During the past decade, advances in the prevention, diagnosis, and treatment of cerebrovascular disorders have led to decreases in the prevalence of stroke (primarily ischemic stroke), but the high rates of morbidity and mortality, despite a number of modifiable risk factors, point to the need for enhanced education for both patients and physicians. Enhancing healthcare professionals' knowledge about evidence-based guidelines, as well as about advances in diagnostic tools, is crucial for improving the outcomes for individuals who are at risk for stroke or in whom a stroke has occurred. A better understanding is needed about the options for patients at risk for stroke, as well as for treatment and rehabilitation. This course explores the roles of diagnosis and screening, evaluation of individuals with suspected stroke, immediate treatment of stroke, and the elements of effective rehabilitation programs. Heightened awareness of variations in the prevalence of stroke according to age, sex, and racial/ethnic groups will help clinicians and healthcare educators target individuals in need of enhanced education about the risks of stroke, especially those that are modifiable.

Education Category: Medical / Surgical
Release Date: 04/01/2014
Expiration Date: 03/31/2017


This course is designed for physicians, nurses, and physician assistants in the primary care setting. Neurologists and other healthcare practitioners will also benefit from this course.

Accreditations & Approvals

NetCE is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians. NetCE is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center's Commission on Accreditation. NetCE is accredited by the International Association for Continuing Education and Training (IACET). NetCE complies with the ANSI/IACET Standard, which is recognized internationally as a standard of excellence in instructional practices. As a result of this accreditation, NetCE is authorized to issue the IACET CEU.

Designations of Credit

NetCE designates this enduring material for a maximum of 10 AMA PRA Category 1 Credit(s)™. Physicians should claim only the credit commensurate with the extent of their participation in the activity. NetCE designates this continuing education activity for 10 ANCC contact hour(s). NetCE designates this continuing education activity for 12 hours for Alabama nurses. Successful completion of this CME activity, which includes participation in the evaluation component, enables the participant to earn up to 10 MOC points in the American Board of Internal Medicine's (ABIM) Maintenance of Certification (MOC) program. Participants will earn MOC points equivalent to the amount of CME credits claimed for the activity. It is the CME activity provider's responsibility to submit participant completion information to ACCME for the purpose of granting ABIM MOC credit. Completion of this course constitutes permission to share the completion data with ACCME. NetCE is authorized by IACET to offer 1 CEU(s) for this program. AACN Synergy CERP Category A.

Individual State Nursing Approvals

In addition to states that accept ANCC, NetCE is approved as a provider of continuing education in nursing by: Alabama, Provider #ABNP0353, (valid through December 12, 2017); California, BRN Provider #CEP9784; California, LVN Provider #V10662; California, PT Provider #V10842; Florida, Provider #50-2405; Iowa, Provider #295; Kentucky, Provider #7-0054 through 12/31/2017.

Special Approvals

This course meets the requirement for California-licensed physicians who must complete 20% of their mandatory CME in the field of geriatric medicine. This activity is designed to comply with the requirements of California Assembly Bill 1195, Cultural and Linguistic Competency.

Course Objective

The early identification and management of the risk factors for ischemic stroke can lead to substantial improvement in health and reductions in cost. However, research has documented gaps between healthcare professionals' knowledge and practice with respect to prevention, with data on adherence to evidence-based or guideline-endorsed recommendations demonstrating underuse or ineffective use of all interventions for primary and secondary prevention. The purpose of this course is to provide needed information about the roles of diagnosis and screening, evaluation of individuals with suspected stroke, immediate treatment of stroke, and the elements of effective rehabilitation programs so that healthcare professionals may implement the necessary interventions appropriately.

Learning Objectives

Upon completion of this course, you should be able to:

  1. Describe the primary types of cerebrovascular disorders and their causes.
  2. Discuss differences in prevalence, morbidity, and mortality according to age, sex, and race/ethnicity.
  3. Identify the nonmodifiable and modifiable risk factors for ischemic stroke.
  4. Implement primary prevention strategies according to evidence-based guidelines.
  5. Discuss the need for education at the community and patient levels.
  6. Apply models of predicting risk of ischemic stroke.
  7. Select the appropriate tools for screening, diagnosis, and early management of ischemic stroke.
  8. Describe the elements of stroke systems of care and a comprehensive stroke center.
  9. Discuss evidence-based treatment options for ischemic stroke.
  10. Describe the benefits and components of a specialized stroke rehabilitation team.
  11. Outline the aspects of patient assessment for stroke rehabilitation.
  12. Discuss evidence-based recommendations for secondary prevention of ischemic stroke.


Lori L. Alexander, MTPW, ELS, MWC, is President of Editorial Rx, Inc., which provides medical writing and editing services on a wide variety of clinical topics and in a range of media. A medical writer and editor for more than 30 years, Ms. Alexander has written for both professional and lay audiences, with a focus on continuing education materials, medical meeting coverage, and educational resources for patients. She is the Editor Emeritus of the American Medical Writers Association (AMWA) Journal, the peer-review journal representing the largest association of medical communicators in the United States. Ms. Alexander earned a Master’s degree in technical and professional writing, with a concentration in medical writing, at Northeastern University, Boston. She has also earned certification as a life sciences editor and as a medical writer.

Faculty Disclosure

Contributing faculty, Lori L. Alexander, MTPW, ELS, MWC, has disclosed no relevant financial relationship with any product manufacturer or service provider mentioned.

Division Planners

John V. Jurica, MD, MPH

Sharon Cannon, RN, EdD, ANEF

Division Planners Disclosure

The division planners have disclosed no relevant financial relationship with any product manufacturer or service provider mentioned.

About the Sponsor

The purpose of NetCE is to provide challenging curricula to assist healthcare professionals to raise their levels of expertise while fulfilling their continuing education requirements, thereby improving the quality of healthcare.

Our contributing faculty members have taken care to ensure that the information and recommendations are accurate and compatible with the standards generally accepted at the time of publication. The publisher disclaims any liability, loss or damage incurred as a consequence, directly or indirectly, of the use and application of any of the contents. Participants are cautioned about the potential risk of using limited knowledge when integrating new techniques into practice.

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It is the policy of NetCE not to accept commercial support. Furthermore, commercial interests are prohibited from distributing or providing access to this activity to learners.

Table of Contents

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#90281: Ischemic Stroke

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Cerebrovascular disease is associated with significant morbidity and mortality in the United States. Stroke occurs in approximately 795,000 individuals each year, of which 610,000 are first-time strokes and 185,000 are recurrent [1]. Stroke is the leading cause of long-term disability in adults; 65% of stroke survivors have some degree of impairment [1,2]. The effect of stroke on mortality is illustrated by the fact that cerebrovascular disease is the fourth leading cause of death in the United States, with an age-adjusted mortality rate of 39.1 per 100,000 population as of 2010 [1]. This represents a 31% decrease in the mortality rate and a 16.78% decline in actual deaths since 2000 but still indicates a substantial healthcare issue, with 1 of every 3 deaths being attributable to stroke [1]. In addition, the financial cost associated with cerebrovascular disease poses a substantial economic burden, with an estimated direct and indirect cost of $315.4 billion in 2010 [1]. Despite the considerable progress being made in the areas of prevention, management, and rehabilitation, it appears that stroke will increasingly cause death and disability in the coming decades as the population ages [3].

The two primary types of stroke are ischemic and hemorrhagic, and ischemic strokes account for the majority (87%) of cerebrovascular disorders [1]. There are several risk factors for ischemic stroke, and predicting risk is an important element in prevention. In predicting risk, consideration should be given not only to comorbidities but also to age, sex, and race/ethnicity, as disparities in prevalence, morbidity, and mortality have been attributed to these patient characteristics [4,5,6,7]. Evidence-based guidelines for primary and secondary prevention have been developed and should be implemented [8,9].

Among the most important risk factors for ischemic stroke is a transient ischemic attack (TIA); approximately 15% of ischemic strokes are preceded by a TIA [1]. The greatest risk for post-TIA stroke is within the first 48 hours, and the risk continues beyond 48 hours to 3 months [10]. Improved understanding of TIAs among both clinicians and patients is needed. A survey of 200 primary care physicians showed that 88% could not correctly identify the typical symptoms and duration of a TIA, and studies have indicated that half of individuals who have a TIA do not report the event to their primary care clinician [1,11].

The early identification and management of the risk factors for ischemic stroke can lead to substantial improvement in health and reductions in cost [12]. For example, the incidence of stroke has been reduced by 30% to 40% with the appropriate use of antihypertensive therapy [9]. Yet, research has documented gaps between physicians' knowledge and practice with respect to prevention, with data on adherence to evidence-based or guideline-endorsed recommendations demonstrating underuse or ineffective use of all interventions for primary and secondary prevention [10,13,14]. Evidence-based guidelines have also been developed for the early management of stroke and for rehabilitation after stroke and should be followed to provide optimum care [15,16,17].

The focus of this course is ischemic stroke, due to its overwhelming prevalence. Advances have been made in tools for the screening and diagnosis of ischemic stroke, and a better understanding of the options for patients at risk is needed. This course explores the role of the physical examination and history, laboratory studies, and imaging techniques in screening and diagnosis. Also discussed are evidence-based guidelines for the early management of ischemic stroke, as well as emerging treatment options. Because data have shown that outcome is improved by care provided in comprehensive stroke centers and by early rehabilitation, these topics are addressed as well [16,17,18,19]. The importance of a multidisciplinary rehabilitation team, appropriate patient assessment, and an exercise program is emphasized.


Although "cerebrovascular disease" is often used interchangeably with the term stroke, the disease encompasses any neurovascular disorder that exists in the presence or absence of an ictus (e.g., carotid artery stenosis, arteriovenous malformations). Despite advances in understanding the pathophysiology of cerebrovascular diseases, the term "stroke" (also known as cerebrovascular accident or brain attack) is inconsistently defined. Stroke has been classically characterized as an injury to the central nervous system (CNS) by a vascular cause. Because this definition is mainly clinical and not inclusive of advances in science and technology, the American Heart Association (AHA)/American Stroke Association (ASA) convened a writing group to develop an updated definition of stroke. The AHA/ASA recommend that the term "stroke" be broadly used to include a variety of definitions (Table 1).


CNS infarction

Brain, spinal cord, or retinal cell death attributable to ischemia, based on:

  • Pathological, imaging, or other objective evidence of cerebral, spinal cord, or retinal focal ischemic injury in a defined vascular distribution; or

  • Clinical evidence of cerebral, spinal cord, or retinal focal ischemic injury based on symptoms persisting ≥24 hours or until death, and other etiologies excluded.

Ischemic strokeEpisode of neurological dysfunction caused by focal cerebral, spinal, or retinal infarction
Silent CNS infarctionImaging or neuropathological evidence of CNS infarction, without history of acute neurological dysfunction attributable to the lesion
Intracerebral hemorrhageFocal collection of blood within the brain parenchyma or ventricular system, not caused by trauma
Stroke caused by intracerebral hemorrhageRapidly developing clinical signs of neurological dysfunction attributable to focal collection of blood within brain parenchyma or ventricular system, not caused by trauma
Silent cerebral hemorrhageFocal collection of chronic blood products within the brain parenchyma, subarachnoid space, or ventricular system on neuroimaging or neuropathological examination, not caused by trauma and without history of acute neurological dysfunction attributable to the lesion
Subarachnoid hemorrhageBleeding into subarachnoid space
Stroke caused by subarachnoid hemorrhageRapidly developing signs of neurological dysfunction and/or headache because of bleeding into the subarachnoid space, not caused by trauma
Stroke caused by cerebral venous thrombosisInfarction or hemorrhage in the brain, spinal cord, or retina because of thrombosis of a cerebral venous structure. Symptoms or signs caused by reversible edema without infarction or hemorrhage do not qualify as stroke.
Stroke, not otherwise specifiedEpisode of acute neurological dysfunction presumed to be caused by ischemia or hemorrhage, persisting ≥24 hours or until death, but without sufficient evidence to be classified as one of the above
CNS: central nervous system


The multiple sources, pathophysiologic mechanisms, and sequelae of stroke are reflected in the diverse types of cerebrovascular disorders. The World Health Organization classifies cerebrovascular diseases under "Diseases of the circulatory system" in the 10th revision of the International Statistical Classification of Diseases and Related Health Problems (ICD-10), the international standard diagnostic classification for all general epidemiologic purposes and many health management purposes (Table 2) [21]. Although TIAs, traumatic intracranial hemorrhage, and vascular dementia pertain to cerebrovascular disorders, they are excluded from the cerebrovascular disease category in the ICD-10. Their exclusion illustrates the heterogeneity of stroke and its sequelae. TIAs are classified under "Diseases of the nervous system: Episodic and paroxysmal disorders." Traumatic intracranial hemorrhage is listed under "Injury, poisoning, and certain other consequences of external causes: Injuries to the head," and vascular dementia, a common sequelae of stroke, is categorized under "Mental and behavioral disorders: Organic, including symptomatic, mental disorders."


ICD CodeDisease
I60Subarachnoid hemorrhage
I61Intracerebral hemorrhage
I62Other nontraumatic intracranial hemorrhage
I63Cerebral infarction
I64Stroke, not specified as hemorrhage or infarction
I65Occlusion and stenosis of precerebral arteries, not resulting in cerebral infarction
I66Occlusion and stenosis of cerebral arteries, not resulting in cerebral infarction
I67Other cerebrovascular disease
I68Cerebrovascular disorders in diseases classified elsewhere
I69Sequelae of cerebrovascular disease

As noted, the two primary types of stroke are ischemic and hemorrhagic. In the United States, approximately 87% of all strokes are ischemic; 10% are hemorrhagic strokes [1,22]. An ischemic stroke occurs when any artery that supplies the brain with oxygen becomes stenosed or occluded, resulting in infarction [23]. In the case of hemorrhagic stroke, bleeding occurs below the arachnoid, the location of the brain's blood supply, allowing blood to directly contact and damage brain tissue. Although ischemic stroke is the focus of this course, a brief overview of hemorrhagic strokes will help to provide context and comparison of the clinical features of both types of stroke. In addition, TIAs are discussed here, as they are often a precursor to ischemic stroke.

Hemorrhagic Strokes

Hemorrhagic stroke is associated with a higher risk of fatality than ischemic stroke, and roughly one-third of patients die within 30 days after the event [1,24]. Hemorrhagic strokes are categorized by the location of the hemorrhage, either intracerebral or subarachnoid, with the former being more common.

Approximately 88% of hemorrhagic strokes are due to intracerebral hemorrhage (ICH), and because of this, the term hemorrhagic stroke often refers to ICH [25]. ICHs are characterized by bleeding directly into the brain parenchyma [26]. Intraventricular hemorrhage describes bleeding that extends into the ventricles [26,27]. Nontraumatic ICH is categorized as primary (unrelated to congenital or acquired lesions), secondary (caused by a congenital or acquired condition), or spontaneous (unrelated to trauma or surgery) [26].

The signs and symptoms of ICH include headache, vomiting, seizures, depressed consciousness, meningeal irritation, and blood-tainted cerebrospinal fluid. The onset of symptoms may occur within seconds to minutes after the start of an ICH. Individuals with this type of stroke often feel more ill than those with an ischemic stroke.

ICH is the least treatable type of stroke [28]. Functional independence is regained within 6 months in approximately 20% of survivors [29]. The morbidity and mortality depend on the volume and location of the hematoma. The 1-year mortality rate varies according to location, with the highest mortality rate (65%) associated with ICH in the brain stem; the rate is 57% for lobar hemorrhage, 51% for deep hemorrhage, and 42% for cerebellar hemorrhage [30].

As many as 80% of primary ICHs occur after small vessels are compromised by chronic hypertension [31]. Hypertension is associated with ICH originating in the periventricular deep white matter, deep subcortical structures, pons, and cerebellum [32]. In individuals older than 70 years of age, cerebral amyloid angiopathy, a condition that leads to amyloid protein infiltration into the cortical arterioles, is responsible for approximately 20% of ICHs [33]. Other causes of ICH include anticoagulant and antiplatelet use, drug use (e.g., cocaine, phenylpropanolamine), and other bleeding diathesis [28,34]. Fewer than 15% of all cases of ICH are secondary to congenital vascular abnormalities and malignant brain lesions [26].

Subarachnoid hemorrhages occur less frequently than ICHs. The hallmark of subarachnoid hemorrhage is the immediate onset of a severe headache with signs of meningeal irritation [35]. Individuals may describe this headache as their "worst ever." Nausea, vomiting, neck pain, and photophobia are also classic symptoms, although they are not always present [35]. Neurologic deficits may be acute or may manifest hours to days after the onset of bleeding.

Nontraumatic subarachnoid hemorrhages are subcategorized as aneurysmal or non-aneurysmal [36]. Aneurysmal subarachnoid hemorrhage is associated with higher rates of morbidity and mortality than non-aneurysmal hemorrhage. Among patients who live 3 months after the event, the risk of death is 8.7% within 5 years and 17.9% within 10 years [37]. In contrast, non-aneurysmal subarachnoid hemorrhages are associated with better outcomes and are less likely to cause death [38].

Most nontraumatic subarachnoid hemorrhages involve rupture of an intracranial aneurysm or cerebral arteriovenous malformation. Congenital arteriovenous anomalies are more likely to cause stroke in adolescents and young adults [39]. The cause of perimesencephalic subarachnoid hemorrhage, a non-aneurysmal type, is unknown [40].


TIAs are sometimes referred to as "mini-strokes" because, like ischemic strokes, they are caused by inadequate cerebral blood flow. TIAs are also called warning strokes, as they often precede an ischemic stroke [41]. The superseded definition of a TIA was "a sudden, focal neurologic deficit that lasts for less than 24 hours, is presumed to be of vascular origin, and is confined to an area of the brain or eye perfused by a specific artery" [42]. The 24-hour time limit was an arbitrary remnant of the time interval used in prospective surveys in the early 1970s [43]. Magnetic resonance imaging (MRI) and computed tomography (CT) have demonstrated that one-third of TIAs, including those that last only minutes, cause infarcts [44].

Because TIA and ischemic stroke are less distinct from one another than once believed, a new TIA definition was proposed, revised, and endorsed in 2009. The proposed definition states that TIA is "a brief episode of neurologic dysfunction caused by focal brain or retinal ischemia, with clinical symptoms typically lasting less than 1 hour, and without evidence of acute infarction" [42]. This definition was designed to better reflect the ischemic pathogenesis of TIA, promote its early management, and support the use of diagnostic imaging techniques to ensure that the patient does not have infarction [42]. The definition was endorsed by the 2009 AHA/ASA guideline, with the omission of "typically less than 1 hour" (as infarction is not necessarily bound by a set period of time) and reads, "Transient ischemic attack (TIA): a transient episode of neurological dysfunction caused by focal brain, spinal-cord, or retinal ischemia, without acute infarction" [9,45].

Research shows that a TIA should be considered a dire condition that requires urgent treatment in order to prevent a more potent ischemic stroke; approximately 15% of ischemic strokes are preceded by a TIA [1]. However, there are several challenges to immediate treatment of TIAs [46]:

  • A wide majority of the general population and many healthcare professionals believe that TIAs are generally benign.

  • Individuals experiencing a TIA often believe they can postpone or forego professional treatment because clinical symptoms usually resolve quickly and without care.

  • Due to the 24-hour arbitrary time limit in the previously accepted definition, healthcare professionals often choose to monitor a patient with a TIA rather than provide immediate treatment.

The risk of ischemic stroke is dangerously high in the period following a TIA. Research indicates that one-half of subsequent strokes occur within the first 48 hours, and a meta-analysis showed that approximately 5% of patients who have a TIA will have an ischemic stroke within 7 days of that event [10,41]. The risk of stroke within 3 months after a TIA is approximately 10% to 20% and is 24% to 29% over the following 5 years [10]. Early initiation of treatment for TIA and minor stroke with existing therapies has been shown to reduce the risk of early recurrent stroke by 80% [47].

As with any stroke, the symptoms of TIA depend on the affected vascular territory. For instance, involvement of the carotid artery causes disturbances in the ipsilateral eye or brain [48]. Although the most common focal neurologic signs of TIA are sudden-onset unilateral weakness and numbness or tingling in a limb, a TIA can cause any of the following symptoms [48,49]:

  • Numbness of the face, hand, or leg, with or without weakness

  • Paralysis

  • Slurred speech

  • Dizziness

  • Double vision

  • Hemianopia

  • Transient monocular blindness

  • Imbalance

  • Aphasia

  • Confusion

  • Head pain

Transient graying or blurring of vision is also common. Occasionally, the line of sight will be shaded. Vertebrobasilar TIAs reflect vestibulocerebellar symptoms such as ataxia, dizziness, vertigo, dysarthria, vision abnormalities (e.g., double vision, hemianopia, bilateral vision loss), and unilateral or bilateral motor and sensory dysfunctions [9].

By the time of evaluation, however, most patients appear asymptomatic because TIAs usually resolve within 5 minutes [50]. A clinician should highly suspect a TIA if the patient says, "I don't know why I'm here. Whatever it was, it is all better now" [51].

TIAs are caused by conditions similar to those leading to ischemic stroke [9]. Among the common causes are atherosclerosis of large vessels, cardioembolism, and atrial fibrillation (AF). Uncommon causes include hypercoagulable states, arterial dissection, sympathomimetic drugs (e.g., cocaine), and arteritis (caused by noninfectious necrotizing vasculitis, drugs, irradiation, or local trauma) [52].

The risk factors for TIA are also similar to those for ischemic stroke and include many modifiable factors, such as hyperhomocysteinemia, hyperlipidemia, smoking, obesity, and diabetes [9]. Risk can be reduced substantially by the treatment of vascular anomalies such as hypertension and AF, two conditions commonly associated with older age. Younger individuals (18 to 45 years of age) who have a TIA or ischemic stroke often have no detectable vascular risk factors [53].

Ischemic Strokes

Within minutes of the onset of ischemic stroke, the core of an infarct can begin to form at the least-perfused site. This site is encircled by an area partially altered metabolically and ionically by cytotoxic edema [54]. This area, the ischemic penumbra, is structurally intact and generally salvageable if reperfusion is achieved promptly. Because cerebral function deficits develop rapidly (within minutes to hours) as an ischemic stroke progresses, these brain attacks are a medical emergency. Each minute that passes results in an average loss of 1.9 million neurons and 14 billion synapses; an ischemic brain ages 3.6 years for every hour that passes after the onset of stroke [55]. For this reason, stroke specialists use the mantra, "time is brain." Although irreversible damage occurs, most individuals with stroke have recoverable penumbral tissue for at least 3 hours following the onset of symptoms [15].

The physical signs, symptoms, and sequelae of ischemic stroke are usually unilateral because of the circulatory anatomy of the brain (Table 3). Anterior circulation is composed of the paired internal carotid arteries and vessels that supply blood to the cerebral hemispheres [56]. Each common carotid artery bifurcates into the internal and external carotid arteries. The ophthalmic artery, posterior communicating artery, and anterior choroidal artery are supplied by the internal carotid artery (Figure 1). Most importantly, the internal carotid artery provides blood to the middle cerebral artery, the largest intracerebral vessel. The middle cerebral artery provides oxygen to the lateral, frontal, parietal, and temporal lobes and the basal ganglia. It also supplies the anterior cerebral artery, which is responsible for the medial part of the frontal and parietal lobes, most of the corpus callosum, the frontobasal cerebral cortex, deep structures, and the anterior diencephalon. The anterior choroidal artery supplies a portion of the thalamus and the posterior limb of the internal capsule.


Affected RegionCommon Signs and Potential Sequelae
Left anterior hemisphere
Aphasia (esp. difficulty reading, writing, calculating)
Right limb weakness and sensory loss Right field visual defect
Right anterior hemisphere
Limb motor weakness or loss
Left field visual neglect
Unable to determine two-point stimuli on left side
Left posterior cerebral artery
Aphasia (esp. difficulty reading, naming objects)
Right visual field defect
Occasionally, right-sided numbness
Right posterior cerebral artery
Left limb sensory loss
Left-sided neglect Left field visual defect
Vertebrobasilar territory (posterior circulation)
Bilateral vision disturbances and nystagmus
Dysarthria and dysphagia
Dizziness, vomiting, headache
No cortical deficits (e.g., aphasia, cognitive impairments)
Caudate nucleus, thalamus, frontal lobe (anterior circulation)Sudden abnormal behavior
Thalamus (posterior circulation)Numbness, decreased sensation on face, arm, leg on same side


Posterior circulation is primarily composed of the vertebrobasilar artery, the posterior cerebral artery, which it supplies, and other branching vessels [56]. The posterior cerebral artery provides blood to the occipital and medial temporal lobes, as well as regions of the midbrain, subthalamic nucleus, basal nucleus, thalamus, mesial inferior temporal lobe, and occipitoparietal cortices. The two main segments of the posterior cerebral artery (P1 and P2) are connected by the posterior communicating artery. The Circle of Willis links the anterior and posterior circulation at the base of the brain.

In general, ischemic strokes are categorized according to etiology: thrombotic and embolic. In addition, they are classified into five subtypes according to a system developed by the Trial of ORG 10172 in Acute Stroke Treatment (TOAST) [60].

Thrombotic Stroke

A thrombotic stroke occurs when a thrombus impairs cerebral blood flow by further narrowing or blocking an artery, typically around an atherosclerotic plaque. The stenosed or occluded artery may be a large vessel (e.g., carotid artery systems, vertebral arteries, the Circle of Willis) or a small vessel (e.g., branches of the Circle of Willis, the posterior circulation). Approximately 21% to 27% of ischemic strokes arise from atherosclerotic disease of the large vessels [61,62]. The cerebral artery branch points, especially those of the internal carotid artery, are the most vulnerable [63]. Small-vessel disease is associated with 21% to 25% of ischemic strokes [61,62]. Thrombotic strokes caused by small-vessel disease are traditionally associated with lacunar infarcts, small, deep, subcortical lesions of 15 mm or less in diameter resulting from occlusion of a single penetrating artery [60,64]. As many as 20% of older individuals who are otherwise healthy have asymptomatic lacunar infarcts unrelated to an ictal event [65]. These silent infarctions were previously believed to be benign with a good long-term prognosis. However, they now have been linked to increased risks of stroke and death and can lead to debilitating cognitive impairments such as vascular dementia [65,66].

Independent risk factors for lacunar infarcts include hypertension, gender, age, diabetes, smoking, and a history of TIA [65]. Although hypertension is strongly associated with the development of small-vessel occlusion, lacunar infarcts also occur in individuals without hypertension. However, normotensive individuals with lacunar infarcts are typically 85 years of age or older, suggesting that hypertension accelerates the arteriopathy underpinning small-vessel disease. Diabetes is an independent risk factor for lacunar infarcts [67].

Embolic Stroke

An embolic stroke occurs when an embolus (i.e., any circulating clot or particle originating from a distal point) blocks an artery that supplies oxygen to the brain. Stroke registries indicate that 26% to 29% of ischemic strokes are embolic [61,62]. Emboli include blood clots, fatty deposits, atherosclerotic plaque fragments, and cancerous cells or infectious materials emanating from conditions such as atrial myxoma and endocarditis, respectively. Clinical symptoms of the resulting infarct correspond to the location of the embolus, not its type. The region of the middle cerebral artery is most frequently blocked by emboli [68].

AF is the most common cause of embolic stroke, increasing the risk of embolic stroke fivefold and doubling the risk of death [69]. Patients with valvular thrombi, from endocarditis or prosthetic valves, or mural thrombi from myocardial infarction (MI), AF, severe heart failure, or patent foramen ovale, are at high risk for the development of emboli [70]. MI is associated with a 2% to 3% incidence of embolic stroke, 70% of which occur in the first week after the event [71].

TOAST Classification

The subtype of ischemic stroke influences treatment decisions, prognosis, and risk of recurrent stroke. The TOAST system was designed to facilitate decision making and standardize ischemic stroke research (Table 4) [60]. Most strokes are subclassified as a large-artery atherosclerosis (caused by either a thrombus or an embolus), a cardioembolism, or an occlusion of a small vessel (lacuna) [60]. Approximately 4% of individuals with stroke have coexisting large-vessel and small-vessel disease [72]. Other determined causes are rare (approximately 3%), and registries have classified up to 36% of ischemic strokes as being of "undetermined etiology" [61].


ClassificationMajor Characteristics
Large-artery atherosclerosis (may be an embolus or thrombus)

Greater than 50% stenosis or occlusion of a major brain artery or branch cortical artery

Cortical, cerebellar, brain stem, or subcortical infarct >15 mm

Cortical or cerebellar dysfunction

Cardioembolism (may be high or medium risk based on evidence of embolism)
Cardiac source of emboli
Cortical, cerebellar, brain stem, or subcortical infarct >15 mm
Cortical or cerebellar dysfunction
Small-vessel (lacuna) occlusion
Patient presents with lacunar syndromea
Subcortical or brain stem infarcts <15 mm may be detected
Other determined cause

May be caused by conditions such as dissection, hypercoagulable states, or sickle cell anemia

May have characteristics of any of the other stroke subtypes

Undetermined etiology
May be any of the following:
Two or more causes identified
Negative evaluation
Incomplete evaluation
aThe five classic lacunar syndromes are pure motor hemiparesis, pure sensory stroke, sensorimotor stroke, ataxic hemiparesis, and clumsy-hand dysarthria.


Approximately 25% of men and 20% of women have a stroke by 85 years of age, and stroke is the fourth leading cause of death in the United States, accounting for nearly 129,000 deaths in 2011 [1,74]. Morbidity associated with stroke is also high, with at least 65% of stroke survivors having some sort of impairment [1,2,9,75]. At 3 months after a stroke, approximately 20% of survivors depend on long-term care. Between 15% and 30% of stroke survivors are permanently disabled [76]. A 6-month follow-up of ischemic stroke survivors (65 years of age and older) demonstrated that [77]:

  • 50% had some degree of hemiparesis

  • 35% had depressive symptoms

  • 30% were unable to walk without some assistance

  • 26% were dependent in activities of daily living

  • 26% were in a nursing home

  • 19% had aphasia

Fortunately, stroke mortality has been declining since the early 20th century. In the United States, stroke has fallen from the third to the fourth leading cause of death, representing a true mortality decline rather than a repositioning of causes of death. This decline is a result of reduced incidence of stroke and lower case-fatality rates, concurrent with cardiovascular risk factor control interventions (e.g., hypertension control). Other efforts (e.g., diabetes control, smoking cessation programs) likely have also contributed to the decline in stroke mortality. The effects of telemedicine and stroke systems of care require additional study but appear to be significant. The decline is observed in both women and men, for all racial/ethnic and age groups, and represents a major improvement in public health and a reduction in years of potential life lost [78].

Disparities in Prevalence and Mortality

Age, gender, and race/ethnicity play major roles in the prevalence of stroke and its associated mortality.


Prolonged damage of the aging cardiovascular system by various risk factors for stroke doubles the risk of ischemic stroke for each decade of life after 55 years of age [8]. Thus, clinicians should be sensitive to their patients' modifiable risk factors, most notably hypertension, starting at an early age [1]. As many as 75% of strokes occur in individuals older than 65 years of age, and the average age at the time of ischemic stroke is 71 years in men and 75 years in women [1].

Clinicians should be particularly aware of silent cerebral infarctions in older individuals, as these infarctions occur more commonly in this population [20].


The lifetime risk of stroke has been reported to be higher for men younger than 85 years of age and higher for women older than 85 years of age, attributable to the greater longevity of women [1,22]. However, a 2007 analysis demonstrated that women 45 to 54 years of age had significantly higher odds of having had a stroke compared with men of the same age [79]. The authors of that study suggested that the disparity may be related to inadequate modification of risk factors among women [79].

Among individuals 65 years of age and older, the median survival time after a first stroke is typically longer for women than for men. For both men and women, the median survival decreases with age (Table 5) [22]. However, the possibility of gender disparities in how health care is provided to individuals who present with stroke symptoms is also being evaluated.


AgeMedian Survival
55 to 64 years7.8 years13.1 years
65 to 74 years7.7 years6.2 years
≥75 years2.3 years2.1 years

Studies suggest that, compared with men, women are evaluated less frequently following a stroke and any evaluation is more likely to be delayed [80,81]. This pattern results from women's presentation with nontraditional symptoms or without traditional symptoms and inappropriate worry by both clinician and patient about treatment-related risks (Table 6) [80,81,82]. Although studies to evaluate differences in strokes between men and women are in early stages, preliminary results indicate that emergency medical service (EMS) personnel and clinicians need an accurate understanding of symptom presentation patterns for men and women. The prevalence of nontraditional symptoms is higher among women than men; nontraditional stroke symptoms include headache, face and limb pain, nausea, and hiccups as well as symptoms typically believed to be unrelated to neurologic deficits (e.g., chest pain, shortness of breath, palpitations) [82].


Symptom on PresentationPrevalence
Overall nontraditional symptoms19%28%
Altered consciousness12%17%
Traditional Symptoms


The decline in stroke mortality has reduced, but not eliminated, the racial/ethnic gap in stroke mortality [78]. Racial/ethnic disparities in the incidence of stroke and its related mortality are substantial, and the factors contributing to the disparities are complex and poorly understood [1,4,5,6,7,83]. The risk of first-time stroke among black and Hispanic individuals approaches 2 times that for white individuals in the United States [22]. The Northern Manhattan Study (NOMAS) showed that the age-adjusted incidence of first ischemic stroke per 100,000 individuals was 191 in the black population, 149 in the Hispanic population, and 88 in the white population [83]. Another study showed that the prevalence of stroke among these three groups also varied according to age [5]. In the black population, the prevalence was 4.8% for individuals 45 to 64 years of age and 10% for individuals 65 years of age and older; the corresponding prevalences were 2.3% and 10% for Hispanic individuals and 2% and 9% for white individuals [5]. Intracranial atherosclerotic strokes were the most common type of strokes among the black and Hispanic populations [83].

According to the AHA 2014 update on statistics for heart disease and stroke, the prevalence of stroke is highest for the American Indian/Alaskan Native population and lowest for Hispanics (of any race) (Table 7) [1]. Data indicate variation among stroke-related mortality rates as well and show that stroke deaths have increased in minority populations while decreasing in the white population. Projections indicate a 20.5% increase in stroke by 2030, with the greatest increase (29%) in Hispanic men [1].


PopulationStroke PrevalenceHypertension Prevalence
American Indian/Alaskan Native5.8%NA
Non-Hispanic Black3.8%40.4%
Non-Hispanic White3.0%27.4%
Hispanic or Latino1.8%26.1%
Asian/Pacific Islander1.9%NA
NA = Not available

Data from 2008–2010 demonstrated an overall rate of 45.3 deaths per 100,000, with a rate of 63.5 for the black (non-Hispanic) population, 44.5 for the white (non-Hispanic) population, 39 for the American Indian/Alaskan Native population, 34 for the Hispanic population, and 31.9 for the Asian/Pacific Islander population [84]. Risk factors, such as hypertension, diabetes, and obesity, vary among these populations as well, but increased risks alone cannot completely explain increased prevalence or mortality [8].


Several modifiable risk factors for stroke have been well-documented in the literature, as well as many that have been less well-documented (Table 8). The well-documented risk factors include many risk factors for cardiovascular disease as well, and proper management of these factors can reduce both the risk of a first-time stroke and the development of a cardiovascular condition [6,8]. Clinicians should discuss the potential for stroke associated with risk factors specific to patients and offer strategies to reduce or eliminate them [8]. Four lifestyle factors warrant brief review because of the substantial role the patient has in helping to manage risk: smoking, diet and nutrition, physical inactivity, and obesity and body fat distribution.


Well-Documented FactorsaLess-Documented Factorsb
Cigarette smoking
Atrial fibrillation (AF)
Cardiac conditions other than AF
Asymptomatic carotid stenosis
Sickle cell disease
Postmenopausal hormone-replacement therapy
Diet and nutrition
Physical inactivity
Obesity and body fat distribution
Metabolic syndrome
Alcohol abuse
Drug abuse
Oral contraception use
Sleep-disordered breathing
Elevated lipoprotein (a)
a Listed in descending order of quality of documentation.
b Information on less-documented risks for stroke can be found in the American Heart Association (AHA) guideline, "Primary Prevention of Stroke."

Cigarette Smoking

Overwhelming evidence shows an undeniable association between cigarette smoking and stroke [85,86]. Smoking doubles the risk for ischemic stroke and increases the risk of hemorrhagic stroke 2 to 4 times [87]. Studies also indicate that repeated exposure to environmental ("secondhand") smoke almost doubles the risk of stroke [88].

Individuals who smoke should be prescribed smoking cessation medications and be informed about cessation programs, counseling, and nicotine replacement products. Epidemiologic studies show that, following smoking cessation, stroke risk decreases over time [8]. Individuals who do not smoke should be encouraged not to start.

Diet and Nutrition

Increased consumption of fruits and vegetables reduces the risk of stroke in a dose-dependent manner. Risk is reduced 6% for each serving of fruits and vegetables per day [89]. Increasing potassium and reducing sodium intake also mitigates the risk of stroke [8,90]. The Dietary Approaches to Stop Hypertension (DASH) diet, which is rich in fruits, vegetables, and low-fat dairy products and which limits saturated and total fat intake, has been shown to lower blood pressure and likely reduce the risk of stroke [91].

Physical Inactivity

A habitually sedentary lifestyle increases an individual's chance of stroke. Physically active men and women generally have a 25% to 30% lower risk of stroke or death than the least active people [92]. Individuals should be strongly encouraged to engage in aerobic exercise at moderate intensity for 150 minutes or more weekly; at vigorous intensity for 75 minutes or more per week; or a combination of both that fulfills these requirements [8]. It should be noted that only moderate-to-vigorous intensity exercise was found to reduce the incidence of stroke in the NOMAS study [83].

Obesity and Body Fat Distribution

One study has found that in the body mass index (BMI) range of 25 to 50 kg/m2, each 5 kg/m2 increase in BMI was associated with a 40% increased risk of stroke mortality; in the BMI range of 15 to 25 kg/m2, there was no relationship between BMI and stroke mortality [93]. Another large epidemiologic study showed that the risk almost doubled for overweight and obese men [94]. Studies have not yet addressed if losing weight reduces this risk. However, it is well-documented that weight loss lowers blood pressure and cholesterol and positively affects other risk factors for stroke. Clinicians should encourage overweight patients to begin a weight-loss program that includes a healthful diet and exercise and provide patients with safe weight-loss strategies, such as those recommended by the AHA [8].

Body fat distribution has proven to be a fairly reliable indicator of stroke risk [95,96]. While some studies support abdominal adiposity as a significant risk factor for stroke only in men, other research indicates that a high concentration of abdominal fat is a significant risk factor in both men and women, independent of BMI. On the other hand, gynoid adiposity in women appears to be associated with a lower risk for stroke, even for women with a higher BMI [96]. A high hip-to-waist ratio may be a more important risk factor for vascular disease, including stroke, than BMI score alone [97].



To decrease the incidence of first-time stroke in the United States, primary prevention should focus on individuals at high risk with modifiable risk factors. In areas of the United Kingdom, the incidence of major stroke has been reduced 40% through a reduction in the incidence of risk factors [98]. The AHA has established evidence-based recommendations for primary prevention of stroke and has developed public campaigns and educational materials to help raise awareness of stroke.

Evidence-Based Recommendations

For most individuals with nonmodifiable stroke risks, the probability of stroke can be decreased substantially with rigorous preventive measures and the treatment of modifiable risks [8,15]. The AHA recommends addressing lifestyle risk factors, as discussed, and medically managing several risk factors, including hypertension, diabetes, AF, other cardiac conditions, dyslipidemia, and asymptomatic carotid stenosis [8].


Hypertension is perhaps the most significant risk factor for stroke, and risk increases as blood pressure increases [8]. Despite compelling evidence since the 1970s of the strong link between hypertension and stroke, 28% of individuals with hypertension are not aware that they have the condition, 39% are not being treated for the condition, and 65% do not have the hypertension in control, defined as blood pressure less than 140/90 mm Hg [8].

The AHA and other professional organizations recommend that all adults 18 years of age and older be screened for high blood pressure. The U.S. Preventive Services Task Force states that the optimal screening interval is not known but notes the recommendation of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7), which is screening every 2 years for adults with a blood pressure less than 120/80 mm Hg and screening every year for people with systolic blood pressure of 120 to 139 mm Hg or diastolic blood pressure of 80 to 90 mm Hg [99,100]. The 2013 update (JNC 8) contains no recommendations for screening. The AHA/ASA recommends that women be screened for high blood pressure before taking birth control pills, as the combination increases the risk of stroke [295].

Appropriate management of hypertension may also include dietary changes, other lifestyle modifications, and pharmacologic therapy. Studies have shown that management is possible for the majority of patients, but most will require treatment that includes two or more drugs [8].


The risk for stroke is 2 to 4 times higher among individuals with diabetes. In 2004, stroke was noted on 16% of diabetes-related death certificates among people 65 years of age or older [101]. Type 2 diabetes is associated with an increased prevalence of atherogenic risk factors, such as hypertension, obesity, and dyslipidemia. The combination of hyperglycemia and hypertension is thought to increase the risk of stroke [8]. The AHA recommends that the target blood pressure for individuals with diabetes be less than 130/80 mm Hg [8]. Pharmacologic therapy with angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) has been shown to be safe and effective in this population [8]. In addition, lipid-lowering statins reduce the risk of first-time strokes in patients with diabetes, irrespective of the baseline lipid levels, pre-existing vascular conditions, and glycemic control [102].

Atrial Fibrillation (AF)

AF is associated with a fourfold to fivefold increased risk of ischemic stroke, and approximately 60,000 strokes occur among the 2.3 million individuals with AF annually [8]. According to the AHA/ASA, women older than 75 years of age should be screened for atrial fibrillation risk due to its link to greater stroke risk [295]. The AHA recommends that individuals with AF who have valvular heart disease (particularly individuals who have mechanical heart valves) should receive anticoagulant therapy [8]. Antithrombotic therapy with adjusted-dose warfarin or aspirin is approved for stroke prevention in individuals with nonvalvular AF based on their calculated risk of stroke and estimated risk of bleeding. The individual's preferences and access to high-quality anticoagulation monitoring should be considered. Warfarin therapy to maintain an international normalized ratio (INR) of 2.0 to 3.0 (target: 2.5) is strongly recommended for high-risk individuals (those with more than a 4% annual risk of stroke) with AF and no significant contraindications to oral anticoagulants [8,103]. Despite the effectiveness of such treatments, anticoagulant therapy continues to remain underprescribed due to overestimation of the associated risks of warfarin (e.g., intracranial, extracranial hemorrhage) and underestimation of stroke risk [103]. Some physicians err on the side of caution and aim for an INR greater than the recommended target, with a corresponding reduction in therapeutic effectiveness.

Other Cardiac Conditions

The management of valvular heart disease, unstable angina, chronic stable angina, acute MI, and other cardiac conditions is a critical factor in stroke prevention. Strategies to prevent postoperative neurologic injury and stroke in patients undergoing surgical revascularization for atherosclerotic heart disease can be found in the American College of Cardiology coronary artery bypass graft surgery guidelines, which are approved by the AHA [8,104]. The AHA states that it is "reasonable" to use warfarin for patients who have had ST-elevation MI and left ventricular dysfunction with extensive regional wall-motion abnormalities [8].


The AHA recommends that statin therapy be prescribed for individuals with known coronary heart disease or high-risk hypertension (e.g., patients with diabetes), including those with normal low-density lipoprotein (LDL) cholesterol levels [8]. In addition, these individuals should be encouraged at every interaction to exercise, eat a healthful diet, and quit smoking. Niacin, bile acid sequestrants, ezetimibe, or fibric acid derivatives may also be considered for individuals with known coronary heart disease and low levels of high-density lipoprotein cholesterol, such as people in whom target cholesterol levels cannot be achieved with statins or people who cannot tolerate statin therapy; however, their effectiveness in decreasing stroke risk has not been established [8].

Asymptomatic Carotid Stenosis

Individuals with asymptomatic carotid artery stenosis should be screened for other modifiable risk factors, and any risk factors identified should be controlled as soon as possible. Antiplatelet therapy with aspirin is recommended, unless contraindicated [8]. Preventive carotid endarterectomy performed by a skilled surgeon is an option for patients when it is determined that the morbidity/mortality risk is less than 6%; however, the reduction in stroke risk is modest at best [9,105]. Comorbidities and life expectancy should be considered when determining if surgery is appropriate. In addition, thorough discussion with the patient and his or her family/caregivers is a necessity. Topics should include the possibility of surgery-related death, the risks and benefits associated with the procedure, and the patient's preferences. For patients with a high surgical risk, carotid angioplasty/stenting may be considered. However, the periprocedural and overall 1-year event rates in some studies have dampened the AHA's enthusiasm for the stenting option [8,9].

Depressive Symptoms

After publication of the AHA guidelines, the findings of a large study showed that depressive symptoms are an independent risk factor for stroke, especially for patients younger than 65 years of age [106]. Clinicians may consider managing depressive symptoms and mood disorders as aggressively as hypertension or diabetes, because mood disorders appear to increase risk for all types of stroke [107].


Although public knowledge regarding the warning signs and risks of stroke has improved, the majority of the general public is still unaware that early treatment can prevent severe disability and death [108,109]. Estimates vary widely, however; the International Stroke Trial found that only 4% of patients with acute ischemic stroke arrive at the emergency department (ED) within 3 hours after the onset of symptoms, and a separate study found that 21% to 25% of individuals with acute ischemic stroke arrive at an ED within the same timeframe [110,111]. Of these individuals, 2% to 4% receive thrombolytic treatment [112,113]. It has been estimated that if all individuals called for emergency help at the onset of symptoms, as many as 29% could realistically receive treatment within 3 hours [112]. In addition, if all patients arrived at the ED within 1 hour after known symptom onset and received optimal treatment, the projected rate of thrombolysis would be 57%.

To improve the rate of early arrival in the ED, public education campaigns designed to help individuals recognize a stroke and seek early treatment often use the "five sudden warning signs" devised by the Brain Attack Coalition, or "FAST," a mnemonic device created by study investigators on the basis of the Cincinnati Prehospital Stroke Scale [114,115]. The AHA uses the five sudden warning signs in their public campaigns, and the National Stroke Association and other organizations use FAST. Early signs and symptoms that comprise the five sudden warning signs include [115,116]:

  • Numbness of the face, arm, or leg (especially on one side)

  • Trouble seeing from one or both eyes

  • Severe headache

  • Dizziness, difficulties with walking, and loss of balance and coordination

  • Confusion and trouble speaking or understanding

FAST was designed to focus on fewer common signs of stroke onset (face numbness, arm numbness, and slurred speech) and to include an action component (time) for lay persons who may have trouble recalling the warning signs and the appropriate action. A retrospective study exploring the capacity of the FAST campaign to facilitate the recognition of stroke suggests that it leads to the identification of approximately 89% of individuals who have a stroke or TIA [115]. The most common stroke symptoms were related to the face, arm, and speech/language. The same study found that a modified version of FAST (with removal of the word "numbness") decreased the number of TIAs identified and targeted ischemic stroke more readily than hemorrhagic stroke. Ultimately, it is unknown whether the general public is more likely to remember FAST or the five sudden warning signs.

In 1989, the United States Department of Health and Human Services Public Affairs launched a National Health Observance to help stimulate awareness of the risk factors, prevention, and early treatment of stroke. For 25 years, May has been recognized as American Stroke Month, with special campaigns to heighten awareness of stroke among the general public. Resources to aid community campaigns can be obtained from the National Stroke Association at http://www.stroke.org/site/PageServer?pagename=awareness.


Patient education should be presented in several forms and focus on modifiable risk factors, patients' needs, lifestyle, and life stage. Healthcare professionals can be most effective in reducing the risk of stroke when they demonstrate an interest in a patient's lifestyle and psychologic status. For instance, if a patient depends on his or her spouse or companion for meals, optimum benefits will result from educating the spouse/companion about healthy diet practices. Clinicians should also consider cultural needs when addressing prevention strategies.

When a patient/caretaker does not speak the same language as the clinician, a professional interpreter should be consulted to ensure accurate communication. A systematic review of the literature has shown that the use of professional interpreters provides better clinical care than the use of informal interpreters, with the former improving the quality of care for patients with limited English language skills to a level equal to that for patients with no language barriers [117]. Use of professional interpreters has been associated with improvements in communication (errors and comprehension), utilization, clinical outcomes, and satisfaction with care [117]. Individuals with limited English language skills have indicated a preference for professional interpreters rather than family members [118].

Whether the education involves stroke prevention, stroke recognition, care after stroke, coping with the effects of stroke, or palliative care, written materials are as important as verbal communication. Several organizations supply general or specialized educational resources, and many also provide patients and family/caregivers with psychosocial, financial, and assisted-living information or aid (Table 9). Clinicians should attempt to obtain materials written in languages appropriate for their patient population and, if appropriate, that target patients in high-risk racial/ethnic populations, especially American Indian/Alaskan native and black individuals. Among new ways for clinicians to heighten awareness in their patients are electronic tips provided by the National Stroke Association that can be sent by e-mail to patients.


American Heart Association
1-800-AHA-USA-1 (242-8721)
American Stroke Association
1-888-4STROKE (478-7653)
Brain Aneurysm Foundation
1-888-BRAIN02 (272-4602)
Brain Attack Coalition
Centers for Disease Control and Prevention
Internet Stroke Center
National Stroke Association
1-800-STROKES (787-6537)
BrightFocus Foundation
Hazel K. Goddess Fund for Stroke Research in Women
National Aphasia Association
1-800-922-4NAA (4622)


When determining the appropriate degree of risk management, information regarding an individual's risk of first stroke is valuable. The goals of risk assessment tools include [8]:

  • Identifying patients who are unaware of their elevated risk

  • Assessing the total risk of multiple factors

  • Discerning the utility of modifications and treatments

  • Projecting a quantitative risk in order to select appropriate treatments or stratification in clinical trials

  • Guiding appropriate use of diagnostic tests

The numerous nonmodifiable and modifiable factors that contribute to the risk of stroke have been discussed. Although many of these are independent risk factors, their interactions can affect predictions and management decisions in unexpected ways. No simple, validated stroke risk-assessment tool is currently available [8]. Although risk-assessment tools may have some utility, it is unknown if they improve primary prevention, especially when applied across subgroups according to age, gender, and race/ethnicity [8,85].

Because TIA is a substantial risk factor for a subsequent stroke, clinicians in many EDs are stratifying such patients by degree of risk with use of the ABCD or ABCD2 assessments [119,120]. The ABCD clinical tool is designed to predict 7-day risk of stroke through assessment of age (1 point for patients 60 years of age or older), blood pressure (1 point for a blood pressure greater than 140/90 mm Hg), clinical features (2 points for unilateral weakness with or without speech impairment or 1 point for speech impairment without weakness), and duration (1 point for 10 to 59 minutes, 2 points for greater than 59 minutes) [121]. The "2" designation in ABCD2 was added to represent the presence or absence of diabetes. The effectiveness of these screening tools is lessened by the fact that some individuals do not seek emergency care for a TIA or do not report a TIA to their clinician. However, the ABCD2 assessment has been shown to identify 21% of individuals with a high 2-day risk of having an ischemic stroke [119]. Individuals with high-risk TIA require the same intensity of evaluation and stroke prevention as individuals with ischemic stroke.


Because the temporal window for effective stroke treatment is short, it is imperative that evaluation and diagnosis are performed promptly and accurately. As noted, fewer than 25% of individuals with ischemic stroke present to an ED or a clinician's office within the optimum 3-hour treatment interval [110]. The AHA has established several evidence-based recommendations for the diagnosis and early management of adult-onset ischemic stroke [15]. These recommendations address the evaluation of the individual before he or she arrives at an ED, diagnosis in the ED, the history and physical examination, laboratory tests, carotid ultrasonography, cerebral angiography, and imaging studies.


The single most important factor influencing the treatment of stroke within 3 hours after the onset of symptoms is the rapid triage and transportation provided by EMS [122]. Stroke assessment should begin with the EMS dispatcher. When stroke or TIA is suspected, the dispatcher is responsible for notifying the appropriate EMS provider and coordinating with an appropriate acute stroke treatment facility (Table 10). Regardless of the degree of the neurologic deficits, an individual with suspected stroke or TIA should be dispatched and triaged as if he or she were a serious trauma patient [15]. If possible, the individual should be taken to a designated stroke center [15,18].


Detection: Recognize stroke signs and symptoms

Dispatch: Call 911 and priority emergency medical services dispatch

Delivery: Prompt pre-hospital notification and transport to hospital

Door: Immediate emergency department triage

Data: ED evaluation, prompt laboratory studies, and computed tomography

Decision: Diagnosis and decision about appropriate therapy

Drug: Administration of appropriate drugs or other interventions

After the individual's airway, breathing, and circulation have been assessed and stabilized, the EMS personnel should initiate a prehospital evaluation [15,123]. If the individual exhibits common signs of stroke and/or a stroke is indicated by a validated prehospital examination tool (e.g., Los Angeles Prehospital Stroke Screen, Cincinnati Prehospital Stroke Scale), EMS providers should notify the ED that an individual with suspected stroke is in transport [123,124]. Any information about coexisting conditions and, most importantly, time of symptom onset should be provided in advance. A blood glucose level should also be determined, as symptoms of hypoglycemia may mimic those of a stroke [15].

Prehospital evaluation expedites the physician's evaluation of the patient on arrival in the ED. If possible, a witness (preferably a close family member or companion) should be transported with the patient to assist with patient history, symptom onset, and contact information. If no witness was present, a family member should be contacted to go to the hospital and should be informed that he or she may need to provide consent for the patient's treatment. History obtained by EMS providers should include [15]:

  • Information about recent events (e.g., stroke, myocardial infarction, trauma, surgery, bleeding)

  • Comorbid diseases (e.g., hypertension, diabetes)

  • Use of medications (e.g., anticoagulants, insulin, antihypertensives)

The patient's medication containers should be transported to the ED as well, especially if medications include anticoagulant, antiplatelet, or antihypertensive drugs. Because 50% of individuals with suspected stroke do not use EMS for initial medical care access, ED staff should be alert to signs of stroke among individuals waiting to be seen in the ED [15].


Organization of the ED's stroke team and assessment protocol is paramount to maximize the likelihood of early and successful management [15]. The acute stroke team should include physicians, nurses, and laboratory/radiology personnel. After the patient has been triaged and stabilized, the inaugural ED evaluation (history and physical examination), laboratory studies, and CT imaging should be performed concurrently. The multimodal approach has three goals [15]:

  • Rapid and careful identification of people with stroke for treatment purposes

  • Determination of the underlying cause of the stroke for secondary prevention

  • Detection of stroke-mimicking conditions that may require immediate care

Within 1 hour of the patient's arrival, the evaluation (including a neurologic examination) and treatment decision should be completed. The AHA recommends that all patients should receive a standardized battery of tests and procedures, with alternative tests performed only if a particular condition is suspected or the patient's history is incomplete (Table 11) [15]. Generally, diagnostic tests should be limited to save time. In addition, all diagnostic tests for stroke should be available 24 hours a day, 7 days a week.


PopulationDiagnostic Test
All patients Cerebral computed tomography or magnetic resonance imaging (without contrast medium)
Blood glucose
Serum electrolytes/renal function tests
Markers of cardiac ischemia
Complete blood count, including platelet count
Prothrombin time/international normalized ratio (INR)
Activated partial thromboplastin time
Oxygen saturation
Selected patients Hepatic function tests
Toxicology screen
Blood alcohol level
Pregnancy test
Arterial blood gas tests (if hypoxia is suspected)
Chest radiography (if lung disease is suspected)
Lumbar puncture (only if stroke is suspected to be secondary to an infectious disease)
Electroencephalography (if seizures are suspected)


In addition to time of onset, other critical historical data that should be obtained include [15]:

  • Information about atherosclerotic and cardiac disease risk factors

  • Prior and current drug abuse and history of migraine, seizure, infection, trauma, or pregnancy

  • Eligibility for treatment of ischemic stroke

If a patient presents with classic signs of stroke and has one or more cardiovascular risk factors, the diagnosis of stroke can be straightforward. However, identifying more unusual cases may be a challenge. If fever and a cardiac murmur are present, the cause of the stroke may be infective endocarditis [126,127]. Giant cell arteritis may be the cause if the patient is 50 years of age or older, has a headache, and has an elevated erythrocyte sedimentation rate. The presence of ptosis and miosis contralateral to the deficit may suggest carotid artery dissection [126,127]. If the symptoms were maximal at their onset, a subarachnoid hemorrhage or embolic stroke should be suspected [128]. In up to 40% of patients with subarachnoid hemorrhage, a severe headache (sometimes called a thunderclap or sentinel headache) that may abate within minutes or hours is the only symptom [128]. Cerebral CT should be immediately performed in any patient with a suspected subarachnoid hemorrhage [35].

The general physical examination should involve assessment of the head, neck, heart, lungs, abdomen, skin, and extremities, as well as the cardiovascular, respiratory, and gastrointestinal systems [15]. Pulse oximetry and body temperature are also important evaluations. When performing the head and neck examination, the clinician should look for physical signs of trauma or seizure activity (e.g., contusions, tongue lacerations) or heart failure (jugular venous distention). Thrombolytic treatment is inadvisable for a seizure in the absence of acute ischemia detected by imaging.

When examining the patient's neck, carotid bruits may be heard. Although these sounds may suggest atherosclerosis, they are not sufficient for diagnosing carotid stenosis [129]. Because the prevalence of asymptomatic carotid bruits increases with advancing age, it is not a reliable clinical marker of stroke risk in individuals older than 65 years of age [130].

The cardiac examination may demonstrate contributing factors or comorbidities, such as myocardial ischemia, valvular conditions, arrhythmias, or aortic dissection (a rare cause of ischemic stroke) [15]. The diagnostic evaluation should include electrocardiography (ECG), because cardiovascular conditions such as AF and MI are prevalent among individuals with stroke [125]. The findings of studies have suggested that the value of chest x-ray as part of the diagnostic workup is debatable, and the 2013 AHA guideline recommends a chest x-ray only if lung disease is suspected [15]. Although cardiac monitoring in patients with stroke has not been evaluated, the AHA recommends its use in the first 24 hours to monitor for AF or MI, either of which can lead to stroke or be a dangerous coexisting condition.

Blood pressure sustained at or above 180/120 mm Hg may signal hypertensive encephalopathy [99,131]. Examination of the respiratory system and the abdomen may lead to the detection of additional conditions. The state of the skin and extremities may indicate systemic conditions, including coagulopathies, platelet disorders, or liver dysfunction [15]. An irregular pulse may be indicative of AF.

If only historical information and/or physical examination are relied on, up to 19% of stroke mimics are mistaken for stroke. Yet, a patient's history and examination may also identify a condition masquerading as a stroke (Table 12) [15,132]. The use of MRI or CT with laboratory studies enhances the accuracy of diagnosis, but detecting mimics with imaging techniques is a challenge if the patient has a history of stroke [15].


Stroke MimicDifferential Symptoms
Brain tumorGradual progression of symptoms
Drug overdoseAltered mental status without focal findings
Conversion disorder
Neurologic findings in a nonvascular distribution
Inconsistent examination
Other psychiatric disorders
Hypertensive encephalopathy
Significant hypertension
Cortical blindness
Cerebral edema
History of diabetes
Low blood glucose level
Decreased level of consciousness
History of similar events
Preceding aura
Hemiplegia that outlasts the headache
Seizures/postictal paresis
History of seizures
Witnessed seizure activity
Drug toxicityHistory of lithium, phenytoin, or carbamazepine use

Another important component of the physical examination is assessment with the National Institutes of Health Stroke Scale (NIHSS). Although initially devised as a research tool to quantify neurologic deficits, this tool is now widely used to measure the severity of a stroke, devise an effective treatment plan that establishes a priority for patient safety, identify the potentially occluded vessel, and predict patient outcome [15,133]. The NIHSS is standardized, reliable, and fast and facilitates communication among healthcare professionals. Any trained healthcare professional can use the scale at the bedside in 5 to 8 minutes. In addition, results are based only on patient evaluation; a history or information from others is not necessary. It is recommended that the scale be used to assess the patient during the ED evaluation and during treatment with recombinant tissue plasminogen activator (rt-PA) or other therapies and that it be repeated often in the first 24 hours. Further information about the NIHSS and a copy of the scale can be obtained from the National Institute of Neurological Disorders and Stroke [134].


For all patients with suspected stroke, the battery of diagnostic tests should be carried out concurrently with laboratory tests, including blood glucose level (to rule out hypoglycemia as a stroke mimic), complete blood count (with platelet count), serum electrolyte levels, renal function studies, and cardiac ischemia biomarkers [15]. Determination of prothrombin time and partial thromboplastin time are of particular importance when considering thrombolysis. Generally, waiting for the results of a diagnostic test should not be a reason to delay thrombolytic therapy. The risk of increased neurologic damage and death caused by ischemic stroke outweighs that of a secondary hemorrhage except when a bleeding or blood disorder is suspected, the patient was given warfarin or heparin, or the patient takes anticoagulant drugs.


Carotid ultrasonography is a noninvasive vascular imaging technique used to measure arterial blood flow and determine the site and degree of stenosis/occlusion of cerebral vasculature. In particular, transcranial Doppler ultrasonography, which can be performed at the bedside, serves multiple purposes in the cerebrovascular setting. Its most common uses are to assess a patient's primary and secondary stroke prevention needs and to monitor a patient's progress during the early post-acute stroke phase [9,15,135]. Additional uses of transcranial Doppler ultrasonography in patients with stroke include [15,135,136]:

  • Detection of intracranial and extracranial vascular disorders

  • Assessment of recurrent stroke risk (e.g., microemboli detection)

  • Identification of candidates for intensive prophylactic interventions (e.g., carotid endarterectomy, angioplasty/stenting)

  • Intraoperative monitoring of carotid endarterectomy

  • Detection of right-to-left shunts

  • Identification of subclavian steal syndrome

  • Measurement of a post-subarachnoid hemorrhage vasospasm

  • Assessment of recanalization (spontaneous or thrombolytically induced)

  • Prognosis of patients with stroke (performed during post-acute phase)

Despite the usefulness of this technique, its performance is highly operator-dependent [135]. Considerable anatomic and physiologic knowledge of the cerebral vasculature is required, as vessel images are not produced, and skill and experience are prerequisites for data interpretation [135,137]. For these reasons, vascular imaging is not practical for the diagnosis of ischemic stroke in most cases. Data acquisition and interpretation tend to be time-consuming and may delay treatment. Thus, the 2013 AHA guidelines do not recommend the use of vascular imaging studies for patients in whom the onset of stroke-related symptoms is less than 3 hours [15]. The guidelines further suggest that carotid ultrasonography should be postponed until a patient has had acute treatment.


Conventional catheter angiography is invasive, uses ionic radiation, and requires a nephrotoxic contrast medium [138]. It is particularly valuable for the detection of pathologic vascular disorders that lead to cerebral hemorrhage or ischemia, including aneurysm, vasculitis, arteriovenous malformation, atherosclerosis, and arterial dissection [9,15]. Digital subtraction angiography (DSA), a type of catheter angiography, remains the standard criterion of conventional angiography for detection of many types of cerebrovascular lesions and diseases [139,140,141]. Its sensitivity and specificity equal or exceed those of noninvasive techniques; however, it can cause serious complications, such as stroke or death [15].

Unlike catheter angiography, magnetic resonance angiography (MRA) is not an x-ray. This technique creates a map of blood flow, not a true image of the vasculature anatomy. Noninvasive time-of-flight MRA is performed without contrast medium, whereas phase-contrast MRA is performed with contrast medium and is minimally invasive (catheter insertion into a blood vessel is unnecessary). Although MRA provides a high-resolution image of many vessels, it cannot reliably resolve distal or branch occlusions of the intracranial vasculature [15]. Another major disadvantage of MRA is that it overestimates the degree and length of high-grade stenosis by signaling loss of flow when blood flow is turbulent, in-plane, or slow [142]. Although MRA continues to advance technologically, in large part through the improvement of contrast media, high-grade stenosis is still overestimated using this technique when compared with DSA [143]. MRA is helpful for detecting less common causes of ischemic stroke or TIAs (e.g., arterial dissection, venous thrombosis) [141].

Computed tomography angiography (CTA) is being investigated in the setting of acute ischemic stroke [15]. This procedure provides a means to rapidly and noninvasively screen intracranial and extracranial vasculature for stenoses and occlusions. Preliminary data suggest that CTA effectively detects large-vessel intracranial occlusions when compared with ultrasound and DSA [144]. Although CTA is fast and can be adapted to conventional CT, contrast medium is required and patients are exposed to additional radiation [15].

Transcranial Doppler (TCD) ultrasonography has been used to detect intracranial vessel abnormalities and to evaluate occlusions and stenoses in intracranial vessels. It is less accurate than CTA or MRA for steno-occlusive disease but can detect microembolic signals that indicate extracranial or cardiac sources of embolism. TCD has been shown to predict and enhance outcomes with intravenous rt-PA [145].

Because the time between the onset of stroke and treatment should be limited, catheter angiography is not recommended by the AHA for the diagnosis of a suspected stroke [15]. In the case of a stroke, the utility of the imaging tool increases after a diagnosis has been made. As with transcranial Doppler ultrasonography, cerebral angiography is particularly useful for confirming the diagnosis, monitoring the progression of thrombolytic therapy, and assisting with the prognosis, particularly during the first 72 hours after a stroke [15].


High diagnostic accuracy of stroke and treatment decisions is optimized by the use of imaging tools such as CT and MRI. Collectively, these neuroimaging options provide detailed information that influences stroke treatment decisions, including infarct age, severity, and distribution; intracranial vascular status; cerebral hemodynamics; estimated reversibility of ischemic damage; and hemorrhage type and distribution [15]. For instance, a widespread distribution of early infarction or edema increases hemorrhagic transformation risk following thrombolytic therapy. CT without contrast medium is readily sensitive to these conditions [15].

For prompt and accurate diagnosis, the use of noncontrast CT or diffusion-weighted MRI is recommended for suspected stroke [15]. Although CT is less expensive, faster, and more widely available, diffusion-weighted MRI more readily detects small cortical, small subcortical, and posterior fossa infarcts and distinguishes chronic ischemia from acute ischemia. MRI is also sensitive to subclinical satellite ischemic lesions that characterize the pathophysiology of the stroke [15,146]. Diffusion-weighted MRI can detect acute ischemic changes within minutes after the onset of stroke; CT may not detect ischemic stroke until up to 1 hour after the event [15]. However, not all patients with suspected stroke may benefit from MRI. Contraindications for MRI include claustrophobia, pacemakers, and metal implants.

If a patient is eligible for rt-PA, the AHA suggests that the CT or diffusion-weighted MRI should be completed within 25 minutes after arrival in the ED and interpreted within 45 minutes [15]. Thus, a physician with expertise in reading these images must be available. The multimodal CT approach (noncontrast CT, perfusion CT, and CT angiography studies) or MRI approach (diffusion-weighted imaging, perfusion-weighted imaging, MRA, gradient echo, and often fluid-attenuated inversion recovery or T2-weighted sequences) may provide additional information to improve the diagnosis of ischemic stroke. However, emergency treatment of stroke should not be delayed by waiting for the results of multimodal imaging [15].

Although CT and MRI are increasingly available in EDs, the AHA states that non-contrast-enhanced computed tomography (NECT) is sufficient to identify contraindications to fibrinolysis and to ensure that patients with ischemic stroke receive timely intravenous fibrinolytic therapy. The AHA recommends that NECT be obtained within 25 minutes of the patient's arrival in the ED [15].


Because strokes are highly heterogeneous, are associated with multiple medical complications, and are time-critical, their effective management depends on organized and comprehensive care. Such treatment is optimally provided in comprehensive stroke centers and stroke systems of care. In 2007, the AHA published evidence-based guidelines to provide recommendations for treatment. These guidelines were updated in 2013 [15].


Comprehensive stroke centers are designed to accommodate the needs of patients with complicated forms of stroke, intracranial hemorrhages, and subarachnoid hemorrhages, as well as patients in need of aggressive intervention measures and intensive care [18]. In general, primary and comprehensive stroke centers have been shown to be associated with better adherence to evidence-based guidelines and with an increased use of intravenous rt-PA [147]. Nationally, only 2% to 3% of individuals with stroke are treated with rt-PA, but the rate is typically greater than 10% at primary and comprehensive stroke care centers [18,113]. Overall care may also be improved at comprehensive stroke centers [147,148]. A formal certification process for comprehensive stroke centers is under development by the Joint Commission and the ASA. The Joint Commission has been certifying primary stroke centers since 2004, and it began providing accreditation for comprehensive stroke centers in 2012 [15]. Because patients are more likely to receive thrombolytic therapy at primary and comprehensive stroke centers, policies mandating the direct routing of individuals with suspected stroke (with onset of symptoms less than 3 hours previously) to either of these types of facilities have been established in seven states (Florida, Maryland, Massachusetts, New Jersey, New Mexico, New York, and Texas) [15]. Telemedicine for stroke (also called telestroke) and air transport are being increasingly used to serve individuals in rural areas that lack local stroke expertise [148].

Stroke centers are commonly part of a comprehensive support network known as a stroke system of care. The system seeks ways to coordinate the highest quality of stroke prevention, community education, EMS, acute care, and post-acute care. Without a system of care, these components often operate less effectively and in isolation. Implementation of a stroke system of care in underserved regions could substantially improve treatment statistics state- or nationwide; for example, one study showed that the additional resources at as few as six target hospitals in the western part of North Carolina would increase patient access to stroke care by 61.5% throughout the state [149].

Guidelines for establishing a stroke system of care were developed by an ASA Task Force [19]. Because of the multidisciplinary aspects of a stroke system, Task Force members were experts in areas of stroke prevention, EMS, acute stroke care, rehabilitation, and healthcare policy. Overall, the recommendations promote the communication and collaboration of patients, clinicians, facilities, and agencies. General ASA recommendations for a stroke system of care are [19]:

  • Coordinate providers of prevention, timely identification, transport, treatment, and rehabilitation of individual patients with stroke in a locality or region, and facilitate interactions among these individuals/agencies.

  • Promote the use of an organized, standardized approach in each facility and component of the system.

  • Identify performance measures (both process and outcomes measures), and include a mechanism for evaluating effectiveness through which the entire system and its individual components can improve.

  • Provide patients and clinicians with the tools needed for effective stroke prevention, treatment, and rehabilitation.

  • Ensure that decisions about protocols and patient care are based on what is in the best interests of patients with stroke.

  • Identify and address potential barriers to successful implementation. Barriers may include costs of developing and maintaining a stroke system, geopolitical lines of service by EMS, adequate legal and political recognition of the system, competition for patients and market share among providers, tensions that may exist among academic and community-based institutions, variable commitment to acute stroke therapy, differences in corporate culture among different facilities and provider groups, and concerns about the adequacy of reimbursement. The involvement of policymakers and stakeholders may be necessary.

  • Customize systems for each state, region, or locality while maintaining universal elements to help ensure optimal prevention of stroke and the timely identification, transport, treatment, and rehabilitation of patients with stroke. For instance, the implementation of transportation services and telemedicine procedures may help individuals in rural areas gain access to needed services.


Thrombolytic therapy with rt-PA is the only treatment approved by the U.S. Food and Drug Administration (FDA) for ischemic stroke [15]. Anticoagulant and antiplatelet agents are also used, but their appropriateness is a source of debate because of limited and inconclusive evidence. The AHA recommendations for the treatment of ischemic stroke are based on an exhaustive review of available studies and emphasize the importance of early management [15].

Recombinant Tissue Plasminogen Activator (rt-PA)

The intravenous administration of rt-PA has been FDA-approved for the treatment of stroke since 1996. Treatment with rt-PA is highly effective if administered within 3 hours. The earlier treatment is initiated, the higher the probability of a full recovery. Treatment within 90 minutes has been associated with a higher rate of favorable outcome at 3 months compared with treatment administered within 180 minutes [150]. However, the therapeutic window may extend to 6 hours [151,152]. Studies to determine the threshold of rt-PA benefits are ongoing. The AHA has changed some of its recommendations regarding rt-PA treatment since its 2003 guidelines (Table 13) [15]. Administration of rt-PA is not recommended for patients who have a systolic blood pressure greater than 185 mm Hg or a diastolic blood pressure greater than 110 mm Hg [15].


Class I Recommendations

Intravenous rt-PA (0.9 mg/kg, maximum dose 90 mg) is recommended for selected patients who may be treated within 3 hours of onset of ischemic stroke (Class I, Level of Evidence A). Physicians should review the criteria outlined in the AHA guidelines to determine the eligibility of patients.

In patients eligible for intravenous rt-PA, benefit of therapy is time dependent; treatment should be initiated as quickly as possible. The door-to-needle time should be within 60 minutes from hospital arrival (Class I, Level of Evidence A).

Intravenous rt-PA (0.9 mg/kg, maximum dose 90 mg) is recommended for administration to eligible patients who can be treated in the time period of3–4.5 hours after stroke onset (Class I, Level of Evidence B). Physicians should review the criteria outlined in the AHA guidelines to determine the eligibility of patients.

Intravenous rt-PA is reasonable in patients whose blood pressure can be lowered safely (to less than 185/110 mm Hg) with antihypertensive agents, with the physician assessing the stability of the blood pressure before starting intravenous rt-PA (Class I, Level of Evidence B).

In addition to bleeding complications, physicians should be aware of the potential side effect of angioedema that may cause partial airway obstruction (Class I, Level of Evidence B).

Class II Recommendations

A patient with a seizure at the time of onset of stroke may be eligible for treatment as long as the physician is convinced that residual impairments are secondary to stroke and not a postictal phenomenon (Class IIa, Level of Evidence C).

The effectiveness of sonothrombolysis for treatment of patients with acute stroke is not well established (Class IIb, Level of Evidence B).

The usefulness of intravenous administration of tenecteplase, reteplase, desmoteplase, urokinase, or other fibrinolytic agents and the intravenous administration of ancrod or other defibrinogenating agents is not well established, and they should only be used in the setting of a clinical trial (Class IIb, Level of Evidence B).

The effectiveness of intravenous treatment with rt-PA is not well established (Class IIb, Level of Evidence C) and requires further study for patients who can be treated in the time period of3–4.5 hours after stroke. Physicians should review the criteria outlined in the AHA guidelines to determine the eligibility of patients.

Use of intravenous fibrinolysis in patients with conditions of mild stroke deficits, rapidly improving stroke symptoms, major surgery in the preceding 3 months, and recent myocardial infarction may be considered, and potential increased risk should be weighed against the anticipated benefits (Class IIb, Level of Evidence C). These circumstances require further study.

Class III Recommendations

The intravenous administration of streptokinase for treatment of stroke is not recommended (Class III, Level of Evidence A).

The use of intravenous rt-PA in patients taking direct thrombin inhibitors or direct factor Xa inhibitors may be harmful and is not recommended unless sensitive laboratory tests such as aPTT, INR, platelet count, and ECT, TT, or appropriate direct factor Xa activity assays are normal, or the patient has not received a dose of these agents for more than 2 days (assuming normal renal metabolizing function). Similar consideration should be given to patients being considered for intra-arterial rt-PA (Class III, Level of Evidence C). Further study is required.

Between 31% and 50% of patients treated with rt-PA have a 4-point or greater improvement on the NIHSS by 3 months after the stroke [15]. These clinical improvements do not recede for at least 1 year after the stroke. In general, the best response to rt-PA has been found for patients who are younger than 75 years of age, with a baseline NIHSS score of less than 20, and no history of diabetes or pre-existing disability [15].

The most common serious medical complication of rt-PA is secondary brain hemorrhage, which occurs in 6% of patients [15,153]. Yet, the risk does not outweigh the benefits of rt-PA. Three months following rt-PA therapy, approximately 30% of patients are neurologically normal or near normal; 30% have mild-to-moderate neurologic deficits; 20% have moderate-to-severe deficits; and 20% have died [154]. Other dangerous complications of rt-PA, although rare, are angioedema, anaphylaxis, systemic hemorrhage, and if rt-PA is administered soon after an acute MI, myocardial rupture [155].


The AHA Task Force reviewed and discussed several studies addressing the use of heparin or low-molecular-weight heparin (LMWH) and danaparoid as an adjunct to a thrombolytic agent in the treatment of stroke [15]. In general, the Task Force concluded that early administration of heparin or LMWH and danaparoid is inadvisable partly due to the increased risk of bleeding complications, especially the hemorrhagic transformation of ischemic strokes. Additionally, early administration has not been shown to prevent recurrent stroke, lessen the risk of neurologic worsening, or improve patient outcome [15].


Although no new data have emerged since the 2003 version of the AHA guidelines for ischemic stroke management regarding antiplatelet treatment, the AHA recommendations for antiplatelet therapy have changed (Table 14) [15]. Data combined from two large clinical trials suggest that administration of aspirin (325 mg) within 48 hours after the onset of stroke slightly reduces mortality and morbidity by preventing early recurrent stroke in some patients [156,157]. The findings of these trials do not suggest the use of aspirin within 24 hours of thrombolytic administration or as a substitute for thrombolytic therapy. A review that summarized the results of nine randomized controlled trials confirmed the findings of these meta-analyses and demonstrated increased odds of complete recovery [158]. Other oral antiplatelet therapies (e.g., ticlopidine, clopidogrel, dipyridamole) have not been tested sufficiently in the setting of acute ischemic stroke. The efficacy of intravenous glycoprotein IIb/IIIa receptor blockers in combination with other interventions or alone is under investigation. These agents may accelerate spontaneous recanalization and improve microvascular patency [159]. If administered alone, these agents have been shown to have an adequate safety profile [160].


Class I Recommendations
The oral administration of aspirin (initial dose is 325 mg) within 24 to 48 hours after stroke onset is recommended for treatment of most patients (Class I, Level of Evidence A).
Class III Recommendations

Aspirin should not be considered a substitute for other acute interventions for treatment of stroke, including the intravenous administration of rt-PA (Class III, Level of Evidence B).

The administration of aspirin as an adjunctive therapy within 24 hours of thrombolytic therapy is not recommended (Class III, Level of Evidence A).

The administration of clopidogrel alone or in combination with aspirin is not recommended for the treatment of acute ischemic stroke (Class III, Level of Evidence C). However, the panel supports research testing the usefulness of emergency administration of clopidogrel in the treatment of patients with acute stroke.

Outside the setting of clinical trials, the intravenous administration of antiplatelet agents that inhibit the glycoprotein IIb/IIIa receptor is not recommended (Class III, Level of Evidence B).


Classification of Interventions
IConditions for which there is evidence for and/or general agreement that the procedure or treatment is useful and effective
IIConditions for which there is conflicting evidence and/or a divergence of opinion about the usefulness/efficacy of a procedure or treatment
IIaThe weight of evidence or opinion is in favor of the procedure or treatment
IIbUsefulness/efficacy is less well established by evidence or opinion
IIIConditions for which there is evidence and/or general agreement that the procedure or treatment is not useful/effective and in some cases may be harmful
Level of Evidence
AData derived from multiple randomized clinical trials or meta-analyses
BData derived from a single randomized trial or nonrandomized studies
CConsensus opinion of experts

Carotid Endarterectomy

In the setting of acute ischemic stroke, justification for emergent (within the first 24 hours) or early revascularization with carotid endarterectomy (CEA) is based on reports of increased risk of recurrent stroke in patients undergoing medical therapy while awaiting revascularization. Some studies have found that CEA is most beneficial when performed within 2 weeks of the last cerebrovascular symptom and that the benefits decline rapidly after 3 weeks [158,161]. However, the risk associated with emergency CEA is believed to be high, for several reasons, particularly in patients with an unstable neurologic status [162]. First, embolic and hemodynamic injuries can occur [163]. Second, detection of an arterial lesion and mobilization of an operating room staff is time-intensive. Lastly, hyperperfusion, which occurs in 0.3% to 1.2% of patients who have CEA, can lead to brain edema and hemorrhagic transformation [163]. Other complications may also develop.

For some patients, however, the benefit of CEA may outweigh the risk. For instance, patients with acute ischemic stroke who have already had previous CEA may be successfully treated with surgical revascularization. Some studies indicate that early CEA may also be appropriate for patients with small, nondisabling stroke in whom the goal is to reduce ongoing thromboembolism or flow-limiting ischemia [162,164,165,166,167,168]. Results of other small studies have suggested that administration of an anticoagulant and delaying surgery until after the patient is stabilized is a better option [169]. Due to the limited and conflicting data, high perceived risk, and unestablished usefulness, the AHA has withheld a recommendation about the use of carotid endarterectomy for treatment of acute ischemic stroke [15].

Angioplasty and Stenting

Scarce research exists regarding emergent endovascular interventions for acute ischemic stroke. Although emergent angioplasty and stenting are high-risk procedures, progressing strokes, which occur when patients' moderate neurologic deficit deteriorates significantly within 72 hours after onset, are associated with very poor outcomes and high mortality rates [170]. Therefore, some case studies suggest that emergency angioplasty followed by immediate or delayed stenting is appropriate for patients with a progressing stroke caused by carotid artery occlusion or stenosis, respectively [171,172]. Angioplasty and stenting may also be appropriate for patients with acute stroke secondary to carotid artery dissection [173].

Emergency angioplasty and stenting of the internal carotid artery performed in conjunction with intra-arterial thrombolysis was associated with more favorable outcomes than pharmacologic treatment alone in patients with acute carotid artery occlusion and secondary artery-to-artery embolism to the middle cerebral artery [174]. In a larger study by the same group of investigators, treatment with urokinase followed by angioplasty and stenting increased recanalization [175].

The AHA has noted that if angioplasty and intra-arterial thrombolytics are introduced into the emergency management of stroke, it believes that the use of these procedures will be limited to comprehensive stroke centers, which have the resources and physician expertise to perform them safely. Any emergent use of these interventions should be confined to the setting of clinical trials [15].


Because stroke is an acute and harrowing event, the emotions and deficits that follow are usually overwhelming to the patient and his or her family members. The multidisciplinary rehabilitation team should therefore develop a treatment strategy to help individual patients based on a consensus model that incorporates family members and caregivers. The likelihood of functional independence and survival is enhanced by organized multidisciplinary rehabilitation; five more patients for every 100 treated are able to live independently with such rehabilitation [176]. Early initiation of rehabilitation is a particularly strong predictor of improved outcome [177].

Rehabilitation in a stroke unit has been associated with better outcomes than rehabilitation in a general healthcare facility, with improved quality of life, survival, and functional status at 5 years [16,178]. Variations in outcomes for inpatient stroke rehabilitation have been found among racial/ethnic populations. Black individuals have less functional improvement at discharge compared with white individuals and are more likely to be discharged to home despite worse functional independence measure (FIM) scores [179]. Asian individuals have functional improvements similar to those for white individuals but have less improvement at 3 months after discharge [179]. These disparities point to the need for focused attention on appropriate rehabilitation services for minority populations.


Because the effects of stroke are multifaceted and unique to each patient, multidisciplinary and organized services play an important role in patient recovery [17,180]. Post-acute stroke care settings include specialized inpatient rehabilitation hospitals, stroke rehabilitation units in acute care hospitals, outpatient therapy clinics, long-term care facilities, and patients' homes. The findings of a systematic review showed that, of these settings, an inpatient specialized stroke unit is best for providing care due to the presence of skilled nursing services, physician care, and variety of therapies [181]. However, the rehabilitation needs of some patients with mild or no disabilities may be addressed effectively in an outpatient facility (e.g., all-day care at a hospital) or in their homes [17,182]. In some cases, recovery may occur without the need for rehabilitation services.

For inpatient and outpatient rehabilitative intervention, the multidisciplinary teams typically consist of several or all of the following: physicians, physical therapists, occupational therapists, kinesiotherapists, speech and language pathologists, social workers, recreational therapists, and nurses [17]. Nursing care for patients in the post-acute phase is particularly intensive. Patients who are triaged to inpatient facilities receive great benefit from 24-hour care by nurses who specialize in stroke care [182,183].

Depending on the patient's and family's/caregivers' specific needs, a clinical psychologist, psychiatrist, dietitian, and other healthcare professionals may join a patient's stroke rehabilitation team [17,183]. However, a team's exact composition is less important in maximizing a patient's outcome than is early intervention and the use of a coordinated, interdisciplinary approach.

The patient and his or her family/caregivers should also be considered part of the team and should be involved in decisions regarding patient care [17]. Securing the family's/caregivers' active involvement early in the rehabilitation process optimizes the patient's chances for recovery and community reintegration [17,184]. After the rehabilitation team has formulated a plan of action for the patient, a team liaison should present its recommendations to the patient and family/caregivers through open discussions [17,185]. Providing patients and families/caregivers with both interactive and written materials is equally important [17,185]. Information to be presented should include [17]:

  • Preferred setting and environment based on the patient's projected recovery

  • Treatment options, including suggested rehabilitation programs, estimated length of stay, frequency of therapy, and discharge criteria

  • Information regarding the patient's prognosis and the anticipated recovery process

Once rehabilitation has commenced, involving the patient's family/caregivers in the rehabilitation sessions and training them to assist the patient with functional activities may aid patient recuperation [186]. During rehabilitation, at least one or two informal meetings per week should be held with family/caregivers to reassess their concerns about the process [17,187].


For individuals who have had a stroke and are medically stable, rehabilitation assessment, prevention of medical complications, and secondary prevention become the focal points [9,15,17]. To begin, the rehabilitation team's systematic evaluation of the patient addresses various issues, including the need for rehabilitation services; the risk of complications; physical functioning, cognition, and communication; and psychosocial conditions [17]. Next, the team works with the patient and family to implement a rehabilitation plan that includes a detailed exercise program and general as well as tailored strategies for secondary prevention [9,17]. Throughout, the team should strive to foster a climate of familial support [17].

Need for Rehabilitation Services

When a patient is medically stabilized, a rehabilitation physician is consulted to assess the patient's rehabilitative needs and recommend the proper rehabilitation setting (Table 15) [16,17]. Additionally, the patient's complete medical history is provided to the rehabilitation physician. If indicated, other rehabilitation specialists may perform specialized or more intensive assessments. Overall, rehabilitation assessments should be [17]:

  • Multidisciplinary, to account for the heterogeneous effects of stroke.

  • Well-coordinated and prompt, so patients can begin a rehabilitation program as soon as possible.

  • Well-documented, to provide the patient's rehabilitation team with accurate and detailed information.


Risk factors for stroke recurrence
Medical comorbidities
Skin assessment and risk for pressure ulcers
Bowel and bladder function
Risk of deep vein thrombosis
Mobility, with respect to the patient's needs for assistance in movement
Safety awareness
Motor function
Cognition and communication status
Psychologic status
History of previous antiplatelet or anticoagulation use, especially at the time of the stroke
Psychosocial status

The Department of Veterans Affairs and Department of Defense (VA/DoD) publication "Clinical Practice Guideline for the Management of Stroke Rehabilitation" is particularly useful for matching patient needs to stroke rehabilitation services [17]. This evidence-based guideline includes algorithms to assess patient rehabilitative needs, including the proper setting and services. Its recommendations are designed to optimize clinical outcomes by facilitating the coordination of early, multidisciplinary stroke-related evaluation and intervention [17]. The guideline emphasizes the use of the NIHSS to assist with patient assessment [17].

The NIHSS is a strong prognosticator of functional outcome, rendering it a valuable tool for determining rehabilitation needs [189,190]. Multiple assessments with the scale provide the rehabilitation team with a sense of the patient's recovery trajectory as he or she enters the rehabilitation stage [17]. For rehabilitation purposes, the VA/DoD guideline recommends that NIHSS assessments be performed during the diagnostic phase, immediately following patient stabilization, and at the time of acute care discharge. If the patient is transferred to rehabilitation without results of this assessment, it is in the team's best interest to evaluate the patient with the scale and begin coordinating its efforts on the basis of the results.

The NIHSS provides detailed information in addition to an overall stroke severity score. A score of less than 6 indicates minor or no functional disability, whereas a score of more than 16 suggests severe disability and an increased probability of death [189]. With the advent of stroke treatment, patients with a score of 6 to 15 are likely to benefit from rehabilitation without the need for a nursing facility [191]. Patients with a score of more than 15 may improve with rehabilitation; however, these patients will likely require long-term care. More than one-half of survivors with a baseline score greater than 20 are initially sent to some form of rehabilitation facility rather than directly discharged to a nursing facility or home [191].

Because the type of stroke affects the usefulness of the NIHSS, its results should be qualified by medical history, examination, and brain imaging data. Specifically, the scale is better suited for predicting functional outcomes at 3 and 6 months after stroke for patients with subcortical lesions than for patients with cortical lesions [192]. Additionally, the reliability of the scale in predicting depressive symptoms and cognitive dysfunctions depends on the hemisphere affected. Because the NIHSS does not include evaluation of weakness of the distal part of the upper extremity, which is common in patients with stroke, a finger extension evaluation should be conducted in addition to the scale [17].

Soon after patient assessment, family/caregivers should be educated [193]. If it is recommended that the patient be discharged from an acute care facility to a nursing facility or the patient's home, relevant contact and background information for nursing home facilities, assisted-living services, social support groups, and stroke-related organizations should be provided to facilitate familial decision-making. Viable options should be presented to the family, especially information about long-term care placement if a severely disabled patient is not a candidate for rehabilitation [17]. If the family/caregivers will be taking care of the patient at a private residence (with or without professional assistance), it is essential to foster discussions about the needs of the patient, challenges the patient and family/caregivers may face, and the benefits of social support programs for the patient and family/caregivers. Whenever possible, written materials should be provided, and they should be in the primary language of the family. Among the important topics to discuss and provide education about include [17]:

  • Secondary prevention and medication administration specifics

  • Nutrition and hydration

  • Symptoms of complications

  • Specifics regarding assistance with activities of daily living (e.g., transfers, positioning, bathing, toileting, dressing, and grooming)

  • Swallowing difficulties

  • Feeding tube use

  • Bladder catheter care

  • Signs of mood disorders

  • Strategies to improve cognitive skills and communication

  • Exercises (range of motion)

The patient's psychosocial status will influence his or her willingness and approach to participating in a rehabilitation program. A psychosocial assessment enables the rehabilitation team to incorporate family/caregivers more effectively into the rehabilitation process [194]. In addition, how the team manages the patient's care may be contingent on the patient's life circumstances and personality profile [17]. Areas of emphasis for the psychosocial assessment should include [17]:

  • Medical history

  • Coping style

  • Therapeutic style and recovery expectations

  • Demographic information

  • Response to treatment

  • Substance use and abuse

  • Psychiatric/psychologic evaluation

  • Emotional and mental status and history

  • Education and employment

  • Spiritual and cultural beliefs

  • Family/caregiver relationship

  • Preferred activities

When designing and implementing the patient's treatment plan, the rehabilitation team should also take into account the residual effects of any difficulties the patient may have had before the stroke, such as drug or alcohol addiction; stress from recent life events, such as divorce, a loved one's death, or retirement; or clinical depression [17]. Individual patients will vary in how well they respond to challenging and demanding therapeutic approaches. After a patient's unique needs and circumstances are determined, relevant specialists will be incorporated into the team. All members of the rehabilitation team should be sensitive to the patient's psychosocial needs.

Risk of Complications

Medical complications related to illness, being bedridden, or lack of proper care/attention can prolong hospitalization, impede rehabilitation, increase disability, or result in death. Living in an inappropriate post-stroke environment also substantially increases a patient's risk for complications. Complications may develop in as many as 85% of hospitalized patients who have had a stroke [195]. Thus, medical examinations before and during a patient's rehabilitation program should assess the most common risks of complications: skin breakdown, deep vein thrombosis (DVT), swallowing dysfunction, bowel and bladder incontinence, falls, and pain [17].

Skin Breakdown

Pressure ulcers are a commonly encountered complication in hospital and long-term care facilities, occurring in approximately 10% and 25% of patients in those settings, respectively [195]. According to the National Pressure Ulcer Advisory Panel, a pressure ulcer is a "localized injury to the skin and/or underlying tissue usually over a bony prominence, as a result of pressure, or pressure in combination with shear" [196,197]. Although ulcers typically occur proximal to osseous prominences (e.g., the sacrum, hips, ankles), skin breakdown at the ears is also common in certain settings [198,199]. Most pressure ulcers are associated with deep tissue injury [200]. Risk factors for pressure ulcers include [195]:

  • Immobility

  • Poor hygiene

  • Urinary incontinence and other sources of moisture

  • Diabetes and other causes of poor circulation

  • Peripheral vascular disease

  • Lower body mass index

  • Localized infection or trauma

  • Edema

  • Poor hydration and/or nutrition

Conditions secondary to pressure ulcers include pain, localized infection, cellulitis, osteomyelitis, sepsis, and even death [201,202]. However, not all pressure ulcers, even those that are severe, will elicit a pain sensation [203].

Ulcers can be prevented or minimized with several measures, including proper positioning, turning, and transferring techniques; good hygiene; proper nutrition and hydration; and the use of barrier sprays, special mattresses, and protective dressings [17]. Good pain management may be necessary to perform correct positioning and frequent turning. Patients should be monitored daily for skin breakdown [17]. Any sign of a pressure ulcer warrants daily treatment [17].

Deep Vein Thrombosis

DVT affects only 2% of patients with stroke; yet, its prevention is critical [195]. The American Academy of Family Physicians recommends that DVT risk be calculated with use of the Well's DVT prediction model, and the results of this model will dictate subsequent DVT testing (Table 16) [204,205]. For patients with symptoms in both legs, the more symptomatic leg should be tested. A score of 3 or more on the Well's test indicates a high clinical probability of DVT; the probability is intermediate for a score of 1 or 2.


Clinical CharacteristicScore
Active cancer (treatment ongoing, within previous 6 months, or palliative)1
Paralysis, paresis, or recent plaster immobilization of the lower extremities1
Recently bedridden >3 days or major surgery in previous 12 weeks requiring general or regional anesthesia1
Localized tenderness along the distribution of the deep venous system1
Entire leg swollen1
Calf swelling 3 cm larger than asymptomatic side (measured 10 cm below tibial tuberosity)1
Pitting edema confined to the symptomatic leg1
Collateral superficial veins (nonvaricose)1
Alternative diagnosis at least as likely as venous thrombosis-2

The D-dimer test alone is not recommended to rule out DVT in patients who have had a stroke. Patients with intermediate-to-high risk for DVT should be screened with use of ultrasonography. This imaging modality may not detect calf-vein DVT, however, and repeat ultrasonography or venography should be used when calf-vein DVT is suspected. Contrast venography was previously the most definitive test for the diagnosis of DVT, but today, Doppler ultrasound is the diagnostic study of choice [205].

Measures such as early mobilization and anticoagulation therapy are recommended to decrease the incidence of DVT after stroke [17]. A patient's risk can be substantially reduced by 50-foot walks daily (with assistance, if necessary), administration of subcutaneous, low-dose unfractionated heparin (5,000 units twice a day, unless contraindicated), and the use of graduated compression stockings (GCS) as an adjunct to medication [17,206]. GCS and intermittent pneumatic compression may be considered for prevention of post-stroke DVT, but their routine prophylactic use requires further study [207].

Swallowing Dysfunction

Based on instrumental testing results, dysphagia may develop in 64% to 78% of patients with stroke [208]. This disorder is strongly linked to the development of malnutrition and pneumonia if not identified early and managed properly [208,209]. Patients with dysphagia often have problems with aspiration, which can cause serious consequences if the stroke has suppressed cough sensations. Although cerebral and cortical strokes can cause dysphagia, brainstem strokes most severely compromise swallowing [208].

The speech and language pathologist on the rehabilitation team should perform a brief swallow assessment on all patients with stroke before oral intake of food and fluids [17,210]. A dysfunctional swallow should be further examined using a complete bedside swallow examination. If bedside swallow screenings indicate an affected swallow, or if the patient has a high risk for aspiration and/or dysphagia, performing a videofluoroscopy swallowing study or fiberoptic endoscopic examination is recommended [17,210,211]. The grade of dysphagia correlates with dysarthria, aphasia, low functional independence, and level of cognitive functioning [211]. The speech and language pathologist may best identify the specific physiologic problem and recommend the necessary management and interventions for treatment [17]. A Cochrane review assessing the effectiveness of a variety of interventions (e.g., acupuncture, neuromuscular electrical stimulation, physical stimulation) on functional outcome found that behavioral interventions and acupuncture reduced dysphagia, and pharyngeal electrical stimulation reduced pharyngeal transit time. However, the authors concluded that data are insufficient to determine the effect of these and other interventions (e.g., nutritional/fluid supplementation) on functional outcome and death [209]. Authors of another review found that acupuncture may be effective for treatment of post-stroke dysphagia, but concluded that the reported benefits should be verified with further studies [212].

Bladder and Bowel Dysfunction

Upon admission to community-based facilities, approximately 50% of stroke survivors have urinary incontinence and 30% have fecal incontinence [213,214]. Almost all patients with fecal incontinence (98%) also suffer from urinary incontinence. Urinary and fecal incontinence can lead to patient discomfort, skin breakdown, and sepsis. Fecal incontinence, in particular, reduces patient and family morale.

Large infarcts, aphasia, cognitive impairment, functional disability, lesions in the frontal cortex or frontoparietal lobes, and advanced age are associated with post-stroke urinary dysfunction [215]. Medications such as diuretics, alpha-adrenoreceptor blockers, and anticholinergic drugs can cause or exacerbate this complication [216,217]. Hyper-reflexia and hyporeflexia are the most common mechanisms of urinary incontinence in stroke survivors [218]. Detrusor sphincter dyssynergia, a cause of incomplete bladder voiding, is uncommon because its pathogenesis involves lesions between the brain stem and spine [217]. When assessing bladder function in patients with acute stroke, it is important to evaluate urinary retention with use of a bladder scanner or an in-and-out catheterization; urinary frequency, volume, and control; and the presence of dysuria [17]. Patients who have urinary incontinence may benefit from bladder-training regimens and scheduled voiding [216,219].

Fecal incontinence can be due to neurogenic impairments or leakage around a fecal impaction (overflow incontinence) [220]. If the underlying cause of fecal incontinence is neurogenic, the signs and symptoms would likely include reduced rectal sensation and tone, inability to voluntarily contract the rectal sphincter, and stool in the rectal vault [220]. A diagnosis of constipation with overflow incontinence is more likely if the patient has rectal sensation and tone.

Risk factors for impaction and constipation include immobility, inactivity, dehydration, some medications, mood disorders, and cognitive deficits [221,222]. Multivariate analysis has shown that advanced age and diabetes are risk factors for fecal incontinence [222]. Patients with persistent constipation or fecal incontinence may benefit from bowel-management programs and psychosocial support [223].


Within 12 weeks of a stroke, approximately 25% of patients will fall [195]. One study found that most falls occur at home in the first 3 months following post-stroke risk assessment [224]. Falls are a common complication for several reasons, including [220,225,226]:

  • Unfamiliar environment and physical state

  • Pain, fatigue, poor balance, and muscle weakness

  • Incontinence

  • Frequent positioning, turning, and transferring, especially in rehabilitative settings

  • Cognitive impairments, mood disorders (including depressive symptoms), visual impairments, spatial neglect, and any other condition that can decrease a patient's safety awareness

The Berg Balance Scale may be the most appropriate screen for patients who are likely to fall [227,228]. This scale tests 14 specific functional movements of daily living of increasing difficulty [229]. The 56-point maximum score indicates adequate balance and low risk of a fall. A score of less than 45 is associated with a proclivity for falling [227,229]. The score at 2 months post-stroke is useful for informing a patient's risk of falls, but it does not account for the multifactorial nature of the problem and should not preclude risk management provided in conjunction with exercise interventions, such as rehabilitation that targets gait coordination, to improve mobility [224,230]. If the patient is able to walk, the Stops Walking When Talking test may further help to identify the risk for a fall [227]. With this test, the examiner initiates a conversation with the patient while walking; if the patient stops walking to respond, the risk of a fall is increased [231]. St. Thomas's Risk Assessment Tool in Falling Elderly Inpatients (known as STRATIFY), a tool used commonly in the rehabilitation setting, has been shown to be a poor predictor of the risk for fall when screening patients with stroke [232].


Pain is one of the most frequently experienced complications. Almost one-half of all stroke survivors experience chronic pain, 65% of whom have shoulder pain [195]. Whether chronic or periodic, pain can delay functional recovery by masking motor function improvement, diminishing a patient's motivation or willingness to perform rehabilitative tasks, or limiting the patient's movement or requiring the use of a cane or wheelchair for ambulation [16]. Pain most often results from joint immobilization and the fixation of tendons and ligaments in one position [75]. In some patients, however, stroke-induced sensorimotor pathway damage leads to the sensation of pain in an affected extremity or side of the body. The most common pain syndrome of this type is central post-stroke pain, which affects 8% of patients, or at least 56,000 stroke patients in the United States each year [233,234]. Four percent of patients with central post-stroke pain experience it as shoulder pain. Central post-stroke pain can be difficult to manage, even with medications. Only amitriptyline and lamotrigine have been shown to be effective in placebo-controlled studies [235].

The VA/DoD guideline recommends using a 0 to 10 scale to assess pain, with 10 representing unbearable pain [17]. Additionally, initial medical examinations should thoroughly document suspected etiology of any pain, its location and characteristics (e.g., burning, tingling, stabbing, dull), its duration and intensity, and what aggravates or relieves the pain. Any pain that interferes with the rehabilitation process should be identified and treated accordingly.

Functional Outcome

Approximately 45% of stroke survivors have residual neurologic deficits that impair mobility [77]. At 6 months, about half of ischemic stroke survivors who are 65 years of age or older have hemiparesis, nearly one-third require assistance with walking, and more than one-quarter need assistance with activities of daily living [77]. Although functional outcome primarily depends on the patient's post-stroke neurologic damage and compensatory capacity, the multidisciplinary rehabilitation team plays a major role in recovery [180]. The team's coordinated and customized efforts can help many stroke survivors adopt an active and social lifestyle. To tailor services to a patient's needs, the team should assess his or her functional abilities during the immediate post-acute stroke phase. Assessment relies on a physical examination and a systematic battery of tests that measure a patient's ability to complete activities of daily living and that screens for cognitive/communication skills as well as visual/spatial neglect disorders [17]. Knowledge of the patient's preferred activities is also helpful.

Several functions/activities are typically measured to assess comprehensive functional status initially and during the rehabilitation process (Table 17) [17]. Although many measurement tools can be used to objectively record a patient's comprehensive functional acuity, the most widely used and trusted instrument in the stroke rehabilitation setting is the FIM [236,237]. Throughout the rehabilitation process, FIM-supported systematic screening can help the rehabilitation team to [17]:

  • Identify functional, cognitive, and visual/spatial deficits not previously detected

  • Set realistic functional goals and document progression toward these goals

  • Deduce discharge or extended care plans

  • Ensure patients' safety as they perform functional tasks and teach proper mechanics to reduce their risk of injury with continued performance


Activities of daily living
Aerobic capacity and endurance
Bladder and bowel management
Circulatory response to position changes and other functional tasks
Communication and social cognition
Joint integrity and mobility
Motor function (agility, coordination, dexterity)
Muscle performance (activation, endurance, power, strength)
Pain response to functional tasks
Range of motion
Reflex integrity
Self-care ability
Sexual activity
Use of assistive and adaptive devices
Visual and spatial neglect

In general, major rehabilitation goals are for patients to regain safe ambulation in their homes and community and to regain the ability to perform activities of daily living with minimal or no assistance. Thus, patients should be reassessed for daily tasks that are appropriate to their expected level of dependency [17]. If a return to independent community or home living is possible, domestic functioning should be evaluated [16,238]. Skills needed to stay home alone include preparing a meal, using safety precautions, properly taking medications, and obtaining emergency services. Patients who may resume driving should be assessed thoroughly for driving-related physical, cognitive, and behavioral functions [17].

Cognition and Communication

Healthy cognition and communication are considered to be essential parts of an individual's well-being. However, stroke frequently has an adverse effect on cognitive and communicative abilities.


Calculation, executive functioning (the integration of multiple and complex processes), and visual perception/construction are the cognitive arenas most often affected during the first several weeks after a stroke [239,240]. Up to 88% of patients with a cerebellar stroke have cognitive deficits, such as impairments in abstract thought, attention, control, memory, planning, and speech [241]. In many cases, patients with stroke-associated right brain damage have anosognosia, a condition in which patients are rendered unaware of their contralateral sensory and motor neurologic deficits (hemiplegia, hemianesthesia, and hemianopia) [242]. Although many survivors regain some or all cognitive skills soon following a stroke, up to 38% remain cognitively impaired at 3 months [243]. Recovery rates may be as high as 80% within 6 months for stroke survivors, with visual perception and visual memory showing the most improvement and language and abstract reasoning showing the least [244,245]. At 1 and 3 years after a stroke, cognitive impairment is one of the factors most strongly linked with poor physical and mental health status [246].

Stroke-induced damage to the brain's cognition centers is second only to Alzheimer's disease as the leading cause of dementia. Stroke-associated dementia manifests with the following symptoms [247]:

  • Memory loss, especially short-term memory

  • Attention deficits and difficulty following instructions

  • Difficulty planning/organizing tasks or solving problems

  • Confusion

  • Poor judgment

  • Behavioral changes, including inappropriate emotions and extreme mood fluctuations

  • Mood disturbances and depression

Areas of cognitive and arousal ability that should be assessed before and during rehabilitation are learning and memory, attention, visual/spatial neglect and impairments, executive functioning, and apraxia (loss of the ability to execute skilled movements despite having the desire and the physical ability to perform them) [17]. In addition to its use in assessing functional ability, the FIM is effective as an initial screen of cognitive and functional communication deficits [248]. Because stroke-related cognition deficits are independently associated with left hemispheric stroke, visual field defect, and urinary incontinence, the presence of any of these conditions should heighten awareness of the possibility of the presence of the others [243].

Visual and spatial dysfunctions may be particularly difficult to identify during the initial post-stroke examination because multiple neuroanatomic systems can be affected to varying degrees. When a standard medical examination does not include the brief, systematic screening for visual and spatial neglects, more than 60% of these dysfunctions remain undiagnosed. However, the use of the FIM may increase their early identification [248]. Patients with neglect deficits are unknowingly inattentive to specific body parts and/or spaces in the external environment. For instance, patients may brush half of their teeth or only eat food on half of their tray. Unilateral neglect is present in almost 50% of patients with right hemispheric stroke [249]. Patients with unilateral neglect are also unaware of limbs contralateral to the site of the brain lesion(s). Neglect disorders are strongly associated with poor functional outcomes and safety issues. Patients with neglect are prone to falls and injuries as well as burns to the affected limbs [226]. Addressing visual and spatial deficits as early as possible in the rehabilitation process using multiple functional adaptation techniques (e.g., visual scanning, external cues) and patient/caregiver education may decrease a patient's risk for injury [17].


As with cognitive difficulties, communication problems strain relationships between stroke survivors and their social system, impede rehabilitation, and lead to poor quality of life. Common communication-related stroke sequelae are aphasia, dysarthria, and apraxia of speech (motor speech disorder in which the muscles required for speech are less coordinated). Patients with communication disorders may also have dysphagia. How these disorders are manifested as well as their severity depends on the location and degree of the stroke. Aphasia affects one-third of stroke survivors and is one of the most common stroke-associated communication deficits [250].

The three types of aphasia are expressive, receptive, and global (Table 18) [251]. Patients with expressive aphasia have difficulties using words and sentences, whereas patients with receptive aphasia struggle to understand what others are communicating to them. Global aphasia is a combination of these two types. Aphasia is typically related to lesions on the left side of the brain, as the language center is located within this hemisphere in most individuals [252]. In many cases, aphasia (mild aphasia in particular) can be an elusive diagnosis because patients may [251]:

  • Be able to carry on normal conversations in many settings

  • Have trouble understanding only when sentences are long or complex

  • Have trouble finding the words to express an idea or may say, "the word is right on the tip of my tongue"


Patients with expressive aphasia may:

  • Use single words or short phrases

  • Omit smaller words like "the," "of," or "and" (the patient's message may sound like a telegram)

  • Say words out of sequence

  • Switch sounds or first letters of words (e.g., dishwasher becomes a "wish dasher")

  • Invent words

  • Create meaningless sentences by fluently stringing nonsense words and real words together

Patients with receptive aphasia may:

  • Require a significant amount of extra time to understand verbal communication, especially if the speech is fast

  • Have difficulty following radio or television news

  • Interpret figurative speech (e.g., "It's raining cats and dogs.") literally

  • Patients frequently have global aphasia, with various combinations of expressive and receptive difficulties.

An additional challenge in assessment is that members of the rehabilitation team typically do not have a clear sense of the patient's communication skills before the stroke. Lastly, reading and writing skills are usually more affected than verbal communication.

Well-trained and organized rehabilitation teams can use alternative methods of communicating to mitigate the effects of cognitive and communication disorders. Ideally, these problems should be recognized and managed early. However, arriving at a diagnosis can be challenging. The speech and language pathologist on the rehabilitation team is best suited to evaluate the patient for cognitive/communication disorders. In some cases, problems are initially undetected or develop after the evaluation. Training the rehabilitation team to recognize symptoms of cognitive and communication deficits (especially those that are subtle) and report findings to the speech and language pathologist can serve as a "safety net" for patients [17]. For proper diagnosis, the speech and language pathologist should also seek the help of the patient's family to gain an understanding of the patient's cognition and communication history.

Through structured observations and other formal tests, the speech and language pathologist comprehensively evaluates the individual's cognition and communication skills in the areas of speech, expression, social communication, and reading/writing (Table 19) [17,253].


CategorySkills to Evaluate
Fluency, vocal quality, clarity, loudness
Strength and coordination of muscles needed for speaking
Use of semantics and syntax
Understanding and answering of different types of questions
Understanding facts and inferences within extended speech
Ability to follow instructions that increase progressively in length and complexity
Language sample of an extended story, written and spoken
Chaining a sequence of events together
Describe the "plot" in an action picture
Message coherency
Word recall
Use of complete sentences, telegraphic sentences or phrases, or single words
Social communication

Ability to interpret jokes and sarcasm, as well as absurdities in stories or pictures

Ability to initiate conversation, take turns speaking and listening during a discussion, and express thoughts clearly

Ability to clarify or restate a message that is initially misunderstood by a conversation partner

Reading and writingReading and writing of letters, words, phrases, sentences, and paragraphs
Swallowing (as needed)
Ability to use an augmentative or alternative communication aid, if necessary

If necessary, the speech and language pathologist formulates remediation strategies to accelerate the patient's recovery of affected communication skills, development of compensatory techniques, or use of residual skills [17,253]. In many cases, patients with stroke-induced attention deficits, visual neglect, memory deficits, executive function deficits, and problem-solving difficulties can be retrained or taught compensation techniques [254]. Strategies to enhance communication with the patient should be taught to the rehabilitation team as well as the family/caregivers [17].

Psychologic Status

Following a stroke, it is understandable that patients and their families experience intense emotions. In many cases, the staff's kindness and helpfulness, familial support, and the passage of time allow patients and their families to deal with the grief and other feelings precipitated by the stroke without medication or psychologic therapy. However, approximately 33% of patients experience post-stroke depression, and other mood disorders also manifest in stroke survivors [1,255,256]. In general, psychologic conditions can have a significant impact on the success of rehabilitation. Thus, all patients should be thoroughly evaluated for psychologic disorders [17].

Detecting post-stroke depression can be particularly challenging, as symptoms often appear to be typical post-stroke symptoms or are subtle. Patients may experience fatigue, sleeping difficulties, loss of appetite, tearfulness, and feelings of hopelessness. They may refuse to participate in therapy. Additionally, cognitive deficits may prevent the patient from recognizing or having the ability to communicate depressive symptoms. Patients with an acquired flat affect may "sound sad" or indifferent to their situation without having post-stroke depression. Although several screening tools for depression in the older population are available (Table 20), a single, universally accepted evaluation tool for post-stroke depression has not been developed. Because little research in this area is available and the condition is underdiagnosed by nonpsychiatric physicians, the diagnosis of post-stroke depression should be based on information from multiple sources, including medical evaluation, patient self-report, observation of patient behavior, patient history, and staff reports of changes in behavior and motivation [17].


Evaluation InstrumentTime RequiredBenefitsDisadvantages
Beck Depression Inventory (BDI)10 minutes
Widely used
Easily administered
Norms available
Good for somatic symptoms

Less useful in elderly and in patients with aphasia or neglect

High rate of false-positive results

Somatic items may not be due to depression

Center for Epidemiologic Studies Depression (CES-D) Scale<15 minutes

Easily administered

Useful in older individuals

Effective for screening in stroke population

Not appropriate for patients with aphasia
Geriatric Depression Scale (GDS)10 minutesEasy to use with older or cognitively impaired individuals, as well as with individuals with visual or physical problems or low motivationHigh rates of false-negative results in minor depression
Hamilton Depression Scale<30 minutes

Observer rated

Frequently used for patients who have had a stroke

Multiple versions compromise interobserver reliability
Folstein Mini-Mental State Examination10 minutesWidely used for screening
Several functions with summed score
May misclassify patients with aphasia

The accompaniment of post-stroke depression with other psychologic disorders is not uncommon. Therefore, the medical evaluation should also screen for other categories of psychiatric symptoms. Generalized anxiety disorder, which affects 20% of survivors, often coexists with post-stroke depression [257]. Generalized anxiety disorder delays the recovery of the ability to carry out activities of daily living and negatively affects social functioning. Additionally, up to 15% of stroke survivors have pseudobulbar affect, characterized by uncontrollable laughing/crying [17].

Both post-stroke depression and pseudobulbar affect respond well to selective serotonin reuptake inhibitors [258]. Although these drugs carry some risk, they are safe in most patients who have had a stroke. However, these medications should not be administered prophylactically [259,260]. Although studies are limited, the use of cognitive-behavioral therapy techniques and brief supportive therapy in conjunction with medication may be beneficial to those with post-stroke depression and other neuropsychiatric sequelae of stroke [17].


Physical inactivity that typically occurs following a stroke can exacerbate muscle weakness (through atrophy and changes in muscle fibers), fatigue, cardiovascular and metabolic deconditioning, and poor balance [261,262]. These complications have been shown to slow physical and social recovery and hinder brain activation over time [263]. Comprehensive fitness training may offset these effects (Table 21) [261,264,265]. Moreover, exercise programs can benefit a stroke survivor by reducing recurrent stroke and cardiovascular risks; preventing injuries and falls; increasing fitness, strength, flexibility, and functional activities; and promoting socialization [261,266]. However, exercise is not without risks. Training programs should be tailored to the patient's capabilities and conditions to promote safety and reduce musculoskeletal injuries [267,268]. For some patients, stroke severity and coexisting conditions may render exercise inadvisable. For instance, silent coronary artery disease, especially in sedentary patients, increases the chance of exercise-induced cardiac death. Because up to 75% of stroke survivors have cardiac comorbidities, the AHA suggests that the medical evaluation for an exercise program should include a graded exercise test with ECG monitoring [261]. Thorough screening, customized exercise program design, monitoring, and patient education should be performed during rehabilitation to maximize benefits and safety.


Mode of ExerciseMajor GoalsIntensity, Frequency, Durationa
Aerobic, large-muscle activities (e.g., walking, treadmill, stationary cycle, combined arm-leg ergometry, arm ergometry, seated stepper)

Increase independence in activities of daily living

Increase walking speed/efficiency

Improve tolerance for prolonged physical activity

Reduce risk of cardiovascular disease

40% to 70% peak oxygen uptake; 40% to 70% heart rate reserve; 50% to 80% maximal heart rate; rating of perceived exertion (RPE) 11–14 (6–20 scale) 3 to 7 days/week 20 to 60 min/session (or multiple 10-min sessions)
Strength (e.g., circuit training, weight machines, free weights, isometric exercise)Increase independence in activities of daily living
1–3 sets of 10–15 repetitions of 8–10 exercises involving the major muscle groups
2 to 3 days/week
Increase range of motion (ROM)
of involved extremities
Prevent contractures 2 to 3 days/week (Before or after aerobic or strength training) Hold each stretch for 10 to 30 seconds
Neuromuscular (coordination and balance activities)Improve level of safety during activities of daily living2 to 3 days/week (Consider performing on same day as strength activities)
aRecommended intensity, frequency, and duration of exercise depend on each individual patient's level of fitness.
Intermittent training sessions may be indicated during the initial weeks of rehabilitation.

As with any rehabilitation program, the degree of a patient's cognitive and communicative deficits can affect an exercise program's success. Although it may misclassify patients with aphasia, the Folstein Mini Mental Status examination can be a useful auxiliary measure of the patient's cognitive status [261]. Some patients may also require professional intervention or psychosocial support to prevent discontinuation of exercise. Barriers that may need to be addressed include lack of familial support, depression, post-stroke fatigue, social integration, and cultural issues [261].

The consequences of inactivity may be most noticeable in patients with hemiparesis or other gait deficits. More than 50% of stroke survivors require rehabilitation to regain a functional level of ambulation [269]. Effects of neural damage underlying gait impairment, spasticity, and poor muscle performance are significantly compounded by muscle weakness, a lack of fatigue resistance, and the increased energy demands of rehabilitation [261]. Patients with mild-to-moderate conditions can benefit from treadmill training with partial body weight support [17]. As the patient walks on a treadmill, his or her body weight is supported by harnesses to facilitate walking at a comfortable speed. This training augments conventional gait rehabilitation therapies by increasing gait speed, muscle performance, and fatigue resistance; however, its effect on long-term walking outcomes requires further study [269,270].

Incorporation of progressive resistance training increases the generalizability of the fitness program and may improve the ability to carry out activities of daily living [271]. Although there are no accepted guidelines, the AHA suggests higher repetitions with reduced loads (10 to 15 repetitions rather than 8 to 12), similar to programs recommended for patients recovering from MI [261]. Additionally, at least one set of at least 8 to 10 exercises should involve the major muscle groups (arms, shoulders, chest, abdomen, back, hips, and legs).

As technology continues to advance, rehabilitation programs may become enhanced with new ways to engage stroke survivors in exercise. A study of virtual reality training sessions was shown to improve arm and hand movement skills in two patients with chronic hemiparesis [272]. The approach was also able to provide individualized, progressive practice based on the patient's level of movement ability and rate of improvement [272].


In the United States, approximately 23% of stroke incidences are recurrent [22]. Due to the high risk of recurrent stroke and its consequences, secondary ischemic stroke prevention tends to follow a risk-stratified model of disease management [273]. Treatment of at-risk patients' conditions is typically aggressive, as inadequate management can have serious implications.

A patient's risk for a recurrent stroke is highest during the first year; 14% of survivors have a recurrent stroke within 1 year after the initial cerebrovascular event, suggesting that secondary prevention is time-critical and should be initiated during the rehabilitation process [274]. After the first year, the chance of recurrent stroke decreases to 4% per year [273]. Because TIA is an important determinant of stroke, the AHA secondary prevention guidelines for patients with TIA tend to be as aggressive as those established for ischemic stroke [9]. The guidelines focus on controlling several important modifiable risk factors.


A major component of secondary prevention is the treatment of modifiable risk factors and the underlying cause of the stroke. For patients who have had an ischemic event, the results of large studies have suggested that addressing hypertension, diabetes, smoking, alcohol consumption, and physical activity can reduce the risk of recurrent stroke [9].


The results of meta-analyses have indicated that lowering blood pressure reduces the risk of stroke 30% to 40% [275,276]. Longitudinal studies suggest that treatment with antihypertensive medications in hypertensive and normotensive patients reduces the incidence of recurrent strokes, MI, and other vascular events [277]. In particular, diuretics or diuretics combined with ACE inhibitors (e.g., ramipril, perindopril) most significantly reduce the risk of recurrent ischemic stroke [9,277]. However, lifestyle modifications that include weight loss; increased intake of fruits, vegetables, and low-fat dairy products; habitual aerobic physical activity; and limited alcohol consumption are crucial components of controlling blood pressure [99]. Although most studies address the prevention of additional ischemic strokes, hypertension management has also been shown to reduce the risk of recurrent hemorrhagic stroke [9,277].

AHA Recommendations

  • Treatment with antihypertensive drugs should be considered for all patients with ischemic stroke or TIA beyond the hyperacute period. The benefits of managing blood pressure are associated with an average reduction of approximately 10/5 mm Hg. A blood pressure of less than 120/80 mm Hg is defined as normal. Target blood pressure for patients with hypertension and without diabetes should be less than 140/90 mm Hg.

  • For patients without contraindications, the available data support the use of diuretics alone or diuretics with an ACE inhibitor.

  • Lifestyle modifications are an integral part of a patient's antihypertensive therapy.


Diabetes is a well-documented independent risk factor for recurrent stroke [278,279]. Aggressive control of hypertension in diabetic patients, with a lower target of 130/80 mm Hg, has been shown to reduce the risk of stroke as well as other cardiovascular events [99]. Including ACE inhibitors in the treatment regimen of patients with diabetes effectively lowers blood pressure, slows the progression of renal disease, and reduces albuminuria [9,280].

AHA Recommendation

  • Use of existing guidelines for glycemic control and blood pressure targets in patients with diabetes is recommended for patients who have had a stroke or TIA.

Cigarette Smoking

Smoking doubles the risk of stroke [281]. Its cessation eliminates the elevated risk after 5 years and reduces the overall risk of stroke-related hospitalization [9,282,283]. Exposure to secondhand smoke also appears to increase the risk of stroke [9,284]. The most effective combination of therapies for smoking cessation is nicotine replacement, social support, and counseling [9,285].

AHA Recommendation

  • All patients with TIA or stroke who smoke should be strongly urged to quit and avoid passive smoke. The use of smoking cessation programs and nicotine replacement therapy should be considered.

Alcohol Consumption

The results of a meta-analysis suggest that the risk of stroke is increased 69% for individuals who have more than five drinks (with one drink defined as 12 ounces of beer, 4 ounces of wine, or 1.5 ounces of liquor) per day compared with nondrinkers [286].

AHA Recommendation

  • Patients with ischemic stroke or TIA who drink heavily should be strongly encouraged to reduce or eliminate their alcohol consumption to lessen risk factors that increase the likelihood of recurrent stroke.

Physical Activity

Habitual exercise clearly prevents stroke [266]. In addition, a sedentary lifestyle impedes functional recovery and places patients at a higher risk for stroke recurrence.

AHA Recommendation

  • An exercise program tailored to a patient's capabilities and comorbidities should be considered.


For patients who have large-artery atherosclerosis, the specific underlying condition should be managed. Similarly, identification and treatment of cardioembolic stroke sources (e.g., AF, cardiomyopathy, acute MI and left ventricular thrombus, valvular heart diseases) is recommended. Patients with ischemic stroke and a high-risk source of cardioembolism generally benefit from anticoagulant therapy.

Extracranial Carotid Artery Disease

Carotid artery revascularization is recommended by the AHA for certain patients with stenosis greater than 50% [9]. However, surgery is not beneficial for patients with stenosis of less than 50%.

AHA Recommendations

  • Carotid endarterectomy (CEA) is recommended for all patients with recent TIA or ischemic stroke within the past 6 months and ipsilateral severe (70% to 99%) carotid artery stenosis if the morbidity/mortality risk is less than 6%.

  • CEA is recommended for certain patients (based on age, gender, and comorbidities) with recent TIA or ischemic stroke within the past 6 months and ipsilateral severe (50% to 69%) carotid artery stenosis if the morbidity/mortality risk is less than 6%.

  • When CEA is indicated for patients with TIA or stroke, surgery within 2 weeks is reasonable rather than delaying surgery if there are no contraindications to early revascularization.

  • Carotid artery stenting (CAS) is indicated as an alternative to CEA for symptomatic patients at average or low risk of complications associated with endovascular intervention when the diameter of the lumen of the internal carotid artery is found to be reduced by more than 70% on noninvasive imaging or more than 50% on catheter angiography.

  • CAS may be considered for patients with symptomatic severe stenosis (greater than 70%) if the stenosis is difficult to access surgically, medical conditions are present that greatly increase the risk for surgery, or other specific circumstances exist (such as radiation-induced stenosis or restenosis after CEA). In this setting, CAS is reasonable when performed by operators with established periprocedural morbidity and mortality rates of 4% to 6%, similar to those observed in trials of CEA and CAS.

Intracranial Atherosclerosis

The rate of stroke recurrence for patients with symptomatic intracranial atherosclerosis is approximately 9% [9]. The findings of retrospective studies have suggested that the greatest rate of recurrence is found among patients with this condition who do not have a response to antithrombotic therapy [287]. Although the results of some studies have indicated that angioplasty or stenting should be considered for such patients, the usefulness of these surgical interventions is unknown and considered investigational [9].

AHA Recommendations

With regard to patients with stroke or TIA due to 50% to 99% stenosis of a major intracranial artery:

  • Aspirin is recommended in preference to warfarin. The optimal dose of aspirin in this population has not been determined. On the basis of the data on general safety and efficacy, daily doses of 50 mg to 325 mg of aspirin are recommended.

  • Long-term maintenance of blood pressure <140/90 mm Hg and total cholesterol level <200 mg/dL may be reasonable.

  • The usefulness of angioplasty and/or stent placement is unknown and is considered investigational.

  • Extracranial-intracranial bypass surgery is not recommended.

Atrial Fibrillation (AF)

The anticoagulant warfarin has a narrow therapeutic margin and numerous food and drug interactions, and these factors (which necessitate frequent INR testing and dose adjustment), combined with the associated significant bleeding risks, has led to the underutilization of this drug despite having been shown to prevent recurrent stroke substantially in patients with ischemic stroke or TIA and AF and despite the adoption of performance measures and guidelines advocating its use in these patients [9,288,289]. Easy-to-use alternative therapies are required and include dabigatran, rivaroxaban, and apixaban [290,291,292]. Significant adverse effects (i.e., serious, sometimes fatal bleeding, acute coronary events) have been associated with some of these agents, making their use inappropriate for some patients [293,294]. However, a 2011 focused update on dabigatran published by the American College of Cardiology, the AHA, and the Heart Rhythm Society recommends this agent as a useful alternative to warfarin for select patients.

Between 35% to 45% of patients with stroke and AF have coexisting conditions that may have caused the stroke [188]. In many cases, both the AF and the other condition (usually stenosis) will require treatment [9].

AHA Recommendations

  • For patients with ischemic stroke or TIA with paroxysmal (intermittent) or permanent AF, anticoagulation with a vitamin K antagonist (target INR: 2.5; range: 2.0 to 3.0) is recommended.

  • For patients unable to take oral anticoagulants, aspirin alone (75 mg to 100 mg per day) is recommended. The combination of clopidogrel plus aspirin carries a risk of bleeding similar to that of warfarin and therefore is not recommended for patients with a hemorrhagic contraindication to warfarin.

  • For patients with AF at high risk for stroke (i.e., stroke or TIA within 3 months; Cardiac failure, Hypertension, Age, Diabetes, Stroke system (CHADS2) score of 5 or 6; mechanical or rheumatic valve disease) who require temporary interruption of oral anticoagulation, bridging therapy with a LMWH administered subcutaneously is reasonable.

  • Dabigatran is useful as an alternative to warfarin for the prevention of stroke and systemic thromboembolism in patients with paroxysmal to permanent AF and risk factors for stroke or systemic embolization who do not have a prosthetic heart valve or hemodynamically significant valve disease, severe renal failure (creatinine clearance <15 mL/min) or advanced liver disease (impaired baseline clotting function).

Noncardioembolic Strokes and TIA

The use of certain antiplatelet therapies rather than oral anticoagulation for noncardioembolic ischemic strokes and TIAs has been shown to reduce the overall risk of recurrent stroke and decrease the incidence of fatal recurrent strokes [9]. Clopidogrel is appropriate for patients who are allergic to aspirin or for patients in whom dipyridamole-associated headaches occur.

AHA Recommendation

  • Aspirin (50 mg to 325 mg per day) monotherapy, the combination of aspirin 25 mg and extended-release dipyridamole 200 mg twice daily, or clopidogrel 75 mg monotherapy are all acceptable options for initial therapy. The selection of an antiplatelet agent should be individualized on the basis of patient risk factor profiles, cost, tolerance, and other clinical characteristics.


Patient M is an active woman, 70 years of age, who lost consciousness and collapsed at home. Her daughter, who was visiting her at the time, did not witness the collapse but found her mother on the floor, awake, confused, and slightly short of breath. The daughter estimated that she called EMS within 5 minutes after the collapse, and EMS responded within 10 minutes. EMS evaluated Patient M, drew blood for a glucose level, and determined that she may have had a stroke. They notified the nearest designated comprehensive stroke center that they would be arriving with the patient within 15 minutes. Patient M's daughter accompanied her.

The triage and transportation of an individual with suspected stroke should be similar to that for an individual with serious trauma, and treatment is recommended within 3 hours after the onset of stroke. Because of the limited time available for assessment and diagnosis before optimal treatment, the EMS dispatcher should notify EMS personnel immediately and coordinate transport of the individual to the closest emergency facility, preferably one that is a designated primary (or comprehensive) stroke care center.

On presentation in the emergency department, Patient M is immediately triaged. Because Patient M is still somewhat confused, her daughter is asked to provide information on the patient's history. The daughter reports that her mother had had an episode of sudden-onset numbness and tingling in the right limb, with slight confusion and slurred speech, 3 days previously. The episode lasted only 5 minutes, and Patient M had not called her primary care physician. Additional information provided by the daughter indicates that Patient M has been treated for hypertension for 10 years but notes that she is often not compliant with her antihypertensive medicine, a diuretic. The patient has never smoked, drinks occasionally, and is of normal weight.

Patient M has two significant risk factors for stroke; one is a long history of hypertension. More than two-thirds of individuals older than 65 years of age are hypertensive, and it is important for individuals with hypertension to have regular blood pressure screening and to maintain a blood pressure of less than 140/90 mm Hg. Antihypertension therapy has been found to reduce the incidence of stroke by 30% to 40%. Patient M's noncompliance with her antihypertension medicine likely includes her among the 65% of known hypertensive individuals in whom blood pressure is not controlled.

Patient M's previous episode of numbness, confusion, and slurred speech appears to be evidence of a TIA, another substantial risk factor for stroke. Research has shown that approximately 5% of patients will have an ischemic stroke within 7 days after a TIA. In addition, the risk of stroke within 7 days is doubled for patients with TIAs who did not seek treatment. As is the case for many individuals who have a TIA, Patient M did not seek medical attention because the clinical symptoms resolved quickly. However, research findings indicate that urgent treatment should be provided for TIAs, as early treatment for TIA and minor stroke has been shown to reduce the risk of early recurrent stroke by 80%.

On physical examination, Patient M's blood pressure is 150/95 mm Hg. She has pain in her left arm and a slight headache. There are slight carotid bruits on the right. She is assessed with use of the NIHSS and found to have left hemiparesis and left visual/spatial neglect. The results of laboratory tests, including a complete blood count, prothrombin time, serum electrolyte levels, cardiac biomarkers, and renal function studies, are all within normal limits. CT of the brain indicates a thrombus in a branch of the right internal carotid artery, with approximately 50% occlusion due to atherosclerosis. There is an area of infarction in the right anterior hemisphere. There is no evidence of a subarachnoid hemorrhage. The diagnosis is made 2 hours after Patient M's arrival in the emergency department. She is treated with intravenous rt-PA at a dose of 0.9 mg/kg, and aspirin antiplatelet therapy is started at an initial dose of 325 mg, 24 hours after thrombolytic therapy, and a maintenance dose of 75 mg per day.

Many of the patient's symptoms, including her loss of consciousness, shortness of breath, pain, and headache, are nontraditional symptoms of stroke. Studies have demonstrated that nontraditional symptoms are more prevalent among women, often leading to a delay in the evaluation for stroke. EMS personnel and clinicians should be aware of the potential for nontraditional symptoms in women and carry out a diagnostic evaluation addressing a suspicion of stroke.

Patient M is eligible for thrombolytic therapy with rt-PA according to evidence-based guidelines developed by the AHA/ASA: her blood pressure is lower than 185/110 mm Hg, the onset of symptoms is less than 3 hours prior to the start of treatment, and the laboratory values are within normal limits. Antiplatelet therapy with aspirin 50 mg to 325 mg daily (versus anticoagulant therapy with warfarin) is recommended for treatment of patients with stroke or TIA due to intracranial atherosclerosis with 50% to 99% occlusion. Antiplatelet therapy is not recommended as an adjunctive therapy within 24 hours of thrombolytic therapy.

When Patient M's condition is stabilized, her primary care physician and consultant neurologist provide a referral for stroke rehabilitation, and a multidisciplinary rehabilitation team is formed to assess her rehabilitative needs, recommend the proper rehabilitation setting, and develop a treatment strategy tailored to her specific needs that includes daily antiplatelet therapy. Patient M is again assessed with the NIHSS, and the score is 12. The patient's cognitive and communication skills are intact on evaluation with the FIM, with the exception of the previously documented left visual/spatial neglect. The assessment also includes evaluation of the patient's risk for complications. Because of her spatial neglect, she is screened with the Berg Balance Scale and the Stops Walking When Talking test. The score on the Berg Balance Scale is 43, and Patient M does stop walking to engage in conversation. Psychosocial assessment includes screening with the Center for Epidemiologic Studies Depression (CES-D) Scale, as well as review of the medical history and conversations with the patient and her children; no signs of depression are present.

Patient M's score of 12 on the NIHSS falls within the range (6 to 15) that indicates she is likely to benefit from rehabilitation. Evaluating a stroke survivor's risk of complications is an important component of the overall assessment, and among the most common complications are falls, deep vein thrombosis, pressure ulcers, swallowing dysfunction, bladder and bowel dysfunction, and depressive symptoms. In assessing the risk of complications, the Berg Balance Scale appears to be the most appropriate screen for patients who are likely to fall, and a score of less than 45 is associated with a likelihood of falling. The risk of a fall is also increased when a patient stops walking to talk, as Patient M did, during the Stops Talking When Walking test.

Screening for signs of depression is also essential, as depression affects approximately 33% of stroke survivors. Signs of depression are subtle and may be vague. Several screening tools are available, but there is no universally accepted tool for use in the post-stroke setting. The CES-D was chosen in this case because it is easy to administer, is useful in older individuals, and has been found to be effective for screening in the stroke population, except for individuals who have aphasia. The diagnosis of depression in stroke survivors should be based on sources in addition to a formal screening tool, such as a medical evaluation, patient self-report, observation of patient behavior, patient history, and staff reports of changes in behavior and motivation.

The rehabilitation team discusses the results of the assessment with Patient M's daughter and son, both of whom live about 45 minutes away from the patient. Together, the team and the family members explore options to determine the best approach to rehabilitation. A decision is made for Patient M to be discharged to an inpatient stroke unit, and a rehabilitation program is developed. The nurse on the team discusses the program with Patient M and her children and explains the course of rehabilitation and the expectations. Rehabilitation will focus on an exercise program consisting of aerobic exercise, strength training, stretching, and coordination and balance activities.

Early initiation of rehabilitation is a particularly strong predictor of improved outcome, and rehabilitation in a stroke unit has been associated with improved quality of life, survival, and functional status at 5 years compared with a general healthcare facility. No studies have demonstrated the superiority of one rehabilitation setting over another, and the inpatient setting was chosen primarily to ensure consistent care, given how far away Patient M's children live, and the limited support she otherwise has for healthcare needs. Decisions about the setting and program for rehabilitation should be shared with family members, and family and other caregivers should be provided with educational resources about the rehabilitation process.

The exercise program developed for Patient M is designed to help her regain the ability to independently carry out activities of daily living safely and to regain a functional level of ambulation. The benefits of an exercise program include increasing fitness, strength, and flexibility; improving function; preventing injuries and falls; and reducing the risk of recurrent stroke.

Patient M gradually resumes the ability to function independently, and after more than 2 weeks in the stroke rehabilitation unit, the score on the NIHSS has improved to 5. Before she is discharged to her home, the rehabilitation team provides instructions for exercises to continue at home and recommends moderate physical activity as a secondary prevention measure. The team also educates Patient M about the importance of maintaining a normal blood pressure through use of her antihypertension medication and lifestyle modifications. At a follow-up visit with her primary care clinician at 3 months, Patient M's blood pressure is 135/80 mm Hg, and she reports that she has been compliant with her antihypertension medicine and antiplatelet therapy and is functioning well at home.


Ischemic stroke remains a significant contributor to morbidity and mortality in the United States. Stroke is associated with several modifiable risk factors, such as smoking, diet, physical inactivity, and obesity, and clinicians should encourage their patients to adopt healthy lifestyle habits, especially patients who are at highest risk. In addition, primary prevention of stroke involves the appropriate management of many medical conditions, such as hypertension, diabetes, dyslipidemia, and AF.

Early diagnosis and appropriate immediate treatment are key to recovery of neurologic function and survival after stroke, making it imperative for both healthcare professionals and the general public to recognize the symptoms of stroke and TIAs, a substantial risk factor for stroke. Clinicians, as well as EMS staff and ED staff, should be skilled in identifying possible stroke-related symptoms, especially noting that women are more apt to have nontraditional symptoms of both TIAs and stroke. Efforts to educate the public about the importance of seeking medical care for TIAs and about the warning signs of stroke are also essential.

Several evidence-based guidelines are available for the primary and secondary prevention of ischemic stroke, as well as for early management and rehabilitation. Adherence to these guidelines will help to reduce the prevalence of stroke and to decrease the morbidity and mortality for individuals who have stroke. Thrombolytic therapy with rt-PA is the cornerstone of treatment for ischemic stroke, and the AHA now recommends beginning antiplatelet therapy with aspirin 24 to 48 hours after the onset of stroke. Other antiplatelet agents, as well as anticoagulant therapy, are not recommended on the basis of the evidence to date.

Outcomes after stroke are improved when care is provided in a comprehensive stroke center and when rehabilitative care is provided by a multidisciplinary team. Effective rehabilitation begins with a systematic evaluation of the patient to determine the need for specific rehabilitation services, the risk of complications, the patient's physical functioning and level of cognition and communication, and the patient's psychosocial status. This evaluation allows for the development of a rehabilitation program that addresses an individual patient's specific needs, with tailored strategies for secondary prevention. When all available resources are utilized, prevention and appropriate treatment of stroke will result.

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