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(Circulation. 1997;96:701-707.)
© 1997 American Heart Association, Inc.

Articles

American Heart Association Prevention Conference IV: Prevention and Rehabilitation of Stroke

Executive Summary

Cathy M. Helgason, MD,; ; Philip A. Wolf, MD, Co-chairs

Key Words: AHA Medical/Scientific Statements • stroke • prevention

	Introduction

Top Introduction Etiology of Stroke Risk Factors Acute Interventions Rehabilitation

 
The American Heart Association Prevention Conference IV, "Prevention and Rehabilitation of Stroke," was held May 1-2, 1996, in Tucson, Ariz. The report of the conference presents the state of knowledge on stroke epidemiology, etiologic basis, treatment, and rehabilitation. The conference report in its entirety is published in the July 1, 1997, issue of Stroke. This executive summary appears in the July 15, 1997, issue of Circulation. Reprints of the executive summary and full text are available from the American Heart Association.

	Etiology of Stroke

Top Introduction Etiology of Stroke Risk Factors Acute Interventions Rehabilitation

 
Stroke results from either ischemia, due to arterial occlusion or stenosis, or hemorrhage, due to leakage or rupture of an artery. Differentiation cannot be reliably made from the history or clinical examination alone. Most—but not all—strokes have a sudden or rapid onset. Differential diagnosis of sudden change in focal neurological status includes seizures or postepileptic paralysis, hemorrhage into a tumor (itself a form of stroke), and migraine. Neuroimaging helps to differentiate between these and the cause of short-lived symptoms (transient ischemic attack [TIA]) usually due to ischemia but possibly due to new-onset infarction or hemorrhage. More precise classification of stroke into a pathogenic subtype evades the best clinical skills.

Ischemic Stroke Mechanism
Embolism to the brain. Embolism to the brain may be arterial or cardiac in origin. Commonly recognized cardiac sources include atrial fibrillation (AF), sinoatrial disorder, recent acute myocardial infarction (AMI), marantic or subacute bacterial endocarditis, cardiac tumors, and valvular disorders, both native and artificial.

Myocardial infarction. Stroke is an important complication in patients with AMI, occurring in 1% to 3% of all infarctions and in 2% to 6% of patients with anterior wall infarctions.

Atrial fibrillation. Pooling of blood in the dysfunctional atrium leads to clots and emboli. AF increases risk of thromboembolism up to 18 times. Risk of stroke in patients with AF can be reduced by up to 70% using oral anticoagulant therapy. Compared with placebo, aspirin reduces risk by 20% to 30%.

Valvular disease. Rheumatic mitral stenosis is the most common valve disorder associated with thromboembolism.

Mitral valve prolapse. Patients with mitral valve prolapse (MVP) who have suffered ischemic brain events should be given prophylactic anticoagulant medication. If they are asymptomatic, MVP patients do not need medication; if they have stroke symptoms, they should receive anticoagulation therapy.

Prosthetic heart valves. Tissue prosthetic valves are believed to be associated with a smaller risk of thromboembolism than mechanical valves.

Repaired cardiac valves. Surgical repair of the mitral valve for mitral insufficiency is lasting and has lower morbidity and mortality and a lower incidence of thromboembolism than valvular replacement. Percutaneous balloon mitral valvuloplasty is associated with significant risk of embolization.

Embolism of aortic arch origin. A causal link between brain infarcts and complicated plaques with highly mobile thrombi in the lumen of the aortic arch is likely. Plaques without mobile components might merely be markers for diffuse atherosclerosis.

Patent foramen ovale. The diagnosis of patent foramen ovale may be suspected in any stroke patient. When the patent foramen ovale is large, surgical closure may be an option.

Cerebral ischemia due to perfusion failure and arterial source for embolism. Stroke due to perfusion failure occurs with severe stenosis of the carotid and basilar artery and when there is microstenosis of the small deep arteries.

Large artery atherosclerotic plaque. Factors that lead these lesions to become symptomatic are not well understood, but stenoses >70% are linearly associated with increased risk of distal brain infarct.

Vasculitis. Inflammatory conditions can involve the cerebral vasculature. Their causes are poorly understood, and the bedside diagnosis is problematic for lack of an accurate noninvasive test and the relatively nonspecific nature of clinical manifestations.

Surgical management of large artery occlusive disease. The North American Symptomatic Carotid Endartectomy Trial (NASCET) demonstrated the benefit of surgery for patients with recent stroke or TIA with extracranial internal carotid artery stenosis ranging from 70% to 99%. The beneficial results in stroke prevention were largely dependent on the skill of the surgeons, who attained an acceptably low rate (5.8%) of perioperative stroke and death. In a European study, medical therapy was clearly superior to surgery at <30% stenosis. Results are awaited for the moderate phase of NASCET, for stenosis ranging from 30% to 69%.

The Asymptomatic Carotid Atherosclerosis Study (ACAS) demonstrated a benefit for surgery for stenosis >60% with low rates of perioperative complications. However, this conclusion is not universally accepted by the stroke community. Some believe the rate of surgical and angiographic complications do not warrant the 1% annual reduction in absolute risk of stroke.

Small artery occlusion. Small, deep cavitary (lacunar) infarcts are mainly due to small arterial occlusions, a fundamental principle in the pathogenesis of small deep infarcts.

Intrinsic small artery disease. Microatheroma may be the most frequent pathology underlying symptomatic lacunar infarcts.

Other causes of small vessel occlusion. Potential causes are (1) cardiogenic embolism; (2) rheumatic heart disease; (3) artery-to-artery embolism; (4) complications of aortic arch plaque; and (5) carotid stenosis and asymptomatic small deep infarcts.

Prothrombotic states. Primary prothrombotic states include abnormalities of certain hemostatic regulatory proteins, including the antithrombins, heparin cofactor II, proteins C and S, and fibrinolytic system derangements. Definitive studies of hemostatic disorders of large populations of subjects with stroke are lacking.

Recommendations

• Patients with MI who are at high risk for systemic embolization should receive oral anticoagulation at a target international normalized ratio (INR) range of 2.5 to 3.5 for 6 months or more.
• Patients with cardiac valvular disorders, prosthetic heart valves, and repaired valves have a variable risk of stroke. Their need for antiplatelet or anticoagulant therapy should be evaluated.
• In the absence of a mobile thrombus, the presence of aortic arch plaque >4 mm should be viewed as a marker of high risk of recurrent stroke, MI, peripheral embolism, and vascular death. The natural history of mobile aortic arch plaques, development of new noninvasive techniques to define plaque composition, and initiation of therapeutic trials may be topics for research in the future.
• When faced with lacunar infarction or syndrome, the possibility of underlying large-vessel, especially intracranial, cardiac source embolism and hypercoagulable state should be considered, as should small-vessel disease.
• Carotid endarterectomy is beneficial for patients with recent cerebral ischemia and ipsilateral carotid artery stenosis of 70% to 99%. It is not beneficial for patients with 0% to 29% stenosis, and it is still uncertain if it is beneficial for those with 30% to 69% stenosis.
• Much work is needed to define the spectrum and role of hypercoagulable states, including that of antiphospholipid antibodies, in stroke.
• The etiology (hemorrhage, ischemia versus non–stroke-related potential causes) of transient cerebral symptoms should be diagnosed in every patient who experiences them. For those for whom the cause is likely to be ischemic and who do not require warfarin, the best dose of aspirin for stroke prophylaxis is debated. Ticlopidine is more effective than aspirin, but the cost and risk of adverse effects are higher.

	Risk Factors

Top Introduction Etiology of Stroke Risk Factors Acute Interventions Rehabilitation

 
Public Health Burden of Stroke
The distribution of the burden of stroke morbidity and mortality is heterogeneous in the US population and is changing dramatically with time. Stroke mortality remains the third leading cause of death in the United States, accounting for 1 in every 15 deaths during 1992. Despite this burden, US stroke mortality rates are among the lowest in the world. The estimated US stroke mortality rate for women was 36.7 per 100 000; for men it was 46.6 per 100 000. There has been a striking 60% decline in US stroke mortality between 1960 and 1990. Despite this decline, nearly 150 000 Americans died of a stroke during 1995, which corresponds to 1 death every 3.5 minutes.

• The burden of stroke is heterogeneous and is greater among the elderly, men, and African-Americans. In the southeastern United States, stroke risk is approximately 1.4 times that of other regions.
• Stroke incidence rates have been level since the mid 1980s, but the decline in stroke mortality has continued at least through 1992.
• Besides mortality, morbidity in 3 890 000 surviving stroke victims is also substantial, making stroke the leading cause of serious disability in the United States. Among long-term (>6 months) stroke survivors, 48% have hemiparesis, 22% cannot walk, 24% to 53% report complete or partial dependence on activity of daily living (ADL) scales, 12% to 18% are aphasic, and 32% are clinically depressed.
• Although stroke incidence appears stable and stroke mortality is slowly declining, the absolute magnitude of stroke is likely to grow over the next 30 years. With the aging of the population and an increased proportion of African-Americans, the number of stroke victims is likely to increase substantially.

Risk Factors for Ischemic Stroke
Nonmodifiable Risk Factors or Risk Markers
Age, gender, race, ethnicity, and heredity have been identified as markers of risk for stroke. These factors cannot be modified.

Potentially Modifiable Risk Factors for Ischemic Stroke
Hypertension. Hypertension is the single most important modifiable risk factor for ischemic stroke.

Cardiac disease. Various cardiac diseases have been shown to increase risk of stroke. AF is the most powerful and treatable cardiac precursor of stroke.

• Cardiac abnormalities, in particular mitral stenosis, are important risk factors for stroke, as discussed in "Etiology of Stroke."
• Another valvular risk factor for stroke is mitral annular calcification.
• The most recent finding suggests that valvular strands are associated with stroke.
• Left atrial enlargement was found to be a risk factor for stroke.
• Epidemiological evidence is growing that the cardiac structural abnormalities of patent foramen ovale (PFO) and atrial septal aneurysm (ASA) increase risk of embolic stroke.
• Myocardial disease has long been recognized as a risk factor for stroke.

Diabetes and glucose metabolism. Case-control studies of stroke patients and prospective epidemiological studies have confirmed an independent effect of diabetes with a relative risk of ischemic stroke in persons with diabetes from 1.8 to 3.0.

Lipids. Although hypercholesterolemia is an important modifiable risk factor for coronary heart disease, the link to ischemic stroke remains uncertain. However, data clearly support the positive relation between total and LDL cholesterol and a protective influence of HDL cholesterol on extracranial carotid atherosclerosis.

Cigarette smoking. Cigarette smoking increases relative risk of ischemic stroke nearly two times, with a clear dose-response relation.

Alcohol. Moderate consumption of alcohol may reduce incidence of cardiovascular disease, including stroke.

Illicit drug use. Drug abuse is a major social problem, with cocaine the substance most commonly associated with stroke. Other drugs linked to stroke include heroin, amphetamines, LSD, PCP, "T's and Blues," and marijuana.

Lifestyle factors (obesity, physical inactivity, diet, and acute triggers). Obesity, physical inactivity, diet, and acute triggers such as emotional stress have been associated with stroke risk. Moderate and heavy levels of physical activity have been associated with reduced incidence of coronary heart disease.

Oral contraceptives. Oral contraceptives with an estrogen content >50 µg, the preparations used in the 1960s and 1970s, were strongly associated with risk for stroke. Recently a study of low-dose oral contraceptives (<50 µg estrogen) disclosed no increased risk of ischemic stroke.

Migraine. Although migraine has been identified as an independent risk factor for ischemic stroke in men older than 40 in the Physicians' Health Study, no association was found in other studies after adjusting for other stroke risk factors.

Hemostatic and inflammatory factors. Hemostatic factors have been related to incidence of cardiovascular disease generally, and in two prospective studies fibrinogen has been linked to increased stroke risk. The endogenous tissue-type plasminogen activator (TPA) system, the primary mediator of intravascular fibrinolysis, has been independently associated with risk of MI and stroke.

Homocysteine. Numerous case-control studies have shown a strong relation between stroke and both basal and postmethionine load hyperhomocysteinemia.

Subclinical disease. Subclinical disease, or disease detected noninvasively and without clinical signs or symptoms, is known to be related to both prevalent and incident stroke. Commonly performed subclinical disease measurements include (1) carotid ultrasonography; (2) ankle-brachial blood pressure ratio or ankle-arm index for assessment of lower extremity arterial disease; and (3) cerebral magnetic resonance imaging (MRI) and computed tomography (CT). Aortic arch atheromas detected by tranesophageal echocardiography (TEE) have also been added to the growing list of stroke risk factors and are discussed in "Etiology of Stroke."

Asymptomatic carotid stenosis. Observational studies suggest the rate of unheralded stroke, ie, stroke without an antecedent TIA ipsilateral to a hemodynamically significant extracranial carotid artery stenosis, is about 1% to 2% annually. Risk of stroke may be higher in patients with progressing and more severe stenosis. In symptomatic carotid artery stenosis, six endarterectomies can be expected to prevent one stroke in 2 years, whereas for asymptomatic patients 67 operations would be needed.

Transient ischemic attacks. After adjustment for major cardiovascular risk factors predisposing a patient to stroke, TIA remains a significant independent risk factor for both stroke and MI. TIA referable to a high-grade carotid artery stenosis carries a higher risk for stroke than those beyond a mild stenosis, and the risk with hemispheric ischemic symptoms is greater than for retinal ischemia.

Multiple Risk Factors
The realization that the probability of stroke is increased severalfold by the presence of multiple risk factors may help both patient and physician to more fully appreciate the need for serious risk factor management.

Intracerebral and subarachnoid hemorrhage. Subarachnoid (SAH) and intracerebral hemorrhage (ICH), which account for only 15% to 25% of total strokes, result in significant morbidity, mortality, and cost. Aneurysms and arteriovenous malformations are the most commonly identified causes of SAH, while hypertensive arteriolar disease, amyloid deposition, intrainfarct hemorrhage, and arteriovenous malformations are the bases of most ICHs. ICH is twice as common as SAH in studies with CT documentation.

Recommendations
Public Policy

• Encourage substantial increases in funding of clinical stroke research appropriate to the major public health burden of this condition.
• Enhance support for screening and follow-up programs for hypertension and other modifiable stroke risk factors, particularly targeting high-risk populations. However, current data do not support mass screening for asymptomatic carotid stenosis.
• Intensify efforts to prevent cigarette smoking and encourage smoking cessation through elimination of advertising, economic disincentives, public education, and other measures.
• Support the prospective collection, monitoring, and reporting of data on surgeon-specific morbidity and mortality after carotid endarterectomy.

Public Education

• Provide more effective education about risk factors for stroke and warning signs and the importance of controlling hypertension and other modifiable stroke risk factors.

Healthcare Providers

• Seek professional education opportunities about risk factors for stroke and warning signs.
• Emphasize the importance of optimal management of AF in persons who are candidates for anticoagulation.
• Increase efforts to reduce coronary heart disease morbidity and mortality among patients with cerebrovascular disease, emphasizing management of risk factors, especially lipids.

Research Priorities

• Collect comprehensive stroke incidence and mortality data to define differences in rates among different racial, ethnic, and socioeconomic groups and in geographic regions of the United States.
• Differentiate ICH and SAH from ischemic stroke in research studies.
• Identify strategies to improve treatments shown to be effective in clinical trials in community practice and improve dissemination of this preventive information to healthcare providers and the public.
• Evaluate genetic stroke risk markers and gene-environment interactions.
• Determine the relation between control of hypertension among stroke survivors and subsequent morbidity and mortality.
• Stress optimal management strategies for patients with AF, during cardiac interventions, and other cardiac contributors to stroke.
• Determine the impact of improved glycemic control on incidence of stroke in persons with type I and type II diabetes.
• Determine the relation between alcohol and ischemic stroke, the dose-response relation, and potential mechanisms.
• Determine the impact of specific illicit drugs on risk of stroke.
• Conduct prospective observational studies of the role of hemostatic or inflammatory markers in the transition from preclinical atherosclerosis to stroke, the effect of intervention on intermediate and clinical end points, and their role in stroke recurrence.
• Clarify the relation between homocysteine metabolism and stroke and research on stroke prevention in randomized clinical trials.
• Clarify the relation between stroke risk and physical activity, diet, obesity, and acute triggers such as stress.
• Clarify the relation between subclinical diseases and stroke risk and the impact of interventions regarding carotid intimal-media thickness; stable and unstable carotid plaque; ankle-brachial blood pressure index; infarctlike lesions, silent stroke, and white-matter disease on MRI; and endothelial dysfunction.
• Develop and investigate genetic and other markers for amyloid angiopathy and lobar hemorrhage.

	Acute Interventions

Top Introduction Etiology of Stroke Risk Factors Acute Interventions Rehabilitation

 
New and Emerging Treatments for Acute Ischemic Stroke
The acute care of patients with stroke aims to control and prevent medical and neurological complications as well as reverse the neurological effects of the stroke itself. The most important advance is the hyperacute administration of r-TPA. A review of thrombolytic drugs and updated guidelines for their use has recently been prepared.

Recent trials of intravenous thrombolysis. The results of five recent clinical trials of intravenous thrombolytic therapy for acute ischemic stroke are conflicting. The National Institute of Neurological Disorders and Stroke (NINDS) study showed that intravenous r-TPA significantly improved stroke outcomes at 3 months in carefully selected patients when administered within 3 hours of onset, following protocol requirements.

Recent studies of intra-arterial thrombolysis. Available evidence suggests that recanalization after intra-arterial delivery is in the range of 60% to 70%, which is superior to the rate for intravenous delivery, which is 30% to 40%. Although these data encourage further testing of intra-arterial thrombolysis, the procedure should still be considered investigational.

Antithrombotic and antiplatelet aggregating drugs. Conclusive data are lacking about the ability of heparin to prevent early recurrent embolism among persons with presumed cardioembolic stroke. Low-molecular-weight heparins and heparinoids have selective antithrombotic actions that may improve safety and reduce the risk of severe symptomatic autoimmune thrombocytopenia. The immediate effects of 325 mg of aspirin on platelet aggregation suggest its usefulness in acute stroke as it has been shown to be in treating acute myocardial ischemia. Drugs such as anti-ICAM-1, which produces effects at the microvasculature level, are being tested.

Neuroprotective drugs. There is no convincing evidence that any current neuroprotective drug is effective in either reducing size of infarction or improving overall outcome.

Calcium entry antagonists. A meta-analysis of nimodipine trials suggests a potential benefit if the drug is given within 12 hours of stroke onset. Additional studies of nimodipine given within 6 hours of onset are under way.

Glutamate antagonists. A major problem with the use of NMDA receptor antagonists in humans is the high rate of neuropsychiatric and hypotensive side effects.

Sodium channel antagonists and glycine antagonists. Inhibition of presynaptic glutamate release by antagonists of presynaptic sodium channels may be useful in stroke.

Opioid antagonists. Nalmafene, an exomethylene derivative of naltrexone, has been tested for safety in patients with acute stroke; a small placebo-controlled, dose-ranging study is nearing completion.

Antioxidants/free radical scavengers. Trials in Europe and North America were halted prematurely after interim analyses suggested a lack of efficacy. Further studies are testing higher doses.

Angioplasty and stenting. Percutaneous transluminal angioplasty and intravascular stenting of the supra-aortic vessels are being examined for safety, feasibility, and long-term durability as an alternative to carotid endarterectomy and other revascularization procedures of the extracranial cerebral vessels.

Intracranial angioplasty. While angioplasty is technically feasible, procedure-related stroke and death rates have been substantially higher in patients having percutaneous transluminal angioplasty of intracranial vessels than for those undergoing extracranial procedures.

Neither angioplasty nor stenting of the extracranial or intracranial vasculature has been evaluated in clinical trials. Their use is considered investigational.

Healthcare system issues of dissemination and implementation of information. State-of-the-art acute stroke care delivery systems are relatively primitive compared with emergency trauma or cardiac care.

Patient factors. The same factors that lead patients to delay seeking medical assistance for AMI also cause them to delay seeking medical help for stroke. Attempts to influence such behavior have had limited success.

Medical System Factors
Prehospital care. Aggressive stroke protocols and educational programs keyed to emergency medical services can markedly reduce the time from stroke onset to initiation of treatment.

Hospital care. It is expedient to treat patients with intravenous thrombolytic agents in the emergency department (ED) before admission to the hospital.

Administrative and triage issues. With high-risk therapies such as thrombolysis, many patients with acute stroke must be treated in an intensive-care setting. The optimal structure and cost-effectiveness of such stroke units have not been well studied.

Diagnostic issues. Early signs of infarction and other CT diagnoses (eg, hemorrhagic infarction versus parenchymal hematoma) are easily missed, even by experienced investigators. Tele-medicine links could provide services for interpreting neuroimaging studies in outlying EDs.

Physician issues. The emergency physician can make the decision to administer thrombolytic therapy, but special training should be required for ED personnel, along with standardization of treatment and diagnostic protocols in conjunction with neurologists. Neurologists and radiologists must also be available to the ED.

Drug administration issues. Stocking the thrombolytic drug in the ED instead of a central pharmacy significantly decreases delay to therapy.

Acute stroke trials with rapidly changing available therapies. Past stroke trials recruited patients for comparison of a therapeutic agent with placebo. A potential therapy must be compared with the best available therapy as defined by recent clinical trials.

Multiple competing studies. An attempt should be made to allow concurrent patient enrollment in multiple studies with a low likelihood of interfering with the primary outcome measure.

Single site with multiple concurrent overlapping studies. Investigators should look for complementary protocols so that most acute stroke patients arriving at their centers will be eligible for some study.

Outcome measures. Functional scales (eg, Barthel and Modified Rankin Scale) are essential for establishing a meaningful benefit to stroke patients and for procuring Food and Drug Administration approval of a new agent.

Evolution of monotherapy to multiple concurrent or sequential therapies. Therapies targeted at only one facet of the complicated process of stroke are likely to be of only limited benefit.

Healthcare system problems and reimbursement issues. In some countries there is a strong tendency to charge all medical costs for treating a patient in a prospective clinical trial to the trial sponsor, even costs that are considered standard treatment and care. If this practice continues, the cost of performing any prospective trial will be prohibitive.

Recommendations
Public Policy
The AHA should

• Establish a multidisciplinary Acute Stroke Care Committee, similar to the Emergency Cardiac Care Committee or the American College of Surgeons' Committee on Trauma, to develop and promote strategies for acute stroke care to be implemented locally.
• Emphasize that emergency treatment of stroke is part of a continuum of care that ranges from risk factor reduction and prevention to rehabilitation.
• Help identify, endorse, educate, and support influential local stroke advocates and charge them with implementing strategies for acute stroke care.
• Disseminate guidelines, consensus statements, and position papers related to acute stroke care to state and regional medical societies, hospital networks, and specialty organizations (eg, community stroke and emergency medicine societies) through local advocates.
• Advocate reimbursement by payers of the usual and customary costs of medical care for patients participating in clinical research.

Education
The AHA and other groups should increase awareness of the importance of early and successful treatment of persons with ischemic stroke to the following groups: the public, especially groups judged to be at the highest risk; physicians; other healthcare providers, including ED personnel; hospital administrators; third-party payers and care organizations; and government.

High-Priority Research
Recent successful developments in acute stroke care are based on advances in basic and clinical research. Continued support and expansion of funding of stroke research by the National Institutes of Health, the AHA, and private sources are urgently needed. The AHA and its affiliates should

• Expand funding of basic and clinical research in stroke.
• Support research on new nonpharmacological interventions, particularly neurointerventional procedures.
• Develop new mechanisms to facilitate and encourage applications from clinical and basic researchers.
• Support research on outcomes after ischemic stroke.
• Endorse the concept of acute treatment of stroke in specialized care facilities.
• Support the funding of demonstration projects that examine the impact of acute stroke care delivery models on stroke outcome and costs.

	Rehabilitation

Top Introduction Etiology of Stroke Risk Factors Acute Interventions Rehabilitation

 
Stroke is a condition with high incidence and moderate mortality rates, leaving a large proportion of survivors with significant residual physical, cognitive, and psychological impairments. The increasing number of older adults and the emergence of new therapies for acute stroke suggest that there will be an increase in the number of stroke survivors living with disabilities. Furthermore, secular trends in stroke severity document a decrease in those most severely affected. This shift to more moderately affected survivors places increased demands on rehabilitation efforts and services, making the issue of how to best limit stroke-related disability and health risks a major concern for healthcare providers in rehabilitation. At this time efforts to prevent stroke must be balanced with the pragmatic effort to prevent disability and maximize quality of life for those who have suffered the consequences of stroke.

The rehabilitation process involves six major areas of focus: (1) preventing, recognizing, and managing comorbid illness and medical complications; (2) training for maximum independence; (3) facilitating maximum psychosocial coping and adaptation by patient and family; (4) preventing secondary disability by promoting community reintegration, including resumption of home, family, recreational, and vocational activities; (5) enhancing quality of life in view of residual disability; and (6) preventing recurrent stroke and other vascular conditions such as MI that occur with increased frequency in patients with stroke. To attain these goals, rehabilitation interventions should assist the patient in achieving and preserving maximum feasible functional independence.

Stroke rehabilitation is an active process beginning during acute hospitalization, progressing for those with residual impairments to a systematic program of rehabilitation services, and continuing after the individual returns to the community. It is an organized effort to help stroke patients maximize all opportunities for returning to an active and productive lifestyle. Because the clinical manifestations of stroke are multifaceted and complex, stroke rehabilitation is best implemented through the coordinated efforts of a team of rehabilitation professionals.

A well-conceived rehabilitation management plan is the basis for all rehabilitation. The first step is to match the patient with the appropriate rehabilitation services and setting. Reasonable medical stability, significant functional disability, and the ability to learn are the primary criteria for rehabilitation. Patients with severe cognitive deficits resulting in the inability to learn new strategies are unlikely to benefit from rehabilitation. A minimal level of physical endurance is also essential.

Scientific Basis for Stroke Rehabilitation
Rehabilitation is effective. At present, however, we cannot easily differentiate between the influence of specific interventions and the natural recovery process. The state of the science in stroke rehabilitation was summarized in the 1995 AHCPR Post-Stroke Rehabilitation Practice Guideline.

Current Issues in Stroke Rehabilitation
Access to and cost-effectiveness of rehabilitation. The effective delivery of post-stroke rehabilitation requires development of an integrated care system that spans acute care, acute rehabilitation, subacute rehabilitation, outpatient services, home care, and community support services.

Recommendations
The rehabilitation panel prepared the following recommendations for clinical practice, public policy, education, and research activities.

Clinical Practice

• Implement interventions during the acute phase of stroke to promote recovery and prevent complications.
• Emphasize the importance of thorough and consistent assessment at each stage of the recovery process to guide treatment decisions and monitor progress.
• Prevent secondary disability by consistently promoting functional independence and opportunities to improve quality of life.
• Maintain a patient and family focus throughout rehabilitation.
• Support demonstration projects of late-stage rehabilitation and evaluate outcomes in terms of functional independence, communication, quality of life, and cost-effectiveness.

Public Policy

• Advocate adoption of the AHCPR Guidelines for Post-Stroke Rehabilitation.
• Support provisions and implementation of the Americans With Disabilities Act.
• Develop a broad-based campaign for reintegrating persons with stroke disabilities into the community.
• Support development and implementation of programs and legislation that address the physical, emotional, and economic burden of stroke.

Education

• Promote continuing education for clinicians who need to change roles and responsibilities in stroke rehabilitation as healthcare delivery changes.
• Establish educational programs for professionals and the general public in collaboration with the AHA and others to address the efficacy of rehabilitation.
• Continue and extend networks such as the AHA Stroke Connection and other communications and support groups for stroke survivors in areas without representation.

Research

• Expand knowledge of brain physiology and neurochemical mechanisms associated with recovery from stroke and the relationship between pathology, impairment, and disability.
• Develop and refine valid, reliable, and sensitive instruments to measure improvement after stroke.
• Design and implement large-scale randomized clinical trial initiatives to (1) identify the elements of care in specialized stroke units that contribute to improved survival and outcome; (2) test the effectiveness and efficacy of different types of rehabilitation interventions, including when, what, and where rehabilitation should take place; (3) examine the effectiveness of various intensities of treatment; and (4) delineate characteristics associated with successful recovery of functional independence.
• Determine differences in outcomes and recovery trajectories for different stroke subtypes (including lesion location, etiology, and associated comorbidity).
• Explore the influence of neuroactive pharmacological agents on recovery of motor, language, and cognitive function.

	Footnotes

 
A full-text version of this report was published in the July 1997 issue of Stroke. A single reprint of this report and the full-text version is available by calling 800-242-8721 (US only) or writing the American Heart Association, Public Information, 7272 Greenville Avenue, Dallas, TX 75231-4596. Ask for reprint No. 71-0126. To purchase additional reprints: up to 999 copies, call 800-611-6083 (US only) or fax 413-665-2671; 1000 or more copies, call 214-706-1466, fax 214-691-6342, or To make photocopies for personal or educational use, call the Copyright Clearance Center, 508-750-8400.

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