Stroke & Vascular Disorders
Stroke associated with cerebral angiography
Mar. 10, 2026
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Intracranial atherosclerosis …
- Updated 03.10.2026
- Released 08.14.2001
- Expires For CME 03.10.2029
Intracranial atherosclerosis
Introduction
Overview
In this article, the authors provide an update on intracranial atherosclerosis. Information on optimal medical management is presented, along with the latest techniques for imaging of intracranial atherosclerosis.
Key points
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• Intracranial atherosclerosis is a common cause of stroke worldwide. | |
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• Aggressive medical therapy is necessary for patients with symptomatic intracranial atherosclerosis. | |
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• Recognition of this cause of stroke is increasing with better neuroimaging methods. |
Historical note and terminology
In 1951, C. Miller Fisher described the clinical findings associated with occlusion of the extracranial internal carotid artery (33). Prior to that, it was generally believed that ischemic stroke in the anterior circulation was invariably caused by intrinsic middle cerebral artery thrombosis. Several studies have subsequently shown that extracranial carotid occlusive disease is a more common cause of stroke than middle cerebral artery or carotid siphon occlusive disease (42; 65); nevertheless, large artery intracranial occlusive disease remains an important cause of ischemic stroke in the United States.
The first clinical descriptions of vertebrobasilar insufficiency were made in the late 1940s and early 1950s (48; 54). Based on the landmark 1946 paper by Kubik and Adams, basilar artery occlusion was considered a fatal disease (48). Subsequent studies, however, have shown that patients can survive basilar artery occlusion and occasionally may have only a minor neurologic deficit (11). Further studies have identified prognostic variables that help predict outcome. One such study conducted at the Mayo Clinic evaluated patients based on their respiratory status. The researchers found that those patients who present with neurologic compromise secondary to basilar artery occlusion and require mechanical ventilation had a high mortality rate. Of the 25 patients evaluated, 22 died. The remaining three persisted in a locked-in state (73).
Before cerebral angiography was first performed in humans in 1927 by Egas Moniz (56; 06), the diagnosis of atherosclerotic intracranial large artery disease could only be established at autopsy. The refinement of cerebral angiography enabled the diagnosis of intracranial large artery disease to be made during life, but the risk of stroke during this procedure, coupled with the lack of proven therapy for intracranial occlusive disease, resulted in limited use of angiography for establishing the diagnosis. The development of transcranial Doppler ultrasound in 1982 by Aaslid and associates (01) and the development of magnetic resonance angiography (62) have enabled noninvasive diagnosis of intracranial occlusive disease. These technological advances, coupled with preliminary data suggesting potential benefits of antithrombotic and thrombolytic therapy and angioplasty for the treatment of intracranial occlusive disease, have led to renewed interest in the pathogenesis and treatment of atherosclerotic intracranial large artery occlusive disease.
Clinical manifestations
Presentation and course
The neurologic syndromes associated with atherosclerotic occlusive disease of the major intracranial arteries are not unique. Other pathologies, such as cardioembolism or artery-to-artery embolism, that cause occlusions of these same arteries produce similar neurologic syndromes. Review of a patient's risk-factor profile, history of transient ischemic attacks, and temporal course of the neurologic deficit may, however, help the clinician distinguish between these different pathologies.
The presence of atherosclerotic risk factors such as hypertension, diabetes, smoking, or hyperlipidemia increases the a priori odds that a transient ischemic attack or stroke may be due to large artery cerebrovascular occlusive disease. Recurrent, stereotypical transient ischemic attacks should always suggest intrinsic large artery disease (extracranial large vessel disease or intracranial large vessel disease) rather than cardioembolism. Transient ischemic attacks tend to be more common in patients with extracranial carotid disease than in those with carotid siphon or middle cerebral artery disease, although there are frequent exceptions. In a study of patients with infarction in the territory supplied by the middle cerebral artery, the rate of transient ischemic attacks preceding stroke in patients with middle cerebral artery occlusive disease was 20% compared to 64% in patients with extracranial carotid occlusive disease (13). Transient ischemic attacks in patients with middle cerebral artery disease also occur over a shorter period than transient ischemic attacks associated with extracranial carotid disease (13).
The rate of transient ischemic attacks preceding stroke in patients with carotid siphon stenosis has not been well studied. In three retrospective studies, transient ischemic attacks were the presenting complaint in 28% to 47% of patients with carotid siphon stenosis (26; 52; 72). However, only one of these studies provided data on the rate of transient ischemic attacks preceding stroke—one of five patients presenting with stroke had a previous transient ischemic attack (72). The rate of transient ischemic attacks preceding stroke in patients with vertebral or basilar stenosis has not been systematically evaluated in a large number of patients; however, a few small series suggest that at least 50% of patients with basilar artery disease have transient ischemic attacks preceding stroke (68; 59).
An understanding of the neurologic syndromes associated with occlusive disease of the major intracranial arteries requires knowledge of the brain territories supplied by each of these vessels. The reader is referred to detailed descriptions of these vascular territories in the monograph by Osborn (58). A brief summary of the common neurologic syndromes associated with occlusive disease of the major intracranial arteries follows.
Atherosclerosis of the carotid siphon typically involves the cavernous section. Infarcts in patients with stenosis or occlusion of the intracranial carotid artery usually involve the middle cerebral artery territory. These patients typically present with hemiparesis, aphasia (dominant hemisphere), anosognosia and neglect (nondominant hemisphere), hemianopia, and hemisensory loss. Partial syndromes are common, depending on which division of the middle cerebral artery is primarily involved. Carotid siphon disease may also cause infarction in the anterior cerebral artery territory (17). Patients with an infarct in this territory often have leg weakness or leg and face weakness with relative sparing of the arm.
Atherosclerosis of the middle cerebral artery typically involves the stem (M1 segment) but occasionally affects the superior division alone (44). Infarction of the entire middle cerebral artery territory causes hemiplegia, hemisensory loss, hemianopia, gaze preference, and global aphasia (left hemisphere) or neglect syndromes (right hemisphere). Infarction in the territory supplied by the superior division of the middle cerebral artery causes hemiplegia and hemisensory loss (sometimes sparing the lower extremity), conjugate gaze preference, contralateral neglect (nondominant hemisphere), and a Broca-type of aphasia (dominant hemisphere). Vision is spared with these infarcts. Infarctions in the territory supplied by the inferior division of the middle cerebral artery in the dominant hemisphere cause Wernicke aphasia, hemianopia, and agitation, whereas the mirror image infarct in the nondominant hemisphere causes confusion, agitation, hemianopia, and poor drawing and copying (15).
Nonstenotic atherosclerotic disease of the middle cerebral artery stem, involving the origins of several lenticulostriate arteries, causes a moderate-sized (2 to 5 cm) infarction involving the internal capsule and basal ganglia (striatocapsular infarction) with sparing of the cortical areas supplied by the middle cerebral artery. Typically, these patients present with pure motor hemiparesis, suggesting small-vessel disease as the cause, but the clue that the vascular pathology involves the middle cerebral artery—rather than a single small penetrating artery—is the relatively large size of the subcortical infarct (22).
The anterior cerebral artery is uncommonly affected by hemodynamically significant atherosclerosis. The majority of infarcts in the anterior cerebral artery territory are caused by emboli from the extracranial carotid artery, heart, or carotid siphon (09). When atherosclerosis is present, it is usually distal to the stem of the anterior cerebral artery (A1 segment) and involves the territories supplied by the pericallosal or callosal marginal branches (46). Infarcts caused by atherosclerotic occlusive disease of these two main branches of the anterior cerebral artery cause weakness, typically involving the foot and thigh and occasionally involving the shoulder, and cortical sensory disturbances. Language dysfunction is also common after left anterior cerebral artery infarction, particularly mutism in the acute stage, which is sometimes followed by a mild mixed transcortical aphasia (09). When the anterior corpus callosum is involved, the following disconnection syndromes may be present: left arm apraxia, poor naming of objects in the left hand, and aphasic writing with the left hand.
When a large infarct involves most of the anterior cerebral artery territory because of an occlusive A1 lesion, there may be abulia and a gaze preference. The caudate and anterior internal capsule are supplied by the anterior cerebral artery through penetrating arteries that arise from the A1 segment. Most infarcts of the caudate or anterior capsule are caused by intrinsic disease of these penetrating arteries and not by intrinsic disease of the anterior cerebral artery stem (16).
Atherosclerosis usually involves the intracranial vertebral artery at the level of the posterior inferior cerebellar artery. The clinical syndromes produced by intracranial vertebral occlusive disease depend on the location of the obstruction, whether the vertebral artery is the source of distal embolism, and whether one or both vertebral arteries are involved. Atherothrombosis of the vertebral artery at the origin of posterior inferior cerebellar artery causes lateral medullary infarction (Wallenberg syndrome) that is often associated with infarction of the inferior cerebellar hemisphere (36). If the thrombus extends from one vertebral artery to the proximal basilar artery, or if both vertebral arteries are occluded, the resultant clinical syndrome may resemble that of intrinsic basilar occlusion. If the vertebral artery is a source of distal embolism, the embolus most commonly lodges at the top of the basilar artery or in the posterior cerebral arteries (18).
The clinical syndromes associated with basilar artery occlusive disease depend on the location of the vascular lesion, whether the brainstem infarction is unilateral or bilateral, and whether distal embolism has occurred. Transient ischemic attacks commonly precede stroke in patients with basilar occlusive disease and typically consist of diplopia, dizziness, dysarthria, perioral numbness, paraplegia, or alternating hemiplegia (04; 68; 59). In patients with a proximal basilar occlusion whose distal basilar artery and superior cerebellar arteries are patent (ie, supplied by retrograde flow from the anterior circulation through the posterior communicating arteries), the infarct is usually limited to the midline and paramedian structures in the pons (17). The pontine tegmentum and cerebellum are usually spared because these structures are supplied by circumferential branches arising from the segment of the basilar artery that is patent and from the posterior inferior cerebellar arteries. Consequently, patients with proximal basilar occlusion usually have combinations of the following signs: quadriparesis (bilateral infarction), hemiparesis (unilateral infarction), pseudobulbar palsy, abnormalities of eye movements (unilateral gaze palsy, internuclear ophthalmoplegia, the one-and-a-half syndrome, skew deviation, ocular bobbing), pupillary abnormalities (bilateral small pupils, Horner syndrome), and reduced level of consciousness, with sparing of sensory and cerebellar function. Occipital headache occurs frequently as well (17).
In some patients with bilateral infarction of the basis pontis from proximal basilar occlusion, severe weakness of the limbs and horizontal eye movements permits only eye blinking or vertical gaze (ie, the "locked-in" syndrome). Nonstenotic atherosclerotic disease of the basilar artery may occasionally cause bilateral basis pontis infarcts by occluding the orifices of paramedian penetrating branches of the basilar artery (34). The deficit in these patients may be similar to that of patients with proximal basilar artery occlusion.
When the distal basilar artery is occluded, infarction may involve the midbrain, thalamus, medial temporal lobes, and occipital lobes. Caplan has described in detail the signs associated with "top of the basilar syndrome" (12). Midbrain involvement causes pupillary abnormalities (decreased reactivity, eccentric shape, altered size), oculomotor abnormalities (vertical gaze palsies, skew deviation, third nerve palsy), and behavioral abnormalities (peduncular hallucinosis). Thalamic involvement causes decreased alertness, amnesia, and sensory abnormalities depending on the size and location of the infarct. The signs associated with temporal lobe and occipital lesions are described below.
Atherosclerosis of the posterior cerebral artery most often affects the proximal (perimesencephalic) segment near the origins of the thalamogeniculate branches (60). Therefore, the ventroposterolateral thalamus, medial temporal lobes, and occipital lobes are at risk of infarction from occlusive disease in this segment of the posterior cerebral artery. Hemianopia or hemisensory transient ischemic attacks are the most common presentation (60). Signs in patients with infarction in the territory supplied by the posterior cerebral artery include hemisensory loss (infarction of ventroposterolateral), memory disturbance and naming difficulties (medial temporal infarction), hemianopia, hemiachromatopsia, alexia without agraphia, and visual agnosias (occipital infarction) (61).
Headache associated with posterior cerebral artery infarction is typically felt around the ipsilateral orbit or forehead (17). Paralysis occurs only when the orifices of the perforating branches to the cerebral peduncle are involved by an atherosclerotic lesion in the proximal part of the posterior cerebral artery. Involvement of the medial thalamoperforating branches of the posterior cerebral artery results in behavioral abnormalities and memory loss (10). Bilateral posterior cerebral artery infarction is associated with cortical blindness, memory loss (due to bilateral medial temporal involvement), and agitation.
Clinical vignette
A 55-year-old African American woman with a history of hypertension, hyperlipidemia, ischemic heart disease, and smoking presented with two episodes of transient quadriparesis and dysarthria. These events lasted about 5 minutes each. She had a prior history of carotid endarterectomy also. MRI of the brain was negative for stroke, but MRA showed signal dropout in the proximal third of the basilar artery. Transcranial Doppler also showed elevated basilar artery flow velocity. The patient was placed on aspirin but had an additional transient ischemic attack with vertigo and dysarthria lasting 4 minutes. She was then switched to warfarin and has been stable for 6 months. She was then placed on aspirin monotherapy with no further transient ischemic attacks. In addition to antithrombotic therapy, the patient’s initial LDL was 127 mg/dl, and she was placed on atorvastatin 80 mg per day with the aim of achieving an LDL of less than 100 mg/dl and preferably less than 70 mg/dl. A target blood pressure of less than 140/90 mm Hg is also being sought.
Biological basis
Etiology and pathogenesis
This topic discusses stroke caused by atherosclerotic occlusive disease of the major intracranial arteries. Other less common causes of intrinsic intracranial occlusive disease (eg, dissection, moyamoya disease) are discussed in other topics.
The pathogenesis and pathophysiology of intracranial atherosclerosis are heavily inferred from research into coronary artery disease. The process of intracranial atherosclerotic disease stems from endothelial injury and then intimal accumulation of cholesterol particles. Initial endothelial injury leads to the recruitment of circulating monocytes that later infiltrate the vessel wall and evolve into macrophages. These macrophages bind to lipoprotein particles and become foam cells. To a degree, T cells play a parallel role in this process. Smooth muscle cells respond to this network of processes and migrate into the intima from the tunica media and promote collagen matrix synthesis that leads to intimal thickening. The continued process of intimal build-up leads to atheroma formation and plaque progression. The degree of stenosis is often not related to the risk of clinical events. Classification and stratification of atheroma severity depend on fibrous cap formation and the extent of lipid-rich necrotic core or the presence of thrombi. Any inflammatory response systemically can erode the fibrous cap via erosion and thinning and boost the risk of rupture to cause acute thrombosis. The presence of intraplaque hemorrhage or plaque neovascularization is a features of plaque vulnerability (21). Further discussion of the pathogenesis and pathophysiology of atherosclerosis is presented in a review article by Ross (63). Compared to extracranial atherosclerotic disease, intracranial atherosclerotic disease is characterized by a higher prevalence of proliferative fibrosis rather than lipid infiltration and inflammation of the vessel wall (45).
Low wall shear stress at arterial branch points and regions of arterial wall opposite to flow dividers are known risks of artherogenesis. In the intracranial arterial circulation, the ventral wall of the middle cerebral artery, regions opposite to the entry of perforating arteries, and the lateral walls of the proximal basilar artery, where the angle of confluence of two vertebral arteries affects flow, are also sensitive areas for intracranial atherosclerotic disease. By contrast, the presence of atheromas in the coronary arteries tends to move away from the lumen and have less of an effect on luminal size. Intracranial arteries tend to readily narrow or exhibit more stenosis with atheroma development. The best explanation may be that intracranial arteries lack an external elastic laminate, thick media, and complex collateral circulation; additionally, intracranial arteries have autoregulatory capabilities of distal cerebral arteries (21). Intracranial arteries have thinner media and adventitia and fewer elastic fibers compared to extracranial arteries. The vessel walls of intracranial arteries have denser internal elastic lamina. There is a smaller vasa vasorum, which is thought to increase the risk of developing more vulnerable atherosclerotic plaque (66).
Intracranial atherosclerosis is usually distal to the circle of Willis and has a lower likelihood of collateral circulation compared to extracranial atherosclerosis. Artery-to-artery embolism from a stenosis segment in the intracranial arteries is considered to be one of the major mechanisms of ischemic stroke in intracranial atherosclerosis (66).
Epidemiology
Atherosclerotic narrowing of the large intracranial arteries is an important cause of ischemic stroke in the United States and worldwide (40). In a prospective study of 405 patients evaluated for stroke, intracranial large artery disease was the cause of 8% of ischemic strokes (65). Subsequent studies suggest that intracranial atherosclerotic disease contributes to 12% to 54% of all strokes in Asian countries. Asians, Hispanics, and Africans tend to have higher rates of intracranial atherosclerotic disease; by contrast, whites of European descent have a higher incidence of extracranial disease. A study performed in New York City, NOMAS, found that intracranial atherosclerotic disease–related strokes are five to six times more prevalent among African Americans and Caribbean Hispanics as compared to whites of European descent.
Race has an important influence on the likelihood of developing intracranial large artery disease. In postmortem studies where most patients were white, it has been shown that atherosclerosis usually involves different arterial trees at different ages. The aorta is involved first, followed by the peripheral arteries, coronary arteries, extracranial carotid and vertebral arteries, and finally the intracranial arteries (35). In contrast to whites, blacks with symptomatic anterior circulation ischemia are more likely to have middle cerebral artery or carotid siphon disease than extracranial carotid disease (43; 38). In a study of patients with anterior circulation ischemia, the rates of middle cerebral artery occlusion were 90% in black males and 12% in white males (43).
Asymptomatic atherosclerotic lesions also tend to occur intracranially in blacks and extracranially in whites (39). Further studies continue to remain limited due to small sample sizes and differing methodologies to measure stenosis. Various studies in different countries reveal the presence of intracranial atherosclerotic disease at a low level. Generally, whites are more prone to large vessel and embolic disease than blacks (03). However, blacks have a higher frequency of intracranial large artery occlusive disease in the posterior circulation. In a study of 27 white and 24 black patients, distal basilar artery and intracranial branch lesions were significantly more frequent in blacks, whereas severe proximal vertebral artery disease was five times more common in whites (37).
Studies of Japanese and Chinese patients have shown that these racial groups are also more likely to develop intracranial large artery disease than extracranial disease (75). In another study comparing Chinese living in the United States with American whites, the Chinese patients had significantly higher rates of intracranial carotid artery and middle cerebral artery stenosis (31). A multicenter study from China found evidence of intracranial stenosis in 46.6% of patients hospitalized with stroke (71). Patients with intracranial stenosis had more severe strokes and a longer length of stay in the hospital.
The explanation for the variance in the distribution of cerebral atherosclerosis in different races is uncertain. Although genetic susceptibility to intracranial large artery disease in blacks and Asians may be important, the influence of lifestyle and risk-factor profiles on the distribution of atherosclerosis may also be significant. Support for the latter theory is provided by the results of studies showing a lower frequency of intracranial large artery disease in black Africans than in black Americans (74) and a strong correlation between the high rate of intracranial large artery disease in Hispanics and the presence of diabetes (65). Most studies, however, that have controlled for the presence of traditional vascular risk factors have found that race is independently associated with site of atherosclerosis in the cerebrovascular circulation (39; 31).
The influence of sex on the risk of developing intracranial large artery disease has not been systematically studied. Data from a few small series suggest that women may be more likely to develop intracranial large artery disease than men, who tend to develop extracranial large artery disease (14). Intracranial atherosclerosis is strongly associated with dementia and Alzheimer disease. The presence of intracranial atherosclerosis in at least two vascular territories is associated with dementia and Alzheimer disease risk and is a contributor to cognitive impairment (66).
Prevention
In general, atherosclerosis of the major intracranial arteries and the extracranial arteries shares traditional risk factors such as hypertension, diabetes, hypercholesterolemia, and smoking. Of these, diabetes and hypertension appear to be the most important risk factors for intracranial large-artery disease (37; 39). Homocysteine has not been well studied in this type of cerebrovascular disease.
Differential diagnosis
The clinical syndromes associated with atherosclerotic intracranial large-artery occlusive disease are not specific. Other vascular pathologies that need to be considered in the differential diagnosis are cardioembolism, extracranial atherosclerotic carotid or vertebral occlusive disease, other extracranial vasculopathies (eg, dissection, fibromuscular dysplasia), nonatherosclerotic intracranial large artery vasculopathies (eg, moyamoya disease, dissection, vasospasm, radiation arteriopathy, infectious or noninfectious vasculitis), intracranial penetrating artery (ie, small vessel) disease, and procoagulant states (eg, antiphospholipid antibody syndrome, oral contraception use, cancer, abnormalities of the circulating anticoagulant system or the fibrinolytic system).
Confusing conditions
Arterial dissection
Vasculitis
Reversible cerebral vasoconstriction syndrome (RCVS)
Diagnostic workup
Brain and vascular imaging studies coupled with data obtained from the history and physical examination usually enable the clinician to establish the diagnosis of atherosclerotic intracranial large-artery occlusive disease. The initial imaging study in patients presenting with one of the clinical stroke syndromes described above is usually a CT of the brain. This enables differentiation between ischemic and hemorrhagic stroke and, in the case of ischemic stroke, provides data on the size and location of the infarct. MRI of the brain is more sensitive than CT at detecting cerebral infarction and is commonly ordered when CT does not reveal the suspected stroke.
In patients presenting with stereotypical transient ischemic attacks, a large (greater than 2 cm) subcortical infarct, or a cortical infarct in the territory of a single intracranial artery, atherosclerotic intracranial large-artery disease should be considered in the differential diagnosis. When the transient ischemic attacks or infarcts are in the territory supplied by the middle cerebral artery or anterior cerebral artery, a carotid ultrasound should be performed to exclude extracranial carotid occlusive disease. Patients with multiple patterns of ischemic lesions on MRI, including concomitant perforating artery infarcts, pial infarcts, and border zone infarcts, are more likely to have combined extracranial and intracranial stenoses (51). Echocardiography should also be considered to exclude a cardiac source of embolus, particularly if brain imaging shows multiple cerebral infarcts in different vascular territories. If an extracranial carotid or cardiac source for the patient's transient ischemic attacks or infarct is excluded, vascular imaging studies of the intracranial vessels should be considered to determine whether the patient has large-artery intracranial occlusive disease.
The gold standard for establishing the diagnosis of intracranial large-artery disease is conventional cerebral angiography or digital subtraction angiography. Angiography enables differentiation between atherosclerotic large-artery occlusive disease and other intracranial vasculopathies such as moyamoya disease, dissection, and vasculitis. Additionally, angiography enables accurate measurement of the degree of stenosis of the diseased artery, diagnosis of arterial occlusion, evaluation of collateral flow patterns, and evaluation of other intracranial and extracranial arteries. The major drawback of angiography is the risk of stroke, which is 0.5% to 1% in patients investigated for cerebrovascular disease. Additionally, this study is invasive, requires intravenous contrast administration, and includes risks related to procedural complications. Digital subtraction angiography is not commonly used for assessing intracranial atherosclerotic disease (02).
CT angiogram is the most commonly used test for intracranial atherosclerotic disease. The sensitivity for assessing intracranial atherosclerosis is high for stenosis greater than 50%. One limitation of CT angiogram is interpreting vascular calcification. This can lead to varying interpretations and is not a reliable indicator of the risk of stroke.
The development of transcranial Doppler in 1982 by Aaslid and associates (01) and the development of MRA have enabled noninvasive diagnosis of intracranial large artery occlusive disease (50; 53; 62; 64; 27). Transcranial Doppler and angiographic correlative studies show that transcranial Doppler has a sensitivity of 85% to 90% and a specificity of 96% to 98% for detecting stenosis (greater than 30%) or occlusion of the carotid siphon or middle cerebral artery stem when performed by experienced ultrasonographers (49). Additional studies, such as the SONIA trial, have demonstrated excellent detection of stenosis ranging from 50% to 99% (32). Focal increases in mean flow velocity with distal reduction in mean flow velocity and increased pulsatility index are classic signs of luminal stenosis. Increasing systemic arterial CO2 by holding one’s breath or administration of CO2 can assess for vasomotor reactivity and identify steal syndrome. The quality of Transcranial Doppler studies varies and heavily depends on the operator. Studies on measuring vessels with Transcranial Doppler reflect this phenomenon. Transcranial Doppler is less reliable for detecting occlusive lesions in the vertebral or basilar arteries (sensitivity 76%, specificity 99%), especially in the distal basilar region (64). Further prospective evaluations with transcranial Doppler have identified other reliable, specific indicators of stenosis in stroke patients (27).
MRA is frequently used to evaluate patients with suspected intracranial occlusive disease. This study does not require intravenous contrast. One study comparing 3D time-of-flight MRA with 3D phase-contrast MRA in 18 patients with stenosis found that 3D time-of-flight MRA diagnosed stenosis with at least 90% sensitivity and correctly graded stenosis with 80% accuracy (57). In the same group of patients, the sensitivity of transcranial Doppler was 76%, and the specificity was 99%. Although transcranial Doppler had a lower sensitivity than MRA, transcranial Doppler provided more complete hemodynamic data (collateral supply, estimations of degree of stenosis) than MRA (64). With the increased sophistication of MRA and transcranial Doppler, the combination of the two may overcome individual shortcomings--MRA’s overexaggeration of stenosis and transcranial Doppler’s insonation window limitations—obviating the need for digital subtraction angiography (08). With the development of high-strength magnets such as 3T MRI, direct thrombus imaging and visualization of intraplaque hemorrhage in symptomatic intracranial stenoses has been demonstrated (05). MRA is sensitive to turbulent blood flow and is known to overestimate the degree of stenosis as a result. Variations on MRA technology, like Zero-echo time MRA, have been shown to be as sensitive as digital subtraction angiogram, with less susceptibility to turbulent blood flow. Additionally, quantitative MRA combines time-of-flight MRA and phase-contrast MR for post-stent placement studies on re-stenosis of vessels; however, this study is not widely used (47).
Perfusion imaging with CT angiogram looks at the mean transit time to infer the degree of stenosis. MRA is also used for perfusion studies and relies on arterial spin labeling to trace blood flow using endogenous magnetically labeled arterial blood water.
Computational fluid dynamics uses reconstruction of source imaging to simulate blood flow through specific blood vessel sections. There is ongoing research into this type of vessel imaging, and it is not routinely used in intracranial atherosclerotic disease assessment.
High-resolution vessel wall MRI (vwMRI) uses a combination of various forms of MR technologies to evaluate vessel walls. Abnormal plaque enhancement is evaluated using T1 sequences. The degree of enhancement is associated with stroke risk. This technology is promising for studying intracranial atherosclerosis; in addition to inferring stroke risk, vwMRI can differentiate from other vasculopathies that can cause vessel stenosis (21).
FDG-PET uses an analog of glucose to study vessel wall stenosis. Studies have shown that FDG naturally accumulates in arteries in the elderly. This substrate is readily taken up in atherosclerotic processes and correlates with macrophage presence.
Management
Therapeutic options for managing patients with acute stroke caused by intracranial occlusive disease are beyond the scope of this section and are reviewed in the acute stroke treatment topics.
The main options for antiplatelet therapy in patients with intracranial atherosclerosis are aspirin, clopidogrel, or dual antiplatelet therapy (either aspirin plus clopidogrel or aspirin plus dipyridamole). The best medical treatment involves aggressive control of risk factors for intracranial atherosclerosis in both asymptomatic and symptomatic variants (45).
Aspirin was used preferentially in the ECIC bypass study. In the past, warfarin was frequently used for the treatment of intracranial large artery disease based on the results of nonrandomized studies of patients with symptoms suggestive of vertebrobasilar disease (55). However, these were small, frequently retrospective studies.
The Warfarin Aspirin Symptomatic Intracranial Disease study mentioned above is a prospective, randomized study in patients with recent transient ischemic attack or stroke and angiographically verified 50% to 99% stenosis (24). Patients were randomly assigned to treatment with warfarin (INR 2-3) or aspirin 1300 mg per day between 1999 and 2003. The study originally planned to enroll 806 patients, but it was halted prematurely due to an increased rate of death and bleeding events in the warfarin arm. At the time of its termination, the Warfarin Aspirin Symptomatic Intracranial Disease study had enrolled 569 patients. The mean follow-up was 1.8 years. The primary outcome was stroke or vascular death, and this outcome was reached in 22% of aspirin-treated patients and 22% of warfarin patients (log rank test, p value 0.82). The rates of systemic bleeding, cardiac ischemic events, and death were higher in the warfarin group. Based on these prospective data, antiplatelet therapy is the preferred antithrombotic treatment for patients with intracranial atherosclerosis.
Modification of stroke risk factors is important in patients with symptomatic intracranial atherosclerosis. Some clinicians have advocated a “relaxed blood pressure” policy for patients with intracranial atherosclerosis, but in WASID, systolic blood pressure > 140 mm Hg was associated with a higher risk of overall stroke and stroke in the territory of the stenotic vessel (70). In data from the WASID study, it was also found that patients with total cholesterol >200 mg/dl had a higher rate of future stroke compared to patients with better risk factor control (19). The importance of regular physical activity has also been demonstrated for patients with intracranial atherosclerosis. In a clinical trial, it was noted that greater physical activity was associated with a 40% decrease in stroke, myocardial infarction, or vascular death (69).
The initial enthusiasm for bypass surgery in patients with intracranial large-artery disease has waned since the Extracranial-Intracranial Bypass Study (30). In that study, patients with extracranial carotid occlusion, distal carotid occlusive disease, or middle cerebral artery occlusive disease were randomized to medical therapy alone (risk-factor management and antithrombotic therapy, usually aspirin 325 mg four times daily) versus medical therapy and extracranial-intracranial bypass. The results demonstrated that extracranial-intracranial bypass was ineffective for preventing stroke in these patients. Subgroup analyses of the stroke rates in patients with distal carotid or middle cerebral artery disease showed that extracranial-intracranial bypass was also ineffective in these groups. In fact, patients with severe middle artery stenosis who underwent extracranial-intracranial bypass had a higher rate of stroke than the medically treated patients with severe middle cerebral artery stenosis (30). Bypass surgery or endarterectomy has also been used for intracranial vertebral artery occlusive disease (67; 07), but the efficacy of these procedures has not been systematically evaluated. Bypass surgery in the posterior circulation usually involves anastomosing the occipital branch of the external carotid artery to the posterior inferior cerebellar artery or the anterior inferior cerebellar artery. These procedures are rarely used today to treat intracranial vertebral disease.
Transluminal angioplasty is another therapeutic option for the treatment of intracranial large artery stenosis. A large retrospective study of 50 patients reported that 49 of them had improved clinical or angiographic outcomes (25). However, 14% of patients had a vessel dissection, and 16% had residual stenosis of more than 50%. Subsequent studies from the VISSIT, VIST, and VAST trials examined angioplasty and stenting in different intracranial circulations; the VAST trial looked at posterior circulation stenosis (both extracranial and intracranial). These studies showed no benefit in reducing stroke risk.
With the development of intracranial stenting, the Stenting and Aggressive Medical Management for Preventing Recurrent stroke in Intracranial Stenosis (SAMMPRIS) trial was launched (23). Patients who had a stroke or transient ischemic attack in the previous 30 days and symptomatic stenosis of 70% to 99% as confirmed by angiography were enrolled and randomly assigned to either aggressive medical therapy (AMT) alone or AMT plus stenting. AMT included a target low-density lipoprotein (LDL) of less than 70 mg/dl and treatment of systolic blood pressure to achieve a target of less than 140 mm Hg in nondiabetics and less than 130 mm Hg in diabetics. Patients in both groups received aspirin and clopidogrel for 90 days, followed by aspirin monotherapy.
The original study hypothesis was that AMT plus stenting would be superior to AMT alone. Four hundred and fifty-one subjects were recruited from 50 sites in the United States. The study was stopped prematurely, however, due to the hazards of stenting. The 30-day stroke/death rate was 14.7% in the stenting arm and 5.8% in the AMT group (p=0.002). Beyond 30 days, the stroke rate in the territory of the stenosed vessel was comparable in the two groups. The rate of the primary endpoint (stroke or death within 30 days or stroke in the territory of the qualifying artery) at 1 year was 20.0% in the stenting group and 12.2% in the AMT group (p=0.009).
Three-year results of SAMMPRIS have confirmed that the benefits of AMT were persistent (28). During a median follow-up period of 32.4 months, the rate of the primary endpoint (including stroke or death within 30 days of enrollment and stroke in the territory of the stenotic vessel beyond 30 days) was 15% in the AMT alone and 23% in the AMT + stenting group (p=0.025). For individual adverse events, each stroke was higher in the AMT + stenting group (26% vs. 19%, p=0.047), and major hemorrhage was higher in the AMT + stenting group (13% vs. 4%, p=0.0009). An additional analysis comparing WASID and SAMMPRIS patients treated medically found that the SAMMPRIS AMT regimen reduced major vascular events by about 42% (21.9% vs. 12.6%, hazard ratio 1.9) (20). Therefore, AMT alone is preferred for patients with severe, symptomatic intracranial disease.
With regard to patients in SAMMPRIS who received stenting, a detailed analysis of the strokes related to the endovascular procedure has been published (29). The three most common mechanisms of stroke were perforating artery occlusion, subarachnoid hemorrhage (due to presumed wire perforation), and delayed cerebral hemorrhage.
Approximately 25% of whites of European descent and up to 60% of Asians carry a loss-of-function polymorphism in the CYP2C19 cytochrome P450 enzyme. This enzyme is necessary for metabolizing clopidogrel to its active form. The presence of this mutation has complicated the interpretation of prior studies on intracranial atherosclerosis treatment, like CHANCE and SAMMPRIS. Further studies on alternative agents like ticagrelor (not dependent on CYP2C19 for metabolism) have been conducted. SOCRATES, PRINCE, and THALES have looked at the utility of ticagrelor as an adjunct to stroke therapy with aspirin. The THALES trial has suggested a role for ticagrelor in reducing stroke risk; further studies are needed for confirmation (41).
Cilostazol has also been studied as an adjunct therapy with aspirin for reducing stroke risk in intracranial atherosclerosis. Studies like TOSS-I, CSPS, CATHARSIS, and TOSS-II have systemically shown no difference in outcomes as compared to clopidogrel and aspirin (21).
The use of low-dose anticoagulation with intracranial atherosclerosis has been studied in the COMPASS trial. Patients with coronary, peripheral, and carotid disease were included in the study. Patients receiving low-dose rivaroxaban and aspirin showed a lower incidence of ischemic and hemorrhagic stroke compared to those who received only aspirin.
Outcomes
In patients with greater than 50% stenosis, the risk of ischemic stroke is 15% overall, and the risk of fatal or disabling stroke is 8% (WASID trial). The degree of stenosis affects the risk of stroke: patients with 70% to 99% stenosis exhibited a higher incidence of transient ischemic attack or stroke as compared to those with 50% to 69% stenosis (WASID trial). The SAMMPRIS trial showed a risk of stroke of 15% and disabling or fatal stroke of 7% in patients with 70% to 99% stenosis. The OXVASC study showed a risk of stroke or transient ischemic attack of 14% in patients with 70% to 99% stenosis. The CICAS study showed an increased risk of stroke with a higher degree of stenosis. This is seen similarly in studies done in Japan and in New York City (NOMAS).
Media
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Contributors
All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.
Author
-
Susan Law DO MPH
Dr. Law of Kings County Hospital in Brooklyn, New York, has no relevant financial relationships to disclose.
See Profile
Editor
-
Steven R Levine MD
Dr. Levine of the SUNY Health Science Center at Brooklyn has no relevant financial relationships to disclose.
See Profile
Former Authors
- J Paul Elliott MD
- Sean Markey MD
- Seemant Chaturvedi MD
Patient Profile
- Age range of presentation
-
- 19 to 65+ years
- Sex preponderance
-
- male>female, >1:1
- Heredity
-
- heredity may be a factor
- Population groups selectively affected
-
- African Americans
- Asians
- White of European descent
- Occupation groups selectively affected
-
- none selectively affected
ICD & OMIM codes
- ICD-10
-
- Vertebro-basilar artery syndrome: G45.0
- Occlusion and stenosis of unspecified cerebral artery: I66.9
- Cerebral atherosclerosis: I67.2
- Occlusion and stenosis of other cerebral artery: I66.8
- Occlusion and stenosis of the basilar artery: I65.1
- Occlusion and stenosis of the vertebral artery: I65.0
- Other transient cerebral ischaemic attacks and related syndromes: G45.8
- Transient cerebral ischaemic attack, unspecified: G45.9
- ICD-11
-
- Asymptomatic stenosis of intracranial or extracranial artery: BD55
- Cerebral ischaemic stroke due to intracranial large artery atherosclerosis: 8B11.1
- Cerebral ischaemic stroke of unknown cause: 8B11.5
- Cerebral ischaemic stroke due to unspecified occlusion or stenosis of intracranial large artery: 8B11.51
- Other specified transient ischaemic attack: 8B10.Y
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