Territorial Strokes as a Tool to Learn Vascular Territories · Territorial Strokes as a Tool to Learn Vascular Territories Behroze Adi Vachha and Pamela Whitney Schaefer* Neuroradiology,

Territorial Strokes as a Tool to Learn Vascular Territories

Behroze Adi Vachha and Pamela Whitney Schaefer*Neuroradiology, Massachusetts General Hospital, Boston, MA, USA

Abstract

Stroke is the fourth leading cause of death in the United States and a leading cause of serious, long-term adult disability. One of the key tasks in establishing the diagnosis of acute ischemic stroke anddetermining its appropriate treatment is establishing the arterial territory affected. Knowledge ofcerebral vascular territories helps identify abnormal vessels on CT and conventional angiograms,confirms that a DWI hyperintense lesion represents an acute arterial stroke, and guides furtherinvestigations and treatment. Factors contributing to understanding vascular territories include theanatomy of the intracranial circulation and its normal variants and the intrinsic variability in theextent of brain supplied by the main branches of the intracranial circulation. This chapter reviews thenormal anatomy of intracranial arteries and describes the vascular distribution as seen on CT andMRI using major territorial strokes as a learning tool.

Keywords

Stroke; Infarct; Vascular territories

Introduction

Stroke is the fourth leading cause of death in the United States and a leading cause of serious, long-term adult disability [1]. Arterial ischemic strokes account for 87 % of all cases; the remainingstrokes are mostly hemorrhagic [2].

Readily available computed tomography (CT) and magnetic resonance imaging (MRI) in emer-gency settings have allowed clinicians to improve correlations between clinical history and preciseanatomic lesion location in stroke patients. One of the key tasks in establishing the diagnosis of acuteischemic stroke and determining its appropriate treatment is establishing the arterial territoryaffected. Knowledge of cerebral vascular territories helps identify abnormal vessels on CT andconventional angiograms, confirms that a DWI hyperintense lesion represents an acute arterialstroke, and guides further investigations and treatment. Factors contributing to understandingvascular territories include the anatomy of the intracranial circulation and its normal variants andthe intrinsic variability in the extent of brain that the main branches of the intracranial circulationsupply.

This chapter reviews the normal anatomy of intracranial arteries and describes the vasculardistribution as seen on CT and MRI using major territorial strokes as a learning tool.

*Email: [email protected]

*Email: [email protected]

Neurovascular ImagingDOI 10.1007/978-1-4614-9212-2_10-1# Springer Science+Business Media New York 2014

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General Overview of Intracranial Arteries

The intracranial circulation can be conveniently divided into the anterior and posterior circulation.The anterior circulation consists of the intradural internal carotid artery (ICA) and its branches, aswell as the two terminal branches of the ICA – the anterior cerebral artery (ACA) and the middlecerebral artery (MCA). The anterior communicating artery (AComm) connecting the two ACAs andthe left and right posterior communicating arteries (PComm) connecting the ipsilateral ICA to theipsilateral posterior communicating artery (PCA) are also considered part of the anterior circulation[3]. The posterior circulation includes the vertebral arteries, the basilar artery and its branches, andthe terminal bifurcation of the basilar artery into the right and left PCAs [3]. Approximate vascularterritories of the major intracranial arteries are depicted in Fig. 1.

At the base of the brain, branches of the internal carotid arteries and the vertebrobasilar trunkanastomose to form an arterial polygon known as the circle of Willis [3]. The circle of Willis isformed by two terminal ICAs, two proximal or horizontal (A1) segments of the ACA, the AComm,two PComms, two proximal or horizontal (P1) segments of the PCAs, and the top of the basilarartery (BA). The MCAs are not considered part of the circle of Willis. The normal circle of Willis isdepicted diagrammatically in Fig. 2.

The following sections discuss the normal anatomy and vascular distributions of the anterior andposterior circulations as seen on CT and MRI.

Anterior Circulation

Intradural Internal Carotid ArteryThe intracranial ICA is divided into six segments: petrous (C2) segment, lacerum (C3) segment,cavernous (C4), clinoid (C5) segment, ophthalmic (C6) segment, and communicating (C7) segment[4]. The ophthalmic (C6) segment is the first ICA segment that lies within the subarachnoid spaceand gives off two important branches: the ophthalmic arterywhich supplies the retina and the opticnerve [4] and the superior hypophyseal artery which supplies the anterior pituitary lobe, theinfundibular stalk, and the optic chiasm [5].

Fig. 1 Approximate vascular territories of the cerebral arteries and their branches as well as the posterior fossa vessels.There is considerable variability in these territories particularly in the basal ganglia, brainstem, and posterior fossa


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The communicating (C7) segment extends from the PComm origin to the ICA terminus. Thissegment has two important branches: the PComm and the anterior choroidal artery.

Posterior Communicating ArteryThe PComm joins the anterior and posterior circulation. It extends from the ICA to the junction ofthe P1 and P2 segments of the PCA. Perforating arteries arise from the posterior PComm and supplythe thalamus and hypothalamus [4].

The tuberothalamic artery or polar artery arises from the caudal part of the PComm, which isclose to the PCA, or from the border between the caudal and middle third of the PComm [6, 7]. It isabsent in approximately one-third of the normal population and is considered to have an anatom-ically complementary relationship with the paramedian artery originating from the P1 segment[7]. The tuberothalamic artery supplies the ventral section of the thalamus including the anteriorthalamic nuclei (i.e., anteromedial, anteroventral, anterodorsal nuclei), ventral anterior nucleus,reticular nucleus, rostral portion of the ventrolateral nucleus, ventral pole of the medial dorsalnucleus, mammillothalamic tract, ventral amygdalofugal pathway, and ventral portion of the internalmedullary lamina [6].

Infarction in the territory of the tuberothalamic artery results in severe neuropsychological deficits[7]. A characteristic feature of tuberothalamic artery infarctions is the impairment of recent memory,

Fig. 2 Anatomic diagram of the normal circle of Willis


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temporal disorientation, and new learning, which is more prominent with left-sided lesions, whileright-sided lesions result in visual memory deficits, hemispatial neglect, and visual spatialprocessing deficits [7, 6]. Language disorders characterized by anomia, impaired fluency, semanticand phonemic paraphasic errors, and impaired comprehension are seen in left-sided lesions. The“amnestic syndrome” is associated with a disconnection between the anterior thalamic nuclei andhippocampal formation, caused by the disruption of the mammillothalamic tract, as well as adisconnection between the amygdala and anterior nuclei by disruption of the amygdalothalamicprojections passing through the internal medullary lamina [8].

Patients with infarctions confined to the ventral anterior nucleus, anterior nuclei, paramediannuclei, mammillothalamic tract, and internal medullary lamina manifest differently from those withthe previously described larger tuberothalamic infarctions. In these patients, there is severe impair-ment of memory and new learning with relative sparing of language [6]. Palipsychism is aphenomenon associated with anterior thalamic infarcts in which patients demonstrate perseverationwhich leads to overlap of sequential cognitive processes [9].

Anterior Choroidal ArteryThe anterior choroidal artery (AChA) arises from the posterior wall of the ICA distal to the origin ofthe PComm (although it occasionally arises from the MCA) and courses laterally in the suprasellarcistern to enter the choroidal fissure of the temporal horn of the lateral ventricle [3, 4].

Although the vascular territory of the AChA shows large variations, the most consistentlydocumented area involves the amygdala, the lateral geniculate body, posterior two-thirds of theposterior limb of the internal capsule, most of the globus pallidus, the origins of the optic radiations,the middle one-third of the cerebral peduncles, and the lateral thalamic border [3, 4, 10, 11]. TheAChA territory is reciprocal with those of the posterolateral and posteromedial choroidal arteriesthat arise from the PCA [4]. Figure 3 depicts an infarct in the vascular territory supplied by theAChA.

Interruption of blood flow from the AChA can result in complete or partial manifestation of theAChA syndrome which includes the triad of hemiplegia (due to involvement of pyramidal tracts in

Fig. 3 Thirty-six-year-old female with right hemiparesis and word-finding difficulties. Diffusion-weighted MRI (DWI)obtained 2 h after onset of symptoms demonstrated restricted diffusion in the left mesial temporal lobe (a) and in the leftposterior limb of the internal capsule (b) consistent with acute infarction in the left anterior choroidal artery distribution


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the posterior limb of the internal capsule), hemisensory loss (due to involvement of the posterolateralnucleus of the thalamus), and homonymous hemianopia (due to involvement of the lateral geniculatebody) [10, 12, 13]. Many AChA territory infarcts present as lacunar syndromes [13].

Normal Variants of the ICAFetal origin of the posterior cerebral artery occurs when the caliber of the PComm may be the sameas or larger than that of the ipsilateral P1 segment of the posterior cerebral artery [14]. This varianthas clinical significance since simultaneous infarcts in the vascular territories of both the anterior andposterior circulation can occur from ICA emboli in the presence of fetal circulation [15].

A “hyperplastic” AChA is defined as a normal cerebrovascular variant in which the temporal-occipital branches of the posterior cerebral artery arise from the AChA [14]. The clinical significanceof this variant is the increased occurrence of intracranial aneurysm formation [16].

In a 4-mm embryo, there are sites of anastomosis between the paired dorsal aortic arches that laterform the internal carotid arteries and the paired longitudinal neural arteries that later form thevertebrobasilar system [17]. With the exception of the PComm, all other primitive arterial connec-tions regress when the definite circulation develops. Failure of these vessels to regress results inpersistent carotid-vertebrobasilar anastomoses. From cephalad to caudal, these are the persistenttrigeminal artery, persistent otic artery, persistent hypoglossal artery, and proatlantal intersegmentalartery [14, 17].

The persistent trigeminal artery (PTA) is seen in 0.1–0.2 % of patients and is the most common ofthe carotid-vertebrobasilar anastomoses [3]. Salas et al. classify the PTA into a medial sphenoidvariation which has an intrasellar or trans-hypophyseal course and a lateral petrosal variation inwhich the artery courses with the sensory roots of the trigeminal nerve and exits the Meckel cavebelow the petroclinoid ligament [18]. Saltzman classifies the PTA into three types: Type I is definedwhen the PTA supplies the distal basilar artery, the proximal basilar artery is typically hypoplastic,and the ipsilateral PComm is absent, Type II is defined when the PTA fills the anterior superiorcerebellar arteries only and the posterior cerebral arteries are supplied by the PComms, and Type IIIdemonstrates a PTA that unites with a remnant of the primitive paired longitudinal neural artery andsupplies an ipsilateral cerebellar artery (usually the anterior-inferior cerebellar artery) [19]. Clini-cally, these anomalies may be responsible for ischemia and trigeminal neuralgia [20].

The persistent hypoglossal artery originates from the ICA at the levels of the C1 through C3vertebral bodies and courses through the hypoglossal canal to anastomose with the basilar artery[3]. This variant is the second most common carotid-vertebrobasilar anastomosis and has beenreported to result in glossopharyngeal neuralgia and hypoglossal nerve paralysis [3, 14].

The proatlantal intersegmental artery arises from the internal carotid artery (Type I) or the externalcarotid artery (Type II) at the levels of the C2 through C4 vertebral bodies and joins the suboccipitalvertebral artery before coursing through the foramen magnum [3, 4].

The persistent otic artery is the least common of the carotid-vertebrobasilar anastomoses. Theactual existence of this variant is controversial, and it may represent overlapping vascular territoriesrather than persistence of an embryonic vessel [4, 14].

Occlusions of the ICA may have clinical manifestations related to embolism or low flow(discussed in border zone infarctions) [15]. Episodes of transient monocular blindness due toembolization to the retinal circulation are typical. An ICA occlusion may be asymptomatic in thepresence of a competent circle of Willis. When a thrombus propagates up to the top of ICA andoccludes both the MCA and the ACA, the occlusion is often called a “T” occlusion [15]. It carries avery poor prognosis unless complete recanalization is achieved very early [21–23].


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Anterior Cerebral ArteryThe ACA is the smaller terminal branch of the supraclinoid ICA. The ACA supplies the anteriortwo-thirds of the medial surface of the cerebral hemisphere extending from the frontal pole to theparieto-occipital sulcus; this region includes the motor and sensory cortical areas for the pelvis andthe lower extremities. The ACA vascular territory includes the anterior four-fifths of the corpuscallosum, the anterior limb of the internal capsule, the anterior-inferior head of the caudate nucleus,and approximately 1 in. of the frontal and parietal cortex of the cerebral convexity adjacent to theinterhemispheric fissure [3, 4]. Figure 4 demonstrates an acute infarct with hemorrhagic conversionin the expected vascular distribution of the ACA. The ACA has three segments: horizontal (A1),vertical (A2), and callosal (A3) segments.

Horizontal (A1) SegmentThe horizontal/A1 segment extends from its origin to the midline where it communicates with thecontralateral ACA by the AComm. The ACA gives rise to the medial lenticulostriate arterieswhich supply the medial basal ganglia and the anterior limb of the internal capsule [3, 4] (Fig. 1).

Fig. 4 Sixty-year-old male with weakness of the right shoulder, leg, and foot. Non-contrast-enhanced CT of the brain(a) obtained 6 h after onset of symptoms demonstrates hypoattenuation with superimposed hyperdensity consistent withhemorrhagic conversion of acute infarct in the left anterior cerebral artery distribution. Diffusion-weighted (b) andFLAIR (c) images obtained 1 h later in the same patient show the full extent of acute left anterior cerebral artery infarct


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The AComm has perforating arteries that supply the anterior hypothalamus, optic chiasm, genu ofthe corpus callosum, cingulate gyrus, and pillars of the fornix.

Vertical (A2) SegmentThe vertical/A2 segment courses in the interhemispheric fissure and gives rise to the orbitofrontaland frontopolar arteries that supply the undersurface and the inferomedial aspect of the frontal lobe[3, 4].

Callosal (A3) SegmentThe callosal/A3 segment curves around the corpus callosal genu and divides into the pericallosaland callosomarginal arteries. The pericallosal artery courses over the superior surface of the▶ corpus callosum in the pericallosal cistern and gives off many small branches to the corpuscallosum [3]. The callosomarginal artery courses within the cingulate sulcus over the cingulategyrus [3]. The cortical branches of the pericallosal and callosal marginal arteries supply the medialportions of the frontal lobes, superior medial portions of the parietal lobes, and the anterior corpuscallosum [24]. Infarctions of these vessels result in hemiparesis and hemianesthesia of the contra-lateral leg due to involvement of the medial precentral and postcentral gyri, respectively.

Recurrent Artery of HeubnerThe recurrent artery of Heubner arises from the proximal A2 or the distal A1 segment [25, 26] andsupplies the anterior part of the caudate nucleus, the anterior third of the putamen, the tip of the outersegment of the globus pallidus, and the inferior anterior limb of the internal capsule [25,26]. Hemiparesis with faciobrachial predominance has been attributed to occlusions within this

Fig. 5 Fifty-five-year-old male with history of atrial fibrillation presented with new onset seizures. Diffusion-weightedMRI obtained 3 h after onset of symptoms demonstrates restricted diffusion in the caudate nucleus, anterior limb of theinternal capsule, and anterior aspect of the putamen and globus pallidus consistent with acute infarct in the expectedvascular distribution of the recurrent artery of Heubner. There is an additional small acute infarct in the right periatrialwhite matter


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artery [26]. Figure 5 depicts an acute infarct in the vascular territory of the recurrent artery ofHeubner.

Normal Variants of the Anterior Cerebral ArteriesThe azygos anterior cerebral artery is a rare variant of the anterior cerebral artery involving acommon trunk in the A2 segment (above the anterior communicating artery) with a prevalence of0.2–4.0 % [14, 27]. Baptista distinguished three types of this anatomical variant: (1) “unpaired”ACA or true azygos artery (Type I anomaly) in which a single unpaired ACA provides branches toboth cerebral hemispheres; (2) “bihemispheric”ACA (Type II anomaly) in which the A2 segment ofone ACA sends branches across the midline, while the contralateral A2 segment either is hypoplasticor terminates early in its course toward the genu of the corpus callosum; and (3) “accessory” ACA(Type III anomaly) where there is an additional vessel arising from the anterior communicatingartery accompanied by two hypoplastic A2 segments [27]. The most common anomaly noted byBaptista was the Type III anomaly, while the Type I anomaly was observed in only 1 of the 381 brainspecimens examined by him [27]. An azygos anterior cerebral artery is associated with a largenumber of cerebral anomalies including agenesis of corpus callosum, porencephalic cysts,hydranencephaly, lobular holoprosencephaly, septo-optic dysplasia, and saccular aneurysms.Being aware of the presence of an azygos ACA is important, as an occlusion of this vessel canresult in infarcts involving the bilateral medial cerebral hemispheres [14].

Trifurcation of the anterior cerebral artery, defined as the presence of three A2 segments of theACA, is seen in 2–13 % cases and most likely represents persistence of the median callosal artery[14]. In the presence of thromboembolic disease, hypoplasia or absence of the A1 segment of theACA typically results in a decreased collateral supply and consequently an increased risk ofinfarction [14].

Clinical manifestations of unilateral ACA territory infarction are spastic hemiparesis of thecontralateral lower limb and to a lesser degree paresis of the arm, with the face and tongue largely

Fig. 6 Sixty-seven-year-old female with left hemiplegia last seen well 9 h prior to presentation in the emergency room.Diffusion-weighted MRI (DWI) demonstrated restricted diffusion within the right frontal and temporal lobe consistentwith acute infarct in the vascular distribution of the superior and inferior divisions of the right middle cerebral artery


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spared [26, 28, 29]. Sensory dysfunction, particularly proprioceptive and discriminative impairmentof the contralateral lower limb, may be present but is usually mild. Other manifestations of unilateralACA territory infarction include speech disturbance with initial mutism, transcortical aphasia,apraxia, apathy, abulia, incontinence, and disinhibition [26]. Bilateral ACA territory infarctioncauses a neurologic syndrome characterized by profound akinetic mutism, paraparesis, and poorrecovery [26].

Middle Cerebral ArteryThe MCA has the largest vascular territory of all of the major intracranial arteries and is the vesselmost commonly affected by cerebrovascular accidents [30]. Cortical branches of the MCA supplytwo-thirds of the lateral surface of the cerebral hemisphere with the exception of a thin 1-in. stripnear the vertex that is supplied by the ACA and the occipital and posteroinferior parietal lobes thatare supplied by the PCA (Fig. 1). Infarcts that occur in different segments of theMCA lead to diverseneurologic outcomes. The following subsections detail the specific MCA territories supplied by thevarious segments of the MCA and their correlation to specific neurologic deficits.

Horizontal (M1) SegmentThe horizontal/M1 segment of theMCA arises from the carotid terminus and extends laterally whereit bifurcates or trifurcates just before it enters the Sylvian fissure. The anterior temporal arteryarises from the M1 segment and supplies the tip of the temporal lobe [4]. Lateral lenticulostriatearteries are deep penetrating branches of the M1 segment that supply the superior part of the headand body of the caudate nucleus, the putamen, and the external capsule [4, 31].

Complete proximal M1 occlusions (Fig. 6) result in sensory, motor, language, and executivefunction deficits due to disruption of both MCA cortical representations and basal ganglia circuit

Fig. 7 Sixty-six-year-old male with right facial droop and expressive aphasia. Diffusion-weighted MRI (DWI) of thebrain obtained 4 h after symptom onset shows an acute infarct involving the left frontal operculum and left anteriorinsula in the expected vascular distribution of the superior division of the left middle cerebral artery


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structures, while distal MCA occlusions spare the lateral lenticulostriate vascular territory butinvolve the distributions of both the superior and inferior division branches (see below).

Insular (M2) SegmentsIn the majority of cases, the MCA divides into two trunks – superior and inferior – althoughoccasionally it trifurcates into superior, middle, and inferior divisions [3, 4, 30, 31]. The superiordivision supplies the frontal and peri-Rolandic regions including the anterior parietal lobe [30]. Theinferior division supplies the lateral temporal and inferior parietal lobes [30]. Figures 7 and8 demonstrate acute infarcts in the vascular territories of the superior and inferior divisions of theMCA respectively.

Opercular (M3) SegmentsThe portions of the superior and inferior divisions that course laterally under the frontal, parietal, andtemporal opercula are termed the opercular/M3 segments [30, 31].

Cortical (M4) SegmentsThe cortical/M4 segments are the portions of the superior and inferior MCA divisions that exit theSylvian fissure and branch over the lateral surface of the hemisphere [3, 4].

Normal Variants of the Middle Cerebral ArteriesAn early bifurcation or trifurcation of the M1 segment close to its origin at the ICA is a commonfinding and is of no definite clinical significance [14]. A middle cerebral artery branch arising fromthe distal internal carotid artery is called a “duplicated”MCA, while a vessel arising from the ACAand coursing parallel to the M1 segment of the MCA is called an “accessory MCA” [14]. Thefrequency of accessory MCA is 0.3–0.4 %, while that of MCA duplication is 0.2–2.9 % [14]. Theaccessory MCA supplies the territory of the orbitofrontal, prefrontal, precentral, and/or central

Fig. 8 Eighty-nine-year-old female with new onset receptive aphasia. Diffusion-weighted MRI (DWI) of the brainobtained 12 h after symptom onset shows an acute infarct involving the left temporal lobe in the expected vasculardistribution of the inferior division of the left middle cerebral artery


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arteries [32]. The duplicatedMCA supplies the territory of the lateral part of the orbital surface of thefrontal lobe and the anterior and/or middle temporal territories. In the setting of MCA infarcts, theaccessory MCA can provide collateral flow to the anterior frontal lobe, but it cannot supply enoughflow to the main MCA territory [32]. Similarly, the duplicated MCA can provide collateral flow tothe anterior temporal lobe, but it cannot supply enough flow to the main MCA territory [32].

Clinical patterns of MCA territory infarcts depend on the location, size, and side of the infarct[30]. If the entire MCA is occluded at its origin, clinical findings are contralateral hemiplegia,hemianesthesia, homonymous hemianopia, and conjugate deviation of the eyes toward the side ofthe infarct in the acute phase [30, 33]. When the speech/language-dominant hemisphere is affected,severe global aphasia is present; when the nondominant hemisphere is affected, the patient presentswith anosognosia, constructional apraxia, and hemineglect [30]. Avariant ofMCA stem infarction ismalignant infarction, a term used to describe those cases with subsequent extensive brain swellingand herniation (Fig. 9) [22].

More distal superior division branch occlusions may produce a clinical syndrome of contralateralhemiparesis and hemianesthesia affecting the lower face and upper extremity more than the leg andcontralateral visual field deficits predominantly affecting the lower fields [30]. For superior divisioninfarcts involving the dominant hemisphere, global aphasia with mutism (aphemia) is seen initially

Fig.9 Seventy-one-year-old man with right hemiplegia and receptive aphasia. (a) Diffusion-weighted MRI (DWI)obtained 3 h after onset of symptoms demonstrates an acute infarct in the territory of the superior and inferior divisionsof the left middle cerebral artery. Non-contrast axial (b) and coronal (c) head CT obtained 4 days later for progressiveworsening mental status in the same patient demonstrate right midline shift with subfalcine and uncal herniationconsistent with malignant edema


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with eventual progression to nonfluent (expressive) aphasia [30], while nondominant hemisphereinfarcts are associated with an acute confusional state and a variable degree of hemispatialneglect [34].

Inferior division infarcts result in visual field defects (contralateral homonymous hemianopia/quadrantanopia) with relative sparing of sensorimotor involvement [30]. Inferior division branchocclusion of the MCA supplying the dominant superior temporal lobe leads to fluent (receptive)aphasia without weakness, while infarcts of the nondominant hemisphere superior temporal lobelead to behavioral disturbances and impairment of visuospatial skills [30]. Sensory aprosody,probably as a result of damage to the right posterosuperior temporal lobe, is a common finding innondominant inferior division territory infarcts [35].

Posterior Circulation

Intradural Vertebral ArteryThe intradural segment of the vertebral artery/V4 segment gives rise to the anterior and posteriorspinal arteries, themedullary perforating branches, and the posterior inferior cerebellar artery(PICA). Occlusions of the anterior spinal artery or vertebral (V4) artery result in infarcts of themedial aspect of the medulla (Fig. 10). The classic triad of the medial medullary syndrome(Déjerine-Roussy syndrome) includes contralateral hemiplegia sparing the face, contralateral lossof posterior column sensation, and ipsilateral tongue paralysis due to involvement of thecorticospinal tract at the medullary pyramid, the medial lemniscus, and the hypoglossal nucleus ornerve [36, 37]. Frequently, however, the clinical syndrome is not confined to the triad and is moreheterogeneous [38].

Posterior Inferior Cerebellar ArteryThe PICA has a variable vascular territory depending on the size of the anterior-inferior cerebellarartery (AICA). PICA territory infarcts involve the lateral medulla (Fig. 11a) as well as the cerebellartonsil and inferior cerebellar hemisphere (Fig. 11b). Lateral medullary infarcts due to occlusion of

Fig. 10 Fifty-five-year-old male with acute onset of nystagmus, right tongue deviation, left-sided ataxia, and sensoryimpairment. Diffusion-weighted MRI (DWI) obtained 6 h after symptom onset demonstrates restricted diffusion in theright medial medulla consistent with an acute infarct in the expected vascular distribution of the intradural vertebralartery


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the PICA result in the lateral medullary (Wallenberg) syndrome characterized by ipsilateral limbataxia, ipsilateral loss of pain and temperature sensation in the face, loss of contralateral pain andtemperature sensation in the body, vomiting, vertigo, nystagmus away from the lesion side,ipsilateral Horner syndrome, dysphagia, and hiccups [38, 39].

Occlusions of the PICA result in infarcts of the inferior cerebellar hemisphere characterized byvertigo, gait ataxia, limb dysmetria, dysarthria, nausea, and vomiting [40]. If the infarct is large,there may be mass effect on the brainstem and hydrocephalus.

Normal Variants of the Vertebral ArteryNormal variations in the distal vertebral artery have been described including C1 and C2 origins ofthe PCIA, duplication of the distal vertebral arteries, and an aberrant course of the distal vertebralartery [41]. Knowledge of these variants is important for both endovascular and surgical planning.

Basilar ArteryThe basilar artery is formed from the union of the two vertebral arteries near the pontomedullaryjunction. The basilar artery courses within the prepontine cistern and bifurcates within theinterpeduncular fossa into the right and left posterior cerebral arteries.

Fig. 11 (a) Thirty-seven-year-old female withWallenberg syndrome. Diffusion-weightedMRI (DWI) obtained 3 h afteronset of symptoms demonstrates restricted diffusion in the left lateral medulla consistent with acute infarct. (b) Thirty-three-year-old female with acute onset of vomiting and gait unsteadiness. DWI demonstrates restricted diffusionconsistent with acute infarct in the inferior left cerebellar hemisphere. Both case (a) and case (b) represent acute infarctsin the vascular territories of the posterior inferior cerebellar artery


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The basilar artery gives rise to several cerebellar branches; occlusions in these vessels result interritorial infarctions that are discussed below.

Superior Cerebellar ArteryThe superior cerebellar arteries (SCA) arise from the distal basilar artery and supply the superiorsurface of the cerebellar hemispheres, the superior vermis, and the dentate nuclei (Figs. 1 and 12a).

SCA occlusion causes ipsilateral ataxia, dysarthria, contralateral pain and temperature sensoryimpairment, nystagmus, nausea, and vomiting [40]. Horner syndrome may be caused by involve-ment of the oculosympathetic fibers [40].With large infarcts, mass effect may lead to compression ofthe midbrain or cause hydrocephalus. Sleep disorders due to lesions involving the locus ceruleushave been documented [40].

Basilar Perforating ArteriesBasilar perforating arteries arise from the dorsal surface of the midbrain to supply the pons and themidbrain.

Anterior-Inferior Cerebellar ArteryThe AICA supplies CN VII and CN VIII as well as a narrow strip of the cerebellar hemisphere thatlies directly behind the petrous temporal bone (Figs. 1 and 12b).

Normal Variants of the Basilar ArteryBasilar artery fenestration is noted in 0.6 % of cases and is most commonly located close to thevertebrobasilar junction [14].

Infarctions of the basilar artery territory result in a wide range of neurologic deficits. Completebasilar artery occlusion leads to infarction of the pons, midbrain, and thalamus. The medial portionsof the temporal, inferior parietal, and occipital lobes also undergo infarction if the PCAs do notreceive sufficient collateralization from the posterior communicating arteries. A combination ofdysarthria, pupillary disorders, lower cranial nerve involvement, or reduced consciousness at initial

Fig. 12 Fifty-seven-year-old male with endocarditis presenting with right-sided ataxia, dysarthria, nystagmus, nausea,and vomiting. Diffusion-weighted MRI (DWI) obtained 3 h after onset of symptoms demonstrates restricted diffusion inthe right superior cerebellar hemisphere consistent with an acute superior cerebellar artery infarct (a) and more inferiorlyin the anterior right cerebellar hemisphere posterior to the temporal bone consistent with acute right anterior-inferiorcerebellar artery infarct (b). Foci of restricted diffusion are also noted within the right brainstem and right occipital lobe(a) and in the left cerebellum (b)


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admission appears to be strongly associated with severe disability or death in the absence ofreperfusion [42].

A constellation of clinical syndromes caused by involvement of brainstem nuclei and ascendingor descending long tracts can be observed with incomplete basilar artery occlusion and more focalinfarction. Several named syndromes are commonly associated with basilar artery occlusions.Occlusions of the proximal and middle segments of the basilar artery result in infarction of thebasis pontis with sparing of the tegmen of the pons (Fig. 13), manifesting as the locked-in syndrome(quadriplegia with spared level of consciousness, preserved eye movements, and blinking) [43].Topof the basilar syndrome (characterized by visual, oculomotor, and behavioral abnormalities, oftenwithout significant motor dysfunction) occurs when there is thromboembolic occlusion of the distalbasilar artery with resultant infarction of the rostral brainstem and/or the posterior cerebral arteryterritory [44]. Infarctions of the dorsolateral pons usually result from occlusion of the AICA (caudalpons) or SCA (rostral pons) and cause the lateral pontine syndrome (ipsilateral limb ataxia,ipsilateral loss of pain and temperature sensation of the face, contralateral loss of pain andtemperature sensation of the body, ipsilateral Horner syndrome, and ipsilateral facial paralysis)[45]. The medial pontine syndrome (contralateral spastic hemiparesis of the body, contralateralloss of position and vibration of the body, and medial strabismus) results from occlusion of theparamedian perforating branches with infarction of the medial pons [45].

Posterior Cerebral ArteryThe PCAs are paired vessels arising from the basilar artery. The PCAs supply parts of the midbrain,subthalamic nucleus, and thalamus. The vascular territory of the PCA includes the posteriortwo-thirds of the medial temporal lobe, nearly the entire occipital lobe and the medial inferiorparietal lobes, as well as the posterior one-fifth of the corpus callosum (Fig. 1). The PComm, arisingfrom the ICA, extends posteriorly to join the PCA at the junction of the P1 and P2 segments, therebycompleting the circle of Willis and providing an important source of collateral circulation for theMCA territory. Infarcts in the region of the PCA result in homonymous hemianopia of thecontralateral visual field with macular sparing. Proximal PCA strokes result in infarcts in thethalamus and/or midbrain as well as in the cortex, while distal PCA strokes involve only corticalstructures. The following subsections describe four distinct PCA segments and their branches.

Fig. 13 Seventy-five-year-old male with acute onset of right arm weakness and dysarthria. Diffusion-weighted MRI(DWI) obtained 3 h after onset of symptoms demonstrates a wedge-shaped acute infarct involving the left paramedianbasis pontis with sparing of the tegmen in the expected vascular distribution of the branches of the basilar artery


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Precommunicating (P1) SegmentThe precommunicating/P1 segment of the PCA extends laterally from the basilar artery to thejunction with the PComm. Branches arising from the P1 segment of the PCA include thalamoper-forating or paramedian arteries to the thalamus and brainstem branches [3, 4].

The paramedian arteries have great variability in terms of the territorial contribution to thethalamus but principally supply the dorsomedial nucleus and internal medullary lamina andintralaminar nuclei (central lateral, centromedian, and parafascicular nuclei) [6]. When thetuberothalamic artery is absent, the paramedian arteries can supply the anterior thalamic areas aswell [6, 7]. The artery of Percheron is an anatomic variant of the paramedian artery in which a singledominant paramedian artery supplies the bilateral medial thalami with variable contribution to themidbrain [4]. Specific ischemic patterns and syndromes that result from occlusion of the artery ofPercheron are discussed in detail in a later section.

Unilateral thalamic infarction in the territory of the paramedian artery is characterized by deficitsin arousal and memory. In the early stages, patients demonstrate decreased and fluctuating levels ofconsciousness, while impaired arousal with confusion, agitation, and apathy are seen in later stagesof the infarct [7]. Left-sided lesions result in language and speech impairments characterized byhypophonia and dysprosody with reduced verbal fluency and perseveration. Syntactic structure ispreserved with occasional paraphasic errors and normal repetition [6]. Right-sided infarcts result invisuospatial deficits.

Bilateral paramedian thalamic strokes are typically characterized by altered mental status, mem-ory impairment, and vertical gaze palsy [6, 46]. Altered mental status may present on a spectrumranging from disorientation and hypersomnolence to deep coma and akinetic mutism [6]. Antero-grade and retrograde memory impairment with confabulation tends to resolve with time but may besevere and persistent. In the late stages, the patient may demonstrate emotional blunting, loss ofinitiative, and inappropriate social behaviors.

Occlusion of the P1 segment of the PCA that supplies the midbrain can result in a CN III palsy orcontralateral ataxia or hemiplegia [47].

Fig. 14 Fifty-year-old male presenting with prosopagnosia. Diffusion-weighted MRI (DWI) obtained 15 h aftersymptom onset demonstrates restricted diffusion in the right occipital and medial temporal lobes consistent withacute right posterior cerebral artery territory infarct


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Ambient (P2) SegmentThe medial and lateral posterior choroidal arteries arise from the P2 segment. The lateralposterior choroidal artery shares a reciprocal relationship with the anterior choroidal artery (whicharises from the ICA) [4].

The anterior and posterior temporal arteries supply the inferior surface of the temporal lobe,while the thalamogeniculate and peduncular perforating arteries supply themidbrain [4]. Occlu-sion of the P2 segment causes visual field defects and more complex visual changes such asprosopagnosia secondary to infarction of the medial temporal and occipital lobes (Fig. 14) [47].

The inferolateral arteries comprise five to ten arteries that arise from the P2 segment of the PCAand supply the thalamus [6]. There are three main groups: the medial geniculate, principalinferolateral, and inferolateral pulvinar arteries. The medial branch supplies the external half ofthe medial geniculate nucleus. The principal inferolateral arteries supply the major part of the ventralposterior nuclei (lateral, medial, and inferior nuclei) as well as the ventral and lateral parts of theventrolateral nucleus. The inferolateral pulvinar arteries supply the rostral and lateral parts of thepulvinar and lateral dorsal nucleus [6].

The Déjerine-Roussy syndrome or thalamic pain syndrome occurs following infarctions related tothe inferolateral arteries and is characterized by contralateral sensory loss followed by agonizingburning pain [6, 47, 48]. This syndrome is usually associated with infarcts of the right thalamus.

Quadrigeminal (P3) SegmentThe quadrigeminal/P3 segment is a short segment without any significant named branches [4].

Calcarine (P4) SegmentThe calcarine/P4 segment divides into the medial and lateral trunks within the calcarine fissure. Themedial trunk gives off medial occipital, parieto-occipital, calcarine, and posterior splenialarteries which supply the regions of the brain represented in their names [4]. The lateral trunkgives rise to the lateral occipital artery [4].

Artery of PercheronThe central artery of Percheron is a rare but clinically important PCAvariant. This occurs when thebilateral, medial thalamic/rostral midbrain perforators arise from a single trunk from one P1 segment

Fig. 15 Sixty-nine-year-old male with waxing and waning mental status progressively worsening over the course of3 days. Diffusion-weighted MRI demonstrates foci of restricted diffusion within the medial aspects of the right and leftthalami (a) and medial midbrain (b) consistent with an acute artery of Percheron infarct


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[4]. Occlusion may result in four distinct patterns of infarction in descending order of frequency:bilateral, paramedian, thalamic, and rostral midbrain infarction (Fig. 15); bilateral, paramedian, andthalamic without midbrain involvement; bilateral, paramedian, and anterior thalamic with midbraininvolvement; and bilateral, paramedian, and anterior thalamic without midbrain involvement[46]. In addition to these four distinct patterns, Lazzaro et al. described a V-shaped hyperintensesignal abnormality on axial FLAIR images along the pial surface of the midbrain in theinterpeduncular fossa in their series of 37 patients with occlusions of the artery of Percheron[46]. Infarctions associated with artery of Percheron occlusions produce long-lasting memorydysfunction, deficits in executive function, and mood changes [49].

Normal Variants of the Posterior Cerebral ArteriesFetal origin of the posterior cerebral artery has been described under normal variants of theICA. Fenestration of the P1 and P2 segments of the PCA has been noted but is a very rareoccurrence [14].

Border Zones

Border zones occur at the junction between two vascular territories. Two distinct border zone orwatershed territories are defined: (1)External (cortical) border zone territories include the frontaland parietal border zone territory between the ACA and MCA territories and the posterior parieto-occipital border zone territory between the MCA and PCA territories. (2) Internal (subcortical)border zone territories include the border zones in the corona radiata and centrum semiovalebetween the penetrating branches (lenticulostriate and medullary perforating and anterior choroidalarteries) and the main cerebral arteries (ACA, MCA, and PCA) [4]. Figure 16 is an example of

Fig. 16 Eighty-seven-year-old man with atrial fibrillation with new onset right hemiplegia. Diffusion-weighted MRI(DWI) obtained 4 h after symptom onset demonstrates bilateral border zone infarcts between the anterior cerebral arteryand middle cerebral artery, presumed to be cardioembolic in origin


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diffusion-weighted MRI sequences demonstrating restricted diffusion consistent with border zoneinfarcts.

Clinical manifestations of patients with border zone infarcts depend upon the location of thelesion. Patients with unilateral precentral cortico-subcortical infarcts present with somnolence,brachial monoparesis, disproportionate motor hemiparesis with face mostly spared, transcorticalmotor aphasia, and focal myoclonic jerks [50]. Unilateral, postcentral cortico-subcortical infarctsresult in sensorimotor hemiparesis with stereoagnosia, cortical hemihypesthesia, visual and tactilehemispatial neglect, anosognosia, hemianopia particularly involving the lower quadrant, Wernicke-like aphasia, and focal myoclonic jerks [50]. Patients with deep border zone infarcts in the dominanthemisphere develop global aphasia, nonfluent aphasia with or without comprehension and/orrepetition deficits, ideomotor apraxia, and acalculia. Patients with internal border zone infarctionsin the nondominant hemisphere demonstrate anosognosia, neglect, or dysprosody depending on theextent of the lesion. Bilateral infarcts in the border zone regions between the MCA and PCA canresult in asimultagnosia (difficulty recognizing several objects at the same time), optical ataxia(difficulty coordinating hand and eye movements), and apraxia of gaze [50]. Bilateral infarcts in theborder zone regions between the ACA and MCA can result in selective weakness of the upper andlower extremities with sparing of the face, hands, and feet referred to as “a man in a barrel”distribution [50].

Summary

Neuroimaging plays a key role in the initial workup of stroke patients. Knowledge of arterialterritories and their associated stroke syndromes is needed to achieve accurate localization ofischemic lesions to guide further management.

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