Clinical-Anatomical Syndromes of Ischemic Infarction

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Chapter 2 Clinical-Anatomical Syndromes of Ischemic Infarction

Alejandro A. Rabinstein, Steven J. Resnick

Ischemic stroke can be defined as a sudden focal neurological deficit corresponding to a vascular distribution. Brain imaging techniques allow us to visualize lesions with great anatomical precision. However, optimal interpretation of the information provided by neuroimaging requires having detailed knowledge of the arterial anatomy (Figures 2-1 through 2-4) and the vascular territories of the brain (Figure 2-5).

Figure 2-1 Anterior circulation, frontal view on conventional angiogram (top) and three-dimensional angiogram (bottom). ICA, internal carotid artery; ACA, anterior cerebral artery; MCA, middle cerebral artery.

Figure 2-2 Anterior circulation, lateral view on conventional angiogram (top) and three-dimensional angiogram (bottom). ICA, internal carotid artery; ACA, anterior cerebral artery; MCA, middle cerebral artery.

Figure 2-3 Posterior circulation, frontal view on conventional angiogram (top) and three-dimensional angiogram (bottom). PICA, posterior-inferior cerebellar artery; AICA, anterior-inferior cerebellar artery; SCA, superior cerebellar artery.

Figure 2-4 Posterior circulation, lateral view on conventional angiogram (top) and three-dimensional angiogram (bottom). PICA, posterior-inferior cerebellar artery; AICA, anterior-inferior cerebellar artery; SCA, superior cerebellar artery; PCA, posterior cerebral artery.

Figure 2-5 Arterial territories of the cerebral hemispheres. Coronal image is shown on the left, axial in the middle, and sagittal on the right. A = anterior cerebral artery territory, M = middle cerebral artery territory, P = posterior cerebral artery territory.

Brain imaging has also enhanced our understanding of clinical-anatomical correlations in patients with ischemic infarctions. Before the development of modern neuroimaging modalities, these correlations could only be established by necropsy studies. In fact, clinical research using radiological data has shown that localization based on classical semiological syndromes may often be incorrect. Similar clinical presentations may occur in patients with strokes in different territories and, conversely, infarctions in the same territory may produce dissimilar manifestations in different patients. Nonetheless, accurate diagnosis relies on the recognition of the brain lesion in a defined vascular territory.

This chapter provides illustrations of ischemic infarctions in all major vascular territories and presents the most common clinical correlations. It is conceived as a practical and concise guide to the correct interpretation of brain imaging and not as a comprehensive anatomical or semiological monograph on this important topic. The reader should keep in mind that the variety of distribution of infarctions encountered in practice is enormous. The boundaries of arterial territories are far from invariable across patients, and anatomical variations in the constitution of the cerebral circulation and its interconnections are relatively common.

CAROTID BIFURCATION OCCLUSION

Case Vignette

A 61-year-old man with history of coronary artery disease, previous myocardial infarction, and multiple vascular risk factors presented to the emergency department with global aphasia and right hemiplegia for more than 6 hours. On examination, he was drowsy and exhibited forced left gaze deviation, right hemianopia, right flaccid hemiplegia involving the arm and the leg to similar degree, and absent response to pain on the right side. Diffusion-weighted imagery (DWI) of the brain revealed a large area of ischemia in the left hemisphere, including the territories of the anterior and middle cerebral arteries (Figure 2-6). Fluid-attenuated inversion recovery (FLAIR) sequence showed no parenchymal hyperintensity but disclosed extensive hyperintense signal in the left middle cerebral artery consistent with fresh thrombus (Figure 2-7). Magnetic resonance angiography (MRA) of the intracranial circulation confirmed the presence of a left carotid terminus occlusion (Figure 2-7). The patient was subsequently diagnosed with acute myocardial infarction and a left ventricular mural thrombus. His neurological condition deteriorated over the following 48 hours, and he expired after care was restricted to palliative measures.

Figure 2-6 Diffusion weighted imaging (left) and apparent diffusion coefficient map (right) of the brain magnetic resonance imaging show extensive areas of restricted diffusion’indicative of cellular edema’in the territories of the left anterior and middle cerebral arteries.

Figure 2-7 Fluid-attenuated inversion recovery magnetic resonance imaging showing hyperintense signal (top row, arrow) in the left middle cerebral artery extending from the top of the intracranial carotid artery caused by acute thromboembolism; regular (left) and enhanced views (right). Hyperintense signal is also seen in the left anterior cerebral artery (lower left panel, arrowhead). Magnetic resonance angiogram of the intracranial circulation confirms the diagnosis of left carotid terminus occlusion (lower right panel).

♦ Occlusion of the carotid bifurcation (carotid terminus or carotid T) typically results in infarction on the anterior cerebral and middle cerebral artery territories, including the deep structures perfused by the lenticulostriate branches (Figure 2-8).

♦ Patients often present with depressed level of consciousness, forced gaze deviation toward the side of the infarction, contralateral homonymous hemianopia, dense contralateral hemiparesis or hemiplegia (face, arm, and leg), and contralateral sensory loss. Aphasia is present when the infarction affects the dominant hemisphere and neglect when the nondominant side is affected.

♦ Decreased alertness and profound leg weakness are the most useful clinical signs to differentiate a carotid T occlusion from the more common middle cerebral artery stroke.

♦ An intravascular hyperdensity at the level of the carotid bifurcation may often be seen on CT scan. Thin-section computed tomography (CT) scans ¹ and T2* gradient echo magnetic resonance (MR) sequence² may reveal intra-arterial thrombus with greater sensitivity.

♦ Early recognition of this massive stroke is essential because mortality is the rule unless prompt recanalization may be achieved (Figure 2-9).

♦ Although intravenous thrombolysis may occasionally be successful, most experts prefer to pursue intra-arterial treatment (pharmacological thrombolysis or mechanical embolectomy) given the large size of the clot responsible for the vascular occlusion.^3,⁴

Figure 2-8 Multiple ascending cuts of a brain magnetic resonance imaging (diffusion-weighted imagery sequence) illustrating the distribution of ischemia in a patient with carotid terminus occlusion.

Figure 2-9 Fifty-eight-year-old man presenting with right carotid T occlusion who expired on the third day after hospitalization. Admission computed tomography scan is shown in the upper row, and magnetic resonance imaging (MRI) obtained a few hours later is displayed in the middle (diffusion weighted imaging on the left and apparent diffusion coefficient map on the right), and lower (T2-weighted MRI) rows.

MIDDLE CEREBRAL ARTERY OCCLUSION

♦ The clinical manifestations of middle cerebral artery (MCA) strokes can vary broadly, depending on the precise location of the vessel occlusion and the strength of the collateral circulation. Proximal occlusion of the horizontal (M1) segment of the MCA typically results in infarction of the lenticular nucleus and internal capsule (Figure 2-10), whereas more distal M1 occlusions spare these deep structures (Figure 2-11).

♦ The MCA supplies most of the cortical convexity, putamen, upper portion of the globus pallidus, posterior head and whole body of the caudate, large parts of the internal capsule (all but the lowest area of the posterior limb, and often the genu and the posterior-superior aspect of the anterior limb), external capsule, capsula extrema, claustrum, and substantia innominata. Figure 2-12 illustrates the topographical patterns of MCA infarction.

♦ The MCA is divided in four segments (see Figures 2-1 and 2-2). The M1 or horizontal segment is a single stem that give rise to the penetrating lenticulostriate branches. It branches into two (or occasionally three) M2 or insular segments as it enters the Sylvian fissure. The M3 or opercular segments ascend following the curvature of the operculum. The M4 or cortical segments travel along the sulci and gyri of the cerebral convexity.

Figure 2-10 Ischemic infarction of the middle cerebral artery territory from proximal occlusion of the horizontal (M1) segment of the vessel. Note that the infarction involves the basal ganglia and internal capsule because the occlusion is proximal to the takeoff of the lenticulostriate braches.

Figure 2-11 Ischemic infarction of the middle cerebral artery territory from distal occlusion of the horizontal (M1) segment of the vessel. Note that the infarction spares the basal ganglia and internal capsule because the occlusion is distal to the takeoff of the lenticulostriate braches.

Figure 2-12 Topographical patterns of middle cerebral artery infarction.

Case Vignette

A 65-year-old man with history of hypertension presented with acute global aphasia and right flaccid hemiplegia involving the lower face, the arm, and, to a lesser degree, the leg. He also had a dense right visual field deficit and profound right sensory loss. Magnetic resonance imaging (MRI) with DWI revealed extensive ischemia in the territory of the left MCA (Figure 2-13). T2* sequence disclosed a hypointense signal in the left MCA indicative of acute vessel thrombosis and MRA confirmed the left M1 occlusion (Figure 2-14). Atrial fibrillation was noted on cardiac telemetry. Over the following 48 hours, the patient developed fatal brain swelling (see Figure 2-14).

Figure 2-13 Brain magnetic resonance imaging showing acute infarction of the left middle cerebral artery territory (diffusion-weighted imaging on the left and matching apparent diffusion coefficient on the right). Note sparing of the deep territory indicating distal M1 occlusion.

Figure 2-14 T2* sequence demonstrates acute thrombus in the distal part of the M1 segment of the left middle cerebral artery (MCA) (upper left, arrow). Fluid-attenuated inversion recovery sequence depicts the extension of the infarction (upper right); notice hyperintense vessel signal in sulcal braches (arrowhead). Intracranial magnetic resonance angiography confirmed the distal MCA occlusion (lower left). Computed tomography scan 2 days later shows massive progression of ischemic brain swelling (lower right).

Territorial MCA Infarction

♦ The largest MCA infarctions (territorial infarctions) result from proximal occlusion of the proximal M1 segment and absence of enough collateral flow to limit the extent of the infarction.

♦ Patients characteristically present with preserved level of consciousness, gaze deviation or strong preference toward the side of the infarction, contralateral homonymous visual field deficit, and contralateral hemiparesis/hemiplegia (leg weakness is caused by involvement of deep capsular fibers) and hemi-hypoesthesia/anesthesia. Aphasia and hemineglect occur in dominant and nondominant infarctions, respectively (see later discussion for more details on deficits of cortical function).

♦ Hyperdense MCA sign may be seen on the initial CT scan. Its presence is associated with less chances of recanalization after thrombolysis ^5,⁶ and worse likelihood of favorable recovery.⁵^–⁷ Still, intravenous thrombolysis remains the standard of care for patients with MCA stroke presenting within 3 hours of symptom onset regardless of the presence of this radiological sign.⁶ Although preferential use of intra-arterial interventions has been advocated by some groups, the benefits of this approach are thus far unproved.⁸

♦ Occlusions of the distal M1 (horizontal) segment of the MCA produce large infarctions involving the cortex and subcortical white matter but sparing the striatocapsular structures perfused by the lenticulostriate branches (Figure 2-11).

♦ Patients present with facial-brachial weakness (relative leg sparing), which tends to be less severe and recover better than in cases of proximal M1 occlusion. Hemisensory loss usually follows a similar distribution. Contralateral homonymous hemianopsia and transient deviation of the eyes and head toward the side of the infarction are also characteristically present.

♦ Complete cortical infarctions of the MCA on the dominant hemisphere cause global aphasia and ideomotor apraxia (Figure 2-13).

♦ Extensive cortical infarctions of the MCA on the nondominant hemisphere manifest with a combination of contralateral visuospatial neglect, anosognosia, motor impersistence, dressing and constructional apraxia, and occasionally sensory aprosodia. Acute confusion, often with pronounced agitation, may predominate upon presentation (Figure 2-15).

♦ Cortical infarctions may have a patchy appearance when some cortical regions are saved by collateral circulation (Figure 2-16).

Figure 2-15 A 54-year-old woman presented to the emergency department with mild confusion, left visual field impairment, left hemiparesis, and left-sided neglect. Computed tomography scan of the brain (upper row) shows early low attenuation changes in the right middle cerebral artery (MCA) distribution, sparing the deep structures. The acute right MCA infarction was subsequently confirmed by magnetic resonance imaging (diffusion-weighted imaging sequence shown, lower left). Intracranial magnetic resonance angiography displayed the occlusion of the right MCA responsible for the ischemic stroke (lower right).

Figure 2-16 Patchy infarction of the right middle cerebral artery territory shown on diffusion-weighted imaging. Although the patient had an occluded right M1 segment, the infarction is discontinuous likely because of preservation of part of the cortex of the arterial territory by perfusion through collateral flow.

Deep Middle Cerebral Artery Infarction

♦ Deep infarctions in the territory of the MCA are caused by occlusion of lenticulostriate branches.

♦ These vessels perfuse the anterior limb, genu, and anterior segment of the posterior limb of the internal capsule (especially its rostral portion); the corona radiata adjacent to the body of the lateral ventricle; the body and upper half of the head of the caudate nucleus, lentiform nucleus, and external capsule.

♦ The anatomical pattern of lenticulostriate arteries is highly variable. Most often, there are two medial and four or five lateral main lenticulostriate branches, all of which arise most commonly from the dorsal aspect of the MCA horizontal trunk.⁹ Lateral branches are generally larger and longer than the medial. Ramifications of these arteries generate an average of more than 20 penetrating vessels.⁹ Often multiple small branches originate from a single common stem.

♦ Deep infarctions are classified as lacunar, when they measure less than 15 mm in maximal diameter on axial cuts, or striatocapsular when they are larger (usually >20 mm in greatest diameter) (Figure 2-17).^10,¹¹

♦ Lacunar infarctions are typically produced by occlusion of a single penetrating artery, whereas striatocapsular infarctions characteristically occur when multiple penetrating branches are occluded. However, this is far from a rule, because infarctions clearly larger than lacunes may originate from occlusion of a common lenticulostriate stem that gives rise to two or more smaller penetrating branches.^10,¹²

♦ Deep infarctions in the MCA territory often present with lacunar syndromes (pure motor, sensorimotor, dysarthria-clumsy hand). Deficits may be more restricted and result in brachiocrural or brachiofacial syndromes. Manifestations traditionally associated with cortical lesions may occur in larger infarctions of the upper internal capsule or even the external capsule, including aphasia, hemineglect, and apraxia. Similarly, subinsular infarctions may present with signs indistinguishable from the anterior opercular syndrome (loss of voluntary control of facial, lingual, pharyngeal, and masticatory muscles, resulting in severe dysarthria and dysphagia). Also, extrapyramidal signs have been noted in patients with putaminal ischemia,¹³ and abulia, akinesia, and, more rarely, chorea have been reported in association with caudate infarctions.¹⁴

Figure 2-17 Examples of deep infarctions in the middle cerebral artery (MCA) territory. The case displayed in the top row is unusual because of concomitant involvement of the head of the caudate’typically perfused by the recurrent artery of Heubner, most often a branch of the anterior cerebral artery’and the lenticular nucleus (diffusion-weighted imaging [DWI] on upper left and matching apparent diffusion coefficient map on the upper right). The case portrayed in the lower row illustrates extension of the infarction into the paraventricular corona radiata (DWI is shown). These cases serve to highlight the various anatomical presentations that can be seen with deep infarctions in the MCA territory.

Superficial Divisional Middle Cerebral Artery Infarction

♦ Occlusions of the superior (or anterior) M2 branch most commonly cause infarctions involving the extensive cortical and subcortical regions of the frontal lobe convexity and the anterior parietal lobe (Figure 2-18). Both the precentral and postcentral gyri are usually affected.

♦ Clinical manifestations are contralateral hemiparesis and hemisensory loss, predominantly faciobrachial. Conjugate eye deviation or gaze preference toward the side of the infarction occurs often, but visual fields tend to be spared. Nonfluent aphasia with oral apraxia and severe dysarthria are frequently disabling deficits in patients with dominant infarctions. Depression is also a common feature in these patients. Acute confusional state, contralateral hemi-inattention, visual perceptual impairment, aprosodia, and anosognosia are prevailing neuropsychological disturbances in infarctions of the nondominant hemisphere.

♦ Superior division MCA infarctions may be caused by large artery atherothrombosis or cardiac embolism; the former mechanism probably predominates.¹⁵

♦ Occlusion of the inferior (or posterior) M2 branch produces infarction involving the parietal and temporal lobes (Figure 2-19).

♦ The most common clinical manifestations include contralateral sensory and visual field deficits. Variable degrees of hypoesthesia with tactile extinction upon double simultaneous stimulation and homonymous hemianopia or superior quadrantanopia are the most characteristic features. Weakness, when present, is usually mild and transient. Fluent (Wernicke’s) aphasia occurs with infarctions of the dominant hemisphere. Hemineglect, constructional dyspraxia and other visual-perceptual difficulties, and sensory aprosody are encountered in patients with nondominant infarctions.

♦ Acute confusional state, often associated with agitated delirium, may predominate in right-sided infarctions of the inferior M2 division.¹⁶ It is important to keep this diagnosis in mind when evaluating any patient presenting with acute confusion and agitation, because detailed neurological examination may be difficult in these cases, and sensory, visual, and perceptual deficits may be easily missed.

♦ Infarctions of the inferior division of the MCA are predominantly caused by cardiac embolism.^15,¹⁶ Carotid artery disease is rarely a cause of infarctions in this vascular distribution.

Figure 2-18 Superior division middle cerebral artery stroke. Diffusion-weighted imaging and apparent diffusion coefficient map shown in the upper row. Fluid-attenuated inversion recovery sequence displayed on the lower left. Conventional angiogram (lateral view, lower right) demonstrates the absence of filling of the occluded superior M2 branch.

Figure 2-19 Inferior division left middle cerebral artery infarction. Diffusion-weighted imaging sequence is shown.

Superficial Cortical Infarctions

♦ Insular infarctions rarely occur in isolation, but insular involvement is seen in close to half of patients with nonlacunar infarctions of the MCA territory (Figure 2-20). Damage to the insular cortex is most frequently found with large MCA infarctions and proximal M1 occlusions.¹⁷

♦ Insular infarctions have received considerable attention because they have been consistently associated with increased likelihood of cardiac arrhythmias, myocardial injury, and adverse outcome including sudden cardiac death.¹⁸^–²⁰

♦ Left ²⁰ and right-sided^18,¹⁹ infarctions have been associated with worse cardiac outcomes in different studies. Hence, the degree of lateralization in the control of autonomic cardiac function in humans remains to be fully elucidated.

♦ It has been reported that MCA infarctions involving the insular territory may be more prone to growth.²¹ The nature of this phenomenon deserves further exploration.

♦ Other cortical branch infarctions may be caused by occlusion of M3 branches (Figure 2-12) and may present with distinctive clinical syndromes. Some common examples of localizing clinical features encountered in practice are shown in Table 2-1.

♦ These cortical infarctions are typically caused by embolism (from arterial or, probably most often, cardiac sources).

♦ Occasionally cortical branch infarctions represent the only sequelae in patients who present with severe hemispheric deficits but later improve dramatically. These cases of “spectacular shrinking deficits” are thought to result from fragmentation of a large embolus that initially occludes the ICA bifurcation or proximal M1 segment.^22,²³

Figure 2-20 Examples of middle cerebral artery infarction with involvement of the insular cortex. Upper row: Early computed tomography scan (left) with a hyperdense vessel sign in the Sylvian fissure (arrow) and loss of differentiation of the right insular ribbon and underlying anatomical boundaries. Diffusion-weighted imagery (DWI) sequence of magnetic resonance imaging (MRI) (right) allows recognition of the extension of the ischemic area. Lower row: DWI sequence of MRI (left) showing a restricted area of ischemia in the right insular region. MRA (right) shows a flow gap in the distal M1 segment (arrowhead) with reduced filling of M2 branches.

TABLE 2-1 Clinical features of MCA branch infarctions.

Hemispheric Border-Zone Infarctions

♦ External border-zone infarctions affect the “watershed” areas between the superficial anterior cerebral artery and MCA territories, and the superficial MCA and posterior cerebral artery (PCA) territories (Figures 2-12 and 2-21).

♦ These cortically based infarctions may be single or multiple simultaneous, in one or both hemispheres.

♦ They typically result from severe hemodynamic failure, often from a combination of ipsilateral vascular stenosis and a drop in systemic blood pressure.

♦ Clinical presentation varies according to the precise location and extension of the ischemic damage. Severe cases may mimic territorial infarctions of the MCA. More characteristically, patients manifest acute transcortical (often mixed) aphasia or conduction aphasia associated with variable degrees of hemiparesis and homonymous visual field deficits. Balint’s syndrome is usually due to bilateral damage to the watershed region between MCA and PCA. It consists of visual disorientation, spasms of fixation (apraxia of gaze), optic ataxia, and simultagnosia with peripheral vision inattention.

♦ Internal border-zone infarctions involve deep frontal white matter between the anterior cerebral artery (ACA) and MCA, often bilaterally (Figures 2-12 and 2-22).

♦ This pattern of ischemia is caused by severe systemic hypotension or prolonged hypoxemia, and it is most commonly seen after cardiopulmonary arrest.²⁴ It may also be encountered after prolonged, complicated cardiac surgery.²⁵

♦ The classical clinical picture is characterized by proximal or complete bilateral brachial paralysis with preservation of leg movements, often described as “man-in-the-barrel syndrome.”²⁴

♦ Also, profound hypoperfusion may induce ischemic lesions between the deep and superficial branches of the MCA. In those cases, variable degrees of hemiparesis tend to be the predominant clinical manifestation.

Figure 2-21 Example of fairly extensive acute external border-zone infarctions in patients who had developed severe hypotension during emergency cardiovascular surgery and who had preexistent bilateral carotid artery stenosis.

Figure 2-22 Three examples of internal border-zone infarctions. Notice the variable distributions of the lesions (unilateral or bilateral, confluent or patchy, purely internal or combined with areas of ischemia in the external border-zone region). Systemic hypotension was the mechanism of infarction in all these cases. Upper row: Diffusion-weighted imaging (DWI) sequence on the left and fluid-attenuated inversion recovery on the right. Middle row: DWI and matching apparent diffusion coefficient map. Lower row: DWI at two levels.

ANTERIOR CEREBRAL ARTERY OCCLUSION

♦ The ACA supplies the entire medial surface of the frontal and parietal lobes, the basal aspect of the frontal lobes, the head and body of the corpus callosum, and various deep structures including components of the olfactory pathway, cingulum, and the anterior portions of the diencephalon (hypothalamic nuclei) and head of the caudate nucleus (irrigated by the recurrent artery of Heubner) (Figure 2-23).

♦ The ACA is typically divided into precommunicating (A1 segment) and postcomunicating portions (distal ACA, A2-A5 segments) by the anterior communicating artery (see Figure 2-1).

♦ Anatomical variations are often present, including unilateral A1 segment hypoplasia (“threadlike” in 6%-8%, absent in 0.2%-2%, and hypoplastic in 6%-10%), multiple anterior communicating arteries (up to 40% in necropsies); unpaired or azygous ACA (1%-5%); and various anomalies in distal branching.²⁶^–²⁸ These variations affect the ability of collateral circulation to compensate for ischemia in the event of a stroke (e.g., patients with poor cross-flow through the anterior communicating artery will suffer greater ischemic damage to the frontal lobe ipsilateral to a carotid occlusion). Additionally, anomalies in the anterior communicating artery region are associated with increased frequency of saccular aneurysm.²⁹

Figure 2-23 Multiple ascending cuts of a brain magnetic resonance imaging (diffusion-weighted imaging sequence) illustrating the distribution of ischemia in a patient with proximal left anterior cerebral artery occlusion.

Case Vignette

A 65-year-old man presented to the hospital with acute onset of left crural paresis. He had suffered a myocardial infarction 2 weeks before and was taking aspirin and clopidogrel for secondary prevention of coronary events. Examination revealed left leg weakness predominantly involving the proximal flexor muscles and associated with hyperreflexia. MRI demonstrated acute infarction in the right ACA distribution (Figure 2-24). Echocardiogram disclosed a mural thrombus overlying a hypokinetic segment of the left ventricle. The patient was anticoagulated and recovered well with physical therapy.

Figure 2-24 Diffusion-weighted imaging sequence of magnetic resonance imaging showing an acute right anterior cerebral artery infarction.

♦ Semiological presentations vary substantially among patients with ACA infarctions. Motor and neurobehavioral manifestations dominate the clinical picture.

♦ Weakness involves predominantly the contralateral leg (hemiparesis with crural predominance), but isolated leg weakness (crural monoparesis) is relatively rare. Leg weakness is more pronounced distally, and tone is flaccid the first few days and spastic later. Even if severe initially, patients usually achieve favorable recovery.

♦ Bilateral ACA infarction should be considered among the causes of acute paraparesis.

♦ Damage to the medial frontal lobe involving the supplementary motor area may produce motor neglect, with decreased utilization of the contralateral limbs. Caudate ischemia manifests with contralateral bradykinesis, clumsiness, and motor perseveration.³⁰

♦ Sensory deficits are milder and mostly affect integrative functions (discriminative and proprioceptive sensations).

♦ Neurobehavioral manifestations are variable and complex. They include expressions of callosal disconnection, such as left ideomotor apraxia, agraphia, and tactile anomia. Antegrade amnesia occurs often and may be disabling. Severe abulia is a characteristic feature, but it is only persistent in cases of bilateral infarctions. Akinetic mutism may be caused by lesions affecting the anteromedial frontal lobes, and it may resemble coma.³¹ Speech subsequently recovers, but milder disturbances may subsist.³² Alien-hand phenomena may be seen in patients with damage to the medial frontal lobe, corpus callosum, or both.

♦ Pathological grasping, sucking, and other frontal release signs; urinary incontinence; and gait apraxia may occur after unilateral ACA infarctions but are more common with bilateral frontal damage.

♦ ACA infarctions, often bilateral, are most commonly seen as a consequence of severe vasospasm following rupture of an anterior communicating artery aneurysm (Figure 2-25).

♦ In the remainder of the cases, cardiac embolism (as illustrated in our vignette) and ICA atherosclerosis are the most frequent mechanisms. Intrinsic disease of the ACA is uncommon.

Figure 2-25 A 46-year-old woman with subarachnoid hemorrhage from rupture of an anterior communicating artery aneurysm developed severe, symptomatic vasospasm 5 days after the bleeding causing extensive ischemia in the territories of anterior cerebral artery. Diffusion-weighted imaging sequence of the magnetic resonance imaging is shown on the left and conventional angiogram confirming severe vasospasm (arrow) is displayed on the right.

ANTERIOR CHOROIDAL ARTERY OCCLUSION

♦ The anterior choroidal artery (AChA) arises from the supraclinoid ICA. It consistently supplies the optic tract, lateral geniculate body, posterior limb of the internal capsule, cerebral peduncle, and the choroid plexus. However, its area of perfusion may be larger and include the middle portion of the medial temporal lobe, medial globus pallidus, lateral thalamus, and the posterior paraventricular corona radiata region (Figure 2-26).

♦ Most AChA infarctions are small (<20 mm) and often manifest clinically as lacunar syndromes.³³ Pure motor and ataxia-hemiparesis syndromes predominate. Sometimes the latter is associated with hypesthesia.

♦ AChA infarcts may also be larger and resemble territorial infarctions. The most common syndrome consists of contralateral homonymous hemianopia (with a spared “beaked” segment), hemiplegia, and hypesthesia.^34,³⁵ Neuropsychological and perceptual deficits may also be found but are less characteristic.

♦ Large AChA infarctions are often deceiving. They can exhibit unexpected manifestations, such as ipsilateral ptosis with or without other signs of Horner’s syndrome, impaired vertical eye movements, and contralateral adventitious movements. These large infarctions with complex clinical manifestations may exhibit a stuttering presentation, which represents a formidable diagnostic challenge for the clinician. Brain imaging becomes invaluable for correct localization in these cases.

♦ Small AChA strokes share the pathophysiology of other small penetrating artery infarctions. Meanwhile, large AChA infarcts are most often related to large vessel atherothrombosis or cardiac embolism.³⁵

♦ Surgical treatment of anterior choroidal artery aneurysm carries a high risk of disabling ischemic complications.³⁶

Figure 2-26 A 59-year-old man with history of hypertension, hyperlipidemia, and insulin-requiring diabetes mellitus presented to the hospital with recurrent episodes of dysarthria and left hemiparesis lasting between 5 and 20 minutes. The latest spell began as the patient was entering the magnetic resonance imaging (MRI) scanner, and the deficits failed to resolve. On examination, the patient had a dense left hemianopia, dysarthria and moderate left hemiparesis involving face, arm, and leg. MRI showed restricted diffusion in the territory of the right anterior choroidal artery (medial temporal lobe, superior peduncle, and posterior limb of the internal capsule).

POSTERIOR CEREBRAL ARTERY OCCLUSION

♦ The PCAs supply the midbrain, thalami, lateral geniculate bodies, posterior portion of the choroid plexus, occipital lobes, inferior and medial aspects of the temporal lobes, and posterior-inferior areas of the parietal lobes. This territory is illustrated in Figure 2-27.

♦ The PCAs constitute the terminal branches of the basilar artery. However, persistence of the fetal origin of the PCA from the internal carotid artery is seen in approximately 10% to 30% of individuals.^37,³⁸ In these patients, the PCA continues a large posterior communicating artery and does not join the basilar artery. Rarely, this variation is present bilaterally.

♦ The PCAs are also conventionally divided in segments: the P1 segment (mesencephalic or precommunicating) extends from the PCA origin on the top of the basilar to the union with the posterior communicating artery, the P2 segment (ambient or postcommunicating) spans from the posterior communicating artery junction until the posterior midbrain. The main branches of these two proximal PCA segments are the central perforating branches (thalamoperforating, thalamogeniculate, and peduncular arteries), posterior choroidal vessels (medial posterior and lateral posterior choroidal arteries), anterior and posterior temporal arteries, and splenial branches to the posterior aspect of the corpus callosum. The distal PCA segments are the short P3 segment (quadrigeminal), extending within the perimesencephalic cistern from the posterior midbrain to the calcarine fissure, and the terminal P4 segment (calcarine or cortical). The latter gives origin to several cortical branches, including the inferior temporal arteries (anterior, middle, and posterior), the parietooccipital artery, and the calcarine artery itself. The PCA trajectory and branches are shown in Figures 2-3 and 2-4.

Figure 2-27 Multiple ascending cuts of a brain magnetic resonance imaging (diffusion-weighted imaging sequence) illustrating the distribution of ischemia in a patient with infarction of the left posterior cerebral artery territory.

Case Vignette

A 68-year-old woman with a history of atrial fibrillation on chronic anticoagulation presented to the hospital with acute behavioral changes, visual disturbances, and right hemiparesis. On examination, she was somnolent, had poor short-term recollection, dense right hemianopia, mild right hemiparesis, and profound right hypoesthesia. Her INR was subtherapeutic because the patient had recently stopped taking warfarin for a dental procedure, and she had opted not to replace it with subcutaneous low-molecular-weight heparin. MRI of her brain showed a large left PCA infarction and MRA disclosed proximal occlusion of this vessel (Figure 2-28). Despite some functional recovery over the following 6 months, her visual and cognitive disturbances remained disabling.

Figure 2-28 Fluid-attenuated inversion recovery magnetic resonance imaging and angiography of the brain showing a large left posterior cerebral artery infarction from embolic occlusion of the P1 segment. Notice thalamic involvement because the occlusion was proximal to the takeoff of the perforating thalamic branches.

♦ Proximal occlusion of a PCA may produce severe neurological deficits including decreased level of consciousness (from mesencephalic and diencephalic involvement), profound disturbances of visual perception, antegrade amnesia, ophthalmoparesis (from damage to the upper midbrain), hemiplegia (typically from peduncular ischemia), hemihypoesthesia, and hemianopia.³⁹

♦ In the acute setting, large PCA infarctions may be clinically indistinguishable from MCA strokes.¹⁵ Thus brain imaging is essential to make the correct diagnosis and direct further evaluations.

♦ PCA occlusions distal to the origin of penetrating arteries irrigating the midbrain and thalamus are much more benign, often presenting with isolated contralateral visual field deficits (Figure 2-29).

♦ Visual field deficits from PCA infarctions present remarkable variability. They result from damage to the lateral geniculate nuclei, visual radiations, and calcarine cortex. Table 2-2 lists the most common visual field disturbances found in practice.

♦ Macular sparing is often encountered in unilateral strokes, presumably thanks to collateral circulation from the MCA perfusing the occipital pole. However, preservation of central vision also requires sparing of the visual radiations connected to the occipital pole.

♦ More complex visual disturbances are characteristic of PCA infarctions and have important localizing value. Visual agnosia, prosopagnosia, color dysnomia and dyschromatopsia, and aberrations of visual perception, such as palinopsia and micropsia, can occur. Anton syndrome is defined by the patient’s denial of cortical blindness.

♦ Sensory manifestations are caused by thalamic injury. Hypoesthesia or anesthesia are the most frequent abnormalities; numbness and paresthesias are the most common complaints. Déjerine-Roussysyndrome is relatively infrequent but distinctive; it consists of severe paroxysmal pain in the hypoesthetic side contralateral to a thalamic lesion caused by a thalamogeniculate branch occlusion. It is typically seen in conjunction with rapidly resolving hemiparesis, choreiform movements, dystonic hand posture, and ataxia.

♦ Patients with left PCA infarctions may experience incapacitating neurocognitive disorders. Alexia without agraphia (from infarction of the splenium of the corpus callosum and related connecting hemispheric fibers) is best known, but alexia with agraphia may also occur (when the infarction extends toward the angular gyrus). Anomic aphasia may be produced by left temporo-occipital strokes. Severe memory impairment can be caused by ischemia of the mesial temporal structures or the thalamus. Left PCA stroke may be responsible for single stroke dementia.⁴⁰

♦ Topographical disorientation and some constructional apraxia may be seen after right PCA infarctions (Figure 2-30).

♦ Midbrain ischemia may express with ipsilateral or bilateral ophthalmoparesis (III nerve palsy, abnormal vertical eye movements) and contralateral hemiplegia (Figure 2-31).

♦ Bilateral thalamic infarctions may result in initial alterations in the level of consciousness and subsequent cognitive (predominantly antegrade memory) and sensory sequelae (Figure 2-32).

♦ Embolism from a cardiac or an arterial (aortic arch, vertebral artery origin) source is the most common mechanism of PCA stroke. Intrinsic atherosclerosis of the PCA is much less common but must be investigated in cases of pure PCA ischemia.

Figure 2-29 Another example of a left posterior cerebral artery infarction (computed tomography scan shown on the left and diffusion-weighted imagery on the right). Notice in his case that there is a large occipital infarction but with no thalamic involvement because the site of the vascular occlusion was distal to the takeoff of the perforating thalamic branches.

TABLE 2-2 Visual field disturbance caused by PCA infarction.

Bilateral PCA infarction

Cortical blindness

Bilateral altitudinal hemianopia

Unilateral PCA infarction

Macular sparing hemianopia

Temporal crescent paring hemianopia

Quadrantanopia

Isolated macular hemianopia (rare)

Figure 2-30 A 64-year-old woman with atrial fibrillation who was brought to the emergency department by her daughter after she was found acutely confused and unable to find her way in her own house. Examination revealed confusion with mild agitation, topographical disorientation, and constructional and dressing apraxia. She also had a left visual field deficit. Magnetic resonance imaging of the brain confirmed the clinical suspicion that the patient had an acute infarction of the right posterior cerebral artery territory (diffusion-weighted imagery and matching apparent diffusion coefficient shown in the upper row, fluid-attenuated inversion recovery sequence shown in the lower row).

Figure 2-31 Patient with left midbrain and small occipital lobe infarction from embolic proximal posterior cerebral artery occlusion.

Figure 2-32 Bilateral thalamic infarction secondary to top of the basilar embolism with spontaneous recanalization. Patient presented with sudden coma, and although he recovered alertness, he remained cognitively disabled.

VERTEBROBASILAR DISEASE

♦ Occlusion of the basilar artery represents the most dreaded form of ischemic stroke. At its worst, it causes massive fatal infarction involving the brainstem, cerebellum, the occipital and posterior temporal lobes, and the thalami (Figure 2-33).

♦ However, these catastrophic results may at times be avoided by prompt recognition of early signs of vertebrobasilar ischemia.

♦ The normal vascular anatomy of the vertebrobasilar system is shown in Figures 2-3 and 2-4.

♦ The vertebral artery is typically divided in four segments: the V1 segment extends from the vessel origin to its entrance into the vertebral foramen of the fifth or sixth cervical vertebra; the V2 or intraforaminal segment transverses the vertebral foramina of C6 to C2; the V3 segment emerges from the C2 foramen and turns to circle the posterior arch of the atlas; the V4 or intradural segment begins as the vessels pierces the dura and ends at the vertebrobasilar junction (at the pontomedullary level).

♦ Asymmetry in the vertebral arteries is commonly seen. Left vertebral artery dominance is present in nearly 45% of people, and in close to 25% the right vertebral artery is larger. Hence, true vertebral artery codominance is encountered in less than one third of the general population. Hypoplastic vertebral arteries, sometimes ending after the origin of the posterior-inferior cerebellar artery, are less frequent but certainly not rare.⁴¹

♦ Infarctions at different levels are caused by different mechanisms:⁴²

♦ Proximal territory infarctions (i.e., involving the medulla and lower cerebellum) are caused by embolism from the heart or atherosclerosis of the extracranial vertebral arteries or by hypoperfusion related to severe intracranial vertebral occlusive lesions.

♦ Middle territory infarctions (i.e., involving pons and anterior cerebellum) are typically due to intrinsic basilar artery disease.

♦ Distal territory infarctions (i.e., involving midbrain, superior cerebellum and posterior cerebral artery territories) are mostly embolic from cardiac or vertebral artery sources.

Figure 2-33 Computed tomography scan of the brain showing a massive infarction in the vertebrobasilar territory.

Case Vignette

A 64-year-old woman was found unresponsive in her bathroom by her husband. She was intubated by the paramedics and transported to our emergency department. On arrival, she was comatose and breathing at a rate of 40 to 45 per minute. She was tachycardic and hypertensive. Her pupils were slightly anisocoric (3.5 mm on the left and 3 mm on the right), and responses to light were minimal on the left and absent on the right. Corneal and oculocephalic reflexes were preserved. Best motor responses to pain were in the form of withdrawal. DWI showed restricted diffusion in the midcerebellum and mesencephalon (Figure 2-34). A hyperintense signal in the basilar artery indicative of acute thrombosis was visualized on FLAIR. Conventional angiography confirmed occlusion of the basilar trunk. She underwent successful basilar recanalization by intra-arterial thrombolysis combined with mechanical disruption of the clot. Despite reperfusion, the patient failed to improve neurologically. Repeat MRI showed established infarction throughout the midbrain. Patient expired shortly after her family requested withdrawal of artificial life support.

Figure 2-34 First row: Diffusion-weighted imaging showing acute brainstem and cerebellar ischemia. Second row: T1-weighted imaging and fluid-attenuated inversion recovery (FLAIR) sequences revealing a hyperintense basilar artery, indicative of acute basilar artery thrombosis. Third row: Conventional angiogram confirming occlusion of the mid to distal basilar artery (left) with subsequent recanalization following intra-arterial thrombolysis (right). Fourth row: Repeat FLAIR disclosing extensive pontomesencephalic infarction.

♦ Early signs of vertebrobasilar ischemia can be subtle and possibly deceiving. Fluctuations with remissions and relapses of symptoms may precede frank progression and irreversible development of severe deficits. Table 2-3 presents a list of common signs that should raise the suspicion of basilar occlusive disease.

♦ Diagnostic imaging modalities other than angiography have limited value in the acute setting. CT scan has poor sensitivity in the posterior fossa but, at times, may reveal a hyperdense clot in the basilar artery (Figure 2-35).

♦ MRI with DWI demonstrates the extension of the ischemic damage (Figure 2-36).

♦ The clinical suspicion of acute symptoms from occlusive basilar artery disease is a medical emergency. If the patient is outside the therapeutic window for intravenous thrombolysis but deemed salvageable, it is advisable to perform catheter angiography without delay to confirm the diagnosis and allow endovascular treatment.

♦ The pattern of acute multiple brain infarctions in the posterior circulation on MRI-DWI is frequently associated with vertebrobasilar atherothrombotic disease.⁴³

♦ The top of the basilar syndrome (or rostral basilar artery syndrome) is characterized by sudden loss of consciousness, sometimes preceded by acute vertigo, ataxia, and diplopia. It is the manifestation of rostral brainstem, occipitotemporal, and thalamic ischemia (Figure 2-37). The area of infarction may also involve the superior cerebellum. Upon awakening, patients may exhibit drowsiness, agitation, disordered visual perception, and oculomotor dysfunction. Motor deficits are typically absent. The mechanism of the stroke is almost invariably embolic (from a cardiac or proximal arterial source).⁴⁴

TABLE 2-3 Signs suspicious for basilar artery occlusion.

Combination of ophthalmoplegia with motor, sensory, or coordination deficits

Crossed motor or sensory findings

Acute ataxia with inability to walk

Sequential appearance of bilateral Babinski signs^*

Sequential appearance of bilateral weakness

Acute reduction in the level of consciousness

* It can also be seen in patients with incipient craniocaudal herniation from massive supratentorial infarctions.

Figure 2-35 A 72-year-old man was brought comatose to the emergency department. He had been found unresponsive at home by his wife in the middle of the night, and paramedics had intubated him upon their arrival. On examination he had anisocoria, absence of corneal reflex on one side, asymmetric oculocephalic reflexes, and bilateral extensor posturing to pain. Computed tomography scan performed nearly 8 hours after the patient had last been seen showed a hyperdense basilar artery sign (left, arrow). Catheter angiography confirmed the suspected occlusion of the basilar artery at its middle segment (right, arrow). Although the basilar artery was recanalized following endovascular therapy (mechanical embolectomy combined with intra-arterial thrombolysis), the patient failed to improve, and the family requested withdrawal of life support measures 2 days later.

Figure 2-36 This example illustrates the value of magnetic resonance imaging (MRI) in revealing the extension of ischemia in patients with basilar artery occlusion. Notice the computed tomography scan (upper left) does not allow clear recognition of brainstem infarction, which is easily visualized on diffusion weighted imaging (upper right) and, to a considerably lesser degree, on fluid-attenuated inversion recovery (lower left). MRI can be combined with magnetic resonance angiography to define the vascular occlusion (lower right).

Figure 2-37 A patient with occlusion of the top of the basilar artery causing infarctions in mesencephalon, bilateral thalami, and bilateral occipital lobes. The mechanism of the stroke was cardiac embolism. Diffusion-weighted imaging is shown in the upper row, fluid-attenuated inversion recovery in the lower left, and magnetic resonance angiography in the lower right. Short arrows indicate areas of ischemia and long arrow signals the top of the embolic occlusion of the basilar top.

CEREBELLAR INFARCTIONS

♦ The cerebellum is normally irrigated by three pairs of long circumferential arteries: the posterior inferior, anterior inferior, and superior cerebellar arteries (PICA, AICA, and SCA). Anatomical variations affecting these vessels are not uncommon.

♦ Pure territorial cerebellar infarctions are most often caused by embolism.

♦ The coexistence of cerebellar infarction and brainstem ischemia constitutes an indication to study the vertebrobasilar circulation for possible atherothrombotic disease.

♦ Imaging with MRI is useful to delineate the true extent of the infarction and recognize the presence of brainstem involvement.

♦ MRI, especially DWI, often discloses multiple areas of cerebellar ischemia.⁴⁵^–⁴⁹ Multiple small cerebellar infarctions are frequently associated with atherosclerotic vertebrobasilar disease.^48,⁴⁹

♦ Mass effect from large cerebellar infarctions can produce rapid herniation. Serial CT scans are valuable aids to serial neurological examinations for the timely diagnosis of cerebellar swelling.

Posterior Inferior Cerebellar Artery Infarction

Case Vignette

A 38-year-old woman presented with severe neck and posterior head pain, dizziness, gait imbalance, and right-hand clumsiness. Her examination predominantly demonstrated right appendicular ataxia. Brain imaging disclosed a large right PICA stroke with incipient mass effect (Figure 2-38). Vascular imaging revealed a right vertebral artery occlusion, most likely due to dissection. The patient was carefully monitored in the stroke unit, and as she developed mild confusion and restlessness, repeat imaging was performed showing worsening swelling with displacement of the fourth ventricle, effacement of the subarachnoid cisterns, distortion of the brainstem, and dilatation of the temporal horn of the right lateral ventricle. The patient immediately underwent suboccipital craniectomy. She improved substantially after surgery and achieved good functional recovery over the ensuing 6 months.

Figure 2-38 Diffusion-weighted imagery and apparent diffusion coefficient map (upper row) and fluid-attenuated inversion recovery (middle left) of the magnetic resonance imaging obtained on admission demonstrating a large area of acute infarction in the right posterior inferior cerebellar artery territory. Computed tomography (CT) scan 36 hours later showed worsening of swelling with brainstem compression (middle right) and obstructive hydrocephalus (lower left). CT scan after suboccipital craniectomy revealed adequate decompression of the posterior fossa (lower right).

♦ The PICA originates from the V4 segment of the vertebral artery. It typically has a medial and a lateral branch. Anatomical variations include a common PICA-AICA trunk, both PICAs arising from a single trunk, and extradural origin of the vessel in one or both sides.

♦ It supplies the dorsal and caudal regions of the cerebellum and the dorsal tegmentum of the medulla.

♦ As illustrated in the presented case, typical initial clinical manifestations are headache, vomiting, vertigo, and ataxia (ipsilateral lateropulsion with inability to walk, ipsilateral dysmetria and dysdiadocokinesis). The elements of Wallenberg’s syndrome may be present in cases involving the dorsolateral medulla.

♦ As swelling progresses, patients may exhibit behavioral changes (confusion, agitation) followed by depressed level of consciousness as obstructive hydrocephalus develops. Compression of adjacent cranial nerve and brainstem structures is manifested by ipsilateral facial palsy, ophthalmoparesis (including ipsilateral VI nerve dysfunction), and contralateral hemiparesis.

♦ When examining brain imaging scans, it is important to focus on the degree of distortion and shift of the IV ventricle, effacement of the quadrigeminal cistern, brainstem deformity, evidence of hydrocephalus, and signs of upward herniation. Presence of these findings predicts neurological deterioration.^50,⁵¹ Infarct volume appears to have lesser prognostic worth.⁵⁰

♦ Decompressive suboccipital craniectomy is indicated in patients with a declining level of consciousness.⁵² However, because clinical decline occurs quickly in these patients, it is reasonable to consider preemptive surgery in patients with incipient clinical signs of swelling or radiological features predictive of deterioration.

♦ Embolism from the heart or a proximal arterial source is the most common mechanism of PICA strokes.⁵³

♦ Prognosis depends on the extent of the infarction. Favorable recovery is possible after timely decompressive surgery.⁵²

Anterior Inferior Cerebellar Artery Infarction

♦ The AICA stems from the inferior third of the basilar artery. Its size is often inversely correlated with the size of the PICA on the same side. As already mentioned, a common PICA-AICA arising from the distal vertebral or proximal basilar arteries is a normal anatomical variation.

♦ It supplies a small region of the anterior and medial cerebellum, typically restricted to the middle cerebellar peduncle and the flocculus, and the inferior lateral portion of the pontine tegmentum (Figure 2-39).

♦ The classical clinical picture is characterized by multiple cranial nerve deficits on the side of the occlusion, which may include facial hypoesthesia, facial weakness, abducens palsy, vestibular syndrome, hearing loss, and occasionally tinnitus. Contralateral hemiparesis, incoordination, and decreased pain and temperature sensations are also fairly common.⁵⁴

♦ AICA infarctions are small and difficult to visualize on CT scan. MRI with DWI offers much better sensitivity for the detection of AICA strokes. It also demonstrates coexistent areas of ischemia; in fact, the combination of PICA and AICA infarctions has been noted to be frequent when patients are examined with MRI-DWI.⁴⁵

♦ Complications from swelling do not occur unless other arterial distributions are involved.

♦ The most common mechanism of ischemia is vertebrobasilar atherothrombosis.^45,⁵³

♦ Pure AICA infarctions have relatively good prognosis.⁴⁵

Figure 2-39 Examples of anterior inferior cerebellar artery (AICA) territory infarctions due to basilar artery disease. The case shown in the upper row illustrates a right AICA infarction on diffusion-weighted imaging (left) with associated pontine ischemia from concomitant compromise of a paramedian penetrating branch; the image on the right is from the fluid-attenuated inversion recovery (FLAIR) sequence displaying a hyperintense basilar artery sign from acute thrombosis of this vessel (arrow). The case shown in the lower row illustrates bilateral AICA infarctions on FLAIR (arrowheads) caused by basilar atherosclerosis visible on magnetic resonance angiography (right, arrow).

Superior Cerebellar Artery Infarction

♦ The SCAs arise from the distal third of the basilar artery shortly before it culminates in its bifurcation giving rise to the PCAs. They are the most constant major cerebellar vessels.

♦ They supply the ventral and rostral vermis and paraventral areas, the anterior-superior aspects of the cerebellar hemispheres (including the dentate, intermediate, and fastigial nuclei and most of the deep cerebellar white matter), and the superior cerebellar peduncles. SCAs also provide branches to the tectum of the midbrain and the dorsolateral tegmentum of the upper pons (Figure 2-40).

♦ Pure SCA strokes manifest with dysarthria, nystagmus, and axial and ipsilateral appendicular ataxia.⁵⁵ SCA-territory ischemia may be part of the rostral basilar artery syndrome (discussed earlier).⁵⁶

♦ MRI scans have shown that SCA infarctions are often multiple, with several lesions in the SCA territory (one or both sides) or other cerebellar territories.^46,⁴⁷ They may remain clinically unnoticed, particularly when they occur in the context of other embolic infarctions in more eloquent areas.

♦ Complications from swelling are infrequent after SCA strokes.

♦ Most SCA infarctions are due to embolism from a cardiac source or proximal vertebrobasilar atherothrombosis.⁴⁶

♦ Prognosis is benign in isolated SCA strokes, especially if partial. However, bilateral SCA infarctions and infarctions extending into the upper brainstem may be fatal or disabling.⁵⁷

Figure 2-40 Patient with paroxysmal atrial fibrillation who presented with sudden onset of dysarthria, dysbasia, and right dysmetria. Magnetic resonance imaging disclosed an acute right superior cerebellar artery (SCA) infarction as shown on diffusion-weighted imagery (upper row) and fluid-attenuated inversion recovery (lower left) sequences. These images illustrate the usual territory perfused by the SCA. Magnetic resonance angiography (lower right) shows the absence of the right SCA; notice clear visualization of the left SCA (arrow).

Cerebellar Border-Zone Infarctions

♦ Infarctions involving the boundary zones between arterial territories are relatively frequent in the cerebellum, but their identification is only possible using MRI scans.

♦ Figure 2-41 illustrates relatively large bilateral infarctions between PICA and SCA territories induced by a major fall in perfusion pressure.

♦ However, border-zone cerebellar infarctions tend to be small and multiple.^48,^49,⁵⁸

♦ They are commonly associated with advanced vertebrobasilar atherosclerosis, likely resulting in microembolism.^43,^48,^49,⁵⁸ Thus their presence should be considered an indication to pursue noninvasive vascular imaging of the posterior circulation.

Figure 2-41 Patient with postoperative stroke following profound intraoperative hypotension blood loss and hypotension. Diffusion-weighted imaging (DWI; left) and fluid-attenuated inversion recovery (FLAIR; right) sequences display bilateral cerebellar infarctions in border-zone distribution. Notice relative apparent discrepancy between the area of restricted diffusion on DWI and the regions with increased signal intensity due to established infarction on FLAIR. This difference is not uncommonly seen in patients with ischemia because of hemodynamic insufficiency and may be due to the presence of areas of subcritical ischemia, which appear bright on DWI.

BRAINSTEM INFARCTIONS

♦ The perfusion of the brainstem is supplied by three pairs of vessels: two paramedian branches, two short circumferential branches, and two long circumferential branches.

♦ Occlusions of these branches at different levels give rise to specific syndromes, which are anatomically purer in their classic descriptions than typically found in practice. In fact, the increasing use of MRI has disclosed that symptoms and signs of traditional syndromes often overlap.

Medullary Infarctions

The main ischemic medullary syndromes are illustrated in Figure 2-42.

Figure 2-42 Medullary anatomy and main medullary stroke syndromes.

Case Vignette

A 75-year-old man was admitted with sudden onset of dysphagia, dysarthria, and gait imbalance. He had long-standing history of hypertension and poorly controlled type 2 diabetes. On examination, he had left miosis and ptosis, dysarthria, difficulty swallowing his saliva, left ataxia, and decreased sensation to pain and temperature on the right side. He developed uncontrollable hiccups in the emergency department. CT scan was not informative, but DWI demonstrated a left lateral medullary infarction with associated ischemia of the left cerebellum (Figure 2-43). The PICA was not seen on noninvasive angiogram and considered to be occluded. Irregularities in other intracranial vessels indicated widespread intracranial atherosclerosis. The patient required temporary placement of a percutaneous gastrostomy tube for safe feeding but subsequently made a favorable recovery with moderate residual dysarthria and ataxia.

Figure 2-43 Diffusion-weighted imaging sequence of magnetic resonance imaging showing an acute left lateral medullary infarction. Notice coexistent left cerebellar ischemia in the posterior inferior cerebellar artery territory.

Wallenberg’s Syndrome

♦ The triad of Horner’s syndrome, ipsilateral ataxia, and contralateral hypalgesia is most useful in the identification of lateral medullary infarction.⁵⁹

♦ Facial weakness and ocular symptoms are frequent and do not necessarily imply that the infarction extends beyond the lateral medulla ⁶⁰ (although presence of those signs often indicates extension up to the pontomedullary junction).⁶¹

♦ When Wallenberg’s syndrome is suspected, the ipsilateral vertebral artery must be investigated because occlusion of this vessel is often responsible for the infarction.⁶¹

♦ Vertebral atherothrombosis is by far the most common mechanism.⁶¹ Vertebral dissection has been found responsible in some cases.^61,⁶² Other mechanisms, including cardiac embolism, are relatively rare.

♦ MRI with DWI is sensitive for the detection of small medullary infarctions in the acute and subacute phases.⁶³ Combined with MRA, this imaging modality may confirm the diagnosis of medullary stroke, delineate the extent of the ischemia, and determine the status of the parent vertebral artery.

♦ Associated cerebellar ischemia is commonly identified on MRI but may remain undetected by CT scan.^61,⁶⁴