Relevance of External Carotid Artery Disease in Internal Carotid Artery Occlusion

Jonathan P. Gertler

Internal carotid artery (ICA) occlusion has long been thought to carry a poor prognosis despite what is often an asymptomatic presentation. However, increasing recognition of segmentation based on cerebrovascular imaging and/or perfusion monitoring techniques, clinical status of initial presentations, and associated extracranial and intracranial vascular disease, has indicated a heterogeneous population that must be approached thoughtfully to understand the prognosis and determine the optimal treatment strategy.

Prospective studies of patients with known ICA occlusions suggest a delayed stroke rate approaching 25% within 2 to 3 years. Some recent data suggest annual stroke rates of 2.4%, but aggregate vascular events including retinal symptoms and limb-shaking transient ischemic attacks (TIAs) were observed at an annual rate of 6.4%. In patients with compromised cerebrovascular reactivity (CVR), stroke rates can approach 10% to 14% annually versus 4% to 6% in patients with preserved CVR.

The mechanism of acute stroke after ICA occlusion is typically embolism to the middle cerebral artery (MCA) circulation, thrombus extension past the ophthalmic artery into the circle of Willis, or hemodynamic insufficiency in association with either an isolated hemisphere or diffuse extracranial cerebrovascular disease. Stroke at an interval following ICA occlusion may be caused by similar mechanisms but can also arise from a diseased external carotid artery (ECA) or embolization from a remnant ICA cul-de-sac containing thrombus and/or platelet or fibrin debris. In either case, turbulent flow at the carotid bifurcation can sweep atheroembolic material into the intracranial vasculature through external carotid collaterals.

The ECA can serve as the major cerebral collateral in the setting of ICA occlusion, and a proximal ECA stenosis can have a hemodynamic impact on cerebral perfusion. Studies have demonstrated that the ECA contributes to cerebral blood flow compensation in up to 80% of patients with a symptomatic ICA occlusion. The increasing importance of focal contributions to cerebral ischemia, rather than hemispheric-based patterns, has also been emphasized, noting the ECA contributions can substantially lower risks associated specifically with compromised collateral beds. In addition, preserved MCA collateral flow, regardless of the source of collaterals (which can emanate from the ECA and be identified as such), is associated with a significantly improved prognosis in patients with acute stroke caused by ICA occlusion as is the preservation of leptomeningeal collaterals. In addition, several studies have demonstrated improvement in cerebral perfusion following restoration of ECA hemodynamics to normal.

Anatomy of Cerebral Collateral Circulation

Although cerebral collateral blood flow can depend on contralateral intracranial supply and/or basilar artery blood flow from either or both vertebral arteries, it is important to recognize that the circle of Willis is incomplete in as many as 60% of patients. The ECA can provide significant ipsilateral collateral blood flow, but it can also be a source of significant-sized collaterals through which atherosclerotic debris can reach the intracranial vessels.

Adult cerebral collateral arterial branches have been categorized by Alksne into large interarterial connections, intracranial–extracranial connections, and small interarterial anastomoses. Other rare collateral vessels are based on persistent trigeminal and hypoglossal arteries, which provide carotid basilar connections.

The ECA serves as a major extracranial arterial collateral primarily through periorbital branches. Periophthalmic channels depend on the superficial temporal, angular, middle meningeal, and infraorbital arteries. Vertebral collateral is provided through the occipital branch of the ECA as well as the costocervical trunk and the contralateral vertebral artery, which communicates at the level of the intervertebral foramen. Perimeningeal, stylomastoid, and anterior tympanic branches of the ECA can all provide collateral channels of varying degrees of significance (Figure 1).

Methodology of grading ECA collateral flow through digital subtraction arteriography is well described. Categories include grade 0 (no filling of the ophthalmic artery), grade 1 (filling of carotid siphon), and grade 2 (filling of anterior or middle cerebral artery).

Evaluation of the Patient With Symptomatic Occlusion of the Internal Carotid Artery

The patient’s history is important to differentiate vague neurologic complaints from specific hemispheric and ocular findings. Ophthalmologic examination to corroborate suspected retinal embolic events is recommended. Limb-shaking TIAs appear to be specifically associated with global hypoperfusion and can add confidence to the need to enhance intracranial collateral flow. Although global cerebral hypoperfusion, manifested by vertebral basilar insufficiency and/or a focal watershed hemodynamic problem, may be correctable by ECA endarterectomy, it is more likely that therapy will benefit specific hemispheric events ipsilateral to an appropriately occluded ICA.

Computed tomography (CT) or magnetic resonance imaging (MRI) should be performed to document baseline existing cerebral tissue loss as well as any unsuspected lesions in the distribution of the occluded ICA. Carotid duplex examination will add hemodynamic data about the degree of ECA stenosis and identify turbulent areas around an ICA cul-de-sac. Transcranial Doppler along with the noninvasive examination can identify cerebral collateral pathways as either contributory or not, and considered with subsequent arteriography through invasive or noninvasive means, it can provide corroborative data to ignore or repair a significant ECA stenosis. It has been suggested that cerebral compensation for carotid occlusion is primarily hemodynamic rather than metabolic. Given that the ECA does not always develop as an important collateral pathway, in the absence of clear embolic events related to a diseased ECA or occluded ICA, hemodynamic assessment of the collateral blood supply increases the accuracy of the decision-making process.

In contrast to the first decade of the 21st century, numerous tools now exist for evaluating the segmentation of patients at risk for stroke after ICA occlusion. Specifically, increased oxygen extraction (OEF) as measured by positron emission tomography (PET) with inhalation of ¹⁵O-labeled gas and low cerebral vascular reactivity (assessed by transcranial Doppler) are associated with an increased risk of recurrent ischemic infraction. Other methodologies include arterial spin labeling for MRI or single photon emission CT (SPECT), both using a vascular challenge (acetazolamide) to assess cerebrovascular reactivity or standard angiographic techniques to assist in identifying collateral scores as well as ultrasound to define plaque characteristics. These evaluations will be critically important for a more accurate prediction of the role of ECA endarterectomy in the setting of global hypoperfusion.

There is an absolute necessity for complete visualization of the proximal vasculature (MRI, spiral CT, and conventional arteriography) in any patient with noninvasively proven diffuse cerebrovascular disease being evaluated for recurrent or new-onset symptoms in the presence of ICA occlusion. Evaluation should include aortic arch views to exclude proximal sources of emboli from the great vessels as well as subclavian stenoses, which can compromise the posterior circulation. Precise definition of the status of the vertebral arteries as well as both carotid bifurcations is necessary, as is a thorough delineation of the intracranial vasculature and their collateral (cross-filling) relationships.

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