Perspective

Transient ischemic events and acute ischemic strokes are separate points on a continuum of cerebral vascular disease and share a relationship similar to that of unstable angina and acute myocardial ischemia.¹ The most common causes are large artery atherosclerosis, cardioembolism, or small vessel (lacunae) disease. Patients with transient ischemic attacks (TIAs) have a significant short-term risk for recurrent stroke, myocardial infarction, and death. Although TIA is typically a reversible process, ischemic stroke is a pathologic process that permanently injures the brain. Ischemic stroke is defined as a permanent cerebral injury secondary to prolonged disruption of cerebral blood flow (typically <10 mL/100 g brain/min).²

Epidemiology

The yearly incidence of TIA in the United States has been estimated to be approximately 200,000 to 500,000 but may be higher because of the high frequency of underreporting of these events by medical professionals.^3–6 The annual incidence of TIA may be less and the annual incidence of stroke may be higher if the tissue-based definition were applied to all patients evaluated for TIA.⁴ It has been estimated that the overall incidence rate of TIA is 1.1 per 1000 U.S. population.⁷ This incidence increases with age from 0.1 per 1000 for patients younger than 50 years to 11.7 per 1000 for patients older than 80 years.³ The incidence of TIA also varies with race and gender: it is significantly greater in blacks and men than in whites and women. The greatest incidence of TIA occurred in black men older than 85 years, who had an incidence of 16 events per 1000.³

TIAs account for 0.3% of all emergency department (ED) visits, and it is estimated that 8.7% to 30% of patients will have a TIA before stroke.^8,9 Only 28% of TIA patients arrive via ambulance, and 36% of patients arrive during daylight hours. Emergency physicians (EPs) obtain computed tomography (CT) scans on 56% to 70% of all TIA patients and magnetic resonance imaging (MRI) scans on 7% of TIA patients. Nearly half of all patients with TIA are admitted to the hospital, although there is geographic variability in this practice; another 20% of patients are referred for follow-up. Finally, patients seen in the ED with TIA receive preventive aspirin therapy in 18% of cases, other antiplatelet therapy in 7%, and no preventive therapy in an estimated 42%.⁷

Clearly defined risk factors for stroke and adverse events following a TIA are now well described in the literature, and several groups of investigators have independently developed short-term risk stratification methods applicable to TIA patients in the ED.^10–13 These investigators reported a 10% rate of stroke in the 90 days following the TIA, with 50% of these strokes occurring in the immediate 48 hours after the TIA.

Recently, the ABCD2 score, which combines elements from existing risk stratification systems, was devised to create a robust prediction standard for determining high-risk populations that will benefit from emergency investigation and therapy to prevent short-term adverse events (Table 100.1).¹² Patients with the following characteristics were at high risk for having a stroke in the next 2 to 90 days: age older than 60 years, blood pressure higher than 140 mm Hg systolic or 90 mm Hg diastolic, clinical features such as unilateral weakness or speech disturbance, longer duration of symptoms of TIA, and diabetes.

Table 100.1 Two-Day Risk for Stroke Stratified According to the ABCD2 Score

Ischemic stroke accounts for 80% to 88% of the total strokes occurring annually.¹⁴ Each year approximately 795,000 people experience a new or recurrent stroke. It is an important cause of death in the United States and ranks third behind heart disease and cancer.¹⁵

Approximately 8% to 12% of all patients suffering an ischemic stroke die within 30 days of the initial stroke. Ischemic stroke disproportionately affects the elderly, with a mean age at onset of 70.5 years. Ischemic stroke affects black and Hispanic populations more frequently than white populations. The age-adjusted incidence of first ischemic stroke per 100,000 population is 88 in whites, 149 in Hispanics, and 191 in blacks.¹⁶ Ischemic stroke is an enormous economic burden, with an average 30-day cost of $20,346 for a severe stroke and mean lifetime cost of $140,048.^15,17 The United States spends approximately $73.7 billion yearly on the direct and indirect cost of stroke care.¹⁵

Pathophysiology

An ischemic injury involving the central nervous system disrupts normal cerebral blood flow to the brain (40 to 60 mL/100 g brain/min). The extent of injury is based on three principles: the duration of disrupted flow, the flow rate, and collateral circulation. Loss of consciousness occurs within 10 seconds and cell death within minutes of disrupted cerebral circulation.

Cerebral tissues with blood flow between 12 and 20 mL/100 g brain/min are termed the ischemic penumbra. These cells are at risk for permanent injury but have the ability to recover if flow is reestablished. When cerebral blood flow falls below 10 mL/100 g brain/min, electrical activity ceases and cell death occurs. Many areas of the brain may be protected by collateral circulation between the anterior and posterior circulation through vessels that make up the circle of Willis.

Classification of TIAs is important because the pathophysiology and risk for recurrent stroke differ among the subtypes. The five mechanisms described are large artery atherosclerosis, cardioembolism, small vessel disease, other rare determined cause, and undetermined cause.^9,18

Large artery atherosclerosis is defined as greater than 50% narrowing of vessel caliber. It accounts for 15% of all ischemic strokes and is the most common cause of low-flow TIA. Symptoms are the result of thrombus formation in a ruptured atherosclerotic plaque. The most commonly affected vascular territories are the origin of the internal carotid and intracranial portion of the internal carotid (siphon), the middle cerebral artery stem, and the junction of the vertebral and basilar arteries. It is found more commonly in men and has a greater incidence in African and Hispanic populations. Patients with large artery atherosclerosis have a higher recurrence rate than do patients with other stroke subtypes: 4%, 12.6%, and 19.2% at 7, 30, and 90 days, respectively.¹⁹ These patients have transient or stuttering symptoms in the same vascular territory. Symptoms and disability may be less severe than those in patients with cardioembolic stroke.¹⁴

Cardioembolic disease represents 20% to 25% of ischemic cerebrovascular events. The most common sources are abnormal cardiac rhythm, abnormal left ventricular wall motion, and aortic and mitral valve disease.²⁰ The clinical features are abrupt in onset, with nonprogressive symptoms that may occur in multiple vascular territories. Cardioemboli affect the anterior circulation in 70% of patients. These patients tend to have more severe symptoms and higher mortality rates; disability is more severe in survivors.¹⁴ Patients with embolic TIA have a lower recurrence rate of 2.5%, 4.6%, 11.9% at 7, 30, and 90 days, respectively.¹⁹

Lacunar strokes represent 20% of all ischemic strokes and are caused by small vessel disease—obstruction of the small vessels that penetrate the brain parenchyma at right angles to major parent arteries and supply the basal ganglia, internal capsule, thalamus, and pons.^21,22 The vessels most commonly involved are small branches of the middle cerebral and basilar arteries.²¹ The most common causes of small vessel disease are microatheroma and lipohyalinosis, which are increased in the setting of older age, hypertension, diabetes, and smoking. Small embolic events rarely cause ischemia in these vessels.^21,22 Patients with lacunar TIA and stroke commonly have hypertension and diabetes. Black populations are affected more than white populations, and there does not seem to be a gender preference in patients with lacunar infarcts. These patients have a favorable prognosis with low, short-term recurrence rates of 0%, 2%, and 3.4% at 7, 30, and 90 days, respectively.^19,21,22

Rare causes of stroke account for approximately 2% to 3% of annual cases. Common causes are nonatherosclerotic vasculopathies (acute arterial dissection, vasculitis, polyarteritis, giant cell arteritis, infectious arteritis), hypercoagulable conditions (deficiencies in proteins C and S and antithrombin III, antiphospholipid antibody syndrome/systemic lupus erythematosus, pregnancy, postmenopausal hormone replacement), hematologic disorders (sickle cell disease, polycythemia, myeloproliferative disorders), and other causes of emboli (patent foramen ovale, endocarditis, air).²³

Cryptogenic stroke is the designation used for stroke without a well-defined etiology despite extensive evaluation. It accounts for 30% to 40% of all strokes in some stroke databases. Patients with cryptogenic stroke have a better 1-year prognosis than do those with other subtypes; the 2-year risk for recurrence is 14% to 20%.¹⁴

Systemic hypoperfusion is an uncommon cause of cerebral ischemia that represents a global decrease in cerebral blood flow. Causes include cardiac arrest and reduced cardiac output as a result of cardiac ischemia, pericardial effusion, arrhythmias, pulmonary emboli, hemorrhage, and medications. Symptoms consist of diffuse brain dysfunction in the setting of unstable vital signs.^14,23

Presenting Signs and Symptoms

Patients who have suffered a TIA often have no physical findings but a variety of historical clinical symptoms. Several studies have demonstrated that interobserver disagreement is high when making the diagnosis of TIA.^24,25

A few basic principles can guide accurate diagnosis of TIA. The symptoms are sudden in onset and vascular in nature. TIAs are commonly brief, lasting less than 1 to 2 hours with many lasting less than 10 to 15 minutes. Symptoms are associated with loss of function such as hemiparesis, hemiparesthesia, dysarthria, aphasia, monocular vision loss, diplopia, and gait and balance disturbances. Symptoms such as shaking, scotomata, and marching of symptoms to other body parts are more consistent with migraine or seizure.²⁶

Approximately 80% of ischemic strokes occur in the distribution of the anterior circulation and give rise to deficits in behavior, sensation, movement, and speech, as well as some elements of visual awareness. The minority of strokes occur in the distribution of the posterior circulation. Common posterior circulation symptoms are limb weakness, gait and limb ataxia, oculomotor palsy, and oropharyngeal dysfunction. In addition, patients often exhibit nausea and vomiting because of brainstem involvement, as well as vertigo and balance disorders related to cerebellar and brainstem injury.

Differential Diagnosis and Medical Decision Making

Evaluation of patients with suspected ischemic injury is summarized in Box 100.1. The results of these fundamental tests combined with risk stratification can guide the EP in determining whether cerebral injury has occurred, as well as the cause of the ischemia.

Patients with TIA and ischemic stroke require rapid and accurate diagnosis to determine the cause and location of the event and the extent of damage. This knowledge allows the EP to estimate the risks and benefits associated with therapies that will reestablish cerebral blood flow and preserve viable brain tissue.

Rapid diagnosis of acute ischemic stroke begins with public education about recognition of the major warning signs of stroke. Prehospital personnel also play a crucial role in early diagnosis and rapid transport of stroke patients to treatment facilities. Tools such as the Cincinnati Prehospital Stroke Scale and the Los Angeles Prehospital Stroke Screen (LAPSS) are used to evaluate facial droop, arm weakness, and speech abnormalities in patients with suspected stroke. In addition, the LAPSS screens for mimics of stroke such as hypoglycemia, hyperglycemia, and seizure and has high sensitivity (93%) and specificity (97%) for the diagnosis of acute stroke.^29,30

EPs caring for patients with acute ischemic stroke are often under enormous time constraints. A systematic method is necessary to distinguish patients with stroke from those with conditions that mimic stroke.³¹ In addition, the EP must combine historical and physical data with the results of neurologic imaging to exclude hemorrhage and determine the extent of injury. These elements, coupled with basic laboratory tests and an electrocardiogram (ECG), as recommended by the American Heart Association (AHA), are the foundation for accurate diagnosis of an acute ischemic stroke.

The history is the cornerstone of accurate stroke diagnosis. Historical evidence that has been identified as being predictive of a patient having a stroke includes persistent focal neurologic deficits, acute onset during the previous week, and no history of head trauma.³¹ Clinical symptoms such as arm and leg weakness and speech impairment are more reliable indicators than subjective isolated sensory symptoms are. The single most important piece of historical information is the time of onset of the symptoms. This is considered to be the last time that the patient was at the previous baseline or symptom-free state. For patients unable to provide this information or awaken with stroke symptoms, onset is defined as time when the patient was last seen to be normal.³² Other key historical factors include contraindications to thrombolytic therapy, medications being taken by the patient, heart disease, previous stroke, TIA, seizures, vomiting, or headache occurring at the beginning of the patient’s acute symptoms.

EPs must use a reproducible standardized physical examination to assess the severity of injury in stroke patients. Three key physical findings—facial paresis, arm drift, and abnormal speech—are highly predictive of an acute stroke. The National Institutes of Health Stroke Scale (NIHSS) (see the Documentation box) is a valid, standardized tool that records clinical findings and provides information that is helpful in determining the prognosis and therapeutic options. This 42-point scale evaluates level of consciousness, cranial nerves, motor function, ataxia, sensation, speech, and neglect. It can be used for serial examinations and is a predictor of patient outcome and risk associated with therapy, which can be useful when discussing treatment options with specialists, patients, and family members.

Patients with an NIHSS score lower than 6 have a predicted excellent outcome at 6 months, and 81% are discharged home. Nearly half the patients with an NIHSS score higher than 15 will require transfer to a nursing facility. Patients with an NIHSS score higher than 20 have a 17% risk for intracerebral hemorrhage when treated with recombinant tissue plasminogen activator (rt-PA). Finally, each additional point on the NIHSS decreases the likelihood of an excellent outcome by 17%.^33–35

Although the history and physical examination are important elements in making an accurate diagnosis of patients with acute neurovascular events, neuroimaging is the key diagnostic tool. The goals of modern neuroimaging evaluation are to (1) obtain evidence of a vascular origin of the symptoms; (2) exclude an alternative nonischemic origin; (3) ascertain the underlying vascular mechanism of the event, which helps guide therapy; (4) identify prognostic outcome categories; and (5) improve selection of patients to be treated with reperfusion therapies by identifying those with regions of salvageable brain tissue, low risk for hemorrhagic transformation, or occlusion of large arteries that might be amenable to therapy.^1,32 Currently, EPs have a multitude of imaging options that are based on availability of the imaging modality and local expertise in interpretation of the images.

Non–contrast-enhanced CT remains the standard imaging technique for evaluating patients with acute stroke. It can be performed in the majority of hospitals, images are acquired rapidly, and it is sensitive in detecting acute hemorrhage. For patients with TIA, CT has been shown to provide an alternative diagnosis in 1% of all cases, and a new infarct has been found within 48 hours in 4% of patients with TIA. Of these patients, 38% eventually experienced a new ischemic stroke in the next 90 days.²⁶ CT findings not associated with an increased short-term risk for stroke include old infarction, periventricular white matter disease, cerebral atrophy, and vascular calcification.³⁶ Unfortunately, CT scans are frequently negative in the first hours after an ischemic stroke, are limited in defining posterior fossa structures and discriminating between infarct and viable at-risk tissue (penumbra), and provide no information on the presence or location of vascular pathology.³²

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