan showing a hyperdensity of the right MCA (arrow) without associated ischemic parenchymal changes. (b) A cerebral angiography, in the early arterial phase, revealed a complete embolic occlusion of M1 of the right MCA (thick arrow), AMCA from ACA (thin arrow), distal MCA branches (arrowhead) from leptomeningeal collateral supply of AMCA, and several perforating arteries from AMCA to the basal ganglia. (c, d) The distal and proximal MCA branches were displayed more clearly in the mid and late arterial phase. (e) A CT scan three days after the onset showed small area of infarction within the basal ganglia (arrow) and temporal lobe (arrowhead).
Liu et al.
Discussion The anatomy of the AMCA was first described by Crompton.6 The origin and clinical significance of the AMCA are still controversial. An incidence of AMCAs of 0.31% was reported by Abanou et al. in their study of 6000 angiograms.7 Abanou et al. classified AMCAs into three subtypes. Type 1 arises from the ICA proximal to its bifurcation, type 2 originates from the proximal portion of the A1 of the ACA, and type 3 arises more distally A1. In this classification, type 1 is actually a duplicated MCA. In addition, Kahilogullari and Ugur reported a case in which AMCA originated from the callosomarginal artery.8 Teal et al. proposed using the term AMCA to describe the anomalous vessel originating from the ACA.9 Several authors have reported that an AMCA coursed along the horizontal portion of the MCA and divided into several branches within the sylvian fissure and supplied the territories of the orbitofrontal, prefrontal, precentral, and central arteries.1,2 Although most AMCAs are smaller than the main MCAs, the occlusion of AMCAs can lead to severe neurological deficit, particularly in the dominant hemisphere.4,5 The MCA is the youngest artery of the brain. It appears later and is in balance with the recurrent artery of Heubner (RAH) with respect to the deep and cortical territories. Handa et al. were among the first authors to suggest that the AMCA forms as a hypertrophied RAH.10 However, there are objections to this idea because of several reasons.11 First, perforating arteries rarely arise from an AMCA. Second, the RAH can coexist with an AMCA. And third, the two vessels have different patterns of distribution. Takahashi et al. proposed that both the RAH and AMCA are persistent anastomoses between the ACA and MCA over the tuberculum olfactorium.12 This explains the developmental variants of these anastomoses, which may result in either an AMCA or a RAH. There are collateral anastomoses between AMCA and MCA through leptomeningeal anastomoses and perforating arteries.13,14 In MCA occlusion, the AMCA may play an important role in supplying collateral blood flow to the territory of the MCA via these collateral anastomoses. Komiyama et al. reported a case of right ICA occlusion with an AMCA,14 which was the sole contributor of collateral blood supply to the right MCA territory. However, the collateral blood supply was not sufficient to spare the rest of the frontal lobe, the temporal lobe, and the basal ganglia.11 The patient had hemidysesthesia, hemianopsia, and hemiparesis, but could walk with a cane two months after symptoms onset. In our case with acute occlusion of MCA, the collateral blood supply revealed by emergency cerebral angiography was mainly from leptomeningeal anastomoses between AMCA and MCA. The collateral supply was so sufficient that the patient only underwent transient ischemic attack and did not need endovascular treatment. There was mild infarction
217 in the basal ganglia and temporal lobe, NIHSS score of the patient at discharge seven days after stroke onset was 0 and modified Rankin scale score at 90 days was 0. To our knowledge, this is the first case report in which AMCA provide sufficient collateral blood supply to the MCA territory to avoid severe disability resulting from the acute occlusion of MCA. Interventional radiologists should bear in mind about this uncommon but important variant. Funding This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.
Conflict of interest None declared.
References 1. Kim MS and Lee HK. The angiographic feature and clinical implication of accessory middle cerebral artery. J Korean Neurosurg Soc 2009; 45: 289–292. 2. Reis CV, Zabramski JM, Safavi-Abbasi S, et al. The accessory middle cerebral artery: anatomic report. Neurosurgery 2008; 63(1 Suppl 1): ONS10–13. 3. Lee IH, Jeon P, Kim KH, et al. Endovascular treatment of a ruptured accessory middle cerebral artery aneurysm. J Clin Neurosci 2010; 17: 383–384. 4. Hiramatsu Y, Wakita M, Matsuoka H, et al. Cerebral infarction associated with accessory middle cerebral arteries: two case reports. Intern Med 2014; 53: 1381–1384. 5. Sharma VK. Transient ischemic attack associated with stenosis of accessory middle cerebral artery. Clin Neurol Neurosurg 2010; 112: 88. 6. Crompton MR. The pathology of ruptured middle-cerebral aneurysms with special reference to the differences between the sexes. Lancet 1962; 2: 421–425. 7. Abanou A, Lasjaunias P, Manelfe C, et al. The accessory middle cerebral artery (AMCA). Diagnostic and therapeutic consequences. Anat Clin 1984; 6: 305–309. 8. Kahilogullari G and Ugur HC. Accessory middle cerebral artery originating from callosomarginal artery. Clin Anat 2006; 19: 694–695. 9. Teal JS, Rumbaugh CL, Bergeron RT, et al. Anomalies of the middle cerebral artery: accessory artery, duplication, and early bifurcation. Am J Roentgenol 1973; 118: 567–575. 10. Handa J, Shimizu Y, Matsuda M, et al. The accessory middle cerebral artery: report of further two cases. Clin Radiol 1970; 21: 415–416. 11. Lasjaunias P, Bereinstein A and ter Brugge K. Surgical neuroangiography. Vol 1. Clinical vascular anatomy and variations, 2nd ed. New York: Springer-Verlag, 2001, pp.590–597. 12. Takahashi S, Hoshino F, Uemura K, et al. Accessory middle cerebral artery: is it a variant form of the recurrent artery of Heubner? Am J Neuroradiol 1989; 10: 563–568. 13. Jain KK. Some observations on the anatomy of the middle cerebral artery. Can J Surg 1964; 7: 134–139. 14. Komiyama M, Nishikawa M and Yasui T. The accessory middle cerebral artery as a collateral blood supply. Am J Neuroradiol 1997; 18: 587–590.
Copyright of Interventional Neuroradiology is the property of Centauro srl and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
Award-Winning Technology
by MicroVention
Trevo Retriever TRUSTED: Used Worldwide • Winner of the Prix Galien Award for Best Medical Technology • The only stent retriever with full-length visibility
Scepter C Scepter XC ®
®
Redefining deliveRability, veRsatility and ContRol Microvention has developed two occlusion balloon catheters. Scepter C® compliant balloon is designed for reliable vessel occlusion yet conforms to vessel anatomy. Scepter XC® x-tra compliant balloon conforms to extremely complex anatomies where neck coverage is more challenging.
Copyright © 2015 Stryker NV00014777.AA
Stroke: Our Only Focus. Our Ongoing Promise.
• Used with
MR CLEAN
1
PROVEN: Level 1 evidence • First Trial to show benefit of intra-arterial therapy + IV-tPA over IV-tPA alone • Largest of the randomized AIS trials, with over 500 patients enrolled For more information or a product demonstration, contact your local MicroVention representative: MICROVENTION, Scepter C, Scepter XC and Headway are registered trademarks of MicroVention, Inc. Scientific and clinical data related to this document are on file at MicroVention, Inc. Refer to Instructions for Use for additional information. Federal (USA) law restricts this device for sale by or on the order of a physician. © 2014 MicroVention, Inc. 11/14
MicroVention, Inc. Worldwide Headquarters 1311 Valencia Avenue Tustin, California 92780, USA MicroVention UK Limited MicroVention Europe, S.A.R.L. MicroVention Deutschland GmbH Web
PH +1.714.247.8000
PH +44 (0) 191 258 6777 PH +33 (1) 39 21 77 46 PH +49 211 210 798-0 microvention.com
• 2x higher chance for a mRS 0-2 and 7x more likely to recanalize* * Adjusted value odds ratio (95% CI) for “no intracranial occlusion on follow-up CT angiography” in the intervention group versus the control group was 6.88 (4.34 to 10.94). Values were adjusted for age, NIHSS at baseline, time from onset to randomization, status with respect to previous stroke, atrial fibrillation, diabetes mellitus and occlusion of the ICAT. Data for follow-up CT angiography were not available for 106 patients. 1
O.A. Berkhemer et al. A Randomized Trial for Intraarterial Treatment for Acute Ischemic Stroke. N Eng J Med December 2014.
Copyright © 2015 Stryker NV00014776.AA
Stroke: Our Only Focus. Our Ongoing Promise.
Case Report
Sufficient collateral blood supply from accessory middle cerebral artery in a patient with acute ischemic stroke
Interventional Neuroradiology 2015, Vol. 21(2) 215–217 ! The Author(s) 2015 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/1591019915583230 ine.sagepub.com
Zhen-Sheng Liu, Long-Jiang Zhou, Yong Sun, Xiong-Wei Kuang, Wei Wang and Cheng Li
Abstract We reported a case of acute embolic occlusion of the middle cerebral artery with a patent accessory middle cerebral artery. Because of the presence of sufficient collateral blood supply from the accessory middle cerebral artery, the patient only underwent transient ischemic attack and did not need endovascular treatment. There was mild infarction in the basal ganglia and temporal lobe, NIHSS score of the patient at discharge seven days after stroke onset was 0, and modified Rankin scale score at 90 days was 0.
Keywords Accessory middle cerebral artery, collateral, ischemic stroke
Introduction The accessory middle cerebral artery (AMCA) is a rare anomalous vessel arising from the anterior cerebral artery (ACA) and running through the sylvian fissure along with the middle cerebral artery (MCA).1,2 Several reports have described cerebral aneurysm and ischemic stroke associated with AMCA.3–5 We report one case of acute embolic occlusion of the MCA in association with an AMCA, in which the AMCA provided sufficient collateral blood supply to the MCA territory to avoid massive cerebral infarction.
Case report A 77-year-old woman was admitted to a primary stroke centre 1 hour after the onset of disturbance of consciousness and left-sided hemiparesis. Physical examination disclosed sensory loss of the left face, arm, and leg, left facial paralysis, and hemiplegia. The National Institutes of Health Stroke Scale (NIHSS) score was 12. The patient had a history of atrial fibrillation for 40 years, which suggested that the cause of the stroke was cardioembolism. A computed tomography (CT) scan showed a hyperdensity of the right MCA without associated ischemic parenchymal changes (Figure 1a). Because of the implantation of an artificial heart pacemaker, a magnetic resonance imaging examination was not performed on the patient. A total dose of 90 mg of rt-PA was administered intravenously without any change in neurological score at the end of the infusion, 2.5 hours after symptoms onset. Therefore, mechanical
thrombectomy was recommended for emergent neurovascular rescue and the patient was transferred to an interventional center for endovascular treatment. When femoral artery puncture was performed 3 hours after symptoms onset, the disturbance of consciousness and left-sided hemiplegia of the patient gradually recovered. The emergency cerebral angiography revealed right MCA occlusion (Figure 1b) and AMCA, which provided sufficient collateral blood supply to the MCA territory through leptomeningeal anastomoses (Figure 1c and d). Furthermore, neurological symptoms of the patient dramatically improved from an NIHSS score of 12 to 2 within 30 min of arrival at the interventional center, and she therefore did not undergo mechanical thrombectomy with the Solitaire device. The patient was discharged to the primary stroke center 24 hours later. A control CT three days after symptoms onset showed small area of infarction within the basal ganglia and temporal lobe (Figure 1e). NIHSS score at discharge seven days after stroke onset was 0 and modified Rankin scale score at 90 days was 0.
Department of Radiology, People’s Hospital, Affiliated Hospital of Southeast University, Yangzhou, China Corresponding author: Zhen-Sheng Liu, Department of Radiology, Yangzhou No.1 People’s Hospital, Affiliated Hospital of Southeast University, 45 Taizhou Road, Yangzhou, Jiangsu 225001, China. Email: [email protected]
216
Interventional Neuroradiology 21(2)
Figure 1. CT scan and emergency cerebral angiography of a 77-year-old female with acute ischemic stroke. (a) CT scan showing a hyperdensity of the right MCA (arrow) without associated ischemic parenchymal changes. (b) A cerebral angiography, in the early arterial phase, revealed a complete embolic occlusion of M1 of the right MCA (thick arrow), AMCA from ACA (thin arrow), distal MCA branches (arrowhead) from leptomeningeal collateral supply of AMCA, and several perforating arteries from AMCA to the basal ganglia. (c, d) The distal and proximal MCA branches were displayed more clearly in the mid and late arterial phase. (e) A CT scan three days after the onset showed small area of infarction within the basal ganglia (arrow) and temporal lobe (arrowhead).
Liu et al.
Discussion The anatomy of the AMCA was first described by Crompton.6 The origin and clinical significance of the AMCA are still controversial. An incidence of AMCAs of 0.31% was reported by Abanou et al. in their study of 6000 angiograms.7 Abanou et al. classified AMCAs into three subtypes. Type 1 arises from the ICA proximal to its bifurcation, type 2 originates from the proximal portion of the A1 of the ACA, and type 3 arises more distally A1. In this classification, type 1 is actually a duplicated MCA. In addition, Kahilogullari and Ugur reported a case in which AMCA originated from the callosomarginal artery.8 Teal et al. proposed using the term AMCA to describe the anomalous vessel originating from the ACA.9 Several authors have reported that an AMCA coursed along the horizontal portion of the MCA and divided into several branches within the sylvian fissure and supplied the territories of the orbitofrontal, prefrontal, precentral, and central arteries.1,2 Although most AMCAs are smaller than the main MCAs, the occlusion of AMCAs can lead to severe neurological deficit, particularly in the dominant hemisphere.4,5 The MCA is the youngest artery of the brain. It appears later and is in balance with the recurrent artery of Heubner (RAH) with respect to the deep and cortical territories. Handa et al. were among the first authors to suggest that the AMCA forms as a hypertrophied RAH.10 However, there are objections to this idea because of several reasons.11 First, perforating arteries rarely arise from an AMCA. Second, the RAH can coexist with an AMCA. And third, the two vessels have different patterns of distribution. Takahashi et al. proposed that both the RAH and AMCA are persistent anastomoses between the ACA and MCA over the tuberculum olfactorium.12 This explains the developmental variants of these anastomoses, which may result in either an AMCA or a RAH. There are collateral anastomoses between AMCA and MCA through leptomeningeal anastomoses and perforating arteries.13,14 In MCA occlusion, the AMCA may play an important role in supplying collateral blood flow to the territory of the MCA via these collateral anastomoses. Komiyama et al. reported a case of right ICA occlusion with an AMCA,14 which was the sole contributor of collateral blood supply to the right MCA territory. However, the collateral blood supply was not sufficient to spare the rest of the frontal lobe, the temporal lobe, and the basal ganglia.11 The patient had hemidysesthesia, hemianopsia, and hemiparesis, but could walk with a cane two months after symptoms onset. In our case with acute occlusion of MCA, the collateral blood supply revealed by emergency cerebral angiography was mainly from leptomeningeal anastomoses between AMCA and MCA. The collateral supply was so sufficient that the patient only underwent transient ischemic attack and did not need endovascular treatment. There was mild infarction
217 in the basal ganglia and temporal lobe, NIHSS score of the patient at discharge seven days after stroke onset was 0 and modified Rankin scale score at 90 days was 0. To our knowledge, this is the first case report in which AMCA provide sufficient collateral blood supply to the MCA territory to avoid severe disability resulting from the acute occlusion of MCA. Interventional radiologists should bear in mind about this uncommon but important variant. Funding This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.
Conflict of interest None declared.
References 1. Kim MS and Lee HK. The angiographic feature and clinical implication of accessory middle cerebral artery. J Korean Neurosurg Soc 2009; 45: 289–292. 2. Reis CV, Zabramski JM, Safavi-Abbasi S, et al. The accessory middle cerebral artery: anatomic report. Neurosurgery 2008; 63(1 Suppl 1): ONS10–13. 3. Lee IH, Jeon P, Kim KH, et al. Endovascular treatment of a ruptured accessory middle cerebral artery aneurysm. J Clin Neurosci 2010; 17: 383–384. 4. Hiramatsu Y, Wakita M, Matsuoka H, et al. Cerebral infarction associated with accessory middle cerebral arteries: two case reports. Intern Med 2014; 53: 1381–1384. 5. Sharma VK. Transient ischemic attack associated with stenosis of accessory middle cerebral artery. Clin Neurol Neurosurg 2010; 112: 88. 6. Crompton MR. The pathology of ruptured middle-cerebral aneurysms with special reference to the differences between the sexes. Lancet 1962; 2: 421–425. 7. Abanou A, Lasjaunias P, Manelfe C, et al. The accessory middle cerebral artery (AMCA). Diagnostic and therapeutic consequences. Anat Clin 1984; 6: 305–309. 8. Kahilogullari G and Ugur HC. Accessory middle cerebral artery originating from callosomarginal artery. Clin Anat 2006; 19: 694–695. 9. Teal JS, Rumbaugh CL, Bergeron RT, et al. Anomalies of the middle cerebral artery: accessory artery, duplication, and early bifurcation. Am J Roentgenol 1973; 118: 567–575. 10. Handa J, Shimizu Y, Matsuda M, et al. The accessory middle cerebral artery: report of further two cases. Clin Radiol 1970; 21: 415–416. 11. Lasjaunias P, Bereinstein A and ter Brugge K. Surgical neuroangiography. Vol 1. Clinical vascular anatomy and variations, 2nd ed. New York: Springer-Verlag, 2001, pp.590–597. 12. Takahashi S, Hoshino F, Uemura K, et al. Accessory middle cerebral artery: is it a variant form of the recurrent artery of Heubner? Am J Neuroradiol 1989; 10: 563–568. 13. Jain KK. Some observations on the anatomy of the middle cerebral artery. Can J Surg 1964; 7: 134–139. 14. Komiyama M, Nishikawa M and Yasui T. The accessory middle cerebral artery as a collateral blood supply. Am J Neuroradiol 1997; 18: 587–590.
Copyright of Interventional Neuroradiology is the property of Centauro srl and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
