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The symptoms of brain ischemia may be transient, lasting seconds to minutes, or may persist for longer periods of time. Symptoms and signs remain indefinitely if the brain becomes irreversibly damaged and infarction occurs. Unfortunately, neurologic symptoms do not accurately reflect the presence or absence of infarction, and the tempo of the symptoms does not indicate the cause of the ischemia [1,2]. This is a critical issue because treatment depends upon accurately identifying the cause of symptoms.
An overview of the evaluation of patients who present with neurologic symptoms that may be consistent with stroke is discussed here. This evaluation includes the following: • Understanding the classification of stroke • An initial quick evaluation to stabilize vital signs, determine if intracranial hemorrhage is present, and, in patients with ischemic strokes, decide if thrombolytic therapy is warranted • Forming a hypothesis of the stroke etiology based upon the history, physical examination, and initial radiologic study (usually noncontrast head CT scan) • Confirming the precise pathophysiologic process with more directed diagnostic testing.
CLASSIFICATION – Cerebrovascular disease is caused by one of several pathophysiologic processes involving the blood vessels of the brain: • The process may be intrinsic to the vessel, as in atherosclerosis, lipohyalinosis, inflammation, amyloid deposition, arterial dissection, developmental malformation, aneurysmal dilation, or venous thrombosis. • The process may originate remotely, as occurs when an embolus from the heart or extracranial circulation lodges in an intracranial vessel. • The process may result from inadequate cerebral blood flow due to decreased perfusion pressure or increased blood viscosity. • The process may result from rupture of a vessel in the subarachnoid space or intracerebral tissue.
The first three processes can lead to transient cerebral ischemia (transient cerebral ischemic attack or TIA) or permanent cerebral infarction (ischemic stroke), while the fourth results in either subarachnoid hemorrhage or an intracerebral hemorrhage (primary hemorrhagic stroke). Approximately 80 percent of strokes are due to ischemic cerebral infarction and 20 percent to brain hemorrhage.
Transient cerebral ischemia – The term transient ischemic attack (TIA) was first introduced in the early 1950s based upon the recognition that transient focal loss of neurologic function often preceded strokes [3]. In the years after this initial description in patients with carotid artery disease, various groups and committees arbitrarily defined TIAs as lasting less than 24 hours, despite subsequent data which clearly demonstrated that ischemic attacks which last longer than one hour are most often associated with brain infarction. Most TIAs last less than five minutes [1,2]. Intracerebral hemorrhage – Bleeding in intracerebral hemorrhage (ICH) is usually derived from arterioles or small arteries. The bleeding is directly into the brain, forming a localized hematoma which spreads along white matter pathways. Accumulation of blood occurs over minutes or hours; the hematoma gradually enlarges by adding blood at its periphery like a snowball rolling downhill. The most common causes of ICH are hypertension, trauma, bleeding diatheses, amyloid angiopathy, illicit drug use (mostly amphetamines and cocaine), and vascular malformations [2,4]. Less frequent causes include bleeding into tumors, aneurysmal rupture, and vasculitis. Neurologic symptoms usually increase gradually over minutes or a few hours.
Subarachnoid hemorrhage – Rupture of arterial aneurysms is the major cause of subarachnoid hemorrhage (SAH). Aneurysm rupture releases blood directly into the cerebrospinal fluid (CSF) under arterial pressure. The blood spreads quickly within the CSF, rapidly increasing intracranial pressure. Death or deep coma ensues if the bleeding continues. The bleeding usually lasts only a few seconds but rebleeding is common. With causes of SAH other than aneurysm rupture (eg, vascular malformations, bleeding diatheses, trauma, amyloid angiopathy, and illicit drug use), the bleeding is less abrupt and may continue over a longer period of time.
Symptoms of SAH begin abruptly, occurring at night in 30 percent of cases. The primary symptom is a sudden, severe headache (97 percent of cases) classically described as the "worst headache of my life." The headache is lateralized in 30 percent of patients, predominantly to the side of the aneurysm. The onset of the headache may or may not be associated with a brief loss of consciousness, seizure, nausea, vomiting, focal neurological deficit, or stiff neck (show figure 1) [5]. There are usually no important focal neurologic signs at presentation unless bleeding occurs into the brain and CSF at the same time (meningocerebral hemorrhage). Ischemia – There are three main subtypes of brain ischemia: • Thrombosis • Embolism • Systemic hypoperfusion
Thrombotic stroke – Thrombotic strokes are those in which the pathologic process giving rise to thrombus formation in an artery produces a stroke either by reduced blood flow distally (low flow) or by an embolic fragment that breaks off and travels to a more distant vessel (artery-to-artery embolism). All thrombotic strokes can be divided into either large or small vessel disease (show table 1).
• Large vessel disease includes both the extracranial and intracranial arterial system; atherothrombosis is by far the most common pathologic process.
• Small vessel disease includes the intracerebral arterial system, specifically penetrating arteries that arise from the distal vertebral artery, the basilar artery, the middle cerebral artery stem, and the arteries of the circle of Willis. These arteries thrombose due to atheroma formation at their origin or in the parent large artery, or by lipohyalinosis (a lipid hyaline build-up distally secondary to hypertension).
Embolic stroke – Embolism refers to particles of debris originating elsewhere that block arterial access to a particular brain region. Since the process is not local (as with thrombosis), local therapy only temporarily solves the problem; further events may occur if the source of embolism is not identified and treated.
Embolic strokes are divided into four categories (show table 1). • Those with a known source that is cardiac • Those with a possible cardiac or aortic source based upon transthoracic and/or transesophageal echocardiographic findings • Those with an arterial source • Those with a truly unknown source in which these tests are negative or inconclusive.
Systemic hypoperfusion – Systemic hypoperfusion is a more general circulatory problem, manifesting itself in the brain and perhaps other organs. Stroke results from a high-grade stenotic lesion that does not completely occlude the vessel, but results in ischemia in the distal "watershed" territories of that vessel. Reduced perfusion can be due to cardiac pump failure caused by cardiac arrest or arrhythmia, or to reduced cardiac output related to acute myocardial ischemia, pulmonary embolism, pericardial effusion, or bleeding. Hypoxemia may further reduce the amount of oxygen carried to the brain.
INITIAL GENERAL ASSESSMENT – Sudden loss of focal brain function is the core feature of the onset of ischemic stroke. However, patients with conditions other than brain ischemia can present in a similar fashion (show table 2). In addition, patients suffering an ischemic stroke may present with other serious medical conditions. Thus, the initial evaluation requires a rapid but broad assessment. The goals in this initial phase include:
• Insuring medical stability • Quickly reversing any conditions that are contributing to the patient's problem • Moving toward uncovering the pathophysiologic basis of the patient's neurologic symptoms.
Diagnosing an intracerebral or subarachnoid hemorrhage as soon as possible can be lifesaving and prevent or minimize permanent neurologic damage. The history may provide clues to these diagnoses, but early triage of the patient to CT scan or MRI is critical. However, it is important to assess and optimize vital physiologic function before sending the patient for an imaging study.
Vital signs – Parameters of particular concern in patients with stroke include blood pressure, breathing, and temperature.
Blood pressure – The mean arterial blood pressure (MAP) is usually elevated in patients with an acute stroke. This may be due to chronic hypertension, which is a major risk factor for ischemic stroke. However, an acutely elevation in blood pressure often represents an appropriate response to maintain brain perfusion. The decision to treat requires a balance between the potential danger of severe increases in blood pressure, and a possible decline in neurologic functioning when blood pressure is lowered. Breathing – Patients with increased intracranial pressure (ICP) due to hemorrhage, vertebrobasilar ischemia, or bihemispheric ischemia can present with a decreased respiratory drive or muscular airway obstruction. Hypoventilation, with a resulting increase in the partial pressure of carbon dioxide, may lead to cerebral vasodilation which further elevates ICP. Intubation may be necessary to restore adequate ventilation and to protect the airway. This is especially important in the presence of vomiting, which occurs commonly with increased ICP, vertebrobasilar ischemia, and intracranial hemorrhage.
Fever – Fever may occur in patients with an acute stroke and can worsen cerebral ischemia [6]. Normothermia should be maintained for at least the first several days after an acute stroke.
History and physical examination – The history and physical examination should be used to distinguish between other disorders in the differential diagnosis of brain ischemia (show table 2). As examples, seizures, syncope, migraine, and hypoglycemia can mimic acute ischemia. The most difficult cases involve patients with focal signs and altered level of consciousness. It is important to ask the patient or a relative whether the patient takes insulin or oral hypoglycemic agents, has a history of a seizure disorder or drug overdose or abuse, medications on admission, recent trauma, or hysteria. The history is also important in separating ischemia from hemorrhage and distinguishing between subtypes of ischemia and hemorrhage.
Ischemia versus hemorrhage – Noncontrast computed tomography (CT) is typically the first diagnostic study in patients with suspected stroke. The main advantages of CT are widespread access and speed of acquisition. CT is highly sensitive for the diagnosis of hemorrhage in the acute setting [7-11]. Intracerebral hemorrhages are evident almost instantly after onset as focal white hyperdense lesions within the brain parenchyma.
Intracerebral hemorrhages can also be defined by magnetic resonance imaging (MRI); the use of susceptibility sequences improves the sensitivity of MRI for early detection of hemorrhage [12-14]. Gradient-echo images can also show the presence of old hemorrhages since this technique is very sensitive to hemosiderin, which can remain in old hemorrhages indefinitely. Small subarachnoid hemorrhages can be missed by either CT or MRI. Lumbar puncture may be needed to make the diagnosis in such patients [15]. MRI is more sensitive than CT for the early diagnosis of brain infarction, although new generation CT scanners may identify subtle indicators of infarction within six hours of stroke onset in a significant number of patients [16,17]. New generation MRI scanners that have the capability to perform fluid-attenuated inversion recovery (FLAIR) images [18] and diffusion-weighted images (DWI-MRI) [19,20] are especially useful in showing infarcts early after the onset of symptoms. In patients with ischemia who do not yet have brain infarction, both CT and MRI may be normal.
Is the patient a candidate for thrombolysis? – Once it has been determined that the patient is suffering from an acute ischemic stroke, consideration should be given to the use of thrombolysis. Thrombolytic therapy with recombinant tissue plasminogen activator (rt-PA) appears to improve outcomes in patients with acute ischemic stroke who meet an extensive list of inclusion and exclusion criteria (show table 3) [21-23]. Prior to rt-PA treatment, all patients require:
• Confirmation that treatment is commencing within three hours of the onset of symptoms or that MR studies show a sizable brain region that is hypoperfused but not yet infarcted (a criterion that currently excludes over one-half of patients from consideration for rt-PA [24,25]) • Confirmation of a persisting and disabling deficit • Confirmation that patient selection criteria are met • Confirmation that the noncontrast head CT is without hemorrhage or major early infarct signs • Two intravenous lines, preferably large bore • Confirmation of blood pressure parameters • Wherever possible, vascular imaging studies (extracranial and intracranial ultrasound, CTA, MRA) should show no occlusive thromboembolus.
Intracranial hemorrhage is the most severe complication of thrombolytic therapy, occurring in approximately 6 percent of patients [21]. No patient characteristics can be identified at presentation that reliably predict whether a patient will or will not suffer a hemorrhage as a result of treatment with rt-PA. However, patients with very severe strokes and those with evidence of major infarction on CT may be at an increased risk for intracerebral hemorrhage following treatment [26,27]. Other predisposing factors for ICH include an elevated baseline serum glucose (>11.1 mmol/L or 200 mg/dL) and a history of diabetes mellitus [28].
Patients need to be advised of the potential risks and informed consent must be obtained prior to administering thrombolytic therapy.
DETERMINING A PRESUMPTIVE DIAGNOSIS OF STROKE SUBTYPE – After completing the initial assessment, the goal of the subsequent evaluation is to determine the underlying pathophysiology of the stroke in order to guide therapy. This part of the discussion assumes that patients with subarachnoid hemorrhage have already been identified by the initial history and physical examination and noncontrast head CT (with or without lumbar puncture). A review of the clinical features and diagnosis of subarachnoid hemorrhage is found separately. In addition, the presence of intracerebral hemorrhage should already be evident by this phase of the evaluation; the diagnostic evaluation in these patients is a separate issue (see below).
In practice, then, this second stage of evaluation is focused upon distinguishing between embolic and thrombotic strokes; in patients with the latter, it is worth differentiating between large vessel and small vessel (penetrating artery or lacunar) infarcts since the causes, outcomes, and treatments are different. A presumptive diagnosis of the stroke subtype can be made following a thorough history, physical examination, and imaging study such as CT or MRI. However, confirmation of the diagnosis requires more extensive testing.
A history of carotid stenosis is a significant risk factor for large artery thrombotic stroke, but these patients need to have other stroke subtypes considered in the differential diagnosis. In the North American Symptomatic Carotid Endarterectomy Trial (NASCET), of patients with 70 to 99 percent stenosis who subsequently experienced an ischemic stroke, 20 and 45 percent of strokes that occurred in the territory of symptomatic and asymptomatic carotid arteries, respectively, were unrelated to carotid stenosis [29].
History – A number of features in the clinical history may be useful in determining the type of stroke:
• Clinical course • Ecology • Previous transient ischemic attack (TIA) • Activity at the onset or just before the stroke • Associated symptoms
Clinical course – The most important historical item for differentiating stroke subtypes is the pace and course of the symptoms and signs and their clearing [30]. Each subtype has a characteristic course [31].
• Embolic strokes most often occur suddenly (show figure 2). The deficits indicate focal loss of brain function that is usually maximal at onset. Rapid recovery also favors embolism.
• Thrombosis-related symptoms often fluctuate, varying between normal and abnormal or progressing in a stepwise or stuttering fashion with some periods of improvement (show figure 3).
• Penetrating artery occlusions usually cause symptoms that develop during a period of hours or at most a few days (show figure 4), compared with large artery-related brain ischemia, which can evolve over a longer period.
• Intracerebral hemorrhage (ICH) does not improve during the early period; it progresses gradually during minutes or a few hours (show figure 5).
• Aneurysmal SAH develops in an instant. Focal brain dysfunction is less common.
Patients often do not give a specific history regarding the course of neurologic symptoms. I may ask if the patient could walk, talk, use the phone, use the hand, etc, as the events developed after the first symptoms occurred [30].
Ecology – Ecology refers to known demographic and historical features that provide probabilities of the patient having one or more of the stroke subtypes. Age, sex, and race are important demographic variables known to the clinician before taking the history [31].
• Most thrombotic and embolic strokes related to atherosclerosis occur in older patients. Individuals under age 40 rarely have severe atherosclerosis unless they also have major risk factors such as diabetes, hypertension, hyperlipidemia, smoking, or a strong family history. In contrast, cardiac-origin embolism is common in young people who are known to have heart disease.
• Hypertensive ICH is more common among blacks and individuals of Asian descent than among whites.
• Premenopausal women have a lower frequency of atherosclerosis than men of similar age unless they have major stroke risk factors. Even after adjusting for age, the incidence of atherosclerotic stroke is four-times higher in men [32].
• Blacks, Asians, and women have a lower incidence of occlusive disease of the extracranial carotid and vertebral arteries than white men.
Hypertension is the most common and most important stroke risk factor [33,34], including isolated systolic hypertension [5,35]. An analysis of nine major prospective observational studies, for example, found a continuously increasing risk of stroke with increasing diastolic blood pressure, even with pressures in the normal range (show figure 6) [33]. Prolonged reductions in the usual diastolic blood pressure of 5, 7.5, and 10 mmHg were associated with at least 34, 46, and 56 percent less stroke, respectively. A second overview of 14 treatment trials concluded that a long-term (mean five years) 5 to 6 mmHg decrease in the usual diastolic blood pressure was associated with a 35 to 40 percent reduction in stroke [34].
Chronic hypertension is a risk factor for both thrombotic extracranial and intracranial large artery disease and penetrating artery disease. Conversely, the absence of a history of hypertension or of present hypertension reduces the likelihood of penetrating artery disease.
Smoking increases the likelihood of extracranial occlusive vascular disease, more than doubling the risk of stroke [36]. The risk of ischemic stroke decreases over time after smoking cessation. In one series of middle-aged women, for example, the excess risk among former smokers largely disappeared two to four years after cessation [36]. Several other risk factors for stroke have been identified: • Diabetes increases the likelihood of large and small artery occlusive disease. • The use of amphetamines increases the likelihood of both ICH and SAH but not brain ischemia. • Cocaine-related strokes are often hemorrhagic (ICH and SAH), due to aneurysms and vascular malformations [4]. Cocaine is also associated with brain ischemia, especially involving the posterior circulation intracranial arteries; this is probably due to vasoconstriction. • Heart disease, including cardiac valvular disease, prior myocardial infarction, atrial fibrillation, and endocarditis, increases the probability of a stroke due to embolism. • Stroke during the puerperium has an increased likelihood of being related to venous or arterial thrombosis. • The presence of a known bleeding disorder or prescription of warfarin or other anticoagulants predisposes to hemorrhage, into either the brain or the CSF.
The link between stroke and oral contraceptive use has been a controversial issue. Initial studies suggesting this association were performed with oral contraceptives containing higher doses of estrogen [37]; excess risk may not be present with current low dose oral contraceptives [38,39].
The presence of these risk factors increases the odds that a stroke is due to a particular mechanism, but the clinician cannot make a firm diagnosis simply on the basis of probability. As examples: some conditions such as hypertension predispose to more than one subtype (thrombosis, intracranial hemorrhage); the presence of a prior myocardial infarction increases the likelihood of cardiac origin embolism, but also increases the likelihood of carotid and vertebral artery neck occlusive disease (thrombosis); and an older patient with severe atherosclerosis may also harbor an unexpected cerebral aneurysm.
Previous transient ischemic attack – A history of TIA (especially more than one) in the same territory as the stroke strongly favors the presence of a local vascular lesion (thrombosis). Attacks in more than one vascular territory suggest brain embolism from the heart or aorta. TIAs are not a feature of brain hemorrhage.
Patients often will not volunteer a prior history of symptoms consistent with a TIA. Many patients, for example, do not relate prior hand or eye problems to subsequent leg problems. Thus, the physician must ask directly about specific symptoms. "Did your arm, hand, or leg ever transiently go numb?" "Did you ever having difficulty speaking?" "Did you ever lose vision? If so, in which part of your vision? Was it in one eye and, if so, which one?"
Activity at the onset or just before the stroke – Hemorrhages (ICH and SAH) can be precipitated by sex or other physical activity, while thrombotic strokes are unusual under these circumstances. Trauma before the stroke suggests traumatic dissection or occlusion of arteries or traumatic brain hemorrhage. Sudden coughing and sneezing sometimes precipitates brain embolism. Similarly, getting up during the night to urinate seems to promote brain embolism (a matudinal embolus).
Associated symptoms – The presence of some associated symptoms are suggestive of specific stroke subtypes. • Fever raises the suspicion of endocarditis and resulting embolic stroke. • Infections activate acute phase blood reactants, thereby predisposing to thrombosis. • Headache is typically a feature of hemorrhagic strokes, but some patients have headaches in the prodromal period before thrombotic strokes. • Vomiting is common in patients with ICH, SAH, and posterior circulation large artery ischemia (show figure 1). • Seizures are most often seen in patients with lobar ICHs or brain embolism; they are rare in patients with acute thrombosis. • Reduced alertness favors the presence of hemorrhage. Accompanying neurologic signs are suggestive of ICH, while the absence of focal signs suggests SAH. Loss of consciousness is also common in patients with thrombotic and embolic strokes that are large or involve the posterior circulation large arteries.
Physical examination – Important clues in the general physical examination include the following: • Absent pulses (inferior extremity, radial, or carotid) favors a diagnosis of atherosclerosis with thrombosis, although the sudden onset of a cold, blue limb favors embolism. • The internal carotid arteries in the neck cannot be reliably palpated but, in some patients, occlusion of the common carotid artery in the neck can be diagnosed by the absence of a carotid pulse. • The presence of a neck bruit suggests the presence of occlusive extracranial disease, especially if the bruit is long, focal, and high pitched. • Palpating the facial pulses is helpful in diagnosing common carotid and internal carotid artery occlusions and temporal arteritis. The facial pulses on the side of the occlusion are often lost with common carotid artery occlusions. In contrast, some patients with internal carotid artery occlusion will have increased facial pulses on the side of the occlusion because collateral channels develop between the external carotid artery facial branches and the carotid arteries intracranially. • Cardiac findings, especially atrial fibrillation, murmurs and cardiac enlargement, favor cardiac-origin embolism. • Careful examination of the optic fundus may reveal a cholesterol crystal, white platelet-fibrin, or red clot emboli. Subhyaloid hemorrhages in the eye suggest a suddenly developing brain or subarachnoid hemorrhage. When the carotid artery is occluded, the iris may appear speckled and the ipsilateral pupil can become dilated and poorly reactive. The retina in that circumstance may also show evidence of chronic ischemia (venous stasis retinopathy).
Neurologic examination – The patient's account of his or her neurologic symptoms and the neurologic signs found on examination tell more about the location of the process in the brain than the particular stroke subtype. The blood supply to various parts of the brain and associated neurologic findings are shown(show figure Anterior cerebral, middle cerebral, posterior cerebral, mid-pontine, inferior pontine, medullary ). Nevertheless, some constellations of symptoms and signs occasionally suggest a specific process (show table 4). • Weakness of the face, arm, and leg on one side of the body unaccompanied by sensory, visual, or cognitive abnormalities (pure motor stroke) favors the presence of a thrombotic stroke involving penetrating arteries or a small ICH. • Large focal neurologic deficits that begin abruptly or progress quickly are characteristic of embolism or ICH. • Vertigo, staggering, diplopia, deafness, crossed symptoms (one side of the face and other side of the body), bilateral motor and/or sensory signs, and hemianopsia suggest involvement of the posterior circulation. • Abnormalities of language suggest anterior circulation disease, as does the presence of motor and sensory signs on the same side of the body. • The sudden onset of impaired consciousness in the absence of focal neurologic signs is characteristic of SAH.
Imaging studies – The location and size of a brain infarct on CT or MRI may further aid in distinguishing between stroke subtypes. • Small subcortical (deep) infarcts are most commonly located in the basal ganglia, internal capsule, thalamus, and pons. They are potentially within the blood supply of a single penetrating artery. The most common cause of a small deep infarct is lacunar infarction due to degenerative changes in the penetrating arteries. • Brainstem and cerebellar infarcts are most commonly caused by brain embolism. On the other hand, large subcortical infarcts, infarcts that are limited to the cerebral cortex, and infarcts that are both cortical or subcortical are commonly caused by thrombosis or embolism. The remainder of this overview, including confirmation of the diagnosis and evaluation of the patient with ICH, is discussed separately. (See "Overview of the evaluation of stroke-II").
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