What EXACTLY did your doctors and hospital implement from this 15 years ago?
NOTHING? So they don't care about improving their stroke recovery program? Not rehab, recovery! Rehab only implies activities, recovery defines itself. Words matter.
The Stroke Rehabilitation Paradigm
2007, Physical Medicine and Rehabilitation Clinics of North America
Brian M. Kelly, DO*,Percival H. Pangilinan, Jr, MD,Gianna M. Rodriguez, MD
Department of Physical Medicine and Rehabilitation, University of Michigan Health System,325 Eisenhower, Suite 200, Ann Arbor, MI 48108, USA
Behind heart disease and cancer, stroke is the third leading cause of death in the Western world and the leading cause of disability. On average, every 45seconds someone in the United States has a stroke. More than 700,000peopleexperience a new or recurrent stoke in the United States each year [1]. Of all strokes,87% are ischemic; intracerebral and subarachnoid hemorrhage make up the remainder. From 1994 to 2004, the stroke death rate fell 20.4% and the annual number of stroke deaths declined 6.7%. The estimated direct and indirect costs of stroke in the United States for 2007 are $62.7 billion [1].
Stroke risk factors
The management of treatable risk factors that contribute to the development and progression of atherosclerotic cerebral vascular disease is important for reducing the risk of ischemic stroke. The major treatable risk factors for cerebral vascular atherosclerotic disease are similar to those for coronary atherosclerosis, including hypertension, cardiac disease, diabetes mellitus,smoking, dyslipidemia, and elevated fibrinogen levels. The risk increasesin patients with two or more of these risk factors [2].
Modifiable risk factors in asymptomatic patients
Hypertension is the most important risk factor [3]. Subjects with bloodpressure less than 120/80 mm Hg have approximately half the lifetime risk of stroke compared with subjects with hypertension [4]. The degree of risk increases with higher levels of pressure and becomes particularly strong with levels higher than 160/95 mm Hg [5]. The choice of antihypertensive agent should be individualized to each patient’s characteristics and comorbidities [6]. There is a high risk of stroke in hypertensive patients withcarotid stenosis [7]. Based on Joint National Commission 7 guidelines,patients who have hypertension at baseline in most cases should be treated;a goal of less than 130/80 mm Hg is targeted as reasonable for most patients.Heart disease is another important risk factor for stroke.The risk of stroke doubles in individuals who have coronary artery disease [5]. Coronary artery disease accounts for the majority of subsequent deaths among stroke survivors. In patients with chronic, stable atrial fibrillation, the risk of stroke increases fivefold [3]. When atrial fibrillation is a manifestation of rheumatic heart disease, the risk of embolic stroke becomes 17-fold greater than normal.Prevention of embolic stroke in these patients is best achieved with longterm anticoagulation. Treatment does carry the danger of intracranial hemorrhage, especially in elderly individuals and persons with impaired balance who are more likely to fall. When the risk of hemorrhage seems to be high; 325 mg of aspirin may be used as an alternative to warfarin. Overall, aspirin is much less effective than warfarin in preventing embolism [5]. Diabetes as an independent risk factor doubles the risk of stroke.Unfortunately, strict glycemic control reduces the risk of microvascular complications such as retinopathy, nephropathy, and neuropathy but does not seem to slow the progression of cerebral vascular disease. The recommended goal for hemoglobin A1c is less than 7%. Rigorous control of blood pressure and lipids is particularly important for patients with diabetes [5]. Smoking has been shown to increase the risk for all stroke subtypes. The relative risk of stroke in heavy smokers (> 40 cigarettes per day) is twice that of light smokers (<10 cigarettes per day). There are no randomized controlled trials of smoking cessation for stroke prevention. The risk for stroke associ-ated with smoking decreases significantly 2 years after cigarette cessationand is at the level of nonsmokers by 5 years [8–10].Hyperlipidemia is a risk factor for coronary artery disease. The relation-ship between serum cholesterol in stroke incidence seems to be morecomplex, however, because cholesterol is an established risk factor inatherosclerosis but seems to be only a weak risk factor for ischemic stroke[11,12]. For patients with transient ischemic attack (TIA), ischemic strokeof atherosclerotic origin, or asymptomatic atherosclerotic cerebral vasculardisease who have a baseline low density lipoprotein (LDL) more than 100mg/dL, statin therapy is recommended [6,13]. Lipid lowering by othermeans, such as fibrates, resins, and diets, does not have an impact on strokeincidence [14,15].Elevated serum levels of homocystine are associated with prematureatherosclerosis, which causes stroke, myocardial infarction, and peripheralvascular disease earlier in life [16,17]. Homocystinemia can be treated withdaily high-dose vitamin therapy, including vitamin B6 (pyridoxine) and folicacid. There is no guarantee this treatment reduces the risk of a recurrent stroke, however [5,18]. Elevated fibrinogen levels correlate with higher riskof stroke, and fibrinogen levels are higher in individuals who smoke andhave a high cholesterol diet [19].
Risk factors in symptomatic patients
Patients admitted to rehabilitation are at risk for a recurrent stroke. Theprobability of stroke recurrence is highest in the postacute period. Forsurvivors of the initial stroke, the annual risk of a second stroke is approx-imately 5%, with a 5-year accumulative rate for recurrence at approximately25% [20]. Risk factors for initial stroke also increase the risk for a recurrentstroke [21]. TIAs and minor stroke are important warning signals of impending completed stroke. Four percent to 8% of patients with TIAsdevelop a completed stroke, and the risk is 30% within the next 5 years[5]. Patients with a TIA should receive prophylaxis against a completedstroke. The most widely accepted intervention is an antiplatelet drug, suchas aspirin. Several trials have reported a reduced incidence of 20% to25% using low- to high-dose daily aspirin. Currently, low-dose or regularstrength aspirin should be recommended [22,23].Ticlopidine is an antiplatelet drug with a different action from aspirin.The Ticlopidine-Aspirin Study confirmed that ticlopidine has a morebeneficial effect on stroke risk reduction over aspirin [24]. It is expensive,however, and has side effects of diarrhea and neutropenia, which maydiminish its value when compared with aspirin. Clopidogrel is another anti-platelet agent similar to ticlopidine. In clinical trials (CAPRIE), clopidog-rel’s efficacy in preventing stroke is slightly 7% better than aspirin aloneand it has fewer side effects [25]. Another agent, dipyridamole, is approxi-mately as effective as aspirin when taken alone, but it has an added benefitfor prophylaxis when taken with aspirin [26–29]. In a large clinical Europeantrial (ESPS-2), anticoagulation was not recommended in the treatment of TIAs unless a patient had a major cardiac source of potential embolism [5].Carotid endarterectomy has reduced the risk of stroke in patients withsingle or multiple TIAs and 70% or more stenosis of the ipsilateral internalcarotid artery [30]. Patients with stenosis of 50% to 70% do not havea hemodynamically significant lesion but may be considered for surgery if symptomatic. Carotid endarterectomy has not been proved superior tomedical treatment in asymptomatic patients, but mortality rates betweenthe two groups were similar [31,32].
Women and risk for stroke
The risk of ischemic stroke or intracerebral hemorrhage stroke duringpregnancy in the first 6 weeks postpartum was 2.4 times greater than fornonpregnant women of similar age and race according to the Baltimore-Washington cooperative stroke study [33]. Clinical trial data indicatedthat estrogen plus progesterone and estrogen alone increased stroke risks n postmenopausal women, including generally healthy women, and do notprovide protection for women with established heart disease [34,35].
Physical activity and stroke prevention
Physical activity reduces stroke risk. The Harvard Alumni Study showeda decrease in total stroke risk in men who were highly physically active [36].Physical activity from sports, during leisure time, or at work was related toa reduced risk of ischemic stroke [37]. The Northern Manhattan Study,which included white, African American, and Hispanic men and womenin an urban setting, showed a decrease in ischemic stroke risk associatedwith physical activity levels across all racial, ethnic, gender, and age groups[36].
Motor recovery
Motor recovery usually occurs in well-described patterns after stroke [38].Within 48 hours of movement loss, muscle stretch reflexes become moreactive in the involved upper and lower extremity in a proximal to distaldirection. The onset of spasticity results in resting postures that have beenidentified as synergy patterns for the upper and lower extremities. Volitionalmovement returns in the same pattern but eventually progresses to isolatedmovement. Spasticity decreases as volitional movement increases, butmuscle stretch reflexes always remain hyperactive despite total recovery.Injections of basic fibroblast growth factor resulted in selective increasesin contralateral sensorimotor cortices to the infarction, which providedevidence of axonal sprouting within the first month of stroke recovery[39]. Functional MRI has demonstrated plastic responses in the brainaround the perimeter of infarcted area during rehabilitation intervention[40]. Primary representation for movement may expand, if spared, and con-tract later as movement continues to improve [41]. Different parts of thebrain may be involved in recovery at different times, and patterns mayvary according to the level of severity and recovery [42–44]. Natural growthfactors may aid in neuroplasticity [44]. It is not intuitively obvious thatgrowth factors should have any effect in the acute stage of stroke or beclinically relevant, but additional information is needed [44]. Because suchpostinjury plasticity can be adaptive or maladaptive, current research isdirected at understanding how plasticity may be modulated to developmore effective therapeutic interventions for neurologic disorders, such asstroke. Behavioral training seems to be a significant contributor to adaptiveplasticity after injury, providing a neuroscientific foundation for the devel-opment of physical therapeutic approaches. Adjuvant therapies, such aspharmacologic agents and electrical and magnetic stimulation, may provideadditional approaches to help functional outcomes through activity therapy.More work has gone into proving plasticity after stroke without a specific n postmenopausal women, including generally healthy women, and do notprovide protection for women with established heart disease [34,35].
Physical activity and stroke prevention
Physical activity reduces stroke risk. The Harvard Alumni Study showeda decrease in total stroke risk in men who were highly physically active [36].Physical activity from sports, during leisure time, or at work was related toa reduced risk of ischemic stroke [37]. The Northern Manhattan Study,which included white, African American, and Hispanic men and womenin an urban setting, showed a decrease in ischemic stroke risk associatedwith physical activity levels across all racial, ethnic, gender, and age groups[36].
Motor recovery
Motor recovery usually occurs in well-described patterns after stroke [38].Within 48 hours of movement loss, muscle stretch reflexes become moreactive in the involved upper and lower extremity in a proximal to distaldirection. The onset of spasticity results in resting postures that have beenidentified as synergy patterns for the upper and lower extremities. Volitionalmovement returns in the same pattern but eventually progresses to isolatedmovement. Spasticity decreases as volitional movement increases, butmuscle stretch reflexes always remain hyperactive despite total recovery.Injections of basic fibroblast growth factor resulted in selective increasesin contralateral sensorimotor cortices to the infarction, which providedevidence of axonal sprouting within the first month of stroke recovery[39]. Functional MRI has demonstrated plastic responses in the brainaround the perimeter of infarcted area during rehabilitation intervention[40]. Primary representation for movement may expand, if spared, and con-tract later as movement continues to improve [41]. Different parts of thebrain may be involved in recovery at different times, and patterns mayvary according to the level of severity and recovery [42–44]. Natural growthfactors may aid in neuroplasticity [44]. It is not intuitively obvious thatgrowth factors should have any effect in the acute stage of stroke or beclinically relevant, but additional information is needed [44]. Because suchpostinjury plasticity can be adaptive or maladaptive, current research isdirected at understanding how plasticity may be modulated to developmore effective therapeutic interventions for neurologic disorders, such asstroke. Behavioral training seems to be a significant contributor to adaptiveplasticity after injury, providing a neuroscientific foundation for the devel-opment of physical therapeutic approaches. Adjuvant therapies, such aspharmacologic agents and electrical and magnetic stimulation, may provideadditional approaches to help functional outcomes through activity therapy.More work has gone into proving plasticity after stroke without a specific increase brain pathology [54]. Some researchers have raised concerns aboutmass practice in the first few days after stroke after an experimental findingin rats demonstrated that more neurons may be damaged or the size of theinfarct may increase by early overuse of a paretic limb [55,56]. The level of exercise of a rat running on a rotating wheel is much greater than whata patient could possibly experience during therapy, however. Could thewrong type of activity be deleterious [57]? We actually may foster a ‘‘learned nonuse’’ by teaching compensatory rather than restorative techniques.There is merit to forced use of the impaired arm and it reinforces long-term use of the upper extremity in ADLs. The constraint-induced (CI) therapy experiment directly supports this concept of ‘‘learned nonuse.’’ Primates whose unaffected arm was restrained until intrinsic recovery occurred showed full use of the now-recovered limb once restraint was removed [57].In addition to timing, there is concern about therapy intensity. Current treatment practices focus on the goals of returning a patient to independence as soon as possible and mitigating the effects of injury and its sequelae, such as spasticity. The current paradigm may need to be challenged. We deliver certain amounts of therapy based on time allotted. Maybe inpatient rehabilitation should offer 4 or 5 hours of therapy per day as a patient gets closer to discharge. Little rigorous evidence supports many of the traditional therapy approach models [58]. Fortunately, many of the newer ‘‘restorative’’ treatments are more rigorous in their study design and may answer tough ques-tions on best practice. For example, studies have compared different therapy protocols for CI therapies and skilled versus unskilled task practice. A newlarge, retrospective study supports the conclusion that conventional therapy has a significant dosage effect that may influence the current paradigm of acute rehabilitation. For example, in a study of outcomes at 70 skilled nursing facilities, an increased intensity of physical therapy and occupational therapy resulted in increased ADL ability and decreased length of stay[59,60]. In two retrospective studies of high- and low-intensity rehabilitation settings, functional gains were significantly related to therapy intensity in rehabilitation duration, but effects were considered small [61,62]. Exercise type also may play a role in rehabilitation. A program of progressive resistance training 1 year after stroke may improve strength of the affected limbs and motor function and balance [63].
Strength training
Strength training (eg, maximal effort, resistance exercise) has benefits at the muscular and neuromuscular levels. Improved recruitment is responsible for torque output within the first 6 weeks of strength training in decondi-tioned limbs. Muscle hypertrophy eventually follows. Neuroadaptationhas been reported after strength training in patients with all types of muscular disorders [63,64] After approximately 4 to 6 weeks of strength training,muscular adaptations produce additional gains in peak torque. The belief that excessive effort exacerbates hypertonia has prevented widespread use of strength training in persons with post stroke hemiparesis [65]. This belief has not been confirmed in studies. Although it is clear that some muscle groups respond to strengthening programs, research has not documented clearly that they improve functional outcomes [66,67].
Fitness training
Fitness often declines in disabled persons, but trials show gains with pro-gressive aerobic exercises (eg, walking on a treadmill 3 days a week) that aretailored to each patient’s tolerance. Benefits are seen even when the exerciseis initiated years after a stroke [68]. Despite consensus that stroke leads toprofound cardiovascular deconditioning, the underlying principle has notbeen concluded. The disability of stroke is widely attributed to brain injuryalone, and the diminished cardiovascular fitness is speculated to be causedby reduced central neural drive. There are, however, several major periph-eral changes in skeletal muscle that could propagate disability and contrib-ute to low fitness levels, including gross muscular atrophy and associatedinsulin resistance [69,70]. One study detailed a home-based exercise interven-tion model to improve fitness. The program consisted of 36 sessions of 90 minutes’ duration over 12 to 14 weeks. Subjects in the usual-care grouphad services as prescribed by their physicians. All sessions for the exercisegroup were supervised by a physical or occupational therapist at home.Components of the program were range of motion and flexibility, strength-ening, balance, upper-extremity functional use, and endurance training(eg, riding a stationary bike for 30 minutes). The intervention and usual-caregroups improved in strength, balance, upper- and lower-extremity motorcontrol, upper-extremity function, and gait velocity. Gains for the interven-tion group exceeded those in the usual-care group in balance, endurance,peak aerobic capacity, and mobility. The study demonstrated the practicalused of home-based interventions compared with the more frequentlyapplied hospital-based intervention programs for improving fitness andfunction after stroke [71]. Another study looked at water-based exercisethat lasted 12 weeks. Individuals in the experimental group exercised ina swimming pool for 1 hour, three times per week. The patients progressedto 30 minutes of water aerobics at 80% heart rate reserve, with the remain-der of the time devoted to stretching, warm-up, and cooling down. Thestudy size was limited but showed promising results, with the greatest rela-tive gains in peak aerobic capacity (23% in the experimental group), perhapsarguing for strong consideration of this form of intervention for strokesurvivors [72].
Constraint-induced therapy
Behavioral research with deafferented primates led to the development of CI therapy for humans with impaired upper limbs after stroke. The CI therapy protocol involves promoting use of the more affected upper extrem-ity for a target of 90% of the waking hours by constraining the less affectedextremity with a padded mitt for 2 to 3 consecutive weeks to prevent use of the hand for compensation during ADLs. The patients received a typeof task practice from therapists
d
termed ‘‘shaping’’
d
for many hours perday. CI therapy was effective for improving movement ability in chronicstroke subjects who met minimal motor criteria of at least 20
extensionat the wrist and at least 10
extension at the finger joint. A patient cannotbe at a risk for falls because the more functional arm is restrained [57].A recent placebo-controlled study showed that the gains from CI therapyare not associated with the amount of therapist attention and so must be theresult of the activity of the training [73]. The automated delivery of CI was just as effective as one-on-one therapist training [74]. Skeptics argue thattraditional training methods currently used by therapists may be just aseffective if delivered at the higher doses that match CI therapy [75]. Thatargument may be flawed because a comprehensive study that involved 66chronic stroke subjects reported that the CI therapy group performedstatistically better than a group of subjects who received an equal dose of neurodevelopmental technique with the arm movement scale [76]. Theyfound that the CI therapy group outperformed a traditional therapy groupduring acute rehabilitation on an arm impairment scale, with the largest dif-ference in the pinch subscale [77,78]. Another study also found advantagesin a modified form of CI therapy than traditional therapy in patients whohave chronic stroke [78–81]. Elderly patients found similar benefits withmodified CI therapy, and the study demonstrated substantial improvementin the abnormal movement patterns and reversed impairments rather thansimply helping patients to adapt to residual impairments [81].The results are attractive for acute and chronic stroke patients for gainswith CI therapy; however, not every patient is eager to start. Compliancewith the mitt restriction schedule has been reported at 32% [80]. An opinionsurvey for therapists and patients reported that many stroke patients wouldnot want to participate in CI therapy but would prefer a therapy protocolthat lasted for more weeks, had shorter activity sessions, and involved fewerhours of wearing the restrictive devices [80]. More than 60% of respondingtherapists also speculated that patients were unlikely to adhere to CI therapy[80]. Some compromises may be needed for safety. Ambulation with a caneand a hemiparetic arm may place a patient at higher risk for balance insta-bility and falls. Reimbursement for CI therapy also may be a limiting factor.
Therapy augmentation
Pharmacology
Pharmacologic interventions may help to facilitate motor recovery byallowing increased participation in therapy. Methylphenidate, a mild central nervous system stimulant whose mode of action is not well understood, maydecrease depression and improve function in the early stages after stroke[82]. Available acetylcholinesterase inhibitors may aid learning of new infor-mation and procedural activities [83,84]. Dopaminergic drugs, such aslevodopa, and drugs that increase the availability of norepinephrine, suchas methylphenidate and amphetamine, have shown some efficacy in strokerehabilitation trials when combined with physical or language therapy[82,85,86]. Augmentation of one of these chemical transmitters, especiallyactivation of
N-methyl d-aspartate (NMDA)
receptors, may help optimizeactivity-dependent relearning of skills after stroke [87]. Selective serotoninreuptake inhibitors have modestly improved motor learning for arm tasksin healthy people and patients with stroke [88,89]. Stroke trials suggest atleast a transient decline in function from antiepileptic drugs (which affectcognitive processing), dopamine blockers (eg, antipsychotics), and alpha-2adrenergic drugs [90,91].The use of amantadine, bromocriptine, and modafinil for more than3 days had no effect on the length of stay in rehabilitation [92]. The useof methylphenidate for moderate strokes did reduce length of stay data[92]; however, these studies were small and larger study populations areneeded to draw definitive conclusions.
Electrical neurostimulation
Motor and limited functional gains have been elicited by electrical neuro-muscular stimulation triggered by feedback. One approach stimulatesa weak muscle to induce movement while another augments existingvolitional movement [93]. Direct neuromuscular electrical stimulation overthe surface of key muscles for a grasp-and-pinch movement may improvemotor skills when combined with task-oriented practice [94]. Functionalelectrical stimulation is also used to activate paretic muscles timed to a move-ment, such as contraction of the tibialis anterior to clear the foot during theswing phase of walking [95]. Implantable electrodes and injectable BIONelectrodes triggered by an external transmitter have shown potential asmuscle-stimulating neuroprostheses [96,97].
Brain stimulation
Brain stimulation may enhance the beneficial effects of motor training inthe rehabilitative process [98]. Studies in animal models showed that motorrecovery after focal lesions in the primary motor cortex can improve withdirect epidural cortical stimulation [99]. There has been increasing interestin testing the effects of noninvasive cortical stimulation in the rehabilitativeprocess. Transcranial magnetic stimulation and transcranial direct currentstimulation have been investigated as potential tools for modulating motorrecovery in stroke or influencing motor, sensory, and cognitive functions[100]. The duration of effects elicited by a single application of either transcranial magnetic stimulation or transcranial direct current stimulationseems to be comparable (up to hours). Both techniques are noninvasiveandseem tobesafe whenused within established safetyguidelines. Themech-anisms underlying their effects, however, may differ. Transcranial magneticstimulationequipmentismoreexpensivebutcanstimulatemorefocally[101].
Robotic trainers and virtual reality practice
Robotic systems may provide cost-effective enhancement of movementrecovery compared with equal doses of conventional treatment. Roboticsmay offer a more cost-effective alternative to hand-over-hand therapyfrom a therapist. This approach may be particularly useful in the upperlimb, in which neurorehabilitation efforts are often abandoned earlier infavor of compensatory strategies. Several small trials with promising resultsconcluded that gains in the robot-trained subjects were partly caused byimproved muscle activation patterns [102]. Patients who received robotictherapy in addition to conventional therapy showed greater reductions inmotor impairment and improvements in functional abilities. The benefitsof this augmented therapy approach were sustained 8 months later [103].Another technologic adjunct to maximize cost-effective, task-specificactivity is computer-guided virtual reality training. Computerized, virtualreality–based activities have a reasonable conceptual basis for rehabilitation[104,105]. A virtual reality system may allow continued practice of task-specific activities and provide feedback on techniques. A few small trialshave suggested possible effectiveness for these forms of practice [106,107].
Complementary medicine
In addition to traditional medical approaches, some studies have con-firmed that acupuncture has a positive effect on motor function, ADLs,and quality of life when administered in the acute and subacute stages of the poststroke period [108]. The benefits were maintained 1 year later, andthere was a decreased length of stay as a result [109]. Acupuncture is notpart of a traditional stroke therapy rehabilitation protocol or covered bymost insurance plans, however.
Predicting disability and function status
Hemiparesis and motor recovery have been the most studied of all strokeimpairments. Twitchell [38] described in detail a pattern of motor recoveryafter stroke. The severity of arm weakness at onset and the timing of thereturn of movement of the hand are important predictors of eventual motorrecovery in the arm. The prognosis for return of useful hand function ispoor when there is complete arm paralysis at onset or no measurable graspstrength by 4 weeks. Even among patients with severe arm weakness at onset, as many as 11% may gain good functional recovery of hand function[110]. Recovery of sensory function maximizes in 1 to 2 months in 50% to67% of stroke survivors [111]. Some other generalizations can be postulated.For patients who show some motor recovery in the hand by 4 weeks, asmany as 70% make a full or good recovery [112,113]. When full recoveryoccurs, it is usually complete within 3 months of onset. For ambulation,95% of patients reach their best neurologic level within 11 weeks of onset[114]. Patients with milder strokes recovered more frequently, and patientswith severe strokes reached their best neurologic level within 15 weeks.The course of motor recovery reaches a plateau after an early stage of progressive improvement. Most recovery takes place in the first 3 months,and only minor additional measurable improvements occur after 6 monthsafter onset [115]. Many patients with ambulatory hemiparesis do not walksafely [116]. Normal casual walking speed for healthy adults is 2.5 to 3.0miles per hour (approximately 130 cm/s) [117]. An interesting study of 147 people 6 months after stroke revealed that patients with hemiparesiswho walk at 25 cm/s achieve only household ambulation. Restrictedcommunity ambulation generally required walking speeds of 40 to 79 cm/s.Unrestricted community ambulation was most likely for persons whowalked at 80 cm/s [116,118]. Only 18% of people achieved unlimitedcommunity ambulation. Across prospective observational studies and inter-ventional experiments, walking speeds at the end of inpatient rehabilitationrange from 25 to 60 cm/s. Recovery of sensory function maximizes in 1 to 2months in 50% to 67% of stroke survivors.
Motor improvements
Formal physiotherapy is often stopped when patients reach functionalgoals or progress too slowly to measure in a certain time frame. Unfortu-nately, some patients are discharged from therapy before a motor plateauis reached. Even then, a plateau in recovery does not necessarily implya diminished capacity for further functional gains. Researchers have foundthat task-specific functional therapy for the arm leads to significant gains inmotor control and strength if patients are allowed to continue treatmentuntil no further gains are made, which required an additional ten sessionsbeyond the standard treatment period [119]. There must be a shift fromthe emphasis on compensatory task-specific activity to the achievement of goal-directed therapy and restorative practice. For patients involved ina CI therapy program, clinical trials have indicated that patients who prac-ticed at an increased intensity increased the amount and efficiency of use of the affected hand by 20% to 50% whether therapy began while they wereacute rehabilitation inpatients or a year after stroke [76,77].Currently, the opportunity to achieve maximal improvement is probablyconstrained by a lack of adequate data to define the optimal intensity (performance time, pace, and duration) of training strategies for specificdisabilities [120]. In the future, functional neuroimaging studies may helpto guide decisions about the type and duration of treatment by providinginsight into the maximal cortical reorganization that can be achieved witha particular therapy over time; however, this possibility requires moreresearch [119,121].
Discharge and additional therapy
Stroke survivors with traditional insurance plans or Medicare are morelikely to be admitted to acute rehabilitation hospitals or units than patientswith managed care [122]. Growing evidence indicates that intensity of reha-bilitation correlates with outcome, which may potentially discriminateagainst patients with limited benefits. Overall, intensive stroke rehabilitationis associated with significantly lower mortality, institutionalization, anddependency [123].In Europe, stroke survivors involved with integrated acute rehabilitationprograms made greater functional gains, were more likely to return home,had decreased 5- and 10-year mortality rates, and reported a better qualityof life than when they were admitted to a less intense program [124–127].The advantages of the stroke unit are improved patient outcomes with fewerdeaths, reduction in disability, and modest decrease in length of stay [123].Outcomes improved when patients were monitored for hypoxia and hypo-tension; and previous unknown cardiac arrhythmias were detected andtreated more frequently [128,129]. Although small, a statistically significantintensity-effect relationship exists between rehabilitation and functionaloutcomes with stroke units [60].The intensity and cost of therapy of individualized programs are consid-erations in the age of managed care. Among inpatient rehabilitationfacilities, data for 2006 indicated that the average Medicare reimbursementper day for a stroke survivor was approximately $1144 and the averagelength of stay was 16.8 days. There may be greater demands to justify thisexpense as Medicare financial constraints arise in the coming years.An observational behavioral mapping study on 64 stroke patients in fiveacute stroke units reported that patients engaged in minimal therapeuticactivity or moderate therapeutic activities for only 12.8% of the therapeuticday (8am to 5pm). Patients were resting in bed 53% of the time and werealone for 60.4% of the time [130]. Therapist contact constituted only5.2% of the day. Previous studies have shown similar limited therapist– patient contact time in stroke units. Poor therapy participation has beenreported and is common during inpatient rehabilitation. Lack of participa-tion resulted in lower improvements in functional independence measurescores and longer lengths of stay, even when controlling for admissionfunctional independence measure scores [130,131].
Patients who participated in acute rehabilitation facilities were morelikely to report higher intensity of therapy, have a community-baseddischarge, and have higher functional outcomes, but costs were higher. Out-comes were similar for patients with minimal motor disabilities and patientswith mild motor disabilities and significant cognitive disabilities betweenacute and skilled rehabilitation facilities, however [132]. This finding propelsthe search for high-quality treatment that is cost effective and may, in somecases, move therapies out of the gym. Other systematic reviews focused onmultidisciplinary community neurorehabilitation and ‘‘early discharge pro-grams,’’ arguing that early discharge programs safely and effectively lowerthe number of inpatient hospital treatment days [133,134].A comparative study of stroke patients admitted to conventional strokerehabilitation versus a full-time integrated treatment program reported pos-itive results. The conventional program offered admission during the workweek, whereas the full-time integrated treatment program offered weekendadmissions and delivered regular day therapy sessions during this time forall patients. Both groups had similar functional independence measurescores at admission; however, the full-time integrated treatment grouphad significantly shorter lengths of stay and was discharged with higheraverage functional independence measure scores and nearly double the func-tional independence measure efficiency scores [135]. This finding wouldinfluence inpatient rehabilitation facilities to move to a full-time, regulartherapy schedule every day of the week and offer more weekend admissionsdespite lack of insurance approval availability.There is a great deal of interest in therapies delivered at home afterdischarge from rehabilitation. Therapy-based rehabilitation services forstroke patients living at home within 1 year of experiencing a stroke resultedin a significant improvement in the ability to manage ADL and reduced thelikelihood of deterioration in ADLs [136]. Low-intensity, home-basedphysical therapy is able to improve lower limb motor function in patients more than 1 year after stroke [137], possibly because the nature of strokemotor therapy itself can be altered at home to be more task specific whileremaining within the typical contact time parameters (ie, 30–45 minutes persession) and be as effective as traditional motor approaches in rehabilitationfacilities [138].In another study, 428 stroke patients and their caregivers were random-ized to rehabilitation from a community stroke team or to routine care,which could include day hospitals or outpatient departments. There were no significant differences between patients who received rehabilitation from community stroke teams and patients who received routine care in their independence in ADL, mood, quality of life, or knowledge of stroke. Patients in the community stroke team group were more satisfied with the emotional support they received. Caregivers of patients in the community stroke team group were under less strain and reported greater levels of overall satisfaction [139].
Summary
There are new challenges to the existing paradigm of stroke rehabilitation, including defining dosage, standardizing treatment parameters acrosssubjects and within treatment sessions, and determining what constitutes clinically significant treatment effects. Exercise type, intensity, duration,and physical location may shift in the future. The long-term goal is to develop prescriptive therapy programs in which specific activities are proven to treat specific motor system disorders. This may change our thinking and practice of what constitutes the current stroke rehabilitation paradigm.
Department of Physical Medicine and Rehabilitation, University of Michigan Health System,325 Eisenhower, Suite 200, Ann Arbor, MI 48108, USA
Behind heart disease and cancer, stroke is the third leading cause of death in the Western world and the leading cause of disability. On average, every 45seconds someone in the United States has a stroke. More than 700,000peopleexperience a new or recurrent stoke in the United States each year [1]. Of all strokes,87% are ischemic; intracerebral and subarachnoid hemorrhage make up the remainder. From 1994 to 2004, the stroke death rate fell 20.4% and the annual number of stroke deaths declined 6.7%. The estimated direct and indirect costs of stroke in the United States for 2007 are $62.7 billion [1].
Stroke risk factors
The management of treatable risk factors that contribute to the development and progression of atherosclerotic cerebral vascular disease is important for reducing the risk of ischemic stroke. The major treatable risk factors for cerebral vascular atherosclerotic disease are similar to those for coronary atherosclerosis, including hypertension, cardiac disease, diabetes mellitus,smoking, dyslipidemia, and elevated fibrinogen levels. The risk increasesin patients with two or more of these risk factors [2].
Modifiable risk factors in asymptomatic patients
Hypertension is the most important risk factor [3]. Subjects with bloodpressure less than 120/80 mm Hg have approximately half the lifetime risk of stroke compared with subjects with hypertension [4]. The degree of risk increases with higher levels of pressure and becomes particularly strong with levels higher than 160/95 mm Hg [5]. The choice of antihypertensive agent should be individualized to each patient’s characteristics and comorbidities [6]. There is a high risk of stroke in hypertensive patients withcarotid stenosis [7]. Based on Joint National Commission 7 guidelines,patients who have hypertension at baseline in most cases should be treated;a goal of less than 130/80 mm Hg is targeted as reasonable for most patients.Heart disease is another important risk factor for stroke.The risk of stroke doubles in individuals who have coronary artery disease [5]. Coronary artery disease accounts for the majority of subsequent deaths among stroke survivors. In patients with chronic, stable atrial fibrillation, the risk of stroke increases fivefold [3]. When atrial fibrillation is a manifestation of rheumatic heart disease, the risk of embolic stroke becomes 17-fold greater than normal.Prevention of embolic stroke in these patients is best achieved with longterm anticoagulation. Treatment does carry the danger of intracranial hemorrhage, especially in elderly individuals and persons with impaired balance who are more likely to fall. When the risk of hemorrhage seems to be high; 325 mg of aspirin may be used as an alternative to warfarin. Overall, aspirin is much less effective than warfarin in preventing embolism [5]. Diabetes as an independent risk factor doubles the risk of stroke.Unfortunately, strict glycemic control reduces the risk of microvascular complications such as retinopathy, nephropathy, and neuropathy but does not seem to slow the progression of cerebral vascular disease. The recommended goal for hemoglobin A1c is less than 7%. Rigorous control of blood pressure and lipids is particularly important for patients with diabetes [5]. Smoking has been shown to increase the risk for all stroke subtypes. The relative risk of stroke in heavy smokers (> 40 cigarettes per day) is twice that of light smokers (<10 cigarettes per day). There are no randomized controlled trials of smoking cessation for stroke prevention. The risk for stroke associ-ated with smoking decreases significantly 2 years after cigarette cessationand is at the level of nonsmokers by 5 years [8–10].Hyperlipidemia is a risk factor for coronary artery disease. The relation-ship between serum cholesterol in stroke incidence seems to be morecomplex, however, because cholesterol is an established risk factor inatherosclerosis but seems to be only a weak risk factor for ischemic stroke[11,12]. For patients with transient ischemic attack (TIA), ischemic strokeof atherosclerotic origin, or asymptomatic atherosclerotic cerebral vasculardisease who have a baseline low density lipoprotein (LDL) more than 100mg/dL, statin therapy is recommended [6,13]. Lipid lowering by othermeans, such as fibrates, resins, and diets, does not have an impact on strokeincidence [14,15].Elevated serum levels of homocystine are associated with prematureatherosclerosis, which causes stroke, myocardial infarction, and peripheralvascular disease earlier in life [16,17]. Homocystinemia can be treated withdaily high-dose vitamin therapy, including vitamin B6 (pyridoxine) and folicacid. There is no guarantee this treatment reduces the risk of a recurrent stroke, however [5,18]. Elevated fibrinogen levels correlate with higher riskof stroke, and fibrinogen levels are higher in individuals who smoke andhave a high cholesterol diet [19].
Risk factors in symptomatic patients
Patients admitted to rehabilitation are at risk for a recurrent stroke. Theprobability of stroke recurrence is highest in the postacute period. Forsurvivors of the initial stroke, the annual risk of a second stroke is approx-imately 5%, with a 5-year accumulative rate for recurrence at approximately25% [20]. Risk factors for initial stroke also increase the risk for a recurrentstroke [21]. TIAs and minor stroke are important warning signals of impending completed stroke. Four percent to 8% of patients with TIAsdevelop a completed stroke, and the risk is 30% within the next 5 years[5]. Patients with a TIA should receive prophylaxis against a completedstroke. The most widely accepted intervention is an antiplatelet drug, suchas aspirin. Several trials have reported a reduced incidence of 20% to25% using low- to high-dose daily aspirin. Currently, low-dose or regularstrength aspirin should be recommended [22,23].Ticlopidine is an antiplatelet drug with a different action from aspirin.The Ticlopidine-Aspirin Study confirmed that ticlopidine has a morebeneficial effect on stroke risk reduction over aspirin [24]. It is expensive,however, and has side effects of diarrhea and neutropenia, which maydiminish its value when compared with aspirin. Clopidogrel is another anti-platelet agent similar to ticlopidine. In clinical trials (CAPRIE), clopidog-rel’s efficacy in preventing stroke is slightly 7% better than aspirin aloneand it has fewer side effects [25]. Another agent, dipyridamole, is approxi-mately as effective as aspirin when taken alone, but it has an added benefitfor prophylaxis when taken with aspirin [26–29]. In a large clinical Europeantrial (ESPS-2), anticoagulation was not recommended in the treatment of TIAs unless a patient had a major cardiac source of potential embolism [5].Carotid endarterectomy has reduced the risk of stroke in patients withsingle or multiple TIAs and 70% or more stenosis of the ipsilateral internalcarotid artery [30]. Patients with stenosis of 50% to 70% do not havea hemodynamically significant lesion but may be considered for surgery if symptomatic. Carotid endarterectomy has not been proved superior tomedical treatment in asymptomatic patients, but mortality rates betweenthe two groups were similar [31,32].
Women and risk for stroke
The risk of ischemic stroke or intracerebral hemorrhage stroke duringpregnancy in the first 6 weeks postpartum was 2.4 times greater than fornonpregnant women of similar age and race according to the Baltimore-Washington cooperative stroke study [33]. Clinical trial data indicatedthat estrogen plus progesterone and estrogen alone increased stroke risks n postmenopausal women, including generally healthy women, and do notprovide protection for women with established heart disease [34,35].
Physical activity and stroke prevention
Physical activity reduces stroke risk. The Harvard Alumni Study showeda decrease in total stroke risk in men who were highly physically active [36].Physical activity from sports, during leisure time, or at work was related toa reduced risk of ischemic stroke [37]. The Northern Manhattan Study,which included white, African American, and Hispanic men and womenin an urban setting, showed a decrease in ischemic stroke risk associatedwith physical activity levels across all racial, ethnic, gender, and age groups[36].
Motor recovery
Motor recovery usually occurs in well-described patterns after stroke [38].Within 48 hours of movement loss, muscle stretch reflexes become moreactive in the involved upper and lower extremity in a proximal to distaldirection. The onset of spasticity results in resting postures that have beenidentified as synergy patterns for the upper and lower extremities. Volitionalmovement returns in the same pattern but eventually progresses to isolatedmovement. Spasticity decreases as volitional movement increases, butmuscle stretch reflexes always remain hyperactive despite total recovery.Injections of basic fibroblast growth factor resulted in selective increasesin contralateral sensorimotor cortices to the infarction, which providedevidence of axonal sprouting within the first month of stroke recovery[39]. Functional MRI has demonstrated plastic responses in the brainaround the perimeter of infarcted area during rehabilitation intervention[40]. Primary representation for movement may expand, if spared, and con-tract later as movement continues to improve [41]. Different parts of thebrain may be involved in recovery at different times, and patterns mayvary according to the level of severity and recovery [42–44]. Natural growthfactors may aid in neuroplasticity [44]. It is not intuitively obvious thatgrowth factors should have any effect in the acute stage of stroke or beclinically relevant, but additional information is needed [44]. Because suchpostinjury plasticity can be adaptive or maladaptive, current research isdirected at understanding how plasticity may be modulated to developmore effective therapeutic interventions for neurologic disorders, such asstroke. Behavioral training seems to be a significant contributor to adaptiveplasticity after injury, providing a neuroscientific foundation for the devel-opment of physical therapeutic approaches. Adjuvant therapies, such aspharmacologic agents and electrical and magnetic stimulation, may provideadditional approaches to help functional outcomes through activity therapy.More work has gone into proving plasticity after stroke without a specific n postmenopausal women, including generally healthy women, and do notprovide protection for women with established heart disease [34,35].
Physical activity and stroke prevention
Physical activity reduces stroke risk. The Harvard Alumni Study showeda decrease in total stroke risk in men who were highly physically active [36].Physical activity from sports, during leisure time, or at work was related toa reduced risk of ischemic stroke [37]. The Northern Manhattan Study,which included white, African American, and Hispanic men and womenin an urban setting, showed a decrease in ischemic stroke risk associatedwith physical activity levels across all racial, ethnic, gender, and age groups[36].
Motor recovery
Motor recovery usually occurs in well-described patterns after stroke [38].Within 48 hours of movement loss, muscle stretch reflexes become moreactive in the involved upper and lower extremity in a proximal to distaldirection. The onset of spasticity results in resting postures that have beenidentified as synergy patterns for the upper and lower extremities. Volitionalmovement returns in the same pattern but eventually progresses to isolatedmovement. Spasticity decreases as volitional movement increases, butmuscle stretch reflexes always remain hyperactive despite total recovery.Injections of basic fibroblast growth factor resulted in selective increasesin contralateral sensorimotor cortices to the infarction, which providedevidence of axonal sprouting within the first month of stroke recovery[39]. Functional MRI has demonstrated plastic responses in the brainaround the perimeter of infarcted area during rehabilitation intervention[40]. Primary representation for movement may expand, if spared, and con-tract later as movement continues to improve [41]. Different parts of thebrain may be involved in recovery at different times, and patterns mayvary according to the level of severity and recovery [42–44]. Natural growthfactors may aid in neuroplasticity [44]. It is not intuitively obvious thatgrowth factors should have any effect in the acute stage of stroke or beclinically relevant, but additional information is needed [44]. Because suchpostinjury plasticity can be adaptive or maladaptive, current research isdirected at understanding how plasticity may be modulated to developmore effective therapeutic interventions for neurologic disorders, such asstroke. Behavioral training seems to be a significant contributor to adaptiveplasticity after injury, providing a neuroscientific foundation for the devel-opment of physical therapeutic approaches. Adjuvant therapies, such aspharmacologic agents and electrical and magnetic stimulation, may provideadditional approaches to help functional outcomes through activity therapy.More work has gone into proving plasticity after stroke without a specific increase brain pathology [54]. Some researchers have raised concerns aboutmass practice in the first few days after stroke after an experimental findingin rats demonstrated that more neurons may be damaged or the size of theinfarct may increase by early overuse of a paretic limb [55,56]. The level of exercise of a rat running on a rotating wheel is much greater than whata patient could possibly experience during therapy, however. Could thewrong type of activity be deleterious [57]? We actually may foster a ‘‘learned nonuse’’ by teaching compensatory rather than restorative techniques.There is merit to forced use of the impaired arm and it reinforces long-term use of the upper extremity in ADLs. The constraint-induced (CI) therapy experiment directly supports this concept of ‘‘learned nonuse.’’ Primates whose unaffected arm was restrained until intrinsic recovery occurred showed full use of the now-recovered limb once restraint was removed [57].In addition to timing, there is concern about therapy intensity. Current treatment practices focus on the goals of returning a patient to independence as soon as possible and mitigating the effects of injury and its sequelae, such as spasticity. The current paradigm may need to be challenged. We deliver certain amounts of therapy based on time allotted. Maybe inpatient rehabilitation should offer 4 or 5 hours of therapy per day as a patient gets closer to discharge. Little rigorous evidence supports many of the traditional therapy approach models [58]. Fortunately, many of the newer ‘‘restorative’’ treatments are more rigorous in their study design and may answer tough ques-tions on best practice. For example, studies have compared different therapy protocols for CI therapies and skilled versus unskilled task practice. A newlarge, retrospective study supports the conclusion that conventional therapy has a significant dosage effect that may influence the current paradigm of acute rehabilitation. For example, in a study of outcomes at 70 skilled nursing facilities, an increased intensity of physical therapy and occupational therapy resulted in increased ADL ability and decreased length of stay[59,60]. In two retrospective studies of high- and low-intensity rehabilitation settings, functional gains were significantly related to therapy intensity in rehabilitation duration, but effects were considered small [61,62]. Exercise type also may play a role in rehabilitation. A program of progressive resistance training 1 year after stroke may improve strength of the affected limbs and motor function and balance [63].
Strength training
Strength training (eg, maximal effort, resistance exercise) has benefits at the muscular and neuromuscular levels. Improved recruitment is responsible for torque output within the first 6 weeks of strength training in decondi-tioned limbs. Muscle hypertrophy eventually follows. Neuroadaptationhas been reported after strength training in patients with all types of muscular disorders [63,64] After approximately 4 to 6 weeks of strength training,muscular adaptations produce additional gains in peak torque. The belief that excessive effort exacerbates hypertonia has prevented widespread use of strength training in persons with post stroke hemiparesis [65]. This belief has not been confirmed in studies. Although it is clear that some muscle groups respond to strengthening programs, research has not documented clearly that they improve functional outcomes [66,67].
Fitness training
Fitness often declines in disabled persons, but trials show gains with pro-gressive aerobic exercises (eg, walking on a treadmill 3 days a week) that aretailored to each patient’s tolerance. Benefits are seen even when the exerciseis initiated years after a stroke [68]. Despite consensus that stroke leads toprofound cardiovascular deconditioning, the underlying principle has notbeen concluded. The disability of stroke is widely attributed to brain injuryalone, and the diminished cardiovascular fitness is speculated to be causedby reduced central neural drive. There are, however, several major periph-eral changes in skeletal muscle that could propagate disability and contrib-ute to low fitness levels, including gross muscular atrophy and associatedinsulin resistance [69,70]. One study detailed a home-based exercise interven-tion model to improve fitness. The program consisted of 36 sessions of 90 minutes’ duration over 12 to 14 weeks. Subjects in the usual-care grouphad services as prescribed by their physicians. All sessions for the exercisegroup were supervised by a physical or occupational therapist at home.Components of the program were range of motion and flexibility, strength-ening, balance, upper-extremity functional use, and endurance training(eg, riding a stationary bike for 30 minutes). The intervention and usual-caregroups improved in strength, balance, upper- and lower-extremity motorcontrol, upper-extremity function, and gait velocity. Gains for the interven-tion group exceeded those in the usual-care group in balance, endurance,peak aerobic capacity, and mobility. The study demonstrated the practicalused of home-based interventions compared with the more frequentlyapplied hospital-based intervention programs for improving fitness andfunction after stroke [71]. Another study looked at water-based exercisethat lasted 12 weeks. Individuals in the experimental group exercised ina swimming pool for 1 hour, three times per week. The patients progressedto 30 minutes of water aerobics at 80% heart rate reserve, with the remain-der of the time devoted to stretching, warm-up, and cooling down. Thestudy size was limited but showed promising results, with the greatest rela-tive gains in peak aerobic capacity (23% in the experimental group), perhapsarguing for strong consideration of this form of intervention for strokesurvivors [72].
Constraint-induced therapy
Behavioral research with deafferented primates led to the development of CI therapy for humans with impaired upper limbs after stroke. The CI therapy protocol involves promoting use of the more affected upper extrem-ity for a target of 90% of the waking hours by constraining the less affectedextremity with a padded mitt for 2 to 3 consecutive weeks to prevent use of the hand for compensation during ADLs. The patients received a typeof task practice from therapists
d
termed ‘‘shaping’’
d
for many hours perday. CI therapy was effective for improving movement ability in chronicstroke subjects who met minimal motor criteria of at least 20
extensionat the wrist and at least 10
extension at the finger joint. A patient cannotbe at a risk for falls because the more functional arm is restrained [57].A recent placebo-controlled study showed that the gains from CI therapyare not associated with the amount of therapist attention and so must be theresult of the activity of the training [73]. The automated delivery of CI was just as effective as one-on-one therapist training [74]. Skeptics argue thattraditional training methods currently used by therapists may be just aseffective if delivered at the higher doses that match CI therapy [75]. Thatargument may be flawed because a comprehensive study that involved 66chronic stroke subjects reported that the CI therapy group performedstatistically better than a group of subjects who received an equal dose of neurodevelopmental technique with the arm movement scale [76]. Theyfound that the CI therapy group outperformed a traditional therapy groupduring acute rehabilitation on an arm impairment scale, with the largest dif-ference in the pinch subscale [77,78]. Another study also found advantagesin a modified form of CI therapy than traditional therapy in patients whohave chronic stroke [78–81]. Elderly patients found similar benefits withmodified CI therapy, and the study demonstrated substantial improvementin the abnormal movement patterns and reversed impairments rather thansimply helping patients to adapt to residual impairments [81].The results are attractive for acute and chronic stroke patients for gainswith CI therapy; however, not every patient is eager to start. Compliancewith the mitt restriction schedule has been reported at 32% [80]. An opinionsurvey for therapists and patients reported that many stroke patients wouldnot want to participate in CI therapy but would prefer a therapy protocolthat lasted for more weeks, had shorter activity sessions, and involved fewerhours of wearing the restrictive devices [80]. More than 60% of respondingtherapists also speculated that patients were unlikely to adhere to CI therapy[80]. Some compromises may be needed for safety. Ambulation with a caneand a hemiparetic arm may place a patient at higher risk for balance insta-bility and falls. Reimbursement for CI therapy also may be a limiting factor.
Therapy augmentation
Pharmacology
Pharmacologic interventions may help to facilitate motor recovery byallowing increased participation in therapy. Methylphenidate, a mild central nervous system stimulant whose mode of action is not well understood, maydecrease depression and improve function in the early stages after stroke[82]. Available acetylcholinesterase inhibitors may aid learning of new infor-mation and procedural activities [83,84]. Dopaminergic drugs, such aslevodopa, and drugs that increase the availability of norepinephrine, suchas methylphenidate and amphetamine, have shown some efficacy in strokerehabilitation trials when combined with physical or language therapy[82,85,86]. Augmentation of one of these chemical transmitters, especiallyactivation of
N-methyl d-aspartate (NMDA)
receptors, may help optimizeactivity-dependent relearning of skills after stroke [87]. Selective serotoninreuptake inhibitors have modestly improved motor learning for arm tasksin healthy people and patients with stroke [88,89]. Stroke trials suggest atleast a transient decline in function from antiepileptic drugs (which affectcognitive processing), dopamine blockers (eg, antipsychotics), and alpha-2adrenergic drugs [90,91].The use of amantadine, bromocriptine, and modafinil for more than3 days had no effect on the length of stay in rehabilitation [92]. The useof methylphenidate for moderate strokes did reduce length of stay data[92]; however, these studies were small and larger study populations areneeded to draw definitive conclusions.
Electrical neurostimulation
Motor and limited functional gains have been elicited by electrical neuro-muscular stimulation triggered by feedback. One approach stimulatesa weak muscle to induce movement while another augments existingvolitional movement [93]. Direct neuromuscular electrical stimulation overthe surface of key muscles for a grasp-and-pinch movement may improvemotor skills when combined with task-oriented practice [94]. Functionalelectrical stimulation is also used to activate paretic muscles timed to a move-ment, such as contraction of the tibialis anterior to clear the foot during theswing phase of walking [95]. Implantable electrodes and injectable BIONelectrodes triggered by an external transmitter have shown potential asmuscle-stimulating neuroprostheses [96,97].
Brain stimulation
Brain stimulation may enhance the beneficial effects of motor training inthe rehabilitative process [98]. Studies in animal models showed that motorrecovery after focal lesions in the primary motor cortex can improve withdirect epidural cortical stimulation [99]. There has been increasing interestin testing the effects of noninvasive cortical stimulation in the rehabilitativeprocess. Transcranial magnetic stimulation and transcranial direct currentstimulation have been investigated as potential tools for modulating motorrecovery in stroke or influencing motor, sensory, and cognitive functions[100]. The duration of effects elicited by a single application of either transcranial magnetic stimulation or transcranial direct current stimulationseems to be comparable (up to hours). Both techniques are noninvasiveandseem tobesafe whenused within established safetyguidelines. Themech-anisms underlying their effects, however, may differ. Transcranial magneticstimulationequipmentismoreexpensivebutcanstimulatemorefocally[101].
Robotic trainers and virtual reality practice
Robotic systems may provide cost-effective enhancement of movementrecovery compared with equal doses of conventional treatment. Roboticsmay offer a more cost-effective alternative to hand-over-hand therapyfrom a therapist. This approach may be particularly useful in the upperlimb, in which neurorehabilitation efforts are often abandoned earlier infavor of compensatory strategies. Several small trials with promising resultsconcluded that gains in the robot-trained subjects were partly caused byimproved muscle activation patterns [102]. Patients who received robotictherapy in addition to conventional therapy showed greater reductions inmotor impairment and improvements in functional abilities. The benefitsof this augmented therapy approach were sustained 8 months later [103].Another technologic adjunct to maximize cost-effective, task-specificactivity is computer-guided virtual reality training. Computerized, virtualreality–based activities have a reasonable conceptual basis for rehabilitation[104,105]. A virtual reality system may allow continued practice of task-specific activities and provide feedback on techniques. A few small trialshave suggested possible effectiveness for these forms of practice [106,107].
Complementary medicine
In addition to traditional medical approaches, some studies have con-firmed that acupuncture has a positive effect on motor function, ADLs,and quality of life when administered in the acute and subacute stages of the poststroke period [108]. The benefits were maintained 1 year later, andthere was a decreased length of stay as a result [109]. Acupuncture is notpart of a traditional stroke therapy rehabilitation protocol or covered bymost insurance plans, however.
Predicting disability and function status
Hemiparesis and motor recovery have been the most studied of all strokeimpairments. Twitchell [38] described in detail a pattern of motor recoveryafter stroke. The severity of arm weakness at onset and the timing of thereturn of movement of the hand are important predictors of eventual motorrecovery in the arm. The prognosis for return of useful hand function ispoor when there is complete arm paralysis at onset or no measurable graspstrength by 4 weeks. Even among patients with severe arm weakness at onset, as many as 11% may gain good functional recovery of hand function[110]. Recovery of sensory function maximizes in 1 to 2 months in 50% to67% of stroke survivors [111]. Some other generalizations can be postulated.For patients who show some motor recovery in the hand by 4 weeks, asmany as 70% make a full or good recovery [112,113]. When full recoveryoccurs, it is usually complete within 3 months of onset. For ambulation,95% of patients reach their best neurologic level within 11 weeks of onset[114]. Patients with milder strokes recovered more frequently, and patientswith severe strokes reached their best neurologic level within 15 weeks.The course of motor recovery reaches a plateau after an early stage of progressive improvement. Most recovery takes place in the first 3 months,and only minor additional measurable improvements occur after 6 monthsafter onset [115]. Many patients with ambulatory hemiparesis do not walksafely [116]. Normal casual walking speed for healthy adults is 2.5 to 3.0miles per hour (approximately 130 cm/s) [117]. An interesting study of 147 people 6 months after stroke revealed that patients with hemiparesiswho walk at 25 cm/s achieve only household ambulation. Restrictedcommunity ambulation generally required walking speeds of 40 to 79 cm/s.Unrestricted community ambulation was most likely for persons whowalked at 80 cm/s [116,118]. Only 18% of people achieved unlimitedcommunity ambulation. Across prospective observational studies and inter-ventional experiments, walking speeds at the end of inpatient rehabilitationrange from 25 to 60 cm/s. Recovery of sensory function maximizes in 1 to 2months in 50% to 67% of stroke survivors.
Motor improvements
Formal physiotherapy is often stopped when patients reach functionalgoals or progress too slowly to measure in a certain time frame. Unfortu-nately, some patients are discharged from therapy before a motor plateauis reached. Even then, a plateau in recovery does not necessarily implya diminished capacity for further functional gains. Researchers have foundthat task-specific functional therapy for the arm leads to significant gains inmotor control and strength if patients are allowed to continue treatmentuntil no further gains are made, which required an additional ten sessionsbeyond the standard treatment period [119]. There must be a shift fromthe emphasis on compensatory task-specific activity to the achievement of goal-directed therapy and restorative practice. For patients involved ina CI therapy program, clinical trials have indicated that patients who prac-ticed at an increased intensity increased the amount and efficiency of use of the affected hand by 20% to 50% whether therapy began while they wereacute rehabilitation inpatients or a year after stroke [76,77].Currently, the opportunity to achieve maximal improvement is probablyconstrained by a lack of adequate data to define the optimal intensity (performance time, pace, and duration) of training strategies for specificdisabilities [120]. In the future, functional neuroimaging studies may helpto guide decisions about the type and duration of treatment by providinginsight into the maximal cortical reorganization that can be achieved witha particular therapy over time; however, this possibility requires moreresearch [119,121].
Discharge and additional therapy
Stroke survivors with traditional insurance plans or Medicare are morelikely to be admitted to acute rehabilitation hospitals or units than patientswith managed care [122]. Growing evidence indicates that intensity of reha-bilitation correlates with outcome, which may potentially discriminateagainst patients with limited benefits. Overall, intensive stroke rehabilitationis associated with significantly lower mortality, institutionalization, anddependency [123].In Europe, stroke survivors involved with integrated acute rehabilitationprograms made greater functional gains, were more likely to return home,had decreased 5- and 10-year mortality rates, and reported a better qualityof life than when they were admitted to a less intense program [124–127].The advantages of the stroke unit are improved patient outcomes with fewerdeaths, reduction in disability, and modest decrease in length of stay [123].Outcomes improved when patients were monitored for hypoxia and hypo-tension; and previous unknown cardiac arrhythmias were detected andtreated more frequently [128,129]. Although small, a statistically significantintensity-effect relationship exists between rehabilitation and functionaloutcomes with stroke units [60].The intensity and cost of therapy of individualized programs are consid-erations in the age of managed care. Among inpatient rehabilitationfacilities, data for 2006 indicated that the average Medicare reimbursementper day for a stroke survivor was approximately $1144 and the averagelength of stay was 16.8 days. There may be greater demands to justify thisexpense as Medicare financial constraints arise in the coming years.An observational behavioral mapping study on 64 stroke patients in fiveacute stroke units reported that patients engaged in minimal therapeuticactivity or moderate therapeutic activities for only 12.8% of the therapeuticday (8am to 5pm). Patients were resting in bed 53% of the time and werealone for 60.4% of the time [130]. Therapist contact constituted only5.2% of the day. Previous studies have shown similar limited therapist– patient contact time in stroke units. Poor therapy participation has beenreported and is common during inpatient rehabilitation. Lack of participa-tion resulted in lower improvements in functional independence measurescores and longer lengths of stay, even when controlling for admissionfunctional independence measure scores [130,131].
Patients who participated in acute rehabilitation facilities were morelikely to report higher intensity of therapy, have a community-baseddischarge, and have higher functional outcomes, but costs were higher. Out-comes were similar for patients with minimal motor disabilities and patientswith mild motor disabilities and significant cognitive disabilities betweenacute and skilled rehabilitation facilities, however [132]. This finding propelsthe search for high-quality treatment that is cost effective and may, in somecases, move therapies out of the gym. Other systematic reviews focused onmultidisciplinary community neurorehabilitation and ‘‘early discharge pro-grams,’’ arguing that early discharge programs safely and effectively lowerthe number of inpatient hospital treatment days [133,134].A comparative study of stroke patients admitted to conventional strokerehabilitation versus a full-time integrated treatment program reported pos-itive results. The conventional program offered admission during the workweek, whereas the full-time integrated treatment program offered weekendadmissions and delivered regular day therapy sessions during this time forall patients. Both groups had similar functional independence measurescores at admission; however, the full-time integrated treatment grouphad significantly shorter lengths of stay and was discharged with higheraverage functional independence measure scores and nearly double the func-tional independence measure efficiency scores [135]. This finding wouldinfluence inpatient rehabilitation facilities to move to a full-time, regulartherapy schedule every day of the week and offer more weekend admissionsdespite lack of insurance approval availability.There is a great deal of interest in therapies delivered at home afterdischarge from rehabilitation. Therapy-based rehabilitation services forstroke patients living at home within 1 year of experiencing a stroke resultedin a significant improvement in the ability to manage ADL and reduced thelikelihood of deterioration in ADLs [136]. Low-intensity, home-basedphysical therapy is able to improve lower limb motor function in patients more than 1 year after stroke [137], possibly because the nature of strokemotor therapy itself can be altered at home to be more task specific whileremaining within the typical contact time parameters (ie, 30–45 minutes persession) and be as effective as traditional motor approaches in rehabilitationfacilities [138].In another study, 428 stroke patients and their caregivers were random-ized to rehabilitation from a community stroke team or to routine care,which could include day hospitals or outpatient departments. There were no significant differences between patients who received rehabilitation from community stroke teams and patients who received routine care in their independence in ADL, mood, quality of life, or knowledge of stroke. Patients in the community stroke team group were more satisfied with the emotional support they received. Caregivers of patients in the community stroke team group were under less strain and reported greater levels of overall satisfaction [139].
Summary
There are new challenges to the existing paradigm of stroke rehabilitation, including defining dosage, standardizing treatment parameters acrosssubjects and within treatment sessions, and determining what constitutes clinically significant treatment effects. Exercise type, intensity, duration,and physical location may shift in the future. The long-term goal is to develop prescriptive therapy programs in which specific activities are proven to treat specific motor system disorders. This may change our thinking and practice of what constitutes the current stroke rehabilitation paradigm.
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