Restorative and Rehabilitative Treatments for Stroke in the Outpatient Setting

Among the nearly 800,000 people who have a stroke annually in the United States, 80% present acutely to the hospital with motor deficits. After acute care management and inpatient rehabilitation, 50% of people who experience a stroke continue to have residual motor deficits that require the use of modified functional techniques to perform mobility and self-care tasks independently or that render the individual partially or wholly dependent on others for assistance. Indeed, many stroke survivors benefit from ongoing lifelong support and care from rehabilitation professionals. The chief purpose of outpatient rehabilitation is to minimize functional decline as persons with stroke age, through prevention of complications and use of rehabilitation therapies as necessary. There is a growing list of outpatient neurorehabilitation interventions that may facilitate further neurologic and functional recovery in select chronic stroke survivors. This review addresses the challenges and opportunities faced by clinicians who care for people with long-term motor impairments from stroke in the outpatient setting.

The Goals of Outpatient Stroke Care and Lifelong Recovery

Most people who have had a stroke are prescribed outpatient rehabilitation services after discharge from either acute hospitalization or the inpatient rehabilitation facility. These outpatient services may continue 2 to 3 days a week for several weeks to months, but inevitably come to an end, either because of insurance coverage limitations or because the individual is no longer showing objective functional gains from week to week. At this juncture, the person who has had a stroke is often counseled that a plateau has been reached in recovery,¹ and aside from a few sheets of paper showing figures illustrating home exercises, and a list of prescribed functional activities to continue practicing, the individual is left with little expert support for ongoing recovery and functional improvement after therapy ends.

Living with stroke-related impairments is challenging and methods to maintain optimal physical function over a lifetime are not intuitive to people and their caregivers. Going to the gym, attending a yoga class, performing stretching exercises, or going for a walk, even if feasible, are insufficient means to sustain functional ability and prevent long-term decline after stroke. Stroke survivors benefit from ongoing clinical monitoring to prevent poststroke complications and to identify when opportunities to improve functional ability arise. Under these circumstances, additional courses of outpatient therapy are often beneficial even months to years after stroke onset.² This monitoring is best provided by a physiatrist or a neurologist with neurorehabilitation training and should include a clinic visit at least annually or more often depending on the complexity of the person’s condition. An outpatient clinic visit should include a review of current functional abilities in both mobility and self-care and note any decline in function, recent medical problems, hospitalizations, or new or ongoing poststroke complications.

Complications after stroke can directly affect functional ability or lead to a decline in function due to a reduction in physical activity. It is generally best to address these complications as early as possible so that restorative rehabilitation therapies can be provided to support improved functional independence. In addition, as rehabilitation science and standards of care in neurorehabilitation advance over time, regular visits offer the opportunity for a patient to be screened for new interventions that may enhance recovery.

The primary goal of lifelong stroke recovery is to maintain and improve flexibility, strength, and motor control and target desired functional skills to maximize independence. Having a goal in one’s life to improve one or more specific skills is beneficial if the goals can be realistically achieved in a reasonable amount of time. People with stroke can improve basic functional skills to some extent at any time poststroke through central neuroplastic processes like those seen in healthy adults who improve in a skilled task, such as learning to play guitar.³

Barriers to Recovery and Function

There are certain common barriers to maintaining functional ability or regaining functional skills. Those most pertinent to the outpatient care of people with stroke include spasticity, soft-tissue contracture, and pain. Others include environmental barriers such physical inability to leave the home, socioeconomic barriers such as lack of insurance or transportation services, and geographic barriers where regional services are limited or unavailable. These later barriers are important, but a discussion of possible solutions goes beyond the scope of this article.

Spasticity

Spasticity is often used loosely in clinical parlance to refer to hypertonia that limits motor control and joint kinematics during functional activities. Spasticity by its formal definition is a velocity-dependent resistance to stretch of a muscle associated with hyperactive reflexes as part of the upper motor neuron syndrome. Defined as such, spasticity contributes to poor motor control and limits joint kinematics during functional activities but is distinguishable from other forms of hypertonia that interfere with function, including spastic dystonia, rigidity, and paratonia. When discussing the clinical management of spasticity, I will be using the term by its formal definition but will refer on occasion to how treatment affects other kinds of hypertonia.

Spasticity is a dynamic condition that is dependent on stroke location and severity of motor paralysis. It is dynamic in that mobilization can help ameliorate the severity of spasticity, and lack of mobilization can cause spasticity to increase. Thus, spasticity is a common reason a person can plateau functionally or have a decline in ability after completing rehabilitation. Spasticity can interfere with comfort, contribute to the development of contractures, interfere with hygiene, cause difficulty with nursing care, and lead to pressure ulcers. At times spasticity can be beneficial when it helps with weight-bearing, standing, or walking, which in turn can improve circulation, reduce the risk for osteoporosis and fracture, and improve mental health. Therefore, it is critical to perform a detailed functional history and examination to determine whether spasticity in a muscle is beneficial, harmful, or of little consequence.⁴

Certain medical complications can trigger spasticity, such as infection, pain, pressure ulcers, urinary retention or stones, ingrown toenails, and venous thromboembolism. Thus, when spasticity develops, these medical complications should be considered. When spasticity is interfering with function and comfort and there are no medical reasons contributing to worsening hypertonia, several tools are available to manage spasticity in the outpatient setting.

The first line of management for spasticity is limb mobilization with weight-bearing and muscle stretching, ideally performed daily.⁵ If spasticity is present in more than one limb and is moderately severe, oral pharmacologic agents can be considered, such as baclofen, tizanidine, diazepam, clonazepam, and dantrolene sodium. Baclofen is a gamma-aminobutyric acid (GABA^B)agonist that works on the interneurons of the spinal reflex. It is generally well-tolerated by people who have had a stroke and easy to titrate, although higher doses can cause lethargy without necessarily achieving adequate spasticity control. Baclofen can also be hepatotoxic, such that liver functions should be monitored until a stable dose is achieved. Tizanidine is an alpha-2 agonist working centrally to increase presynaptic inhibition of motor neurons. This drug must be titrated slowly to avoid sedation, which is the primary limitation in its use for spasticity. It can also cause hallucinations, hypotension, and prolonged QT interval.

The other oral medications are used less often due to less efficacy or higher risk for complications. Benzodiazepines work postsynaptically on GABA^A receptors, reducing central nervous system (CNS) drive. Medications such as diazepam and clonazepam can be sedating and are often chosen for nighttime use to reduce painful spasms common at the end of the day. Use of benzodiazepines is limited due to risk of dependence and tolerance. Dantrolene sodium is the only peripherally acting agent used for spasticity that reduces calcium release from the sarcoplasmic reticulum of the muscle fiber, which uncouples excitation and contraction. Its use is generally as an adjunct to other medications in more severe refractory spasticity. Tolerance can be limited because higher doses can lead to generalized weakness and dantrolene can cause liver failure.

There is a consensus among practitioners that the first line of treatment for focal spasticity is injection of botulinum toxin into specified muscles.⁶ Furthermore, botulinum toxin may be injected into muscles of both upper and lower limbs when spasticity is not too severe. Botulinum toxin is clinically available in two subtypes, A and B, and works by inhibiting release of acetylcholine from presynaptic neuromuscular terminals. These neurotoxins have advantage over oral agents as they are well-tolerated and cause few side effects. Rarely, botulinum toxin can disseminate, and when used in the upper limb or neck can lead to temporary dysphagia. Muscle selection for injection is based on a careful examination identifying those contributing to spasticity, spastic dystonia, or paratonia. Dosing is selected based on severity of resistance to stretch, the size of the muscle, and the functional goals to be achieved.

Goals can include improved motor control, easier positioning for activities, or to improve comfort and fit of orthotics. Botulinum toxin can be used in combination with oral agents or with intrathecal baclofen pump. The use of an intrathecal baclofen pump is considered when spasticity is severe and cannot be managed with oral agents or neurotoxins. Because baclofen does not readily cross the blood-brain barrier, concentrations in the CNS are about 8.5 times less than in the serum following oral administration. Direct intrathecal administration allows dosing in the range of micrograms instead of milligrams and provides effective reduction of spasticity. Placement of the catheter tip in people with stroke may be as high as the C6 level without delivering excessive brain concentrations of baclofen or affecting respiratory drive, but the clinical effect of intrathecal baclofen on upper limb spasticity is less than that achieved in lower limbs.⁷ If additional spasticity control is necessary in the upper limb, focal chemoneurolysis with botulinum can be helpful.

Most surgical approaches to treat spasticity are not necessary given the numerous options that are less invasive and permit better titration to achieve optimal spasticity control. However, achilles tendon lengthening and the split anterior tibial tendon transfer (SPLATT) are simple outpatient surgical procedures that can correct equinovarus posturing in ankle spastic dystonia or ankle contracture and can be an alternative method to control spasticity in ambulatory people who have had a stroke.⁸ In cases of severe upper limb spasticity for which focal neurolysis is ineffective and when the limb is otherwise nonfunctional, tendon release and surgical neurolysis are a valid choice.

Joint and Muscle Contracture

Despite best efforts to prevent joint and muscle contracture in individuals with stroke, to a certain extent some loss of range is inevitable, particularly in shoulder, wrist, fingers, hip, ankle, and spine. The foundation of preventing contracture is to pass the hemiplegic limbs through a full functional range at least once daily. Spasticity can make achieving full range of motion challenging for a caregiver and painful for the patient. Although a resting wrist-hand splint is commonly used to prevent contracture of the wrist and fingers, the existing data suggest poor efficacy.⁹

Serial casting is a process whereby a fiberglass cast is applied across a joint that is positioned with the muscle at a modest stretch near end range to provide a prolonged consistent stretch. The cast is removed after 5 to 7 days and reapplied while the joint is stretched further. The casting is typically repeated 3 to 5 times with the goal to improve joint range and reduce muscle hypertonicity. Serial casting has been shown effective for improving range of motion in children with cerebral palsy,¹⁰ but evidence in adults with stroke is lacking. An alternative to serial casting in the lower limb is the use of a static adjustable ankle-foot orthosis (AFO), which is an adjustable orthotic that can be locked down at any given angle to apply a consistent stretch to the ankle. This orthotic can improve ankle range by an average of 20 degrees, as shown in a small series of adults with confirmed contractures.¹¹

Orthotics may also be used to accommodate for fixed contractures to permit better function. For example, the addition of a wedge at the heal of an AFO used for walking assistance can accommodate an ankle plantarflexion contracture to allow more normal foot placement during gait and protect the knee and hip proximally. Because the wedge functionally lengthens the limb, a lift is usually placed on the other shoe to avoid a functional leg length discrepancy.

In cases of severe contracture when functional use of the limb is not a goal, tendon lengthening, tendon release (tenotomy), and joint capsule release can be used to allow comfortable positioning for daily activities or care.

Pain Syndromes

There is a 30% prevalence of pain following stroke, occurring primarily in the chronic phase. Pain can be nociceptive in nature, commonly from joint or muscle strain and inflammation. Less commonly, individuals with stroke can have chronic neuropathic pain. The most common causes of both nociceptive and neuropathic pain are listed in Table 1. Some sources of pain after stroke can have characteristics that are both nociceptive and neuropathic in nature, such as hemiplegic shoulder pain or spasticity. In either case, early pain management can prevent what is primarily a nociceptive pain from becoming a chronic neuropathic pain syndrome.

Hemiplegic shoulder pain is the most common nociceptive pain generator poststroke, with an incidence in the first year up to 22% and a prevalence as high as 84%.¹² The onset of shoulder pain is associated with subluxation and motor weakness, although these are not mutually exclusive, and evidence suggests that weakness is the dominant predictive factor. The cause of shoulder pain is multifactorial and several causes can be involved in pain for any one individual. Numerous treatments have been evaluated for the treatment of hemiplegic shoulder pain with little evidence to support any one approach.¹³ Based on current guidelines, early shoulder care should include proper positioning in bed and wheelchair with the use of arm boards to protect the shoulder. Maintaining passive range of motion in normal movement planes is important, with family and caregivers being familiar with proper ranging technique. Mild pain can be managed with pain medication and targeted motor training whereas more severe and persistent shoulder pain requires diagnostic assessment. Diagnostic tests include radiographs to evaluate for bony pathology and ultrasound to evaluate for soft tissue injury and inflammation. Targeted injection of steroid into inflamed regions of shoulder (eg, subacromial space, glenohumeral joint, biceps tendon sheath) using ultrasound guidance can be considered, followed by manual therapy and motor training. Early treatment of shoulder pain can reduce the risk for chronic hemiplegic shoulder pain, which is more resistant to treatment.¹³

Hip pain after stroke is less common than shoulder pain and typically appears in the more chronic phase of recovery. In individuals with no previous hip pathology, the cause of pain in the hemiplegic hip is often from a greater trochanteric syndrome, defined as pain associated with inflammation of the trochanteric bursae along with adjacent tendinopathy.¹⁴ Pain will be present over the lateral aspect of the thigh and exacerbated by prolonged sitting, walking, or stair climbing. Examination reveals point tenderness posterior to the greater trochanter and tenderness along the iliotibial band. A positive Ober test may be observed where the affected hip remains in an abducted position in side-lying when the hip is passively extended and the knee is flexed. People who have had a stroke can have a positive Ober test without pain. The pain usually resolves with therapy that targets stretch of the iliotibial band and strengthening of hip musculature.

Many people who have had a stroke will walk with the hemiplegic knee in a hyperextended position during the stance phase of gait (genu recurvatum). This is caused by quadriceps weakness and ankle plantarflexion hypertonia or tightness. These mechanics do not cause pain for many people, but some will develop posterior knee pain with chronic knee recurvatum. Treatment is to improve knee mechanics through strengthening, improved ankle flexibility, and reduction of plantarflexion spasticity (often using botulinum toxin injection). AFOs can be adjusted to drive the knee into relative flexion during the stance phase of gait.

Another source of lower limb pain is hammertoes (static toe flexion at interphalangeal joints), which, although common in people over age 65, can develop early in people who have had a stroke. Although these people may not have noticeable spasticity in toe flexors on examination at rest, many will have dynamic flexion of the toes during standing and walking, causing pressure on the tips of toes distally and on the interphalangeal joints within the shoe. If not managed, joint contractures may develop. In people without joint contractures, botulinum toxin may relieve the hypertonia to help maintain proper position of the toes during gait. A hammertoe pad, available at many pharmacies, may be helpful as well. With fixed toe contractures, widening the toe box of the shoe, use of a hammertoe pad, or surgical correction is the best strategy.

Neuropathic pain, in contrast to nociceptive pain, can originate from either chronic tissue injury that leads to CNS sensitization or direct central or peripheral neurologic injury. The pain may be spontaneous or elicited, with elicited pain being characterized by allodynia and hyperpathia.¹⁵ Neuropathic pain induces a high amount of emotional distress and can be disabling. The neuropathic aspect of spasticity is often associated with severe pain during passive range of the affected limb or in the context of muscle spasms. Although the medical treatment of spasticity can help, the addition of progressive stretching and strengthening is usually required to reduce the neuropathic characteristics over time.

Persistent poststroke headache (PPSH), defined as headache lasting longer than 3 months, can be related to ischemic stroke, hemorrhagic stroke, cervical artery dissection, reversible cerebral vasoconstriction syndrome (RCVS), or cerebral venous thrombosis (CVT).¹⁶ The prevalence of PPSH is up to 23%. Clinical risk factors include preexisting headache disorder, headache at stroke onset, and stroke caused by dissection or CVT. PPSH more often meets the clinical criteria for tension headache than migraine but can be characterized by either. The pain is typically located ipsilesional for anterior circulation strokes and occipital for posterior circulation strokes. Headaches with migraine characteristics can be treated using common migraine medications, apart from vasoactive drugs such as triptans or dihydroergotamine. Botulinum toxin injection may be useful for either migraine or tension-type headaches. Nonpharmacologic options, such as exercise, cognitive-behavioral therapy, meditation, and biofeedback, are additional options often available through chronic pain management programs.

In central poststroke pain syndrome (CPSPS), pain is referred to a location in the body that originates from the stroke lesion itself. CPSPS occurs in about 8% of people after stroke, with an onset usually in the first month after stroke. The diagnosis of CPSPS should only be made if the pain began after the stroke, is located in an area of the body corresponding to the CNS lesion, and is not accounted for by another nociceptive or peripheral neuropathic cause.¹⁷ If sensory changes are not identified in the painful region, causes other than CPSPS should be explored. Pharmacology in addition to exercise and psychosocial support is the foundation of treatment. Low doses of amitriptyline at bedtime have been shown to improve global functioning and reduce ratings on pain scales. Lamotrigine can also reduce daily pain ratings and cold-induced pain. Studies evaluating the effect of pregabalin for CPSPS are mixed but this drug can improve sleep and anxiety. Gabapentin is a frequent choice for treating CPSPS; clinical trials are lacking, but it has been shown effective in other causes of central pain. Other options include carbamazepine, phenytoin, and baclofen. The best option for any one individual may need to be determined by sequential trial. A good strategy is to trial drugs with different mechanisms of action or drug classes sequentially.¹⁸ Motor cortex stimulation has been explored and shows promise but is not used clinically.

Complex regional pain syndrome type 1 is a rare cause of pain after stroke, with an incidence of less than 2%, which is lower than historical reports, which have ranged from 12% to 15%. The lower incidence is likely due to a shift in clinical practice to providing earlier mobilization and rehabilitation care after acute stroke.¹⁹ As such, the need to manage CRPS in outpatients who have had a stroke is unusual. When chronic cases occur, the clinical symptoms can be challenging to manage; the effectiveness of pharmacology, psychological support, or rehabilitation care are limited. However, if these interventions are provided in a multimodal manner as part an intensive comprehensive pain management program, clinically meaningful improvement in pain control and function can be achieved.²⁰

Novel Interventions for Stroke Recovery in the Outpatient Setting

Muscle strengthening, motor control training, cognitive training, and task-oriented therapy are the key interventions used in stroke rehabilitation both in the early inpatient phase and in the outpatient setting. Inpatient rehabilitation focuses on basic mobility and self-care; outpatient rehabilitation focuses on dynamic mobility, complex functional activities, and community reintegration. Although few new therapeutic approaches have been developed over the past decade in stroke recovery, there are some worth noting, including the incorporation of high-intensity gait training, use of virtual reality to improve motor control, and neuromodulation using vagal nerve stimulation (VNS) combined with upper limb training. Robotics is an emerging area that currently plays a supportive role in outpatient rehabilitation.

High-Intensity Gait Training

The historical assumption that people who have had a stroke, who are usually older and are likely to have cardiovascular disease, should train at modest levels of intensity with a focus on functional gait has been challenged in recent years. Recently there has been a greater understanding that training individuals in the postacute care setting (>6 months poststroke) at high cardiovascular intensities can improve walking function better than low-intensity training.²¹ Perry et al.²² noted that the gait speed necessary for community ambulation needs to exceed 0.8 m/s, making higher comfortable walking speeds a target for functional gait recovery. Evidence from numerous clinical trials suggests that gait training on a treadmill, with or without a safety harness, at 60% to 80% of heart rate reserve or 70% to 85% of heart rate maximum is superior to passive or low-intensity training for improving timed walking distance as measured by the 6-minute walk test. Before a high-intensity gait program can be initiated, people with stroke and known cardiovascular disease should be cleared via graded exercise testing with electrocardiogram. They should also be free of active musculoskeletal disease or injury. Provision of a high-intensity program has added costs in terms of equipment and personnel, but the costs are low at $155 per 0.1 m/s gain in self-selected walking speed, suggesting a high benefit to cost ratio.²³

Motor Training With Virtual Reality

If advancing ambulation skill to the level of community mobility is a poststroke goal, training with exposure to a wide variety of environmental demands seems appropriate. Training with a skilled therapist in an outdoor setting is ideal but not always practical in the clinical setting. The advancement of virtual reality (VR) technology has allowed for novel approaches to motor training in people who have had a stroke. Using immersive 3-dimensional VR technology during treadmill training and exposing people who have had a stroke to different virtual walking conditions can improve walking speed and distance in people with chronic stroke (Figure 1). Some people do not tolerate virtual environments due to vertigo or dizziness.

There is higher utilization of VR in clinical settings for upper limb motor training than for walking and typically in the form of gaming. The most common type of training is with standard home video games on a 2-dimensional television screen using a hand-held device. Others have utilized counterbalanced arm support systems with video games and sometimes with 3-dimensional immersive goggles.^24,25 In a systematic review, it was concluded that VR and interactive video gaming may be beneficial in improving upper limb function.²⁶ It was noted that gaming is superior to other VR systems that provide only visual feedback during training, suggesting that VR games enhance the level of engagement that people have during therapy, which in turn may facilitate therapeutic effectiveness. However, without larger clinical trials, which are lacking, it remains unclear whether VR is superior to conventional training for upper limb recovery after stroke.

Implanted VNS for Upper Limb Recovery

Neuromodulation is the application of electrical energy to direct targets within the nervous system to modulate neural function. In stroke recovery, neuromodulation has been studied as an adjunct to conventional rehabilitation for the enhancement of functional recovery. Numerous modalities for neuromodulation have been studied, including both invasive and noninvasive methods. There is insufficient evidence to support the efficacy of transcranial magnetic stimulation, transcranial direct current stimulation, cortical stimulation, or deep brain stimulation to improve recovery after stroke.²⁷ In contrast, triggered VNS applied during therapy via an implanted pulse generator has demonstrated superiority over conventional therapy alone.²⁸

The pivotal clinical trial VNS-REHAB followed 108 people with unilateral ischemic stroke implanted with a VNS device over 9 months. Participants were randomized to VNS stimulation during rehabilitation therapy 3 times a week for 6 weeks vs sham stimulation with therapy. Therapy sessions included a trigger of the stimulator by the therapist, carefully timed with individualized high-repetition, functional tasks, such as reach and grasp, simulated eating, opening and closing containers, and other skilled activities (Figure 2). Following in-clinic therapy, participants were instructed in a home exercise program performed independently. During home exercises, a small magnet swipe over the device either activated VNS or sham VNS for 30 minutes. The active VNS group showed significantly greater improvements in the upper extremity Fugl-Meyer assessment and Wolf motor function test immediately after in-clinic therapy and at 90-day follow-up. Approximately 50% of the active VNS participants achieved minimal clinically important improvements in motor function 90 days posttreatment, compared with only about 20% of those receiving sham VNS (number need to treat = 4.3). Only one participant had a serious adverse event of vocal cord paralysis following device implant. These findings led to approval for VNS use in upper limb recovery by the Food and Drug Administration (FDA) in 2021. Appropriate candidates for VNS implant are people with ischemic stroke who are medically stable, without swallowing difficulties, and have some ability to move the arm along with a minimal amount of active wrist extension and flexion and some thumb and finger extension. Because the device can be activated for 30-minute sessions by a magnet swipe, people are able to continue using VNS for the lifetime of the device battery.

Robotics in Stroke

There is an allure surrounding the use of robotics in stroke rehabilitation with the idea that therapy can be fully customized and automated, reducing the need for human therapists and expanding access to highly intensive therapy at a low cost. This ideal has not yet been achieved due to the complexity and limitations of most robotic devices on the market. Several barriers need to be overcome to improve access, usability, and utilization of therapeutic robots in clinical rehabilitation.

There are different types of robotic trainers. The main two categories are exoskeletons, where forces operate across joints in the limb, and end-effector robots, where forces are applied to the most distal segment of the limb, such as through a handle or a footplate. Exoskeletons can be installed on a larger device, such as a treadmill or gaming console, whereas some are fully applied to the body, such as overground exoskeletons (Figure 3).

Robotics theoretically have a high potential for enhancing the application of certain therapies in people who have had a stroke. Robots can provide highly repetitive motor training and are essentially indefatigable. Robotic therapy can be prefunctional to improve strength for functional range and accuracy of movement or can simulate functional activities. Robots can assist movement or add resistance to movement and can provide complex multisensory feedback including visual or sensory (haptic feedback). Robots can accurately measure and record performance from session to session, allowing precise tracking of recovery. Several problems with robots are their size and weight. Robots utilize motors and sensors, which require large housing within the device. Thus, robots can take up a lot of space in a clinic, are bulky, and can be heavy, in addition to being expensive, all limiting their usefulness.

Current evidence supports the use of robotic devices to improve arm strength, functional use, and activities after stroke, but they are not superior to conventional therapy. No optimal upper limb robotic device has been identified and the long-term benefits are not known.²⁹ Gait training robotics have a limited role in stroke, with the benefit primarily to advance nonambulatory individuals to some walking capacity, especially early after stroke. In the chronic ambulatory outpatient phase, there is little evidence for the benefit from robotic gait training as there is little evidence to suggest they help increase walking speed or function.³⁰

Conclusion

Rehabilitation and recovery after stroke is a lifelong process that is best achieved through coordinated outpatient care following the acute period of recovery. Management and prevention of medical and physical problems that commonly arise in stroke survivors can help maintain opportunities for individuals to improve or maintain functional ability at an optimal capacity. When problems arise, such as spasticity, pain, or contracture, combining medical management with outpatient physical or occupational therapy will lead to the best response to treatment. A thorough knowledge of newer targeted therapies that can enhance walking ability or arm and hand function allow for appropriate patient selection and referral, which can translate to a higher quality of life for many individuals after stroke.