Stroke rehabilitation is simultaneously a complex, challenging, and gratifying experience, which is often both physically demanding and emotionally charged. As stroke is often the most common diagnostic category on an acute inpatient rehabilitation unit,¹ it is typically considered a “prototype” rehabilitation condition. The disorder serves as a model for the development and application of principles and practices that can be applied to the rehabilitation care of patients with other diagnoses.

Stroke is defined by the World Health Organization² as a syndrome consisting of rapidly developing clinical manifestations reflecting disturbances in cerebral functioning derived from vascular disease origin and lasting more than 24 hours. Roughly 80% or more of all strokes are ischemic in nature; most of the remainder are hemorrhagic.³ The ischemic strokes can be further divided into common and uncommon causes (Table 10–1). Determining the particular cause is of great importance to rehabilitation physicians, as it will eventually determine the medical treatment strategy, including the type and duration of anticoagulation utilized for the secondary prevention of a subsequent stroke.

Transient ischemic attacks (TIAs), in contrast, last briefly and are characterized by stroke symptoms or signs that last less than 24 hours in duration; most TIAs last less than an hour.⁴ Regardless of the duration of symptoms, once brain imaging has identified cerebral infarction, the condition is classified as a stroke. TIAs are generally ischemic in nature and result as a consequence of a temporary occlusion of an intracranial vessel. Most alarming for the rehabilitation team is that almost 15% of patients who suffer a TIA will have a stroke within 3 months, with the majority of stroke occurrence occurring within 48 hours.⁴

The temporal course, acuity level, and combinations of presenting symptoms generally differ between ischemic and hemorrhagic causes of stroke. The specific residual neurologic deficits that result from the acute events are more dependent on the location and extent of the lesion than on the type of stroke. Chief among the characteristics of stroke is the multidimensional and diverse nature of its presenting symptoms and enduring problems, requiring involvement of virtually all members of the typical interdisciplinary rehabilitation team to address them successfully and comprehensively.

Much of the initial management algorithm for stroke is focused on stabilizing the patient, establishing a cause, and providing acute treatment; notably virtually all cases of stroke benefit from eventual rehabilitation (Fig. 10–1).

Early brain imaging in an evolving stroke is critical. A noncontrast computerized tomography (CT) scan is commonly utilized to rule out an acute intracerebral hemorrhage (ICH) and will determine initial medical management, including the potential use of intravenous tissue plasminogen activator (tPA) for thrombotic strokes (Fig. 10–2).

Magnetic resonance imaging (MRI) diffusion-weighted images are superior to conventional T2-weighted images in the detection of acute ischemic strokes within the first 24 hours (Fig. 10–3).

Stroke is the second leading cause of death and a major cause of serious long-term disability worldwide, affecting nearly 26 million people around the world.³ Recent evidence indicates that stroke has dropped to become the fifth most common cause of death in the United States,³ where approximately 795,000 people experience a stroke every year; of these annual cases, 610,000 are new strokes and 185,000 are recurrent attacks.³ Interestingly the incidence figures have changed very little in the past few years, whereas the stroke death rate has fallen slightly.³ Mortality rate, reflecting the number of patients who die within the first month following stroke, is about 135,000.³ More relevant for rehabilitation professionals is that stroke remains a major cause of serious long-term physical disability in the United States and worldwide. Stroke incidence increases with increasing age, and the overall number of deaths attributed to stroke is estimated to double by 2030.⁴ There are significant racial and ethnic disparities in incidence figures, with stroke affecting blacks and Hispanics with greater frequency than whites.³

Perhaps most notably, prevalence figures for stroke (reflective of the number of stroke survivors in the United States) have demonstrated steady increases in recent years. Current prevalence estimates for stroke in the United States approach an estimated 7.2 million Americans, or 2.7% of the U.S. population over 20 years of age.³ These trends are attributable to several likely reasons; among these are reduced early mortality resulting from better acute management and increased poststroke longevity resulting from more attention to lifestyle issues, improved methods of rehabilitation, and more effective methods to prevent complications.

It is extremely difficult to obtain reliable figures on the prevalence of permanent disability, but it is estimated that more than one-half of all stroke survivors in the United States receive some form of rehabilitation services, although there is evidence that these services are being underutilized.

At present, an estimated 1.1 million Americans report difficulty with activities of daily living resulting from stroke.³ Stroke was among the top 18 diseases contributing to years lived with disability in 2010; of these 18 causes, only the age-standardized rates for stroke increased significantly between 1990 and 2010.⁵ Estimates for the cost of stroke in the United States are approximately $36.5 billion, of which about one-half is derived from the direct medical cost of stroke and the remainder from lost productivity (Fig. 10–4).³

Interestingly, prevalence figures for silent stroke in the United States are relatively high, approaching 11% between 55 and 64 years of age, 22% between 65 and 69 years of age, 28% between 70 and 74 years of age, 32% between 75 and 79 years of age, 40% between 80 and 85 years of age, and 43% above 85 years of age. It is estimated that 13 million people are alive today in the United States with prior silent stroke.³ Also interesting is the recent and somewhat surprising trend that the incidence of stroke in young adults is increasing.^6,7 Kissela and associates⁶ found an increase in stroke in young adults from 4.5% in 1993 to 1994 to 7.3% in 2005.

The major pathophysiologic mechanisms of ischemic stroke include intracranial vessel occlusion by an embolus, in situ thrombosis (usually affecting small vessels), and hypoperfusion secondary to vascular stenosis (Fig. 10–5).

Stroke is typically characterized by the vascular territory affected; each vessel is accompanied by typical symptoms, which correspond to the area of infarction. Strokes are further categorized into large vessel disease (affecting the internal carotid artery or vertebrobasilar system), medium vessel disease (affecting the middle, posterior, or anterior cerebral arteries), or small vessel (or lacunar) disease, each with their own corresponding constellation of signs and symptoms (Fig. 10–6).

Neurologic deficits associated with major brainstem stroke syndromes and lacunar strokes are presented in Tables 10–2 and 10–3; of note, lacunar strokes arise from occlusion of smaller branches of the major cerebral arteries.⁸

Cerebral infarctions occur when cerebral blood flow has been diminished for a long duration; border zones between distributions of major cerebral arteries may be affected in more severe cases. This rim of mild-to-moderate neural ischemic tissue, which interfaces the normally perfused area and the area of infarction, which is evolving, is called the ischemic penumbra. This area may be visible on a MRI diffusion-weighted image for several hours after the original insult (Fig. 10–7).

Cerebral ischemia, in turn, leads to a cascade of events culminating in neuronal cell death (Fig. 10–8).

In contrast to ischemic stroke, intracranial hemorrhage results in cerebral infarction secondary to a mass effect on the neural structures and increasing intracranial pressure.⁴

This particular constellation of deficits involved after cerebral vascular occlusion can be explained by the anatomic relationship of the different zones of the brain. For example, a middle cerebral artery stroke is often characterized by facial and arm hemiparesis due to its involvement of the primary motor area, hemisensory deficit of the face and arm (due to its involvement of the adjacent primary sensory area), and either Wernicke’s or Broca’s aphasia (dependent upon whether the dominant hemisphere was involved or not) (Fig. 10–9).

In contrast to middle cerebral artery syndromes, anterior cerebral artery syndromes predominantly affect the legs, whereas posterior cerebral artery syndromes cause vision deficits, cranial nerve palsies, and homonymous hemianopsia (Figs. 10–10 and 10–11).

It surprises some to learn that a great deal of natural neurologic recovery occurs spontaneously following onset of stroke. Thus, for example, at the time of stroke, 73% to 88% of patients experience hemiparesis, 30% to 36% have aphasia, and 13% have dysphagia; in contrast, at 6 months poststroke only 37% to 48% have hemiparesis, 18% to 30% have aphasia, and 4% have dysphagia.^9–12 As many as 9% of patients with severe upper extremity (UE) weakness at onset may gain good recovery of hand function, and up to 70% of patients showing some motor recovery in the hand by 4 weeks make a good recovery.¹³

Some of this natural recovery likely occurs because of normal physiological processes that enable recovery of tissues, including the resorption of edema, local chemical toxins, and debris in the injured areas of the brain, in addition to the repair of injured neurons and recanalization of local blood supply. This natural recovery generally takes place during the first few months following stroke onset. Other recovery is thought to occur as a result of neuroplasticity, which is the capacity of the central nervous system to reorganize and remodel itself after injury. Recent years have witnessed an explosion in the amount of evidence that demonstrates the ability of the nervous system to adapt and modify after injury. Neuroplasticity likely results from a variety of mechanisms, including resolution of diaschisis (i.e., functional deactivation of brain areas remote from the damage),¹⁴ peri-infarct neural reorganization,^15,16 sprouting of new neurons, development of new synapses or increased activation of existing synapses, awakening of previously dormant neural pathways, and increased activity in the contralesional hemisphere or other less involved locations of the brain resulting from the injury itself.^17–19

Additionally, neuronal stem cells are now known to be present in the adult central nervous system and are located in the ependymoma; these cells may be able to differentiate into nascent neurons, astrocytes, and oligodendrocytes.²⁰ The true extent to which these stem cells contribute to functional recovery is still not completely known.

Of great interest to rehabilitation professionals and scientists is the extent to which neuroplasticity can be favorably affected by external means, that is, how we or our interventions can influence the brain’s recovery potential. Also known as experience-dependent plasticity, examples of such interventions include activity or exercise (as performed, for instance, during standard rehabilitation programs), electrical or magnetic stimulation, chemical or pharmacological intervention, and cell therapies. There is now extensive and mounting evidence that external influences can affect the capacity of the brain to heal.^21–23 This forms the mechanistic basis for many of our rehabilitation interventions.

It is important to recognize that most traditional rehabilitation efforts focus heavily on compensation for the neurologic deficits that result from stroke. Stroke survivors are taught how to perform daily functions in the presence of impairments in body structure or function. A great deal of the training after stroke, for example, involves teaching people with hemiparesis how to walk, dress, bathe, communicate, and perform other activities of daily living despite impairments such as weakness or aphasia. More recent theory and practice, however, have emphasized the capacity of many of our rehabilitation interventions to influence the primary body structures and functions, likely by remediating the mechanistic cause of the deficits. Ideally, current rehabilitation programs emphasize elements of each intervention strategy. This combination approach is critical in view of the need to provide practical solutions to the problems causing physical dependence, disability, and lack of community participation, combined with the desire—and recently discovered capacity—to reverse some of the physical impairments.

Despite the spontaneous recovery that occurs most often in the first few months following stroke, it is estimated that most people with stroke have substantial residual impairments with subsequent significant human and economic burden.^24,25 While individual impairments that result from stroke can be managed through the implementation of specific rehabilitation interventions, an important common characteristic of rehabilitation programs is their emphasis on addressing the totality of the poststroke patient experience, making rehabilitation a holistic undertaking. Managing stroke rehabilitation is therefore an intensive and complex process. Other characteristics of stroke rehabilitation include an interdisciplinary nature and reliance on a comprehensive but coordinated team approach to care; a goal-directed focus on outcomes (especially those goals that focus on functional restoration, community reintegration, and quality of life); use of education and training interventions that are based heavily on principles derived from adult learning theory and motor control; an emphasis on enhancing the patient experience and addressing psychological issues; recognition of the importance of motivation and psychological state; a focus on family, social interactions, and recruiting community resources; and an attention to quality-of-life issues.²⁶

It is important to note that these rehabilitation practices can be implemented in many diverse locations. In the idealized “continuum of care,” rehabilitation interventions begin immediately after the stroke during the acute poststroke phase. Initial rehabilitative interventions typically include patient and caregiver education, motor assessment and activation, exercises, and an assessment of swallowing capacity. For many, transfer to a hospital-based acute inpatient rehabilitation facility follows, where patients typically receive several hours of multimodality therapy per day. Alternatively or additionally, if or when the rehabilitation needs are lower or tolerance is limited, patients may be transferred to subacute rehabilitation programs. Such programs typically provide 1 to 2 hours of therapy per day up to 5 days per week and take place in skilled nursing facilities. Subsequently, stroke patients often receive therapy in the home and/or in outpatient rehabilitation facilities, which can have varying degrees of frequency and intensity. Both of these are becoming more popular levels of rehabilitation care. The directions of patients’ pathways among these facilities might vary as well and are driven by cost and availability of services.

To an extent, utilization of post-acute inpatient rehabilitation is determined greatly by insurance statutes and coverage determinants. In the United States, Medicare beneficiaries (many of whom are elderly) must meet strict criteria to qualify for one of the five levels of post-acute inpatient rehabilitation. Although studies have demonstrated clear functional benefits for stroke patients who have undergone inpatient rehabilitation, stringent, constantly changing, and time-specific documentation standards must demonstrate the need for rehabilitation.^27,28

In all of the settings, stroke rehabilitation programs have in common five broad sets of objectives: (1) preventing, recognizing, and managing risk factors, medical comorbidities, and secondary complications; (2) training people with stroke to enable them to achieve maximal independence in functional tasks; (3) facilitating psychological and social adaptation and coping for not only the patient but also the family; (4) promoting the resumption of prior life roles and reintegration into the community; and (5) the ultimate overriding goal of enhancing quality of life for people afflicted with stroke. Each of these goals will be considered systematically in this chapter.

Stroke risk factors are typically divided into modifiable and nonmodifiable categories. Although no preventive measures can be undertaken for nonmodifiable factors, physiatrists may be in the position to play a key role in the secondary prevention of stroke survivors through addressing modifiable risk factors (Table 10–4).

Modifiable risk factors for ischemic stroke include hypertension, diabetes, cardiac arrhythmia (atrial fibrillation), carotid stenosis, sleep apnea, tobacco use, and a sedentary lifestyle.²⁹ Smoking cessation is critical, as smokers have anywhere between two and four times the likelihood of developing a stroke. Control of hyperlipidemia, a sedentary lifestyle, and subsequent cardiovascular disease can decrease the likelihood of a future stroke by up to 25%.^8,30,31 Uncontrolled diabetics can have up to three times the risk of future stroke development.³² Research has suggested that symptomatic carotid stenosis (>70%) substantially increases the risk of ipsilateral stroke development. The risks and benefits of carotid endarterectomy in this patient population should be weighed carefully; perioperative stroke risk during a carotid endarterectomy is roughly 1.9% while the absolute risk reduction over 5 years is 5.9%.³³

Special consideration of the use of antiplatelet therapy in stroke is warranted, and typically the benefits of agents such as low-dose aspirin (81–325 mg daily) and clopidogrel must be weighed carefully; combining the two not only substantially increases the risk of future ICH but also decreases the risk of a secondary stroke.³⁴

Nonmodifiable risk factors for ischemic stroke include age above 55 (the risk doubles every decade after 55), male gender, race, family history of stroke, and the geographic location. African Americans are twice as likely to develop stroke than Caucasians, while Hispanics are 1.5 times more likely to have a stroke. Those Americans who live in the Southeastern United States are more likely to develop a stroke than people in the rest of the country.⁸

Hypertension is a primary risk factor for ICH. In older individuals, angiodysplasia from cerebral amyloid angiopathy is more common and often presents as lobar hemorrhage at multiple sites. Other risk factors for ICH include vascular malformations (cerebral angiomas and aneurysms), coagulation deficits (e.g., hemophilia, von Willebrand’s disease, and medical anticoagulation), and alcoholism.^8,35,36

Rehabilitation patients who have suffered a TIA must also be appropriately managed with anticoagulants, as roughly 15% of these patients will develop a stroke within 3 months (many will have a stroke within 48 hours). The risk of developing a subsequent stroke can be assessed by the use of the ABCD² score³⁷ (Table 10–5).

Because of the high risk of imminent stroke within 48 hours, those patients hospitalized on an inpatient rehabilitation unit must have appropriate care (e.g., consultation with a neurologist and consideration of aggressive anticoagulation treatment). Of note, TIA patients managed with aspirin and clopidogrel have been found to have superior functional outcome and quality of life when compared to those who have been managed with aspirin alone, but they also have a greater risk of ICH.³⁸

The occurrence of stroke is nearly always associated with comorbid medical conditions that require medical attention.^26,39,40 Although these comorbidities vary in type, severity, and impact, they have been found to occur more frequently among people with stroke than in the general population.¹¹ Many of these comorbidities carry the potential to influence the outcome of people with stroke unfavorably.^9,41–43 These problems can be categorized as (1) preexisting medical conditions that require ongoing care, or at least awareness, by professionals during rehabilitation; (2) general health functions, such as nutrition, hydration, and bowel and bladder management; (3) secondary poststroke complications, such as venous thromboembolism and pneumonia, resulting from either the stroke or the immobilization or treatment of the patient following the stroke; and (4) acute exacerbations of preexisting chronic medical conditions such as angina in patients with coronary disease and hyperglycemia in patients with diabetes.²⁶ Table 10–6 summarizes recently reported figures of frequencies of various complications.

Perhaps most common but also usually underrecognized is the occurrence of profound physiological deconditioning, which can result in loss of normal postural reflexes leading to orthostatic hypotension on arising, increased pulse rate at rest and with activity, catabolic nutritional state, psychological depression, reduced pulmonary vital capacity, slowing of gastrointestinal tract and urinary stasis, and venous stasis.^47,48

Venous thromboembolism constitutes the complication for which more evidence exists for the implementation of prevention methods than for any other complication. Occurring in between 10% and 45%,^49,50 there is now strong evidence that pharmacological interventions, using repeated low doses of unfractionated, or (preferably) fractionated, heparins or other anticoagulants can reduce the frequency of this potentially dangerous complication.^51,52 Particular recommendations for anticoagulation are dependent upon the cardiac condition that the stroke is attributed to; anticoagulation in stroke cases attributed to valvular atrial fibrillation are calculated by the Congestive heart failure, Hypertension, Age>75, Diabetes mellitus, and prior Stroke Score (CHADS2 Score)⁵³ (Table 10–7).

Pneumonias occur in up to one-fourth of all people with stroke,⁴⁵ largely because of aspiration of food and stomach contents, but probably partially also resulting from weakness of the muscles of the chest and abdominal wall, causing reduced strength of expiratory muscles and, therefore, cough.^54–60

Cardiac conditions occur in a sizeable proportion of people with strokes. These conditions constitute the second most common cause of death in the first month and the most common cause of death in later phases following stroke.^40,61–63 Because of the commonality of etiologies between ischemic stroke and ischemic heart disease, it is not surprising that coronary heart disease is found in about two-thirds of all people with strokes. Perhaps of most importance, the presence of heart disease has been found to adversely affect survival and rehabilitation outcomes after stroke.⁶¹ Despite this finding, it is also important to recognize that even people with significant heart disease have been found to make improvements during rehabilitation.⁴¹