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Stroke Imaging

Practice Essentials

Stroke, or cerebrovascular accident (CVA), is a clinical term that describes a sudden loss of neurologic function persisting for more than 24 hours that is caused by an interruption of the blood supply to the brain (see the images below). Stroke is the third leading cause of death worldwide, with considerable disability among survivors.
 

The etiologies of stroke are varied but can broadly be categorized into ischemic or hemorrhagic infarctions. Approximately 80-87% of strokes are from ischemic infarction due to thrombotic or embolic cerebrovascular occlusion. Hemorrhagic infarctions constitute most of the remainder of strokes, with a smaller number due to aneurysmal subarachnoid hemorrhage.

Furthermore, 20-40% of patients with ischemic infarction may develop hemorrhagic transformation within one week after ictus.
Differentiating between these different types of stroke is an essential part of the initial workup of these patients because the subsequent management of each patient is vastly different. The scope of this article mainly focuses on ischemic and hemorrhagic stroke.

Neuroimaging plays a vital role in the workup of acute stroke by providing information essential to accurately triage patients, expedite clinical decision making with regard to treatment, and improve outcomes in patients presenting with acute stroke. Rapid and accurate diagnosis is crucial.
 CT allows time-critical decision-making in stroke patients, informing decisions on thrombolytic therapy with tPA, which has a narrow therapeutic index.

Axial noncontrast computed tomography (NCCT) demon

Axial noncontrast computed tomography (NCCT) demonstrates diffuse hypodensity in the right lentiform nucleus, with mass effect upon the frontal horn of the right lateral ventricle. The patient is a 70-year-old female with history of left-sided weakness for several hours duration.

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MRI was subsequently obtained in the same patient.

MRI was subsequently obtained in the same patient. An axial T2 FLAIR image (left) demonstrates high signal in the lentiform nucleus with mass effect. The axial diffusion-weighted image (middle) demonstrates high signal in the same area with corresponding low signal on the apparent diffusion coefficient (ADC) maps, consistent with true restricted diffusion and an acute infarction. Maximum intensity projection from a 3D time-of-flight MRA (right) demonstrates occlusion of the distal middle cerebral artery (MCA) trunk (red circle).

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Pathophysiology

Ischemic stroke

Acute ischemic strokes are the result of vascular occlusion secondary to thromboembolic disease. Ischemia results in cell hypoxia and depletion of cellular adenosine triphosphate (ATP). Without ATP, energy failure results in an inability to maintain ionic gradients across the cell membrane and cell depolarization. Influx of sodium and calcium ions and passive inflow of water into the cell ensues, resulting in cytotoxic edema. Further, cell depolarization leads to the release of glutamate and free radicals, mitochondrial membrane disruption, and a cascade that ultimately leads to apoptotic cell death.

Ischemia also directly results in dysfunction of the cerebral vasculature, with breakdown of the blood-brain barrier occurring within 4-6 hours after infarction. Following breakdown of the blood-brain barrier, proteins and water flood into the extracellular space, leading to vasogenic edema. Vasogenic edema produces greater levels of brain swelling and mass effect that peak at 3-5 days and resolves over the next several weeks with resorption of water and proteins.

Infarction results in the death of astrocytes as well as the supporting oligodendroglia and microglia cells. The infarcted tissue eventually undergoes liquefaction necrosis and is removed by macrophages with the development of parenchymal volume loss. A well-circumscribed region of cerebrospinal-fluidlike low density is eventually seen, consisting of encephalomalacia and cystic change. The evolution of these chronic changes may be seen in the weeks to months following the infarction.

Ischemic penumbra

Ischemic tissue can be functionally divided into the irreversibly damaged infarct core and the ischemic penumbra surrounding it. The infarct core is the central zone of dead or dying tissue in an ischemic area. Surrounding the infarct core is tissue with less severe reduction in blood flow that may be salvaged with early reperfusion, termed ischemic penumbra, and oligemic tissue at the periphery. Without reperfusion, the zone of infarct core may extend to involve the penumbra. The goals of modern ischemic stroke diagnosis and therapy lie in identifying the infarct core and determining if any significant salvageable tissue exists.

Ischemic stroke classification

Ischemic strokes may be divided into 3 major subtypes, based on the TOAST classification system, adopted from the system of categorizing stroke developed in the multicenter Trial of Org 10172 in Acute Stroke Treatment. These include large artery infarction, small-vessel or lacunar infarction, and cardioembolic infarctions.

Large vessel occlusive disease

Large artery occlusion typically results from embolization of atherosclerotic debris originating from the common or internal carotid arteries or from a cardiac source. A smaller number of large artery occlusions may arise from plaque ulceration and in situ thrombosis. Large-vessel ischemic strokes more commonly affect the middle cerebral artery territory, with the anterior cerebral artery territory affected to a lesser degree (see the images below).

Noncontrast CT in this 52-year-old male with histo

Noncontrast CT in this 52-year-old male with history of worsening right-sided weakness and apahasia demonstrates diffuse hypodensity and sulcal effacement involving the left anterior and middle cerebral artery territories consistent with acute infarction. Scattered curvilinear areas of hyperdensity are suggestive of developing petechial hemorrhage in this large area of infarction.

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MRA in the same patient (left) demonstrates occlus

MRA in the same patient (left) demonstrates occlusion of the left precavernous supraclinoid internal carotid artery (ICA, red circle), occlusion or high-grade stenosis of the distal middle cerebral artery (MCA) trunk and attenuation of multiple M2 branches. The diffusion-weighted image (right) demonstrates high signal confirmed to be true restricted diffusion on the ADC map consistent with acute infarction.

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This 60-year-old female underwent NCCT after an ep

This 60-year-old female underwent NCCT after an episode of left upper extremity weakness. NCCT demonstrates cortical and subcortical hypodensity involving the right mid to anterior temporal lobe.

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MIP image from a CTA demonstrates a filling defect

MIP image from a CTA demonstrates a filling defect or high-grade stenosis at the branching point of the right MCA trunk (red circle), suspicious for thrombus or embolus. CTA is highly accurate in detecting large vessel stenosis and occlusions, which comprise approximately one third of ischemic strokes.

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Lacunar infarction

Lacunar infarctions are small infarcts resulting from occlusion of deep, penetrating end arteries (see the image below). They may be caused by small vessel atherosclerosis and lipohyalinosis related to hypertension or embolic occlusion. Because of the limited area supplied by these perforating end arteries, their obstruction results in a small area of infarction ranging from about 5 mm in diameter up to approximately 15 mm. The most common locations for lacunar infarctions include the basal ganglia, internal capsule, thalamus, and the corona radiata.

Axial noncontrast CT demonstrates a focal area of

Axial noncontrast CT demonstrates a focal area of hypodensity in the left posterior limb of the internal capsule in this 60-year-old male with new onset of right-sided weakness. The lesion demonstrates high signal on the FLAIR sequence (middle image) and DWI (right image), with low signal on the ADC maps, indicating an acute lacunar infarction. Lacunar infarcts are typically no more than 1.5 cm in size and can occur in the deep gray matter structures, corona radiata, brainstem, and cerebellum.

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Cardioembolic infarction

Cardiogenic emboli are a common source of recurrent stroke (see the image below). They may constitute up to 20% of acute stroke and have been reported to have the highest 1-month mortality. Risk factors include atrial fibrillation and recent cardiac surgery. Cardioembolic strokes may be isolated, multiple and in a single hemisphere, or scattered and bilateral; the latter two indicate multiple vascular distributions and are more specific for cardioembolism. Multiple and bilateral infarcts can be the result of embolic showers or recurrent emboli. Other possibilities for single and bilateral hemispheric infarctions include emboli originating from the aortic arch and diffuse thrombotic or inflammatory processes that can lead to multiple small vessel occlusions.

Cardioembolic stroke: Axial diffusion-weighted ima

Cardioembolic stroke: Axial diffusion-weighted images demonstrate scattered foci of high signal in the subcortical and deep white matter bilaterally in a patient with a known cardiac source for embolization. An area of low signal in the left gangliocapsular region may be secondary to prior hemorrhage or subacute to chronic lacunar infarct. Recurrent strokes are most commonly secondary to cardioembolic phenomenon.

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Watershed infarction

Vascular watershed or border-zone infarctions occur at the most distal areas between arterial territories (see the image below). They are believed to be secondary to embolic phenomenon or due to severe hypoperfusion, such as in carotid occlusion or prolonged hypotension.

MRI was obtained to evaluate this 62-year-old hype

MRI was obtained to evaluate this 62-year-old hypertensive and diabetic male with history of transient episodes of right-sided weakness and aphasia. The FLAIR image (left) demonstrates patchy areas of high signal arranged in a linear fashion in the deep white matter, bilaterally. This configuration is typical for deep borderzone or watershed infarction; in this case, the anterior and posterior middle cerebral artery (MCA) watershed areas. The left-sided infarcts have corresponding low signal on the ADC map (right), signifying acuity. An old left posterior parietal infarct is noted as well.

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Hemorrhagic transformation of ischemic stroke

Hemorrhagic transformation represents the conversion of a bland infarction into an area of hemorrhage. Proposed mechanisms for hemorrhagic transformation include reperfusion of ischemically injured tissue, either from recanalization of an occluded vessel or from collateral blood supply to the ischemic territory or disruption of the blood brain barrier. With disruption of the blood-brain barrier, red blood cells extravasate from the weakened capillary bed, producing petechial hemorrhage or more frank intraparenchymal hematoma.

Hemorrhagic transformation of an ischemic infarct occurs within 2-14 days post ictus, usually within the first week. It is more commonly seen following cardioembolic strokes and is more likely with larger infarct size.
Hemorrhagic transformation is also more likely following administration of tPA and with noncontrast CT demonstrating areas of hypodensity (see the image below).

Noncontrast CT (left) obtained after this 75-year-

Noncontrast CT (left) obtained after this 75-year-old male was admitted for CVA; scan demonstrates a large right middle cerebral artery distribution infarction with linear areas of developing hemorrhage. These become more confluent on day 2 of hospitalization (middle image), with increased mass effect and midline shift. Massive hemorrhagic transformation occurs by day 6 (right) with increased leftward midline shift and subfalcine herniation. Obstructive hydrocephalus is also noted with dilatation of the lateral ventricles, likely due to compression of the foramen of Monroe. Intraventricular hemorrhage is also noted, layering in the left occipital horn. Larger infarctions are more likely to undergo hemorrhagic transformation and are one contraindication to thrombolytic therapy.

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Hemorrhagic stroke

The most common etiology of primary hemorrhagic stroke (intracerebral hemorrhage) is hypertension, with at least two thirds of patients with primary intraparenchymal hemorrhage reported to have preexisting or newly diagnosed hypertension. Hypertensive small vessel disease results from tiny lipohyalinotic aneurysms that subsequently rupture and result in intraparenchymal hemorrhage. Typical locations include the basal ganglia, thalami, cerebellum, and pons (see the images below). The remaining cases of spontaneous intraparenchymal hemorrhage may be secondary to vascular malformations (eg, arteriovenous malformations and cavernous malformations) or amyloid angiopathy.

Axial noncontrast CT scan of the brain in a 60-yea

Axial noncontrast CT scan of the brain in a 60-year-old male with history of acute onset of left-sided weakness demonstrates 2 areas of intracerebral hemorrhage in the right lentiform nucleus with surrounding edema and effacement of the adjacent cortical sulci and right sylvian fissure. Mass effect is present upon the frontal horn of the right lateral ventricle with intraventricular extension of hemorrhage.

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Noncontrast CT of the brain (left) demonstrates an

Noncontrast CT of the brain (left) demonstrates an acute hemorrhage in the left gangliocapsular region with surrounding white matter hypodensity consistent with vasogenic edema. T2-weighted axial MRI (middle image) demonstrates the hemorrhage with surrounding high-signal edema. The coronal gradient echo image (right) demonstrates susceptibility related to the hematoma with markedly low signal adjacent the left caudate head. Gradient echo images are highly sensitive for blood products.

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Subarachnoid hemorrhage

The most common cause of atraumatic hemorrhage into the subarachnoid space is rupture of an intracranial aneurysm. Aneurysms are focal dilatations of arteries, with the most frequently encountered intracranial type being the berry aneurysm or saccular aneurysms. Aneurysms may less commonly be related to altered hemodynamics related to arteriovenous malformations, collagen-vascular disease, polycystic kidney disease, septic emboli, and neoplasms.

Nonaneurysmal perimesencephalic subarachnoid hemorrhage may also be seen and is thought to arise from capillary or venous rupture. It has a less severe clinical course and, in general, better prognosis.

Berry aneurysms are most commonly isolated lesions that form due to a combination of hemodynamic stresses and acquired or congenital weakness in the vessel wall. Saccular aneurysms typically occur at vascular bifurcations, with more than 90% occurring in the anterior circulation. These include the junction of the anterior communication arteries and anterior cerebral arteries most commonly, the middle cerebral artery bifurcation, the supraclinoid internal carotid artery at the origin of the posterior communicating artery, and the bifurcation of the ICA.

The pathologic effects of SAH on the brain are multifocal. SAH results in elevated intracranial pressure and impairs cerebral autoregulation. This, in combination with acute vasoconstriction, microvascular platelet aggregation, and loss of microvascular perfusion, results in profound reduction in blood flow and cerebral ischemia (see the images below).

Noncontrast CT scan was performed emergently in th

Noncontrast CT scan was performed emergently in this 71-year-old male who presented with acute onset of severe headache and underwent rapid neurologic deterioration requiring intubation. The noncontrast CT (left image) demonstrates diffuse, high-density subarachnoid hemorrhage in the basilar cisterns and both Sylvian fissures. Diffuse loss of gray-white differentiation is present. The FLAIR image demonstrates high signal throughout the cortical sulci, basilar cisterns, and in the dependent portions of the ventricles. FLAIR is highly sensitive to acute subarachnoid hemorrhage because of the suppression of high CSF signal lending to greater conspicuity of SAH compared with conventional MRI sequences.

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This patient subsequently underwent a CTA and subs

This patient subsequently underwent a CTA and subsequent cerebral angiography. Multiple aneurysms were identified, including a 9-mm aneurysm at the junction of the anterior cerebral and posterior communicating arteries seen on this lateral view of an internal carotid artery (ICA) injection. Balloon-assisted coil embolization was performed.

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Lateral view of a selective injection of the left

Lateral view of a selective injection of the left internal carotid artery demonstrates a microcatheter passing distal to the aneurysm neck. This lateral view from an angiogram performed during balloon-assisted coil embolization demonstrates significantly diminished filling of the aneurysm.

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Mortality and Morbidity

Each year in the United States, approximately 795,000 people experience new or recurrent stroke. Of these, approximately 610,000 represent initial attacks, and 185,000 represent recurrent strokes. The incidence of stroke varies depending on age, gender, ethnicity, and socioeconomic status. Approximately 87% of strokes in the United States are ischemic, 10% are secondary to intracerebral hemorrhage, and another 3% may be secondary to subarachnoid hemorrhage.

The global incidence of stroke has at least modest variation from nation to nation, suggesting the importance of genetics and environmental factors, such as disparities in access to healthcare for developing countries. According to the World Health Organization, 15 million people suffer stroke worldwide each year. The age-adjusted incidence of total strokes per 1000 person-years for people 55 years or older has been reported in the range of 4.2–6.5. The highest incidences have been reported in Russia, Ukraine, and Japan.

The increased survival among stroke victims places an increased demand on healthcare systems globally.

Stroke subtypes also vary greatly in different parts of the world. For example, the proportion of hemorrhagic strokes may be even higher in certain populations, such as in China, which was reported to be up to 39.4%, and up to 38.7% in Japan.

Stroke is the second leading cause of death and the third leading cause of disability in the world. In 2010, there were 16.9 million incident stroke cases, 33.0 million prevalent stroke cases, and 5.9 million deaths attributed to stroke. According to a report from the American Heart Association, approximately 87% of all strokes were ischemic strokes. Stroke accounts for approximately 9% of deaths around the world. The mortality approaches 50-100 deaths per 100,000 people per year worldwide but varies significantly regionally. Mortality is highest in many developing nations, likely due to genetic and socioeconomic factors, prevalence of modifiable risk factors, and differences in available healthcare resources for diagnosis and treatment.

The decline in US stroke death rates for more than 4 decades has begun to slow. According to the Centers for Disease Control and Prevention (CDC), in adults aged 35 years or older, stroke death rates declined 38% from 2000 to 2015. The annual percent change (APC) in stroke death rates changed from a 3.4% decrease per year during 2000-2003, to a 6.6% decrease per year during 2003-2006, to a 3.1% decrease per year during 2006-2013, to a 2.5% increase per year during 2013-2015. The last trend indicated a reversal from a decrease to a statistically significant increase in Hispanics (APC = 5.8%) and in persons in the South Census Region (APC = 4.2%). Declines in stroke death rates failed to continue in 38 states. During 2013-2015, an estimated 32,593 excess stroke deaths might not have occurred if the previous rate of decline had been sustained.

Approximately 25% of ischemic strokes are fatal within a month, nearly one third by 6 months, and 50% by 1 year. Stroke mortality is even higher for those with primary intracerebral hemorrhage and subarachnoid hemorrhage, which approach 50% mortality by one month.

For subarachnoid hemorrhage, the mortality is approximately 35% after the initial bleed.
Vasospasm is the leading cause of death in those who survive the initial hemorrhage,
with the peak incidence occurring 5-12 days after the aneurysm rupture. Rebleeding is also associated with a significantly increased mortality of approximately 70% in survivors of the initial bleed.

Estimates of population-based studies have shown that approximately 500 per 100,000 live with the consequences of stroke with the age-adjusted prevalence for people aged 65 years or more ranging from 46.1 to 73.3 per 1000 population. It has been estimated that stroke-related disability is the sixth most common cause of reduced disability-adjusted life-years.

Race, Sex, and Age

According to data published by the American Heart Association, blacks have a risk of first-ever stroke that is nearly double that for whites. The age-adjusted incidence of first ischemic stroke per 100,000 was 88 in whites, 191 in blacks, and 149 in Hispanics, according to data from the Northern Manhattan Study (NOMAS) of stroke and stroke risk factors. In a US study, researchers found that blacks had a 3-fold higher multivariate-adjusted risk ratio of lacunar stroke than whites.
 An increased proportion of intracerebral hemorrhage and lacunar infarcts have been reported in Asia.

Stroke is an important health issue in women because their incidence of stroke exceeds that in men at older ages. This may in part be secondary to the greater lifespan of women compared to men and the effects of hormone status on cardiovascular disease following menopause. Women 45-54 years are reported to be more than twice as likely as men to suffer a stroke. Overall, 55,000 more women than men have a stroke annually in the United States.

Stroke is a disease of increasing importance in the elderly population, with approximately 75% of strokes occurring in those older than 65 years. Numerous studies have demonstrated that the age-specific incidence of stroke increases with each decade of life.

Anatomy

Arterial distributions

Knowledge of cerebrovascular arterial anatomy and the territories supplied by each is useful in determining which vessel or vessels are involved in acute stroke. Atypical patterns that do not conform to a vascular distribution may indicate another diagnosis, such as venous infarction.

The cerebral hemispheres are supplied by 3 paired major arteries: the anterior, middle, and posterior cerebral arteries. The anterior and middle cerebral arteries comprise the anterior circulation and arise from the supraclinoid internal carotid arteries. The anterior cerebral artery supplies the medial portion of the frontal and parietal lobes and anterior portions of basal ganglia and anterior internal capsule. The middle cerebral artery supplies the lateral portions of the frontal and parietal lobes and the anterior and lateral portions of the temporal lobes and gives rise to perforating branches to the globus pallidus, putamen, and internal capsule.

The posterior cerebral arteries arise from the basilar artery and form the posterior circulation. The posterior cerebral artery gives rise to perforating branches that supply the thalami and brainstem and cortical branches to the posterior and medial temporal lobes and occipital lobes. The cerebellar hemispheres are supplied inferiorly by the posterior inferior cerebellar artery (PICA) arising from the vertebral artery, superiorly by the superior cerebellar artery, and anterolaterally by the anterior inferior cerebellar artery (AICA) (see the images below).

Frontal view of a cerebral angiogram with selectiv

Frontal view of a cerebral angiogram with selective injection of the left internal carotid artery illustrates the anterior circulation. The anterior cerebral artery consists of the A1 segment proximal to the anterior communicating artery with the A2 segment distal to it. The MCA can be divided into 4 segments: the M1 (horizontal segment) extends to the limen insulae and gives off lateral lenticulostriate branches, the M2 (insular segment), M3 (opercular branches) and M4 (distal cortical branches on the lateral hemispheric convexities).

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Lateral view of a cerebral angiogram illustrates t

Lateral view of a cerebral angiogram illustrates the branches of the anterior cerebral artery and Sylvian triangle. The pericallosal artery has been described to arise distal to the anterior communicating artery or distal to the the origin of the callosomarginal branch of the anterior cerebral artery (ACA). The segmental anatomy of the ACA has been described as follows: the A1 segment extends from the internal carotid artery (ICA) bifurcation to the anterior communicating artery; A2 extends to the junction of the rostrum and genu of the corpus callosum; A3 extends into the bend of the genu of the corpus callosum; A4 and A5 extend posteriorly above the callosal body and superior portion of the splenium. The Sylvian triangle overlies the opercular branches of the middle cerebral artery (MCA), with the apex representing the Sylvian point.

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Frontal projection from a right vertebral artery a

Frontal projection from a right vertebral artery angiogram illustrates the posterior circulation. The vertebral arteries join to form the basilar artery. The posterior inferior cerebellar arteries (PICA) arise from the distal vertebral arteries. The anterior inferior cerebellar arteries (AICA) arise from the proximal basilar artery. The superior cerebellar arteries (SICA) arise distally from the basilar artery prior to its bifurcation into the posterior cerebral arteries.

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The anterior cerebral artery supplies the following structures:

Cortical branches – Medial frontal and parietal lobe

Medial lenticulostriate branches – Caudate head, globus pallidus, anterior limb of the internal capsule

The middle cerebral artery supplies the following structures:

Cortical branches – Lateral frontal and parietal lobes, lateral and anterior temporal lobe

Lateral lenticulostriate branches – Globus pallidus and putamen, internal capsule

The anterior choroidal artery supplies the following structures:

Optic tracts

Medial temporal lobe

Ventrolateral thalamus

Corona radiata

Posterior limb of the internal capsule

The posterior cerebral artery supplies the following structures:

Cortical branches – Occipital lobes, medial and posterior temporal and parietal lobes

Perforating branches – Brainstem, posterior thalamus, and midbrain

The posterior inferior cerebellar artery supplies the following structures:

Inferior vermis

Posterior and inferior cerebellar hemispheres

The anterior inferior cerebellar artery supplies the following structure:

Anterolateral cerebellum

The superior cerebellar artery supplies the following structures:

Superior vermis

Superior cerebellum (see the image below)

The supratentorial vascular territories of the maj

The supratentorial vascular territories of the major cerebral arteries are demonstrated superimposed on axial (left) and coronal (right) T2-weighted images through the level of the basal ganglia and thalami. The middle cerebral artery (MCA; red) supplies the lateral aspects of the hemispheres, including the lateral frontal, parietal and anterior temporal lobes, insula, and basal ganglia. The anterior cerebral artery (ACA; blue) supplies the medial frontal and parietal lobes. The posterior cerebral artery (PCA; green) supplies the thalami and occipital and inferior temporal lobes. The anterior choroidal artery (yellow) supplies the posterior limb of the internal capsule and part of the hippocampus extending to the anterior and superior surface of the occipital horn of the lateral ventricle.

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(Images below illustrate vascular distributions.)

Vascular distributions: Middle cerebral artery (MC

Vascular distributions: Middle cerebral artery (MCA) infarction. Noncontrast CT scan demonstrates a large acute infarction in the MCA territory involving the lateral surfaces of the left frontal, parietal, and temporal lobes as well as the left insular and subinsular regions with mass effect and rightward midline shift. The caudate head is spared, and at least part of the lentiform nucleus and internal capsule, which receive blood supply form the lateral lenticulostriate branches of the M1 segment of the MCA. Note the lack of involvement of the medial frontal lobe (anterior cerebral artery territory), thalami and paramedian occipital lobe (posterior cerebral artery territory).

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Vascular distributions: anterior cerebral artery (

Vascular distributions: anterior cerebral artery (ACA) infarction. Diffusion-weighted image on the left demonstrates high signal in the paramedian frontal and high parietal regions. The opposite diffusion-weighted image in a different patient demonstrates restricted diffusion in a larger ACA infarction involving the left paramedian frontal and posterior parietal regions. Infarction of the lateral temporoparietal regions bilaterally (both MCA distributions) also exists; it is greater on the left, indicating multivessel involvement suggesting emboli.

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Vascular distributions: posterior cerebral artery

Vascular distributions: posterior cerebral artery (PCA) infarction. The noncontrast CT images demonstrate PCA distribution infarction involving the right occipital and inferomedial temporal lobes. The image on the right demonstrates additional involvement of the thalamus, also part of the PCA territory.

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Vascular distributions: Anterior choroidal artery

Vascular distributions: Anterior choroidal artery infarction. The diffusion-weighted image (left) demonstrates high signal with associated signal dropout on the apparent diffusion coefficient (ADC) map involving the posterior limb of the internal capsule. This is the typical distribution of the anterior choroidal artery, the last branch of the internal carotid artery before bifurcating into the anterior and middle cerebral arteries. The anterior choroidal artery may also arise from the middle cerebral artery (MCA).

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Stroke in the young patient

A number of different diseases can result in ischemic stroke in the young patient. These include cardioembolic disease, dissection, inherited structural and metabolic abnormalities, thrombophilias, pregnancy, and drug use, as follows
:

Cardioembolic strokes can be seen in patients with risk factors such as arrhythmias; congenital structural defects such as patent foramen ovale; and valvular heart disease, including both native and prosthetic valves.

Dissection can be seen with trauma and connective tissue disorders, such as Marfan and Ehler-Danlos syndrome.

Inherited abnormalities include inherited forms of hyperlipidemia, such as autosomal dominant hypercholesterolemia, cerebral autosomal dominant arteriopathy with subcortical infarcts, and leukoencephalopathy (CADASIL), and numerous other congenital metabolic abnormalities.

Hematologic disorders include deficiencies of protein C and S, antithrombin III deficiency, antiphospholipid antibody syndrome, hyperviscosity syndromes, and sickle cell anemia.

Vasculitides, including lupus and Behçet disease can also produce ischemic infarction.

Pregnancy creates a hypercoagulable state by increasing the amounts of certain clotting factors, with stroke and hypertensive encephalopathy being potential complications of pregnancy induced hypertension and eclampsia.

Drugs, both prescribed and illicit (especially cocaine), may result in ischemic infarction.

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