Rafael H. Llinas
Constance J. Johnson
Overview
Epidemiology
Cerebrovascular disease (CVD) is a major cause of disability and the third leading cause of death in the United States. According to 2005 American Heart Association (AHA)
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estimates, the annual cost is more than $393.5 billion in direct and indirect costs and there are 4.7 million stroke survivors (2.3 million men, 2.4 million women) (1). Approximately 28% of strokes occur in people younger than age 65 years; men have a 26% greater odds of sustaining a first stroke than women (2). The annual death rate from stroke is higher in African Americans; compared with whites, young African Americans have a two- to threefold greater risk of ischemic stroke, and African American men and women are more likely to die of stroke (1).
Stroke incidence and death rate from stroke have decreased in recent years. This epidemiology of stroke reflects changing risk and demographics as well as more universal application of preventive measures. From 1992 to 2002 death rates from CVD (International Classification of Diseases (and Related Health Problems), 10th edition [ICD-10]) declined 18.0%, while actual CVD deaths increased 0.8% in the same period, (probably reflecting the aging population). Studies in the 1980s showed that stroke incidence had decreased nationwide and worldwide, but this decline stabilized after 1990 (3). Factors that may have contributed to the initial decline include more aggressive treatment of hypertension, more effective and early delivery of health care, and better management and recognition of the cardiogenic sources of cerebral embolization. This is supported by the finding of a community-based study that found a 40% reduction in the incidence of stroke in the past 20 years, as well as significant reductions in smokers, mean total cholesterol, mean systolic and diastolic blood pressures, and increases in preventive treatments (4). Unfortunately, among adults age 18 years and older, the prevalence of two or more risk factors increased from 23.6% in 1991 to 27.9% in 2002 (1).
Ischemic CVD presents two major challenges in ambulatory practice: the prevention of stroke in the large number of people with risk factors that make them prone to stroke and the optimal care of the many stroke survivors in each community. Brain hemorrhage is an acute problem usually presenting to the emergency room and requiring hospitalization and is not covered in this chapter.
Risk Factors and Prevention
A major goal of patient evaluation in ambulatory practice is the identification of the patient with an increased risk of stroke. Stroke risk factors identified in the Framingham study are age, systolic blood pressure, use of antihypertensive therapy, diabetes mellitus (DM), smoking, prior cardiovascular disease, atrial fibrillation, and left ventricular hypertrophy by echocardiogram (5). Subsequent observational data indicated the importance of blood cholesterol, especially for those younger than the age of 45 years (6). In the United States, ethnicity is an important risk factor; blacks have the highest stroke mortality rates, followed by non-Hispanic whites and Asians; Native Amricans and Hispanics have the lowest stroke mortality rates (3).
Patients who have previously had a stroke or transient ischemic attack (TIA) are an important subgroup of this high-risk population. A population-based study found that the risk of stroke after TIA was 9.5% at 90 days, and 14.5% at 1 year (7). The risk of combined stroke, myocardial infarction (MI), or death in this population was 21.8% at 1 year. One in six survivors of a first-ever stroke experience a recurrent stroke over the next 5 years, of which 25% are fatal. The greatest risk of recurrence is in the first 6 months after first stroke (8).
Prevention of stroke includes attention to modifiable risk factors as discussed below, and can be separated into primary prevention and secondary prevention (Table 91.1) (9,10).
Hypertension
Data accumulated during the Framingham study indicate that the risk of stroke is strongly related to hypertension. Atherothrombotic brain infarction occurred in hypertensive subjects (blood pressure greater than 160/95 mm Hg) four times more often than in normotensive subjects (5). Evidence from large controlled trials shows that stroke risk and other cardiovascular disease risk is significantly reduced by the treatment of hypertension in all patients, including those with a history of CVD (11, 12, 13, 14, 15, 16). The risk reduction for first stroke with treatment of hypertension was 35% to 47% in these trials. Reduction in stroke risk with treatment of hypertension occurs rapidly, and the lower the blood pressure, the lower the risk of stroke, with no apparent threshold below which there is no further reduction in risk (17). A meta-analysis of nine randomized trials (62,605 hypertensive patients) revealed that calcium channel blockers (CCBs) and angiotensin-converting enzyme inhibitors (ACEIs) reduced cardiovascular events including stroke with reduction in systolic blood pressure. Although all antihypertensive agents were believed to have similar long-term efficacy and safety, a combination of ACEIs and diuretics have been shown very effective in preventing stroke (18). The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack (ALLHAT) trial indicated that blacks may derive greater blood pressure reduction and stroke risk reduction from chorthalidone than lisinopril (19). Chapter 67discussses the evaluation and long-term management of hypertension.
Lipids
There have been many trials studying β-hydroxy-β-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (see Chapter 82), all of which have shown benefit in lowering chances of having first or recurrent stroke. A meta-analysis of three placebo-controlled randomized
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trials (19,768 patients) concluded that pravastatin 40 mg/ day reduced ischemic stroke risk 23% across a range of lipid levels with no evidence for benefit in hemorrhagic stroke or stroke of unknown type (6,20). Unfortunately, control of lipids through diet or bile acid sequestering agents have not been found to reduce stroke rates. Target levels of low-density lipoprotein (LDL) cholesterol have not been specified for stroke risk reduction, but should follow similar guidelines to those for cardiac risk reduction (see Chapter 82).
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TABLE 91.1 Effectiveness of Stroke Prevention Strategies |
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Diabetes Mellitus
Although the presence of DM confers additional risk of stroke, there are no randomized controlled trials (RCTs) demonstrating that tight glucose control in itself reduces risk of stroke. The UK Prospective Diabetes Study found that tight blood sugar control improves microvascular but not macrovascular endpoints in diabetes (21). This same cohort has found that diabetic patients with fatal stroke had higher glycosylated hemoglobin (HbA1c) levels, than those with nonfatal stroke (odds ratio 1.37 per 1% HbA1c) (22). Tight control of glucose with metformin in overweight and obese patients is the only regimen that has been shown to reduce the incidence of macrovascular complications in diabetes (23,24).
Smoking
Cigarette smoking is a predictor of the presence of significant intracranial and extracranial vascular stenosis (25). The duration of cigarette smoking is predictive of extracranial carotid artery stenosis detected by duplex scanning (26). In the Heart Outcomes Prevention Evaluation (HOPE) trial, the risk of stroke among smokers was 1.42 (95% confidence interval [CI] 1.00–2.04) compared with nonsmokers (27). Importantly, the risks for former smokers were the same as for those who had never smoked,
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suggesting the importance of smoking cessation in this population. As noted below, the major risk to survival in stroke patients is cardiac morbidity, so the implementation of smoking cessation counseling is indicated for this reason alone (see Chapter 27).
Cardiac Impairment
Patients with previous MI and/or cardiac impairment are predisposed to stroke, either directly because of emboli from the heart that lodge in cerebral arteries and lead to cerebral infarction, or indirectly because chronic atherosclerotic cardiac disease is associated with atherothrombotic cerebral disease. Cardioembolic stroke accounts for 15% to 30% of all ischemic strokes and is highly associated with cardiac arrhythmias, particularly atrial fibrillation with or without valvular disease, valvular disease, recent MI, and dilated cardiomyopathy (25). Data from the Framingham study identified cardiac impairment as a significant risk factor in the occurrence of the more common nonembolic atherothrombotic brain infarction. Subjects with electrocardiographic evidence of left ventricular hypertrophy were nine times more likely to develop atherothrombotic brain infarction than those without this abnormality. Patients with coronary artery disease (CAD) had five times the risk of atherothrombotic brain infarction, and those with radiographic evidence of cardiomegaly had three times the risk. When the contribution of concomitant hypertension was eliminated, left ventricular hypertrophy and CAD were each associated with a threefold increase in the risk of atherothrombotic brain infarction; the contribution of cardiomegaly on radiograph was not found to be significant when other variables were controlled. On the basis of these findings it was concluded that cardiac impairment, especially if associated with hypertension, significantly heightens the risk of stroke occurrence.
One of the most important modifiable risk factors is the presence of nonvalvular atrial fibrillation. A meta-analysis of five randomized trials of warfarin or aspirin in nonrheumatic atrial fibriallation concluded that the use of warfarin resulted in a 68% reduction in the risk of stroke (28). The annual rate of stroke in the control group was 4.5%, which was similar to the Framingham study, which found an annual stroke rate of 5%. Risk factors that predicted stroke were age, hypertension, previous history of stroke or TIA, and diabetes. Patients younger than age 65 years with none of these risk factors had an annual stroke rate of 1%. Risk reduction for aspirin in this population was not as consistent, averaging 36%. The current recommendations are to use long-term anticoagulation in all patients with chronic atrial fibrillation, with the exception of those at low risk, targeting an international normalized ratio (INR) = 2.0 to 3.0 (29,30). Patients younger than age 60 years with no risk factors may be treated with aspirin 325 mg daily (29,30).
Other Factors
Elevated blood hemoglobin and hematocrit levels have been implicated as possible risk factors, but a cause-and-effect relationship has not been established. Oral contraceptive use is associated with a five- to 10-fold increase in the risk of vascular diseases, including stroke (see details in Chapter 100). Observational studies initially indicated a decreased risk of ischemic stroke for postmenopausal hormone replacement therapy users (31). The Women's Health Initiative study, however, which studied 10,739 postmenopausal women, age 50 to 79 years of age, found a significant increased effect on the risk for stroke (32). Finally, it is generally accepted that the presence of an asymptomatic cervical bruit correlates with an increased incidence of subsequent stroke, but there is controversy regarding the approach to patients with this finding (see Asymptomatic Carotid Stenosis).
Asymptomatic Carotid Stenosis
Asymptomatic carotid stenosis is detected by the presence of a cervical bruit or because a vascular screening test was performed (seeChapter 86). Bruits occur in 4.5% of the population older than 45 years of age (33). A bruit is not pathognomonic of underlying stenosis (Table 91.2). A duplex scan (see description in Chapter 86) can define which patients with bruits have carotid stenosis and require further evaluation. Stenosis exceeding 75% to 80% of the lumen is associated with an annual risk of ipsilateral stroke of 2% to 3%. A large controlled trial (Asymptomatic Carotid Atherosclerosis Study [ACAS]) demonstrated that, for asymptomatic patients with more than 60% stenosis of the carotid artery, the combination of medical management (risk factor reduction and 325 mg aspirin per day) and carotid endarterectomy was superior to medical management alone (34). Over 5 years, the projected
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incidence of morbid events (perioperative death or stroke) was 5.1% for carotid endarterectomy patients, and the incidence of ipsilateral stroke was 11.0% for patients treated medically (an aggregate risk reduction of 53%). Patients to whom carotid endarterectomy is offered should be told that in ACAS there was approximately a 3% risk of perioperative stroke or death with carotid endarterectomy and that the benefit found in the ACAS trial accrued over 5 years.
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TABLE 91.2 Possible Causes of Cervical Bruit |
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Patients with excess cardiac risk were excluded from the ACAS trial. Medical management alone would probably benefit the latter group. Information about the symptoms of TIA should be given to any patient with a cervical bruit so that the patient does not ignore warning symptoms. The American Heart Association (AHA) has excellent patient education materials on TIA.
Classification of Cerebrovascular Events
Type of Event
Symptoms and signs of vascular origin are characterized by the rapid onset of deficits in a vascular distribution. The following classification has been developed based on duration:
Vascular Territory
Cerebrovascular events are also classified on the basis of the vascular territory involved. Table 91.3 lists symptoms and signs referable to the two major vascular territories. There is overlap in the symptoms that may make the distinction between carotid and vertebrobasilar disease difficult. The history alone often provides the evidence necessary to identify the arterial territory involved.
A subgroup of ischemic events, called lacunar syndromes, is caused by occlusion of penetrating nonanastomosing branches of the major cerebral arteries. The pathology of the involved vessels has been characterized: occlusion is caused either by miniature atherosclerotic plaques at the origin of vessels 400 to 1000 µm in diameter or, more commonly, by a degenerative process called lipohyalinosis affecting vessels 200 µm or less in diameter. These changes correlate strongly with the presence of hypertension. At least 20 clinical lacunar syndromes have been described (35); lacunar infarctions may also be silent, identified only by computed tomography (CT) or magnetic resonance imaging (MRI). The common syndromes include the following:
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TABLE 91.3 Clinical Features of Ischemia Involving the Major Vascular Territories |
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Symptomatic Patients
Transient Ischemic Attack and Stroke
Most TIAs and strokes are caused by artery-to-artery embolization, cardiogenic embolus, or small vessel (lacunar)
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disease. The distinction between TIA and stroke is becoming less important because a rigorous search for cause is indicated in both and many patients with TIA have evidence of brain infarction on imaging. Treatment is based on cause of the event regardless of whether the patient has had a TIA or stroke. Both events signal brain ischemia; stroke occurs when blood supply from collateral vessels is insufficient or the occluding thrombus is too large to be rapidly cleared.
For patients with TIA, other transient neurologic events described elsewhere, such as seizure (see Chapter 88), hypoglycemia (see Chapter 81), syncope (see Chapter 89), and migraine (see Chapter 87) must be considered. A Todd paralysis (transient focal weakness after a focal motor seizure or secondarily generalized tonic–clonic seizure) is diagnosed when the primary event is a seizure. Transient episodes with altered consciousness are almost never vascular in nature. Migraine occurs primarily in younger patients, is associated with headache, and must conform to defined criteria (see Chapter 87). A mass lesion such as a tumor or subdural hematoma may present with transient neurologic symptoms; however, these patients usually have persistent signs and symptoms. CT or MRI (see Chapter 86) is diagnostic. Occasionally, an acute exacerbation of multiple sclerosis may mimic TIA; however, these patients are usually younger and have had multiple episodes with nonvascular localization (e.g., optic neuritis).
Evaluation
Initial evaluation of the patient with TIA or stroke may be in the hospital (the patient who presents within hours or days of the event) or in the ambulatory setting (the patient who presents within weeks of the event). A detailed history is essential to identify risk factors for CVD and to delineate and classify the focal symptoms. The physical examination should include assessment for hypotension, hypertension, cardiac disease, CVD, and peripheral vascular disease, and any persisting neurologic abnormality. The patient should also have a careful funduscopic evaluation to assess the status of the retinal vessels and to detect emboli that suggest atherothrombotic carotid occlusive disease or cardiac disease. A brain MRI or CT (see Chapter 86) can localize the event, demonstrate previous silent events, and rule out other causes of neurologic symptoms that mimic CVD.
If there is clinical evidence of heart disease, in particular a murmur, atrial fibrillation, or left ventricular dysfunction, a transesophageal echocardiogram should be obtained to look for a cardiac source of arterial emboli. Transesophageal echocardiogram can also evaluate the aortic arch as a source of embolism. In patients with heart disease, ambulatory cardiac monitoring to check for arrhythmias may be beneficial when the cause of the stroke remains unknown after duplex and transesophageal echocardiogram.
Screening tests to check for treatable causes of occlusive CVD include a serologic test for syphilis, hematocrit measurement (polycythemia), and erythrocyte sedimentation rate (vasculitis). If a hypercoagulable state is suspected, anticardiolipin antibodies, anti-nuclear antibodies (AN) and homocysteine levels should be obtained (36).
Patients with carotid territory events should have a noninvasive carotid evaluation, using the available technique with the best performance characteristics. A meta-analysis of the various available procedures shows that the preferred noninvasive technique is duplex ultrasonography (37). Chapter 86 describes the characteristics of duplex ultrasonography and the patient experiences associated with it and other noninvasive diagnostic tests.
Cerebral angiography (see description in Chapter 86) should be considered in patients who do not have a definite source of brain embolus identified in the heart, aortic arch, or carotid arteries. Although a duplex scan can rule out carotid stenosis, intracranial vascular disease cannot be identified conclusively by duplex. A limited (noninvasive) evaluation can be justified if the patient's event was so devastating that further evaluation and treatment are precluded.
Early Management
Atherothrombotic Events
Patients with atherothrombotic events, either cortical or lacunar, may be treated medically or surgically.
Medical Therapy
This aspect of management includes risk factor modification and anticoagulant and antiplatelet drugs.
Antihypertensive therapy after an acute ischemic stroke is usually deferred until the patient's neurologic deficit is stable. In a small controlled study of hypertensive patients who had sustained a nonembolic ischemic stroke, 44% of the untreated patients, compared with 20% of the treated patients, suffered another major stroke, and at the end of a 2- to 5-year followup period, 46% of the untreated patients and 26% of the treated patients had died (38). Although the number of recurrent strokes was small, the difference in mortality was statistically significant in favor of the treated group. A meta-analysis of nine trials of blood pressure–lowering agents in hypertensive and nonhypertensive stroke survivors revealed a 28% reduction in stroke recurrence with treatment of hypertension (39). The Preventing Strokes by Lowering Blood Pressure in Patients with Cerebral Ischemia (PROGRESS) trial, a large, randomized, placebo-controlled trial of the ACEI perindopril with and without the diuretic indapamide demonstrated a 43% decrease in recurrent stroke risk in both hypertensive and nonhypertensive stroke and TIA survivors who received both drugs. Perindopril alone lowered
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blood pressure without affecting stroke recurrence (40). A subsequent meta-analysis found similar reductions in risk of stroke (21% to 24%) with antihypertensive treatment, with ACEIs and diuretics being the most effective (41). Although questions remain about subgroups and specific medications, treatment of hypertension in stroke survivors appears beneficial. (See Chapter 67 for details on the treatment of hypertension.)
The antiplatelet drugs aspirin, aspirin and dipyridamole (42), ticlopidine (43), and clopidogrel (44,45) are effective in reducing the recurrence of TIA or stroke. Aspirin is the most widely studied and cheapest agent, with effectiveness in doses of 50 to 1,500 mg (46). Ticlopidine's side-effect profile (fatal neutropenia, diarrhea) outweighs its modest statistical advantage. Clopidogrel's efficacy in secondary stroke prevention was only evident as a combined reduction in MI, stroke, or vascular death (44). The combination of aspirin and clopidogrel has been shown not only not to be more protective but to lead to higher rates of intracerebral and extracerebral hemorrhages (45). In the European Stroke Prevention Study II (ESPS II) trial, aspirin plus dipyridamole (25 mg plus 200 mg twice daily) was compared with aspirin alone (25 mg twice daily), extended-release dipyridamole alone (200 mg twice daily), or placebo. There was a 23.1% reduction of stroke in those on combination therapy compared with aspirin alone. Side effects were minor: headache and gastrointestinal (GI) events with dipyridamole and bleeding and GI events with aspirin, with the combination not significantly affecting side-effect incidence (42). Chapter 57lists additional details regarding the use of and efficacy of antiplatelet drugs.
Anticoagulant therapy with warfarin (INR 1.4 to 2.8) was compared with aspirin (325 mg/day) in a large, double-blind, randomized trial (Warfarin-Aspirin Recurrent Stroke Study [WARSS]) in patients with prior noncardioembolic stroke, most with lacunar (55% in warfarin group, 56% in aspirin group) or cryptogenic (25% in warfarin group, 26% in aspirin group) stroke. Over 2 years of followup there was no difference in the rates of ischemic stroke, death, or major hemorrhage (approximately 17% in both groups) (47). Warfarin has been recommended for symptomatic patients (TIA or stroke) with known high-grade intracranial stenosis or preocclusive extracranial carotid bifurcation disease that cannot be addressed surgically (e.g., in patients who have cardiac disease precluding surgery). The prospective trial (Warfarin-Aspirin Symptomatic Intracranial Disease [WASID]) trial, however, showed no benefit of warfarin over aspirin and indeed found that there were more fatal events on warfarin than aspirin (48). Ongoing trials of higher on-treatment INRs and of warfarin in subgroups of patients will determine whether warfarin should be recommended for some patients. Based on all available data, aspirin appears superior in most patients with noncardioembolic strokes. Patients with significant intracranial disease probably should not be treated with warfarin unless recurrent events occur without remission; intracranial angioplasty is probably indicated in these patients. A role for cholesterol lowering in secondary stroke prevention was examined in a meta-analysis that included patients with stroke. Risk was reduced by 25% (49).
Surgical Therapy
Carotid endarterectomy can be recommended to patients with hemispheric or retinal TIAs or nondisabling stroke with ipsilateral severe (70% or greater) stenosis at the carotid bifurcation. This recommendation is supported by a large clinical trial (North American Symptomatic Carotid Endarterectomy Trial [NASCET]) in which 9% of carotid endarterectomy patients versus 26% of patients receiving antiplatelet treatment experienced an ipsilateral stroke during the 2 years after initiation of treatment (50). For symptomatic patients with moderate (50% to 69%) stenosis, the rate of stroke (average followup of 5 years) was 15.7% in the surgical group compared with 22.2% in the medical group (p = 0.045), a modest benefit compared with the benefit in patients with more severe stenosis. For stenosis less than 50%, there was no benefit (51). Patients who have undergone carotid endarterectomy are usually continued on long-term antiplatelet therapy.
In patients with recurrent TIAs or strokes and arteriographic evidence of severe vertebral or basilar artery stenosis, bypass procedures, angioplasty, and stenting have been undertaken. The efficacy of these procedures has not yet been established. Because the guidelines for the treatment of patients with TIAs and survivors of stroke are still evolving, the advice of a neurologist who specializes in CVD should be sought.
Cardioembolic Events
Patients with cardioembolic events who benefit from anticoagulation with warfarin include those with atrial fibrillation (both valvular and nonvalvular disease), recent MI, dilated cardiomyopathy, and rheumatic and prosthetic valves. Clinical trials consistently show a reduction in expected events in anticoagulated patients with atrial fibrillation; for those who have had a TIA or minor stroke the annual incidence of a new event is reduced from 12% to 4% and for those with no history of TIA or stroke, the annual incidence is reduced from approximately 5% to 2% (52). Chapter 57 describes specific aspects of anticoagulant therapy to prevent cerebrovascular accident; other chapters cover postinfarct mural thrombi (see Chapter 63), atrial fibrillation (see Chapter 64), and valvular heart disease (see Chapter 65). For patients with both a cardiac source and high-grade carotid stenosis (70% or higher) proximal to the territory of a TIA or stroke, carotid endarterectomy should be considered.
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Stroke Prognosis
Morbidity in Stroke Survivors
A number of studies have evaluated stroke survivors on the basis of the degree of neurologic, functional, and psychosocial impairment. In a 1975 study of stroke survivors, half of the patients (63 of 123) had no motor defecit when examined 6 months to 33 years (mean, 7 years) after the event (53). Right and left hempiparesis were equally represented; dysarthria and dysphasia were associated with right hemiparesis in 13 and 9 of 27 survivors respectively. These findings are probably representative of the situation in other communities.
In a classic study of overall function, Katz et al. (54) found that of patients who survive a stroke, approximately 50% are independent 2 years later and can ambulate and perform activities of daily living with minimal or no assistance. Spontaneous improvement is most rapid in the first few months after the stroke and is rarely noted after 2 years. Only a small percentage of stroke survivors remain bedridden and completely dependent. These findings were corroborated by results from the Mayo Clinic, where only 4% of the community-dwelling survivors of a stroke required total care at 6 months, 36% had some degree of neurologic deficit yet were able to work, and 29% were functioning normally (55). On the basis of the authors’ assessment, 54% of their patients may have benefited from rehabilitative care, including the 10% who were aphasic.
The Framingham study provided information on the equally important social and psychologic sequelae of stroke (53). A significant decrease in the levels of vocational function and socialization outside the home was noted among stroke survivors (compared with age- and sex-matched control subjects), and the decrease exceeded that anticipated based on the levels of neurologic deficit. In a prospective study, the social and psychologic difficulties facing the stroke survivor were evaluated in more detail (56). Within the first 6 months after hospital discharge, 37% of the patients demonstrated moderate or severe depression, 32% anger or anxiety, 56% social isolation, 43% reduction in community involvement, 46% economic strain causing life-style alteration, and 52% disruption of normal family functions. Additional studies have confirmed the high incidence of moderate or severe depression in the first year after stroke and have shown that the risk of depression is particularly high in patients with damage in the left frontal hemisphere. Longitudinal studies show that poststroke depression lasts up to 2 years (57). Patients with poststroke depression respond well to antidepressant therapy (see Management of Psychologic and Behavioral Sequelae). Recognition and treatment of the psychosocial problems of the stroke patient and family are discussed in more detail below.
Mortality in Stroke Survivors
The death rate among stroke survivors is significantly greater than that expected for the general population matched for age and sex. The 5-year cumulative mortality is approximately 50% to 60%, with the greatest number of deaths occurring in the first year. With time, however, the mortality rate approaches that of the general population, and in at least one study, the increased rate of death after a stroke subsided completely after 24 to 30 months (54).
Studies that classified strokes on the basis of type of vascular pathology indicate that the early prognosis is much better for thrombotic or embolic disease than for hemorrhage (55). There is evidence that the type of pathology is a less reliable predictor of late prognosis. Eisenberg et al. (58) reported that patients with cerebral hemorrhage who lived 1 month had a 5-year survival equal to or better than patients with cerebral thrombosis.
The leading cause of death in stroke survivors is cardiovascular disease, with cardiac-related deaths exceeding deaths attributed to CVD by a factor of 2 to 1. Because cardiac disease is a major contributor to the cause of the stroke, stroke recurrence, and the survival from stroke, thorough evaluation and management of cardiac disease are of great importance in the care of stroke survivors.
Long-term Management
Management of the patient who has survived a stroke involves the evaluation and treatment of physical and psychosocial sequelae and the selection of appropriate therapy to lessen the risk of recurrence. Once the patient has been discharged from the hospital, the patient's personal physician plays a critical role in coordinating care. Reduction in a patient's disability and dependency often requires the concerted efforts of the patient's family, physical, occupational, and speech therapists, and occasionally a psychiatrist. Patients with significant deficits persisting for 3 months or longer may qualify for disability insurance under Social Security (see Chapter 9).
Role of the Family
At the time of discharge from the hospital, appropriate education is especially important for the stroke survivor and the patient's family. At this juncture, patients are confronted with the full extent of their functional loss. By dispelling myths regarding stroke and supplanting them with accurate information, physicians and therapists can ensure that the actions of well-meaning family members do not foster the patients’ feelings of inadequacy.
The following general suggestions can be helpful for the family of a stroke patient with residual disability:
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Role of Rehabilitation
Success in stroke rehabilitation often depends on the extent of permanent damage and the patient's ability to use alternative methods of function to compensate for fixed deficits. As noted above, spontaneous improvement in the stroke survivor may continue to occur for the first 6 to 12 months after the stroke, yet the mechanisms underlying such gains remain obscure. In studies to determine whether intensive rehabilitation results in functional gains after the period of spontaneous improvement, it has been found that even significantly impaired patients admitted to a rehabilitation program 12 months after a stroke may show marked improvement in dressing skills, bladder and bowel function, and walking. These findings form the basis for the conclusion that a program of rehabilitation does improve the outcome of the stroke survivor. It is estimated that the savings derived in returning a patient to the family or to independent living more than equals the costs of rehabilitation.
It is clear that not all patients in a rehabilitation program show significant functional improvement. A number of patient characteristics correlate with poor rehabilitation results, including bowel and bladder incontinence, low self-care status on admission, right hemispheric involvement, intellectual and perceptual deficits, heart failure, signs of generalized arteriosclerosis, and lower educational levels. However, because none of these factors correlates strongly with poor outcome, the best approach is to offer rehabilitation services when possible to each stroke survivor with significant functional impairments.
It is generally agreed that, except for patients with evidence of subarachnoid bleeding, for whom bed rest and mild sedation are indicated, aprogram of functional rehabilitation should begin as soon as possible after a stroke occurs and the patient is stable. There are several reasons for the early initiation of a program of rehabilitation. First, it is generally accepted that patients who are provided with rehabilitation services early are likely to experience greater long-term functional improvement. Second, early transfer from bed to chair coupled with physical therapy reduces the complications that can develop in the immobile bedridden patient and that can subsequently limit the extent of functional recovery. Stretching of tight muscles, passive range of motion, and active or resistive exercises minimize the degree of muscle atrophy and prevent the development of contractures. Additionally, even limited mobility of the patient reduces the risk of circulatory complications such as thrombophlebitis, postural hypotension, and pressure sores. Third, early rehabilitation is of particular benefit to the patient who demonstrates an impaired ability to communicate because of either aphasia or dysarthria. Approximately one third of stroke patients exhibit some form of communication disorder, and many of these remain severely impaired beyond the period of spontaneous recovery. Such patients may feel desperately isolated because of their loss of ability to communicate. Therapists who specialize in speech and hearing are skilled in the evaluation and management of these problems and play an integral role in daily interactions with the patient and in recommending appropriate strategies to the patient's family and physician.
Everyone involved in the rehabilitation process must appreciate the significance of the functional losses sustained by the patient, so the losses must be viewed from the patient's perspective. This requires an awareness of the patient's usual activities before the stroke; this essential information should be obtained in conjunction with a social worker who can evaluate the patient's role at home before the stroke and can project how the stroke will alter that role when the patient returns home.
The rehabilitation initiated in the hospital can be continued after discharge. Most communities have physical, occupational, and speech therapists available for both home and ambulatory followup. For patients meeting eligibility criteria, these services are covered by third-party payers. The patient and family should be acquainted with the goals and plans for continued rehabilitation before discharge. Chapter 9provides information about home health services. The comprehensive text of Brandstater and Basmajian (http://www.hopkinsbayview.org/PAMreferences) provides details about the many individualized approaches available for rehabilitation.
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Management of Psychologic and Behavioral Sequelae
The high incidence of psychologic and behavioral problems among stroke survivors has been noted above. These problems often hinder rehabilitation efforts. Fear of a second stroke and depression caused by loss of functional ability are readily understandable in the context of the patient's predicament. Appropriate counseling of the patient and family (as outlined in Role of Rehabilitation), coupled with participation in an active rehabilitation program, are the best ways to minimize the adverse psychologic reactions to a stroke.
A number of stroke survivors experience mood disturbances that do not correlate with the level of functional disability, and there is evidence that for many patients the mood disorder is a specific complication of cerebral damage rather than a reaction to functional loss (57). This mood disorder may augment the cognitive impairment of the patient or on occasion may be expressed as an apparent cognitive impairment (pseudodementia of depression, described in Chapter 26). Response in such patients to antidepressant treatment may be dramatic. Earlier observations suggested that the type of mood disorder depends on the side of the brain affected by the stroke. Gainotti (59) reported that behavior denoting a catastrophic reaction (see Chapter 26) and anxious depressive orientation of mood (anxiety reactions, bursts of tears, provocative utterances, depressed renouncements, or sharp refusals to go on with the examinations) are more common among patients withleft (dominant) hemisphere damage. Symptoms denoting an opposite emotional reaction (denial of illness, minimization, indifference reactions, and tendency to joke) and expressions of hate toward the paralyzed limbs are more common among patients suffering from a lesion of the right (nondominant) hemisphere. Most authorities agree, however, that both psychological and physiologic factors contribute to the development of mood disorders after strokes. Tricyclic antidepressants have been shown to benefit patients with poststroke depression (57). Chapter 24 lists practical information about these and other antidepressant drugs.
The AHA booklet, How Stroke Affects Behavior, is particularly helpful for the family and for health care professionals caring for the patient who has survived a stroke.
Management of Late Complications
A number of complications may occur during the months to years after a stroke.
Shoulder Problems
The painful shoulder is one of the most disturbing complications encountered in the patient with a residual hemiparesis. Shoulder pain is often caused by increased traction on the shoulder capsule secondary to abnormal positioning of the paralyzed arm. The normal alignment of the joint can be restored through the use of a sling and proper positioning of the arm at night. Physical therapy, after initial symptomatic treatment with analgesics and the application of heat, can limit the extent of permanent structural damage (see Chapter 69 for additional details).
The shoulder–hand syndrome occurs in approximately 5% of stroke patients. It is characterized by the occurrence of a painful shoulder associated with stiffness and swelling of the hand and fingers. Onset is acute or subacute (developing over 3 to 6 months) and may involve the hand and shoulder simultaneously or one followed by the other. Although a number of conditions can result in shoulder discomfort, the dystrophic changes in the hand are characteristic of the development of a complex regional pain syndrome. There is swelling below the wrist, and the intrinsic muscles of the hand atrophy with extension deformities in the metacarpophalangeal joints. At this stage radiographic examination of the hand often shows spotty demineralization of the carpal bones. The severe pain associated with this condition greatly hinders rehabilitation efforts. Therefore, early recognition and treatment are important. A nonsteroidal anti-inflammatory drug (NSAID), local heat, and medications for chronic pain may be helpful.
Complications of Inactivity
The partially paralyzed stroke survivor often leads a sedentary existence, conducive to the development of vascular complications such as thrombophlebitis and pressure sores. Use of elastic stockings and frequent repositioning of the immobile patient by an informed family member minimizes these problems.
Neurologic Complications
Prolonged pressure on a paralyzed limb may lead to a peripheral nerve lesion, which may be difficult to recognize when superimposed on brain damage resulting from the stroke. An awareness of this potential complication can expedite its recognition, and electrodiagnostic studies can confirm the lower motor neuron damage (see Chapter 92). Once a diagnosis is made, prompt initiation of physical therapy limits the degree of functional loss resulting from this potentially reversible lesion.
Approximately 3% to 10% of stroke survivors develop seizures (epilepsy) as a late complication (60). Patients with damage to their sensorimotor cortex are the most likely to develop epilepsy, with the first seizure usually occurring 6 to 12 months after the stroke. Transient neurologic dysfunction after a seizure in a stroke survivor is often attributed to a second stroke. The rapid resolution of symptoms and electroencephalographic evidence of an
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epileptogenic focus point to seizure activity rather than ischemia as the cause. Recurrent seizures in the stroke survivor confirm the diagnosis of epilepsy. Seizure control can usually be achieved through the use of anticonvulsant medication (see Chapter 88).
Finally, stroke-related deficits may transiently worsen when the patient develops a major intercurrent illness such as pneumonia or myocardial infarction. In this instance, neurologic status returns to baseline after resolution of the intercurrent illness. (See discussion of upper motor neuron symptoms in Chapter 86.)
General Surgery
Chapter 93 addresses the approach to general surgery in patients who have a history of stroke.
Specific References*
For annotated General References and resources related to this chapter, visit http://www.hopkinsbayview.org/PAMreferences.
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