Stroke: Comprehensive Guidelines for Clinical Assessment and Emergency Managemen
Stroke: Comprehensive Guidelines for Clinical Assessment and Emergency Management (Part I)
Authors: John E. Duldner, Jr., MD, Emergency Physician, Department of Emergency Medicine, MetroHealth Medical Center, Cleveland, OH.
Charles L. Emerman, MD, Chairman, Department of Emergency Medicine, MetroHealth Medical Center, Cleveland, OH; Associate Professor, Case Western Reserve University, Cleveland, OH.
Peer Reviewers: Edward Jauch, MD, MS, Assistant Professor, Department of Emergency Medicine, University of Cincinnati Medical Center; Member, Greater Cincinnati/Northern Kentucky Stroke Team, Cincinnati, OH.
Sydney Starkman, MD, FACEP, Associate Clinical Professor of Emergency Medicine and Neurology, UCLA Medical Center; Chairman, Stroke Group, UCLA Stroke Center, Los Angeles, CA.
Thrombotic and embolic infarction of the brain is a major cause of morbidity and mortality in the United States, with the estimated annual medical costs of stroke care reaching approximately $30 billion per year. About 20% of these expenditures occur in the first 90 days after an acute event.1 Cerebral vascular disease is a leading cause of death, second only to cardiovascular disease and cancer.2 Overall, approximately 500,000 strokes of all types occur each year, and they are responsible for about 150,000 deaths. Seventy-five percent of all strokes occur in patients over the age of 65.
The ED is frequently the first point of contact for stroke victims. Although many patients currently present after a substantial delay following onset of symptoms, the role of the emergency physician in the acute management of stroke is likely to expand as newer therapies are shown to improve morbidity and mortality.3 Though patients may present to the ED with a devastating neurological picture, substantial improvement may occur over time, even in the absence of specific therapy. About 20% of patients who survive the initial event eventually have full or partial resolution of hemiparesis. Hemineglect, a common finding in early stroke, resolves in most patients.4 Although the risk of repeated stroke is highest within the first 30 days, 25-40% of patients will have a repeat stroke within five years.5 Early recurrence is associated with a significant increase in morbidity and mortality.
Eighty-five percent of strokes are ischemic in origin whereas hemorrhagic strokes occur in about 15% of patients.1 The one-month mortality rate for stroke varies according to etiology. It is approximately 15% for ischemic stroke, 50% for subarachnoid hemorrhage, and may be as high as 80% for intracerebral hemorrhage.4,6,7 Cardiovascular complications account for 35% of stroke deaths, recurrent stroke for 25%, and pulmonary complicationseither pneumonia or embolismfor another 25%.8
With these clinical challenges in focus, this two-part article will provide a comprehensive review of diagnostic and management considerations in patients with ischemic stroke syndromes. Part I will provide a systematic review of clinical presentations and stroke syndromes, while part II will provide guidelines and protocols for patient evaluation and management.
The Editor
The goals for prehospital management of stroke patients include priority dispatch, early recognition, brief evaluation, appropriate intervention and rapid transport. In fact, stroke is considered a medical emergency and the prehospital response should be commensurate with this urgency. Prehospital care for stroke begins with EMS dispatch, for which the priority should be high. Although the majority of prehospital providers will recognize symptoms of a large hemispheric stroke, prehospital personnel should be taught basic neurological assessment skills to detect subtle presentations. A brief neurological examination including assessment of level of consciousness, Glasgow Coma Scale, pupil size and reactivity, and gross motor function may suffice, but a more specific neurological exam may improve diagnostic sensitivity. Several cities have implemented prehospital stroke scales to improve detection, and their sensitivity is being tested. A stroke-specific prehospital protocol may improve clinical outcomes in the field.
The field evaluation should be focused. In addition to evaluating the patient for evidence of cardiovascular or traumatic illness, EMS personnel should evaluate the patient for conditions that mimic stroke and can be readily reversed. These conditions include hypoglycemia, drug overdose, and seizures. In addition to evaluating the ABCs, patients should receive at least the following: cardiac monitor, placement of intravenous catheter, supplemental oxygen, and a rapid blood sugar screen. Providers should avoid administration of excess intravenous (IV) fluids or inappropriate use of dextrose (D50). Scene time should not be delayed with field interventions, and patients should be transported rapidly to an appropriate facility with the capability to manage acute stroke. Prehospital personnel should be instructed to notify the receiving hospital to facilitate prompt mobilization of resources, particularly specialized stroke teams where available.
According to the World Health Organization (WHO) definition, stroke is characterized by a neurological deficit of sudden onset accompanied by focal dysfunction and symptoms lasting more than 24 hours that are presumed to be of a non-traumatic vascular origin.9 A transient ischemic attack (TIA) is diagnosed on the basis of neurological events that have a duration shorter than 24 hours, followed by complete return to baseline. An additional sub-category of stroke includes reversible ischemic neurological deficit (RIND), a category that is used when the deficit resolves completely, usually within three days, but always within three weeks.
It should be stressed that a variety of disorders may mimic strokes. In general, the diagnosis of stroke is correctly made on the basis of the initial clinical examination by non-neurologists in more than 95% of the cases. A few trials have found higher misdiagnosis rates, although these studies were performed at tertiary referral centers, which tend to see more complicated patients. Misdiagnosis occurs more commonly in younger patients and those with complex or atypical symptomatology.10 The differential diagnosis includes complex migraine headache with hemiparesis, post-ictal paresis (Todd’s paralysis), hypoglycemia, cerebral tumor, cerebral infection, subdural hematoma, drug intoxication, and malignant hypertension.
The risk of stroke increases with age, particularly in patients older than 65. In patients younger than 60, there is a male predominance to stroke in a 3:2 ratio. There is a familial association with stroke including both a paternal and maternal history of cerebral vascular and cardiovascular disease.11
It is estimated that almost 50% of strokes can be prevented by control of treatable risk factors.12 (See Table 1.) Hypertension is the primary risk factor for stroke. Patients with hypertension have 4-5 times the risk of stroke than that of nonhypertensive patients. Even in patients with normal blood pressures, the risk of stroke diminishes as the diastolic blood pressure falls. In addition, isolated systolic hypertension has also been recognized as a risk factor for stroke. Cardiovascular and cerebrovascular disease coexist in more than 80% of stroke patients.13 Atrial fibrillation occurring in the setting of mitral stenosis, congestive heart failure, or cardiomyopathy, as well as in patients with mechanical cardiac valves, carries a risk of stroke on the order of 6% per year.14,15 The annual risk of atrial fibrillation-associated stroke increases with age and is as high as 36% in the very old.
Cigarette use and diabetes also increase the risk of stroke, particularly in women. Diabetics have a four-fold increase in stroke risk. The incidence and mortality of stroke is higher in African-Americans.16 This may be attributable to differences in access to health care, although there may be a higher incidence of hypertension, glucose intolerance, and hyperlipidemia in this population.16 The association between hypercholesterolemia and stroke is less clear, and reduction of cholesterol has recently been shown to reduce stroke risk.17 Heavy alcohol use increases the risk of stroke, especially subarachnoid hemorrhage.18 TIAs are strong predictors of stroke with an annual risk that is around 8%, although most strokes are not preceded by a TIA.
Stroke usually involves the development of a focal neurological deficit, the nature of which can help localize the involved vascular territory. Although transient loss of consciousness may occur from global cerebral hypoperfusion, it is not generally a symptom of stroke unless accompanied by other vertebrobasilar symptoms that localize the vascular insult. Seizures may accompany stroke, although again, in the absence of focal neurological deficits, this finding alone does not confirm the diagnosis of stroke. Headache occurs in a substantial minority of patients with stroke and is most common in patients under the age of 70, in non-smokers, and in patients with cerebellar infarcts.19 Headache that occurs with stroke is frequently, though not always, diffuse in nature. Vomiting, seizures, headache, or coma occur more commonly with hemorrhagic stroke but may be seen on occasion with ischemic infarction.
Careful clinical evaluation can identify the site of infarction in about 90% of the cases.(See Table 2.) The variety of neurological deficits seen in stroke relate to the area of the brain involved and the vascular territory perfused by cerebral vessels. Among patients undergoing angiography for atherosclerotic stroke, 62% have stenosis or occlusion of the internal carotid artery (ICA), 10% have occlusion or stenosis of the middle cerebral artery (MCA), whereas 15% have blockage of the vertebrobasilar (VB) arteries.23
Conditions Causing Focal Neurologic Lesions
Overview. The most common cause of focal neurologic deficits is thrombotic cerebral infarction.20-28 Because most thrombotic strokes cause abrupt neurologic deficits, that is an important differential point for establishing the diagnosis. Metabolic disorders, however, may also have an abrupt onset, so it is necessary first to distinguish stroke from other conditions, such as brain tumors, brain abscess, and intracranial lesionsin which neurologic dysfunction usually progresses gradually but may initially manifest as seizures or postictal focal paralysis.
Once conditions mimicking primary neurologic disorders have been eliminated, the emergency physician should attempt to identify which of the three categories of cerebro-occlusive disease has occurredthrombosis, embolism, or hemorrhagebecause initial therapy will depend upon the underlying cause.
Physical Examination. A rapid but comprehensive neurologic exam includes assessment of the following nine major neurologic functions: mental status, station and gait, skull and spine, meninges, motor function, sensation, proprioception, cranial nerves, and cerebellar function. Nonspecific, initial vital signs may also give important information. For example, reflex sinus bradycardia and elevated systemic blood pressure frequently occur with catastrophic intracranial events, such as subarachnoid intracerebral hemorrhage. And blood pressure discrepancy between the arms may herald a dissecting aortic aneurysm. The carotid pulses may reveal bruits, and the cardiac exam may suggest embolic causes for focal neurologic deficits:: atrial fibrillation, paradoxical movement of the left ventricle (aneurysm with possibility of mural thrombus), and murmurs suggesting valvular disease associated with bacterial or marasmic endocarditis.
Thrombotic Infarction. Cerebral occlusions result in well-described, sudden, focal neurologic deficits. They occur without or with less severe headache and vomiting than intracerebral hemorrhages. Significant obtundation or depression of consciousness is unusual unless the occlusion involves a massive amount of brain, the brainstem, or a previously diseased brain. A full-blown deficit usually develops in seconds with emboli, and from minutes to hours with cerebral thrombotic infarction.
Cerebral artery thrombosis usually develops at night during sleep, with symptoms perceived by the patient or family upon awakening in the morning.23-25 As a rule, the patient falls asleep without a deficit and awakens with a hemiparesis or speech disturbance.
Usually, thrombotic cerebral infarction does not present with severe depression of consciousness unless the basilar artery system is involved or unless there has been massive internal carotid thromboembolism resulting in acute cerebral edema and secondary compression of the brainstem structures.26 Moreover, thrombotic infarction rarely causes seizures in the acute phase of the illness, although focal seizures do occur as sequelae in regions that have been scarred as a result of the previous cerebral infarction.
Suspect a diagnosis of thrombotic cerebral infarction in patients with extensive arteriosclerosis and in those with hypercoagulable states due to malignancy, thrombocytosis associated with collagen vascular disorders, and hyperosmolar states, which can lead to venous thrombosis.
Embolic Infarction. Embolic infarction is the next most common cause of focal neurologic deficits.28-32 In contrast to thrombotic infarction, cerebral embolism is apt to occur at any time of the day or night and frequently occurs during periods of vigorous physical activity.25
When evaluating the possibility of cerebral embolic infarction, identifying a source, if possible, is essential. Common sources include atrial thrombi in elderly patients with long-standing chronic atrial or paroxysmal atrial fibrillation, valvular vegetations caused by bacterial endocarditis, thromboembolism in myocardial infarction, and, in patients with extracranial vascular disease, ulcerated plaques in the carotid system. It is, at present, a neurologic axiom that when atrial fibrillation and focal neurologic deficits co-exist, cerebral embolization has occurred.27,29
As mentioned, embolic infarction usually occurs when the patient is awake, and does not present with severely impaired mental status unless there has been a complette occlusion of the carotid artery, leading to massive cerebral edema, or unless the vasuclar insult involves the ascending reticular activating system (ARAS). The acute phase of embolic infarction may be accompanied by seizures, which can be either focal of diffuse, in up to 20% of cases.27 At present, it is recommended that patients who have had cerebral embolism due to an intracardiac thrombosis associated with atrial fibrillation be anticoagulated immediately with heparin therapy.25,28 Anticoagulation should be preceded by CT scanning to exclude the possibility of hemorrhagic infaction.
Transient Ischemic Attacks. TIAs manifest as stereotyped, short-lived, focal neurologic deficits lasting, by definition, less than 24 hours. The time from onset to the maximal deficit is usually only a few minutes, and TIAs rarely last more than eight hours. Most resolve within 15-60 minutes.30
Although the definition of TIA is straightforward, management is complex and controversial. In one study, 30% of patients originally diagnosed as having TIAs were subsequently considered misdiagnosed on review of their medical records by a stroke specialist.29,31,32 Physicians, including neurologists, perceive the management of TIAs as difficult, and many are frequently uncertain about how to best evaluate and manage such patients.
From the viewpoint of emergency practice, the greatest clinical significance of TIAs is that they are harbingers of ischemic cerebral infarction, with its potentially devastating consequences. Estimates of the incidence of infarction following TIA vary, but in the absence of systematic treatment, approximately 5-10% of patients will have a stroke within a month and 12% within a year. At the end of two years, stroke will have occurred in an estimated 20-40% of TIA patients.31,32 Therefore, emergency physicians must recognize the occurence or increasing frequency of TIAs and institute appropriate measures to reduce the patient’s risk of stroke.
Transient focal deficits may be caused by neurologic disorders other than focal ischemia. Features in the history and physical examination may provide clues to underlying disorders. For example, a throbbing unilateral headache (often occurring after disappearance or improvement of a focal deficit) and scintillating scotomas and accompanying nausea suggest migraine, especially in younger patients. Clonic motor activity and abrupt loss of consciousness followed by confusion, or a history of epilepsy or traumatic brain surgery suggest a seizure disorder. A recent history of headache, a clouded sensorium, or depressed level of consciousness with a focal neurologic deficit following a head injury may indicate a subdural hematoma. Remember, they may also occur without any preceding head injury, especially in the elderly.
Although systemic hypotension rarely produces focal symptoms, hemodynamic obstruction of a cerebral artery may decrease regional blood flow enough to cause dysfunction. In addition, cardiogenic emboli are well-known causes of TIA and stroke. Emboli arising from the heart may occur in association with valvular or nonvalvular atrial infarction, cardiomyopathy, mitral stenosis or prosthetic heart valves. Mitral valve prolapse, especially in younger patients, may also be associated with cerebral embolism. Occasionally, septic emboli will originate from a diseased endocardium. So-called paradox emboli originating in the lung or venous system and traveling through a patent foramen ovale may also occur.
Intracranial Hemorrhage. Hemorrhagic strokes, subarachnoid and intracranial hemorrhage, typically occur during stress or exertion. Precipitating events include sexual intercourse, Valsalva’s maneuver, and labor and delivery. Recent evidence also suggests that alcohol consumption contributes to hemorrhagic stroke, especially subarachnoid.33,34 In most cases, focal deficits rapidly evolve and many are associated with confusion, coma, or immediate death.
Excruciating headache is the cardinal symptom of intracranial hemorrhage and is classically described as "the worst" in the patient’s life. It may be accompanied by nuchal rigidity on physical exam. Arteriovenous malformations (AVM) may bleed into the subarachnoid space, but when they involve the cerebral parenchyma, lateralizing signs will be present. Lack of focal findings and young age at presentation help distinguish subarachnoid from intracerebral hemorrhage. Except for the occasional field cut, oculomotor palsy of aneurysmatic compession, or focal seizure, lateralizing focal neurologic lesions are notably absent with subarachnoid hemorrhage. On the other hand, intracranial hemorrhage is characterized by prominent focal findings because of its intraparenchymal location.
There are two main types of intracranial hemorrhage: intracerebral and extracerebral. In the elderly population, intracerebral hemorrhage is most common as a complication of long-standing hypertension or anticoagulation therapy. Hypertensive intracerebral hemorrhage has a predilection for certain sites and usually occurs, in order of frequency, in the thalmus, putamen, cerebellum, or brainstem. It most often develops when the patient is awake and active. Detecting cerebellar hemorrhage or hematoma is especially important, as intracranial bleeding in that location is amenable to neurosurgical intervention.35
Spontaneous subarachnoid hemorrhage usually results from a ruptured intracranial aneurysm. Onset usually consists of a sudden severe headache during vigorous activity, which is sometimes likened by patients to an abrupt blow on the head. Hemorrhagic infarction, which is the third most common cause of focal deficits in patients with cerebrovascular disease, should be considered in patients with hypertension or those who are taking anticoagulants, who have had previous craniocerebral trauma, or who have a history of unexplained headaches. Unlike thrombotic and embolic cerebral infarction, hemorrhagic infarction frequently presents with severely impaired consciousness and/or seizures and may be accompanied by severe headache and nuchal rigidity.
Noncerebrovascular Causes of Focal Neurological Deficits
Hyperosmolar states (hypernatremia, hyperglycemia), hypoxia, hypotension, carbon monoxide poisoning, hyponatremia, hypoglycemia, hypocalcemia, and hypophosphatemia can cause focal neurologic deficits.27,28,36-38 CNS findings in patients with metabolic disorders may be diffuse or focal, with diffuse involvement producing alteration in consciousness that range from drowsiness to psychosis to coma. In general, those changes progress in severity as the metabolic derangement worsens, but they may, at times, develop rapidly. The vast majority of diffuse and focal CNS abnormalities caused by metabolic derangements clear completely and promptly once the derangement is corrected.
Symptoms and signs of focal brain dysfunction resulting from metabolic derangement are especially common in the elderly. Those abnormalities probably represent the unmasking of preexisting subclinical structural brain damage by profound metabolic changes within the brainchanges induced by electrolyte or osmolar derangements.39 The biochemical basis for focal neurologic deficits in metabolic disorders is unclear. However, alterations in brain cell volume seem to play a major role. In hyperosmolar states, intracellular water moves into the extracellular space across the semipermeable cell membrane to maintain equality in tonicity between the two compartments. The resulting shrinkage in intracellular volume then leads to cerebral dysfunction. Conversely, hypo-osmolarity results in fluid movement into the cellular compartment and leads to cerebral edema and CNS symptoms.
Syndromes of Ischemia and Infarction in the Acute Stroke
Cerebral Arterial Anatomy. The anterior portion of the brain involving the frontal, temporal, and parietal lobes, is usually supplied by the carotid arteries, whereas the posterior portion including the occipital lobe, cerebellum, and brainstem is perfused by the VB system. (See Figure 1.) The carotid artery arises from the innominate artery on the right and directly from the aortic arch on the left. It divides into the internal and external carotid arteries at its extracranial bifurcation. The ICA courses through the skull in segments termed the carotid siphon. The first two branches of the ICA are the ophthalmic and anterior choroidal arteries. The MCA is the largest of the two terminal branches of the carotid artery and divides into two or three main trunks. The MCA perfuses the cortex, parietal lobe, temporal lobe, internal capsule, and portions of the basal ganglia along its course. The anterior cerebral artery (ACA) is the second of the terminal branches of the ICA. It forms the anterior portion of the circle of Willis and supplies portions of the frontal lobe. The posterior cerebral artery (PCA) occasionally arises from the carotid system, although typically it is the terminal portion of the basilar artery, supplying the occipital lobe and selected areas of the thalamus. There may be collateral flow provided to these vascular territories by the circle of Willis.
The vertebral arteries (VA) arise from the subclavian arteries and give off branches supplying the medulla and portions of the cerebellum. The basilar artery (BA) is formed by the junction of the two vertebral arteries and gives off a variety of penetrating arteries supplying the brainstem and portions of the basal ganglia before dividing into the posterior cerebral arteries. (See Figure 2.)
The carotid artery. Obstructing lesions of the carotid artery frequently occur at bifurcation points. In asymptomatic patients, ICA disease may be diagnosed on the basis of a carotid bruit. Approximately half of patients with moderate stenosis (greater than 50% occlusion) will have a carotid bruit, and about 90% of patients with a carotid bruit have at least moderate stenosis.40,41 Recent studies have demonstrated that treatment of patients with asymptomatic, high-grade carotid stenosis (more than 70% stenosis) can reduce the risk of stroke.42,43 Patients with carotid artery stenosis may also present with TIA. TIAs occurring in the distribution of the ICA usually have focal symptoms that are rapid in onset and last 2-15 minutes. In general, episodes that last only seconds are not due to TIAs. Attacks in the ICA distribution that involve the dominant hemisphere may present with myriad symptoms such as motor dysfunction, amaurosis fugax, numbness, and/or aphasia. TIAs in the distribution of the ICA of the non-dominant hemisphere have similar symptomatology but without aphasia.
Clinical symptoms of ICA occlusion vary greatly due to variation in collateral flow. Major deficits at initial presentation may resolve partially as emboli migrate to smaller branch vessels. Most symptoms of ICA occlusion reflect ischemia in the middle cerebral artery territory and present with hemiparesis and, in the case of dominant hemispheric lesions, aphasia. Other patterns may occur including hemiparesis with hemianopia or a variety of aphasic patterns without hemiparesis.
Watershed Infarctions. High-grade stenosis of the ICA may also render the brain susceptible to infarction during periods of relative hypotension. These so called "watershed" infarcts occur in vulnerable areas supplied by distal distribution of the anterior and middle cerebral arteries, the distal distribution served by the middle and posterior cerebral arteries, and the superficial and deep branches of the middle cerebral artery.44 Patients with watershed infarction between the anterior and middle cerebral arteries present with hemiparesis, predominantly in the leg.45 There is usually an associated decrease in sensation in the same distribution. In dominant hemisphere infarctions, there is a decrease in verbal ability with preserved comprehension. Infarction involving the posterior watershed area presents with homonymous hemianopia. There may be hypoesthesia in the face and legs. Motor weakness is rare in this type of infarction. Finally, watershed infarction may also occur in the area between the deep and superficial branches of the MCA and nearly all of these patients present with hemiparesis. Hemisensory deficit and language disorder are common in dominant hemisphere infarctions.
The Anterior Cerebral Artery. The ACA forms the anterior portion of the circle of Willis and supplies portions of the frontal lobe and medial portions of the parietal lobe. (See Figure 3.) Infarction in the distribution of the ACA leads primarily to symptoms involving the distal leg, such as weakness or clumsiness. There may be speech disturbances. The anterior limb of the internal capsule may be affected leading to face and arm weakness. Lesions of the anterior choroidal artery can cause hemiplegia and sensory loss, along with homonymous hemianopia. Frontal lobe infarctions are estimated to occur in about 20% of initial cerebral vascular accidents.46 About 15% of patients with symptomatic strokes involving other areas of the brain also have frontal lobe infarctions on computed tomography.47
A variety of frontal lobe syndromes may occur with anterior cerebral artery infarction. The superior medial syndrome is associated with higher cortical dysfunction: difficulty in task preparation, apraxia, agraphia, volitional movement, loss of bi-manual coordination, and grasp reflex. Aphasia may occur in ACA stroke involving the dominant hemisphere. Facial palsy and hemi-neglect may also be present. Patients with bilateral ACA infarcts may present with docile behavior, indifference to surroundings, incontinence, confabulation, and akinetic mutism. Patients with infarction in the superficial territory of the ACA may present with contralateral weakness, primarily involving the leg, sensory loss, and mutism. Ischemia in the deep distribution of the ACA may lead to movement disorders such as hemichorea or hemiballism. Infarction in the area of the anterior communicating artery presents with amnesia, a Korsakoff-like picture, and loss of volition.
In summary, lesions in the distribution of the ACA lead to weakness of the leg, which is occasionally associated with proximal muscle weakness in the upper extremities. There may be associated sensory involvement or change in affect. Language impairment is also a common, but not invariable, finding.
The Middle Cerebral Artery. The MCA supplies most of the convex surface of the brain and a significant amount of "deep" brain tissue. It supplies blood to almost the entire basal ganglia, the putamen, the upper parts of the globus pallidus, a portion of the head, and all the body of the caudate nucleus, and a substantial part of the anterior and posterior rims of the internal capsule. Not surprisingly, occlusion of the MCA is responsible for the majority of stroke syndromes, with embolism from either the ICA or the heart to the MCA being the most common cause of cerebral infarction. Thrombosis of the MCA accounts for only 2% of ischemic events in the MCA territory.45 Usually, occlusion of the MCA results in a large infarct that affects both superficial and deep areas supplied by this vessel. However, in some cases, adequate collateralization can minimize the degree of tissue loss.
Occlusion of the trunk or upper division of the MCA produces a large infarct characterized by contralateral hemiplegia, deviation of the head and eyes toward the side of the infarct, global aphasia (in the dominant hemisphere), hemianopia, hemianesthesia, and hemineglect. Hemiparesis affects the leg less than the arm and face. While dominant hemisphere infarction results in aphasia of the Broca-type, occlusion of the lower division of the MCA results in a Wernicke-type aphasia when occlusion involves the dominant hemisphere and hemianopia. Interruption of blood flow in the small penetrating arteries results in lacunar infarction and manifests clinically as pure hemiparesis without sensory, language, or behavioral manifestations.48,49
Common findings in MCA infarction include loss of consciousness, hemiplegia and hemiparesis, eye and head deviation, sensory disturbances, visual field disturbances, neglect, and movement disorders. These findings are typical for infarction occurring in either the dominant or nondominant hemisphere.45,48,49 Immediate loss of consciousness at the onset of the ischemic insult is uncommon. However, delayed loss of consciousness occurring at a point 36 hours to several days after the ischemic insult is more consistent and is usually caused by increased peri-infarct edema, elevated intracranial pressure, and cerebral herniation.
Hemiplegia and hemiparesis can result from infarction of the deeper arterial distribution as well as the superficial distribution. Only when infarction of the lower division of the MCA occurs is a motor deficit unlikely. Head and eye deviation are well-described in middle cerebral artery occlusion and should be expected after massive infarction of the entire middle cerebral artery territory.44 Eye deviation tends to be more common in right hemispheric infarction, and it may be accompanied by a neglect syndrome of the contralateral side, which, in most cases, resolves after 1-2 weeks. Although sensory deficits are frequently overshadowed in MCA infarctions, profound loss of sensory modalities are common with MCA infarction, particularly if there is involvement of the anterior parietal cortex.50 Visual field disturbances are common in large infarcts of the middle cerebral artery. Hemianopia is the most common visual field disturbance, however, parietal infarction can result in a quadrantanopia due to involvement of parietal radiations of visual fibers.48
As mentioned previously, patients suffering a stroke in the territory of the MCA may develop neglect syndromes. These may involve motor, verbal, or visual neglect. Neglect is manifested clinically by a patient’s partial or complete inability to respond or recognize stimuli from one side of the patient’s body. Frequently, a patient will fail to respond to a stimulus presented on the right side, for example, in response to motor or auditory stimulus on that side, or a deficiency in naming objects that lie or are positioned on the right side of the patient. Movement disorders including hemichorea, athetosis, or dystonia are infrequently observed after MCA occlusion.48-52
Dominant vs. Nondominant Hemisphere Infarction
Characteristics of Dominant Hemispheric Infarction. Because the two middle cerebral arteries supply opposite hemispheres, infarction of the dominant hemisphere will demonstrate clinical findings different from that of infarction of the nondominant hemisphere. Although the contralateral hemiplegic syndromes and other associated abnormalities described earlier still occur, hemisphere-specific symptoms and signs permit more accurate determination of right- or left-hemispheric involvement.
Speech Disorders. It is important to note the patient’s hand dominance in order to infer hemisperhic dominance. The majority of right-handed, and most left-handed patients, have dominance for speech and language located in the left hemisphere. Left hemispheric infarction is characterized by aphasia, both motor and sensory, and apraxia. Speech and language dominance located in the right hemisphere is found infrequently.49 Global or total aphasia usually results from occlusion of the trunk of the middle cerebral artery or its upper division. Motor aphasia, also known as Broca’s aphasia, results from infarction of the insular cortex and fronto-parietal operculum. During the period of acute infarction, total aphasia is more likely, with a true motor aphasia evolving over time. Broca’s speech disturbance manifests as hesitant and broken responses. This is especially true when a patient attempts to speak polysyllabic words and is due to the dyspraxia between the oropharynx and the respiratory elements that permit smooth vocalization.49,53 This speech pattern is nonfluent and displays agrammatism, characterized by simple utterings, usually single words or nouns that are spoken in short and disjunctive phrases.
Wernicke’s aphasia, also known as sensory aphasia, occurs with occlusion of the lower division of the middle cerebral artery and generally results from a large infarct encompassing the posterior temporal, inferior parietal, and lateral temporo-occipital regions.49,53 These patients show no deficit in the ability to vocalize, speak in phrases, make smooth transitions, or properly pronounce their words. However, in the acute phase, attempts at speech contain few understandable words. This condition, known as jargon paraphasia, results in distorted phonetic structure, involves consonants, substituted words, and perseveration.33 In some cases, the extent of the language disturbance is not evident in simple conversation and requires more extensive evaluation. Generally, there is a deficit in writing that parallels the spoken element. In cases where hemiparesis is not involved, the writing is legible with abnormal content.
Apraxia represents an abnormality in the execution of a task. It is generally an acquired problem in that it results in an inability to perform a previous task that cannot be explained by loss of coordination, weakness, dementia, or aphasia. Apraxia results from a loss of motor programs stored in left hemisphere dominant individuals.51,52 The most common type of apraxia is ideomotor apraxia where the affected brain area contains the idea for movement and the motor areas that lead to this movement. Ideomotor apraxia is tested by asking the patient to perform a basic task such as combing hair.
Characteristics of Nondominant Hemispheric Infarction. Syndromes produced by nondominant hemispheric infarction are less predictable and may include defects of attention, including directed and focused attention, spacial operations, and confabulatory behaviors. Two common, characteristic forms of defects in attention include extinction and neglect. Extinction is the inability to perceive a stimulus when a second stimulus is presented simultaneously.54 Neglect is manifested by a lack of response to stimuli from one side of the body in the absence of any pre-existing sensory or motor deficit severe enough to account for this imperception.49 Neglect usually involves auditory, visual, and tactile stimuli, and patients are frequently found to act to stimuli only in the field or space opposite the affected side. These patients can only relate to one side of their body or surroundings. Damage to the nondominant hemisphere can also affect the ability to localize objects in space. Patients have a diminished capacity to determine spacial orientation and are unable to localize sounds in space.
Behavioral changes due to infarction of the nondominant hemisphere include acute confusion and delirium manifested by impaired orientation, diminished attention, and altered perception. Memory and thought processes are impaired, but alertness is maintained.48 The incidence of behavioral abnormalities is greater when the temporal lobe is affected, and this is likely due to the proximity of these lesions to the limbic system. Constructional apraxia may occur and results in the inability to arrange, draw, or build objects due to the inability to manipulate objects in space.
The Posterior Cerebral Artery. The posterior cerebral artery generally arises from the VB system. Among the clinically significant areas supplied are the occipital lobe and thalamus.55
Thalamic Lesions. Posterior communicating artery infarction may lead to a number of thalamic syndromes. These patients usually have sensory symptoms involving loss of tactile, temperature, and pain sensation. Patients typically complain of numbness and tingling on one side of the body, occasionally associated with dysesthesia. Proprioception is frequently spared. There may be some motor weakness or ataxia, which may indicate involvement of the adjacent internal capsule. Infarction in the paramedian area may involve transient loss of consciousness followed by confusion, amnesia, and confabulation. Hypoesthesia is common and movement disorders may also be associated with this lesion.
Occipital Lesions. The superficial portion of the PCA supplies the occipital area.56 Typically, lesions in this area lead to a homonymous visual field defect which may be a hemianopia or a quadrantanopia. Macular vision tends to be spared in PCA infarction due to collateral supply from the MCA. Dominant hemisphere lesions may lead to alexia. Bilateral lesions can cause cortical blindness or tunnel vision. Lesions of the PCA may cause midbrain disturbances including oculomotor palsy or internuclear ophthalmoplegia. There may be associated dyslexia, memory loss, and confusion.
The Vertebrobasilar Circulation
Vascular anatomy of the vertebrobasilar system is complex and therefore leads to heterogeneous syndromes and presentations characteristic of posterior circulation ischemic disease. Clinical syndromes arising from occlusion in this arterial distribution can vary greatly due to the combination of areas in the brain perfused, variability within this circulatory bed, and collateral blood flow.
The most common site of atherosclerotic stenosis in the vertebral arteries is at their origin, whereas stenotic lesions in the basilar artery affect all three segments equally. Thrombosis rarely involves the trunk of the basilar artery but may occur in branching arterioles. Embolic phenomena are usually found within the distal basilar branches, specifically the posterior cerebral arteries. There are occasional cases where neck rotation, trauma, or chiropractic manipulation to the neck has resulted in vertebrobasilar infarction. These patients tend to be younger and without evidence of bony abnormalities or pre-existing vascular disease.45
Transient Ischemic Attacks. The most common transient symptom is dizziness or vertigo; however, chronic recurrent spells of vertigo unaccompanied by other neurological signs or symptoms are seldom due to vascular disease.45,48 Furthermore, transient vertigo when occurring in solitary episodes, should not be considered a transient ischemic attack. Dizziness may also occur from TIA associated with a carotid distribution, although usually not in the absence of other associated findings. Drop spells or syncope that present in the absence of other signs or symptoms of brain stem ischemia are infrequently due to occlusion of the vertebrobasilar system.
Embolization of fibrin-platelet material from atherosclerotic sites is one proposed explanation in the pathogenesis of transient ischemia attacks.57 Other etiologies include cerebral vasospasm, arterial hypotension with fixed stenotic lesions, and, more rarely, TIAs induced by exercise, emotional outbursts, and polycythemia.58,59 Multiple episodes of transient neurologic dysfunction consisting of different patterns suggest an embolic phenomenon, whereas a fixed patterns of signs and symptoms suggests atherosclerotic or thrombotic lesions.
The classic findings of vertebrobasilar TIA include perioral numbness, dizziness or vertigo, horizontal or vertical diplopia, dysarthria, paresis of either one complete side or both sides of the body, or numbness of all of one or both sides of the body. Other manifestations may include headache, ataxia, decreased vision including darkening, blurring and tunnel vision, partial or complete blindness, pupillary and gaze abnormalities, vomiting, hiccups, and impaired hearing.45
Weakness or numbness may involve the fingers and face in some TIA episodes but only the fingers in others. Dizziness and ataxia may occur in some attacks, while in others diplopia may be part of the picture. TIAs due to basilar artery disease may affect each side of the body alternately, and affected parts may be involved simultaneously or spread from one region to another. The attacks may cease abruptly or fade gradually.57,58
Infarction Syndromes of the Vertebrobasilar System. Subclavian steal presents with symptoms referable to the posterior circulation. Classically, stenosis of the subclavian artery proximal to the origin of the vertebral artery results in augmented flow through the opposite vertebral artery and reversal of flow through the vertebral artery on the same side as a subclavian stenosis. In this case, activity in the upper extremities results in flow reversal and blood being "stolen" from the intended cerebral bed. Patients with subclavian steal present with headache, intermittent episodes of cerebral ischemia, or claudication pain in the ischemic arm. Subclavian steal is more common in the left subclavian artery.45 The cerebral manifestations of subclavian steal are worse when patients have coexistent carotid artery disease. Diagnosis is based on physical examination that reveals a diminished pulse and blood pressure in the affected extremity; clinical suspicion is required, and Doppler ultrasonography can confirm the diagnosis.
The vertebral arteries are the main source of blood flow to the medulla. Consequently, occlusion can lead to several clinical syndromes, including the lateral medullary syndrome and the medial medullary syndrome. In 80% of cases, the lateral medullary syndrome, also known as Wallenberg syndrome, is usually caused by lesions in the vertebral artery near the take-off of the PICA.48 This lesion produces infarction in a lateral wedge of the medulla and results in vertigo, headache, facial pain, feelings of disequilibrium, nausea and vomiting, ataxia, and hiccups; diminished sensation in the ipsilateral face, diminished pain and temperature sensation of the contralateral body, Horner’s syndrome, ataxia of gait and limb, nystagmus, slight weakness of the ipsilateral face, paralysis of the ipsilateral vocal cord and weakness of the ipsilateral palate may also occur.45,48 Contralateral hemiparesis or a positive Babinski’s sign are not components of the lateral medullary syndrome. The medial medullary syndrome results in contralateral hemiparesis sparing the face, loss of tactile, proprioceptive, and vibratory sense. There is preservation of pain and temperature sensation, and ipsilateral tongue paralysis.47,48,60-63
PICA Syndrome. Occlusion of the posterior inferior cerebellar artery (PICA) is the most common cerebellar artery syndrome and may lead to the lateral medullary syndrome described above. PICA infarcts are associated with greater involvement of the cerebellum and have a worse prognosis. Involvement of the anterior inferior cerebellar artery (AICA) generally results in pontine and cerebellar infarction. Extensive cerebellar infarction is uncommon with AICA occlusion, and it tends to have a more benign prognosis. Patients with AICA infarction have ipsilateral facial weakness and hypesthesia, deafness, Horner’s syndrome, ataxia, vertigo, nystagmus, and contralateral limb and trunk hypesthesia.45,48 Occasionally, infarction of the AICA or the PICA results in a pure vestibular syndrome and patients may be misdiagnosed as having labyrinthitis.45,48 Isolated superior cerebellar artery (SCA) occlusion is unusual. The SCA infarction syndrome includes ipsilateral limb ataxia, a Horner’s syndrome, contralateral thermoanalgesia involving the face, arm, trunk and leg, and a fourth cranial nerve palsy.48,64
Vertebrobasilar infarction is usually due to occlusion of a branch of the basilar artery rather than complete infarction of the trunk (basilar branch disease). The basilar artery supplies portions of the midbrain, the pons, and regions of the cerebellum. Three branches are involved: small paramedian penetrators, short circumferential branches, and long circumferential branches (AICA and SCA). Occlusion of the basilar artery trunk results in bilateral infarction of the basis pontis and cerebellar tegmentum. Clinical manifestations include coma, abnormal breathing patterns, quadriplegia with decerebrate posturing ,and bilateral sensory loss. Cranial nerve abnormalities include bilateral reactive pupillary miosis, horizontal ophthalmoplegia (not overcome by oculocephlic maneuvers) and ocular bobbing.45,48,58 The "locked-in" syndrome results from sparing of the tegmentum with infarction of the basis pontis. Patients are conscious, however they are quadriplegic, anarthric, and have complete sensory impairment but may communicate using eye movements. Occlusion of the distal end of the basilar artery results in the "top of the basilar" syndrome. Patients with bilateral infarction present with motor, sensory, visual, oculomotor, and behavioral findings, absent vertical gaze palsy, nystagmus, third nerve palsy, bilateral ptosis, internuclear ophthalmoplegia, unreactive pupils, homonymous hemianopia, cortical blindness, and hemianesthesia or hemihypesthesia.45,48,65,66 Pontine lesions due to occlusion of small perforating arteries results in several minor syndromes, indistinguishable from those seen in cerebral lacunar infarction.45,60
While large vessel occlusions have stereotypical symptomatology, there is a separate set of symptoms associated with lesions of the small penetrating branch arteries, commonly termed lacunar infarctions. Lacunar strokes are characterized by the lack of impairment of consciousness, aphasia, or visual disturbances.67-69 Lacunar infarctions are very common and involve the deep central regions of the brain, particularly the basal ganglia, basis pontis, and thalamus, leading to characteristic syndromes. Pure motor hemiparesis is a frequent result of lacunar infarction. These rarely involve monoplegia, and usually result in hemiparesis of the face, arm, and leg. Pure sensory stroke is the most common lacunar infarction in some series again involving the face, arm, and leg. A third variety of lacunar infarction involves ataxia and leg hemiparesis. Finally the clumsy hand-dysarthria syndrome, is caused by a lesion in the basis pontis or in the anterior limb of the internal capsule. Lacunar infarctions tend to have a good prognosis. The mortality rate in patients with lacunar infarction is markedly lower than in patients with middle cerebral artery infarction and tend to be due to non-neurologic causes such as pneumonia or cardiovascular events. Patients with lacunar infarction are more likely to recover fully than are patients with large artery occlusions. Approximately 60% of patients with lacunar infarctions will be independent at one year following the stroke.
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Physician CME Questions
49. Primary risk factor for stroke include all of the following except:
A. hypertension.
B. alcohol use.
C. marijuana use.
50. Lacunar infarctions present with:
A. aphasia.
B. pure motor hemiparesis.
C. cranial nerve palsies.
51. Neglect syndromes are common in
A. MCA infarctions.
B. lateral medullary syndrome.
C. PICA infarction.
D. posterior cerebral artery infarction.
52. The World Health Organization definition of stroke is:
A. a neurological deficit accompanied by focal dysfuncion.
B. a neurological deficit of sudden onset accompanied by focal dysfunction and symptoms lasting more than 24 hours.
C. neurological events that have a duration shorter than 24 hours.
D. neurological deficit of sudden onset that is unaccompanied by or accompanied by focal dysfunction.
53. In patients younger than 60, the predominance of stroke is:
A. male to female, 3:2.
B. female to male, 2:4.
C. female to male, 3:2.
54. The most common cause of focal neurologic deficits are:
A. embolic infarctions.
B. intracranial hemorrhage.
C. thrombotic cerebral infarctions.
55. Patients with Wernicke’s aphasia:
A. show no deficit in the ability to vocalize, but, in the acute phase, use speech containing few understandable words.
B. demonstrate an abnormality in the execution of a task.
C. demonstrate deficits of attention.
56. The most common transient symtom of a TIA is:
A. paresis.
B. dizziness or vertigo.
C. headache
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