Ischemic stroke syndromes and their anatomic localization …

Stroke & Vascular Disorders

Updated 08.23.2023
Released 05.10.2004
Expires For CME 08.23.2026

Ischemic stroke syndromes and their anatomic localization

Authors: Aneesh B Singhal MD, Eva A Rocha MD PhD

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Editor: Steven R Levine MD

Ischemic stroke syndromes and their anatomic localization

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Introduction

Overview

The original description of stroke syndromes followed the phenomenological approach to clinical diagnosis that characterized classical neurology. Accurate diagnostic localization of injuries or lesions of the nervous system required clinicians to piece together the different deficits into well-defined, recognizable, and predictable syndromes based on pattern recognition. Stroke syndromes had the singular advantage of directly relating to specific vessels and their branches. The introduction of advanced imaging techniques improved our understanding of how clinical syndromes relate to specific vascular processes, incorporating elements of mechanism (ie, pathogenesis), causation (ie, etiology), and prognosis (ie, outcome) into the cerebrovascular clinical evaluation. In this article, the authors describe a process by which the recognition of ischemic stroke syndromes is linked to relevant diagnostic and therapeutic choices destined to optimize outcomes.

Key points

	• Because the vascular supply to different brain regions is predictable, the identification of ischemic stroke syndromes, by inference, allows cerebrovascular localization diagnosis.
	• The evolution of increasingly sophisticated imaging techniques provides certainty about the anatomic relationship between each stroke syndrome and its underlying pathologic substrate.
	• Stroke syndrome recognition allows inference of the mechanism (ie, pathogenesis) and causation (ie, etiology) of the stroke and facilitates management decisions.
	• Stroke syndromes optimize benefit versus risk assessment of therapeutic interventions by providing perspective of the natural history of the stroke.

Historical note and terminology

The traditional approach to neurologic diagnosis is centered on the use of bedside neurologic findings to localize the brain lesions responsible for them. The most frequent scenario for the application of such a paradigm is the care of stroke patients, and it is not surprising that stroke syndromes drove the progress of localization diagnosis in both neurology and neurosurgery (38; 37). The 19th century witnessed an exponential growth in clinical neurology, and it is within this period that a number of the classic stroke syndromes were first described. However, the idea that lesions in specific areas of the brain could produce discrete yet predictable neurologic deficits was still a subject of controversy. It gained importance in large part due to the efforts of Charcot, who introduced a 2-part approach to the study of neurologic diagnosis; the méthode anatomoclinique (anatomoclinical method) involved cataloging patients based on their neurologic deficits and then correlating the lesions found at autopsy with those deficits (25). His pathologic characterization of cerebral infarctions led to the concept of neurologic localization becoming widely accepted.

Advances in stroke localization during the earlier part of the 20th century followed the work of Foix, who was considered by many to be the first modern stroke neurologist (13). His contributions included detailed descriptions of the vascular supply of specific cerebral arteries, together with the clinical syndromes resulting from their occlusion. Later in the 20th century, many of his original ideas were further defined by C Miller Fisher, who introduced definitions for transient ischemic attack, lacunar syndromes, and the etiopathogenic importance of extracranial carotid atherosclerosis (22). Julien Bogousslavsky and Louis Caplan later categorized the clinical manifestations of cerebrovascular disease in their book Stroke Syndromes (09). In parallel, advances in neuroimaging provided a more dynamic dimension to the day-to-day application of the anatomoclinical method of Charcot, arguably becoming the equivalent to bedside neuropathology.

Clinical manifestations

Presentation and course

The hallmark of presentation of stroke is its temporal profile, typically characterized by suddenness of onset, with symptoms appearing with sufficient abruptness as to leave no doubt about the estimated time of onset. The temporal profile of ischemic stroke also includes the deficit evolution over time, which can follow 1 of several patterns: (1) rapid recovery, (2) improvement, (3) plateau, (4) stuttering (ie, waxing and waning), and (5) worsening. Each of these has diagnostic and therapeutic implications, and, when associated with specific stroke syndromes, they help guide management.

In addition to their temporal profile, the second attribute of stroke syndromes is that they indicate a focal deficit, one that can be produced by the compromise of a single vascular territory. Conversely, global neurologic symptoms are more likely the result of generalized processes. The components of stroke syndromes can be categorized in one of several clinical domains, closely following the pattern of the bedside neurologic evaluation: (1) consciousness and cognition, (2) speech and language, (3) vision and eye movements, (4) cranial nerve function, (5) motor function, (6) sensation and perception, and (7) coordination.

Transient ischemic attacks are clinically characterized by acute loss of focal brain or monocular function lasting less than 24 hours resultant from inadequate cerebral or ocular blood supply (09). The vascular territories of transient ischemic attacks may be identified according to clinical symptoms (Table 1).

Table 1. Probable Arterial Territory of Transient Ischemic Attacks According to Neurologic Symptom

	Arterial territory
Symptom	Carotid	Either	Vertebrobasilar
Dysphasia	+
Monocular visual loss	+
Unilateral weakness		+
Unilateral sensory disturbance		+
Dysarthria		+
Homonymous hemianopia		+
Unsteadiness/ataxia		+
Dysphagia		+
Diplopia			+
Vertigo			+
Bilateral simultaneous visual loss			+
Bilateral simultaneous weakness			+
Bilateral simultaneous sensory disturbance			+
Crossed sensory/motor loss			+
From (09)

To address the presentation and course of numerous stroke syndromes, we divide our discussion into the carotid and vertebrobasilar circulations while acknowledging that certain overlap may result from anomalous or variant arterial architecture. We cover both general and specific criteria for stroke localization and then merge the latter into the management continuum.

General stroke semiology

Carotid circulation. Patients with stroke syndromes in the carotid circulation present certain characteristic deficits, either in isolation or combined, to form more complex syndromes:

(1) Language abnormalities (left hemisphere). Most patients harbor neurologic control of language function within the left cerebral hemisphere (32). Therefore, stroke syndromes involving the left hemisphere usually include some type of language disorder (ie, aphasia). In these cases, language output (ie, expression) and input (ie, comprehension) are more selectively affected by lesions rostral or caudal to the rolandic sulcus respectively.

Table 2. Main Language and Speech Stroke Syndromes

Type of aphasia	Fluency	Comprehension	Repetition	Naming	Other features	Location
Broca aphasia – expressive aphasia	-	+	-	-	agrammatic, associated with hemiparesis	posterior-inferior frontal
Transcortical motor aphasia	-	+	+	+/-	not paraphasic, eventually associated with hemiparesis (crural involvement)	anterior and superior to Broca area (supplementary motor area)
Global aphasia	-	-	-	-	mute or stereotypy, associated with hemiparesis hemianopia, hemi-hypoesthesia, apraxia	Perisylvian region (middle cerebral artery territory)
Wernicke aphasia – sensory aphasia	+	-	-	-	paraphasic, associated with homonymous hemianopia, apraxia, anosognosia	posterior-superior temporal
Pure word deafness – cortical deafness	+	-	-	-	better reading	middle third of superior temporal gyrus
Transcortical sensory aphasia	+	-	+	+/-	semantic jargon, eventually associated with hemianopia and visual agnosia	Watershed areas of middle cerebral artery and posterior cerebral artery
Anomic aphasia	+	+	+	-	only naming deficit, associated with homonymous hemianopia	inferior parietal (angular gyrus)
Conduction aphasia	+	+	-	+	mainly repetition deficit, associated with hemi-hypoesthesia, apraxia hemianopia	arcuate fasciculus – supramarginal gyrus
Isolation or mixed transcortical aphasia	-	-	+	-	only repetition spared, eventually associated with hemianopia, visual agnosia and hemiparesis	watershed areas of middle cerebral, anterior cerebral and posterior cerebral artery
Apraxia of speech	-	+	-	-	articulatory difficulties, eventually associated with apraxia and face or tongue paresis	inferior part of precentral gyrus and nearby areas
Thalamic aphasia	+	+/-	+	-	dysarthria, initially with mutism	thalamus in the dominant hemisphere
Subcortical aphasia	+	+	+	-	dysarthria, hypophonia	basal nuclei in the dominant hemisphere
Adapted from (09)

(2) Perceptual disorders (right hemisphere). In most individuals, the right hemisphere is more involved in: (A) processing and interpreting sensory inputs from the outside world and (B) channeling the resulting perceptual tapestry in a way that modulates behavior and movement (ie, motor planning and execution). Patients with strokes involving the right hemisphere, particularly posteriorly, have abnormalities of multimodal sensory integration, commonly manifested as contralateral neglect.

(3) Gaze paresis. The paramedian pontine reticular formation, also known as the pontine gaze center, drives both eyes conjugately toward the same side and receives contralateral excitatory inputs from the frontal eye field and the inferior parietal lobule. Strokes affecting the cerebral hemispheres cause contralateral gaze paresis, often accompanied by forced ipsilateral eye deviation (52).

(4) Visual field defects. Lesions that affect the posterior portions of the cerebral hemispheres commonly result in homonymous field cuts. The characteristic attribute of geniculo-parieto-temporal visual field defects is that they are incongruous. Because approximately 20% of the population has a persistent fetal origin of the posterior cerebral artery, directly from the internal carotid artery via the posterior communicating artery, congruous field defects can be seen in a minority of cases.

Vertebrobasilar circulation. The structures supplied by the vertebrobasilar system represent a complex array of loci with discrete functional implications; involvement of these structures typically leads to very characteristic deficits (11). In general, the concurrent presence of any two of the following criteria is highly suggestive that the stroke involved the vertebrobasilar system:

(1) Deficits of cranial nerves II through XII. This includes two different components: (A) cranial nerve II, producing congruous visual fields defects, and (B) cranial nerves III to XII, whose nuclei and fascicles are located within the brainstem itself. The cranial nerves affected allow localization of the lesion along the distribution of the vertebrobasilar system.

(2) Deficits exclusive to the brainstem. Certain structures exist only in the brainstem and have no counterpart elsewhere in the nervous system. Due to this particularity, any injury to them leads to pathognomonic clinical findings (eg, internuclear ophthalmoplegia due to injury of the medial longitudinal fasciculus).

(3) Deficits of cerebellar function. Blood supply to the cerebellum derives from the vertebrobasilar system. Therefore, any deficit attributable to cerebellar dysfunction generally results from a derangement in the vertebrobasilar circulation.

(4) Deficits of long tracts disconnection. Many of the stroke syndromes characteristic of brainstem involvement typically affect one or another function that depends on long tract integrity (eg, hemibody strength or sensation), and, distinctly, this is contralateral to a lesion affecting ipsilateral cranial nerves (ie, “crossed” syndromes).

Other focal signs and symptoms. Some signs and symptoms can result from lesions in either the carotid or the vertebrobasilar circulations and do not allow, by themselves, specific lesion localization:

(1) Motor weakness. Present in 80% to 90% of all stroke patients, it is the most frequent clinical manifestation of stroke. Faciobrachial predominant paresis usually indicates damage to the motor cortex due to involvement of the middle cerebral artery. Pure motor hemiparesis has been associated with lesions in the internal capsule or in the basis pontis. Hemiparesis with conjugate gaze palsy may occur from lesions on the cerebral hemisphere (when eyes are deviated to the side of the lesion) or pons (when eyes are deviated contralaterally). Bilateral hemiparesis is uncommon after stroke and may represent lesions in both hemispheres, brainstem or spinal cord. Isolated monoparesis is relatively rare, representing 1% to 2% of all strokes. Upper extremity arm weakness (usually distal more than proximal) is the most common type of isolated monoparesis and is usually associated with lesions in the “hand-knob” area in the contralateral precentral gyrus. Stroke mechanism may vary; however, contralateral motor-strip infarcts have been associated with non-stenosing carotid stenosis, often with plaque ulceration or thrombus (53). This entity of “SYmptomatic Non-stenosing Carotid artery stenosis” or SYNC is being increasingly recognized with advances in carotid artery plaque imaging.

(2) Dysarthria. This pure motor abnormality of speech occurs in about one quarter of stroke cases and represents weakness of the oropharyngeal musculature from loss of suprasegmental control (33). It can result from dysfunction of the following structures: lips, tongue, jaw, and palate, which are innervated by the facial, glossopharyngeal, vagal, and hypoglossal nerves. Patients with dysarthria have inarticulate or unintelligible speech but are able to understand, read, and write.

(3) Sensory loss. This is a very common manifestation of stroke and affects over 50% of the patients. Both motor and sensory pathways are somatotopically organized; therefore, lesions result in loss of function with predictable patterns.

(4) Pseudobulbar features. “Pseudo-bulbar palsy” refers to lower cranial nerve palsy due to supranuclear lesions. There are three types of pseudo-bulbar palsy according to lesion location: the cortical form is characterized by a faciopharyngoglossomasticatory diplegia with automatic voluntary dissociation; the striatal form has the same features and also pyramidal signs, emotional lability, and intellectual impairment; and the pontine form is characterized by faciopharyngoglossomasticatory diplegia with emotional lability, pyramidal signs and sometimes cerebellar signs, without dementia. Inappropriate laughing and crying are very characteristic of pseudo-bulbar palsy. Most frequently pseudo-bulbar palsy is associated with multiple recurrent ischemic strokes although it may also have acute onset. A severe type of acute pseudo-bulbar palsy caused by bilateral opercular lesions is Foix-Chavany-Marie syndrome. Patients with this syndrome present with anarthria and bilateral central voluntary paresis of lower cranial nerves with preserved involuntary and emotional innervation (09).

Spinal cord lesions may evolve with flaccid para- or tetraplegia with complete loss below the level of the lesion and bowel and bladder dysfunction in case of transverse spinal cord infarction. The anterior spinal artery syndrome leads to the same symptoms, but sensation of touch, vibration, and proprioception is preserved (09).

Specific stroke semiology

Recognition of stroke syndromes is the cornerstone of patient care, providing a portal to the identification of important attributes about each patient. Among these, prompt diagnosis of large arterial occlusion is of paramount importance due to the patient's potential benefit from endovascular treatment (ie, thrombectomy).

Stroke syndromes. The following constitute the most important stroke syndromes, grouped by arterial systems and presented according to hierarchical position (ie, first-order vessels preceding second- and third-order branches) of the involved vessels.

(1) Anterior circulation syndromes. The large arterial occlusion syndromes associated with the internal carotid artery and middle cerebral artery can be virtually indistinguishable, depending on a variety of collateral patterns and often differing in a matter of magnitude (Table 1).

Large arterial territories of the cerebral hemispheres (axial section)

(Contributed by Dr. Camilo Gomez.)
Small and composite arterial territories of the cerebral hemispheres (coronal section)

(Contributed by Dr. Camilo Gomez.)

They are characterized by major cerebral hemispheric dysfunction, contralateral gaze paresis, hemianopia, and a motor deficit that affects the face and upper limb to a greater degree. Occlusion of either of the two middle cerebral artery divisions (ie, M2) results in partial forms of the full syndrome, largely motor dysfunction for the anterosuperior division, and sensory or perceptual deficits for the posteroinferior division (03). Anterior cerebral artery syndrome leads to contralateral hemiparesis, selectively affecting the lower limb and, at times, to abulia. Finally, the anterior choroidal artery syndrome includes contralateral hemiparesis (with or without ataxia), hemisensory loss, and, infrequently, incongruous hemianopia (34). With the advent of mechanical thrombectomy for acute stroke, distinguishing features of large vessel occlusion on admission has become extremely important. The Field Assessment Stroke Triage for Emergency Destination (FAST-ED) scale for pre-hospital evaluation of large vessel occlusion includes the following criteria: facial palsy, arm weakness, speech changes, eye deviation, and extinction/neglect (35).

Table 3. Carotid Stroke Syndromes from Large and Medium Artery Occlusions

Vessel Involved	Semiology
Internal carotid artery or middle cerebral artery	• Impaired consciousness • Global aphasia (left hemisphere) and severe dysarthria • Contralateral incongruent hemianopia and gaze paresis • Contralateral hemiparesis (face> arm> leg) • Contralateral multimodal neglect (right hemisphere)
Anterior cerebral artery	• Variable lethargy • Abulia--atypical subtle aphasia (left hemisphere) and dysarthria • No visual or ocular motor changes • Contralateral hemiparesis [leg>>arm (proximal)>face] • Contralateral crural neglect (right hemisphere) • Contralateral alien hand sign
Anterior choroidal artery	• Normal level of consciousness • Infrequent atypical aphasia (left hemisphere) and moderate dysarthria • Infrequent contralateral incongruent sectoranopia • Contralateral hemiparesis (face=arm=leg) ± ataxia • Contralateral hemisensory loss
Anterosuperior middle cerebral artery division	• Minimally impaired consciousness • Nonfluent aphasia (left hemisphere) and severe dysarthria • Contralateral gaze paresis • Contralateral hemiparesis face> arm> leg • Relatively preserved perception (right hemisphere)
Posteroinferior middle cerebral artery division	• Minimally impaired consciousness • Fluent aphasia (left hemisphere) and moderate dysarthria • Contralateral incongruent hemianopia • Contralateral intent hemiparesis face> arm> leg • Contralateral multimodal neglect (right hemisphere) • Contralateral alien hand sign

Table 4. Carotid Stroke Syndromes from Smaller Occlusions and Composite Territories

Vessel Involved	Semiology
Lenticulostriate arteries	• Atypical aphasia (left hemisphere) and variable dysarthria • Contralateral hemiparesis
Rolandic artery	• Contralateral hemiparesis face>>hand>>arm>leg
Opercular or insular branches	• Nonfluent aphasia (left hemisphere) and mild dysarthria • Apraxia • Contralateral discrete neglect (right hemisphere)
Angular artery (left hemisphere)	Gerstmann syndrome • Agraphia • Acalculia • Left-right disorientation • Finger agnosia
Superficial anterior arterial (MCA-ACA) borderzone (unilateral)	• Transcortical aphasia (left hemisphere) and mild dysarthria • Contralateral hemisensory loss • Loss of contralateral volitional saccades • Prosopagnosia
Superficial anterior arterial (MCA-ACA) borderzone (bilateral)	“Man-in-the-barrel” syndrome • Bilateral proximal weakness of the upper limbs
Deep arterial (MCA-ACA) borderzone	• Transcortical aphasia • Contralateral sensory loss
Bilateral anterior cerebral artery	• Abulia and akinetic mutism • Bilateral hemiparesis (atypical paraparesis) • Urinary incontinence

(2) Vertebrobasilar syndromes. Large arterial occlusion in the vertebrobasilar system results in syndromes with catastrophic implications (Table 5). Proximal or mid-basilar artery occlusion compromises the entire brainstem and cerebellum as it also does an “isolated” vertebral artery (ie, no contralateral collateral flow) (05). Otherwise, occlusion of the vertebral artery and its most important branch (ie, posterior inferior cerebellar artery) results in Wallenberg syndrome.

Large arterial territories of the vertebrobasilar system

(Contributed by Dr. Camilo Gomez.)
Stroke syndromes associated with medullary infarctions

(Contributed by Dr. Camilo Gomez.)

The syndromes that accompany occlusion of the anterior inferior cerebellar artery and superior cerebellar artery overlap because their territories complement each other and supply common structures. Occlusion of the top of the basilar artery leads to a combination of: (A) altered sensorium, (B) visual and ocular motor abnormalities, and (C) long tract dysfunction (12; 26; 28). Unilateral posterior cerebral artery syndromes are characterized by highly congruous visual fields defects with concurrent disorders of eye movement control or behavioral abnormalities. Bilaterally, they encompass cortical blindness, with or without the patient’s awareness. Rarely, occlusion of the posterior choroidal artery is associated with hemisensory loss and homonymous sectoranopia (23; 39).

Table 5. Vertebrobasilar Stroke Syndromes from Large and Medium Artery Occlusions

Vessel Involved	Semiology
Proximal and mid-basilar artery	• Severely depressed consciousness • Bilateral gaze palsy • Quadriparesis Locked-in syndrome • Quadriparesis and preserved consciousness
Isolated vertebral artery	• Same as basilar artery (“isolated” system) Wallenberg syndrome • Vertigo, nausea and vomiting • Hoarseness and dysphagia (CN IX, X, XI) • Horner syndrome (ipsilateral) • Ipsilateral ataxia • Crossed hemisensory loss (ipsilateral CN V)
Posterior inferior cerebellar artery	Wallenberg syndrome • Vertigo, nausea and vomiting • Hoarseness and dysphagia (CN IX, X, XI) • Horner syndrome (ipsilateral) • Ipsilateral ataxia • Crossed hemisensory loss (ipsilateral CN V)
Anterior inferior cerebellar artery	• Ipsilateral ataxia • Vertigo, nausea, and vomiting • Ipsilateral hearing loss, and tinnitus • Ipsilateral fascicular VII • Horner syndrome
Superior cerebellar artery	• Vertigo, nausea, and vomiting Benedikt syndrome • Ipsilateral CN III • Contralateral hemiparesis • Contralateral tremor - chorea - athetosis
Top of the basilar artery	• Decreased consciousness • Pseudosixth phenomenon (thalamic esotropia) • Variable unilateral or bilateral visual field defects • Hemiparesis (unilateral or bilateral)
Posterior choroidal artery	• Contralateral incongruous sectoranopia • Contralateral hemisensory loss
Posterior cerebral artery	• Contralateral congruous hemianopia (± macular sparing) • Agitated delirium • Alexia without agraphia • Peduncular hallucinosis Balint syndrome • Simultagnosia • Ocular apraxia • Ocular ataxia
Posterior cerebral artery (bilateral)	• Cortical blindness Anton syndrome • Visual anosognosia • Confabulations

The most important syndromes resulting from small arterial occlusions in the vertebrobasilar system are listed in Table 6.

Stroke syndromes associated with medullary infarctions

(Contributed by Dr. Camilo Gomez.)
Stroke syndromes associated with pontine infarctions

(Contributed by Dr. Camilo Gomez.)
Stroke syndromes associated with midbrain infarctions

(Contributed by Dr. Camilo Gomez.)

These “penetrators” can be divided into 2 distinct bundles, paramedian and lateral, that supply the brainstem at all levels (08; 31; 45). The cranial nerves affected in their syndromes localize the lesion, both rostrocaudally (ie, medulla, pons, or midbrain) and transversely (ie, paramedian vs. lateral; tegmental vs. tectal).

Table 6. Vertebrobasilar Stroke Syndromes from Small Artery Occlusions

Vessel Involved	Semiology
Paramedian medullary perforators	Dejerine syndrome • Ipsilateral CN XII • Ipsilateral ataxia • Contralateral hemiparesis
Lateral medullary perforators	Wallenberg syndrome • Vertigo, nausea, vomiting, hiccups • Hoarseness and dysphagia (CN IX, X, XI) • Horner syndrome (ipsilateral) • Ipsilateral ataxia
Paramedian pontine perforator	Raymond syndrome • Ipsilateral CN VI • Contralateral hemiparesis
Paramedian pontine perforator (bilateral)	Locked-in syndrome • Quadriparesis and preserved consciousness
Lateral pontine perforators	Millard-Gubler syndrome • Ipsilateral CN VII • Contralateral hemiparesis Foville syndrome • Ipsilateral gaze paresis • Ipsilateral CN VII • Contralateral hemiparesis
Paramedian midbrain perforators	• Peduncular hallucinosis Weber syndrome • Ipsilateral CN III • Contralateral hemiparesis • Seldom vertical gaze paresis • Seldom convergence nystagmus
Paramedian midbrain perforators (ventromedial tegmental lesion)	Benedikt syndrome • Ipsilateral CN III • Contralateral hemiparesis • Contralateral tremor - chorea - athetosis
Paramedian midbrain perforators (dorsomedial tegmental lesion)	Claude syndrome • Ipsilateral CN III • Contralateral hemiparesis • Contralateral ataxia
Paramedian midbrain perforators (tectal lesion)	Parinaud syndrome • Loss of upward (± downward) gaze • Loss of convergence
Lateral midbrain perforators	• Contralateral hemisensory loss (multimodal) • Seldom contralateral hemiparesis
Thalamic perforators	• Contralateral sensory loss • Contralateral ataxia • Choreoathetoid movements Dejerine-Roussy syndrome • Contralateral paroxysmal pain
Thalamogeniculate perforator	• Contralateral sensory loss • Contralateral ataxic hemiparesis • Choreoathetoid movements Dejerine-Roussy syndrome • Contralateral paroxysmal pain
Artery of Percheron (anatomical variation in which a single artery supplies both paramedian thalami and rostral midbrain)	• Coma • Ocular gaze palsy • Neuropsychiatric manifestations • Recurrent somnolence

(3) Lacunar syndromes. Lacunar syndromes result from small and deep-seated infarctions, and the most important are listed in Table 7, together with their frequency of occurrence. They have been described following infarcts in numerous locations, thereby limiting their localization value (21; 36; 04).

Table 7. Lacunar Stroke Syndromes

Semiology	Infarct location
Pure motor stroke (50%): • Contralateral hemiparesis	• Internal capsule • Basis pontis • Less frequently: corona radiata, cerebral peduncle, and medullary pyramid
Pure sensory stroke (15%): • Contralateral sensory loss	• Thalamus • Anterior limb of the internal capsule
Sensorimotor stroke (15%): • Contralateral motor and sensory deficit	• Internal capsule • Corona radiata • Thalamus
Ataxic hemiparesis (15%): • Contralateral hemiparesis • Contralateral ataxia	• Internal capsule • Thalamus • Corona radiata • Lentiform nucleus • Cerebellum • Basis pontis
Dysarthria-clumsy hand syndrome (5%): • Contralateral ataxia of the upper limb • Dysarthria	• Basis pontis • Internal capsule

Headache and stroke syndromes

The association of cerebrovascular diseases with headache in fairly common. Migraine related strokes are uncommon but may represent 25% of all stroke etiologies in patients below 50 years of age. Migrainous infarction is a diagnosis of exclusion and more frequently occurs in patients with migraine aura, smokers, and those using oral contraceptives (10). Cerebral arteriopathies presenting with stroke are frequently associated with headache, including reversible cerebral vasoconstriction syndrome (RCVS) and primary angiitis of the central nervous system. Although reversible cerebral vasoconstriction syndrome is frequently associated with recurrent thunderclap headaches, primary angiitis of the central nervous system is more associated with insidious and progressive headache (50). Patients with cervical artery dissection frequently have cervical pain or headache preceding stroke. Patients with carotid artery dissection may present with Horner syndrome and low cranial nerve palsy. Hemorrhagic strokes often present with headaches and in subarachnoid hemorrhage there is a typical sudden onset high intensity headache. Rupture of posterior communicating artery aneurysms can lead to ipsilateral third nerve palsy along with sudden severe headache. Table 8 summarizes headache characteristics in cerebrovascular diseases (09).

Table 8. Headache Characteristics in Cerebrovascular Disease

	Subarachnoid hemorrhage	Intracerebral hemorrhage	Ischemia	RCVS	Migraine	Cerebral venous thrombosis
Headache	Most patients	Half of patients	One third of patients	Most patients	Most patients	Most patients
Onset	Sudden	Acute to subacute	Acute to subacute	Sudden	Subacute	Variable
Intensity	Severe	Variable	Variable	Severe	Moderate to severe	Moderate to severe
Duration	Hours	Hours to days	Hours to days	Recurrent (hours to days)	Minutes to hours	Days to weeks
Location	Diffuse	Variable	Variable	Diffuse	Unilateral (could be bilateral)	Diffuse
Nausea/vomit	At onset	Variable (more common in posterior fossa ICH)	Unusual	Uncommon	Frequent	Not uncommon
Prior headache	Very frequent (sentinel headache)	Uncommon	Uncommon	Common	Always	Uncommon
Associated neurologic finding	Neck rigidity, third nerve palsy in posterior communicating aneurysm	Present According to hematoma location	Present According to ischemic location	Variable	Migraine aura (visual, sensory, motor or vestibular)	Variable Papilledema Visual disturbances
Adapted from (09)

Atypical locations and manifestations

Infarcts of the corpus callosum splenium are rare, representing less than 1% of ischemic strokes location. Patients may present with encephalopathy, alexia without agraphia, and color anomia (51).

Usually stroke manifests with loss of function (“negative symptoms”), although positive symptoms such as hyperkinetic movement disorders may also occur. Infarcts in the putamen, subthalamic nucleus, caudate, or the posterior nucleus of the thalamus can cause movement disorders such as chorea/ballism or tremor. Limb shaking can occur, triggered by position change or exercise, and indicates decreased cerebral perfusion, most frequently caused by carotid high-grade stenosis (57).

Alien limb syndrome can be caused by a stroke in about 10% of cases. Reflexive grasping, groping, and manipulations can localize in the supplementary motor area, anterior cingulate gyrus, medial prefrontal cortex, and anterior corpus callosum of the dominant hemisphere. Alternatively, antagonistic action between the hands, extremity levitation, and uncontrolled grasping usually occur after anterior corpus callosum lesions (57).

Anton syndrome is characterized as a denial of blindness and confabulation and can occur after bilateral occipital lobe infarcts. Charles-Bonnet syndrome is characterized by visual hallucinations after loss of input into the visual cortex and can be precipitated by strokes affecting visual field. Gerstmann syndrome comprises the symptoms: agraphia, acalculia, finger agnosia, and right–left confusion and occurs due to lesions on the angular gyrus of the dominant hemisphere (57).

Bacterial and nonbacterial endocarditis often manifests with sudden confusion or somnolence, or an ‘embolic encephalopathy’, without localizing features to specific arterial territories. Imaging in such patients typically shows multiple scattered infarctions (49).

Certain etiologies can be recognized by their stroke features. For example, patients with fixed arterial stenosis (eg, intracranial middle cerebral artery stenosis, Moyamoya disease) typically develop recurrent stereotyped focal deficits. Patients with the genetic syndrome CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy) accrue small-vessel strokes with psychiatric and cognitive change, leading to dementia (14). Stroke-like episodes with hearing or vision loss are seen in patients with mitochondrial disorders such as mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) (40).

Poststroke recrudescence is the phenomenon of transient reemergence or worsening of prior stroke deficits in clinical settings such as systemic infections (eg, urinary tract infection), benzodiazepine exposure or sleep cycle disruptions, and electrolyte imbalance. It is believed to result from failure of stroke recovery pathways from these systemic factors; removal of the systemic trigger results in clinical improvement to baseline. It is important to distinguish this syndrome from recurrent stroke or transient ischemic attacks, and other mimics such as seizures (54).

Stroke-like migraine attacks after radiation therapy (SMART) syndrome is a rare but reversible complication occurring several years after radiation therapy. Patients manifest with headaches, seizures, or other focal neurologic deficits concerning stroke or recurrence of the underlying disease such as tumor (19).

Besides neurologic involvement, an acute stroke may lead to systemic changes, such as the stroke-heart syndrome. This syndrome is probably due to an autonomic dysregulation caused by stroke manifesting as myocardial necrosis, coronary demand ischemia, and arrhythmia. There has been an association of stroke-heart syndrome and worst short-term prognosis (46).

Cerebrovascular localization diagnosis

The diagnosis of stroke begins with the semiologic recognition of the presenting syndrome in the context of the appropriate temporal profile.

Cerebrovascular localization diagnosis

The clinician, on recognition of the stroke syndrome, uses inductive reasoning to localize the lesion and match it to its corresponding vascular territory. This is confirmed by the ancillary imaging data and followed by integratio...

This leads, by inductive reasoning, to presumptive lesion and vessel localization, both of which are then confirmed by supportive imaging results. Next, factoring the patient’s risk profile and the natural history of the specific vascular syndrome, deductive reasoning allows the clinician to: (A) generate an etiopathogenic construct of the patient’s clinical scenario, (B) derive a set of prognostic possibilities based on the available therapeutic alternatives, and (C) choose the best course of management based on a rigorous benefit and risk assessment.

The Bamford/Oxfordshire classification categorizes stroke based on initial clinical signs (Table 9) (07). A computerized algorithm has been created to aid clinicians in this classification. The application is available and can be accessed at www.compact-stroke.com (18).

Table 9. Bamford / Oxfordshire Stroke Classification

Classification	Arterial territory	Findings
Total anterior circulation stroke	Middle and anterior cerebral arteries	All 3 of the following: • Unilateral weakness (and/or sensory deficit) of the face, arm, and leg • Homonymous hemianopia • Higher cerebral dysfunction (dysphasia, visuospatial disorder)
Partial anterior circulation stroke (PACS)	Only part of the anterior circulation has been compromised	Two of the following need to be present for a diagnosis of a PACS: • Unilateral weakness (and/or sensory deficit) of the face, arm, and leg • Homonymous hemianopia • Higher cerebral dysfunction (dysphasia, visuospatial disorder)
Posterior circulation syndrome (POCS)	Vertebrobasilar system	One of the following needs to be present for a diagnosis of POCS: • Cranial nerve palsy and a contralateral motor/sensory deficit • Bilateral motor/sensory deficit • Conjugate eye movement disorder (eg, horizontal gaze palsy) • Cerebellar dysfunction (eg, vertigo, nystagmus, ataxia) • Isolated homonymous hemianopia
Lacunar stroke	Small vessel involvement	One of the following needs to be present for a diagnosis of a lacunar stroke: • Pure sensory stroke • Pure motor stroke • Sensorimotor stroke • Ataxic hemiparesis

In addition to the above stroke syndromes, an “embolic encephalopathy” (multiple cerebral infarcts causing encephalopathy without focal deficits) and “combined stroke syndromes” (multiple infarcts with a combination of the classic Oxfordshire stroke syndromes) have been described in patients with bacterial and nonbacterial thrombotic endocarditis.

Biological basis

Etiology and pathogenesis

Ischemic stroke accounts for almost 90% of all strokes, but it is hardly a homogeneous condition, having numerous potential causes (ie, etiology). There are, however, only two mechanisms (ie, pathogenesis) for the production of ischemic stroke: (A) in situ occlusion due to local vascular pathology (eg, atherothrombosis) and (B) embolic occlusion by a particle originated in an upstream source (eg, atrial fibrillation). The operational application of etiopathogenic information to bedside diagnosis requires using a robust stroke classification scheme. The most frequently used criteria is the TOAST (Table 10) (01; 02).

Table 10. Ischemic Stroke Classification Used in the TOAST

Stroke Type
	• Large artery atherothromboembolic • Cardioembolic • Lacunar • Other causes • Unknown or undetermined cause due to (a) incomplete evaluation, (b) competing causes, (c) no evident cause despite adequate tests for stroke etiology

The bulk of stroke patients seen in daily practice correspond to either atherothromboembolic or cardioembolic types, as reported in the majority of the published series, and both are largely self-explanatory. Lacunar infarctions are considered small deep-seated infarcts directly resulting from in situ occlusion secondary to chronic arteriolopathy (ie, lipohyalinosis and fibrinoid necrosis).

The category of stroke of “other cause” constitutes a heterogeneous group of causative factors and underlying conditions that are capable of precipitating cerebral arterial occlusions, including: (A) thrombophilic disorders (eg, antiphospholipid antibodies), (B) inflammatory conditions (eg, vasculitides), (C) traumatic injuries (eg, dissection), (D) genetically transmitted conditions (eg, CADASIL), (E) perfusion catastrophes (eg, borderzone infarction following cardiac arrest), (F) transient dynamic arterial dysfunction (eg, reversible cerebral vasoconstriction syndrome), and (G) drug-induced arteriopathies (eg, cocaine).

The Causative Classification of Ischemic Stroke (CCS) is an automated and more detailed version of the TOAST system, with higher inter-rater reliability (Table 11). The CCS system can be accessed online (ccs.mgh.harvard.edu) and relates stroke etiology to different stroke syndromes (06).

Table 11. Ischemic Stroke Classification Used in the Causative Classification of Ischemic Stroke System

Large artery atherosclerosis	Evident	(1) Either occlusive, or stenotic (≥ 50% diameter reduction or < 50% diameter reduction with plaque ulceration or thrombosis or plaque with ≤ 50% diameter reduction that is seated at the site of the origin of the penetrating artery supplying the region of an acute lacunar infarct) vascular disease judged to be due to atherosclerosis in the clinically relevant extracranial or intracranial arteries, and (2) The absence of acute infarction in vascular territories other than the stenotic or occluded artery
	Probable	(1) Prior history of 1 or more transient monocular blindness, transient ischemic attack, or stroke from the territory of index artery affected by atherosclerosis within the month preceding the index stroke, or (2) Evidence of thrombosis, near-occlusive stenosis, or nonchronic complete occlusion judged to be due to atherosclerosis in the clinically relevant extracranial or intracranial arteries (except for the vertebral arteries), or (3) The presence of ipsilateral and unilateral acute internal watershed infarctions or multiple, temporally separate infarctions exclusively within the territory of the affected artery
	Possible	(1) The presence of an atherosclerotic plaque protruding into the lumen and causing mild stenosis (< 50%) in the absence of any detectable plaque ulceration or thrombosis in a clinically relevant extracranial or intracranial artery and prior history of 2 or more transient monocular blindness, transient ischemic attacks, or stroke from the territory of index artery affected by atherosclerosis, at least 1 event within the last month
Cardio-aortic embolism	Evident	(1) The presence of a high-risk cardiac source of cerebral embolism
	Probable	(1) Evidence of systemic embolism, or (2) The presence of multiple acute infarctions that have occurred closely related in time within both right and left anterior or both anterior and posterior circulations in the absence of nonembolic occlusion or near occlusive stenosis of all relevant vessels. Other diseases that can cause multifocal ischemic brain injury such as vasculitides, vasculopathies, and hemostatic or hemodynamic disturbances must not be present.
	Possible	(1) The presence of a cardiac condition with low or uncertain primary risk of cerebral embolism
Small artery occlusion	Evident	(1) Imaging evidence of a single and clinically relevant acute infarction less than 20 mm in greatest diameter within the territory of basal or brainstem penetrating arteries in the absence of any focal pathology in the parent artery at the site of the origin of the penetrating artery (focal atheroma, parent vessel dissection, vasculitis, vasospasm, etc.), or
	Probable	(1) The presence of stereotypic lacunar transient ischemic attacks within the last week, or (2) The presence of a lacunar syndrome
	Possible	(1) Presenting with a classical lacunar syndrome in the absence of imaging that is sensitive enough to detect small infarctions
Other uncommon causes	Evident	(1) The presence of a specific disease process that involves clinically appropriate brain arteries
	Probable	(1) A specific disease process that has occurred in clear and close temporal or spatial relationship to the onset of brain infarction such as arterial dissection, cardiac or arterial surgery, and cardiovascular interventions
	Possible	(1) Evidence for an evident other cause in the absence of complete diagnostic investigation for mechanisms listed above
Undetermined causes	Unknown	Cryptogenic embolism: (i) Angiographic evidence of abrupt cut-off consistent with a blood clot within otherwise angiographically normal looking intracranial arteries, or (ii) Imaging evidence of complete recanalization of previously occluded artery, or (iii) The presence of multiple acute infarctions that have occurred closely-related in time without detectable abnormality in the relevant vessels Other cryptogenic: Those not fulfilling the criteria for cryptogenic embolism Incomplete evaluation: The absence of diagnostic tests that, up to the examiner’s judgment, their presence would have been essential to uncover the underlying etiology
	Unclassified	The presence of more than 1 possible or evident mechanism where there is either probable evidence for each or no probable evidence to be able to establish a single cause

The clinical application of this information must take into account that: (A) certain large arterial occlusion syndromes commonly result from in situ occlusion (eg, internal carotid artery at its origin) whereas others frequently imply embolism (eg, middle cerebral artery); and (B) small artery syndromes may result from in situ occlusion (eg, lacunar infarction), embolism (eg, atrial fibrillation), or even large parent artery pathology (eg, basilar artery atheroma compromising pontine penetrators).

In 2014 the designation “embolic stroke of undetermined source” (ESUS) was created to identify patients with nonlacunar cryptogenic ischemic strokes with a probable embolic mechanism (30). The following criteria are used to classify a stroke as embolic stroke of undetermined source:

(1) Ischemic stroke detected by CT or MRI that is not lacunar

(2) Absence of extracranial or intracranial atherosclerosis causing ≥ 50% luminal stenosis in arteries supplying the area of ischemia

(3) No major risk cardioembolic source of embolism

(4) No other specific cause of stroke identified

Some stroke syndromes are more frequently related to specific etiologies. Border zone infarcts are more frequent in large artery atherosclerotic disease but may also occur from severe hypotension or arteriopathies such as reversible cerebral vasoconstriction syndrome, Moyamoya disease, and radiation-induced arteriopathy.

Episodes of transient monocular blindness entitled amaurosis fugax are usually related to carotid occlusion or stenosis.

Lacunar infarcts and stroke syndromes are usually related to small vessel disease and hypertensive arteriolosclerosis. These patients are often affected by cognitive impairment, due to white matter disease or strategically located lacunar infarcts. For example, the presence of lacunes in the thalamus, putamen, or pallidum have been associated with a decrease in cognitive performance (41). Lesions in the fornix has also been associated with acute amnestic syndrome presenting with anterograde amnesia often accompanied by confabulation (24). Apathy, fatigue, and delirium has also been associated with white matter disease in a metanalysis (15; 16).

Lacunar infarcts and stroke syndromes are usually related to small vessel disease and hypertensive arteriolosclerosis.

As noted above, isolated upper limb paresis has been more frequently associated with symptomatic nonstenosing carotid artery atherosclerosis (SYNC) with artery-to-artery embolism (carotid plaque rupture syndrome) (53). Failure to recognize nonstenosing carotid artery plaque rupture as a stroke mechanism may result in misclassification as embolic stroke of undetermined source instead of large artery atherosclerosis. This has management implications.

Patients presenting with vesicles in the ophthalmic root of the trigeminal nerve most and contralateral hemiparesis most probably have herpes zoster-related vasculitis.

Multiple cerebral infarcts may occur from different etiologies. In patients presenting with multiple infarcts involving the anterior circulation unilaterally the most frequent etiology is ipsilateral carotid atherosclerosis. In patients with multiple cortical infarcts in different arterial territories the most frequent etiology is cardioembolism. Frequent causes of cardiac embolism are atrial fibrillation and infectious endocarditis. A type of embolic encephalitis may occur in patients with bacterial endocarditis due to multiple infectious emboli (49). Patients with multiple deep infarcts due to microangiopathy may evolve with cognitive decline and vascular dementia.

The bow-hunter’s syndrome is characterized by ischemia in the vertebrobasilar territory after head rotation, causing dynamic vertebral artery stenosis. It is usually due to a mechanical compression from a bony structure (42). Beauty parlor stroke syndrome, also named hairdresser-related ischemic cerebrovascular events (HICE), is caused by cervical artery dissection or hemodynamic compromise related to preexisting arterial disease (17).

Patients with COVID-19 typically have thrombosis or cardioembolism to the large cerebral arteries due to hypercoagulability and endotheliopathy (48). A propensity towards large vessel occlusion, multi-territory stroke, and involvement of otherwise uncommonly affected vessels has been shown. Case reports have described atypical neurovascular presentations such as bilateral carotid artery dissection, the reversible cerebral vasoconstriction syndrome, and posterior reversible encephalopathy syndrome (PRES) (55).

Differential diagnosis

Generally speaking, the diagnosis of acute ischemic stroke should be easily made at the bedside if two categorical criteria are met: (A) the syndrome has an abrupt (ie, sudden) onset and (B) the syndrome conforms to one of those described above (ie, it is consistent with occlusion of a single vessel as its root cause). That said, published series have reported alternative diagnoses (ie, “stroke mimics”) in 30% to 50% of patients evaluated (29). The primary causes of these “mimics” include seizures (with postictal paralysis), toxic or metabolic encephalopathies, space occupying lesions, acute confusional state, migraine, inflammatory or demyelinating lesions, and hypoglycemia among others. The efficient use of ancillary studies, particularly imaging, should allow clinicians to differentiate between stroke and its “mimics.”

Transient worsening or reemergence of previous stroke-related deficits in patients with toxic and metabolic factors may be frequently misdiagnosed as a new acute stroke. The following criteria are used for diagnosis of poststroke recrudescence:

(1) Transient worsening of residual poststroke focal neurologic deficits or transient recurrence of previous stroke-related focal neurologic deficits

(2) Chronic stroke on brain imaging

(3) No acute lesion on DWI

(4) Cerebral ischemia considered unlikely (eg, symptom duration > 1 hour without new DWI lesion; no suspicion for low flow transient ischemic attack from cerebral artery stenosis or occlusion)

(5) No clinical or electroencephalographic evidence of seizure around the time of the event

The main triggers for poststroke recrudescence are infections, hypotension, hyponatremia, insomnia or stress, and benzodiazepine use (54). Neurologic deficits in poststroke recrudescence patients are usually mild to moderate and never exceed the deficits from the prior stroke.

The main differential diagnosis to transient neurologic deficits after prior stroke are described in Table 12.

Table 12. Differential Diagnosis of Transient Neurologic Deficits After Previous Stroke

Feature	Poststroke recrudescence	Seizure-related deficits (eg, Todd paralysis)	Transient ischemic attack, aborted stroke, or cerebral ischemia without infarction	Migraine-related deficits	Functional neurologic symptom disorder	Amyloid spells
Onset	Usually abrupt; deficits may initially progress	Usually abrupt; associated with seizure disorder; maximum at onset	Abrupt	Gradual over 5-20 min	Variable	Abrupt, with symptoms spread to contiguous body areas, usually arm
Symptoms and signs	New deficits that are mild to moderate; a subset of previous stroke symptoms; and mainly affect motor, sensory, or language function	New deficits that may be severe, extending beyond the original stroke symptoms; may be associated with confusion, tongue bite, incontinence, and other ictal or postictal phenomena	New deficits that are usually different from previous stroke symptoms	Migraine aura: positive visual/sensory symptoms or language deficits (more symptoms if basilar-type migraine) but no motor weakness; hemiplegic migraine: motor weakness with ≥1 migraine aura symptom	Variable symptoms; presence of give-way weakness, Hoover sign, etc	“Marching” paresethesias; weakness, or other positive or negative symptoms; may resemble migraine aura
Clinical course	Gradual resolution with removal of the triggering factor; less often waxing-and-waning deficits; complete return to baseline usually within 1-2 days	Gradual resolution of deficits over minutes to hours, return to baseline within 2 days	Prompt resolution, usually within 1 hour; may occur after stroke thrombolysis (aborted or averted stroke)	Migraine aura: resolution < 1 hour, usually followed by headache; hemiplegic migraine: resolution < 24 hours, accompanied with headache; persistent aura without infarct: > 1 week	Variable	Recurrent, lasting minutes
Brain and vascular imaging	Chronic infarct or hemorrhage; no evidence of new stroke; no new cerebral artery occlusion or hemodynamically significant stenosis	Chronic infarct or hemorrhage; no evidence of new stroke although DWI may be abnormal if seizure is prolonged	Chronic infarct or hemorrhage; no evidence of new stroke; rarely, evidence for arterial reperfusion (eg, dilated collateral vessels), or new cerebral artery occlusion (aborted stroke) or significant stenosis	Chronic infarct or hemorrhage; no evidence of new stroke; no new cerebral artery occlusion or hemodynamically significant stenosis	Chronic infarct or hemorrhage; no evidence of new stroke; no new cerebral artery occlusion or hemodynamically significant stenosis	Chronic infarct or hemorrhage; no evidence of new stroke; presence of cortical microbleeds, convexal subarachnoid hemorrhage or superficial siderosis
Scalp EEG	No evidence of electrographic seizure activity	Ictal or postictal epileptic or epileptiform patterns	No evidence of electrographic seizure activity	No evidence of electrographic seizure activity	No evidence of electrographic seizure activity	No evidence of electrographic seizure activity
From (54)

Diagnostic workup

Presently, during the hyperacute phase of ischemic stroke management, CT-based techniques continue to be the most practical and informative. Nonenhanced CT allows: (A) assessment of the integrity of the neural tissue (ie, documents the presence or absence of infarction); (B) detection of alternative diagnoses (eg, intracerebral hemorrhage); and (C) qualification of stroke patients for treatment with intravenous tPA. Immediately adding CTA allows the identification of large arterial occlusion and streamlines the selection process for endovascular treatment (20; 56). CT perfusion studies provide the means to assess the ischemic penumbra, theoretically discriminating between salvageable and infarcted tissue.

Large arterial occlusion in the carotid system

(A) The initial CT of a patient with a left middle cerebral artery syndrome shows a dense middle cerebral artery sign (arrow). The source (B) and 3D rendering (C) of the CTA confirm the LMCA occlusion (arrows). Angiography before ...

In MRI, the introduction of diffusion-weighted imaging sequences and apparent diffusion coefficient maps increased the sensitivity of detecting ischemic brain tissue, even in the hyperacute stage (58; 44). In addition, gradient refocusing echo sequences can easily demonstrate even small areas of hemorrhagic transformation, of critical importance in planning the application of antithrombotic therapy, whereas MRA provides an anatomic rendition of the flow in the large arteries.

Infarction patterns in the vertebrobasilar system

(A) Occlusion of the proximal BA produces extensive infarction of the brainstem, cerebellum and posterior cerebral hemispheres. (B) Infarction of the superior cerebellar artery territory exemplifies a medium sized infarction. (C) ...

Ultrasound-based techniques, extracranial neurovascular ultrasound, and transcranial Doppler provide alternative methods for acquiring real-time information about cerebral hemodynamics and the vascular wall of the extracranial arteries. Catheter cerebral angiography is reserved for individuals whose noninvasive testing does not provide all of the diagnostic information necessary to make appropriate therapeutic decisions.

In-depth assessment of cardiogenic embolism is best accomplished using transesophageal echocardiogram due to its increase sensitivity for cardiac and aortic sources of embolization (27). Cardiac MRI is increasingly becoming an even greater asset in the diagnostic evaluation of ischemic stroke. Finally, data suggest that occult atrial fibrillation may be more prevalent than suspected, and long-term cardiac rhythm monitoring via 30-day event monitors or using implantable loop recorders is justified in many cases (47; 43).

Media

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Contributors

All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.

Authors

Aneesh B Singhal MD

Dr. Singhal of Harvard Medical School has no relevant financial relationships to disclose.
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Eva A Rocha MD PhD

Dr. Rocha of Universidade Federal de São Paulo has no relevant financial relationships to disclose.
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Editor

Steven R Levine MD

Dr. Levine of the SUNY Health Science Center at Brooklyn has no relevant financial relationships to disclose.
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Former Authors

Patrick Pullicino MD, Catalina Ionita MD, Karen D Orjuela MD, and Camilo R Gomez MD MBA

Patient Profile

Age range of presentation: 19 to 65+ years
Sex preponderance: Female > Male, >1.25: 1
Heredity: Heredity may be a factor, particularly in certain genetically transmitted arteriopathies
Population groups selectively affected: African Americans

Persons living in the southeastern United States (ie, Stroke Belt)
Occupation groups selectively affected: None selectively affected

ICD & OMIM codes

ICD-9: Occlusion and stenosis of unspecified precerebral artery: 433.9

Cerebral artery occlusion, unspecified: 434.9

Acute but ill-defined cerebrovascular disease: 436
ICD-10: Cerebral infarction: I63

Cerebral infarction due to thrombosis of vertebral artery: I63.01

Cerebral infarction due to thrombosis of basilar artery: I63.02

Cerebral infarction due to thrombosis of carotid artery: I63.03

Cerebral infarction due to thrombosis of middle cerebral artery: I63.31

Cerebral infarction due to thrombosis of anterior cerebral artery: I63.32

Cerebral infarction due to thrombosis of posterior cerebral artery: I63.33

Cerebral infarction due to thrombosis of cerebellar artery: I63.34

Cerebral infarction due to thrombosis of other cerebral artery: I63.39

Cerebral infarction due to embolism of vertebral artery: I63.11

Cerebral infarction due to embolism of basilar artery: I63.12

Cerebral infarction due to embolism of carotid artery: I63.13

Cerebral infarction due to embolism of middle cerebral artery: I63.41

Cerebral infarction due to embolism of anterior cerebral artery: I63.42

Cerebral infarction due to embolism of posterior cerebral artery: I63.43

Cerebral infarction due to embolism of cerebellar artery: I63.44

Cerebral infarction due to embolism of other cerebral artery: I63.49

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Ischemic stroke syndromes and their anatomic localization

Associated Disorders

arterial dissection
atherosclerosis
atrial fibrillation
cardiomyopathy
coronary artery disease
- diabetes
- hypertension
- peripheral vascular disease
- vascular dementia

Differential Diagnosis

intracerebral hemorrhage
seizure with postictal paralysis
complex migraine
primary or metastatic tumors
inflammatory and demyelinating disorders
- toxic/metabolic encephalopathies
- hypoglycemia

Also Relevant

Anterior cerebral artery stroke syndromes
Aortic atherosclerosis and stroke
Ischemic stroke
Lacunar infarction
Medical complications of stroke
- Primary prevention of stroke
- Stroke therapy
- Supportive care for ischemic stroke patients

Ischemic stroke syndromes and their anatomic localization

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Table 1. Probable Arterial Territory of Transient Ischemic Attacks According to Neurologic Symptom

General stroke semiology

Table 2. Main Language and Speech Stroke Syndromes

Specific stroke semiology

Table 3. Carotid Stroke Syndromes from Large and Medium Artery Occlusions

Table 4. Carotid Stroke Syndromes from Smaller Occlusions and Composite Territories

Table 5. Vertebrobasilar Stroke Syndromes from Large and Medium Artery Occlusions

Table 6. Vertebrobasilar Stroke Syndromes from Small Artery Occlusions

Table 7. Lacunar Stroke Syndromes

Headache and stroke syndromes

Table 8. Headache Characteristics in Cerebrovascular Disease

Atypical locations and manifestations

Cerebrovascular localization diagnosis

Table 9. Bamford / Oxfordshire Stroke Classification

Biological basis

Etiology and pathogenesis

Table 10. Ischemic Stroke Classification Used in the TOAST

Table 11. Ischemic Stroke Classification Used in the Causative Classification of Ischemic Stroke System

Differential diagnosis

Table 12. Differential Diagnosis of Transient Neurologic Deficits After Previous Stroke

Diagnostic workup

Media

References

Contributors

Authors

Editor

Former Authors

Patient Profile

ICD & OMIM codes

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