Table of Contents  
CASE REPORT
Year : 2021  |  Volume : 8  |  Issue : 1  |  Page : 90-92

Cerebral collateral circulation in acute stroke with occlusive internal carotid artery disease


Department of Neurology and Emergency Care, Ramkrishna Care Hospital, Raipur, Chhattisgarh, India

Date of Submission05-Feb-2020
Date of Decision10-Feb-2020
Date of Acceptance11-Mar-2020
Date of Web Publication20-Feb-2021

Correspondence Address:
Rahul Pathak
Department of Neurology and Emergency Care, Ramkrishna Care Hospital, Raipur, Chhattisgarh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijves.ijves_15_20

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  Abstract 


Acute brain infarction due to carotid artery occlusion has been associated with poor outcome in the absence of cerebral collaterals. The incipient development of collaterals does not guarantee their persistence while available data are strongly indicative that good collateral flow is key in cerebral perfusion, and in reducing infarct size, this knowledge has resulted in only limited therapeutic applications.

Keywords: Acute stroke, cerebral collaterals, external carotid artery, internal carotid artery, internal carotid artery occlusion


How to cite this article:
Pathak R, Thakur SD, Imade A, Sen LC. Cerebral collateral circulation in acute stroke with occlusive internal carotid artery disease. Indian J Vasc Endovasc Surg 2021;8:90-2

How to cite this URL:
Pathak R, Thakur SD, Imade A, Sen LC. Cerebral collateral circulation in acute stroke with occlusive internal carotid artery disease. Indian J Vasc Endovasc Surg [serial online] 2021 [cited 2021 Mar 1];8:90-2. Available from: https://www.indjvascsurg.org/text.asp?2021/8/1/90/309701




  Introduction Top


Cerebral collateral circulation has been reported to alter the risk of stroke in many studies. The circle of Willis constitutes the main network of collateral circulation and is immediately available to maintain perfusion in case of acute large artery occlusion, while other collateral networks are also available, but optimal functioning may develop over time.[1] In patients with occlusion of the internal carotid artery (ICA), the collateral circulation plays a pivotal role in the pathophysiology of cerebral ischemia.[2] Inadequate collateral blood flow distal to the ICA occlusion may be due to poor function of collateral pathways. In ICA occlusion, the circle of Willis, including the anterior and posterior communicating arteries, is the major collateral pathway that can compensate for decreased cerebral perfusion pressure rapidly. While collateral pathways through the ophthalmic artery and leptomeningeal vessels may be recruited when there is inadequate collateral flow through the circle of Willis.[2] Thus, an inadequate function of Willisian collaterals, which may lead to the recruitment of ophthalmic or leptomeningeal collaterals, may cause hemodynamic impairment.

We report a case of middle-aged male with left middle cerebral artery (MCA) acute ischemic stroke with complete occlusion of the left ICA with robust collaterals and his clinical aspect.


  Case Report Top


A 58-year-old male was admitted to the emergency department with sudden onset of headache, giddiness, right-sided weakness, and speech difficulty for 2 h. The patient was chronic alcoholic and hypertensive. On admission, the patient's conscious level was equal to a Glasgow Coma Scale (E4V5M6) score of 15, with a power of the right upper and lower limbs being 3/5. Blood pressure was 110/80 mmHg. A 12-lead electrocardiogram was unremarkable. Initial brain noncontrast computed tomography (CT) scan showed subtle hypodensity in the left medial basal ganglia without any evidence of hemorrhage [Figure 1]. The patient was diagnosed as an acute ischemic stroke, and there were no other contraindications, making the patient eligible for thrombolysis. The patient was given rt-PA (alteplase: 0.6 mg/kg) intravenously according to the Japanese guideline for thrombolysis in patients with acute ischemic stroke. CT angiography was done and showed nonenhancement of the left ICA from the bifurcation of the common carotid artery to the supraclinoid segment [Figure 2] and [Figure 3]. Bilateral common carotid artery, right-sided carotid bifurcation, right internal and external carotid arteries, and bilateral vertebral arteries had normal flow [Figure 2]. The left MCA was supplied by the right ICA through the anterior communicating artery [Figure 3],[Figure 4],[Figure 5],[Figure 6]. Transthoracic echocardiography revealed mild diastolic dysfunction with an ejection fraction of 60%. Postthrombolysis CT head showed no hemorrhage [Figure 7]. The patient was managed with antiplatelets, anticoagulants, lipid-lowering drugs, and other supportive management. On progressive days, weakness was improved significantly, and the patient was discharged after 1 week, with a power of 5/5.
Figure 1: Hypodensity in the left medial basal ganglia (orange arrow)

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Figure 2: Three-dimensional computed tomography angiography showing complete occlusion of the left internal carotid artery from the origin (white arrow)

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Figure 3: Fluoroscopic angiography shows Willisian collateral (red arrow) supplying the left middle cerebral artery distally while complete occlusion of the left internal carotid ar tery up to the supraclinoid segment (green arrow)

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Figure 4: Partial recanalization of the left middle cerebral artery through anterior communicating artery postthrombolysis

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Figure 5: Normal filling of the left cortical branches distally

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Figure 6: Three-dimensional computed tomography angiography shows Willisian collateral supplying the left middle cerebral artery and distal cortical branches (black arrow) through the anterior communicating artery (blue arrow)

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Figure 7: Computed tomography head postthrombolysis (day 1)

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  Discussion Top


Recent advances in imaging techniques have allowed for the prompt evaluation of cerebral perfusion and indirectly the status of collateral circulation and provide valuable anatomical and functional information.[1] However, evaluation of the cerebral collateral circulation may not alter the treatment for most patients with occlusive carotid artery disease, but it may serve a prognostic role and in a selected group of patients and may provide additional information for risk stratification and therapeutic decisions.[2]

The protective role of the cerebral collateral circulation depends on several factors including anatomical variations, systemic arterial pressure, age, and the rate of development of occlusion and collaterals from the external carotid artery to the petrous segment of the ICA. After occlusion of a large artery, the subsequent drop in perfusion pressure distally generates a pressure gradient between neighboring arterial fields, resulting in changes in flow direction and rate; collateral flow changes occur almost immediately, within 1–4 s.[1]

Cerebral collateral circulation has been reported to alter the stroke risk.[3] Distal fragmentation of a thrombus within the parent vessel may occlude distal branches supplying retrograde collateral flow from cortical arteries. Hemodynamic fluctuation may influence the endurance of collaterals and possibly impairment of cerebral blood flow.[3] The efficacy of collateral vessels likely depends on age, duration of ischemia, and associated comorbidities.[3] The presence of collaterals on cerebral angiography has been associated with a lower risk of hemispheric stroke and transient cerebral ischemia in patients with carotid stenosis.[4]

Apart from the circle of Willis, ophthalmic and leptomeningeal collaterals, other cerebral collaterals may include: (1) ipsilateral vertebral artery – occipital artery – ECA – ICA, (2) ipsilateral thyrocervical trunk or costocervical trunk – ascending cervical artery or deep cervical artery – occipital artery – ECA – ICA, (3) contralateral ECA – contralateral superior thyroid artery – ipsilateral superior thyroid artery – ipsilateral ECA – ICA, and (4) ipsilateral thyrocervical trunk – inferior thyroid artery – superior thyroid artery – ECA – ICA.[5]

With the progressive degrees of carotid stenosis, the presence of collateral circulation was found to increase; next to nil collaterals were seen in patients with no stenosis, whereas collaterals were seen in >50% of patients with the most severe stenosis.[6] The rate of development of carotid occlusion may also play a pivotal role in development of persistent collaterals.


  Conclusion Top


In those developing carotid independence, intervention is not needed, while with largely carotid dependence, intervention could be feasible and justified. Different collateral circulation pathways, and to analyze how compensation affects patients' neurological symptoms, benefits from invasive and noninvasive treatment and prognosis need further research. The presence of primary collaterals in acute stroke with complete ICA occlusion remains to be a good prognostic factor along with thrombolysis.

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.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Romero JR, Pikula A, Nguyen TN, Nien YL, Norbash A, Babikian VL. Cerebral collateral circulation in carotid artery disease. Curr Cardiol Rev 2009;5:279-88.  Back to cited text no. 1
    
2.
Yamauchi H, Kudoh T, Sugimoto K, Takahashi M, Kishibe Y, Okazawa H. Pattern of collaterals, type of infarcts, and haemodynamic impairment in carotid artery occlusion. J Neurol Neurosurg Psychiatry 2004;75:1697-701.  Back to cited text no. 2
    
3.
Henderson RD, Eliasziw M, Fox AJ, Rothwell PM, Barnett HJ. Angiographically defined collateral circulation and risk of stroke in patients with severe carotid artery stenosis. North American Symptomatic Carotid Endarterectomy Trial (NASCET) group. Stroke 2000;31:128-32.  Back to cited text no. 3
    
4.
Liebeskind DS. Collateral circulation. Stroke 2003;34:2279-84.  Back to cited text no. 4
    
5.
Wang J, Zheng C, Hou B, Huang A, Zhang X, Du B. Four collateral circulation pathways were observed after common carotid artery occlusion. BMC Neurol 2019;19:201.  Back to cited text no. 5
    
6.
Norris JW, Krajewski A, Bornstein NM. The clinical role of the cerebral collateral circulation in carotid occlusion. J Vasc Surg 1990;12:113-8.  Back to cited text no. 6
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7]



 

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