eMedicine Specialties > Neurology > Neuro-vascular Diseases

Anterior Circulation Stroke

Author: Alison Elizabeth Baird, MB, BS, PhD, MPH, FRACP, Professor of Neurology and Physiology/Pharmacology, Director of Division of Cerebrovascular Disease and Stroke, State University of New York Downstate Medical Center
Contributor Information and Disclosures

Updated: Sep 17, 2008

Introduction

Background

The anterior circulation of the brain describes the areas of the brain supplied by the right and left internal carotid arteries and their branches. The internal carotid arteries supply the majority of both cerebral hemispheres, except the occipital and medial temporal lobes, which are supplied from the posterior circulation (see Image 1). Ischemic strokes occurring in the anterior circulation are the most common of all ischemic strokes, accounting for approximately 70% of all cases.

The internal carotid artery originates at the bifurcation of the common carotid artery at the level of the thyroid cartilage in the neck. The extracranial portion of the artery passes into the carotid canal of the temporal bone without giving off any branches. The intracranial portion of the artery consists of the petrosal, cavernous (ie, S-shaped carotid syphon), and supraclinoid portions. The major intracranial branches arise from the supraclinoid portion, the first being the ophthalmic artery that enters the orbit through the optic foramen to supply the retina and optic nerve. Next, the posterior communicating artery arises just distal to the ophthalmic artery and joins the posterior cerebral artery.

The anterior choroidal artery arises prior to the terminal bifurcation of the internal carotid artery into the middle cerebral and anterior cerebral arteries. The middle cerebral artery (MCA) is the direct continuation of the artery, while the anterior cerebral artery (ACA) branches medially at the level of the anterior clinoid process. The circle of Willis consists of a vascular communication of blood vessels at the base of the brain connecting the major vessels of the anterior and posterior circulations. 

The collateral circulation is an important potential source of blood supply in cases of internal carotid artery occlusive disease. The 2 primary sources of collateral flow via the circle of Willis are the anterior and the posterior communicating arteries. Blood may flow from the contralateral ICA via the A1 segment of the contralateral anterior cerebral artery through the anterior communicating artery to the ipsilateral ACA (appears as reversal of flow). Blood may come from the posterior circulation (posterior cerebral arteries) via the posterior communicating artery (reversal of flow). Note that a high degree of variation exists in the normal vascular anatomy of the circle of Willis. For example, in as many as 20% of patients, the posterior cerebral arteries (ie, fetal variant) arise from the internal carotid artery as normal vascular variants. Therefore, some variation exists in the exact parts of the brain supplied by the anterior circulation.

If the primary collateral circulation fails, secondary sources of collaterals may come from the branches of the ipsilateral external carotid artery. Branches from the maxillary artery anastomose with the ophthalmic artery leading to reversal of flow in the ophthalmic artery and into the occluded ICA. Leptomeningeal collaterals may also anastomose with distal MCA branches and lead to reversed flow in the MCA.

For additional resources, visit Stroke/Cerebrovascular Disease.

Pathophysiology

Ischemic strokes in the anterior circulation are caused most commonly by occlusion of one of the major intracranial arteries or of the small single perforator (penetrator) arteries. The most common causes of arterial occlusion involving the major cerebral arteries are (1) emboli, most commonly arising from atherosclerotic arterial narrowing at the bifurcation of the common carotid artery, from cardiac sources, or from atheroma in the aortic arch and (2) a combination of atherosclerotic stenosis and superimposed thrombosis. Lacunar strokes are believed to be caused by lipohyalinotic intrinsic disease of the small penetrating vessels.

The most common sites of occlusion of the internal carotid artery are the proximal 2 cm of the origin of the artery and, intracranially, the carotid siphon. Factors that modify the extent of infarction include the speed of occlusion and systemic blood pressure. Occlusion of the internal carotid artery is not infrequently silent, because external orbital-internal carotid and willisian collaterals can open up if the occlusion has occurred gradually over a period of time. Mechanisms of ischemia resulting from internal carotid artery occlusion are, most commonly, artery-to-artery embolism or propagating thrombus and perfusion failure from distal insufficiency.

The MCA is the largest of the intracerebral vessels and supplies through its pial branches almost the entire convex surface of the brain, including the lateral frontal, parietal, and temporal lobes; insula; claustrum; and extreme capsule. The lenticulostriate branches of the MCA supply the basal ganglia, including the caput nuclei caudati, the putamen, the lateral parts of the internal and external capsules, and sometimes the extreme capsule. Occlusion of the MCA commonly occurs in either the main stem (M1) or in one of the terminal superior and inferior divisions (M2). Occlusion of the M1 segment of the MCA prior to the origin of the lenticulostriate arteries in the presence of a good collateral circulation can give rise to the large striatocapsular infarct.

Occlusion of the MCA or its branches is the most common type of anterior circulation infarct, accounting for approximately 90% of infarcts and two thirds of all first strokes. Of MCA territory infarcts, 33% involve the deep MCA territory, 10% involve superficial and deep MCA territories, and over 50% involve the superficial MCA territory.

The ACA supplies the whole of the medial surfaces of the frontal and parietal lobes, the anterior four fifths of the corpus callosum, the frontobasal cerebral cortex, the anterior diencephalon, and the deep structures. Occlusion of the ACA is uncommon, occurring in only 2% of cases, often through atheromatous deposits in the proximal segment of the ACA.

The anterior choroidal artery supplies the lateral thalamus and posterior limb of the internal capsule. Occlusion of the anterior choroidal artery occurs in fewer than 1% of anterior circulation strokes. Often, ischemia in the distribution of the ophthalmic artery is transient in the setting of symptomatic internal carotid artery occlusion (ie, transient monocular blindness, occurring in approximately 25% of patients), but central retinal artery ischemia is relatively uncommon, presumably because of the efficient collateral supply.

Occlusion of single penetrating branches of the middle and anterior cerebral arteries that supply the deep white and gray matter produce the lacunar type of stroke. These occlusions account for as many as 20% of ischemic strokes.

The acute ischemic process varies markedly from patient to patient. Patients with similar clinical syndromes may have markedly different pathophysiological profiles. Many new pathophysiological insights have been obtained from studies using functional brain imaging (eg, magnetic resonance imaging [MRI], positron emission tomography [PET], single-photon emission computed tomography [SPECT]). Several pathophysiological ischemic stroke syndromes can be identified on the basis of imaging parameters of perfusion and tissue injury that could be used to target stroke treatment. Using new MRI methods, the following 3 patterns have been identified:

• Perfusion-diffusion mismatch, which may represent a situation of viable but ischemic tissue that could be salvaged by timely reperfusion. In this pattern, a larger area of hypoperfusion surrounds a zone of ischemic injury on diffusion-weighted imaging. This pattern occurs in approximately 70% of patients in the first 24 hours.  In many patients an arterial occlusion is identified on MR angiography (MRA).
• Complete ischemia, in which the perfusion and diffusion lesions are of equivalent size, likely representing a complete infarct. This pattern has been identified in approximately 10-20% of patients in the first 24 hours.  In many patients an arterial occlusion is identified on MR angiography (MRA).
• Reperfusion pattern, in which a perfusion deficit no longer exists and the MRA is normal. This pattern occurs in approximately 10-15% of patients in the first 24 hours

Reperfusion is an important part of the ischemic process, and by 24 hours, 20-40% of arterial occlusions have begun to clear, with recanalization rates of 70% by 1 week and 90% by 3 weeks. Early reperfusion (<24 h) may have significant prognostic benefits and is associated with improved outcome and smaller infarct size, but later reperfusion may not alter outcome significantly and may be associated with hemorrhagic conversion of the infarct and edema formation.

Frequency

United States

Approximately 750,000 new and recurrent cases of stroke occur each year in the United States. Approximately 80% of these are ischemic strokes. Anterior circulation ischemic stroke accounts for approximately 70% of all ischemic strokes. Approximately 420,000 new cases of anterior circulation ischemic stroke per year are reported in the United States.

International

The risk of stroke is highest in Eastern Europe, followed by Western Europe, Asia, the rest of Europe, and North America.

Mortality/Morbidity

• Stroke is the third leading cause of death in the United States and the leading cause of adult disability. High rates of morbidity and mortality are associated with all types of ischemic strokes, but the prognosis varies among subtypes. For example, mortality rates after intracerebral hemorrhage are as high as 30% at 1 month. Conversely, the ischemic lacunar syndromes (ie, caused by occlusion of a single small penetrating artery) quite often are associated with a good prognosis and have a better prognosis than MCA syndromes.
• Overall, at 6 months after a stroke, as many as 30% of patients have died, 20-30% are moderately to severely disabled, 20-30% have mild to moderate disability, and 20-30% are without deficits.
• Stroke recurs in as many as 10% of stroke survivors in the first 12 months after stroke, with an incidence of 4% per year thereafter. After transient ischemic attack, the risk of stroke is 10.5% over the next 3 months, with the highest risk in the 2 days following TIA.

Race

Stroke risk is highest in African Americans, being up to 4-fold higher than in whites. This may relate in part to higher rates of some vascular risk factors such as hypertension and diabetes.  Stroke risks are also higher in Hispanics and Asians relative to whites.

The patterns of arterial occlusion are different in African Americans and Asians than in whites.

• Asians and African Americans have higher rates of intracranial arterial occlusive disease than whites. The intracranial arterial occlusive disease in these populations typically involves the main stem of the MCA or the ACA.
• In whites, the arterial occlusive disease typically involves the extracranial carotid arteries, and lesions in the middle and anterior cerebral arteries are usually of embolic origin.

Sex

Strokes at all ages are more likely to occur in men, but overall more strokes occur in women. This is because strokes occur more commonly at older ages and females have a longer life span than males (the native protective effect of estrogen is lost at menopause). This disparity may become greater in the future with the aging of the population.

Age

The incidence of stroke rises exponentially with age, particularly in individuals older than 55 years.

• However, 25% of all strokes occur in individuals younger than 65 years of age; so stroke is not just a condition of the elderly.
• Strokes can occur at any age.

Clinical

History

Patients typically present with sudden onset of focal neurological symptoms. Specific features of the time course and evolution, focal neurological symptoms, and global symptoms are listed below.

• Time course and evolution
  • Sudden or rapid onset
  • Reaches maximal intensity within 24 hours
  • Gradual or stepwise worsening in as many as 30% of patients
• Focal neurological symptoms
  • Cognitive impairment - Difficulty with speech
  • Weakness or incoordination - Unilateral
  • Numbness or loss of sensation, typically unilateral
  • Dysarthria
  • Visual loss, either in one eye or in one visual field
• Global symptoms
  • Headache
  • Altered mental status
  • Syncope
  • Seizure
  • Coma

Physical

• Left hemisphere (ie, dominant)
  • Right hemiparesis, variable involvement of face and upper and lower extremity
  • Right-sided sensory loss, in a similar pattern to the motor deficit; usually involves all modalities, decreased stereognosis, graphesthesia
  • Right homonymous hemianopia
  • Dysarthria
  • Aphasia, fluent and nonfluent
  • Alexia
  • Agraphia
  • Acalculia
  • Apraxia
• Right hemisphere (ie, nondominant)
  • Left hemiparesis (same pattern as on right)
  • Left-sided sensory loss (similar pattern as the motor deficit)
  • Left homonymous hemianopia (same pattern as on right)
  • Dysarthria
  • Neglect of the left side of environment
  • Anosognosia
  • Asomatognosia
  • Loss of prosody of speech
  • Flat affect
• Cortical and subcortical: Findings consistent with both cortical and subcortical localization can be seen in this clinical scenario.
• ACA territory
  • Crural paresis > arm paresis
  • Frontal signs (eg, abulia)
• Anterior choroidal artery territory
  • Hemiparesis
  • Hemianesthesia
  • Homonymous hemianopia
• Lacunar syndromes
  • Pure motor hemiparesis
    • Contralateral, usually affecting the face and upper and lower extremities equally
    • Also associated with dysarthria
    • No sensory or visual loss or cognitive impairment
  • Pure sensory stroke
    • Contralateral loss of all sensory modalities, equally affecting the face and upper and lower extremities
    • No motor signs, dysarthria, visual loss, or cognitive impairment
  • Dysarthria-clumsy hand syndrome - Dysarthria, dysphagia, contralateral tongue and facial weakness and paresis, and clumsiness of the contralateral arm and hand
  • Homolateral ataxia and crural paresis - Paresis of the contralateral leg and side of the face, prominent ataxia of the contralateral leg and arm—also called "ataxic hemiparesis," meaning ataxia and weakness on the same side.
  • Isolated motor/sensory stroke
    • Paralysis and sensory loss of the contralateral leg, arm, and face
    • No visual loss or cognitive impairment

Causes

Risk factors include epidemiologic risk factors (ie, not modifiable) and potentially modifiable risk factors.

• Epidemiologic risk factors
  • Age (risk rises exponentially with age)
  • Sex (more common in males at all ages)
  • Race (African American > Asian > Caucasian)
  • Geographic (Eastern Europe > Western Europe > Asia > rest of Europe or North America)
  • Genetic risk factors (stroke or heart disease in individuals younger than 60 y; some familial syndromes, eg, cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy [CADASIL])
• Potentially modifiable risk factors
  • Hypertension (diastolic or isolated systolic)
  • Diabetes mellitus type 1 or 2
  • Atrial fibrillation
  • Smoking
  • Coronary artery disease
  • Hypercholesterolemia
  • Alcohol abuse
  • Drug abuse (eg, cocaine)
  • Oral contraceptive use
  • Pregnancy

• Search for CME/CE on This Topic »

• Frontal Lobe Syndromes (Neurology)

• Stroke Center
• Stroke Overview
• Stroke Causes
• Stroke Symptoms
• Stroke Treatment
• Transient Ischemic Attack Overview

• The Course and Outcome of Unilateral Intracranial Arteriopathy in 79 Children With Ischaemic Stroke