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Exercise Training and Parkinson's Disease

Placebo or Essential Treatment?

Iris Reuter, MD
Martin Engelhardt, MD, PhD

THE PHYSICIAN AND SPORTSMEDICINE - VOL 30 - NO. 3 - MARCH 2002


In Brief: Exercise training is often recommended for patients who have Parkinson's disease. Until the debate about the pathophysiologic cause of impaired movement in parkinsonism is settled, it is difficult to develop a specific exercise treatment for symptoms that include hypokinesia, tremor, and muscular rigidity. Most of the published studies show a benefit of exercise training, and we provide an overview of the most essential studies and present conclusions for a practical approach to exercise training in parkinsonism.

Parkinson's disease (PD) is a neurodegenerative condition with clinical features that include resting tremor, rigidity, bradykinesia, and loss of postural reflexes. The pathogenesis is the loss of dopaminergic neurons in the substantia nigra with a subsequent lack of the neurotransmitter dopamine. The onset is usually in the sixth or seventh decade of life, but earlier onset is well known. Actor Michael J. Fox was diagnosed with early-onset PD at age 30.

Pre-exercise Clinical Assessment

Motor difficulties. Considerable debate still exists about the pathophysiology of movement impairment in PD.1-3 Electrophysical studies in monkeys2,3 showed when specific neurons of the basal ganglia were active during the movement cycle; however, it is still difficult to develop a training program to improve motor disability. Some symptoms are directly related to PD, but others are functional problems from aging or are factors secondary to the disease, such as muscle atrophy caused by impaired movements, contractures, osteoporosis, and cardiovascular deficits.4

Most PD patients are elderly, and even healthy older adults have more balance problems during walking and a greater risk of falling5 than do younger people. Studies by Woollacott and Tang5 and by Azulay et al6 showed that older people depend on their visual systems more often to get additional information to maintain balance, and they have more difficulties increasing step length than do younger people. Coordination, muscle strength, and flexibility also decrease with age,7,8 and deficits are more pronounced in parkinsonism because of bradykinesia, increased muscle rigidity, and loss of postural reflexes. Table 1 shows the requirements for locomotion and the motor deficits in PD.

TABLE 1. Requirements for Locomotion and Motor Deficits in Parkinson's Disease

TaskImpairments

Initiation and termination of locomotionFreezing before walking or after turn of direction
Reduced muscle-force production
Loss of heel strike, which impairs braking
Impairment of ballistic movements

Generation and maintenance of continuous
movement toward destination
Reduced speed forward caused by diminished stride length and
  increased double-limb support phase
Instability of upper trunk caused by lack of transverse
  pelvis rotation
Fixed shoulder-elbow position

Adaptation to a changing environment or to
concurrent tasks
Difficulties in performing two tasks at the same time
Insufficient function of sensory-motor association cortex,
  less focused cortical activity

Cardiovascular considerations. Abnormal cardiovascular reflexes are common in PD and more frequent than in healthy older people.9 Cardiovascular abnormalities in patients who have PD include orthostatic hypotension, postprandial hypotension, cardiac arrhythmias, and, less commonly, exercise-induced hypotension. Dopaminergic drugs can worsen all cardiovascular symptoms. Frequently, a fixed pulse rate prevents an adequate tachycardia response to exercise in PD patients.10

Patients, especially the elderly, should be evaluated for cardiac problems before exercise training commences. Because of possible involvement of the autonomic nervous system, clinicians must be aware of the risk of exercise-induced hypotension. Figure 1 presents the blood pressure curves observed by Reuter et al11 in an exercise test of three patients who had exercise-induced hypotension. Patients became symptomatic at a higher submaximal level, maximal level, or during recovery. Subjects who had rigid heart rate variability and the akinetic-rigid phenotype were more prone to develop exercise-induced hypotension than were subjects who had normal heart rate variability.

Many PD patients also suffer from obstructive respiratory diseases.12 Rigidity and muscle stiffness affect not only the limbs, but also the trunk and respiratory muscles. In exercise tests, peak cardiovascular and metabolic responses of PD patients were comparable to those of controls,11,13 but PD patients had higher submaximal VO2 and higher submaximal oxygen consumption.13,14 This might be due to decreased mechanical efficiency or to mitochondrial dysfunction.15 Patients who have PD, therefore, need to improve their efficiency of movement to train at an intensity level that increases their cardiovascular endurance. In contrast to previous opinion, cardiovascular and metabolic parameters can improve in elderly patients.16

How Medication and Exercise Relate

In PD patients, endogenous dopamine is more than 60% reduced. The treatment for PD is symptomatic, and drug therapy aims to supply the lacking dopamine. The two mainstream drug therapies are levodopa (a precursor drug of dopamine) and dopamine agonists that work at the level of the dopamine receptors in the striatum. Medication influences motor performance markedly; however, drug treatment cannot abolish all symptoms, and physical therapy is often recommended.

To assess their stage of disease, patients are asked if their motor disability fluctuates and if they feel the onset and wearing off of the medication. If so, the clinician can determine when the patient is in an optimal "on" state (best medication effect) and when the patient is in an "off" state (without medication or when medication has no effect on motor disability). Critical times are when medication is being altered or when patients have infections. Understandably, patients will not be motivated to exercise during "off" states because their movements are impaired. Patients who experience "on" and "off" periods are sometimes not able to walk during "off" periods but can perform activities well during "on" periods. Therefore, patients should be in an "on" period when they participate in sports. Some patients use sports to reduce drug-induced dyskinesia. Some patients benefit from exercise when they experience dyskinesia; others trigger dyskinesia with exercise.

Patients are sometimes concerned that the effect of medication taken before exercise will not last as long as under normal daily activity. Carter et al17 and Goetz et al18 did not find any significant influence of exercise on levodopa absorption and clinical efficacy, but Carter et al reported marked interindividual differences in levodopa absorption. In a more detailed pharmacokinetic and dynamic study, Reuter et al19 reported two counterbalancing tendencies under exercise: better levodopa absorption and increased EC50 (EC50 is the concentration of agonist required to provoke a response halfway between the baseline and maximum responses). This suggests that the same dose of levodopa that provoked the half-maximal motor effect at rest produced less than 50% of the effect under exercise. To achieve the same half maximal effect under exercise, the dose of levodopa has to be increased.

Symptoms Influence Sports Activities

A striking reduction in physical activity occurs, even in patients with low motor disability scores.20 Although some patients feel an urge to exercise to become mobile, especially in the morning, others feel fatigued, and many give up their usual physical activities such as playing tennis, skiing, running, and walking. The suggestion of physical therapy or sports therapy is often perceived less than favorably by some patients who perceive that their motor impairment is more severe while exercising than at rest.

In studies by Kuroda et al21 and Sasco et al,22 some patients were anxious that physical activity might worsen the course of the disease. These studies showed a slight protective effect of physical activity on the risk of developing PD, but high-performance athletes had the same risk as nonathletes. However, early in the disease, athletic patients noticed impairments in their usual sports activity. They lost the ability to change location quickly during a tennis game or to brake during downhill skiing, and the distance of free and easy walking during hiking was reduced. Invincible fatigue after mountaineering followed by a period of stiffness and immobility was also reported. There was no difference in sports performance between parkinsonian patients with an akinetic-rigid, tremor-dominant, or akinetic-rigid-tremor phenotypes.20

Depression

Every physician who treats PD patients must be prepared to assess fatigue and depression. Prevalence of depression among patients who have PD ranges from 20% to 70%. The effect of depression and anxiety on motor disability was observed by Mohr et al,23 and they noted improvement of rigidity and motor function using behavioral therapy for anxiety.

Improved emotional condition can subsequently improve coordination and motor disability per se, and a patient might put more effort into a task when motivated. However, a task, such as rising from a chair using one leg, can be performed only if the patient has adequate strength. Although evidence suggests that physical therapy benefits patients who have PD, psychological factors might confound the data.

Evaluations of the effect of sport (especially endurance activities) among depressed patients showed significant improvement of mood.23 Positive feedback and inclusion in group sports reduced anxiety and feelings of social isolation, and often reduced motor disability.23 Group physical therapy has a social integrative function. Patients appreciate the attention of the therapist and the social contacts in the group.18,24 When evaluated, exercise therapy improved well-being and mood.23

Beneficial Effects of Physical Therapy

Physical therapy comprises several specialities: single and group physical therapy, sports therapy, therapeutic swimming, ergotherapy, occupational therapy, and speech therapy. Physical therapy for PD aims to:

  • Preserve the remaining functions on a high level,
  • Improve motor function, including initiation of movement, trunk mobilization, and range of motion,
  • Reduce tremor and rigidity,
  • Improve activities of daily living, and
  • Prevent secondary complications caused by posture changes or muscle atrophy.

The recommended intensity of exercise training in PD is controversial, and the benefit of intensive exercise as treatment for motor disability is not clear, but the benefit of exercise as treatment for PD is generally accepted. In one of the first reports in the literature on physical therapy for PD, Doshay25 compared 100 PD patients who did not receive any physical therapy with 100 privately insured PD patients who had had intensive physical therapy for several years. He found, on average, less severely disabled patients in the exercising group in short- and long-term assessments. Although this study lacks objective measures and has many methodologic flaws, it is a remarkable observation, especially regarding the long-term assessment and the limitation of confounding effects of different drugs and drug-treatment regimens. These patients probably had similar treatment because of the few drugs available for PD in 1962.

In the following years, the effect of physical therapy was always assessed in carefully selected patients. Patients with serious concomitant diseases, atypical PD syndromes, or dementia were excluded. In general, patients had to be able to commit themselves to the program and to be sufficiently mobile to attend the exercise sessions. These factors need to be considered when results of these studies are applied to clinical practice with nonselected PD patients. The training of high-performance athletes indicates that a frequency of two to three times per week is necessary for a training effect, and at least 6 weeks of activity is required to improve performance. Most of the studies had these prerequisites.

Only a few studies had an appropriate control group and blinded raters to assess motor disability during the study. Comella et al26 conducted a randomized, single-blind, crossover study over 4 weeks with three 1-hour sessions per week in 18 patients who had Hoehn and Yahr stage 2 or 3 PD, a mean age of 66 years, and a mean PD duration of 10 years. They found a significant improvement in the Unified Parkinson's Disease Rating Scale (UPDRS) for activities of daily living and motor scores. Without continued training, the clinical improvement returned to baseline after 6 months. (To see these scales, go to https://neurosurgery.mgh.harvard.edu/pdstages.htm.)

In a controlled study of 33 patients, Formisano et al27 found that intensive physical therapy—three 1-hour sessions per week for 4 months—improved motor disability. The program included active and passive mobilization exercises (flexion and extension of hips, knees, ankles, elbows, and wrists), abduction and adduction of the shoulders, and balance and coordination exercises in supine and quadrupedic positions. No correlation existed between exercise benefit and the patients' ages. Severity and duration of the disease influenced the benefit of the treatment in the improved measures. Patients with a low Columbia University Rating Scale (CURS) score (<23) improved markedly in the walking test, and patients with a high CURS score (>23) improved in fitting cubes with the left hand. Patients who had PD up to 5 years showed improvements in walking, and patients who had PD longer than 5 years improved in the cube-fitting task.

Palmer et al28 compared effects of upper body karate training with a United Parkinson Foundation stretching program in 28 patients in a randomized, controlled, blind study. The 12-week training period included three 1-hour sessions per week of either stretching or karate. At the end of the training period, improvements in both groups were similar. Functional improvement occurred in gait, arm tremor, and coordination, but function in complex arm-trunk movements deteriorated. The authors theorized that the deterioration resulted from increased stiffness after an exhausting exercise program and that stiffness was a limiting factor of the exercise program; however, muscle rigidity remained unchanged.

In an open pilot trial of 14 weeks with two training sessions per week, Reuter et al29 reported an improvement of PD-specific disability and general muscle strength, flexibility, and coordination as assessed by a sport-specific rating scale. An unexpected side effect of the training program was that levodopa-induced involuntary movements and so-called dyskinesias improved; dystonia and fluctuations of motor disability remained the same. The effects lasted 6 weeks beyond the active training period. External stimuli improved gait initiation and performance of simultaneous tasks. This confirms the results of a study by Thaut et al,30 who demonstrated that externally cued movements are the best retained. Rhythmic auditory stimulation was used to entrain gait patterns that significantly improved the velocity, stride length, and step cadence during a 3-week home-based program. Patients who have PD are more impaired and, therefore, benefit more from movement cues than unaffected elderly people. External stimulus music was advantageous in all studies in which it was used.

Axial symptoms are often regarded as difficult to treat with physical therapy, but two studies that targeted axial symptoms reported improvements. In a controlled study, Schenkman et al31 showed that axial rotation and flexibility can be improved over 10 weeks in patients who had PD. In a 5-week, uncontrolled study, Viliani et al32 reported improvement in the straightening-up process in patients who had PD. Müller et al33 noted positive effects of motor planning strategies for task preparation.

In contrast to outpatient-group treatment studies, Banks and Caird34 administered an individual home-training program and found a significant increase in position change and walking ability. However, 50% of the patients stopped their exercise program within 3 months, mainly due to fatigue or lack of benefit. Lack of motivation might have contributed as well. Individual home programs lack the social integrative factor of group therapy.

Conflicting Evidence

Gibberd et al35 reported no benefit of physical therapy compared with occupational therapy in 24 patients with stable PD who participated in a 4-week therapy program of two sessions per week and crossed over after a 3-month gap. The authors did not find a significant difference between the two treatments and concluded that physical therapy does not improve the physical condition of stable PD patients. The crossover design of the study is good, but it is questionable whether the control group was suitable for physical therapy. The goal of the active occupational-therapy group was to improve independence and functional activities such as mobility, dressing, and feeding. Patients likely received considerable physical training as well. The assessments used specific tasks that were trained with both programs. In addition, the short duration of the program may have been insufficient to show improvement in an elderly population.

Pedersen et al36 reported a deterioration of stride length and gait velocity after physical therapy in 10 PD patients, despite participants' reported subjective impressions that the training was beneficial. There was no statistically significant improvement in the motor tasks. These results suggest that increased well-being contributes to the benefits of exercise therapy but is not the only decisive parameter. It is not obvious why this study's results disagree, because the training program did not differ from those of more successful group studies.

Reasons for varying study results might be that the training programs and assessment parameters were partially different. One might wonder how well motor disability in a fluctuating disease like PD could be reliably and reproducibly measured. Schenkman et al37 found that many impairment measures were relatively stable during the early and middle stages of PD. Assessments of common PD rating scales (CURS, UPDRS, Hoehn and Yahr stage) have shown that they are reliable and reproducible.38 However, evidence suggests that the scales often measure different aspects of PD, and that it is not feasible to compare patients who have been rated by different scales.

In addition, the PD rating scales are not designed to measure improvements from a physical program. Most do not evaluate specific musculoskeletal impairments and are not sensitive for short-term PD alterations. For example, the steps on the Hoehn and Yahr scale are too large to measure subtle changes. In a controlled trial of physical therapy and occupational therapy for PD, Gibberd et al35 performed assessments with PD rating scales. They found no difference in motor performance between groups, despite patient improvements.

Compelling Questions

Many studies have methodologic deficits and inadequate power because of the small number of individuals studied. Most studies lack an appropriate placebo group. A large, placebo-controlled study should be designed to include at least 40 patients in each treatment arm. To assess if one treatment is superior to another, a study should include two treatment arms: one with PD-specific exercises and the other with nonspecific training. A specific impairment will always limit the function and the performance capacity of patients with parkinsonism. To improve performance, we need to know which type of exercise has a specific effect and which exercises may be helpful but are nonspecific. One might argue that success is the most important factor, whatever the reason might be, but to improve treatment further, we must analyze the effect of a program and separate the general factors from the specific.

Outcome measures should be relevant to activities of daily living and be based on more than just general PD scales that are too insensitive to assess short-term alteration of motor disability. Musculoskeletal rating scales should clearly assess the desired outcome measures, and the chosen exercises must clearly be effective for the deficit being measured.

Practical Aspects of Exercise Therapy

In our experience, several pragmatic issues affect the optimal planning of physical training for patients with PD. Patients should exercise during an optimal "on" period, and each session should be no longer than 45 to 60 minutes. The intensity should be between 60% and 80% of VO2max.39 Training frequency should be at least twice a week, though three times per week is better. Elderly patients benefit from a gradual increase of intensity and duration. We recommend flexibility and balance exercises and low-intensity strength training (table 2). Teaching external cues, splitting complex movements into simple motor tasks, and incorporating simultaneous movements are also beneficial. PD patients are more impaired in these areas than healthy elderly and, therefore, benefit more from training than healthy elderly.6

TABLE 2. Strategies to Improve Specific Deficits in Parkinson's Disease

DeficitCorrective Exercise

Initiation of movementsPolysensory cueing

HasteningSelection of cueing frequencies
Gait preparation exercise with different gait types (forward, backward, sideways)
Position change (lying to sitting or sitting to standing)

BrakingAlternate gait types (forward, backward, walking on toes and heels)

Muscle rigidityStretching exercises to aid flexibility
Exercises in warm water to aid relaxation

Trunk stiffnessRotational and straightening-up exercises

Complex and compound movements,     
dual and/or sequential tasks
Training with simple motor sequences

Simultaneous movements and
coordination
Forming complex and simultaneous movements from simple motor sequences

Miscalling of movementsTraining of large-amplitude movements

BalanceRoll exercises, reach exercises
Pezzi ball (also called gymnastic ball or physiotherapy ball) exercises
Pool exercises with paddles and swim noodles

StrengthIsometric exercises in supine, prone, and quadruped positions
Rollover exercises
Training against water resistance

The group should not be too heterogeneous; otherwise, it is too much for some patients, and others feel bored. Patients enjoy partner exercises, such as dancing or ball games, if both partners are in similar physical condition. External stimuli, like music, is advantageous. Although many PD patients like ball games or bicycling, they must be aware of the risk of falls.

Training in water helps detonate muscles and decrease trunk stiffness and rigidity.30 Water improves body perception, and water resistance can be used for strength training. The pool should have a railing, and patients should be able to stand. The water temperature should be between 81° and 88°F (27° and 31°C) to aid muscle relaxation. There should be at least one therapist for every six patients, and tools, such as swim noodles, are helpful. Patients will need extra time for changing clothes before and after training sessions.

Key Points

Most studies show that physical therapy benefits PD patients, though sometimes only modestly. The studies are not designed to assess the quality and specificity of different exercise programs or to show that one program is clearly superior to others.

Improvements after training programs were found in global scores rather than for single items; however, global scores are more vulnerable to confounders and placebo effects. The various exercise programs described in the studies target the same goals: improving bradykinesia, rigidity, flexibility, and balance. Learning external cues helped patients to initiate movements, continue moving, and overcome obstacles.

The effect of exercise outlasted the training period in studies that included follow-up exams. Gait improvement with visual cues lasted about 2 hours after training. After 2 hours, the increased attention may have dropped to a "normal" level. However, only specific cue patterns improve gait, which refutes the hypothesis that the effect of visual cues was purely based on improved attention.6,40 The duration of this long-term effect remains unclear, because without specific training, the patients in the studies returned to baseline within 3 to 6 months. The data support that there are exercise benefits specific to the pathophysiology of PD; however, we are not aware of an exercise program suitable to overcome the specific motor deficits in PD.

It is well known that PD patients can perform much better when they are aware of the task. Patients in follow-up investigations may be less anxious and more focused on the tasks, but this is difficult to measure. Improvement seems to be more than would be expected from increased alertness. A way to resolve this might be to use two baseline assessments.

No clear data indicate which patients benefit most from training. Apart from one study41 of bedridden and wheelchair-bound patients, all were conducted in PD patients at Hoehn and Yahr stage 2 or 3 (early or moderately advanced patients). Reuter et al29 did not find any correlation between demographic data and symptom improvement. Other authors found a correlation between improvement and disease severity,42 but not between disease duration or patient age. Because elderly patients can improve as much as younger subjects, we encourage physicians to initiate physical therapy in all their PD patients.

References

  1. Marsden CD, Obeso JA: The functions of the basal ganglia and the paradox of stereotaxic surgery in Parkinson's disease. Brain 1994;117(Pt 4):877-897
  2. Parent A, Hazrati LN: Functional anatomy of the basal ganglia. I. The cortico-basal ganglia-thalamo-cortical loop. Brain Res Brain Res Rev 1995;20(1):91-127
  3. Parent A, Hazrati LN: Functional anatomy of the basal ganglia. II. The place of subthalamic nucleus and external pallidum in basal ganglia circuitry. Brain Res Brain Res Rev 1995;20(1):128-154
  4. Handford F: Towards a rational basis for physiotherapy in Parkinson's disease. Baillierres Clin Neurol 1993;2(1):141-158
  5. Woollacott MH, Tang PF: Balance control during walking in the older adult: research and its implications. Phys Ther 1997;77(6):646-660
  6. Azulay JP, Mesure S, Amblard B, et al: Visual control of locomotion in Parkinson's disease. Brain 1999;122(Pt 1):111-120
  7. Hollmann W, Liesen H, Rost R, et al: Uber das Leistungsverhalten und die Trainierbarkeit im Alter. Z Gerontol 1978;11:312-324
  8. Daubney ME, Culham EG: Lower extremity muscle force and balance performance in adults aged 65 years and older. Phys Ther 1999;79(12):1177-1185
  9. Turkka JT, Tolonen U, Myllyla VV: Cardiovascular reflexes in Parkinson's disease. Eur Neurol 1987;26(2):104-112
  10. Tanner CM, Goetz CG, Klawans HL: Autonomic nervous system disorders in Parkinson's disease, in Koller WC (ed): Handbook of Parkinson's Disease. New York, Marcel Dekker, 1992, pp 185-215
  11. Reuter I, Engelhardt M, Freiwald J, et al: Exercise test in Parkinson's disease. Clin Auton Res 1999;9(3):129-134
  12. Neu HC, Connolly JJ Jr, Schwertley FW, et al: Obstructive respiratory dysfunction in parkinsonian patients. Am Rev Respir Dis 1967;95(1):33-47
  13. Protas EJ, Stanley RK, Jankovic J, et al: Cardiovascular and metabolic responses to upper- and lower-extremity exercise in men with idiopathic Parkinson's disease. Phys Ther 1996;76(1):34-40
  14. Stanley RK, Protas EJ, Jankovic J: Exercise performance in those having Parkinson's disease and healthy normals. Med Sci Sports Exerc 1999;31(6):761-766
  15. Schapira AH: Evidence for mitochondrial dysfunction in Parkinson's disease—a critical appraisal. Mov Disord 1994:9(2):125-138
  16. Liesen H, Heikkinen E, Suominen H, et al: Der Effekt eines zwolfwochigen Ausdauertrainings auf die Leistungsfähigkeit und den Muskelstoffwechsel bei untrainierten Männern des 6. und 7. Lebensjahrzehnts. Sportarzt und Sportmed 1975;2:26-40
  17. Carter JH, Nutt JG, Woodward WR: The effect of exercise on levodopa absorption. Neurology 1992;42(10):2042-2045
  18. Goetz CG, Thelen JA, MacLeod CM, et al: Blood levodopa levels and unified Parkinson's disease rating scale function: with and without exercise. Neurology 1993;43(5):1040-1042
  19. Reuter I, Harder S, Engelhardt M, et al: The effect of exercise on pharmacokinetics and pharmacodynamics of levodopa. Mov Disord 2000;15(5):862-868
  20. Fertl E, Doppelbauer A, Auff E: Physical activity and sports in patients suffering from Parkinson's disease in comparison with healthy seniors. J Neural Transm Park Dis Dement Sect 1993;5(2):157-161
  21. Kuroda K, Tatara K, Takatorige T, et al: Effect of physical exercise on mortality in patients with Parkinson's disease. Acta Neurol Scand 1992;86(1):55-59
  22. Sasco AJ, Paffenbarger RS Jr, Gendre I, et al: The role of physical exercise in the occurrence of Parkinson's disease. Arch Neurol 1992;49(4):360-365
  23. Mohr B, Müller V, Mattes R, et al: Behavioral treatment of Parkinson's disease leads to improvement of motor skills and to tremor reduction. Behav Ther 1996;27:235-255
  24. Szekely BC, Kosanovich NN, Sheppard W: Adjunctive treatment in Parkinson's disease: physical therapy and comprehensive group therapy. Rehabil Lit 1982;43(3-4):72-76
  25. Doshay LJ: Current concepts in therapy: Method and value of physiotherapy in Parkinson's disease. N Engl J Med 1962;Apr 26:878-880
  26. Comella CL, Stebbins GT, Brown-Toms N, et al: Physical therapy and Parkinson's disease: a controlled clinical trial. Neurology 1994;44(3 pt 1):376-378
  27. Formisano R, Pratesi L, Modarelli FT, et al: Rehabilitation and Parkinson's disease. Scand J Rehabil Med 1992;24(3):157-160
  28. Palmer SS, Mortimer JA, Webster DD, et al: Exercise therapy for Parkinson's disease. Arch Phys Med Rehabil 1986;67:(10)741-745
  29. Reuter I, Engelhardt M, Stecker K, et al: Therapeutic value of exercise training in Parkinson's disease. Med Sci Sports Exerc 1999;31(11):1544-1549
  30. Thaut MH, McIntosh GC, Rice RR, et al: Rhythmic auditory stimulation in gait training for Parkinson's disease patients. Mov Disord 1996;11(2):193-200
  31. Schenkman M, Cutson TM, Kuchibhatla M, et al: Exercise to improve spinal flexibility and function for people with Parkinson's disease: a randomized, controlled trial. J Am Geriatr Soc 1998;46(10):1207-1216
  32. Viliani T, Pasquetti P, Magnolfi S, et al: Effects of physical training on straightening-up processes in patients with Parkinson's disease. Disabil Rehab 1999;21(2):68-73
  33. Müller V, Mohr B, Rosin R, et al: Short-term effects of behavioral treatment on movement initiation and postural control in Parkinson's disease: a controlled clinical study. Mov Disord 1997;12(3):306-314
  34. Banks MA, Caird FI: Physiotherapy benefits patients with Parkinson's disease. Clin Rehabil 1989;3:11-16
  35. Gibberd FB, Page NG, Spencer KM, et al: Controlled trial of physiotherapy and occupational therapy for Parkinson's disease. Br Med J 1981;282(6271):1196
  36. Pedersen SW, Oberg B, Insulander A, et al: Group training in parkinsonism: quantitative measurements of treatment. Scand J Rehabil Med 1990;22(4):207-211
  37. Schenkman M, Cutson TM, Kuchibhatla, et al: Reliability of impairment and physical performance measures for persons with Parkinson's disease. Phys Ther 1997;77(1):19-27
  38. Baas H, Stecker K, Fischer PA: Value and appropriate use of rating scales and apparative measurements in quantification of disability in Parkinson's disease. J Neural Transm Park Dis Dement Sect 1993;5(1):45-61
  39. American College of Sports Medicine: Position stand: the recommended quantity and quality of exercise for developing and maintaining cardiorespiratory and muscular fitness, and flexibility in healthy adults. Med Sci Sports Exerc 1998;30(6):975-991
  40. Morris ME, Iansek R: Characteristics of motor disturbance in Parkinson's disease and strategies for movement rehabilitation. Human movement Science 1996;15:649-669


Dr Reuter is a neurologist in the department of neurology at King's College Hospital in London, and Dr Engelhardt is an orthopedic surgeon in the department of orthopedics at the University of Frankfurt. Address correspondence to Iris Reuter, MD, Dept of Neurology, Clinical Neurosciences, Mapother House, King's College Hospital, Denmark Hill, London SE5 9RS, UK; e-mail to [email protected].

Disclosure information: Dr Reuter discloses no significant relationship with any manufacturer of any commercial product mentioned in this article. No drug is mentioned in this article for an unlabeled use.


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