Sue Ann Sisto
INTRODUCTION
Physical therapists are responsible for the exercise prescription and management of patients with neurological disorders. Physical therapists can best treat patients with neurological illnesses by focusing on neurological impairments, functional limitations, and participation outcomes while considering the cardiopulmonary system. The cardiopulmonary system plays an important role in functional activities because of its role in transporting oxygen to skeletal muscle. Abnormalities in the cardiopulmonary system can produce limitations in movement and thus functional outcomes.
Patients with neurological deficits have a particular problem of deconditioning due to hospitalization or inactivity as a result of their disease or illness. This deconditioning could mean the difference between independence and dependence in activities of daily living (ADL). Physical therapists are the first health care professionals to note the functional impact of cardiopulmonary limitations because of the way that their patients are challenged through exercises and position changes in the provision of physical therapy.
Furthermore, physical therapists can contribute to the prevention of cardiopulmonary complications of immobility, weakness, and exercise intolerance. Individuals with neurological injuries, who are within age ranges where cardiac risk factors are high, may be even more at risk during activity or exercise. In the existing health care environment, these neurological patients may be discharged from the acute care hospital in a fragile cardiopulmonary state. Therefore, significant focus must be placed on the cardiopulmonary status of patients with neurological illnesses who demonstrate activity and exercise risk factors.
It is ultimately the intent of this chapter to make the reader familiar with the Guide to Physical Therapist Practice (2nd ed.) as it relates to evidence-based treatment of cardiopulmonary disorders for neurological patients. Therapists must select the primary practice pattern that is evident at the time of intervention, taking into account all comorbid conditions. When patients with neurological disorders are “triaged” into the cardiopulmonary practice patterns, it is assumed that the cardiopulmonary status becomes the primary focus of the intervention. With this in mind, this chapter provides guidelines regarding the factors associated with activity and exercise that influence the exercise ability for patients with neurological impairments. This chapter also makes recommendations for common tests and measures used for exercise testing and describes the physiological responses to exercise, including the effect of medications. Finally, the intent is to make recommendations for exercise training interventions and identify other benefits of exercise for patients with neurological disorders.
NEUROLOGICAL DIAGNOSTIC CATEGORIES
Stroke (Practice Patterns 5A, 5D, 5I, 7A; ICD-9-CM Code: 342)
Stroke, or cerebrovascular accident (CVA), is the result of a thrombus or hemorrhage in the brain, producing an area of infarct. This region produces neurological impairments that may result in significant disability. Indeed, stroke is the leading cause of serious, long-term disability in the United States, where 15% to 30% of stroke survivors are permanently disabled1 with $3.8 billion paid to Medicare beneficiaries.2 According to the World Health Organization (2002), 15 million people suffer stroke worldwide each year.1
There are nearly 4.7 million stroke survivors alive in the United States and 2.3 million are men and 2.4 million are women. There are approximately 700,000 new strokes annually where 500,000 are new strokes and 200,000 are recurrent strokes. Approximately 15% to 30% of individuals who sustain a stroke are permanently disabled (Survey of Income and Program Participation [SIPP]).2 When considered separately from other cardiovascular diseases (CVDs), stroke ranks as the third leading cause of death after diseases of the heart and cancer. The mean age of onset of stroke is 66 years, and 28% of people who suffer a stroke in a given year are younger than 65 years. At all ages, more women die of stroke than do men. Compared with white men 45 to 54 years old, African American men in the same age group have a threefold greater risk of ischemic stroke. The proportion of strokes that result in death within 1 year is approximately 29% and is less if the stroke occurs before the age of 65 years.3
Physical activity, including moderate-intensity exercise such as walking, is associated with a substantial reduction in risk of ischemic stroke in women.4 Studies have found an association between physical inactivity and the risk of stroke5,6 and have estimated that 79% of strokes could be averted through regular exercise and avoidance of both smoking and obesity. Walking for the prevention of CVD, in particular ischemic stroke, was related to the higher walking duration, distance, pace, and energy expenditure.7 A study of 37,000 women aged 45 years and older participating in the Women’s Health Study (2006) suggests that a healthy lifestyle consisting of a low body mass index (BMI), regular exercise to name a few, significantly reduced the risk of total and ischemic stroke but not hemorrhagic stroke.8 A meta-analysis of reports of 31 observational studies conducted mainly in the United States and Europe found that moderate and high levels of leisure time and occupational physical activity protected against all stroke types.9
CVD is the most common cause of death in long-term survivors of stroke, which argues for the importance of exercise and activity when guided by an optimal cardiopulmonary examination.10 Because atherosclerosis is typically the underlying disease process, coronary artery disease (CAD) frequently coexists in patients with stroke. Approximately 75% of individuals who have had a stroke have heart disease11 (ICD-9-CM Code 411). Besides cardiac disease, other risk factors for developing CVA include hypertension (ICD-9-CM Code 401), abnormal plasma lipid profiles (ICD-9-CM Code 272), obesity (ICD-9-CM Code 278), and insulin resistance, potentially resulting in diabetes (ICD-9-CM Code 250).12 Reduction of these risk factors could be addressed through the use of Practice Pattern 6A, Primary Prevention/Risk Reduction for Cardiovascular/Pulmonary Disorders.
The Guide to Physical Therapist Practice (2nd ed.) focuses on the practice patterns for stroke in the neuromuscular section (Patterns 5A, 5D, and 5I). This is because, early after a stroke, interventions primarily address the paralysis involving the neuromuscular system. However, a patient who sustained a stroke beyond 3 to 6 months will continue a downward course of deconditioning, requiring greater focus on the cardiopulmonary system practice patterns. Practice Pattern 6B would address those patients with stroke whose aerobic capacity and endurance were limited because of deconditioning. If comorbid conditions such as a previous myocardial infarction or ventilatory pump dysfunction were also present, Practice Patterns 6C, D, and E should be considered.
Factors That Influence Ability to Exercise
There are morphological changes that exist with aging and that affect the stroke population because of the average age of onset (66 years). Cardiac-related changes affect cardiac tissue and chambers, the conduction system, and the coronary arteries. Cardiac function in healthy older people may be adequate to meet the body’s need while at rest and is maintained by increases in stroke volume and ejection fraction because of increased cardiac filling (preload).13This, however, may be inadequate for patients with neurological disorders when participating in exercise tasks such as ambulation that is commonly prescribed by physical therapists. The energy demands placed on individuals who have suffered a stroke are thought to be at least 50% greater for walking because of the biomechanical challenges of gait.14 Standard exercise, such as ambulation training, may place a significant demand on an already-compromised cardiovascular system. Therapists must be aware of the potential for patients with stroke who have a compromised cardiovascular system and provide proper monitoring of exercise intensity.
Changes in muscle composition following stroke may also limit exercise participation. Ryan and associates observed a strong relationship of 
to thigh lean tissue mass as measured by dual X-ray absorptiometry (DXA). There was gross muscular atrophy and metabolic and muscle phenotype changes that were reported to possibly predispose patients with stroke to fatigue. Computed tomography (CT) scans of the mid-thigh muscle area in 30 patients with stroke were 20% lower in the hemiparetic thigh, with a 25% relatively higher fat content, compared with those of the non–hemiparetic thigh (P < 0.001).15 Heydrick identified, based on a shift to a lower frequency and higher amplitude, spectral profile of electromyography signals. This change corresponded with improved muscle recruitment after treadmill training, a loss of slow-twitch (oxidative) muscle fibers, and anaerobic metabolism in the hemiparetic leg.16 However, more research is needed to demonstrate the effects of strength training on muscle adaptation in patients with hemiparesis and its effect on exercise capacity. Gerrits and colleagues (2009) studied the strength of the knee extensors bilaterally after stroke by using maximal voluntary torque and half relaxation time compared with controls.17 The authors reported that aside from bilateral weakness in the stroke group, the knee extensors showed a lower rate of torque development and relaxation bilaterally compared with controls and concluded that these changes may be related to changes in the muscle reported in other studies.
The level of motor impairments is a definitive factor for patients with stroke participating in exercise. For example, patients with stroke frequently demonstrate flaccid and/or spastic limbs with sensory impairments. Walking on a treadmill the sound limb may propel the paretic limb because of the cyclical nature of walking and the use of momentum; however, the contribution of the paretic limbs can be limited. In more severe cases of motor impairment, treadmill walking is limited by reduced trunk balance. In this case, seated ergometry may be used. Furthermore, the hemiparetic/hemiplegic leg may make very little contribution to the walking or cycling motion. Despite the lesser contribution of the hemiparetic limb to exercise, there still may be enough work output to produce aerobic conditioning.
Other comorbid pathologies common to this age group may limit exercise participation. Endocrine abnormalities, in the form of insulin resistance, have been reported to further potentiate the risk of CVD.18 Almost all patients with neurological dysfunction have a form of restrictive lung disease due to decreased chest wall movement resulting from the paralysis. Patients with neurological disease are, therefore, at risk for atelectasis and pneumonia. Osteoarthritis may limit an individual’s ability to ambulate, propel a stationary bicycle, or climb stairs. Peripheral vascular disease may limit walking or cycling ability due to leg pain or swelling. Diabetes or hypertension will put the patient with stroke at greater risk of cardiac pathology or exercise intolerance. The practice patterns and ICD-9-CM codes of the potential comorbid conditions of patients with stroke are summarized in Table 14-1.
TABLE 14-1 Common Comorbid Pathologies, Practice Patterns, and ICD-9-CM Codes Associated with Stroke
Impairments such as the loss of proprioception may not only limit motor performance during exercise but also lead to injury. For example, the patient may lack awareness that the ankle is excessively inverted during gait, which may predispose the patient to an ankle sprain. Mental confusion or dementia may be present in addition to the cognitive limitations that are coincident with stroke. This often limits a patient’s ability to either follow directions during exercise or adhere to an unsupervised exercise program. Special attention must be paid to these age- or diagnostic-related changes that are noncardiopulmonary precautions during exercise.
Tests and Measures for Exercise Testing
A few studies have measured peak exercise capacity in patients with stroke, resulting in lower functional capacities.14,19 This is most likely due to the reduced number of motor units available for recruitment during exercise. Additionally, reduced oxidative capacity and overall poor endurance further limit functional capacity. Patients with stroke are unable to achieve the same workload as age-matched control subjects during leg ergometry.20,21
Exercise testing is necessary to determine the presence and severity of cardiac disease and resultant functional limitation, if any. A few studies have examined the exercise capacity of hemiparetic populations. MacKay-Lyons et al.22evaluated exercise capacity in 29 patients with acute stroke (<1 month), using open-circuit spirometry during maximal treadmill walking effort with 15% body weight support. Mean 
was 14.4 mL/kg/min or 60% of age-predicted normative values for sedentary individuals. These values were similar to past values reported for patients with myocardial infarction.20–26 Comparisons are difficult when the modes of exercise used for testing are different (ie, leg ergometry vs arm or supine ergometry). A summary of published data of the acute peak exercise responses in patients with hemiparesis can be found in Table 14-2.
TABLE 14-2 Cardiovascular Responses at Peak Exercise Testing in Stroke
Because of the presence of CAD, a physician trained in using continuous electrocardiogram (ECG) monitoring should supervise exercise testing. The reasons for implementing an exercise test for patients with stroke would be either to determine the presence and severity of heart disease and/or to determine functional status. If there is a previous history of myocardial infarction with resultant myocardial ischemia, ST-segment depression will appear on the ECG during the test. The level of exercise, at which these ECG changes become significant, can provide guidelines for a safe exercise prescription.
CLINICAL CORRELATE
Exercise testing should be coupled with Borg’s28 ratings of perceived exertion (RPE) at each workload (see Chapter 9).
This will allow the therapist and the patient to use this perceived intensity rating during subsequent exercise training sessions or when ECG monitoring is not possible. As the patient’s fitness level increases, the ratings of perceived exertion (RPE) will diminish at the same submaximal exercise level. This should signal the therapist to increase the training workload, while maintaining the target RPE level.
If peak or maximal exercise cannot be accomplished during the test, a submaximal exercise test can be used to determine a safe level for the patient’s exercise program. Nomograms29 can be used to determine estimates of maximal aerobic power (
) from the submaximal oxygen consumption. Some caution must be taken because this nomogram applies to healthy individuals. Because nomograms are not available for patients with stroke, exercise capacities are likely to be overestimated. However, Birkett and Edwards30 determined that unilateral arm-cranking exercise could be used to predict an individual’s upper-body aerobic exercise capacity by using heart rate (HR). This is particularly helpful in hemiplegia when arm-crank exercise is accomplished by a single arm. Furthermore, a comparison of the HR at the same submaximal workload before and after an exercise training program can document changes in cardiorespiratory fitness. A decrease in the HR after exercise training for the same workload as prior to training is interpreted as improvement in aerobic capacity or fitness. See Chapters 9 and 10 for general guidelines for exercise testing.
The choice of exercise modality will be dependent on the degree of motor impairment. Treadmill walking, for example, may be appropriate only for patients with mild-to-moderate functional impairments. However, the recent introduction of overhead harness devices enables severely involved patients to be treadmill tested. These devices support the patient by means of a metal frame surrounding the treadmill, from which is suspended a canvas vest. The patient is fitted into the vest, which is used to unweigh the body. Harness devices allow the patient with hemiplegia to ambulate safely on a treadmill and also facilitate gait training. Patients should be able to walk independently with a cane or be able to sustain independent ambulation with the support of a treadmill handrail. Walking speeds are typically much slower, and energy expenditure usually is approximately 55% to 65% higher than that in age-matched healthy subjects. It is recommended that the workload increments are organized so that the total exercise time is between 8 and 12 minutes. Therefore, exercise protocols may need to increase the intensity very gradually using protocols such as the Naughton–Balke or modified Balke,31 where the velocity remains constant and only the grade is increased gradually. Target velocity can be determined by a preliminary treadmill exercise test.14
In target cases where patients fatigue easily, an intermittent protocol may be appropriate. This protocol intersperses brief rests between progressively increasing workloads. For example, a patient with stroke may begin a treadmill exercise test at 1 mph for 2 minutes. After a 1-minute rest, the treadmill may be advanced to the next workload, 1.5 mph, again followed by a rest. This progression/rest approach allows for the HR to progress to the highest possible rate, while accommodating for those neuromuscular deficits requiring intermittent rest.
For leg cycle ergometry, a pedaling rate of 50 rpm, starting at 20 W and increasing by 20 W per stage is the general guideline; however, test protocols may have to be determined individually. Maximal HR is similar to the treadmill walking protocol, but the peak oxygen uptake is 10% to 15% higher with treadmill testing.32
Combined arm and leg ergometry can be used when spasticity and weakness prohibit sufficient elevation of the HR by using a single upper or lower limb individually. When combining the arm and leg, patients can use both limbs to achieve a maximal effort. Because of muscle fatigue, an intermittent protocol again may be advisable. If the person has poor sitting balance, arm ergometry can be done from the wheelchair and leg ergometry can be done in the supine or semireclined position.33
To estimate the workload for leg ergometry, several equations have been proposed.34–37 These equations involve the use of specific anthropomorphic information to estimate the maximal workloads. For example, Jones and associates34 determined that maximal power output could be estimated by the following equations:
Work capacity (kpm/min) for males = 1,506 × [height (m) × 2.7] × [age − 0.46];
Work capacity (kpm/min) for females = 969 × [height (m) × 2.8] × [age − 0.43].
Caution must be taken when using these equations to estimate maximal workloads for arm ergometry. These equations may overestimate the maximal workload because arm ergometry work capacity is less than that accomplished by the legs. Furthermore, these equations are based on samples of healthy men and women without neurological disability. Therefore, these equations could significantly overestimate the work capacity of individuals with stroke. Workload is often determined empirically, in which case the tester identifies a comfortable workload and increases the workload until the person can no longer continue.
The functional disability of stroke is compounded by the presence of CAD in some individuals. In some cases, patients with stroke and cardiac pathology may wear a Holter monitor, a portable device that is worn around the neck with chest electrode attachments that records continuous 24-hour ECGs. Cardiac monitoring could then be conducted during physical therapy. This would enable the physician to determine the HRs of functional tasks that produce either ischemia or arrhythmia.11 Continuous ECG monitoring can thus provide the physical therapist with an HR limit to the exercise prescription that is specific to functional tasks.
Assessment of peak oxygen consumption () by using traditional modes of testing such as treadmill or cycle ergometer can be difficult in individuals with stroke due to balance deficits, gait impairments, or decreased coordination. Billinger et al. (2008) found that a total-body recumbent stepper may be a safe, feasible, and valid exercise test to obtain measurements of and prescribe aerobic exercise in people with stroke.38 Eleven participants performed two maximal-effort–graded exercise tests on separate days to assess cardiorespiratory fitness. The authors reported a strong relationship between the total-body recumbent stepper and the cycle ergometer exercise test for and peak HR (r = 0.91 and 0.89, respectively); however, the mean was significantly higher for the total-body recumbent stepper. Therefore, the mode of testing must be considered when comparing changes in cardiorespiratory fitness within patients and across studies. A summary of exercise testing guidelines can be found in Table 14-3.
TABLE 14-3 Summary of Exercise Testing Guidelines for Stroke
Potential Physiological Responses to Exercise
Hemiparesis resulting from stroke produces physiological changes in muscle fibers and muscle metabolism during exercise. One study found that there was a greater percentage of type 2 fibers of the anterior tibialis muscle of 10 ambulatory patients with hemiparesis and spastic gait compared with young and older healthy controls.39 This study suggested that many motor units are never recruited in the paretic muscle during slow walking. This reduced proportion of type 1 fibers leads to diminished capacity for oxidative metabolism and low endurance. High-intensity aerobic exercise has the potential to minimize these effects by enhancing motor unit recruitment favoring the development of high-oxidative muscle fibers. Ambulatory persons with stroke may be able to perform approximately 70% of the peak power output that can be achieved by age-matched persons without CVA. Paretic muscles are deconditioned and demonstrate increased lactate production, reduced blood flow, and altered fiber-type composition. These physiological changes could be due to changes in the relative proportion of fiber types.40 However, Sunnerhagen and colleagues41 did not find major differences in fiber-type composition between the affected and the less-affected legs in high-functioning patients with stroke. These individuals did, however, demonstrate underlying weakness, and the authors concluded that strength training might be indicated. At present, we do not completely understand the effects that exercise has on fiber-type proportion poststroke. It may be possible to impact the muscle fiber–type proportion of patients with stroke as a result of strengthening exercises with more severely involved patients.
Interventions for Exercise Training
Clinical evidence of CVD may delay intensive exercise and limit functional recovery. However, when patients with stroke have progressed beyond the initial rehabilitation phase, a monitored aerobic training program may not only improve endurance and functional capacity but also reduce the risk for subsequent cardiovascular and cerebrovascular events. Therefore, endurance training is recognized as an important component of rehabilitation and long-term maintenance of health.
Potempa and colleagues reported approximately a 13% increase in 
after a 10-week supervised aerobic training program. The improvements were related to improvements in sensory motor function, therefore suggesting that aerobic training can also improve these neuromuscular impairments.25 Fletcher and colleagues42 demonstrated an increase in exercise endurance and reduction in resting HR as a result of a home exercise program consisting of arm ergometry for 5 days a week for 6 months. Using an adapted bicycle ergometer, Fletcher and colleagues found that a 10-week long, gradually progressive training program produced an increase in maximal oxygen consumption, workload, exercise duration, and a reduction in systolic blood pressure (BP) at submaximal workloads.26 Duncan et al.27 studied 100 patients with subacute stroke for recovery of function. She stratified them according to whether they received structured, physiologically based exercise or “usual care.” The exercise group showed improvement in , duration of exercise, 6-minute walk velocity, and gait velocity.
Survivors of stroke exhibit a peak oxygen uptake of about half their age-matched counterparts, leaving tremendous room for improvement. Peak fitness levels have been reported to be 44% lower than that of age- and gender-matched sedentary controls10 with levels of 14.7 ± 4 mL/kg/min. Furthermore, Macko et al.14 reported that 31 patients with stroke used 66% of peak oxygen capacity to walk on a treadmill with handrail support at a pace that is 75% slower than their self-selected floor-walking velocity. If patients with stroke could participate in exercise training, emerging studies project that there would be as much as a 60% to 70% increase in and a 100% to 150% increase in self-selected walking speed. Additionally, an overall reduction in the amount of assistive devices and physical assistance needed would result from participating in exercise training.33
Macko et al.19 studied fitness reserve in 21 patients with chronic stroke to evaluate whether treadmill training reduced the energy cost and improved peak fitness during gait. increased from 15.4 to 17.0 mL O2/kg/min and lowered oxygen demand at submaximal levels. Patients were able to use 20% less peak exercise capacity to accomplish more work.
Rimmer et al. (2009) compared the effects of three different exercise training regimens on cardiorespiratory fitness and coronary risk factor reduction in subjects with unilateral stroke. Participants exercised three times per week on either a stationery bike or a recumbent stepper.43 Participants were assigned to a moderate-intensity, shorter duration (MISD) exercise group where they gradually increased exercise intensity while keeping exercise duration constant or to a low-intensity, longer duration (LILD) exercise group where they gradually increased the duration to 60 minutes while keeping exercise intensity constant or to a conventional therapeutic exercise (TE) group consisting of strength, balance, and ROM activities. The MISD group attained improvements in BP and total cholesterol (TC) compared with the other groups and both MISD and LILD groups showed significant reductions in total cholesterol compared with the TE group. However, in this study there was no significant change in and submaximal 
in any of the groups despite the significant gains in coronary risk reduction compared with TE group. Thus, aerobic exercise after stroke may reduce cardiac risk factors even if there is no significant change in fitness. This approach could have potential to reduce the occurrence of recurrent strokes and other neurological events.
Training modality—The training modality depends on the severity of the motor impairments. Typical modalities include treadmill, arm- or leg-crank ergometry, or a combination of the two. Body weight–supported (BWS) ambulation may be useful for moderate to severely impaired patients with stroke, where the body weight is supported by an overhead harness while walking on a treadmill or overground if the harness system is mobile. As the patient progresses in their ambulation independence, more body weight can progressively be assumed by the patient by decreasing the overhead support. However, Hesse and associates44 compared a machine BWS device to a standard treadmill with support provided by two therapists. The machine providing the partial BWS that allowed for the improved ambulation of severely disabled patients with hemiparesis and requiring only one therapist for assistance.
Treadmill training with partial body weight support in subjects with hemiparesis allows practice of gait characterized by greater balance, higher symmetry, and less spasticity as compared with floor walking. Visintin and colleagues45reported better mobility outcomes with BWS treadmill training when compared with traditional treadmill training with full weight bearing of 100 patients with stroke. Walking speed and overground walking endurance improved significantly after 6 weeks of training.
Electrical stimulation (ES) on a recumbent bicycle has been explored in chronic stroke. Janssen et al. (2008) demonstrated that a short cycling training program on a semirecumbent cycle ergometer could markedly improve cycling performance, aerobic capacity, and functional performance of people with chronic stroke.46 The authors evaluated whether leg cycling training in 12 subjects with chronic stroke can improve cycling performance, aerobic capacity, muscle strength, and functional performance and determined whether ES to the contralateral (paretic) leg during cycling has additional effects when performed twice a week for 6 weeks compared with a group who also received ES but with no visible contraction. Aerobic capacity and maximal power output significantly increased but muscle strength was not significantly enhanced after training. The use of ES had no additional effects in this specific group of subjects with chronic stroke and it should be noted that the aerobic and cycling performance effects were not related to functional performance.
Duration—The duration of training will depend on initial fitness level and may initially require intermittent bouts during each session. Cardiopulmonary exercise may last 20 minutes for 10 to 12 weeks. Most exercise programs demonstrate their efficacy by improving fitness, increasing oxygen utilization by muscle, decreasing the need for myocardial work, and reducing the progression of CAD using a frequency of exercise for 3 to 5 times per week.26,42
Intensity—HR, as a percentage of the age-predicted maximum, is a useful guide to establish the intensity of exercise. The window to produce aerobic training effects is approximately 60% to 85% of this predicted maximum. This guideline should be adhered to provided the patient is not on medication that restricts HR, in which case RPE should be used. If a or was obtained, the HR at 40% to 60% of the measured or of continuous or discontinuous exercise would be recommended. The training intensity should be increased as tolerated. Wearing a portable chest-worn HR monitor allows for continuous monitoring of HR during training and has the benefit of feedback to the patient as to the gains in fitness. As fitness improves, patients will either be able to walk faster or farther at the same absolute HR. Sufficient warm-up and cool-down periods (10 minutes each) should be included to prevent negative musculoskeletal and cardiovascular effects. A summary of the exercise training for cardiovascular fitness is found in Table 14-4.
TABLE 14-4 Exercise Training Studies for Patients with Stroke
Influence of medications on ability to exercise—Patients on vasodilators will require a longer cool-down period after exercise to prevent hypotension. Patients on medications to reduce cardiac output by reducing HR will demonstrate lower peak HRs during exercise. Patients using diuretics may exhibit arrhythmias due to lower fluid volume that alters electrolyte balance. Interactions of all pharmacological agents to each other during exercise must be understood. For a complete review of medications that impact on the cardiovascular and pulmonary systems, see Chapter 8.
Other responses to exercise—Exercise risk factors such as hypertension can be reduced through exercise intensities of 40% to 70% peak O2 consumption.49 There is a discrepancy between the self-perception of physical activity that was measured using self-report questionnaires, step activity monitors, self-efficacy expectations related to exercise, and from treadmill testing. Resnick reported that there were significant discrepancies between subjective (self-efficacy expectations) and objective findings helping to understand the perspective of stroke survivors with regard to physical activity.50
The effects of exercise on patients with stroke may also have an effect on the immune system. Physical exercise has been reported to activate the immune system. Therefore, exercise should be considered for its possible prevention of infectious diseases that are often complications for patients with stroke.51 Approximately 33% of these patients suffer from depression during their rehabilitation period.52 The benefits of exercise for patients with depression in general have been established.53 Therefore, it is likely that exercise will ameliorate depression in patients with stroke. Although no studies have published the effects of exercise on bone mineral density, we know that bone mineral density decreases with age and inactivity for patients with CVA.54 Therefore, it is reasonable to expect that exercise would reduce this loss in these patients who are at increased risk of osteoporotic fractures.
General Effects of Exercise Training on Impairment, Disability, and Quality of Life
Studies have demonstrated a very positive effect of exercise in patients with stroke, including improvements in gait and endurance. One study examined the effect of 6 months of low-intensity aerobic exercise in patients with chronic stroke and found a substantial and progressive decrease in energy cost and cardiovascular demands.14 Six weeks of treadmill training with up to 40% body weight support for approximately 15 minutes, four times per week, resulted in better gait and overground walking endurance. Walking speed was measured by taking the middle 3-m velocity while subjects walked on a 10-m walkway. Walking endurance was recorded as the amount of distance an individual could walk until they could no longer continue, up to a maximal distance of 320 m.45 BWS treadmill training, in addition to neurological physical therapy, was also reported to improve functional gait and walking velocity in seven nonambulatory patients with stroke.44
Another 8-week study of supervised home exercise, three times a week, produced an increase in median gait velocity, an increase in the 6-minute walk test time, and an increase in the health-related effects impact physical functioning on quality of life (QOL).48 Perceived quality impact life relating to health factors was also improved after 10 weeks, three times a week, of aerobic exercise and lower extremity strengthening in patients with chronic stroke (post 9 months). This was in addition to improved gait speed, rate of stair climbing, and increased activity.47 Silver and colleagues55 reported an improvement with patients in the get up and go test, whereas Smith and colleagues56 demonstrated an increase in torque-generating capacity across the knee of patients with chronic stroke who participated in treadmill training.
The activity profiles of walking for patients with stroke are 571 steps/d; 99% of the time is spent at less than 99 steps/min as measured by a step activity monitor. This activity profile may be compared to the findings of Gardner and associates,57 who found that healthy subjects completed 8,672 steps/d compared with those with peripheral arterial occlusive disease. Therefore, general real-world activity is significantly reduced in stroke.
Exercise appears to have great benefit on patients with stroke, provided it is implemented cautiously. Screening for the appropriateness of exercise must be made on patients with unstable cardiopulmonary symptoms: respiratory distress, hypo- or hypertension, dyspnea, unstable angina, congestive heart failure, or unstable arrhythmias. HR and BP should be monitored before, during, and after exercise. If exercise is progressed prudently, it may also have additional health benefits through the reduction of significant cardiac risk factors.
Traumatic Brain Injury (Practice Patterns 5D; ICD-9-CM Codes: 800, 801, 803, 804, 850, 851, 852, 853, 854, 994)
Traumatic brain injury (TBI) occurs at a rate of approximately 500,000 new cases per year in the United States. The most frequent cause of TBI is motor vehicle accidents closely followed by gunshot wounds. TBI can result in motor impairments similar to that which occurs in stroke; however, the major difference is that patients with TBI are primarily young people who usually do not have underlying medical problems. Cognitive disturbances are the primary disability resulting from TBI and may include agitation, memory disturbances, and learning difficulties. One retrospective 10-year follow-up study of recovery of function following patients with severe TBI demonstrated continued improvement in social, cognitive, physical, and emotional functioning for at least 10 years postinjury. This implies that exercise intervention could promote improvement of function throughout this extended recovery period.58
Factors That Influence Ability to Exercise
As in all cases of neurological disease or illness, the ability to exercise depends on the severity of neurological impairment and cognitive disturbance. Factors that might affect exercise performance are listed in Box 14-1.
BOX 14-1
Summary of Factors That Influence Exercise Performance in Patients with TBI
•Cognitive deficits
•Emotional lability
•Communication deficits
•Dysautonomia
•Orthopedic deficits
•Respiratory difficulties
•Malnutrition
•Seizure disorder
Significant cognitive limitations can cause intellectual deficits, making exercise instructions difficult to comprehend and therefore, limiting compliance. Behavioral/emotional problems can impede the success of an exercise intervention program because of the patient’s inability to maintain stable emotions, making communication during exercise training difficult. Dysautonomia or dysregulation of the autonomic nervous system because of severe diffuse axonal injury and brain hypoxia is associated with a poorer outcome,59 limiting the effectiveness of an exercise program because of the severity of brain damage. TBI can result in significant orthopedic deficits occurring at the time of the injury, which can impair the patient’s ability to exercise or require modifications to the exercise modality.33
Most individuals who had suffered a TBI had been intubated and had a subsequent tracheostomy during the acute and subacute phases of recovery. The tracheostomy tube may remain in place for some time because of ongoing build-up of pulmonary secretions or because of sleep apnea. Ideally, the tracheostomy tube decreases both dead space and resistance from the oral cavity, making exercise more tolerable. However, a patient with a tracheostomy tube may find it uncomfortable to exercise because of the expulsion of secretions through the tracheostomy tube brought about by increased ventilation. In some cases, adequate respiration can be accomplished by temporarily closing the tube with the cap to achieve full ventilation by mouth. However, in other cases, it may be necessary to refrain from excessive exertion until the tracheostomy tube is removed.
Another factor associated with TBI that can influence exercise performance is relative malnutrition. A marked catabolic response with a negative nitrogen balance can result in subsequent dietary muscle wasting. Therefore, the appropriate fuel substrate may not be available during exercise training to enhance fitness or the development of muscle mass. This relative malnutrition may persist for a number of months after injury and may require dietary supplementation.
Patients with TBI also may be prone to seizures, especially during exercise testing where hyperventilation is usually induced. Although there is little evidence of the effect of exercise on seizure activity in TBI, one study of 204 patients with epilepsy determined that in a majority of the patients physical exercise had no adverse effects.60 A considerable proportion (36%) claimed that regular exercise contributed to better seizure control. However, in approximately 10% of the patients, exercise appeared to be a seizure precipitant. The authors concluded that for individuals with epilepsy, the risk of sustaining serious seizure-related injuries during exercise seemed modest. Because similar studies have not been conducted in TBI, caution is advised to ensure appropriate therapeutic anticonvulsant medication levels before exercise testing and training. Appropriate medical supervision should be present during initial testing when rigorous exercise is involved, even when anticonvulsant medications have been taken.
Tests and Measures for Exercise Testing
A consensus statement by rehabilitation professionals from Quebec identified four health-related risk factors that should be included in fitness screening for patients with TBI.61,62 These include angina pectoris, aortic stenosis, and exertional syncope. Outward aggression, pulmonary embolism, uncontrolled epilepsy, and ventricular arrhythmias can also be exacerbated by exercise. Identifying these risk factors prior to the implementation of an exercise program may help either to exclude inappropriate candidates for exercise or to trigger increased medical supervision during the initial prescription period.
There are few exercise studies that have evaluated the effects of exercise on cardiopulmonary function for patients with TBI. Hunter and colleagues63 performed progressive exercise tests on 12 subjects with closed TBI by using a treadmill, a bicycle ergometer, and mechanical stairs. The treadmill and stairs produced the higher oxygen consumption and may be a more accurate measure of maximal exercise performance in this population. Jankowski and colleagues64 tested 14 sedentary adults with TBI for submaximal peak rate of oxygen consumption. These authors determined that the TBI patients demonstrated a subnormal oxidative capacity and an above-average oxygen cost of locomotion.
The 20-m shuttle walk/run test has been demonstrated as a reliable field test for aerobic capacity of patients with TBI.61 This is a cardiovascular field test that involves walking or running a 20-m shuttle course while maintaining the pace determined by signals from an audiotape (see Chapter 9). The initial slow walking pace of 2.4 km/h was gradually increased each minute until the patient could no longer continue. The shuttle walk/run test, when compared with ergometer and treadmill tests,65 has been reported to produce an underestimation of peak for healthy fit males. However, when standardized exercise testing equipment may not be available, the shuttle walk/run test may be the most reliable alternative. The key to the reliability of all walk tests is the standardization of testing methods and instructions.
In general, the considerations in exercise testing in TBI that may be different from those in stroke are that motor impairments may involve all limbs rather than affecting one side. In addition, cognitive behavior may limit a patient’s ability to understand the purpose of a maximal exercise test. If agitation is present, patients with TBI may not be willing to wear a face mask or mouthpiece necessary for metabolic testing. Finally, there may be significant dysautonomia due to involvement of the subcortical and brainstem structures at the time of the brain trauma. These autonomic problems may present with abnormal HR and BP responses during exercise testing. Careful monitoring with the supervision of a physician is recommended.
Otherwise, an incremental graded exercise test will be sufficient to achieve a maximal effort because CVD is likely not a problem in this population, who generally are young and not at risk. A discontinuous protocol is usually not required because of the young age but may be required if there are significant motor impairments. In this case, other modes of exercise testing such as bicycle or leg ergometry may allow the patient to reach a higher workload.
Interventions for Exercise Training
Few studies exist that evaluate the effect of exercise training in TBI. This is likely due to the wide variability in physical performance across patients and because of the important focus on the cognitive behavior of these patients in the earlier stages of recovery. The physical impairments generally are not as severe as the cognitive. However, Hunter and colleagues63 evaluated a 3-month conditioning program in 12 patients with TBI and closed head injury. The exercise consisted of aerobic and flexibility exercises for 50 minutes for 12 weeks. Maximal power output increased on the treadmill, bicycle ergometer, and mechanical stairs and resting HR decreased. Maximal oxygen consumption increased to 75% to 85% of their predicted values.
Jankowski and colleagues64 conducted a 16-week circuit-training program of moderate intensity (2 hours) and prolonged duration (three times a week for 6 weeks). The aerobic stations of the circuit consisted of cycling, rope skipping, jogging, and stair climbing. While there was an increase in oxidative capacity, there was a failure to reduce oxygen cost while walking. Wolman and associates66 found improvements in exercise duration and maximal workload for patients with TBI who participated in a 6-week program of biking. However, Mossberg et al.67 evaluated the cardiorespiratory response to treadmill exercise on admission and discharge in 40 individuals with acquired brain injury. Total ambulation time increased and submaximal HR decreased, suggesting improved aerobic capacity. Peak HR and 
did not change. Mossberg et al. later (2008) studied the effect of body weight–supported treadmill training (BWSTT) on cardiorespiratory adaptations on two patients with TBI.68 Each patient received two to three sessions of BWSTT per week. Aerobic capacity was measured while they ambulated on a treadmill without BWS before and after BWSTT and both patients’ submaximal and peak responses improved including treadmill work performed, peak oxygen uptake, and estimated cardiac stroke volume (oxygen pulse). This case report suggests that BWSTT has the potential to favorably change cardiorespiratory capacity after TBI.
The results of these studies indicate that patients with TBI can tolerate and benefit from intense exercise training programs.69 For this reason, exercise training is warranted in TBI to overcome the general deconditioning for the injury and recovery period. Patients with TBI often complain of fatigue that may be central in origin; however, exercise training may cause a reduction of these complaints of fatigue and allow for greater involvement in social and occupational activities. More studies are needed to address the efficacy of exercise training in TBI, particularly those that include measurements of functional limitations and disability. A summary of these exercise training studies is given in Table 14-5.
TABLE 14-5 Summary of Evidence for Exercise Training for Patients with TBI
Influence of Medications on Ability to Exercise
No studies have addressed the pharmacological effects of medications taken by patients with brain injury as they relate to exercise performance. Although most patients with TBI are on many medications to manage brain damage during the early stages after the injury, many patients are on few, if any, medications for the long term.
The primary condition that distinguishes TBI from brain injury associated with stroke is the common use of medications to control seizures and agitation. These medications are often taken for the long term. Further discussion of medications and their effects on exercise can be found in Chapter 8.
General Effects of Exercise Training on Impairment, Disability, and Quality of Life
Gordon and colleagues70 conducted a retrospective study of a community-based sample of 240 individuals with TBI (64 exercisers and 176 nonexercisers) and 139 individuals without a disability (66 exercisers and 73 nonexercisers). The researchers found that the exercisers with TBI were less depressed, reported fewer symptoms, and their self-reported health status was better than that of the nonexercising individuals with TBI. There were no differences between the two groups of individuals with TBI on measures of disability and handicap. These findings suggest that exercise improves mood and aspects of health status and also improves aspects of disability and handicap for patients with TBI.
Spinal Cord Injury (Practice Patterns 5H, 5A, 5E, 7A; ICD-9-CM Codes: 344, 806, 952, 741, 336)
Spinal cord injury (SCI) produces neuromuscular, skeletal, hormonal, and psychological changes in the injured individual. Injury at the highest level (C1 through C7) causes tetraplegia with impairment of the arms, trunk, legs, and pelvic organs. Injury to the thoracic segments leads to paraplegia with impairments of the legs and pelvic organs.
CLINICAL CORRELATE
SCI leads to partial or complete loss of volitional control of muscles innervated below the level of the lesion resulting in loss of muscle strength and endurance. This loss also alters the cardiopulmonary system’s response to exercise because local fatigue of remaining intact musculature often prevents patients from maintaining prescribed workloads.
Stimulation of the cardiopulmonary system is also impaired in SCI due to lack of innervation to the autonomic nervous system, thereby reducing the ability to support higher rates of aerobic metabolism. Regular exercise through either voluntary activity or ES of paralyzed muscles can increase the strength and endurance of these muscles. However, the potential benefits from exercise are drastically altered. Injuries below C7 result in paraplegia. Certain patients with paraplegia may suffer from loss of autonomic control (T6 and above) similar to that in tetraplegia (C1 through C7). Figure 14-1 illustrates lesion levels and resultant functional limitations. A summary of the practice patterns and ICD-9-CM codes for SCI are given in Table 14-6.
TABLE 14-6 Summary of Spinal Cord Injury Practice Patterns and ICD-9-CM Codes
FIGURE 14-1 Spinal cord injury lesion levels and resultant functional limitations. (C = Cervical; T = Thoracic; L = Lumber; S = Sacral)
Factors That Influence Ability to Exercise
SCI impairs thermoregulation due to loss of autonomic nervous system control for vasomotor (vascular dilation/constriction) and sudomotor (sweating) responses in the areas of lost sensation. Therefore, a person with SCI has a reduced ability to handle thermal extremes and to perform aerobic exercise. Because patients with SCI must rely on their upper body for locomotion, they may be at a thermal risk.71
Other factors, including relatively small muscle mass and deficient cardiovascular reflex and inactivity of the venous skeletal muscle pump (resulting in hypokinetic circulation), can cause early onset of fatigue during arm exercise in patients with SCI. Exercise responses to arm-crank ergometry (ACE) are significantly related to the level of lesion of SCI. The higher the lesion level, the lower the physical work capacity and mean exercise systolic and diastolic blood pressure.72
Tests and Measures for Exercise Testing
In general, wheelchair ergometry (WCE) is less metabolically efficient than arm-crank ergometry at submaximal intensities.73 However, arm-crank ergometry imposes a greater central circulatory stress. Higher peak HRs are elicited by arm-crank ergometry than by WCE, suggesting that exercise testing needs to be ergometer specific when the results are to be used for exercise prescription.74 If the subject’s neurological level of injury is T10 through L2, the maximal exercise test will progress as conducted for an able-bodied individual. If the injury level is T6 or above, exercise performance may be influenced by lack of sympathetic outflow to the adrenal medulla, resulting in impaired release of catecholamines during exercise. For these individuals, the Borg Perceived Exertion Scale should be applied (see Chapter 9).
McClean and colleagues75 found that an RPE of 10 to 12 was both linearly related to a 50% to 60% peak power output in tetraplegia and associated with a higher power output than that predicted by HR or oxygen consumption. Therefore, a Borg RPE of 14 to 15 is most often used to represent a sufficient intensity to terminate the test for patients with tetraplegia when other cardiac and metabolic measures are unobtainable due to impaired cardioregulatory responses. However, in 2007 Lewis et al. contradicted the well-accepted relationships between RPE and both HR and during exercise by people without disabilities and challenged its use as a valid index of perceived exertion in persons with SCI.76 Their study examined the relationship between HR, , minute ventilation (
), and RPE (Borg categorical 6–20 scale) during a peak-graded arm ergometry in persons with paraplegia and tetraplegia. There were inconsistent associations for subjects with tetraplegia, where the RPE related positively to HR at the initial work rate, but there were no other significant correlations and for subjects with paraplegia where RPE did not correlate significantly with HR, , or 
. In general, HR, , and increased as the exercise intensity increased and were more pronounced in subjects with paraplegia. While RPE values increased with increasing work rates for each group, no differences between groups were found. Therefore, RPE does not appear to be a valid surrogate for physiological stress in SCI during a maximal exercise test.
Generally, subjects whose neurological level is thoracic (T1) and lower can propel a manual wheelchair and complete a maximal wheelchair treadmill exercise test to determine aerobic capacity. However, subjects whose neurological level is cervical (C5 through C8) usually require arm-crank ergometry to determine aerobic capacity, securing the upper extremities as needed. Subjects should refrain from food, caffeine, nicotine, or alcohol for a 4-hour period before testing. The exercise test protocols usually consist of incremental graded workloads of 3-minute stages with the initial power output at 10 or greater for paraplegia. The workload should be progressed by 6 W per stage with the WCE and progressed to 12 W per stage for the arm-crank ergometry because it elicits a higher maximal power out-put when compared with the wheelchair exercise.77,78 For tetraplegia, the initial power output is 1 to 3 W with a work rate progression of between 4 and 6 W.79 The testing protocols for paraplegia and tetraplegia are summarized in Table 14-7. Cycling rates for both exercise modalities can be maintained by a metronome. Figures 14-2and 14-3 illustrate wheelchair and arm-crank ergometry systems for exercise testing and training.
TABLE 14-7 Summary of Suggested Guidelines for Exercise Testing in Paraplegia and Tetraplegia
FIGURE 14-2 Wheelchair ergometry modality for exercise testing or training. (From Keyser RE, Rodgers MM, Gardner ER, Russell PJ. Oxygen uptake during peak-graded exercise and single-stage fatigue tests of wheelchair propulsion in manual wheelchair users and the able-bodied. Arch Phys Med Rehabil. 1999;80:1289. Used with permission from WB Saunders Company and Randall E. Keyser.)
FIGURE 14-3 Arm-crank ergometry modality for exercise testing or training. (Reprinted with permission from Lamont LS, Going A, Kievit J. A comparison of two arm exercises in patients with paraplegia. Cardiopulm Phys Ther J. 1996;7:3.)
CLINICAL CORRELATE
Because of the absence of thermoregulatory sweating and vasoconstriction below the level of the lesion, a fan and spray-water system can be used to facilitate heat loss by convection and production of a cooling effect through vaporization of “artificial sweat.” Blankets should also be used during the cool-down and postexercise periods to avoid hypothermia. To avoid problems associated with autonomic hyperreflexia such as hyper-or hypotension and venous pooling, subjects with neurological injury of T6 and above should wear an abdominal binder and leg-compressive stockings. In some cases, where hypotension due to venous pooling is persistent, arm-crank ergometry with the legs either elevated or in a semi-reclined position can facilitate venous return and make additional blood available to the exercising arms.73
King and colleagues24 studied exertional hypotension in four lesion levels of patients with SCI who performed a continuous maximal arm ergometry exercise test. Exertional hypotension, defined in this case as a maximal BP lower than the highest submaximal BP, was present in all patients with SCI regardless of lesion level. Patients who experience hypotension can report a sense of dizziness, nausea, visual changes, and/or sweating. Still other patients with SCI who experience hypotension do not report any symptoms. Therefore, it is important to monitor BP throughout the test. This is typically done during arm-crank ergometry by therapist-assisted cranking, while the arm remains still to measure BP.
Aerobic power during maximal exercise was studied in 58 males with traumatic spinal cord lesions from C4 through L4. Twenty-five well-trained “world-class athletes” and 33 untrained subjects were compared with five arm-trained and five arm-untrained able-bodied subjects.80 During maximal wheelchair exercise, the aerobic power (
), pulmonary ventilation, and blood lactate concentration were higher in subjects with lower levels of SCI. At each injury level above C6 through C7, nearly all trained subjects reached a higher than did untrained subjects with the corresponding level of lesion. The peak HR in the tetraplegia groups was lower than that in the paraplegia group with no or only small differences between trained and untrained subjects at the same level of SCI. Therefore, the expectations of individuals with paraplegia are much the same as that of a healthy group; however, significant limitations in cardiorespiratory responses occur with tetraplegia ergometry; therefore, a Borg perceived exertion scale should be used.
Other studies have demonstrated that exercise capacity is dependent on spinal injury level. Yamasaki and colleagues81 determined that individuals with high paraplegia (T3 through T8) compared with those with low paraplegia (T10 through L2) who performed arm-crank exercise had low work efficiency. This was attributed to increased ventilation, which yielded an increase in oxygen uptake. In 1998, Yamasaki and colleagues82 later found that years since injury are not as important in determining cardiorespiratory responses during maximal arm cranking as is level of SCI and training. Gass and colleagues83 compared arm-crank and treadmill wheelchair propulsion in a homogeneous group of nine men with paraplegia (T4 through T6). This study found that, unlike previous studies, there were no significant differences in oxygen consumption, ventilation, or HR between the two modes of ergometry during the last minute of incremental exercise to exhaustion. This conclusion was most likely due to the study of paraplegics versus tetraplegics and to the fact that the lesion level was homogeneous.
Interventions for Exercise Training
With the growing interest in exercise and sport and the significance of CVD in the spinal cord–injured population, the role of endurance training in improving cardiovascular health is of particular interest. Ordinary daily activities of those with SCI are usually not adequate to maintain cardiovascular fitness, and lack of participation in a regular activity program may result in a debilitative cycle.84 As this occurs, there is a reduction in functional work capacity that may limit independence, and the reduction in cardiovascular fitness may increase the risk for CVD.
Work capacity in those with SCI is limited by loss of functional muscle mass and sympathetic control. Sympathetic nervous system impairment limits control of regional blood flow and cardiac output, and maximum HR following cervical lesions may be reduced to 110 to 130 beats per minute (bpm). However, endurance training in patients with tetraplegia and paraplegia can elicit improvements in exercise performance similar to those observed in able-bodied individuals.
A HR chest monitor (Polar CIC, Inc; Port Washington, NY) should be worn during all training periods to ensure maintenance of target HR during each training session. Subjects should be progressed from 60% of target HR up to 85% over the course of the training period, usually lasting between 8 and 12 weeks. Training targets will also depend on whether subjects have a neurological level of injury at or above T6 or below T6 because of the potential for autonomic dysreflexia. BP should be measured at intervals throughout exercise. In subjects with tetraplegia, HR may rise to a limited degree during arm-crank ergometry.
A review of 13 cardiorespiratory training studies involving subjects with SCI84 revealed average improvements of 20% in and 40% in physical work capacity after 4 to 20 weeks of training. On the basis of the positive results of these studies, the general endurance training guidelines for the normal population appear also to be appropriate for the spinal cord–injured population. These guidelines can be followed during participation in a number of different activities and sports including wheelchair pushing, arm-crank ergometry, aerobic swimming, ambulation training, canoeing, and wheelchair basketball.
There is no evidence that intense training and competition are harmful, but special areas of risk as a result of impairments in sensation, cardiovascular function, autonomic function, and temperature regulation must be considered. The long-term benefits of endurance training in those with SCI have not been adequately studied, but there is suggestion that similar physiological and psychological changes may occur in able-bodied individuals.
Taylor and colleagues85 studied the effects of an arm-crank ergometry training program on several physiological variables of recreational wheelchair subjects. Ten subjects with paraplegia (five experimental and five control) were tested prior to and immediately after a 2-month exercise regimen at 80% of peak HR (30 min/d, 5 d/wk, for 8 consecutive weeks). The results demonstrated significant increases in and workload but only mild improvements in maximal HR and postexercise blood lactate levels. The results indicate that physiological variables of subjects with paraplegia following an arm ergometer endurance training program are similar to changes previously observed in healthy subjects. These values, when compared with those of healthy individuals, are low as a result of the relative inactivity.
Eight men with tetraplegia participating in an 8-week arm-crank ergometry training program demonstrated improved cardiopulmonary function including exercise HR, physical work capacity, and maximal oxygen uptake. Additionally, wheelchair propulsion endurance improved as evidenced by distance covered in 12 minutes on a circular track.86 Different exercise effects among persons with paraplegia and tetraplegia have been noted. After a training protocol, subjects with paraplegia had cardiorespiratory responses that were similar to those of individuals without SCI, whereas subjects with tetraplegia exhibited increased resting HR and systolic BP.
Twenty individuals with SCI were tested for by using a WCE.87 The subjects were divided into four groups: (1) a group with tetraplegia (four subjects); (2) an untrained female group with paraplegia (five subjects); (3) an untrained male group with paraplegia (seven subjects); and (4) a trained male group with paraplegia (four subjects). for the group with tetraplegia was significantly lower than that for the other groups. for the untrained female group was significantly lower than that for both the untrained male group with paraplegia and the trained male group with paraplegia. The untrained male group with paraplegia had a significantly lower than the trained male group with paraplegia. The present study, combined with the findings from research, gives strong evidence that in untrained patients with SCI is highly related to the level of injury.
Hjeltnes and colleagues88 studied 10 male patients with tetraplegia who completed arm-crank ergometry three times per week. Aerobic capacity was compared to 10 patients with paraplegia who received traditional rehabilitation. Peak workload increased in the group with quadriplegia, but oxidative capacity did not. It was not surprising that peak oxygen capacity was greater in the group with paraplegia and significantly increased as a result of the training.
Price and Campbell89 examined the thermoregulatory responses of able-bodied athletes, athletes with paraplegia, and athletes with tetraplegia at rest, during prolonged upper-body exercise, and recovery. Exercise was performed on an arm-crank ergometry at 60% for 60 minutes. Peak oxygen uptake values were greater for the able-bodied individuals when compared with that of the subjects with paraplegia and least for the subjects with tetraplegia.
Dallmeijer and colleagues90 studied the effect of rehabilitation on physical capacity, mechanical efficiency of manual wheelchair propulsion, and performance of standardized ADL. Nineteen recently injured subjects with SCI were tested on a WCE for peak oxygen uptake and performance time at the beginning and at the end of the active rehabilitation period. Mechanical efficiency of submaximal wheelchair exercise was significantly higher after rehabilitation compared with that before. Performance time showed a significant decrease for most tasks. The results of this study show considerable improvements in physical capacity, mechanical efficiency of manual wheelchair propulsion during rehabilitation, and a concomitant lower performance time during standardized ADL. The higher mechanical efficiency and the decrease in performance time during standardized ADL suggest improvement in wheelchair propulsion techniques.
Bernard and colleagues91 characterized the influence of neurological lesion level on the cardiorespiratory and ventilatory responses of two groups of athletes with paraplegia during incremental exercise on a treadmill and under the usual conditions for wheelchair exercise. Cardioventilatory responses were evaluated in two groups of wheelchair sports—men with paraplegia designated as athletes with high paraplegia and in athletes with low paraplegia. With the exception of respiration, there were no significant differences in the classic cardiorespiratory parameters (, 
, HR, ) between the two groups. For the ventilatory parameters, there were significant differences between the two groups. A ventilatory disturbance was observed that was manifested by values of breathing frequency and tidal volume during exercise that were significantly different between groups.
During maximal exercise, no significant differences between the two groups concerning cardiorespiratory and ventilatory values were observed. The achievement of a greater number of workload levels and the higher maximal values indicated a better capacity for adaptation to exercise in the group with lower thoracic paraplegia. These results raise questions about the influence of neurological level, and further research is needed to define with more precision the capacities of readaptation of cardiovascular and respiratory functions as well as the training methods best adapted to the optimization of physical capacities.
Barstow and colleagues92 studied the peak and submaximal responses of oxygen uptake and HR in patients with SCI performing arm-crank ergometry and functional electrical stimulation (FES) leg cycling exercise. The purpose was to test whether the blunted HR response and slower rate of adjustment of oxygen uptake seen by using FES leg cycling exercise are also characteristic of arm exercise in these patients. Eight patients with paraplegia performed incremental and constant work rate (CWR) exercise with the legs and arms. Peak HR was higher during incremental arm exercise and was not correlated with that observed during incremental FES leg cycling.
For the same increase in , constant work rate arm exercise was associated with faster (and normal) kinetics, greater increase in HR, and lower end-exercise blood lactate compared with FES leg cycling. Therefore, the consistently higher peak HR and and faster kinetics for voluntary arm exercise compared with FES leg cycling exercise suggest no intrinsic dysfunction of HR control in subjects with paraplegia. Rather, these data suggest that during FES leg cycling, the changes seen are due to some characteristic specific to the injury, such as reduced muscle mass and/or deconditioning of the remaining muscle.
Muraki and colleagues93 studied the main factors that influence physical work capacity (PWC) in wheelchair-dependent subjects with paraplegia by using multivariate analysis. Thirty-two male subjects with paraplegia performed a submaximal arm exercise test on an arm-crank ergometry to determine their physical work capacity at 150 bpm and level of physical activity, occupation, level of SCI, and time since SCI. There was a high correlation between physical work capacity and the level of SCI and physical activity level compared to other factors. These results indicate that the level of SCI and physical activity are the most important factors in determining physical work capacity in wheelchair-dependent males with paraplegia.
Other forms of exercise training, such as ES, have emerged as promising interventions for improving fitness in SCI. Janssen et al. (2008) found that interval training using a modified versus a standard ES leg cycle ergometry can elicit marked improvements, not in peak metabolic and cardiorespiratory responses in men with SCI.94 Modifications to a standard ES protocol included increasing the current amplitude, adding shank muscle activation, and increasing angular motion. The training consisted of a 6-week interval training program with both experienced and novice riders. The modified protocol elicited significantly higher peak values for oxygen uptake, carbon dioxide production, pulmonary ventilation, cardiac output, HR, and blood lactate concentration. These changes occurred even with the experienced riders who had plateaued with a standard ES protocol. Frotzler et al. (2008) also reported a partial reversal of bone loss in chronic SCI after high-volume ES cycling, especially at the location of the distal femur where the bone is actively loaded during cycling versus the proximal tibia that was passively loaded.95
On the subject of dosing, Valent and colleagues (2008) found that regular hand cycling (once a week or more) appeared to be beneficial for improving aerobic physical capacity in persons with paraplegia during clinical rehabilitation.96 The authors investigated the influence of hand cycling use (questionnaire) on outcome measures of physical capacity during and after rehabilitation and 1 year later in 162 persons with paraplegia and tetraplegia. Peak oxygen uptake and peak power output determined in a hand-rim wheelchair peak exercise test, peak muscle strength of the upper extremities (triceps), and pulmonary function showed a significantly larger increment in paraplegia, not in tetraplegia and not at 1-year follow-up. A summary of parameters of exercise training studies in SCI can be found in Table 14-8.
TABLE 14-8 Summary of Parameters of Exercise Training Studies in SCI
Influence of Medications on Ability to Exercise
The primary medication that may influence exercise performance in subjects with spasticity is Baclofen. This medication has a tendency to make patients with SCI tired and weak. If possible, physicians often try to reduce or discontinue this medication if spasticity can be maintained under control. In some cases, patients have reported a decrease in spasticity as a result of FES of the lower limbs or even during upper-body exercise. Any medication change should be monitored and recorded to evaluate the influence on exercise capacity and training.
Other Responses to Exercise
Musculoskeletal changes such as decreased rate or possible cessation of bone loss97 occur as a result of exercise. From a neurological point of view, reports by Daly and colleagues98 have reported a decrease in spasticity and accelerated peripheral nerve regeneration as a result of exercise. Research also indicates that exercise in SCI produces an enhanced insulin sensitivity, which can lead to the prevention of diabetes.99 Daly et al. (1996) also reports accelerated wound healing. Kocina100 demonstrated an increase in weight loss and an increase in fat loss and lean body mass for patients with SCI who participated in an exercise training protocol.
During exercise, aural temperature changes in patients with SCI are important to monitor. One study of athletes with tetraplegia demonstrated a gradual rise of 0.9°C in aural temperature throughout exercise. During 30 minutes of passive recovery, the able-bodied athletes demonstrated greater decreases in aural temperatures than those for the athletes with paraplegia. Aural temperatures for the patients with tetraplegia increased, peaking at 5 minutes of recovery and remained elevated until the end of the recovery period. Fluid consumption and weight loss were similar for the able-bodied subjects and patients with paraplegia, whereas changes in plasma volume were greater for the able-bodied athletes. The results of this study suggest that under experimental conditions, athletes with paraplegia are at no greater thermal risk than able-bodied athletes. A relationship between the available muscle mass for heat production and sweating capacity appears evident for the maintenance of thermal balance. During recovery from exercise, decreases in aural temperature were greatest for the able-bodied athletes with the greatest capacity for heat loss and lowest for the athletes with tetraplegia with a lesser capacity for heat loss. A summary of other responses to exercise in patients with SCI can be found in Box 14-2.
BOX 14-2
Summary of Other Responses to Exercise in Patients with SCI
•Reduced bone-density loss
•Decrease in spasticity
•Enhanced insulin sensitivity
•Accelerated wound healing
•Weight loss
•Decrease in fat mass
•Increase in lean body mass
General Effects of Exercise Training on Impairment, Disability, and Quality of Life
Noreau et al.101 found an increased employability and independence in ADL without assistance in patients with SCI who exercised. Spinal cord lesions with paresis reduce the total active skeletal muscle mass. This can cause physical inactivity, medical complications, and social isolation. As a consequence, cardiovascular disorders as a cause of death are higher in this group compared with the general population. Therefore, one aim of rehabilitation is to increase the individual’s performance in daily life activities. It has been shown that the normal daily life activities of individuals with tetra- and paraplegia with no additional physical training are not intense enough to maintain a satisfactory level of physical fitness.
Manns and Chad102 studied 38 individuals with paraplegia and tetraplegia to determine the relationships among fitness, physical activity, subjective QOL, and handicap. Physical activity, measured by a leisure time exercise questionnaire, played an important role in the determination of handicap, measured by the Craig Handicap Assessment Reporting Technique (CHART) in SCI. It appears that the greater the time spent in leisure activity, the greater the likelihood that the associated handicap will be lower.
Tawashy et al. (2009) studied 49 individuals with SCI who were community dwellers and were primarily wheelchair users to determine the relationship of self-report physical activity and secondary conditions such as pain, fatigue, and depression.103 The authors found that those who engaged in heavy-intensity activity within the community had lower pain and fatigue and higher levels of self-efficacy, whereas high amounts of mild-intensity activity led to less depression. Therefore, even mild activity has QOL gains such as less depression and if we can encourage higher-intensity activities, there is potential to thwart pain and fatigue.
Multiple Sclerosis (Practice Patterns 5A, 5E, 6C, 6E, 7A; ICD-9-CM Code: 340)
Multiple sclerosis (MS) is an autoimmune demyelinating disease of the central nervous system. The loss of myelin reduces the speed of nerve conduction, thus interfering with smooth, rapid, and coordinated movement. Therefore, MS is associated with minimal-to-severe levels of disability as defined by the expanded disability rating scale (EDSS).104 MS has an estimated prevalence of 58 per 100,000 in the United States, occurring most frequently in women who are in their third and fourth decades of life. Three patterns of MS have been identified: (1) relapsing/remitting, (2) progressive, and (3) a combination of relapsing/remitting and progressive.105 Symptoms vary depending on the type and severity of MS and on the location of lesions. Symptoms include spasticity, tremor, weakness, fatigue, visual disturbances, bowel and bladder dysfunction, and pain. The most common and debilitating symptom of MS is a generalized sense of fatigue, frequently resulting from heat sensitivity.
Factors That Influence Ability to Exercise
It has been reported that 75% to 95% of persons with MS have fatigue, whereas 50% to 60% report that fatigue is their worst symptom. Fatigue in MS has been described as different from normal fatigue in that it comes on easily, prevents sustained physical functioning, is worsened by the heat, interferes with physical functioning, and causes frequent problems.106 Freal and colleagues107 found that fatigue was most likely to occur in the afternoon and evening as opposed to in the morning. This may be related to the body’s core temperature being the lowest in the morning. To avoid fatigue, the morning may be the best time to perform exercise.
Surprisingly, the severity of the illness (EDSS score) is not related to the severity of the fatigue. Therefore, even individuals with milder MS might suffer as much from fatigue as those who are more severe. Furthermore, MS fatigue has been found to be separate from depression because if depression is present, it is not related to the presence or severity of fatigue.106 Iriarte and colleagues108 found that fatigue was a symptom in 118 out of 155 patients with clinically diagnosed MS (76%). Twenty-two percent had fatigue at rest (asthenia), 72% described fatigue with exercise, and 6% described worsening of symptoms with effort. Finally, some authors have suggested that local skeletal muscle changes may contribute to the global sense of fatigue. These changes may include decreased oxidative capacity, slowed relaxation time, and a decrease in the number of slow-twitch muscle fibers. These changes may be due to inactivity resulting from the CNS dysfunction, leading to deconditioning and disuse. However, reconditioning by increasing the oxidative capacity of skeletal muscles may be warranted.
An estimated 80% of patients with MS are sensitive to changes in core body temperature, either from external environmental factors or from vigorous exercise. Aerobic exercise increases body heat due to an increase in metabolic rate. Without normal thermoregulatory responses from the autonomic nervous system, such as sweating, hyperthermia can result. The change in body temperature that elicits neurological signs varies between 0.1°C and 2.3°C. This rise in temperature causes a decrease in nerve conduction and is directly related to the degree of nerve conduction loss.109 Therefore, it is important that physical therapists assess temperature sensitivity prior to the beginning of an exercise regimen. Dysautonomia can also cause cardiac acceleration and reduction in the BP response.110
Neurological signs such as spasticity, muscle weakness or paralysis, and sensory loss may contribute to an inability to participate in exercise. Additionally, impaired balance and tremor may require modifications to traditional exercise modes. Fear of fatigue or worsening of symptoms can lead patients with MS to avoid exercise, which can lead to deconditioning and disuse atrophy. If the physical therapist can communicate an understanding of the pathophysiology of MS and the expected response to exercise to the patient, the patient’s concerns will be put to rest and allow for greater compliance with the exercise program. Box 14-3 summarizes the factors that can influence exercise performance in MS.
BOX 14-3
Summary of Factors That Can Influence Ability for Patients with MS to Exercise
•Fatigue
•Depression
•Pain
•Temperature insensitivity
•Spasticity
•Muscle weakness
•Sensory loss
Tests and Measures for Exercise Testing
Treadmill testing is often impossible for patients with MS who exhibit motor and sensory impairments of the lower limb such as spasticity or paresis. Therefore, as in severe stroke or head injury, upright or recumbent leg ergometry or a combination of arm and leg ergometry may be more practical. As in all exercise testing, arm ergometry often produces arm muscle fatigue before a cardiopulmonary maximum is reached. Recommendations for exercise testing110 include the use of a discontinuous protocol of 3- to 5-minute stages, beginning with a warm-up of unloaded pedaling. The work rate should be increased at each stage by approximately 12 to 25 W for legs and 8 to 12 W for arms. Foot stabilization may be necessary to counteract spasms or tremor.
There is very little research on the exercise capacity of patients with MS, most likely due to the wide variability of severity and disease fluctuation. However, most indications are that in the absence of severe paresis and cardiovascular dysautonomia, many individuals have been able to reach 85% to 90% of their age-predicted maximal HR. For physical therapists who may not have access to metabolic testing apparatus, HR is often a more feasible way of measuring maximal exercise capacity.110
Tantucci and colleagues111 found that there was no significant increase in the metabolic cost of exercise for patients with mild MS (EDSS score 0–2). This may have been attributed to minimal spasticity or ataxia. However, there was a significant increase in at rest and during exercise that could not be explained. In addition, Morrison et al. (2008) found that despite greater reported fatigue levels, participants with MS showed similar RPE and physiologic responses to submaximal and maximal exercise compared with controls.112 All participants underwent a graded aerobic exercise test on a cycle ergometer with breath-by-breath gas measurements and continuous HR monitoring. After completing the modified fatigue impact scale, participants rated their effort sense every 30 seconds during exercise using the modified Borg 10-point scale. The two study groups showed similar baseline characteristics except for higher fatigue scores in the MS group. There were no significant differences for any fitness measure, including oxygen cost slope. Neither HR nor RPE—measured at 25%, 50%, 75%, and 100% of peak—differed between groups. Therefore, the Borg 10-point scale may help improve evidence-based exercise prescriptions, which otherwise may be limited by fatigue, motor impairment, heat sensitivity, or autonomic dysfunction.
Temperature sensitivity should be assessed before exercise testing and training. This can be done through patient interviews to determine a past history of temperature sensitivity or through tympanic membrane thermometry during moderate-to-high exercise intensities. Measures should be taken before, during, and after exercise. This will allow for the determination of tolerable exercise intensities. HR and BP should be monitored because of the potential presence of autonomic cardioregulatory dysfunction.
Interventions for Exercise Training
There is a paucity of information in the literature concerning appropriate exercise rehabilitation for individuals with MS. Previous reports have indicated that there are no deleterious effects of exercise on the disease course of MS,113implying that individuals with MS can participate in exercise. In fact, limited studies of aerobic exercise in patients with MS have shown increases in cardiorespiratory and muscular functioning.110 Although incorrect exercise may increase fatigue in subjects with MS, it also may decrease fatigue if performed at an appropriate intensity.
Exercise programs have also not been shown to improve the course of the disease process in most patients. This may be due to the generalized nonspecific low-intensity exercise programs that are typically given to patients with MS.80 These individuals may begin exercising too late in the progression of the disease, exercise at too low or too high intensity, or perform the exercise incorrectly. It has been shown that persons with MS can lose up to 75% of their muscle strength before typical clinical tools detect it.
If possible, exercises should be initiated early on in the disease process when the greatest gains in strength and endurance can be achieved before the onset of severe disability. Exercises should focus on maintenance and when possible, on increasing flexibility, strength, and endurance. It appears that these kinds of exercises can be performed safely and should help to combat the effects of deconditioning.
The manner in which an exercise program progresses or regresses varies among individuals. During a remission, patients can generally maintain and even increase the intensity of the exercise program, and a new exercise baseline should be established for each remission. Likewise, if a patient is undergoing an exacerbation, the exercise intensity should be reduced. The use of an HR monitor can be an easy guide to help the patient maintain the appropriate exercise intensity. If a patient has significant dysautonomia, other ratings, such as RPE, may be useful for the patient to use in guiding exercise intensity; however, these ratings may not be valid when there are significant cognitive deficits.
Patients should be encouraged to hydrate before, during, and after exercise and should be provided fans when needed to prevent overheating. Precooling, or immersing heat-sensitive patients in cool water before exercise, tends to produce greater increases in physical work and greater comfort, when compared with a noncooled control group.114 The Schwinn Air-Dyne cycle may be useful because it blows cool air on the user. However, the rise in temperature should not exceed approximately 9°F. Aquatic exercise may also be useful if the water temperature is maintained around 90°F. Considerations should be made for possible cognitive deficits such as memory loss. Writing home instructions will ensure better compliance with prescribed exercises.110 Expiratory muscle function may also improve if respiratory muscle training is a part of the exercise program. This may subsequently improve exercise capacity and cough efficiency, thus preventing pulmonary complications associated with MS.115
Exercise intensity should fall between 60% and 85% of peak HR and between 50% and 70% for three sessions a week at 30 minutes each for 4 to 6 months.101 Generally, those patients who have minimal impairments have the best exercise tolerance. Complaints of muscular or general fatigue should not last longer than 30 minutes. If it does, this may indicate that the exercise intensity was too high, indicating a need for subsequent adjustment of intensity at the next session.
The effectiveness of a home aerobic exercise program on exercise capacity was studied by Schapiro and colleagues.116 The 50 subjects with mild-to-moderate MS participated in 16 weeks of a home program for 15 to 30 minutes per day, 4 to 5 times per week. The exercises were not supervised and their intensity was not controlled. The results showed that there was a 10% increase in maximal workload on the bicycle ergometer test following the intervention. It was noted that those subjects with lower baseline EDSS scores (1.0–3.5) had better results (greater peak workloads and exercise times) than those subjects with EDSS scores greater than 3.5.
Gehlsen and colleagues117 studied the effects of a 10-week aquatic exercise program on 10 ambulatory subjects with MS. Lower extremity peak torque, work, and fatigue in knee flexors and extensors were determined with a Cybex dynamometer. Upper-limb muscular force, work, fatigue, and power were determined using a biokinetic swim bench. After subjects participated in freestyle swimming and shallow-water calisthenics three times per week for 1 hour per session, an increase in peak knee extensor torque from baseline to the midpoint of the training was measured. No such training effect at the knee was found at 10 weeks. However, reduction in systemic fatigue and total work improved significantly after 10 weeks. The upper limbs showed increased muscle function from pre- to postintervention; however, there was no change in upper-limb fatigue levels.
One uncontrolled study reported on five patients with MS who completed a 4- to 6-week lower-limb endurance training program.118 Very low resistance was used by all subjects, who performed three sets of 10 repetitions of knee flexion at each exercise session. The results showed that subjects demonstrated a decreased perception of peripheral fatigue, an increased perception of well-being, and higher peak knee flexor torque levels after the exercise program.
Petajan and colleagues119 conducted a randomized controlled trial of 15 weeks of aerobic exercise on 54 subjects with mild-to-moderate MS (EDSS ≤ 6.0) to examine its effects on and isometric strength. The exercise group exercised three times per week for 40 minutes per session. The exercise group showed significant increases in (22%), physical work capacity (48%), and upper- and lower-extremity strength. Typically, in the MS population, decreased , HRmax, and workload are affected by the disease process.120
Gappmaier and colleagues121 studied the effect of a 15-week aerobic exercise program on fitness, strength, body composition, and lipid profiles in patients with MS. There was a 20% increase in maximal exercise capacity and maximal isometric force of the prime movers activated during cycle ergometry. The authors recommended exercise that combines upper- and lower-limb work because it appears to allow patients to compensate for deficits involving primarily the lower limbs. Table 14-9 summarizes exercise training studies relevant to patients with MS.
TABLE 14-9 Summary of Exercise Training Studies for Patients with MS
Influence of Medications on Ability to Exercise
Patients with MS may have amantadine HCL prescribed to temporarily reduce fatigue. Amantadine HCL, fluoxetine HCL, and hyoscyamine sulfate may also cause muscle weakness. Baclofen is often prescribed to reduce spasticity but in high doses may worsen muscle weakness and fatigue. Prednisone, prescribed as an anti-inflammatory, may also cause muscle weakness, reduced sweating, hypertension, diabetes, and/or osteoporosis. Consideration of these medications, as they relate to exercise prescription, is important. Questioning the patient and confirming with the neurologist optimize care when monitoring medications for patients with MS.
Other Responses to Exercise
There may be attenuated HR, BP, or sudomotor responses that require careful monitoring and hydration during exercise. Such exercise should take place in a temperature-controlled room. Also, it has been shown that physical activity may decrease the risk of developing other chronic health conditions119 such as CAD. There is usually significant weight gain after the onset of MS because of inactivity and sudomotor medications. Exercises that maintain or increase muscle mass may halt weight gain and reduce fat mass. Gappmaier and colleagues121 found favorable body composition changes with 15 weeks of exercise training, which was sufficient to achieve or maintain proper body weight and a normalization of certain lipid profiles. Weight loss has a psychological benefit but also has an important functional benefit. Patients with MS who are overweight or obese and are moderately to severely disabled have a greater chance of exacerbating fatigue due to the effort required for mobility. Depression may affect exercise adherence, so constant reinforcement to sustain the exercise regimen is necessary for some patients.
General Effects of Exercise Training on Impairment, Disability, and Quality of Life
Fatigue often leads to a reduction in physical activity. This leads to muscle atrophy and weakness, decreases in flexibility, cardiovascular deficits, sleep abnormalities, increases in depression and anxiety levels, and ultimately, more fatigue. By in-creasing physical activity levels, even in a chronic disabling disease, improvements in physical and psychosocial factors can be obtained.
Petajan and associates119 demonstrated that there was a de-crease in depression, anger, and fatigue after aerobic exercise. This controlled study demonstrated that moderate aerobic exercise could improve physiological function, emotional behavior, fatigue levels, and daily activity functioning.
Aerobic exercise and strengthening have the potential of benefiting patients with MS. Although aerobic exercise can cause an increase in temperature and strengthening muscles can cause muscle fatigue, these effects can be minimized when the exercises are performed correctly. Therefore, it is important to develop exercises that take into consideration the symptoms (especially muscular fatigue and weakness) and pathophysiology of the disease, while maintaining or increasing the functional independence and functional capabilities of the individuals. Because of the early age of onset of MS, the goal should be to maintain functional independence, limit disability, and maintain a high QOL.
Parkinson Disease (Practice Patterns 5A, 5E, 6B, 6E, 7A; ICD-9-CM Code: 332)
Parkinson disease (PD) is a progressive neurological disease of the extrapyramidal system. There is an associated reduction in endogenous dopamine, a neurotransmitter primarily located in the substantia nigra of the basal ganglia. Loss of dopamine results in bradykinesia (slowness of movement), tremor at rest, rigidity, and gait and postural deformities. Gait is usually described as slow, shuffling, and festinating (involuntary hurrying). With more severe PD, freezing or the inability to continue or initiate walking, especially when passing through doors and narrow spaces, is predominant. Standing posture is characterized by increased kyphosis, and the hips, knees, and elbows are maintained in the flexed position. The Hoehn and Yahr122 scale is used to classify severity of PD. This scale is illustrated in Table 14-10. The Unified Parkinson’s Disease Rating Scale (UPDRS) is a PD behavioral rating scale consisting of four categories: (1) mentation, behavior, and mood, (2) ADL both on and off medication, (3) motor examination, and (4) complications of therapy in the previous week. This scale is used to track PD longitudinally and is evaluated by interview. Total disability is 199 and 0 represents no disability. This scale, although more complicated, has supplanted the Hoehn and Yahr scale.
TABLE 14-10 Hoehn and Yahr Grades
Factors That Influence Ability to Exercise
Exercise response studies are fraught with the problem of both significant variability between patients and medication levels. The autonomic nervous system can be dysfunctional in PD, where there may be problems with thermoregulation. Therefore, sweating patterns as well as HR and BP responses should be monitored during exercise.
Muscular rigidity can reduce exercise efficiency. Walking limitations can even produce falls during treadmill exercise. Overground walking where rapid turns are involved can result in loss of balance in more severe cases. Because of inefficient gait patterns, higher HRs and increased oxygen consumption may be evident during exercise. If a patient is severely kyphotic, lung capacity and thereby exercise capacity may be further reduced.
Tests and Measures for Exercise Testing
Patients who have balance or freezing problems should not be tested on a treadmill; a cycle ergometer is a safe alternative unless there is an overhead harness support to prevent injury from potential near falls. When metabolic exercise testing is indicated, it may be advisable to use a mask rather than a mouthpiece because of the patient’s inability to coordinate oral musculature. If patients with PD are in the age group where they are at risk for CVD, appropriate precautions regarding ECG and physician monitoring should be considered. Most importantly, if more than one exercise test is going to be conducted, the time of day and time after medication during “on” or “off” periods should remain consistent. Preferably, testing should begin 45 minutes to 1 hour after medication has been taken. Some patients experience peak-dose tachycardia and dyskinesias. Appropriate cardiac and physical supervision is necessary. Skidmore et al. reported in a pilot study an asymptomatic drop of >20 mm Hg during treadmill exercise in 8 of 9 patients with PD participating in treadmill exercise, indicating a need for autonomic monitoring.123Caution should be used when testing individuals who have had a recent change in medication because their physiological performance may be unpredictable. Optimally, if the exercise performance of patients with PD fluctuates significantly on medication, testing should be done both on and off medication to determine exercise response ranges.
Reuter and colleagues124 studied the cardiovascular performance and metabolic response in 15 patients with PD after exercise training using a cycle ergometer ramp protocol exercise test. The results did not show differences in cardiovascular adaptation to physical work in these patients compared with their healthy counterparts. Therefore, it should be possible to improve cardiovascular endurance in patients with PD.
Stanley and colleagues125 compared the cardiopulmonary function of individuals with PD to that of healthy normals (HN) on a stationary bicycle by using an incremental exercise protocol. For men and women, there were no significant differences in between those having PD and the HN. Likewise, there was no significant difference in time to achieve a maximal effort. Patients with PD reached their earlier than did HN, indicating that individuals with PD may be less efficient during exercise.
Canning and associates126 evaluated the exercise capacity of 16 subjects with mild-to-moderate PD to determine whether abnormalities in respiratory function and gait affect exercise capacity. Subjects were categorized according to exercise history, disease severity, and presence/absence of upper airway obstruction. Subjects performed a maximum exercise test on a cycle ergometer, together with respiratory function tests and a walking test. 
and peak workloads achieved by subjects with PD were not significantly different from normal values, despite evidence of respiratory and gait abnormalities typical of PD. Sedentary subjects produced scores lower than exercising subjects. Despite their neurological deficit, individuals with mild-to-moderate PD have the potential to maintain normal exercise capacity with regular aerobic exercise.
Protas and colleagues127 studied the aerobic capacity of eight individuals with PD. This study (1) compared maximal exercise performance in individuals with and without PD, (2) compared exercise performance during upper and lower extremity exercise, and (3) described submaximal exercise responses. Subjects performed a lower extremity ergometer test (LE test) and an arm-crank ergometry test. Peak power was less for the PD group than for the control group for both tests. Submaximal HR and oxygen consumption were higher for the PD group than for the control group. The authors concluded that individuals with mild-to-moderate PD can be tested with both exercise protocols to peak exercise capacity and that there are differences in upper and lower extremity peak power and submaximal responses among persons with and without PD.
Werner et al. (2006) studied differences in vital signs and RPE between 16 individuals with PD compared with a group of healthy individuals during treadmill exercise test (modified Bruce protocol).128 HR, systolic BP, and the RPE were measured at submaximal exercise (defined as stage 2 of the modified Bruce protocol) and at peak exercise (defined as 85% of age-predicted target HR). During submaximal exercise, no significant differences were found between the PD group and the control group; however, at peak exercise, one half of the subjects with PD exhibited blunted cardiovascular responses (HR, BP, or RPE), despite reaching a comparable intensity of exercise thus displaying abnormal cardiovascular responses at the higher exercise intensities. This exercise protocol could help guide the exercise prescription using BP, HR, and RPE as the rate-limiting parameters.
Interventions for Exercise Training
Exercise training is generally designed to reduce the indirect effects of inactivity and immobility associated with PD but may not affect the disease process directly, for example, tremor and rigidity. Because this disease is progressive, exercise interventions should not be short-term; rather, exercise should become part of the everyday lifestyle. Most clinicians and researchers believe that physical therapy should begin as soon as the diagnosis is made to prevent muscle atrophy, weakness, and reduced exercise capacity.118
CLINICAL CORRELATE
In some cases, patients with PD may display bradycardia in response to aerobic exercise activity, making it difficult to reach the target heart rate. Heart rates can be extremely variable and should be monitored closely during exercise. In this case, the rating of perceived exertion should be used to identify exercise intensity. Exercise is best planned at the same time after medication intake to maximize its benefit. In some cases, motor planning and memory may be impaired and repeated demonstrations along with written and visual cues are needed to ensure adherence. Exercise groups can also avoid the feelings of isolation so prevalent in patients with PD.127
Koseoglu and colleagues129 studied the effects of exercise training, as a part of a pulmonary rehabilitation program, on pulmonary function tests and exercise tolerance including subjective RPE among patients with PD and nine age-matched healthy controls. After the training program, there was an improvement in some pulmonary function test parameters, exercise tolerance, and RPE for patients with PD.
Skidmore et al. (2008) conducted a pilot study where they evaluated the safety and feasibility of a 3-month progressive treadmill aerobic exercise (TM-AEX) program for persons with PD with gait impairment.123 Eight subjects underwent a treadmill stress test to determine eligibility, of which three were referred for further cardiac evaluation and five were enrolled. In 136 subjects, treadmill aerobic exercise sessions significantly improved the subjects’ total UPDRS scores and peak ambulatory workload capacities. The results of this study suggested that an aerobic exercise program is feasible for persons who have PD and gait impairments as long as precautions are taken to prevent falls through the use of an overhead harness. Thus, this pilot study shows promise that treadmill aerobic exercise may reduce symptom severity and improve fitness for persons with PD.
Kurtais et al. (2008) studied whether gait training on a treadmill would improve functional tasks of lower extremities in patients with PD.130 Twenty-four patients diagnosed with idiopathic PD were enrolled in group I, where they attended a training program on a treadmill for 6 weeks, or group II that served as the control group. Both groups were instructed in home mobility exercises. The primary study outcome measures were timed functional lower extremity tasks and the secondary outcome measures were exercise tests and patient’s global assessment. Graded exercise tests (Naughton protocol) were performed on a treadmill. There were significant improvements in exercise test parameters in the exercise group only which carried over to the functional lower extremity activities. Specifically, , exercise duration, and METS improved significantly in the exercise group, indicating a benefit of treadmill training on fitness in persons with PD.
Schenkman and colleagues (2008) described three case reports of patients with early PD who completed 4 months of supervised endurance exercise training and 12 months of home exercise, with monthly clinic follow-up sessions for 16 months.131 The main outcome measure was economy of movement (rate of oxygen consumption during gait) measured at four treadmill speeds. One secondary outcome measure included the UPDRS among others. Economy of movement improved for all three patients and remained above baseline at 16 months. Two patients also had scores that were above baseline for UPDRS total score, even at 16 months. The authors concluded that their study suggested that gains might occur with a treadmill training program that is coupled with specific strategies to enhance adherence to exercise.
Influence of Medications on Ability to Exercise
Medications have been the best way to treat PD to correct dopamine imbalances, decreased epinephrine and norepinephrine, and increased acetylcholine. The most common drugs are dopaminergics like Sinemet, anticholinergics, and monoamine oxidase type B inhibitors. Side effects include upset stomach, confusion, delusional states, and insomnia. Long-term use can actually produce movement disorders such as dyskinesias. Unfortunately, there is a declining effect of these drugs over the years. Drug absorption can be reduced by strenuous exercise, use of anticholinergic drugs, autonomic nervous system dysfunction, food intake, protein and iron supplements, and aerobic fitness.132
Enhanced fatigue on performance of motor tasks is a very frequent and disabling complaint of patients with PD and is poorly characterized and understood. Ziv and colleagues133 found that increased muscle fatigue should be recognized as an integral part of the spectrum of motor impairment of PD and is associated with a central dopamine deficiency.
LeWitt and colleagues134 studied weakness, easy fatiguing, and lack of endurance perceived by patients with PD. Although the slowed motor repertoire in PD may underlie these experiences, other abnormalities in skeletal muscle utilization may also be involved. The authors investigated whether an index of metabolic efficiency during a continuous exercise task, the latency until anaerobic threshold (AT), is altered by levodopa (LD) while pedaling a bicycle ergometer against a uniform workload. When compared to an unmedicated state, LD treatment delayed anaerobic threshold. Subjects did not differ in their perceived exertion upon reaching anaerobic threshold. In addition to relief of symptoms by LD, the efficiency of energy utilization in exercising skeletal muscle is also increased.
Goetz and colleagues135 studied 10 regular exercising men with PD on LD under two conditions—at rest and during vigorous exercise started 1 hour after LD ingestion. There was a high degree of agreement between plasma LD level and the patients’ disability scores 30 minutes later under both conditions, with no difference between the two. The authors concluded that LD levels accurately reflect disability and motor function in these patients and that vigorous exercise, started 1 hour after LD ingestion, does not influence LD or motor scores.
Carter and colleagues136 studied the effect of exercise, using cycle ergometry on LD absorption in 10 patients with PD. Oral LD was administered during exercise and at rest on separate days. Exercise-delayed LD absorption in five patients increased it in three and did not influence it in two. The authors concluded that exercise can either increase or decrease LD absorption. Further research is needed on the exercise effects of CD in PD.
Other Responses to Exercise
Comella and colleagues137 conducted a randomized, single-blind, crossover study, evaluating physical disability in patients with moderately advanced PD after 4 weeks of normal physical activity and after 4 weeks of an intensive physical rehabilitation program. Following physical rehabilitation, there was significant improvement in ADL and motor scores, but there was no change in the mentation score. During the 6 months following physical rehabilitation, patients did not exercise regularly, and the disability scores returned to baseline. The authors concluded that physical disability in patients with moderately advanced PD objectively improves with a regular physical rehabilitation program, but this improvement is not sustained when normal activity is resumed.
Inzelberg et al. (2005) found a reduction in the perception of dyspnea (POD) of individuals with PD when inspiratory muscle training was performed six times per week for 30 minutes for 3 months compared with a control group who received a sham treatment.138 The investigators evaluated the effect of this inspiratory muscle training on pulmonary functions, inspiratory muscle performance, dyspnea, and QOL in patients with PD. Following the training period, there was a significant improvement in the training group but not in the control group, in inspiratory muscle strength, inspiratory muscle endurance, and the perception of dyspnea. Patients with PD who can achieve reductions in dyspnea may improve their QOL or the willingness to engage in activity without experiencing shortness of breath, especially for those activities that require a large effort.139
General Effects of Exercise Training on Impairment, Disability, and Quality of Life
Reuter and colleagues140 studied the influence of intensive exercise training on motor disability, mood, and subjective well-being in patients with PD over a 20-week period. Sixteen slightly to moderately affected idiopathic patients with PD received intensive exercise training twice weekly. They found that motor disability as well as mood and subjective well-being can be significantly improved by intensive sports activities in early- to medium-stage PD patients.
Kuroda and colleagues141 reported on data obtained from public health nurse visits, including a 1-year follow-up for 438 patients with PD living in Japan. The follow-up period averaged 4.1 years, during which 71 deaths were observed. The patients were classified according to the degree of physical exercise they performed, and the ratios of observed to expected deaths were calculated. The exercising group showed the lowest ratio for patients able to walk independently compared with that for those who could not.
Sasco and colleagues142 conducted a case control study of patients with PD. Physical exercise was conducted in a cohort of 50,002 men who attended either Harvard College or the University of Pennsylvania between 1916 and 1950, and who were followed up in adulthood for morbidity and mortality. Cases of PD were identified from responses to mailed questionnaires and death certificates through 1978. The association between physical activity at the time of college and subsequent risk of PD was evaluated. Those playing on a varsity sports team or participating in regular physical exercise in college were associated with a lower though nonsignificant risk of PD. In adulthood, participation of moderate or heavy sports activities was linked to a reduced risk. These results, which require further confirmation, are compatible with a slight protective effect of physical exercise on the risk of PD, although the lack of association cannot be refuted.
Schenkman and colleagues143 reported that task-specific training in addition to aerobic exercise may be more beneficial than standard exercise training. Future research is needed to evaluate the effects of adding external cues, cognitive strategies, task-specific training, and environmental modifications to aerobic exercise for people with PD.
Rodriques de Paula et al. (2006) evaluated changes in different domains of QOL for 20 persons with PD (stages 1–3 on the Hoehn and Yahr scale) after a program of physical activity consisting of 36 group sessions of aerobic conditioning and muscular strengthening.144 QOL was measured using the Nottingham Health Profile, a generic questionnaire composed of six domains. There were significant gains associated with the program on the total score and those related to emotional reactions (ER), social interactions (SI), and physical ability (PA). Social interaction was the domain that showed the greatest program gains (41.4%). The authors concluded that a light-to-moderate intensity program of physical activity resulted in improvements in their perception of QOL.
Herman et al. (2007) conducted a study of QOL with nine patients with PD who participated in intensive treadmill training four times per week for 30 minutes, each session for 6 weeks. QOL was measured using the Parkinson’s Disease Questionnaire (PDQ-39). The PDQ-39 is the most widely used PD-specific measure of health status. It contains 39 questions, covering eight aspects of QOL including mobility, ADL, emotions, stigma, social support, cognitions, communication, and bodily discomfort. The instrument was developed on the basis of interviews with people diagnosed with the disease. Herman and colleagues found that the PDQ significantly improved as a result of the intensive treadmill training from a score of 32 to 22.145
Guillain–Barré Syndrome (Practice Patterns 4A, 5E, 5H, 6B, 6E, 7A, 7B, 7C; ICD-9-CM Codes: 341, 344)
Guillain–Barré syndrome (GBS) is an autoimmune disorder of the peripheral nervous system causing progressive weakness of limbs with diminished/absent tendon reflexes and has no known etiology. This inflammatory process affects the Schwann cells. The process of remyelination occurs rapidly. The patient may also experience secondary axonal damage. The regrowth rate is slow: approximately 1 mm/d. Despite profound deficits and paralysis, there is a 65% chance of full recovery.146
Factors That Influence Ability to Exercise
Physical therapists must consider issues of overwork, avoidance of eccentric contractions, and performance of antigravity muscle training before progressing to the addition of weights. Overwork weakness is a prolonged deficit in the absolute strength and endurance of a muscle as a result of excessive activity.147 Because GBS affects the peripheral nerve, motor unit recruitment is impaired, leaving fewer muscle fibers available to provide sufficient force during exercise. This puts these muscle fibers at risk for overwork.
Tests and Measures for Exercise Testing
To avoid muscle damage or overuse weakness, maximal exercise testing is not recommended. Submaximal tests like those recommended by Noonan and Dean148 may be possible once a patient has passed the acute phase of recovery. Testing should include rest intervals and evaluation of reports of muscle soreness. For example, a therapist should compare reports of muscle soreness immediately after exercise and after a weekend of rest. Repeated muscle testing across days should corroborate whether muscle weakness is increasing, thus requiring additional rest. Initially, rest periods should be frequent. As the patient continues to recover, demonstrated by a reduction in complaints of soreness and weakness, rest periods may be withdrawn and continuous exercise instituted.
There should be a general avoidance of eccentric muscle strengthening and an emphasis on fast-twitch muscle fiber recruitment, such as that obtained from fast contraction concentric exercise on an isokinetic dynamometer. Other functional tasks often involve eccentric contractions and should be avoided if soreness and weakness increase.
Potential Physiological Responses to Exercise
Ropper and Wijdicks studied a 76-year-old man with severe GBS, who demonstrated extremes of hypotension alternating with hypertension.149 The BP paralleled both systemic vascular resistance and cardiac output. HR, rather than stroke volume, was the major determinant of cardiac output over a wide range of BPs. These findings suggest that hypotension resulted from a vasodepressor response with a vagotomized heart and that hypertension was the result of increased sympathetic activity. Both extremes were caused by parallel changes in vascular resistance and HR. Dysfunction of baroreflex buffering may have accounted for the rapid swings in pressure. The authors caution that BP should be monitored before, during, and after exercise to avoid hypo- or hypertensive reactions.
Interventions for Exercise Training
Pitetti et al.150 reported a case study of an individual who had residual deficits following an acute incidence of GBS to determine if there would be improved physiological adaptations following aerobic endurance training. A 57-year-old man, who for 3 years needed the aid of a crutch for walking, following an acute bout of GBS, participated in this study. Peak work level (W), oxygen consumption, and ventilation were determined on a bicycle ergometer, a Schwinn Air-Dyne ergometer (SAE), and an arm-crank ergometry before and after exercise training. The subject trained for 16 weeks at an approximate frequency of 3 d/wk at an average duration of 30 minutes and at an average intensity of 75% to 80% of pretraining peak HR.
Approximately a 10% improvement was seen in for the SAE and bicycle ergometer, respectively. For peak ventilation, a 23% and 11% improvement was seen for the SAE and bicycle ergometer, respectively. For the arm-crank ergometry, a 16% increase in peak ventilation was seen, with no improvement in aerobic capacity. Total work capacity on the bicycle ergometer was improved by 29% following training. This study demonstrated that patients with GBS may be able to improve cardiopulmonary function and work capacity following a supervised training program using the SAE. The subject also reported improvements in ADL.
It is the peripheral denervation process that links GBS to polio and peripheral neuropathy. Irreversible weakness is believed to be due to muscle damage in patients who are post-polio following strenuous activity. In fact, animal studies have demonstrated short-term detrimental responses to intense exercise on the reinnervation of myelinated fibers. Therefore, physical therapists are cautioned against overworking skeletal muscles of patients with GBS.
Postpolio Syndrome (Practice Patterns 4A, 5H, 5G, 6B, 6E, 7A, 7B, 7C; ICD-9-CM Codes: 344, 357.4)
Poliomyelitis is an acute viral disease that attacks the brain and the ventral horn of the spinal cord. Damage to the lower motor neurons usually results in atrophy and weakness of muscle groups, perhaps paralysis and possibly deformity. A second type, bulbar poliomyelitis, infects the medulla oblongata and may result in dysfunction of the swallowing mechanism along with respiratory and circulatory distress. Minor forms of poliomyelitis result in fever, sore throat, headache, and upper-body stiffness, but leave no significant atrophy or paralysis.
The most common features of postparalytic syndrome (PPS) for more than 350,000 afflicted survivors include general fatigue, weakness, and joint/muscle pain. The primary reasons for these symptoms include (1) destruction of the anterior horn cells by the polio virus, leaving fewer motor neurons to induce muscle contraction; (2) unaffected motor unit enlargement by reinnervation through terminal sprouting; and (3) defective transmission at the neuromuscular junction secondary to failure of terminal axonal sprout.
Postpolio syndrome is a group of related signs and symptoms occurring in people who had paralytic poliomyelitis years earlier. New weakness, fatigue, poor endurance, pain, reduced mobility, increased breathing difficulty, intolerance to cold, and sleep disturbance in various degrees and expressions make up the syndrome. The reported incidence is between 25% and 80%. The origins are multifactorial and can be associated with underexertion, overexertion, inactivity due to intercurrent illness or injury, hypo-oxygenation, sleep apnea, deconditioning, and the failure of sprouted, compensatory large motor units. The exercise question in postpolio syndrome is related to the experience of new weakness or loss of muscle function due to overuse, which is often associated with injudicious repeated challenges to weakened musculature. Carefully prescribed exercise can be used for increasing strength and endurance and improving cardiopulmonary conditioning.
Birk (1993) reviewed the literature involving postpolio syndrome and exercise. The authors concluded that acute responses to resistive exercise suggest significant muscle strength decrements in the knee extensors of individuals with polio compared with similar-aged people without polio. Although there is extremely limited research on training studies, there is a suggestion that low-level training induces significant strength increases for the following at least 6 weeks of training. This should not imply that only the knee extensors are weakened in the lower extremities; however, training research is limited to this muscle group. Birk also reported that acute aerobic responses of individuals with polio also differ significantly from those observed in age-matched control studies. Studies of aerobic training suggest the potential of significant elevations in maximal oxygen uptake.151
The manifestations of postpolio syndrome typically occur between 20 and 40 years after an acute episode of poliomyelitis and are confined to previously affected muscles. Because of motor unit remodeling and direct mechanical damage, weakness increases in individual muscles until it exceeds their narrow margin of reserve and becomes clinically apparent. Although the exact cause is not clear, generalized weakness often occurs when several muscles are affected and various postural limb strategies used by the patient are no longer able to compensate for the loss of muscle strength. The mainstays of treatment are lifestyle changes to avoid overexertion and use of lightweight orthoses and assistive aids to unload the extremities.152
Factors That Influence Ability to Exercise
Weinberg and colleagues153 evaluated the factors limiting exercise performance and analyzed the respiratory strategies adopted during exercise in five patients postpolio with severe inspiratory muscle dysfunction at rest and during leg or arm cycle exercise. Gas exchange was measured by arterial blood gas analysis and mass spectrometry of expired air. Ventilatory mechanics were studied by measurement of esophageal and gastric pressures. Blood gases at rest were found to be normal, except for subnormal partial pressure of oxygen (PO2) levels in three patients. In all but one patient, ventilatory insufficiency was the limiting factor for exercise. A compensatory breathing pattern with abdominal muscle recruitment during expiration was present at rest in three of the patients. The pressures generated by the diaphragm were below the fatigue threshold, that is, the level that can be sustained for at least 45 minutes in healthy subjects. The extent of ventilatory dysfunction was evident in blood gas values during the exercise test. In summary, diaphragmatic fatigue seems to be avoided, but at the cost of impaired blood gases.
Willen and Grimby154 described pain and its relationship to the effects of polio, physical activity, and disability of 32 individuals with late effects of polio. More than 50% of the individuals had pain every day, mostly during physical activity. In the lower limbs, cramping pain was the most common pain characteristic in both polio-affected and non–polio-affected limbs. In the upper limbs and in the trunk, aching pain was the most common pain characteristic, especially in the polio-affected areas. The degree of muscle weakness had no correlation to pain experience. The walking test demonstrated a relatively small difference between self-selected and maximal walking speed. Pain and physical mobility were both strongly correlated with energy expenditure. There is a relationship between physical activity in daily life and experience of pain. In many postpolio individuals who experience a high level of pain, self-selected and maximal walking speeds are approximately the same. It is strongly recommended that individuals with late effects of polio, experiencing aching and especially cramping pain, modify their level of physical activity.
Stanghelle et al.155 studied subjective symptoms, medical and social situations, pulmonary function, and physical work capacity during a period of 3 to 5 years in patients with post-polio syndrome. The patients answered a questionnaire about their subjective symptoms and medical and social situations and underwent spirometry as well as symptom-limited exercise stress testing. Most patients experienced increasing symptoms and physical disability related to their polio, and the majority reported that their mental health was unchanged or improved. Lung function was, on average, moderately reduced and of the restrictive type, and only minor changes were found during 3 to 5 years. A pronounced reduction in peak oxygen uptake was seen at the first evaluation, especially among the women.
At the second examination, peak oxygen uptake was further decreased, especially in men, more than that predicted from increasing age. The patients increased their BMI significantly during the same period. These results indicate that subjective symptoms and physical disability related to polio increased with increasing age in these patients with the post-polio syndrome, and cardiorespiratory deconditioning and weight gain also became increasing problems in most patients. However, the mental status of the patients remained stable or improved, possibly due to a comprehensive re-rehabilitation and educational program.
Tests and Measures for Exercise Testing
Willen and associates156 studied the physical performance in individuals with late effects of polio; specifically, they evaluated the effects of reduced muscle strength in the lower limbs. Thirty-two individuals performed a bicycle exercise test. Muscle strength in the quadriceps and the hamstrings was measured on an isokinetic dynamometer. Reductions in peak workload, peak oxygen uptake, and predicted HR were seen. The AT was within or slightly lower than normal limits in relation to predicted maximal oxygen uptake, indicating that the cardiorespiratory system was not limiting performance. Muscle testing of the test group demonstrated a significantly lower ability to perform muscle actions compared with individuals from a reference group, and strong correlations were found among muscle strength, peak , and peak workload. It appears that adjusted peripheral muscle endurance training might improve the work capacity in those individuals with weak leg muscles and low oxygen uptake, whereas individuals with relatively good muscle strength would improve their aerobic fitness in a general fitness program.
Stanghelle and colleagues155 studied 68 subjects who were admitted to a rehabilitation hospital with a presumptive post-polio syndrome who were examined with pulmonary function and symptom-limited exercise stress testing to study how many of these subjects could be classified as suffering from cardiorespiratory deconditioning. The subjects had moderately reduced lung function of the restrictive type, and none of the subjects had forced expiratory volume for 1 second below 30% of predicted value, indicating that hypoventilation would probably not occur. A pronounced reduction in maximal oxygen uptake was seen, especially in women. The maximal HR values were above 70% of predicted values in all but one subject, indicating that subjects might benefit from endurance training. Fifteen subjects had a suspected pulmonary limitation due to the exercise, with the ratio of ventilation to maximal voluntary ventilation greater than 70%. These results indicate that cardiorespiratory deconditioning was considerable in most of the subjects with postpolio syndrome.
Interventions for Exercise Training
Recent studies have shown that judicious exercise can improve muscle strength, cardiorespiratory fitness, and the efficiency of ambulation in postpolio patients. It may also add to the patient’s sense of well-being. These benefits appear to occur when patients stay within reasonable bounds while exercising to avoid overuse problems. In particular, patients should be instructed to avoid activities that cause increasing muscle or joint pain or excessive fatigue, either during or after their exercise program.
Patients seen in postpolio clinics frequently complain of new fatigue, weakness, muscle pain, and/or joint pain. The most frequent complaints involving ADL include new difficulties with walking and stair climbing. The therapeutic benefit of exercise to these patients is to minimize or reverse decline in function.
Patients with postpolio syndrome have unique problems, which need to be considered when prescribing an exercise program for an individual patient. A number of functional etiologies for declining function have been hypothesized including disuse weakness, overuse weakness, weight gain, and chronic weakness. Because of the variability in which the motor neurons to different muscle groups may have been affected in a particular patient, both asymmetric and scattered weaknesses may be present. The challenge in prescribing exercise for the patient with postpolio syndrome comes in recognizing these unique factors in each patient and modifying the prescription accordingly.
One must protect muscles and joints experiencing the adverse effects of overuse, and body areas with very significant chronic weakness, while exercising areas experience the deleterious effects of disuse. Weight gain is to be avoided if at all possible in this population because increased weight only leads to further difficulty in the performance of daily activities.
Kriz and colleagues157 studied the cardiorespiratory responses of 10 subjects postpolio participating in a 16-week upper-extremity aerobic exercise program and compared them with 10 nonexercised controls. The subjects trained three times a week for 20 minutes per session. Exercise intensity was prescribed at 70% to 75% of HR reserve plus resting HR. After training, the exercise group had higher oxygen consumption, carbon dioxide production, , power, and exercise time. There was no reported loss of muscle strength. It was concluded that subjects postpolio can safely achieve an increase in aerobic capacity with a properly modified upper-extremity exercise program. This improvement is comparable to that demonstrated by able-bodied adults.
Many individuals with disabilities may be unable to achieve maximal oxygen uptake in an exercise test, and maximal exercise testing may cause increased fatigue, pain, and muscle weakness. Sasco et al.142 examined the role of submaximal exercise testing and training based on objective as well as subjective parameters in survivors of polio. Subjects participated in a 6-week exercise training program for 30 to 40 minutes, three times a week. The program consisted of treadmill walking at 55% to 70% of age-predicted maximum HRs; however, exercise intensity was modified to minimize discomfort/pain and fatigue. Neither objective nor subjective exercise responses were significantly different in the control group over the 6 weeks. No change was observed in cardiorespiratory conditioning in the experimental group. However, movement economy, which is related to the energy cost of walking, was significantly improved and walking duration was significantly increased at the end of training. Modified aerobic training may have a role in enhancing endurance and reducing fatigue during ADL in polio survivors.
A final study of clinically stable patients with dermatomyositis/polymyositis who underwent a long-term physical training program (6 months) improved muscle strength and increased aerobic capacity by 28% compared with untrained patients. The authors point out that physical training should be a part of their comprehensive rehabilitation management, particularly in view of the cardiopulmonary risk in these patients.158
General Effects of Exercise Training on Impairment, Disability, and Quality of Life
Oncu and colleagues (2009) were one of the first to investigate the impact of a hospital and a home exercise program on functional capacity (), fatigue (fatigue severity score), and QOL (Nottingham Health Profile) on 32 patients with postpolio syndrome in Izmar, Turkey.159 Half the patients each received either hospital or home aerobic exercise programs. Parameters of fatigue and QOL improved in both the home- and hospital-based exercise program, but the energy subscore on the Nottingham Health Profile improved only in the hospital exercise. Furthermore, the functional exercise capacity improved only in the hospital-based environment. This may have been attributable to the PT supervision of the program. Thus the authors concluded that the physical exercise with the goal of increasing functional capacity that leads to positive changes in fatigue and QOL should be conducted under supervision in a hospital environment. Since this health care delivery model may not be feasible in the United States, certainly the implementation of such an exercise program on an outpatient basis might have similar effects.
SUMMARY
Evidence of the potential effectiveness of exercise for neurological populations has been presented. Therapists should consider cardiopulmonary testing and training as part of their therapeutic armamentarium. Training neurological patients with respect to their cardiopulmonary system should lead to a reduction in coronary heart disease risk factors and improvement in other secondary conditions. This improvement in energetics will likely lead to improved functional status, community mobility, and QOL.
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