Rehabilitation of the Older Adult with Stroke
aDepartment of Physical Medicine and Rehabilitation, Baylor College of Medicine,
1333 Moursund Avenue, D-111, Houston, TX 77030, USA
bTraumatic Brain Injury and Stroke Program, The Institute for Rehabilitation and Research,
1333 Moursund Avenue, D-111, Houston, TX 77030, USA
cLong-Term Acute Care Brain Injury Program, Kindred Hospital, Baylor College of Medicine,
1333 Moursund Avenue, Houston, TX 77030, USA
Stroke is an increasing public health concern throughout the world as the
leading cause of long-term disability. There is estimated to be over 3.5 millionsurvivors of stroke in the United States. It is responsible for 10% to 12% of alldeaths in industrialized countries. Almost 90% of these deaths are among peopleaged over 65 years. It is well known that there exist differences related toepidemiology, pathophysiology, comorbidity, and functional outcome of patientswith advanced age compared with the young. Factors that have been suggested toinfluence this disparity include age-related complications, availability of re-sources, lack of aggressive management, and possible diminished capacity forneuroplasticity. Despite these differences across age groups, there is compellingevidence that good outcomes can be achieved after comprehensive stroke re-habilitation The number of individuals aged N65 years is projected toincrease from 39 million in 1995 to 69 million, or 20% of the total population, in2030. The fastest growing age group will be the population aged N85 years,doubling its 1995 size by 2025 and increasing fivefold by 2050. This articlereviews the current medical and rehabilitative aspects of stroke and the possibledisparities related to advanced age.
T Department of Physical Medicine and Rehabilitation, Baylor College of Medicine, The Institute
for Rehabilitation and Research, 1333 Moursund Avenue, D-111, Houston, TX 77030.
0749-0690/06/$ – see front matter D 2006 Elsevier Inc. All rights reserved.
Cerebrovascular disease is divided into ischemic or hemorrhagic lesions.
Ischemic lesions comprise 80% of strokes and are caused by thrombotic (60%) orembolic (20%) mechanisms. Hemorrhagic strokes have an incidence of ap-proximately 15% and are divided into intracerebral (10%) or subarachnoid (5%).
Other causes (5%) of stroke include tumor, aneurysm, and arteriovenous mal-formation. The incidence of each stroke subtype and its etiology vary with age.
Overall, cerebral infarction accounts for most strokes across all age groups. Thereis an increased incidence of hemorrhagic stroke with younger age when com-pared with the elderly primarily because of the differences in risk factors. Strokesare classified further by the brain’s anatomic blood supply and related neurologicstructures. They can be divided generally into anterior, middle, and posteriorcerebral artery distributions (
The outcome of a patient with a treated stroke may never be as good as that of
someone in whom a stroke is prevented The identification and modificationof risk factors should begin as a primary prevention measure and continue after astroke as a secondary prevention measure during the acute care and rehabilitationphase. There are specific and well-defined risk factors for stroke, both modifiableand unmodifiable, that are well-known to most clinicians. Advanced age,hypertension, atrial fibrillation, statin use, and alcohol consumption are discussedin terms of their impact on the elderly.
Age is the most important unmodifiable risk factor for all stroke types in-
cluding ischemic stroke. For each successive 10 years after the age 55, the strokerate more than doubles in both men and women Approximately 65% ofall strokes occur in those who are over the age of 65. Data from Rochester,Minnesota, demonstrated that more than half of the strokes in this population
Table 1Common stroke syndromes by territory
Contralateral weakness (legN arm) and hemianesthesia, contralateral cortical sensoryloss, incontinence, abulia, apraxia, personality changes, frontal release signs,conjugate eye deviation toward lesion
Contralateral hemiplegia (arm and faceN leg) and hemianesthesia, homonymoushemianopsia, conjugate eye deviation toward lesion, aphasia (d), aprosody (n),apraxia (d), hemineglect (n), visuoperceptual deficits (n), anosognosia
Contralateral visual field defects (hemianopsia) with macular sparing, language ormemory deficits, alexia with or without agraphia (d)
Abbreviations: ACA, anterior cerebral artery; MCA, Middle cerebral artery; PCA, posterior cerebralartery; (d), dominant; (n), nondominant.
affected subjects aged N75 years and nearly one quarter affected subjects agedN85 years. Furthermore, elderly stroke patients are reported to have more severestrokes, higher case-fatality rates, and larger proportion discharged to long-terminstitutional care. In general, the frequency of stroke is higher in males thanfemales until the age of 55. After the age of 55, the risk is nearly equal for bothmen and women. Because women tend to live longer than men, however, morewomen die of stroke each year.
Hypertension is considered the most important modifiable risk factor. The
efficacy of antihypertensive treatment in preventing stroke is well established inall age groups. Using blood pressure of over 140/90 mm Hg to define hy-pertension, about 20% of the adult population has hypertension, whereas forpeople over the age of 65 years the prevalence is as high as 65% Since 1991,the results of three major trials (the British Medical Research Council trial oftreatment in older adults, the Swedish Trial in Old Patients with Hypertension,and the Systolic Hypertension in the Elderly Program) have conclusively es-tablished the benefits of treating older patients (N60 years) with both diastolic andisolated systolic hypertension. International guidelines for the management ofhypertension (including the Fifth Report of the Joint National Committee, the1993 report of the World Health Organization and the International Society ofHypertension, and the second report of the British Hypertension Society WorkingParty) have all been modified to reflect the emerging evidence concerning thebenefits of treating older patients. Cost-effectiveness data are similarly in accordwith giving high priority to the treatment of older individuals with hypertension.
Atrial fibrillation is an important cardiac risk factor in the elderly and is
estimated to cause almost half of all cardioembolic strokes. The prevalence ofatrial fibrillation in people over 60 is approximately 5% and rises to almost 15%after the age of 75. Studies have shown that stroke patients with atrial fibrillationare significantly more likely to be dead, disabled, or handicapped at 3 monthsthan those without atrial fibrillation There is an increased risk of subsequentstroke in the elderly patient with atrial fibrillation, yet many are not being treated.
Although warfarin therapy with international normalized ratio between 2 and 3dramatically reduces the risk of stroke, the risk of intracranial hemorrhage isincreased in patients older than 75 years and in those anticoagulated with an in-ternational normalized ratio above 3. The decision to treat with warfarin ther-apy should be made by weighing the benefits against the risks for that individual.
There is compelling evidence that 3-hydroxy-3-methylglutaryl-CoA reductase
inhibitors (statins) are strongly associated with lower risk of coronary disease. Inthe Prospective Study of Pravastatin in the Elderly at Risk trial, pravastatin wasshown to reduce the risk of coronary events in elderly people with a history orrisk of vascular disease Until recently, data regarding the specific rela-tionship between hypercholesterolemia and stroke were less robust. Accordingto data from the Heart Protection Study, there was an overall 25% reduction offirst event rate for stroke. Among patients with pre-existing cerebrovasculardisease there was no apparent reduction in the stroke rate, but there was a sig-nificant reduction in the rate of any major vascular event The association
between plasma cholesterol levels and risk of stroke seems to diminish with in-creased age Statins have shown worsening of cognitive function in tworandomized trials and several case reports The Heart ProtectionStudy and Prospective Study of Pravastatin in the Elderly at Risk trial, however,did not show favorable or deleterious effects on cognitive measures that weretested. There is still controversy over the finding that statins increased the fre-quency of new cancer diagnoses in elderly individuals although recentexperience in long-term trials allay concerns that there was a cause and effectrelationship. Although there are clear benefits of statin therapy after a stroke, thepotential side effects should be considered in the elderly.
There is a variable association between alcohol consumption and stroke. Al-
cohol has been reported to be a possible risk factor for thromboembolic strokeand as a protective factor for stroke with light or moderate consumersModerate consumption of alcohol (one to two drinks per day) mayreduce cardiovascular disease including ischemic stroke; however, there seems tobe a dose-response relationship between moderate consumption and the risk ofintracerebral and subarachnoid hemorrhage. There is only limited evidence thatmoderate amount of drinking may have a protective effect among those olderthan 65 Alcohol should not be considered as a preventive agent for stroke.
There are serious concerns of alcohol use in the elderly including alcohol-medication interactions, acceleration of age-related postural instability, andincrease in falls It is recommended that the elderly abstain from alcohol use.
The work-up for an older adult with stroke may be quite different from that of
a young person. It is generally accepted that a hypercoagulable work-up in anelderly person with otherwise obvious stroke etiology, such as carotid stenosis,has a low yield. The differential diagnosis in young adults may include hema-tologic abnormalities and drug abuse, whereas advanced age may boast its ownspecific causes for stroke that warrant further investigation. The differential di-agnosis of an elderly stroke patient may include such causes as hyperhomo-cysteinemia, amyloid angiopathy, and multi-infarct dementia.
Hyperhomocysteinemia is now established as a major risk factor for stroke
It has been attributed to dietary deficiency of vitamin B6, vitamin B12, orfolic acid, especially in older patients with poor nutritional intake. The interplayof folate, vitamin B12, and vitamin B6 helps control blood levels of homocysteine.
Some individuals may have an inherited deficiency and develop premature ath-erosclerosis and often experience a stroke early in life. The use of antiepilepticdrugs, such as phenytoin, has also been shown to increase the level of homo-cysteine in the blood Patients with stroke can have homocysteine levels1.5 times those of age- and sex-matched controls Two large randomizedmulticenter trials, the Vitamin Intervention for Stroke Prevention and the Vita-mins to Prevent Stroke studies, are designed to determine if, in addition to best
medical and surgical management, high-dose folic acid, vitamin B6, and vitaminB12 supplements reduce recurrent stroke or transient ischemic attack
Cerebral amyloid angiopathy is caused by deposition of b-amyloid sheets in
media and adventitia of small to mid-sized arteries of the cerebral cortex and theleptomeninges. Vessels become more rigid and fragile increasing the risk of rup-ture. Advanced age increases the incidence of cerebral amyloid angiopathy,which has been reported as 5% of those in the seventh decade of life, and up to50% of those older than 90 years. Fifteen percent of all intracerebral hemorrhagesin patients older than 60 years and about 50% of nontraumatic lobar intracerebralhemorrhages in those older than 70 years are attributable to cerebral amyloidangiopathy. Incidence remains elusive because definitive diagnosis is madeonly by histologic examination or postmortem brain biopsy. The most commonsymptoms are headache, occurring 60% to 70% at onset, followed by dementia,transient neurologic symptoms, or coma. The most common and devastatingeffect of cerebral amyloid angiopathy is lobar intracerebral hemorrhages, but it isassociated with a lower mortality rate and a better functional outcome thanhypertensive deep ganglionic bleeds. It is estimated that at least 40% of pa-tients with intracerebral hemorrhages–related hemorrhage have some degree ofdementia. Although patient management is unchanged from standard intra-cerebral hemorrhages, priority should be given to reversing anticoagulation.
Blood thinners, such as warfarin, and antiplatelet agents, such as aspirin, shouldbe avoided if possible. If these medications are required for other conditions, suchas heart disease, the potential benefits must be carefully weighed against theincreased risks.
Multi-infarct dementia, or vascular dementia, is the second most common
cause of dementia in the elderly after Alzheimer’s disease. The diagnosis requires(1) cognitive loss, often subcortical; (2) imaging studies demonstrating vascularbrain lesions; and (3) exclusion of other causes of dementia, such as Alzheimer’sdisease It affects people between the ages of 60 and 75 with a slight pre-dilection for men. Multi-infarct dementia is caused by small, multiple cerebralinfarcts with the progression of cognitive impairment being insidious, stepwise,or both, usually affecting executive dysfunction, memory loss, or aphasia. Afamilial form of dementia associated with cerebrovascular disease is observed ina rare genetic condition, cerebral autosomal-dominant arteriopathy with subcor-tical infarcts and leukoencephalopathy. This condition is less common in theelderly because recurrent strokes usually begin before the age of 50.
Effective rehabilitation of the stroke patient with dementia is dependent on
motivation and cognitive ability even more than on remaining motor or sensoryfunction. Specifically, there should be a meaningful engagement with the thera-pist. Neuropsychologic evaluation commonly identifies impairment in executivedysfunction, memory, and language. Given its strong vascular component, thediagnosis of multi-infarct dementia is believed to be more preventable and of-fers a better likelihood for cognitive improvement compared with Alzheimer’sdisease Treatment often involves control of risk factors, such as hyper-tension, diabetes, smoking, hyperfibrinogenemia, hyperhomocysteinemia, ortho-
static hypotension, and cardiac arrhythmias and pharmacologic management.
Medications currently being used are similar to Alzheimer’s disease. Anti-cholinergic medications, atypical antipsychotic agents, and antidepressants (eg,selective serotonin reuptake inhibitors) may be useful in some patients Pentoxifylline has been studied to slow the progression of dementia in patientswho meet Diagnostic and Statistical Manual-III criteria for multi-infarct dementiaand have clinical and neuroradiologic evidence of cerebrovascular disease Small open-label studies using rivastigmine, a second-generation acetylcholines-terase inhibitor, have shown improved attention, executive function, and apathyin vascular dementia Memantine is an N-methyl-d-aspartate receptor an-tagonist, approved in October 2003 by the US Food and Drug Administration fortreatment of moderate to severe Alzheimer’s disease. In Alzheimer’s disease ithas been shown to promote less cognitive deterioration with early benefit onmood and behavior with a low incidence of adverse effects All of thesemedications seem to be promising agents in vascular dementia, but their effectsneed to be established in double-blind, placebo-controlled clinical trials.
Medical issues during stroke rehabilitation
Medical management of the stroke patient goes beyond the acute care period.
This is especially true with the recent trend toward earlier discharge from acutecare to a rehabilitation facility. The goals during the rehabilitation phase of astroke patient include (1) ensuring medical stability by implementing secondarystroke prevention measures and controlling risk factors, (2) preventing andtreating complications that may increase morbidity and mortality, and (3) pro-moting neurologic and functional recovery. Ensuring medical stability of a patientdemands a thorough review of clinical history, physical examination includinga detailed neurologic assessment, laboratory studies, imaging results, and diag-nostic testing. Specific treatments should be noted, including use of tissue plas-minogen activator or interventional procedures and initiation or discontinuationof medications. Secondary stroke prevention measures, including risk factormodification, pharmacologic management, and surgical management (ie, carotidendarterectomy), should be implemented or confirmed.
Specialized stroke units are associated with better prognosis than general
medical units Effective early management of acute stroke and transientischemic attack reduces morbidity and mortality and can reduce use of scarcehealth and social services resources. Stroke-related mortality has decreased inrecent years partly because of better risk factor management, the advent of tissueplasminogen activator, and improvement in acute medical management afterstroke. Despite this overall reduction in mortality, stroke still remains an impor-tant cause of death worldwide. Approximately 20% of first-ever stroke patientsdie within 30 days. In the first few days, mortality is usually caused by the strokeitself from edema, herniation, or disruption of brainstem centers. Patients whohave suffered a stroke remain at an increased risk of recurrent stroke at 30% to
40% within 5 years. An individualized strategy for secondary stroke preventionshould be implemented within a maximum of 7 days of acute stroke or transientischemic attack.
Pneumonia, cardiac disease, and pulmonary embolism are the most frequent
causes of death during the first 30 days. Pneumonia may occur in approximatelyone third of patients, commonly caused by aspiration secondary to dysphagia. Allstroke patients should undergo a bedside screening before initiation of oral intakefollowed by a full bedside swallow study if needed. Cardiac disease after stroke ismanifested as myocardial infarction, arrhythmias, or heart failure. Full cardiacwork-up should be completed during the acute care of a stroke patient. Theincidence of pulmonary embolism after stroke is between 10% and 15%. Its peakis usually during the first week after stroke; initiation of prophylactic measuresfor deep vein thrombosis should be done as soon as possible. The total durationof prophylaxis is still unknown, because the risk of deep vein thrombosiscontinues well beyond the first week. Risk factors for deep vein thrombosisshould be assessed during the rehabilitation phase and at the time of discharge. Itis generally accepted that an ambulation distance of 50 ft per day significantlyreduces the risk of deep vein thrombosis after stroke Contraindications tochemical prophylaxis may warrant mechanical (sequential compression device)or surgical (inferior vena cava filter) interventions.
Early recovery after a stroke is caused by spontaneous mechanisms related
to resolution of harmful local factors (ie, local edema, resorption of local toxins,improved local circulation, and resolution of arterial spasm). Motor recoveryhas been well-described and the most studied of all stroke impairments. Theclassic paper by Twitchell in 1951 first described the pattern of motorrecovery following stroke from a flaccid state to progressive increase in tone. Thephases of recovery described by Twitchell were later formalized into stagesby Brunnstrom in 1970 The general pattern of recovery in a classic mid-dle cerebral artery infarction is as follows: (1) proximal recovery occurs be-fore distal; (2) the lower extremity recovers earliest and most completely; and(3) synergy patterns, stereotyped mass movements, occur before isolated, volun-tary movements.
Neural plasticity is the potential of the central nervous system to reorganize its
structure and function based on the idea that the brain is responsive, flexible, anddynamic. There is modification of neural networks that are use-dependent. Afterearly, spontaneous recovery after stroke, several mechanisms are thought to oc-cur. Bach-Y-Rita described several theories on recovery and neuroplasticity,including collateral sprouting, unmasking, and diaschisis. Regeneration or col-lateral sprouting describes when a neighboring axon branches to assume theterritory of a denervated region or injured axon. Unmasking of pathways is theactivation of previously latent pathways when the dominant system fails. There
may exist redundant pathways in which there is unmasking of the uninjuredparallel pathway. The concept of diaschisis, coined by Constantin Von Monakowin 1914, describes how a site away from the primary injury may be affected whenthere is loss of neural input from the injured part of brain. Reversal of this processmay contribute to neurologic and functional recovery after a stroke
There is a clinical perception that these restorative processes are age-
dependent. The question remains whether brain plasticity still exists and to whatextent in the aging human brain because most studies have reported on younganimals. Animal studies by Popa-Wagner and coworkers report quantitativechanges in the hippocampus and qualitative changes in the cortex with increasedage. There seems to be a regenerative potential of the aged brain that is competentbut attenuated after a stroke. Human studies further evaluate the ability of theaging motor cortex to reorganize. It is now well-known that cortical reorgani-zation underlies functional recovery after a stroke and is elicited by motortraining that uses practiced movements. The influence of age on this form ofplasticity has been specifically studied by Sawaki and coworkers who founda significant decrease in training-dependent plasticity as a function of age. Fur-ther studies are needed to delve into the mechanism and to quantify these changesin the aged brain.
An important goal during rehabilitation is to identify and minimize the use of
pharmacologic agents that may impede recovery after stroke. Many drugs com-monly used to treat new or chronic conditions have central nervous system sideeffects. Studies in laboratory animals indicate that certain centrally acting drugs(ie, clonidine, prazosin, neuroleptics, and other dopamine receptor antagonists;benzodiazepines; phenytoin; and phenobarbital) impair behavioral recovery afterfocal brain injury. Even single doses may have long-term harmful effects Consistent with previous reports, haloperidol retards motor recovery after sen-sory motor cortex injury in rats. The use of low doses of atypical antipsychotics
Table 2Clinical practice guidelines for pharmacologic management of stroke patients during rehabilitation
1. Recommend against the use of neuroleptics, benzodiazepines, phenobarbital, and phenytoin during
the stroke recovery period. The benefit of these drugs versus the risk of potential adverse effectshould be considered.
2. Recommend against centrally acting a2-adrenergic receptor agonists as antihypertensive medica-
tions, such as clonidine, and a1-receptor antagonists, such as prazosin, as antihypertensive medi-cations. There is a potential to impair recovery in stroke patients.
3. Because there is insufficient evidence on the optimal dosing and safety of neurostimulant agents, no
clear recommendation can be made. A trial of neurotransmitter-releasing agents should beconsidered in patients to improve participation in stroke rehabilitation or to enhance motor recovery.
Adapted from Duncan PW, Zorowitz R, Bates B, et al. Management of adult stroke rehabilitation care:a clinical practice guideline. Stroke 2005;36:e100–43.
provides a safer alternative to haloperidol in the treatment of agitated strokepatients The Stroke Council of the American Heart Association endorses theclinical practice guidelines for the pharmacologic management of stroke reha-bilitation (
The practice of neurorehabilitation is unique in that it provides an opportunity
to enhance intensive rehabilitation with pharmacologic interventions that facili-tate the recovery of damaged neurons and plastic responses in underused andunused brain tissue. Animal studies reveal that norepinephrine, amphetamine, andother a-adrenergic stimulating drugs can enhance motor performance after uni-lateral ablation of the sensory motor cortex. Although widely used, there arelimited data to support the use of neurostimulants in stroke recovery. The moststudied in clinical trials is dextroamphetamine, which has been shown both toexpedite motor recovery and improve aphasia Other agents commonlyused and studied in small controlled trials or case series to treat motor, language,and cognitive-behavioral syndromes include methylphenidate, amantadine, levo-dopa, selective serotonin reuptake inhibitors, and modafinil
General rehabilitation principles in the stroke patient
Stroke rehabilitation begins as soon as the diagnosis of stroke is established.
Rehabilitation during the acute phase should be to prevent recurrent stroke, avoidmedical complications, mobilize the patient, encourage the resumption of self-care activities, and provide emotional support to the patient and family. Duringthis phase, specific goals may include measures to prevent deep vein thrombosisor pressure sores, to minimize spasticity or contracture, to manage bowel andbladder issues, and to prevent respiratory complications. Therapy involves range-of-motion exercises and bed positioning with progressive increase in intensity astolerated. A study of 145 patients with first-ever strokes showed better effec-tiveness on a functional outcome scale, the Barthel Index, with early reha-bilitation treatment compared with delayed initiation of services Pooling theresults of nine controlled trials revealed a small, but statistically significantintensity-effect relationship in the rehabilitation of stroke patients Sub-sequent studies support higher intensity of upper and lower limb training toimprove activities of daily living, walking ability, and dexterity The generalconsensus is that greater intensity of rehabilitation produces slightly better out-comes It is still unknown whether there is a minimum threshold of inten-sity, below which there is no benefit.
There are several rehabilitation models for treatment of central nervous system
dysfunction. The basis for the appropriate model and its concomitant goalsshould be a combined effort of the patient, family, or caregiver, and the multi-
disciplinary rehabilitation team. The general approach to rehabilitation of a strokepatient may include one or more of the following methods: (1) compensatorystrategies; (2) strengthening exercises; (3) facilitation and neurophysiologictechniques (Bobath); and (4) task-oriented approaches. Advanced age shouldnot preclude any of these strategies, including upper- and lower-extremity task-oriented training.
Compensation refers to the use of alternate strategies to complete a task. The
initial functional training of a hemiplegic patient should emphasize compensatorystrategies. For example, self-care is performed using the unaffected arm andmobility is achieved using a wheelchair. Some experts suggest that compensa-tion is detrimental for the patient because it may lead to ‘‘learned nonuse.’’ It isgenerally believed that there are some compensatory strategies that are necessaryfor function, whereas others that are detrimental should be avoided.
A decline in general fitness often occurs in the disabled and in the elderly.
In randomized trials, progressive resistance exercises performed three to fourtimes weekly for a period of 6 to 12 weeks by patients with adequate motorcontrol improved strength and functional activities Even in chronic strokepatients, trials show gains in walking ability with progressive aerobic exercisesthat are tailored to each patient’s tolerance Lower-extremity muscle strengthhas been correlated with gait speed in stroke patients Lower-extremitystrength has also been inversely correlated with a risk of falling in older post-stroke patients. An appropriate strengthening program can be implemented ata variable point in the rehabilitation process of a stroke patient.
Neurophysiologic and facilitation techniques
The neurodevelopmental training, or Bobath, approach focuses on the pro-
gression of movement through inhibition of primitive reflexes and facilitationof higher-level control. With neurodevelopmental training, the stroke patient isencouraged to use the affected side of their body to promote and relearn normalmovement and to reduce muscle spasticity. Although widely used, no randomizedcontrolled studies have shown this to be more effective than any other approachto stroke rehabilitation.
Emerging evidence suggests that new models of task-oriented exercise have
the potential to improve motor function even years after stroke. There is evidence
supporting the efficacy of task-specific training protocols emphasizing the use ofthe more affected limb Constraint-induced movement therapy and body-weight–supported treadmill training use this model of high intensity, task-specifictraining for the upper and lower extremity, respectively. Protocols for constraint-induced movement therapy are based on the theory of learned nonuse associatedwith the great effort required to perform tasks with the affected hand Thisapproach involves intensive task-specific practice with the affected hand for 3 to6 hours a day over a period of 2 to 6 weeks. The therapy progresses graduallyfrom small approximations to full movement. The protocol may additionallyrestrain the unaffected hand to force greater use of the affected hand. There arespecific inclusion criteria, which greatly limits the application of this trainingprotocol The clinical benefit of this treatment may be present if initiatedearly or even 1 year poststroke.
Recovery of walking is a complex phenomenon. Even after significant neuro-
logic improvement, walking requires considerable practice to improve motorcontrol. Body-weight–supported treadmill training uses task-specific training toallow patients to take more steps at faster speeds than may otherwise be feasible.
The effectiveness of this therapy is still inconclusive. A recent Cochrane reviewin 2003 on body-weight–supported treadmill training showed that it may improvewalking speed among people with stroke who could walk independently at thestart of treatment, but not those who were dependent walkers. There were nostatistically significant adverse events, which is an important concern in theelderly who may have cardiac comorbidties Emerging evidence suggeststhat new models of task-oriented exercise, including the introduction of robotics,have the potential to improve motor function and cardiovascular health evenyears after stroke. Still, there is a need for well-designed large-scale studies toevaluate the effects further.
Stroke-related dysphagia may cause complications, such as aspiration, de-
hydration, and nutritional deficiencies. In stroke patients, aspiration usually oc-curs from dysfunction of the pharyngeal phase of swallowing and is likely tooccur without clinical manifestation, called ‘‘silent aspiration.’’ Nearly one thirdof patients with dysphagia have aspiration, which in addition to impaired coughand gag reflex, becomes a major risk factor for pneumonia. Formal evaluation ofswallow function and compensatory strategies should be implemented before theinitiation of any oral intake. Video fluoroscopic swallow study can reveal delayedinitiation of swallow with alteration in pharyngeal transit time.
Elderly patients are particularly susceptible to the effects of dehydration and
malnutrition. Dehydration may be due to lowered response, impaired ability toconcentrate urine, use of diuretics, or decreased intake due to fear of incon-
tinence. Malnutrition is most commonly related to depression followed by use ofmedications that decrease appetite. Age-related reduction in laryngeal elevationalso increases risk of aspiration.
Communication disorders are present in more than one third of patients, with
aphasia being the most common. Aphasia is a disorder of language, typicallyassociated with lesions of the left or dominant hemisphere. It is also recognizedthat some aspects of language, such as prosody of speech, may be affected ifthe nondominant side is affected. The Boston School of Aphasia is a commonlyused classification system that assesses fluency, comprehension, repetition, andword-finding ability to make a diagnosis. In addition, the Western Aphasia Bat-tery is used to evaluate the severity of the impairment. Generally, the progno-sis for recovery is worse for the patient with delayed treatment or with advancedage. Regardless, a speech-language pathologist can provide interventions tomaximize recovery and prevent inappropriate compensatory strategies. Anotherimportant goal is the education of family, caregivers, and staff on the facili-tation of communication to meet the patient’s needs. Although drug therapy isunlikely to revolutionize the treatment of aphasia, it may serve to supplementintense treatment or strategies to improve performance. Trials using bromocrip-tine, amphetamines, piracetam, and donepezil have been promising Additional studies are necessary, however, to assess the full potential of apha-sia pharmacotherapy. Until then, the initial severity of aphasia timeliness oftherapy intervention and age are the main factors influencing speech recovery.
The incidence of bladder incontinence is 50% to 70% during the first month
after stroke, but returns to the level of the general population by about 6 months.
Supraspinal injury, as in stroke, causes an uninhibited or hyperreflexic bladderthat is best treated with a timed voiding schedule. Postvoid residuals shouldbe carefully monitored initially until safe bladder volume can be documented.
Urinary retention is much less common, but may require intermittent catheteri-zation initially. The frequency of urinary tract infections increases as a resultof prolonged catheter use, alterations in bladder emptying, or reduced fluidintake. Elderly patients may have increased risk of bladder dysfunction dueto premorbid bladder incontinence retention from medications, infections orprostatic problems in males. Bladder incontinence can increase skin breakdown,decrease socialization, increase rate of depression, and eventually increase chanceof institutionalization. Medication should be used with caution unless previouslyindicated because of premorbid conditions.
Bowel incontinence occurs in up to one third of patients. Unlike bladder
incontinence, bowel dysfunction usually resolves in the first few weeks af-ter stroke. Even more common is bowel impaction. This is usually related to
the relative inactivity; decreased nutrition, especially fiber; and diminishedfluid intake. Appropriate dietary modifications, the use of regular bowel medi-cations, and progressive increase in activity level can aid in managingbowel dysfunction.
Approximately 65% of individuals develop spasticity after a stroke
In 1980, Lance published this frequently cited definition: ‘‘Spasticity is amotor disorder characterized by a velocity-dependent increase in tonic stretchreflexes (muscle tone) with exaggerated tendon jerks, resulting from hyper-excitability of the stretch reflex, as one component of the upper motor neuronsyndrome.’’ Treatment should be based on realistic goals for the patient, whichmay include reducing pain, simplifying activities of daily living, improvinghygiene, or improving function. It is notable that some patients do not requiretreatment because they may rely on their spasticity for improved function (ie,‘‘walk on their tone’’).
Management of spasticity begins with two fundamental interventions: daily,
prolonged stretching program; and avoidance or management of noxious stimuli(ie, ingrown toenail, distended bowel or bladder, pressure sore, or even tightclothing). It was once thought that a step-wise approach should be taken next,consisting of trial of oral medications, then local injections of phenol or botu-linum toxin, to surgical options (rhizotomy, orthopedic surgery). The currentmanagement for spasticity of cerebral origin now minimizes the role of oralantispasticity agents because there is only mild reduction of spasticity with sig-nificant impairment of cognition. Even dantrolene, which is thought to actperipherally, may cause sedation and muscle weakness. The side effects of oralagents may be magnified in the elderly patient. Weight-bearing exercises andserial casting are commonly incorporated in the treatment program. Focal injec-tions with phenol or botulinum toxin can be more effective when appropriatelyadministered. Serial casting can and should be used adjunctively with otherspasticity interventions. Intrathecal baclofen pumps are now more widely usedfor generalized spasticity Preliminary studies have shown intrathecal bac-lofen pumps to be effective in improving walking speed and functional mobilityin ambulatory stroke patients when combined with physical therapy
Hemiplegic shoulder pain is a frequent pain syndrome seen in poststroke
patients with a prevalence of 34% to 84%, affecting both motor rehabilitation andpsychologic well-being. It interferes with activities of daily living, balance, andambulation and is associated with poorer outcome and increased length of stay inhospital Major risk factors for hemiplegic shoulder pain are advanced age,muscle tone changes after stroke, and sidedness of stroke. Age-related changesinclude decreased range of motion, degenerative changes of the acromioclavicu-
lar joint and glenoid labrum, and calcified tendons that may exacerbate the paincondition. Spastic hemiplegic shoulder is more commonly associated with paincompared with a flaccid shoulder because the humeral head is displaced an-teriorly, posteriorly, or medially. Still, Tobis in 1957 proposed the ‘‘maincause of shoulder pain in hemiplegia is flaccidity.’’ The weight of the unsup-ported arm stretches the capsule and ligaments causing inferior subluxation.
Right-sided lesions are thought to cause increased risk of trauma-related hemi-plegic shoulder pain, especially if associated with visuospatial deficits or neglect.
The differential diagnosis of hemiplegic shoulder pain may include adhesivecapsulitis, rotator cuff tears, neuropathic damage, chronic regional pain syn-drome, and musculoskeletal imbalances. Clinical history, palpation, and plainradiographs with arms unsupported are reliable tools in making the diagnosis.
Treatment of hemiplegic shoulder pain starts with proper positioning and
handling. There is evidence that hemiplegic shoulder pain increases during thefirst few weeks following discharge from a hospital, usually because of lessskilled transfers, less therapy, and less medications Early range-of-motionexercises can prevent immobility, spasticity, and contracture. Slings and supports,if used appropriately, can reduce subluxation and protect from trauma; how-ever, they also reduce upper-extremity mobility and sensory feedback, encour-age flexor tone, and impair gait and body image. Functional electrical stimulationhas been shown to maintain muscle bulk and tone in flaccid shoulder and en-hance functional recovery through cortical feedback. More recently, intra-muscular neuromuscular electric stimulation has been shown to reduce poststrokeshoulder pain with improvement lasting at least 6 months Oral analgesicmedications are limited by their cognitive and sedative side effects, especiallyin the elderly. Local steroid injections can provide temporary relief, but atro-phic effects of repeated injections further weaken the cuff. In chronic regionalpain syndrome, sympathetic nerve block of the stellate ganglion may be effec-tive if more conservative measures fail. Botulinum toxin injections have beenused to relieve hemiplegic shoulder pain at rest and with range-of-motion insome patients.
Stroke has been associated with a higher fall risk in both the acute care and
rehabilitation settings The incidence of falls has been reported as 14% inacute care 24% during inpatient rehabilitation and 39% in geriatricrehabilitation setting These numbers are quite dramatic because the numberof hospital falls in stroke patients is a strong predictor of falls after discharge.
Studies have shown increased age, male gender, visuospatial neglect, right hemi-sphere strokes, urinary incontinence, bilateral motor involvement, posturalinstability, impaired activities of daily living, impulsivity, and use of certain medi-cations (ie, diuretics, antidepressants, or sedatives) to be positively associatedwith fall risk Because rehabilitation has become an increasingly sig-nificant part of stroke care and falls are one of the most common complications,
there is a unique obligation to work on fall prevention strategies without lower-ing activity levels. Fall prevention measures begin with a fall assessment screen-ing to identify patients at risk, implementing fall prevention strategies thatminimize the use of restraints and sedating medications, and making ongoingreassessments at scheduled intervals. Despite these interventions, falls remain asignificant complication after stroke.
Poststroke depression is a frequent complication after stroke that is associated
with a negative impact on rehabilitation and functional recovery Overthe years, literature has supported a relationship between stroke and depressionwith an incidence between 15% and 70%. According to a population-based study,the prevalence of major depression was 25% at hospital discharge, 30% at3 months after stroke, 16% at 1 year, and 29% at 3 years with a mean age of73 The Framingham study reported a 47% incidence of depression at6 months poststroke with no difference between left- and right-sided lesions Other studies reported predisposition to depression after left anterior or rightposterior infarcts The pathophysiology is not entirely elucidated and mightinvolve several mechanisms including direct consequences of brain lesions,neuroendocrine mechanism, or even psychologic reaction to the stress or dis-ability. Other causes include damage to left cerebral cortex, proximity of lesion tofrontal pole, and premorbid history of a psychiatric disorder. Confounding factorsmay include medical comorbidities, impaired attention and initiation, or drugsthat may depress mood (
Treatment should be comprehensive to include patient and caregiver edu-
cation, therapeutic exercises, psychotherapy, and pharmacologic agents. Coun-seling during rehabilitation may decrease the risk of depression, especially whendirected toward concerns of being a burden on family or society. Several drugshave been shown to be effective in treating depression with a potential benefit ofimproving short-term motor recovery after stroke Currently, such drugs asmethylphenidate, nortriptyline, citalopram, and fluoxetine are commonly used totreat poststroke depression
Table 3Medications commonly associated with worsening of depressive symptoms
Estrogen, progesterone, prednisone, anabolic steroids
The search for depression should be systematic and early to ensure appropri-
ate treatment. The elderly population may already be at high risk for depres-sion because of associated chronic disease. Even more, advanced age is oftenaccompanied by loss of key social support systems because of the death of aspouse or siblings, retirement, or relocation of residence at a time when it ismost needed. Older adults with depression are more likely to commit suicidethan are younger people with depression. Within 10 years after a stroke, the riskof death is 3.5 times higher in depressed patients than in those without depres-sion
A comprehensive rehabilitation program should include appropriate commu-
nity and social integration. A history of the patient’s prior community activitiesand interests serves to guide the clinician in planning appropriate measures. Thepoststroke family support, financial status, and community resources should beevaluated to optimize successful return to the community. There are both physi-cal and cognitive benefits associated with community participation. It has beenshown that participation in physical activities can improve a patient’s balance,decrease anxiety and depression, assist with pain management, and increase one’sability to maintain functional independence There is also a potential de-creased risk of dementia with certain leisure activities
The ability to drive is a vital aspect of maintaining functional independence in
the community. Although many older adults voluntarily stop driving, there arestill several elderly patients who wish to resume. The elderly are the fastestgrowing segment of the driving population. A person’s crash risk per mileincreases starting at age 55, exceeding that of a young, beginning driver by age80 The effect of adding disability to these statistics is obvious. Counselingpatients about their new disability and discussing alternative options may be ap-propriate. Driving assessment can be coordinated through a multidisciplinarydriver’s rehabilitation program, which may include an assessment of vision, at-tention, hearing, visuospatial skills, and motor function, followed by a behind-the-wheel assessment Opinions on driving fitness may be required by thephysician; current licensing policies, liability, and reporting procedures for po-tentially ineligible drivers should be reviewed for each state
Because only thrombolytics have been demonstrated to be effective in mini-
mizing brain damage and maximizing functional outcome, intensive rehabilita-tion remains the most significant means by which stroke survivors may recover.
Previously, the rehabilitation approach to the older stroke patient was supportiveand focused on prevention of complications while spontaneous recovery occurs.
Now, even these older stroke patients are undergoing relatively aggressive re-
habilitation with good outcomes in morbidity, mortality, and function. In ad-dition, the quality of life of these individuals is significantly improved. Therecently published National Service Framework for Older People specificallyhighlights the importance of preventing age discrimination, encouraging respectand dignity, and promoting general health and well-being to ensure a well-coordinated approach to providing services that address conditions that are sig-nificant for older people. The Stroke Treatment and Ongoing Prevention Act iscurrently in the approval process with the 109th Congress, which will provideresources to improve stroke education, research, and patient care. In the mean-time, it is important for clinicians to understand the current state of stroke reha-bilitation so they can continue to provide quality care and improve outcomes.
The author acknowledges the assistance of Richard L. Harvey, MD, and the
staff at the Rehabilitation Institute of Chicago for their support in preparation ofthis article.
 Di Carlo A, Lamassa M, Pracucci G, et al. Stroke in the very old: clinical presentation and
determinants of 3-month functional outcome: a European perspective. European BIOMED Studyof Stroke Care Group. Stroke 1999;30:2313 – 9.
 Ergeletzis D, Kevorkian CG, Rintala D. Rehabilitation of the older stroke patient: functional
outcome and comparison with younger patients. Am J Phys Med Rehabil 2002;81:881 – 9.
 Lieberman D, Lieberman D. Rehabilitation following stroke in patients aged 85 and above.
J Rehabil Res Dev 2005;42:47 – 54.
 Paolucci S, Antonucci G, Troisi E, et al. Aging and stroke rehabilitation. a case-comparison
study. Cerebrovasc Dis 2003;15:98 – 105.
 Bronner LL, Kanter DS, Manson JE. Primary prevention of stroke. N Engl J Med 1995;333:
 Brown RD, Whisnant JP, Sicks JD, et al. Stroke incidence, prevalence, and survival: secular
trends in Rochester, Minnesota, through 1989. Stroke 1996;27:373 – 80.
 Wolf PA, D’Agostino RB, O’Neal MA, et al. Secular trends in stroke incidence and mortality.
The Framingham Study. Stroke 1992;23:1551 – 5.
 Goldstein LB, Adams R, Becker K, et al. Primary prevention of ischemic stroke: aA statement
for healthcare professionals from the Stroke Council of the American Heart Association. Stroke2001;32:280 – 99.
 Lamassa M, Di Carlo A, Pracucci G, et al. Characteristics, outcome, and care of stroke associated
with atrial fibrillation in Europe: data from a multicenter multinational hospital-based registry(The European Community Stroke Project). Stroke 2001;32:392 – 8.
 Shepherd J, Blauw GJ, Murphy MB, et al. Pravastatin in elderly individuals at risk of vascular
disease (PROSPER): a randomised controlled trial. Lancet 2002;360:1623 – 30.
 Collins R, Armitage J, Parish S, et al. Effects of cholesterol-lowering with simvastatin on stroke
and other major vascular events in 20536 people with cerebrovascular disease or other high-riskconditions. Lancet 2004;363:757 – 67.
 Sacks FM, Pfeffer MA, Moye LA, et al. The effect of pravastatin on coronary events after
myocardial infarction in patients with average cholesterol levels. Cholesterol and RecurrentEvents Trial investigators. N Engl J Med 1996;335:1001 – 9.
 Schatz IJ, Masaki K, Yano K, et al. Cholesterol and all-cause mortality in elderly people from the
Honolulu Heart Program: a cohort study. Lancet 2001;358:351 – 5.
 Muldoon MF, Barger SD, Ryan CM, et al. Effects of lovastatin on cognitive function and
psychological well-being. Am J Med 2000;108:538 – 46.
 Muldoon MF, Waldstein SR, Ryan CM, et al. Effects of six anti-hypertensive medications on
cognitive performance. J Hypertens 2002;20:1643 – 52.
 King DS, Wilburn AJ, Wofford MR, et al. Cognitive impairment associated with atorvastatin
and simvastatin. Pharmacotherapy 2003;23:1663 – 7.
 Orsi A, Sherman O, Woldeselassie Z. Simvastatin-associated memory loss. Pharmacotherapy
 Wagstaff LR, Mitton MW, Arvik BM, et al. Statin-associated memory loss: analysis of 60 case
reports and review of the literature. Pharmacotherapy 2003;23:871 – 80.
 Ben-Shlomo Y, Markowe H, Shipley M, et al. Stroke risk from alcohol consumption using
different control groups. Stroke 1992;23:1093 – 8.
 Camargo Jr CA, Hennekens CH, Gaziano JM, et al. Prospective study of moderate alcohol
consumption and mortality in US male physicians. Arch Intern Med 1997;157:79 – 85.
 Stampfer MJ, Colditz GA, Willett WC, et al. A prospective study of moderate alcohol con-
sumption and the risk of coronary disease and stroke in women. N Engl J Med 1988;319:267 – 73.
 Fried LP, Kronmal RA, Newman AB, et al. Risk factors for 5-year mortality in older adults: the
Cardiovascular Health Study. JAMA 1998;279:585 – 92.
 Malmivaara A, Heliovaara M, Knekt P, et al. Risk factors for injurious falls leading to hos-
pitalization or death in a cohort of 19,500 adults. Am J Epidemiol 1993;138:384 – 94.
 Green D. Thrombophilia and stroke. Top Stroke Rehabil 2003;10:21 – 33.
 Tamura T, Aiso K, Johnston KE, et al. Homocysteine, folate, vitamin B-12 and vitamin B-6 in
patients receiving antiepileptic drug monotherapy. Epilepsy Res 2000;40:7 – 15.
 Coull BM, Malinow MR, Beamer N, et al. Elevated plasma homocyst(e)ine concentration as a
possible independent risk factor for stroke. Stroke 1990;21:572 – 6.
 Spence JD, Howard VJ, Chambless LE, et al. Vitamin Intervention for Stroke Prevention (VISP)
trial: rationale and design. Neuroepidemiology 2001;20:16 – 25.
 Roman GC. Vascular dementia revisited: diagnosis, pathogenesis, treatment, and prevention.
Med Clin North Am 2002;86:477 – 99.
 Schut LJ. Dementia following stroke. Clin Geriatr Med 1988;4:767 – 84.
 Black RS, Barclay LL, Nolan KA, et al. Pentoxifylline in cerebrovascular dementia. J Am Geriatr
 Roman GC. Rivastigmine for subcortical vascular dementia. Expert Rev Neurother 2005;5:
 Areosa Sastre A, McShane R, Sherriff F. Memantine for dementia. Cochrane Database Syst Rev
 Indredavik B, Bakke F, Solberg R, et al. Benefit of a stroke unit: a randomized controlled trial.
 Reding MJ, Potes E. Rehabilitation outcome following initial unilateral hemispheric stroke: life
table analysis approach. Stroke 1988;19:1354 – 8.
 Twitchell TE. The restoration of motor function following hemiplegia in man. Brain 1951;74:
 Brunnstrom S. Movement therapy in hemiplegia: a neurophysiological approach. Philadelphia
 Bach y Rita P. Central nervous system lesions: sprouting and unmasking in rehabilitation. Arch
 Seitz RJ, Azari NP, Knorr U, et al. The role of diaschisis in stroke recovery. Stroke 1999;30:
 Popa-Wagner A, Schroder E, Schmoll H, et al. Upregulation of MAP1B and MAP2 in the rat
brain after middle cerebral artery occlusion: effect of age. J Cereb Blood Flow Metab 1999;19:425 – 34.
 Sawaki L, Yaseen Z, Kopylev L, et al. Age-dependent changes in the ability to encode a novel
elementary motor memory. Ann Neurol 2003;53:521 – 4.
 Goldstein LB. Common drugs may influence motor recovery after stroke. The Sygen In Acute
Stroke Study Investigators. Neurology 1995;45:865 – 71.
 Goldstein LB, Bullman S. Differential effects of haloperidol and clozapine on motor recovery
after sensorimotor cortex injury in rats. Neurorehabil Neural Repair 2002;16:321 – 5.
 Duncan PW, Zorowitz R, Bates B, et al. Management of adult stroke rehabilitation care: a clini-
cal practice guideline. Stroke 2005;36:e100 – 43.
 Crisostomo EA, Duncan PW, Propst M, et al. Evidence that amphetamine with physical ther-
apy promotes recovery of motor function in stroke patients. Ann Neurol 1988;23:94 – 7.
 Sonde L, Nordstrom M, Nilsson CG, et al. A double-blind placebo-controlled study of the
effects of amphetamine and physiotherapy after stroke. Cerebrovasc Dis 2001;12:253 – 7.
 Walker-Batson D, Curtis S, Natarajan R, et al. A double-blind, placebo-controlled study of the
use of amphetamine in the treatment of aphasia. Stroke 2001;32:2093 – 8.
 Smith BW. Modafinil for treatment of cognitive side effects of antiepileptic drugs in a patient
with seizures and stroke. Epilepsy Behav 2003;4:352 – 3.
 Grade C, Redford B, Chrostowski J, et al. Methylphenidate in early poststroke recovery:
a double-blind, placebo-controlled study. Arch Phys Med Rehabil 1998;79:1047 – 50.
 Scheidtmann K, Fries W, Muller F, et al. Effect of levodopa in combination with physiotherapy
on functional motor recovery after stroke: a prospective, randomised, double-blind study. Lancet2001;358:787 – 90.
 Pariente J, Loubinoux I, Carel C, et al. Fluoxetine modulates motor performance and cerebral
activation of patients recovering from stroke. Ann Neurol 2001;50:718 – 29.
 Pleger B, Schwenkreis P, Grunberg C, et al. Fluoxetine facilitates use-dependent excitability of
human primary motor cortex. Clin Neurophysiol 2004;115:2157 – 63.
 Bassetti CL. Sleep and stroke. Semin Neurol 2005;25:19 – 32.
 Greener J, Enderby P, Whurr R. Pharmacological treatment for aphasia following stroke.
Cochrane Database Syst Rev 2001;4:CD000424.
 Paolucci S, Antonucci G, Grasso MG, et al. Early versus delayed inpatient stroke rehabilitation:
a matched comparison conducted in Italy. Arch Phys Med Rehabil 2000;81:695 – 700.
 Kwakkel G, Wagenaar RC, Koelman TW, et al. Effects of intensity of rehabilitation after stroke:
a research synthesis. Stroke 1997;28:1550 – 6.
 Kwakkel G, Wagenaar RC, Twisk JW, et al. Intensity of leg and arm training after primary
middle-cerebral-artery stroke: a randomised trial. Lancet 1999;354:191 – 6.
 Langhorne P, Wagenaar R, Partridge C. Physiotherapy after stroke: more is better? Physiother
 Patten C, Lexell J, Brown HE. Weakness and strength training in persons with poststroke
hemiplegia: rationale, method, and efficacy. J Rehabil Res Dev 2004;41:293 – 312.
 Saunders DH, Greig CA, Young A, et al. Physical fitness training for stroke patients. Cochrane
 Bohannon RW, Walsh S. Nature, reliability, and predictive value of muscle performance mea-
sures in patients with hemiparesis following stroke. Arch Phys Med Rehabil 1992;73:721 – 5.
 Page SJ. Intensity versus task-specificity after stroke: how important is intensity? Am J Phys
 Wolf SL, Blanton S, Baer H, et al. Repetitive task practice: a critical review of constraint-induced
movement therapy in stroke. Neurologist 2002;8:325 – 38.
 Grotta JC, Noser EA, Ro T, et al. Constraint-induced movement therapy. Stroke 2004;35(Suppl 1):
 Moseley AM, Stark A, Cameron ID, et al. Treadmill training and body weight support for
walking after stroke. Cochrane Database Syst Rev 2003;3:CD002840.
 Albert ML, Bachman DL, Morgan A, et al. Pharmacotherapy for aphasia. Neurology 1988;38:
 Enderby P, Broeckx J, Hospers W, et al. Effect of piracetam on recovery and rehabilitation after
stroke: a double-blind, placebo-controlled study. Clin Neuropharmacol 1994;17:320 – 31.
 Berthier ML. Poststroke aphasia: epidemiology, pathophysiology and treatment. Drugs Aging
 McGuire JR, Harvey RL. The prevention and management of complications after stroke. Phys
Med Rehabil Clin N Am 1999;10:857 – 74.
 Lance JW. Symposium synopsis. Chicago7 Year Book Medical; 1980.
 Francisco GE, Hu MM, Boake C, et al. Efficacy of early use of intrathecal baclofen therapy for
treating spastic hypertonia due to acquired brain injury. Brain Inj 2005;19:359 – 64.
 Francisco GE, Boake C. Improvement in walking speed in poststroke spastic hemiplegia after
intrathecal baclofen therapy: a preliminary study. Arch Phys Med Rehabil 2003;84:1194 – 9.
 Roy CW, Sands MR, Hill LD, et al. The effect of shoulder pain on outcome of acute hemi-
plegia. Clin Rehabil 1995;9:21 – 7.
 Tobis JS. Posthemiplegic shoulder pain. N Y State J Med 1957;57:1377 – 80.
 Wanklyn P, Forster A, Young J. Hemiplegic shoulder pain (HSP): natural history and
investigation of associated features. Disabil Rehabil 1996;18:497 – 501.
 Yu DT, Chae J, Walker ME, et al. Intramuscular neuromuscular electric stimulation for post-
stroke shoulder pain: a multicenter randomized clinical trial. Arch Phys Med Rehabil 2004;85:695 – 704.
 Mayo NE, Korner-Bitensky N, Becker R, et al. Predicting falls among patients in a rehabilitation
hospital. Am J Phys Med Rehabil 1989;68:139 – 46.
 Salgado R, Lord SR, Packer J, et al. Factors associated with falling in elderly hospital patients.
 Vlahov D, Myers AH, al-Ibrahim MS. Epidemiology of falls among patients in a rehabilitation
hospital. Arch Phys Med Rehabil 1990;71:8 – 12.
 Tutuarima JA, van der Meulen JH, de Haan RJ, et al. Risk factors for falls of hospitalized stroke
patients. Stroke 1997;28:297 – 301.
 Nyberg L, Gustafson Y. Fall prediction index for patients in stroke rehabilitation. Stroke 1997;
 Byers V, Arrington ME, Finstuen K. Predictive risk factors associated with stroke patient falls in
acute care settings. J Neurosci Nurs 1990;22:147 – 54.
 Nyberg L, Gustafson Y. Patient falls in stroke rehabilitation: a challenge to rehabilitation strate-
 Rapport LJ, Webster JS, Flemming KL, et al. Predictors of falls among right-hemisphere stroke
patients in the rehabilitation setting. Arch Phys Med Rehabil 1993;74:621 – 6.
 Parikh RM, Lipsey JR, Robinson RG, et al. A two year longitudinal study of poststroke mood
disorders: prognostic factors related to one and two year outcome. Int J Psychiatry Med 1988;18:45 – 56.
 Robinson RG, Lipsey JR, Rao K, et al. Two-year longitudinal study of post-stroke mood dis-
orders: comparison of acute-onset with delayed-onset depression. Am J Psychiatry 1986;143:1238 – 44.
 Robinson RG, Starr LB, Kubos KL, et al. A two-year longitudinal study of post-stroke mood
disorders: findings during the initial evaluation. Stroke 1983;14:736 – 41.
 Robinson RG, Starr LB, Lipsey JR, et al. A two-year longitudinal study of post-stroke mood
disorders: dynamic changes in associated variables over the first six months of follow-up. Stroke1984;15:510 – 7.
 Astrom M, Adolfsson R, Asplund K. Major depression in stroke patients: a 3-year longitudinal
 Kase CS, Wolf PA, Kelly-Hayes M, et al. Intellectual decline after stroke: the Framingham
 Robinson RG, Kubos KL, Starr LB, et al. Mood disorders in stroke patients: importance of
location of lesion. Brain 1984;107(Pt 1):81 – 93.
 Robinson RG, Schultz SK, Castillo C, et al. Nortriptyline versus fluoxetine in the treatment of
depression and in short-term recovery after stroke: a placebo-controlled, double-blind study. AmJ Psychiatry 2000;157:351 – 9.
 Lazarus LW, Moberg PJ, Langsley PR, et al. Methylphenidate and nortriptyline in the treatment
of poststroke depression: a retrospective comparison. Arch Phys Med Rehabil 1994;75:403 – 6.
 Andersen G, Vestergaard K, Lauritzen L. Effective treatment of poststroke depression with the
selective serotonin reuptake inhibitor citalopram. Stroke 1994;25:1099 – 104.
 Raj A. Depression in the elderly: tailoring medical therapy to their special needs. Postgrad Med
 Bean JF, Vora A, Frontera WR. Benefits of exercise for community-dwelling older adults. Arch
Phys Med Rehabil 2004;85(7 Suppl 3):S31 [quiz: S3–4].
 Verghese J, Lipton RB, Katz MJ, et al. Leisure activities and the risk of dementia in the elderly.
 Waller PF. Alcohol, aging, and driving. In: Gomberg ESL, Hegedus AM, Zucker RA, editors.
Alcohol problems and aging. NIAAA Research Monograph No.33. Bethesda7 NIAAA; 1998.
 Carr DB. The older adult driver. Am Fam Physician 2000;61:141–6, 8.
 Kelly R, Warke T, Steele I. Medical restrictions to driving: the awareness of patients and doctors.
Developing World Bioethics ISSN 1471-8731 (print); 1471-8847 (online) Volume 4 Number 1 2004 PATENTS AND ACCESS TO DRUGS IN DEVELOPING COUNTRIES: AN ETHICAL ANALYSIS More than a third of the world’s population has no access to essentialdrugs. More than half of this group of people live in the poorest regionsof Africa and Asia. Several factors determine the accessibility of drugs indeveloping
SBS INSIGHT ARCHIVES - May 22, 2007 DOSE OF REALITY There are now more people being treated for attention deficit hyperactivity disorder than ever before. In 10 years the number of Australians taking medication for ADHD has doubled. Recently the biggest increase has been in adults and girls. Some are worried the condition is being over diagnosed and that the medication is potentia