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LETTERS TO THE EDITOR
Year : 2022  |  Volume : 25  |  Issue : 2  |  Page : 298-300
 

If nothing goes right, it goes to the left: A case of left anterior cerebral artery stroke due to right internal carotid artery stenosis


Department of Neurology, Comprehensive Stroke Care Program, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Thiruvananthapuram, Kerala, India

Date of Submission26-Apr-2021
Date of Acceptance06-Aug-2021
Date of Web Publication13-Jan-2022

Correspondence Address:
P N Sylaja
Professor of Neurology, Comprehensive Stroke Care Program, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum - 695 011, Kerala
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/aian.aian_307_21

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How to cite this article:
Ramachandran H, Pavuluri H, Sreedharan SE, Sylaja P N. If nothing goes right, it goes to the left: A case of left anterior cerebral artery stroke due to right internal carotid artery stenosis. Ann Indian Acad Neurol 2022;25:298-300

How to cite this URL:
Ramachandran H, Pavuluri H, Sreedharan SE, Sylaja P N. If nothing goes right, it goes to the left: A case of left anterior cerebral artery stroke due to right internal carotid artery stenosis. Ann Indian Acad Neurol [serial online] 2022 [cited 2022 Jul 1];25:298-300. Available from: https://www.annalsofian.org/text.asp?2022/25/2/298/335392




Dear Editor,

Symptomatic carotid disease with more than 50% stenosis usually causes neurological symptoms in the form of minor stroke or transient ischaemic attacks in the ipsilateral anterior circulation territory and the most common location of plaque is in the carotid bifurcation and proximal internal carotid artery (ICA).[1] The mechanism of stroke is an artery to artery embolism, thrombosis or hemodynamic fluctuations. Azygos anterior cerebral artery (AACA) is a variant of Willisian circle anatomy characterised by absence of the anterior communicating artery (ACom) and the bilateral anterior cerebral arteries (ACAs) join to form a single trunk which travels superiorly in the interhemispheric fissure and has implications in the arterial haemodynamics. We report a case of left ACA territory infarction caused by right ICA stenosis in a patient with azygos ACA.


   Case Report Top


A 55-year-old gentleman with past history of hypertension and dyslipidaemia for the last 5 years, poorly compliant to treatment, with acute onset right-sided weakness of predominantly lower limb along with speech disturbance, presented outside the window period. On examination, the patient had apathy, global aphasia, right upper motor neuron facial weakness and right-sided weakness predominantly in the lower limb. CT brain at admission showed evolved infarct in the left ACA territory involving the left parasagittal frontal lobe [Figure 1]. CT angiogram showed right ICA hypodense plaque causing about 80% stenosis at origin and azygous ACA with occlusion of the left division of azygos ACA [Figure 1]. Cardiac evaluation including 2D-echo and 24 hours Holter monitoring were normal. MR plaque imaging of the right ICA plaque showed lipid-rich core without any ulceration or intraplaque haemorrhage. The patient was managed with dual antiplatelets, statins and antihypertensives. In view of the symptomatic right carotid stenosis, carotid revascularisation was considered. Over the next 1 month, the patient improved to NIHSS of 9 and modified Rankin scale of 3. He is planned for right carotid endarterectomy.
Figure 1: CT brain with angiogram of the patient. (a) Axial CT brain on admission showing left mesial frontal hypodensity (arrow) suggesting an evolved ACA territory infarct. (b) CT angiogram of extracranial vessels in sagittal section showing right proximal (white arrow) ICA plaque causing 80% stenosis. (c) CT angiogram axial section at the level of carotid bifurcation showing hypodense plaque (white arrow) in the right proximal ICA. (d) CT angiogram coronal section of intracranial vessels showing azygos ACA and left division occlusion (arrow)

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   Discussion Top


Anterior circulation comprises of ACA and middle cerebral artery (MCA) formed from ICA. The ACAs are connected by the ACom which is a primary collateral along with the posterior communicating artery in cases of occlusions or stenosis in the vascular network.[2] Arteria termatica or AACA was first described by Wilder with a reported incidence of less than 2%.[3] AACA is characterised by A1 segments of bilateral ACAs joining to form a single stem (A2 segment) which ascends in the interhemispheric fissure as a result of the persistence of the embryonic median artery of the corpus callosum. The anatomical variations in the ACA were described by Baptista.[4] Type I anomaly is the true azygos ACA, from which ACA branches supply both hemispheres. Type II anomaly is the bihemispheric ACA, where both right and left ACA are present, but most of the major branches to the bilateral hemispheres arise from one ACA and the other one is rudimentary. In type III, an accessory ACA arises from Acom [Figure 2]. Our patient had a Type I anomaly.
Figure 2: Schematic depiction of normal ACA and anomalous variants. 1 – terminal ICA, 2 – left MCA M1, 3 – right A1 ACA, 4 – left A1 ACA, 5 – right A2 ACA, 6 – left A2 ACA, 7 – Acom artery, 8 – true azygos ACA, 9 – left A2 azygos (bihemispheric) ACA, 10 – rudimentary right A2 ACA and 11 – accessory third median azygos ACA. (a) Normal ACA pattern. (b) Type I variant showing true azygos ACA from which ACA branches supply both hemispheres. (c) Type II variant showing bihemispheric ACA where most of the major branches to the bilateral hemispheres arise from one A2 ACA and contralateral rudimentary A2 ACA. (d) Type III variant showing an accessory ACA arising from Acom artery

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The left ACA territory infarct could be explained by right ICA stenosis due to the coexistent true azygos ACA with probable embolisation from the right ICA plaque as the mechanism causing the infarct and thus the aetiology of stroke is large artery atherosclerosis. In a patient with high-grade carotid stenosis, with infarct in the opposite hemisphere, carefully analysing the vascular anatomy may give a clue to the aetiology which can help in the management of the patient.


   Conclusion Top


AACA is a rare variant, which can produce unilateral or bifrontal infarctions.[5] The anatomical variations in the ACA should be carefully looked into in cases of ACA territory strokes that affect the arterial haemodynamics and a proper etiological evaluation aids in the optimal management of the patient.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Acknowledgements

We thank Mr. Krishnakumar N for his assistance in obtaining high quality images.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
   References Top

1.
Abbott AL, Paraskevas KI, Kakkos SK, Golledge J, Eckstein H-H, Diaz-Sandoval LJ, et al. Systematic review of guidelines for the management of asymptomatic and symptomatic carotid stenosis. Stroke 2015;46:3288-301.  Back to cited text no. 1
    
2.
Moreira de Sousa CS, Mendes de Miranda CLV, Avelino MC, Bastos BB, Moreira de Sousa RS, Mendes de Miranda CVV. Thrombosis of the azygos anterior cerebral artery. Case Rep Radiol 2017;2017:5409430.  Back to cited text no. 2
    
3.
Baptista AG. Studies on the arteries of the brain. Neurology 1963;13:825-35.  Back to cited text no. 3
    
4.
Beyhan M, Gökçe E, Karakuş K. Radiological classification of azygos anterior cerebral artery and evaluation of the accompanying vascular anomalies. Surg Radiol Anat 2020;42:1345-54.  Back to cited text no. 4
    
5.
Khaliq A, Gul P, Gul P. Azygos anterior cerebral artery causing Bifrontal infarcts: A case report. PJNS 2018;13:20-2.  Back to cited text no. 5
    


    Figures

  [Figure 1], [Figure 2]



 

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