Motor Recovery in Stroke

1/9/12 Motor Recovery In Stroke

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Motor Recovery In Stroke

Author: Auri Bruno-Petrina, MD, PhD; Chief Editor: Denise I Campagnolo, MD, MS more...

Updated: Dec 6, 2011

Recovery Considerations

Stroke rehabilitation is a combined and coordinated use of medical, social, educational, and vocational measuresto retrain a person who has suffered a stroke to his/her maximal physical, psychological, social, and vocationalpotential, consistent with physiologic and environmental limitations. The cellular mechanisms behind stroke areseen in the image below.

When the brain suffers an injury, such as a stroke, neurons release glutamate onto nearby neurons, w hich become excited and

overloaded w ith calcium, after w hich they die (left). Normal neurotransmission (above) is altered during injury, causing excess calcium

to activate enzymes, eventually leading to destruction of the cell. Since this process occurs via glutamate receptors, including N-Methyl-

D-aspartate (NMDA) receptors, scientists believe that damage can be stopped through the use of agents that block these receptors.

Evidence from clinical trials supports the premise that early initiation of therapy favorably influences recovery fromstroke. When the initiation of therapy is delayed, patients may in the interim develop avoidable secondarycomplications, such as contractures and deconditioning.

In addition, many studies show that stroke rehabilitation can improve functional ability even in patients who areelderly or medically ill and who have severe neurologic and functional deficits.

The initial clinical examination of a patient with an acute stroke includes a thorough, detailed neurologicexamination. The neurologic findings are used by the rehabilitation team for prognostication, development of thespecific details of the rehabilitation plan, and selection of the appropriate setting for rehabilitation.

Reassessment of the patient's condition during rehabilitation provides a means of monitoring progress andsubsequently evaluating outcome. The initial rehabilitation assessment should begin immediately following onset,within 2-7 days, and then subsequently at repeated intervals.

Go to Stroke, Ischemic, for more complete information on this topic.

Timing, extent, and types of recovery

Patients recover after stroke in 2 different, but related, ways.

A reduction in the extent of neurologic impairment can result from spontaneous, natural neurologic recovery (viathe effects of treatments that limit the extent of the stroke) or from other interventions that enhance neurologic



functioning. A patient demonstrating this form of recovery presents with improvements in motor control, languageability, or other primary neurologic functions.

The second type of recovery demonstrated by stroke patients is the improved ability to perform daily functionswithin the limitations of their physical impairments. A patient who has sensorimotor, cognitive, or behavioraldeficits resulting from stroke may regain the capacity to carry out activities of daily living (ADL), such as feedinghimself/herself, dressing, bathing, and toileting, even if some degree of residual physical impairment remains.

The ability to perform these tasks can improve through adaptation and training in the presence or absence ofnatural neurologic recovery, which is thought to be the element of recovery on which rehabilitation exerts thegreatest effect.

Hemiparesis and motor recovery have been the most studied of all stroke impairments. As many as 88% ofpatients with acute stroke have hemiparesis.

In a classic report, Twitchell described in detail the pattern of motor recovery following stroke.[1] At onset, theupper extremity (UE) is more involved than the lower extremity (LE), and eventual motor recovery in the UE is lessthan in the LE. The severity of UE weakness at onset and the timing of the return of movement in the hand areimportant predictors of eventual motor recovery in the UE. The prognosis for return of useful hand function isunfavorable when UE paralysis is complete at onset or grasp strength is not measurable by 4 weeks.

However, as many as 9% of patients with severe UE weakness at onset may gain good recovery of hand function.As many as 70% of patients showing some motor recovery in the hand by 4 weeks make a full or good recovery.Full recovery, when it occurs, usually is complete within 3 months of onset.

Bard and Hirshberg asserted that if no initial motion is noticed during the first 3 weeks or if motion in one segmentis not followed within a week by the appearance of motion in a second segment, the prognosis for recovery of fullmotion is not favorable.

Although most recovery from stroke takes place in the first 3 months, and only minor additional measurableimprovement occurs after the 6 months following onset, recovery may continue over a longer period of time insome patients who have significant partial return of voluntary movement.

Criteria for admission to a comprehensive rehabilitation program

Criteria for a patient’s admission to a comprehensive rehabilitation program may include the following:

Stable neurologic statusSignificant persisting neurologic deficitIdentified disability affecting at least 2 of 5 functions, including mobility, self-care activities, communication,bowel or bladder control, and swallowingSufficient cognitive function to learnSufficient communicative ability to engage with therapistsPhysical ability to tolerate the active programAchievable therapeutic goals

Theories of Recovery

One theory of motor recovery is that collateral sprouting from intact cells to the denervated region occurs aftersome or all input has been destroyed.

Another theory suggests that there is an unmasking of neural pathways and synapses that are not normally usedbut that can be called upon when the dominant system fails (excitability to capture effects of remaining input).

Mechanisms of Recovery

The first recovery mechanism is resolution of harmful local factors, which generally accounts for early spontaneousimprovement after stroke (usually within the first 3-6 mo). These processes include resolution of local edema,



resorption of local toxins, improvement of local circulation, and recovery of partially damaged ischemic neurons.

Neuroplasticity

The second recovery mechanism, which may continue for many months, is neuroplasticity, which can take placeearly or late. Brain plasticity is the ability of the nervous system to modify its structural and functionalorganization. The 2 most plausible forms of plasticity are collateral sprouting of new synaptic connections andunmasking of previously latent functional pathways.

Other mechanisms of plasticity include assumption of function by undamaged, redundant neural pathways,reversibility from diaschisis, denervation supersensitivity, and regenerative proximal sprouting of transectedneuronal axons. Experimental evidence indicates that plasticity can be altered by several external factors,including pharmacologic agents, electrical stimulation, and environmental stimulation.

A key aspect of neuroplasticity that has important implications for rehabilitation is the fact that the modifications inneuronal networks are use-dependent. Animal experimental studies and clinical trials in humans have shown thatforced use and functional training contribute to improved function. On the other hand, techniques that promotenonuse may inhibit recovery.

In the past, the conventional wisdom was that benefits from rehabilitation were achieved primarily through trainingpatients in new techniques that compensate for impairments (for example, using the uninvolved hand to achieveself-care independence). This approach avoided intense therapy on the weak upper limb.

Currently, it is recognized that repeated participation by patients in active physical therapeutic programs probablyprovides direct influence on the process of functional reorganization in the brain and enhances neurologic recovery.

Pattern of Disability

After stroke occurs, total loss of voluntary movement may be noted in involved extremities, with loss or decreasein muscle stretch reflexes (MSRs). Within 48 hours, MSRs and finger jerks are more active on the involved side,although they may require 3-29 days to develop. Within a short period, tone appears in the wrist and finger flexors,as well as in the ankle plantar flexors. As a result, the UE is prone to demonstrate the adductor/flexor pattern, andthe LE is prone to demonstrate the adductor/extensor pattern.

Development of spasticity

In 1-30 days, spasticity appears, resulting in resting posture. In the upper extremity, this posture takes thefollowing form:

Shoulder - In adduction and internal rotationElbow - In flexionForearm - In pronation/supinationWrist and fingers - In flexion

In the lower extremity, resting posture develops as follows:

Hip - In adduction and extensionKnee - In extensionAnkle - In plantar flexionFoot - In inversion

Within 1-38 days after stroke, clonus appears in ankle plantar flexors, and the onset of clasp-knife phenomenonoccurs within 3-31 days.

Spasticity in the lower extremity decreases with increased volitional movement, but MSRs always remainincreased, despite total recovery.

Pattern of Recovery



Recovery of function in the UEs

Recovery of UE flexor synergy occurs as follows:

Shoulder flexion - 6-33 daysElbow flexion - 1-6 days laterFinger and wrist flexion - 1-13 days laterShoulder adduction/internal rotation

Clinically, flexor synergy can also present as follows:

Scapula retraction/elevationShoulder abduction (90°)/external rotationElbow flexion (acute angle)Forearm supination (full range)

Recovery of UE extensor synergy occurs as follows:

ShoulderElbowWrist/finger extension

Clinically, extensor synergy presents as follows:

Scapula protractionHumerus flexion/internal rotationElbow extensionForearm pronation

In a study of 188 patients with stroke, Nijland et al found that assessment of finger extension and shoulderabduction within 72 hours after stroke can help to predict upper limb recovery. If, by the second day followingstroke, patients in whom upper limb motor function was affected were capable of some voluntary extension of thefingers and some abduction of the hemiplegic shoulder, there was a 0.98 probability that they would regain some

dexterity by 6 months.[2]

Patients with no such voluntary movement on the second day, according to the study, had only a 0.25 probabilityof regaining dexterity by 6 months. Full recovery at 6 months was achieved in 60% of patients with some earlyfinger extension.

Recovery of function in the LEs

Recovery of LE flexor synergy occurs as follows:

Hip flexion/adduction - 1-31 daysKnee flexion - 1-2 days laterAnkle/toe dorsiflexion - 25-90 days

LE extensor synergy is recovered first in hip/knee extension and then in ankle plantar flexion.

PT Options in Stroke

Rehabilitation should include physical therapy (PT) that is directed at specific training of skills and at functional

training.[3] Therapy should be given with sufficient intensity to promote skill acquisition. Major theories ofrehabilitation training include the following:

Traditional therapyBobath Concept– Neurodevelopmental trainingProprioceptive neuromuscular facilitationBrunnstrom



Traditional therapy

This form of therapy employs range-of-motion (ROM), strengthening, mobilization, and compensatory techniques.

The process of mental practice may also be used to improve the performance of certain activities.[4] This is when apatient mentally rehearses an action without physically performing the action. Current evidence is not clear onwhether this practice, in conjunction with physical practice, actually improves motor capacity of the upper limbregion. Further studies are required.

Bobath concept

According to the Bobath concept, muscle patterns, not isolated movements, are used for motion. The theorystates that persons with motor deficiencies following stroke are unable to direct nervous impulses to muscles inthe different combinations used by persons with an intact central nervous system (CNS).

The therapy, therefore, is meant to suppress abnormal muscle patterns before normal patterns are introduced.Abnormal patterns are modified at proximal key points of control, such as the neck, spine, shoulder, and pelvis.

Proprioceptive neuromuscular facilitation

This form of therapy aims to stimulate nerve/muscle/sensory receptors to evoke response through manual stimulito increase ease of movement and promote function.

Brunnstrom movement therapy

This therapy involves central facilitation using Twitchell's recovery. It aims to enhance specific synergies throughthe use of cutaneous/proprioceptive stimuli.

Studies

Every patient should avoid strenuous exercise after stroke, but it is a good idea to participate in an individualizedexercise program. At 1 year post stroke, improvement in functional walking ability was seen in stroke patients whounderwent either locomotor training, including body weight supported treadmill, or a progressive home exerciseprogram supervised by a physical therapist. No significant differences in improvement were found between the two

groups.[5] Reports in the literature state that for young stroke survivors who participated in an aerobic fitnessprogram, improvement in fitness levels, ambulatory speed, and life satisfaction was statistically significant.

Results from a randomized, controlled, assessor-blinded study indicated that even long after a stroke, kinestheticability training, administered in combination with a conventional rehabilitation program, can improve balance in

hemiparetic stroke patients.[6]

The inclusion of breathing retraining (BRT) and inspiratory muscle training (IMT) in the rehabilitation program ofpatients who have suffered a stroke can result in improved respiratory muscle function, exercise capacity, andquality of life, according to a study by Sutbeyaz et al. In this study, patients received BRT and IMT training for half

an hour daily, 6 times a week for 6 weeks.[7]

Results from a systematic review indicate that modified constraint-induced movement therapy (CIMT) is more

effective than traditional rehabilitation in reducing a patient's disability level.[8] It can improve upper extremity abilityand increase movement spontaneity. Further studies are needed on CIMT’s effectiveness in kinematic analysis.

In a pilot, randomized, clinical trial, with a 6-month follow-up, the practicality and efficacy of conventionalneurological therapy, constraint-induced therapy, and therapeutic climbing to improve minimal-to-moderate armand hand function in stroke patients was evaluated. The study concluded that improvement of arm and hand

function in the intermediate term was best achieved using the constraint-induced therapy approach.[9]

Occupational Therapy in Stroke

Most patients with significant neurologic impairment who survive a stroke are dependent on others for performanceof basic ADL (ie, bathing, dressing, feeding, toileting, grooming, transfers). The capacity of individuals to perform



these activities usually is scored on disability rating scales, such as the Functional Independence Measure.Almost all patients show improved performance of ADL as recovery occurs.

Most improvement is noted in the first 6 months, although as many as 5% of patients show continued measurableimprovement up to 12 months postonset. Other patients may show some functional improvement beyond 6months, even though the disability scales usually fail to detect further improvement because of their limitedsensitivity at the upper end of the functional range.

Reports of the levels of functional independence eventually reached by stroke patients after recovery vary from oneauthor to another. This variability probably reflects differences between study populations, methods of treatment,follow-up, and data reporting. In most reports, 47-76% of patients achieve partial or total independence in theperformance of ADL.

Most authors who have attempted to determine which factors predict ultimate ADL functional outcome have usedmultivariate analysis. Of the many independent variables tested, those listed below have been reported to have themost influence on outcome. However, not all of these factors have been shown to predict outcome statusstatistically in every study. Factors predicting poor ADL outcome include the following:

Advanced ageComorbiditiesMyocardial infarctionDiabetes mellitusSevere strokeSevere weaknessPoor sitting balanceVisuospatial deficitsMental changesIncontinenceLow initial ADL scoresDelay in initiating rehabilitation following onset

Aphasia Therapy

Approximately one third of patients with acute stroke have clinical features of aphasia. Language function in manyof these patients improves, and, at 6 months or more after stroke, only 12-18% of patients have identifiableaphasia.

Skilbeck and colleagues reported that patients with aphasia continue to show some late improvement in languagefunction even more than 1 year after onset.

Patients who are classified initially as having Broca aphasia have variable outcomes. In patients with largehemisphere lesions, Broca aphasia persists with little recovery. Patients with smaller lesions confined to theposterior frontal lobe often show early progressive improvement, but the impairment may evolve into a milder formof aphasia with anomia and difficulty finding words. Patients with global aphasia tend to progress slowly, withcomprehension often improving more than expressive ability does.

The communicative ability of patients who initially have global aphasia improves over a longer period of time, up toa year or more postonset. Patients with global aphasia associated with large lesions may show only minorrecovery, but recovery may be quite good in patients with smaller lesions. The extent of language recoveryassociated with Wernicke aphasia is variable.

Associated Conditions

Most patients with stroke who undergo rehabilitation have many other associated medical conditions that requireprofessional attention. These problems might be preexisting medical illnesses that necessitate ongoing care (eg,hypertension, diabetes mellitus [DM]), secondary poststroke complications (eg, deep venous thrombosis,pneumonia), or acute poststroke exacerbations of preexisting chronic diseases (such as angina in a patient withischemic heart disease).



Management of these conditions can constitute major portions of the rehabilitation effort. Some patients may bemore disabled by certain associated comorbid diseases than by the stroke itself.

The occurrence of these associated conditions has several implications for management of stroke cases duringand after rehabilitation. First, these problems can detract from the benefits of rehabilitation. Some medicalproblems, such as heart disease, have been found to affect the course and outcome of rehabilitation adverselyfollowing a stroke. Intercurrent medical complications can limit the patient's ability to participate in therapeuticexercise programs, inhibit functional skill performance, and reduce the likelihood of achieving favorable outcomesfrom rehabilitation.

The rehabilitation interventions also might affect the medical condition adversely, causing an exacerbation of thedisease or necessitating an adjustment in the treatment program. Patients who are treated in a stroke unit have

better outcomes at discharge than do patients who are not.[10]

Surgical Options

Tendon release can be performed in cases of severe spasticity or contractures.

Carotid endarterectomy can be carried out in patients with stenosis of 70% or greater.

There is no longer any clear indication for carotid artery bypass to prevent stroke or in patients who have had aTIA. No benefit has been demonstrated from the surgery.

Although there have been reports of successful cases involving surgical bypass or endarterectomy involving theposterior circulation, these procedures remain largely experimental.

Consultations in Stroke

Consultations with neurologists and physiatrists are important aspects of treatment in patients who have sufferedstroke.

Consultations with psychologists are also essential. Psychosocial issues obviously are very important in cases ofstroke. Numerous studies have reported on the influence of the psychological adjustment and coping mechanismsof the patient, as well as those of his/her spouse and other family members, in determining the patient’s outcome.

Other Treatment Options

Biofeedback attempts to modify autonomic functions, pain, and motor disturbances through acquired volitional

control, using auditory, visual, and sensory clues.[11]

Functional electrical stimulation commonly is employed in the UEs and LEs to improve strength, encourage andaugment early active ROM, assist in the management of dependent peripheral edema through forceful isotonic

muscle contraction, and establish early proprioceptive joint sense in the sensory-compromised patient.[12]

Rehabilitation programs are offered in different settings, such as acute inpatient rehabilitation units, subacuteinpatient rehabilitation units, home care environments, and outpatient centers. The acute rehabilitation setting isappropriate for patients who meet the admission criteria and are able to tolerate 3 hours or more of active therapyper day.

An acute rehabilitation setting is preferred if the patient requires close monitoring of his/her medical status bymedical and nursing professionals. If the patient's medical status is stable but the patient is unable to toleratemore than 1 hour of therapy a day, a subacute rehabilitation or skilled nursing setting is more appropriate. Patientswho are independent or require only minimal assistance in self-care tasks and mobility are suited for outpatienttherapy or a home care program.

Rehabilitation units

Medical stability traditionally has been required for admission of a patient to a specialized rehabilitation unit;



however, hospitals increasingly are transferring patients from acute wards to rehabilitation units at earlier stages,often when the patients still have unresolved medical problems.

This practice has forced rehabilitation centers to expand their resources to care for these more complex casesand to provide closer medical and nursing monitoring. Local institutional referral patterns and practices usuallydetermine the timing of transfer, but if earlier transfer to rehabilitation can be accomplished safely, patient care

may be enhanced by earlier active participation of the patient in the rehabilitation program.[13]

Planning for discharge from the inpatient rehabilitation program should begin on admission. Discharge functionalstatus, destination of discharge, and length of hospital stay are comparable in patients with a good prognosis.Discharge functional status is comparable in patients with an unfavorable prognosis, but mortality is higher and thehospital stay is longer in medical wards.

Discharge from the hospital often is thought of as the end of rehabilitation, with the assumption that a goodprogram prepares the patient for reintegration into the home and community; however, hospital discharge insteadshould be looked at as the end of the beginning of a new life in which the patient faces the challenge of adapting todifferent roles and relationships and of searching for new meaning in life.

This adaptation involves resuming former roles in the family and with friends as much as possible and finding waysto live a meaningful life in the community.

Postacute rehabilitation

During postacute rehabilitation, all patients should be monitored carefully for evidence of cardiac disease. Theclassic features of coronary artery disease and congestive heart failure may be present, but often they are not.

Ischemia may be silent.[14]

The clinical clues to significant coexisting heart disease may be subtle (eg, slower than expected progress,excessive fatigue, lethargy, mental changes). These cardiac complications can be treated successfully and arenot contraindications to rehabilitation. The patient should undergo appropriate cardiac investigation withelectrocardiography, Holter monitoring, and echocardiography and also should receive optimal therapy.

Early initiation of therapies is desirable. Beginning rehabilitation early minimizes secondary complications, suchas contractures and deconditioning, and helps to motivate the patient. Whether more intense therapy as an

independent variable improves ultimate functional recovery is not known.[15]

Evaluation of neurologic impairments should be made repeatedly during the course of the rehabilitation program.Ideally, evaluation should be made weekly in the early phases of rehabilitation to allow monitoring of the recoveryprocess and to guide the therapeutic intervention. A clear need for committed medical direction is evident inpatients who have sustained strokes.

The role of the clinician includes provision of medical care. Many patients have ongoing associated medicalproblems that require appropriate monitoring and therapy. The clinician must act as a medical counselor, offeringreasonable prognostication to patient and family, along with guidance in reduction of stroke risk factors andongoing medical care. The clinician also must give leadership to the team and assist in developing treatmentprotocols and setting treatment expectations.

The multiple problems that a patient can have following stroke require the active participation of a team ofprofessionals. The treatment activities of the team members must be coordinated so that detailed evaluations areshared and agreements made regarding goals and treatment interventions.

Each of the professional therapists on the team should be knowledgeable about the appropriate interventionswithin his/her discipline for treating the disabilities of patients following stroke. The interventions should be directedat achieving specific therapeutic goals, which may be for the short term (for example, weekly goals) or longer term(for instance, goals to be reached by discharge). Having achieved those goals, the patient moves on to the nextphase of rehabilitation or is discharged home to continue treatment as an outpatient.

Rehabilitation requires a functional approach. When impairments cannot be altered, every effort should be made toassist patients in compensating for deficits and adapting to alternative methods so that they can achieve optimal



functional independence.

Home Care in Stroke

A study by Young and Forster found home care to be cheaper than day hospital services (£385 vs £620

[approximately $546 vs $880]).[16]

Outcome measurements have indicated a modest advantage in favor of home care.

No difference in outcome was found between home care and hospital-based rehabilitation following acute care.

Hospital-based services are 27% more expensive than home care services.

Geriatric ward patients are 2.4 times less likely to die or to become institutionalized by 6 months if placed in dayhospital service.

Stroke unit patients demonstrate superior ADL performance at 6 months with home care (2.6 times moreexpensive) than they do with outpatient therapy.

General medical ward patients had similar outcomes, although outpatient services cost 56% of home care.

Home care risks

Risks for suboptimal home care (72.6% prediction/validation rate) include the following:

A depressed caregiverInadequate knowledge of how to care for a family member following a strokeA dysfunctional family

Cardiac Precautions

The rehabilitation management of patients with identified cardiac complications should include formal clinicalmonitoring of pulse and blood pressure during physical activities. Brief electrocardiac monitoring during exercisecan add more specific information.

Note that in deconditioned patients, the resting heart rate may be high, and, in an elderly patient, the estimatedlimit for heart rate based on 50% above resting may be too high. For patients on beta blockers, a reasonable limitmight be a heart rate of around 20 beats above the resting level.

A useful set of cardiac precautions in patients undergoing rehabilitation was developed by Fletcher and colleagues.Activity should be terminated if any of the following symptoms develop:

New onset of cardiopulmonary symptomsHeart rate decreases to less than 20% of baselineHeart rate increases to greater than 50% of baselineSystolic BP increases to 240 mm HgSystolic BP decreases 30 mm Hg from baseline or to less than 90 mm HgDiastolic shortening fraction increases to 120 mm Hg

Complications During Rehabilitation

Medical complications frequently occur during the postacute phase of rehabilitation, affecting up to 60% of patients(and up to 94% of patients with severe lesions).

Common medical complications include the following:

Pulmonary aspiration, pneumonia - 40%Urinary tract infection - 40%Depression - 30%



Musculoskeletal pain, reflux sympathetic dystrophy - 30%Falls - 25%Malnutrition - 16%Venous thromboembolism - 6%Pressure ulcer - 3%

The means of treating depression in patients following stroke remains uncertain. One study found evidence thatpharmacotherapy can reduce depressive symptoms in these patients but that it can also increase adverse

events.[17] The report found no evidence that psychotherapy reduces depression.

Common neurologic complications include the following:

Toxic or metabolic encephalopathy - 10%Stroke progression - 5%Seizures - 4%

In ischemic stroke patients who were followed over the course of 2-4 years, seizures developed in 6-9% ofpatients. Seizures developed in 26% of patients with cortical lesions and in 2% of patients with subcorticallesions. Risk factors include the following:

Lobar hemorrhage (acute)Cortical lesions (chronic)Persistent paresis (50%)

Other risk factors include the following:

Language function deficit, dysarthriaVisual field defect (20%), hemianopiaPosture and balance deficitSensory, cognitive, and perceptual function deficitsBowel and bladder incontinenceDeconditioningCongestive heart failureHypertensionDMDysphasiaSpasticityContracturesHeterotopic calcification

Prognosis in Stroke

Significant improvement in UE function usually is seen only in the first 3 months poststroke. If no return of motorfunction is noted after more than 6 months, prognosis for useful function is unfavorable. If no return of voluntarymotor function is noted after more than 1 week, it is unlikely that full use of the affected UE will return.

Poor prognostic indicators include the following:

Proprioceptive facilitation (tapping) response for more than 9 daysTraction response (shoulder flexors/adductors) in more than 13 daysProlonged flaccid periodOnset of motion at longer than 2-4 weeksSevere proximal spasticityAbsence of voluntary hand movement for more than 4-6 weeks

Stroke rehabilitation outcome

Predictors of outcome include the following:



Type, distribution, pattern, and severity of physical impairment[18]

Cognitive, language, and communication abilitiesNumber, types, and severity of comorbid conditionslevel of motivation or determinationCoping ability and coping styleNature and degree of family and social supportsType and quality of the specific training and adaptation program provided

Remarkable recoveries have been reported in 3-6 years. (Patients have returned to work 3 years poststroke).

Starting rehabilitation early correlates with better outcome but may be confounded by case severity. (See thegraphs below.) However, stroke rehabilitation improves functional ability even in patients who are elderly ormedically ill, as well as in those who have severe neurologic/functional deficits. Significant gains that are achievedare not attributable only to spontaneous recovery.

The bar graphs show the percentages of patients w ith stroke w ho demonstrated different outcomes on the modif ied Rankin Scale of

global disability. These results w ere recorded 3 months follow ing treatment of patients w ith tissue plasminogen activator (tPA) or

placebo, in the National Institutes of Neurological Disorders and Stroke tPA trials 1 and 2. Rankin 0 = no symptoms; 1 = no signif icant

disability, despite symptoms (able to perform all usual duties and activities); 2 = slight disability (unable to perform all previous activities

but able to look after ow n affairs w ithout assistance); 3 = moderate disability (requires some help, but able to w alk w ithout assistance);

4 = moderately severe disability (unable to w alk w ithout assistance and unable to attend to ow n bodily needs w ithout assistance); 5 =

severe disability (bedridden, incontinent, and requires constant nursing care and attention); 6 = dead. Image courtesy of UCLA Stroke

Center.

Of patients who survive stroke by more than 30 days, 10% demonstrate complete spontaneous recovery, 10%show no benefit from any treatment, and 80% may benefit from treatment. Stroke survivors who do not undergorehabilitation are more likely to be institutionalized.

Eighty-five percent of patients went home after 3 months of participation in a stroke rehabilitation program. After 43days, 80% of patients returned home, 85% were ambulatory, and 50-62% were independent in performance ofADL. Functional state improved in the stroke unit from 6-52 weeks.

Patients in outpatient and nonoutpatient therapy groups showed statistical improvement between stroke onset,discharge to home, and 1-year follow-up. The outpatient therapy group required a longer rehabilitation stay, wasmore impaired at onset, and did not perform as well as the nonoutpatient group. The outpatient therapy group wasassociated with complete UE/LE hemiplegia, unilateral neglect, impaired proprioception, and urinary incontinence.

Sphincter function, level of neurologic impairment, and capacity to perform ADL related to outcome are assessed,but these measures are not useful to anticipate the outcome of each patient.

Patients unable to walk 3 months poststroke received therapy up to 2 years after the stroke. Seventy-four percentof patients walked without assistance. Seventy-nine percent of patients had a modified Barthel score below 70.

Rehabilitation should include therapy directed at specific training of skills and functional training. Therapy shouldbe given with sufficient intensity to promote skill acquisition.

A population-based study by Dhamoon et al suggests that within a group of patients who have suffered ischemicstroke, there will be an annual decline for up to 5 years in the proportion of patients who are functionally

independent that is unrelated to recurrent stroke and other risk factors.[19]

In the study, 525 patients aged 40 years or older (mean age, 68.6 y) with incident ischemic stroke were



prospectively followed at 6 months and annually for 5 years. During that time, the proportion of patients with aBarthel score of 95 or higher declined. The decline was independent of age, stroke severity, and other predictors offunctional decline, occurring even in patients who did not suffer recurrent stroke or myocardial infarction. Theauthors also found that the decline occurred in patients who were receiving Medicaid or who had no healthinsurance but did not occur in those with Medicare or private insurance.

Degree of recovery

The degree of recovery of independent functioning during rehabilitation has been found to be greater than thatwhich might have been expected through a reduction in neural impairments alone, suggesting that rehabilitationinterventions play an important role in the patient's recovery of function.

The 2 types of improvement are related in subtle and complex ways. Alternative compensatory functionalstrategies, such as 1-handed dressing techniques for the hemiplegic patient, assume a major role in theperformance of functional tasks when neurologic improvement is minimal or absent.

The degree of natural recovery of neurologic function varies, but figures on the relative frequencies of neurologicdeficits during the early and later poststroke stages offer some insight into the degree of recovery that might beseen. The number of these deficits generally declines by approximately 33-50%. For example, the followingreductions in prevalence from initial presentation have been found at 1-year follow-up:

Hemiparesis - From 73% at presentation to 37%Aphasia - From 36% at presentation to 20%Dysarthria - From 48% at presentation to 16%Dysphagia - From 13% at presentation to 4%Incontinence - From 29% at presentation to 9%

As previously mentioned, the time required for recovery also varies. Although most improvements in physicalfunctioning occur within the first 3-6 months, later recovery also is commonly observed. Although it is tempting tospecify a definitive prognosis in a stroke patient, it is important to recognize that a multiplicity of variablesdetermine ultimate outcome, which is why expectations for recovery often are inaccurate.

Recovery and Diet

No special diet is required to improve the patient's motor recovery after stroke; however, the patient should avoidexcessive weight gain and remain on the regular diet for conditions such as DM, hypertension, and hyperlipidemia.

A study did find evidence that intensive nutritional supplementation can improve motor recovery in previously

undernourished patients who have suffered stroke and who are undergoing intensive inpatient rehabilitation.[20]

For excellent patient education resources, visit eMedicine's Stroke Center. Also, see eMedicine's patienteducation article Stroke.

Contributor Information and DisclosuresAuthorAuri Bruno-Petrina, MD, PhD Clinical Trainee, Pemberton Marine Medical Clinic, N Vancouver

Auri Bruno-Petrina, MD, PhD is a member of the following medical societies: American Academy of PhysicalMedicine and Rehabilitation, Canadian Association of Physical Medicine and Rehabilitation, College ofPhysicians and Surgeons of British Columbia, and International Society of Physical and Rehabilitation Medicine

Disclosure: Nothing to disclose.

Specialty Editor BoardMilton J Klein, DO, MBA Consulting Physiatrist, Heritage Valley Health System-Sewickley Hospital and OhioValley General Hospital

Milton J Klein, DO, MBA is a member of the following medical societies: American Academy of Disability



Evaluating Physicians, American Academy of Medical Acupuncture, American Academy of Osteopathy,American Academy of Physical Medicine and Rehabilitation, American Medical Association, AmericanOsteopathic Association, American Osteopathic College of Physical Medicine and Rehabilitation, AmericanPain Society, and Pennsylvania Medical Society


Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical CenterCollege of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Richard Salcido, MD Chairman, Erdman Professor of Rehabilitation, Department of Physical Medicine andRehabilitation, University of Pennsylvania School of Medicine

Richard Salcido, MD is a member of the following medical societies: American Academy of Pain Medicine,American Academy of Physical Medicine and Rehabilitation, American College of Physician Executives,American Medical Association, and American Paraplegia Society


Chief EditorDenise I Campagnolo, MD, MS Director of Multiple Sclerosis Clinical Research and Staff Physiatrist, BarrowNeurology Clinics, St Joseph's Hospital and Medical Center; Investigator for Barrow Neurology Clinics; Director,NARCOMS Project for Consortium of MS Centers

Denise I Campagnolo, MD, MS is a member of the following medical societies: Alpha Omega Alpha, AmericanAssociation of Neuromuscular and Electrodiagnostic Medicine, American Paraplegia Society, Association ofAcademic Physiatrists, and Consortium of Multiple Sclerosis Centers

Disclosure: Teva Neuroscience Honoraria Speaking and teaching; Serono-Pfizer Honoraria Speaking andteaching; Genzyme Corporation Grant/research funds investigator; Biogen Idec Grant/research fundsinvestigator; Genentech, Inc Grant/research funds investigator; Eli Lilly & Company Grant/research fundsinvestigator; Novartis investigator; MSDx LLC Grant/research funds investigator; BioMS Technology CorpGrant/research funds investigator; Avanir Pharmaceuticals Grant/research funds investigator

References

1. TWITCHELL TE. The restoration of motor function following hemiplegia in man. Brain. Dec 1951;74(4):443-80. [Medline].

2. [Best Evidence] Nijland RH, van Wegen EE, Harmeling-van der Wel BC, Kwakkel G. Presence of fingerextension and shoulder abduction within 72 hours after stroke predicts functional recovery: earlyprediction of functional outcome after stroke: the EPOS cohort study. Stroke. Apr 2010;41(4):745-50.[Medline].

3. Ada L, Dean CM, Morris ME, Simpson JM, Katrak P. Randomized trial of treadmill walking with bodyweight support to establish walking in subacute stroke: the MOBILISE trial. Stroke. Jun 2010;41(6):1237-42. [Medline].

4. Barclay-Goddard RE, Stevenson TJ, Poluha W, Thalman L. Mental practice for treating upper extremitydeficits in individuals with hemiparesis after stroke. Cochrane Database Syst Rev. May 112011;5:CD005950. [Medline].

5. Duncan PW, Sullivan KJ, Behrman AL, Azen SP, Wu SS, Nadeau SE, et al. Body-weight-supportedtreadmill rehabilitation after stroke. N Engl J Med. May 26 2011;364(21):2026-36. [Medline].

6. [Best Evidence] Alptekin N, Gok H, Geler-Kulcu D, Dincer G. Efficacy of treatment with a kinaesthetic



ability training device on balance and mobility after stroke: a randomized controlled study. Clin Rehabil.Oct-Nov 2008;22(10-11):922-30. [Medline].

7. [Best Evidence] Sutbeyaz ST, Koseoglu F, Inan L, Coskun O. Respiratory muscle training improvescardiopulmonary function and exercise tolerance in subjects with subacute stroke: a randomizedcontrolled trial. Clin Rehabil. Mar 2010;24(3):240-50. [Medline].

8. Shi YX, Tian JH, Yang KH, Zhao Y. Modified constraint-induced movement therapy versus traditionalrehabilitation in patients with upper-extremity dysfunction after stroke: a systematic review and meta-analysis. Arch Phys Med Rehabil. Jun 2011;92(6):972-82. [Medline].

9. Khan CM, Oesch PR, Gamper UN, Kool JP, Beer S. Potential effectiveness of three different treatmentapproaches to improve minimal to moderate arm and hand function after stroke - a pilot randomizedclinical trial. Clin Rehabil. Nov 2011;25(11):1032-41. [Medline].

10. Kalra L, Dale P, Crome P. Improving stroke rehabilitation. A controlled study. Stroke. Oct1993;24(10):1462-7. [Medline]. [Full Text].

11. Woodford H, Price C. EMG biofeedback for the recovery of motor function after stroke. CochraneDatabase Syst Rev. Apr 18 2007;CD004585. [Medline].

12. Pomeroy VM, Cloud G, Tallis RC, Donaldson C, Nayak V, Miller S. Transcranial magnetic stimulation andmuscle contraction to enhance stroke recovery: a randomized proof-of-principle and feasibilityinvestigation. Neurorehabil Neural Repair. Nov-Dec 2007;21(6):509-17. [Medline].

13. Davidoff GN, Keren O, Ring H, Solzi P. Acute stroke patients: long-term effects of rehabilitation andmaintenance of gains. Arch Phys Med Rehabil. Oct 1991;72(11):869-73. [Medline].

14. Dam M, Tonin P, Casson S, Ermani M, Pizzolato G, Iaia V, et al. The effects of long-term rehabilitationtherapy on poststroke hemiplegic patients. Stroke. Aug 1993;24(8):1186-91. [Medline].

15. Paolucci S, Grasso MG, Antonucci G, Bragoni M, Troisi E, Morelli D, et al. Mobility status after inpatientstroke rehabilitation: 1-year follow-up and prognostic factors. Arch Phys Med Rehabil. Jan 2001;82(1):2-8.[Medline].

16. Young J, Forster A. Day hospital and home physiotherapy for stroke patients: a comparative cost-effectiveness study. J R Coll Physicians Lond. Jul 1993;27(3):252-8. [Medline].

17. [Best Evidence] Hackett ML, Anderson CS, House A, Xia J. Interventions for treating depression afterstroke. Cochrane Database Syst Rev. Oct 8 2008;CD003437. [Medline].

18. Sze KH, Wong E, Or KH, Lum CM, Woo J. Factors predicting stroke disability at discharge: a study of793 Chinese. Arch Phys Med Rehabil. Jul 2000;81(7):876-80. [Medline].

19. [Best Evidence] Dhamoon MS, Moon YP, Paik MC, Boden-Albala B, Rundek T, Sacco RL, et al. Long-term functional recovery after first ischemic stroke: the Northern Manhattan Study. Stroke. Aug2009;40(8):2805-11. [Medline]. [Full Text].

20. [Best Evidence] Rabadi MH, Coar PL, Lukin M, Lesser M, Blass JP. Intensive nutritional supplementscan improve outcomes in stroke rehabilitation. Neurology. Dec 2 2008;71(23):1856-61. [Medline].

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Motor Recovery in Stroke

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