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Year : 2013  |  Volume : 16  |  Issue : 4  |  Page : 521-524

Cerebral revascularization with superficial temporal - middle cerebral artery anastomosis for complete carotid occlusion: An emerging modality for preventing recurrent stroke

1 Department of Neurosurgery, Jawaharlal Institute of Postgraduate Medical Education and Research, Puducherry, India
2 Department of Neurology, Jawaharlal Institute of Postgraduate Medical Education and Research, Puducherry, India

Date of Submission08-Jul-2013
Date of Decision29-Jul-2013
Date of Acceptance20-Aug-2013
Date of Web Publication25-Oct-2013

Correspondence Address:
V R Roopesh Kumar
Department of Neurosurgery, Jawaharlal Institute of Postgraduate Medical Education and Research, Puducherry - 605 006
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0972-2327.120450

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Complete long segment carotid occlusion presents a treatment challenge. These patients cannot be managed adequately by endarterectomy or stenting. Despite best medical management, many continue to develop recurrent strokes. In this select group of patients, there may be role for flow augmentation techniques like superficial temporal-middle cerebral artery bypass. We report a patient who was thus successfully treated and remains asymptomatic. The relevant literature is reviewed.

Keywords: Extra cranial-intracranial bypass, recurrent stroke, superficial temporal - middle cerebral artery bypass, total carotid occlusion

How to cite this article:
Roopesh Kumar V R, Narayan SK, Madhugiri VS, Sasidharan GM, Gundamaneni SK. Cerebral revascularization with superficial temporal - middle cerebral artery anastomosis for complete carotid occlusion: An emerging modality for preventing recurrent stroke. Ann Indian Acad Neurol 2013;16:521-4

How to cite this URL:
Roopesh Kumar V R, Narayan SK, Madhugiri VS, Sasidharan GM, Gundamaneni SK. Cerebral revascularization with superficial temporal - middle cerebral artery anastomosis for complete carotid occlusion: An emerging modality for preventing recurrent stroke. Ann Indian Acad Neurol [serial online] 2013 [cited 2021 Jun 12];16:521-4. Available from:

   Introduction Top

Complete occlusion of the internal carotid artery (ICA) is an important cause of stroke. [1],[2],[3] Ultrasonography, magnetic resonance (MR) imaging and contrast angiography digital subtraction angiography (DSA) and functional imaging of the brain (positron emission tomography) help understand hemodynamic factors involved in the pathophysiology of brain ischemia. [4],[5],[6],[7] Recently, there has been a resurgence of interest in the role of extra cranial-intracranial (EC-IC) bypass surgery for flow augmentation in patients with a completely occluded ICA. [8] With advances in the measurement of cerebral hemodynamics, it may be possible to identify high-risk patients who could benefit from the bypass surgery. [9],[10],[11] We report a patient with complete ICA occlusion and recurrent stroke who ultimately benefited from EC-IC bypass.

   Case Report Top

A 60-year-old man presented with recurrent episodes of transient ischemic attacks (TIA) in the form of weakness involving the left side of the face, upper limb and lower limb since 3 months. He had recently been detected to be hypertensive and was on antihypertensive medications. He had no other risk factors for stroke (diabetes, hypercholesterolemia, smoking, alcoholism, hyperhomocystenemia). He continued to have episodes of hemodynamic TIA despite best medical management. These were not related to exertion or valsalva maneuver and were thought to be postural, related to hemodynamic factors. While under evaluation in the hospital, he developed a major stroke involving the left upper and lower limbs from which he recovered only partially (power 3/5).

Routine blood investigations were normal. Computed tomography (CT) brain revealed multiple infarcts in the right cerebral hemisphere [Figure 1]. Echocardiogram and electrocardiography were normal. Color Doppler scan of the carotid arteries revealed total occlusion of the right ICA. This was confirmed with CT angiogram (CTA) and MR angiogram (MRA). DSA revealed total occlusion of the right ICA at its origin. There was poor collateral flow to the right hemisphere from the left ICA (across the anterior communicating artery) and from vertebrobasilar system due to an incomplete circle of Willis. There was no evidence of thrombus or embolus in any IC vessel [Figure 2]. This led to an inadequate perfusion of the right cerebral hemisphere resulting in recurrent TIAs. After the major stroke in the hospital, a repeat CT brain revealed a right middle cerebral artery (MCA) territory infarct. Single Photon Emission CT (SPECT) CT of the brain also revealed ischemia of the entire right cerebral hemisphere.
Figure 1: Computed tomography brain plain, showing multiple lacunar infarcts in the right cerebral hemisphere, (a) in the centrum semiovale, (b) in the basal ganglia, (c) in the medial temporal lobe

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Figure 2: Digital subtraction angiography of the right common carotid artery. (a) Anteroposterior view, (b) lateral view, showing total occlusion of the right internal carotid artery, (c) the left A1 is not well visualized, indicating poor flow

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It was decided that medical management alone would not be sufficient to improve the cerebral vascularity of the right cerebral hemisphere and prevent further ischemic events. Hence a decision was made to revascularize the right cerebral hemisphere by performing a bypass procedure from superficial temporal artery (STA) to the MCA. Pre-operative trans-cranial Doppler (TCD) could not pick up any flow in the MCA. The STA was localized using Doppler and superficial temporal-MCA (ST-MCA) anastomosis performed in the standard fashion [Figure 3] and [Figure 4].
Figure 3: Pre-operative marking of right superficial temporal artery. (a) The incision, (b) the Doppler waveforms used to localize the course of the artery

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Figure 4: Final anastomosis of superficial temporal artery (black arrow) with middle cerebral artery (white arrow)

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Post-operative recovery was uneventful. Aspirin was continued throughout the peri-operative period to prevent graft thrombosis. Post-operative CT and MRA and DSA confirmed good flow across the graft [Figure 5]. Post-operative TCD was not performed so as not to apply any pressure over the anastomotic area that would lead to thrombosis of the anastomosis. He did not develop any further episodes of TIA and was discharged after 10 days of hospital stay. At 2 months follow-up, he was asymptomatic and was improving from his previous deficits with grade 4/5 power in the left upper and lower limbs and was ambulant. SPECT is planned at the 6 monthly follow-up visit.
Figure 5: Post-operative imaging. (a) Magnetic resonance angiogram, (b) digital subtraction angiography, showing good flow across the graft and re-establishment of cerebral cortical vasculature on the right side

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   Discussion Top

The accurate prevalence and incidence rates of complete ICA occlusion are difficult to ascertain as this can remain asymptomatic. In a retrospective, population-based study on patients with symptomatic ICA occlusion, an incidence rate of 6/100,000 has been reported. [1] However, many patients with TIA do not seek medical attention or undergo carotid imaging. The same study suggests that about 15% of large-vessel infarctions may be caused by ICA occlusion. In a study in Manchester, UK, Mead et al., [2] reported ICA occlusion in 50 of 380 consecutive patients with ischemic stroke over a year. In a study on the correlation of arteriographic findings and symptoms in patients with cerebrovascular disease, 25% of patients with ischemic stroke had ICA occlusion. [3] The prevalence of asymptomatic ICA occlusion is unknown.

ICA occlusion can produce brain ischemia by the two mechanisms:

Embolism from the distal or proximal stump or from atherosclerotic plaques in the common carotid artery or external carotid artery (most common mechanism accounting for nearly two-thirds of strokes in ICA occlusion. This is less common with complete ICA occlusion

A compromised cerebral blood flow (CBF) resulting in perfusion failure (misery perfusion syndrome) with distal insufficiency as seen in the present case.

Sometimes both the above factors act synergistically in causing cerebral ischemia.

Ultrasonography is usually the initial imaging modality for the evaluation of symptomatic ICA disease. Gadolinium-enhanced MRA is probably better than ultrasonography at diagnosing near-occlusions. Recently, CTA has been used to diagnose ICA disease with a high degree of accuracy. DSA remains the "gold standard" for the evaluation of carotid occlusive disease. However, it is an invasive procedure and therefore should be used only when ultrasonography or MRA fail to provide a definitive distinction between a near-occlusion and a complete occlusion. [3]

Symptomatic ICA occlusion increases the risk of future cerebrovascular events. In a study on angiographically proved ICA occlusion, the rate of recurrent stroke was 4.8% at 1 year, 12.2% at 3 years and 17.1% at 5 years. [9],[10],[11],[12] In a meta-analysis of 20 follow-up studies on patients with symptomatic ICA occlusion, the annual risk of stroke was 5.5% and that of ipsilateral stroke was 2.1%. Those with evidence of hemodynamic compromise on functional imaging are at an even higher risk (all strokes, 12.5%; and ipsilateral stroke, 9.5%). [13] Patients with bilateral carotid occlusion have a high-risk of stroke.

   Management of ICA Occlusion Top

As it is technically difficult to open a chronically occluded ICA, the management of a chronic ICA occlusion mainly includes strategies to reduce the risk of future strokes and other cardiovascular events. In patients with previous stroke or TIA, antiplatelet treatment leads to a 22% reduction in the risk of future non-fatal stroke. Addition of dipyridamole may further reduce the risk of strokes. Although anticoagulants are often used in ICA occlusion caused by dissection, the evidence base for this is poor. Similarly, it is unclear whether antithrombotic agents reduce the risk of future strokes in the subset of patients with a hemodynamic basis for the cerebral ischemia.

There is, thus, a definite role for flow-augmentation bypass procedures in select patients with complete carotid occlusion. The ST-MCA bypass can improve CBF in patients with symptomatic unilateral carotid occlusion. An ongoing carotid occlusion surgery study is aiming to re-examine its effectiveness in reducing subsequent ipsilateral ischemic stroke in patients with recent cerebral ischemic symptoms. [14] Endarterectomy or stenting is only useful if the occlusion involves a short segment. Long segment stenosis as in the present case may not be suitable for the endarterectomy. The addition of encephaloduroarteriosynangiosis to an ST-MCA anastomosis is of doubtful value, especially since the muscle could compress and compromise the patency of the anastomosis.

   Conclusion Top

ICA occlusion is an important cause of cerebral ischemia. The clinical course of ICA occlusion is variable, from being a completely asymptomatic to one leading to devastating strokes. Our understanding of the role of hemodynamic factors in the pathogenesis has greatly improved in recent years which resulted in developing newer modalities of management like STA-MCA bypass which greatly helps in revascularizing the ischemic cerebral hemispheres, thereby preventing further strokes.

   References Top

1.Flaherty ML, Flemming KD, McClelland R, Jorgensen NW, Brown RD Jr. Population-based study of symptomatic internal carotid artery occlusion: Incidence and long-term follow-up. Stroke 2004;35:E349-52.  Back to cited text no. 1
2.Mead GE, Shingler H, Farrell A, O'Neill PA, McCollum CN. Carotid disease in acute stroke. Age Ageing 1998;27:677-82.  Back to cited text no. 2
3.Thiele BL, Young JV, Chikos PM, Hirsch JH, Strandness DE Jr. Correlation of arteriographic findings and symptoms in cerebrovascular disease. Neurology 1980;30:1041-6.  Back to cited text no. 3
4.Weimar C, Mieck T, Buchthal J, Ehrenfeld CE, Schmid E, Diener HC, et al. Neurologic worsening during the acute phase of ischemic stroke. Arch Neurol 2005;62:393-7.  Back to cited text no. 4
5.Yanagihara T, Piepgras DG, Klass DW. Repetitive involuntary movement associated with episodic cerebral ischemia. Ann Neurol 1985;18:244-50.  Back to cited text no. 5
6.Yanagihara T, Klass DW. Rhythmic involuntary movement as a manifestation of transient ischemic attacks. Trans Am Neurol Assoc 1981;106:46-8.  Back to cited text no. 6
7.Tatemichi TK, Young WL, Prohovnik I, Gitelman DR, Correll JW, Mohr JP. Perfusion insufficiency in limb-shaking transient ischemic attacks. Stroke 1990;21:341-7.  Back to cited text no. 7
8.Furlan AJ, Whisnant JP, Kearns TP. Unilateral visual loss in bright light. An unusual symptom of carotid artery occlusive disease. Arch Neurol 1979;36:675-6.  Back to cited text no. 8
9.Klijn CJ, Kappelle LJ, van Huffelen AC, Visser GH, Algra A, Tulleken CA, et al. Recurrent ischemia in symptomatic carotid occlusion: Prognostic value of hemodynamic factors. Neurology 2000;55:1806-12.  Back to cited text no. 9
10.Fisher CM. Facial pulses in internal carotid artery occlusion. Neurology 1970;20:476-8.  Back to cited text no. 10
11.Klijn CJ, Kappelle LJ, van Schooneveld MJ, Hoppenreijs VP, Algra A, Tulleken CA, et al. Venous stasis retinopathy in symptomatic carotid artery occlusion: Prevalence, cause, and outcome. Stroke 2002;33:695-701.  Back to cited text no. 11
12.Kashiwazaki D, Kuroda S, Terasaka S, Ishikawa T, Shichinohe H, Aoyama T, et al. Carotid occlusive disease presenting with loss of consciousness. No Shinkei Geka 2005;33:29-34.  Back to cited text no. 12
13.Tatemichi TK, Desmond DW, Prohovnik I, Eidelberg D. Dementia associated with bilateral carotid occlusions: Neuropsychological and haemodynamic course after extracranial to intracranial bypass surgery. J Neurol Neurosurg Psychiatry 1995;58:633-6.  Back to cited text no. 13
14.Younkin D, Hungerbuhler JP, O'Connor M, Goldberg H, Burke A, Kushner M, et al. Superficial temporal-middle cerebral artery anastomosis: Effects on vascular, neurologic, and neuropsychological functions. Neurology 1985;35:462-9.  Back to cited text no. 14


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


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