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Postural control and falls in individuals with chronic stroke : neural mechanisms and effects of exercise Marigold, Daniel S. 2003

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POSTURAL CONTROL AND FALLS IN INDIVIDUALS WITH CHRONIC STROKE: NEURAL MECHANISMS AND EFFECTS OF EXERCISE by DANIEL S. M A R I G O L D B.Sc. (Kinesiology), University of Waterloo, 2001 A THESIS SUBMITTED IN PARTIAL FULFILMENT OF THE REQUIREMENTS FOR THE DEGREE OF M A S T E R OF SCIENCE in THE F A C U L T Y OF G R A D U A T E STUDIES (Graduate Program in Neuroscience) , We accept this thesis as conforming to the required standard THE UNIVERSITY OF BRITISH C O L U M B I A December 2003 © Daniel S. Marigold, 2003 In presenting this thesis in partial fulfilment of the requirements for an advanced degree at the University of British Columbia, I agree that the Library shall make it freely available for reference and study. I further agree that permission for extensive copying of this thesis for scholarly purposes may be granted by the head of my department or by his or her representatives. It is understood that copying or publication of this thesis for financial gain shall not be allowed without my written permission. ABSTRACT n Although falls and fall-related injuries are an enormous burden for individuals with stroke, we do not know the neural mechanisms underlying these events. While impairments in postural control presumably contribute to falls, the type of exercises most effective for improving postural control in individuals with chronic stroke are unclear. The purpose of this thesis was (1) to understand how individuals with chronic stroke modulate postural control and determine the underlying neural mechanisms contributing to falls and (2) to determine the effects of two different exercise interventions on postural control and physical function. In each of the three experiments conducted, postural reflexes were evoked by unexpected translations of a platform upon which participants were standing. Experiment I examined the effects of different weight-' bearing load on the modulation of lower limb postural reflexes. We revealed that individuals with stroke could modulate ankle extensor, but not ankle dorsiflexor reflex magnitude. In Experiment II we discovered that reduced tibialis anterior reflex magnitude and delayed non-paretic rectus femoris onset latency contribute to falls in individuals with stroke. In addition, reduced maximum volitional muscle strength, particularly the paretic lower limb, contributed to falls induced by platform translations. Based on the results from the first two experiments, we hypothesized that deficits in supraspinal centres are responsible for the impaired postural control observed. Experiment HI was a 10-week randomized clinical trial in individuals with chronic stroke. The results demonstrated that regardless of intervention (Agility or Stretching/weight-shifting program), exercise resulted in faster paretic lower limb postural reflexes, improved functional balance and mobility, faster step reaction time, and improved balance confidence and quality of life. However, there was a greater change in paretic rectus femoris postural reflex onset latency and step reaction time for the Agility exercise group. Although there was no difference in the number of fallers between groups when the entire sample was included, a sub-analysis of those with a history falls demonstrated a reduction in the number of fallers in the Agility group. These results suggest that an Agility-based exercise intervention may be more beneficial for individuals with stroke. Further, the results suggest exercise-induced neural plasticity. ' Ill TABLE OF CONTENTS A B S T R A C T i i T A B L E OF CONTENTS i i i List of Tables vii List of Figures viii Contribution of the Author ix Acknowledgements x CHAPTER 1 - Introduction and Purpose .;1 1.1 Overview of Thesis 1 1.2 Purpose |1 1.3 Introduction 1 1.3.1 Cerebrovascular Accident 1 1.3.2 Postural Control 2 1.4 Literature Review 3 1.4.1 Falls in individuals with stroke •] .3 1.4.2 Exercise in individuals with chronic stroke 4 1.4.3 Postural control following stroke 7 1.5 Research Questions 9 1.5.1 Research Question #1 (Chapter 2) .9 1.5.2 Research Question #2 (Chapter 3) 10 1.5.3 Research Question #3 (Chapter 4 - primary study) 10 CHAPTER 2 - Experiment 1 11 2.1 Abstract 11 2.2 Introduction 11 2.3 Method 13 2.3.1 Participants 13 2.3.2 Protocol 14 2.3.3 Data Analysis 14 2.4 Results 16 2.4.1 The effect of weight-bearing load on the magnitude of postural reflexes 18 2.4.2 The effect of weight-bearing load on muscle onset latency 20 2.5 Discussion 21 IV 2.5.1 Modulation of ankle muscle postural reflex magnitude following stroke 22 2.5.2 Altered supraspinal control due to stroke affects timing of postural reflexes independent of load 23 2.6 Bridging Summary 24 CHAPTER 3 - Experiment II 25 3.1 Abstract 25 3.2 Introduction 26 3.3 Methods 27 3.3.1 Participants 27 3.3.2 Protocol 28 3.3.3 Data Analyses 29 3.3.4 Statistical Analyses 30 3.4 Results 31 3.4.1 Muscle postural reflexes 31 3.4.2 Muscle strength 32 3.5 Discussion 35 3.5.1 Postural reflexes evoked from forward platform translations: contribution to falls... 35 3.5.2 Muscle weakness contributes to falls 37 3.5.3 Future directions and implications 38 3.6 Bridging Summary 38 C H A P T E R 4 - Experiment III 40 4.1 Summary 40 4.2 Introduction 41 4.3 Methods 42 4.3.1 Participants 42 4.3.2 Study design 42 4.3.3 Intervention 43 4.3.4 Outcome measures.. 43 4.3.5 Statistical analysis 46 4.4 Results 47 4.4.1 Participant characteristics 47 4.4.2 Clinical outcome measures 47 4.4.3 Muscle onset latencies 50 4.4.4 Falls 50 4.5 Discussion 54 4.6 Platform-induced falls 55 CHAPTER 5 - Conclusions and General Discussion 56 5.1 General Findings 56 5.2 Evidence of altered supraspinal control contributing to impaired postural control in stroke 56 5.2.1 Peripheral mechanisms contribute minimally to the impaired postural control following stroke 57 5.2.2 Supraspinal deficits are responsible for the impaired postural control following stroke : 58 5.2.3 Implications for rehabilitation 59 5.3 Exercise interventions for individuals with chronic stroke 59 5.3.1 Program adherence, safety, and exercise instructors 60 5.3.2 Types of exercises used in the intervention and their effectiveness 61 5.4 Exercise-induced Neural Plasticity 63 5.4.1 Reasons for exercise-induced neural plasticity 64 5.4.2 Potential mechanisms for exercise-induced neural plasticity 66 5.5 Limitations 69 5.6 Future directions 71 5.7 Final thoughts 72 C H A P T E R 6 - References 73 Appendix I: Literature table - Falls in individuals with stroke 94 Appendix II: Literature table - Exercise in individuals with stroke 98 Appendix III: Literature table - Postural control following stroke 114 Appendix IV: Test re-test reliability for standing postural reflexes 12^ 7 Appendix V : Berg Balance Scale 128 Appendix VI: Nottingham Health Profile (NHP) 132 Appendix VII: Activities-specific Balance Confidence (ABC) Scale 135 Appendix VIII: Informed consent for Experiment 1 136 Appendix IX: Platform translation protocol for Experiment I 138 Appendix X : E M G electrode placement guidelines 139 Appendix XI: American Heart Association Stroke Functional Classification (AHASFC) 140 vi Appendix XII: Informed consent for Experiment II and III 141 Appendix XIII: Platform translation protocol for Experiment II and III 144 Appendix XIV: Recruitment for Experiment II and III 145 Appendix X V : Mini-Mental State Exam 146 Appendix X V I : Experiment II and III physician consent 148 Appendix XVII: Exercise interventions 150 Appendix XVIII: Platform-induced falls for Experiment III 152 vii List of Tables Table 2.1 Mean (SD) of participant characteristics 13 Table 2.2 Weight-bearing load in percent body-weight (SD) 16 Table 2.3 Mean (SD) onset latencies (msec) for backward & forward platform translations .. ..21 Table 3.1 Participant characteristics of the non-fallers (N = 42) and fallers (N = 14) 28 Table 3.2 Postural reflex differences between Fallers and Non-fallers 33 Table 4.1 Participant characteristics 49 Table 4.2 Changes over time with clinical measures for both exercise groups 52 Table 4.3 Effects of the exercise interventions on postural reflex muscle onset latencies 53 Table 4.4 Fall data over one year from the start of the exercise interventions for the Stretching/weight-shifting and Agility groups 54 Table 1.1: Falls in individuals with stroke 94 Table n. 1: Persons with chronic stroke 98 Table H2: Persons with acute stroke - relevant and important articles only I l l Table III. 1: Postural control following stroke 114 Table IV. 1: Test re-test reliability 127 Table V I . l . N H P 132 Table IX. 1: Experiment I protocol 138 Table X . l : Electrode placement 139 Table XIII. 1: Experiment II and III protocol 144 Table XVIII. 1: Falls on platform 152 Vll l List of Figures Figure 2.1 (A) Diagrammatic definitions of the onset latency and postural reflex magnitude (hatched is the postural reflex magnitude calculated from a 75 msec area from the onset latency). Typical postural reflex responses of the (B) paretic M G and (C) non-paretic M G under the three load conditions for one individual with stroke 17 Figure 2.2 Postural reflex magnitude from M G and T A for the stroke and control groups. Values normalized to the Neutral condition are shown, although statistical analyses were performed on the non-normalized data. Note that background muscle activity was removed prior to calculating the magnitude 19 Figure 2.3 Background muscle activity from M G and T A for the stroke and control groups. Values normalized to the Neutral condition are shown 20 i Figure 3.1 Sample paretic limb postural reflexes evoked from a forward platform translation for (A) a Non-faller and (B) a Faller. Time zero represents the onset of the platform movement 32 Figure 3.2 Isokinetic joint torques normalized to body mass for the ankle dorsiflexors, knee extensors, and hip flexors. (A) Paretic limb joint torque for the Non-fallers and Fallers. (B) Non-paretic limb joint torque for the Non-fallers and Fallers 34 Figure 4.1 Trial profile ..48 Figure 4.2 Changes in paretic limb postural reflex muscle onset latencies following the exercise intervention. A typical filtered E M G profile (sample from one participant within the Agility group) demonstrating the faster postural reflexes with exercise training. The solid thick line represents the postural reflex during baseline testing and the dashed line represents the postural reflex during post-intervention testing 51 ix Contribution of the Author This thesis contains three experiments that have been conducted by the candidate Daniel S. Marigold, under the supervision of Janice J. Eng (Associate Professor, School of Rehabilitation Sciences). The collection, analysis, and documentation of all experiments were primarily the work of the candidate. The above statement was written by Daniel S. Marigold and agreed upon by the undersigned. Janice J. Eng, Ph.EtX^ References Marigold DS, Eng JJ, Inglis JT. Modulation of ankle postural reflexes in stroke: implications for falls. J Physiol (in review). Marigold DS, Eng JJ. Neural mechanisms contributing to falls in individuals with chronic stroke. J Neurophysiol (in review). Marigold DS, Eng JJ, Dawson AS, Inglis JT, Harris JE, Gylfadottir S. Exercise leads to faster standing postural reflexes and better functional balance and mobility in persons with chronic stroke: a randomized clinical trial. In preparation for submission, November 2003. X Ackn owledgements I would like to start by thanking my thesis committee, Drs. Janice Eng, Tim Inglis, Drew Dawson, and Alan Kingstone, for their help and guidance throughout my degree. In particular, I am forever grateful to my supervisor Dr. Janice Eng for her mentorship, support, encouragement, and guidance. Furthermore, I wish to thank Dr. Janice Eng for giving me the opportunity to run the exercise clinical trial and for putting up with my constant bombardment of ideas, questions, and manuscript drafts. I wish to thank our three exercise instructors, Sif Gylfadottir, Erica Botner, and Atila Ozkaplan for their hard work and dedication to the program. I would also like to thank all my colleagues in the Rehab Research Lab at GF Strong Rehab Centre for their support and help in data collection, particularly Jocelyn Harris, Patrick McCrea, Craig Tokuno, Catherine Donnelly, and Kelly Chu. In addition, I would like to thank Dr. Jon Money for his time and help with the statistical analyses of our experiments. A special thanks goes to Cheryl Louis who was involved in screening, data collection, data inputting, and providing any help when needed. I cannot forget the help and support of my fiancee Erica, my parents Wayne and Pat, and my sister Denise throughout my degree. They all have inspired and encouraged me to reach for and obtain my goals. I am grateful to the Michael Smith Foundation for Health Research and the Natural Sciences and Engineering Research Council of Canada for financial support. Last, but certainly not least, I wish to thank all the participants that took the time to be involved in our studies. CHAPTER 1 - Introduction and Purpose 1 1.1 Overview of Thesis The thesis begins with the overall purpose followed by introductory information regarding stroke and postural control. Subsequently, three sections are presented which are devoted to background research under the following areas, (1) falls in individuals with stroke, (2) exercise in individuals with chronic stroke, and (3) postural control following stroke. Further information for each of these sections can be obtained in the literature tables in Appendices I -in. Background research is followed by a description of the research questions and their hypotheses. Methodology is addressed in each chapter with regard to the particular experiment. Chapters two through four are experimental chapters. Chapter five integrates the findings from each experiment and provides some suggestions and implications for rehabilitation research. 1.2 Purpose The objective of this thesis was (1) to understand how individuals with chronic stroke modulate postural control and determine the underlying neural mechanisms contributing to falls and (2) to determine the effects of two different exercise interventions on postural control and physical function. 1.3 Introduction 1.3.1 Cerebrovascular Accident Cerebrovascular accident (or stroke) results from restricted blood supply to the brain leading to impaired neurologic function (O'Sullivan 1988). There are between 40,000 to 50,000 strokes each year in Canada and there are currently 300,000 individuals living with stroke (Heart and Stroke Foundation^ Canada 2003). Stroke-related impairments include muscle weakness, spasticity, pain, sensorimotor dysfunction, visual deficits, and balance impairments (O'Sullivan 2 1988). Individuals with stroke are at a high risk for falls, presumably due to stroke-related impairments. Recovery occurs fastest during the first 90 days but continues up to six months post-stroke (Duncan and Lai 1997; Jorgensen et al. 1999; Wade et al. 1985). Ninety percent of stroke survivors have some functional disability (Gresham et al. 1975). 1.3.2 Postural Control Postural control has been defined as a complex neural process involved in the organization of the stability and orientation of the body in space (Allum et al., 1998). Postural control occurs continuously with movement; whether during quiet standing (quiet standing postural control), during preparation to move positions (anticipatory postural control), or in response to an : external disturbance or perturbation applied to the body (reactive postural control) and is the primary means of maintaining stability. Postural stability (synonymous with balance) is the ability to maintain the body's centre of mass within the base of support (i.e. the feet) or boundaries in which the base of support doesn't require repositioning (Shumway-Cook and Woollacott 2001). During human stance postural stability is imperative, as large centre of mass excursions outside the base of support may result in a fall. The central nervous system (CNS) utilizes somatosensory, vestibular, and visual input for postural control over a wide range of movements and in response to various destabilizing events (Allum et al., 1998; Dietz et a l , 1992). This is accomplished by generating torques at the joints of the supporting legs and trunk through muscle activity and possible modifications of the base of support by stepping and/or reaching/grasping movements of the upper extremities (Maki and Mcllroy 1996, 1997). The responses generated by the CNS in the form of muscle activity and/or limb movements are referred to as postural responses (or postural reflexes). The functional coupling of muscles that comprise these movements are known as muscle synergies and can change depending on the task and/or environmental constraints (Shumway-Cook and Woollacott 2001). The effects of neurological conditions, such as stroke, on postural control are largely unknown. Reactive postural control is the first line of defense against unexpected balance-threatening disturbances that have the potential to lead to falls. Falls and fall-related injuries are major concerns in individuals who have suffered a stroke. Whether postural reflexes utilized to maintain postural stability in response to unexpected destabilizing events could be modified or -improved through exercise remains uncertain. Although two studies (Eng et al. 2003; 1 3 Tangeman et al. 1990) have shown that exercise improves functional balance in individuals with chronic stroke, the advantages of different types of exercise programs are unknown. 1.4 Literature Review 1.4.1 Falls in individuals with stroke Stroke is the number one cause of neurological disability in Canada (Mayo et al. 1999). Falls and fall-related injuries are a frequent occurrence in individuals with stroke. The incidence of falling among individuals with stroke in a hospital/rehabilitation setting ranges from 39% to 44% (Nyberg and Gustafson 1995; Ugur et al. 2000). Individuals with stroke who fall during this time are twice as likely to fall after discharge (Forster and Young 1995). The incidence of falling for community-dwelling stroke survivors has been reported to be between 23% and 73% (Forster and Young 1995; Hyndman et al. 2002; Jorgensen et al. 2002; Yates et al. 2002). Once an individual falls, a fear of falling may develop (of course, fear of falling may also lead to falls) contributing to activity restriction (Friedman et al. 2002; Murphy et al. 2002). Unfortunately, i f an individual is at high risk for falling more than one fall is a likely scenario. Forster and Young (1995) have reported an average of 3.4 falls per person with stroke during a six-month period following hospital discharge. In fact, the incidence of multiple falls among individuals with stroke is approximately 50% (Hyndman et al. 2002; Yates et al. 2002). Nyberg and Gustafson (1995) have reported the leading cause of falls in individuals with stroke while in a rehabilitation setting is transferring or changing positions. In community-dwelling stroke survivors, 77% of falls occur during walking (Jorgensen et al. 2002). The majority of falls in individuals with stroke appear to be directed sideways and towards their affected side or on their hands and knees (Hyndman et al. 2002). Not surprisingly, Kanis et al. (2001) found a greater than 7-fold increase in fracture risk within the first year after hospitalization with stroke. In older adults, approximately 2 - 6 % suffer fractures as a result of falling (Lord et al. 2001). Impairments such as muscle weakness, pain, spasticity, visual disturbance, and sensorimotor dysfunction may contribute to poor postural control and a high rate of falls in individuals with stroke. Yates et al. (2002) found that individuals with stroke who demonstrated motor and 4 sensory impairments were three times as likely to fall compared to those individuals who exhibited no impairments. Understanding the nature of the postural control problems that result in falls and determining strategies for falls-reduction are vital in reducing health care costs and ensuring quality of life and mobility for individuals with stroke is improved. 1.4.2 Exercise in individuals with chronic stroke There is abundant research in healthy older adults demonstrating the beneficial effects of exercise on postural control through a reduction in falls (Campbell et al. 1997; Campbell et al. 1999; Hu and Woollacott 1994a; Robertson et al. 2001a; Robertson et al. 2001b; Steinberg et al. 2000) , increased muscle strength (Lord et al. 1993; Schlicht et al. 2001), and improved functional balance (Hopkins et al. 1990; Lord et al. 1993, 1995, 1996; Rogers et al. 2001). Surprisingly, there is a lack of research and implementation of community-based group exercise programs for individuals with chronic stroke even though the incidence of falls in this population is very high. Several different approaches to exercise training have been implemented in individuals with chronic stroke including treadmill or over-ground gait training (Ada et al. 2003; Hesse et al. 1995; Macko et al. 1997, 2001; Miller 2001; Miller et al. 2002; Mudge et al. 2003; Silver et al. 2000; Smith et al. 1998b, 1999, 2000; Sullivan et al. 2002; Trueblood 2001), muscle strength training (Badics et al. 2002; Engardt et al. 1995; Kim et al. 2001; Sharp and Brouwer 1997; Weiss et al. 2000), functional exercise training (Bassile et al. 2003; Dean and Shepherd 1997; Monger et al. 2002; Potempa et al. 1995; Rodriquez et al. 1996; Tangeman et al. 1990), and combined functional exercise and muscle strength training (Bastien et al. 1998; Carr and Jones 2003; Dean et al. 2000; Eng et al. 2003; Rimmer et al. 2000; Teixeira-Salmela et al. 1999, 2001) . These studies have encompassed both home-based (Dean and Shepherd 1997; Monger et al. 2002; Rodriquez et al. 1996; Tangeman et al. 1990) and community-based group programs (Ada et al. 2003; Bassile et al. 2003; Bastien et al. 1998; Dean et al. 2000; Eng et al. 2003; ;' Rimmer et al. 2000; Teixeira-Salmela et al. 1999, 2001) as well as individual lab-based programs (Carr and Jones 2003; Engardt et al. 1995; Hesse et al. 1995; K i m et al. 2001; Macko et al. 1997, 2001; Miller 2001; Miller et al. 2002; Mudge et al. 2003; Potempa et al. 1995; Sharp and Brouwer 1997; Silver et al. 2000; Smith et al. 1998b, 1999, 2000; Sullivan et al. 2002; Trueblood 2001). These programs have ranged in duration from 2-24 weeks of training with •5 the exception of the study by Rodriquez et al. (1996) in which training at home lasted for between 10 and 65 months. Simple physical/occupational therapy assessment and treatment in the home has also been used and promising results including improved functional mobility have been reported (Green et al. 2002; Wade et al. 1992). Exercise in individuals with chronic stroke has shown significant benefits including improvements in gait (Rodriquez et al. 1996; Teixeira-Salmela et al. 2001; Trueblood 2001), v increased gait speed (Ada et al. 2003; Bassile et al. 2003; Dean et al. 2000; Eng et al. 2003; Hesse et al. 1995; Miller et al. 2002; Miller 2001; Monger et al. 2002; Sullivan et al. 2002; Teixeira-Salmela et al. 1999, 2001), increased muscle strength (Badics et al. 2002; Carr and Jones 2003; Engardt et al. 1995; Kim et al. 2001; Rimmer et al. 2000; Sharp and Brouwer 1997; Smith et al. 1998b, 1999; Teixera-Salmela et al. 1999; Weiss et al. 2000), faster chair stand time (Weiss et al. 2000), faster stair climbing speed (Eng et al. 2003), increased peak VO2 (Macko et al. 2001; Potempa et al. 1995; Rimmer et al. 2000), reduced steady state V 0 2 (Macko et al. 1997), decreased energy expenditure (Macko et al. 2001), increased weight bearing ability or force production from the paretic limb (Dean and Shepherd 1997; Dean et al. 2000; Tangeman et al. 1990), increased balance ability (Tangeman et al. 1990), and increased muscle activation in the affected limb (Dean and Shepherd 1997). Moreover, improvements in clinical > assessments including the Get Up and Go test (Silver et al. 2000), Berg Balance (Bastien et al. 1998; Eng et al. 2003; Miller 2001; Miller et al. 2002; Mudge et al. 2003; Weiss et al. 2000), Activities of Daily Living Index (Tangeman et al. 1990), and the Nottingham Health Profile (Teixeira-Salmela et al. 1999) have also been observed with exercise. While it is clear that exercise has substantial benefits for individuals with chronic stroke, whether different types o f exercise programs have different effects remains uncertain. Unfortunately, the majority of the existing research on exercise training in individuals with chronic stroke has not focused specifically on postural control and none have investigated falls-reduction. In fact, only a few studies have investigated the effects of exercise on functional balance or postural control in individuals with chronic stroke (Bastien et al. 1998; Dean and Shepherd 1997; Eng et al. 2003; Smith et al. 2000; Tangeman et al. 1990). The majority of the exercise-training studies are not controlled; rather, they have one group and are a pre-, post-test' design. Consequently, it is difficult to assess whether changes are due to the exercise intervention or from the attention from the therapists or from the act of attending the exercise sessions. Nonetheless, in a study by Tangeman et al. (1990), functional balance ability (measured using a scale designed for the study) was significantly improved following a four-week (2hr/session, 4x/week) individual home-based training program focusing on weight shifting, balance, and functional activities. In a feasibility study by Bastien et al. (1998), individuals with chronic stroke performed functional balance exercises (dance and Tai Chi) in combination with muscle strengthening tasks and group discussions. This community-based group exercise program demonstrated an increase in Berg Balance over the 6 - 8 weeks of training. However, in a later study, Smith et al. (2000) examined the influence of a 12-week (3x/wk) progressively graded treadmill aerobic exercise program on postural control. Participants were subjected to horizontal platform perturbations pre- and post-intervention and , reaction and recovery times were analyzed; however, no significant differences were discovered (Smith et al. 2000). These authors suggested that task-specific training might be necessary to improve balance ability. This has been demonstrated in acute stroke survivors, where participants underwent 15 sessions over three weeks of platform translation training and demonstrated an increased ability to withstand increasing magnitude translations compared to acute stroke survivors who did not receive the intervention (Hocherman et al. 1984). In chronic stroke survivors, Dean and Shepherd (1997) examined sitting postural control in a randomized controlled study, where the experimental group practiced exercises over two weeks designed to improve sitting and loading the affected leg while reaching and the control group performed cognitive manipulative tasks while seated. The exercise training increased the loading ability of the affected leg and led to greater muscle activation in the experimental group compared to the control group (Dean and Shepherd 1997). Recently, Eng et al. (2003) "ci evaluated the effect of an eight-week community-based group exercise intervention (involving walking, strength training, and balance exercises) on functional capacity and balance in individuals with chronic stroke; their results demonstrated improvements in both. Interestingly, this last study is the only one to investigate retention effects and the results suggest that the exercise effects are retained for at least one month following the intervention. Although the consequences of a fall due to an unexpected perturbation to balance are detrimental, there exist no studies on the influence of exercise on standing postural reflexes in individuals with chronic stroke. Promising results from a study in healthy older adults has shown that multi-sensory training can increase stability, decrease falls, and decrease muscle onset latencies of postural reflexes (Hu and Woollacott 1994a, b). ' Therefore, one of the objectives of this thesis was to examine the influence of exercise training in individuals with chronic stroke on the reactive postural control system and determine which types of exercise programs are effective in improving postural control. A large emphasis 7 on community-based group exercise programs for individuals with chronic stroke is necessary, as acute phase rehabilitation is shortening and individuals have many years with their injury without easy access to these types of programs. 1.4.3 Postural control following stroke There is very little research on postural control following stroke. In contrast, extensive c literature exists for healthy young and older adults in which much of our understanding of how the body controls movement stems from. Challenging postural stability through destabilizing forces induced while standing on a moveable platform (i.e. perturbations) provides an indication about an individual's reactive postural control capabilities. Original work by Horak and Nashner (1986) defined two types of postural responses to perturbations during stance: the ankle and hip strategies. The ankle strategy re-establishes stability by moving the centre of mass back within the base of support (i.e. the feet) through movement primarily about the ankle joint (Horak and Nashner 1986). Muscle activity originates in muscles surrounding the ankle followed by a sequential activation of muscles controlling the knee, hip, and trunk (Horak and Nashner 1986). When perturbations are larger, faster, and/or the individual is standing on a smaller surface, centre of mass is moved to re-establish stability through movement about the <'• hip joints (Horak and Nashner 1986). Muscle activation in this case, the hip strategy, originates in the muscles surrounding the hip and controlling the trunk followed by muscles controlling the knee and minimal involvement of ankle musculature (Horak and Nashner 1986). Recent work has extended the idea of these 'feet-in-place' strategies and focused more on responses termed 'change-in-support' strategies that move the base of support to maintain stability during perturbed stance (Maki and Mcllroy 1997). These researchers argue that individuals preferentially use stepping strategies, termed 'compensatory stepping reactions', and/or reaching/grasping movements to control stability (Maki and Mcllroy 1997). Hence, there are multiple strategies available in an individuals' repertoire for postural control. ; In healthy older adults, postural control is compromised due to decreased musculoskeletal .• capacity (e.g. muscle weakness), sensory function, visual impairments, neural processing, and cognitive abilities, which result in a large number of falls in this population (Alexander 1994; Campbell et al. 1989; Maki and Mcllroy 1996, 1997, 1999; Tinetti et al. 1988). Muscle onset latencies are delayed and the strength of the postural responses is diminished with aging (Lin 8 and Woollacott 2002). Furthermore, older adults often require multiple steps to recover balance following sudden platform movements (Maki and Mcllroy 1999). The investigation into the postural responses of individuals with stroke following platform perturbations that challenge the reactive postural control system have only recently started to be investigated. Early studies have sought to characterize the patterns and timing of the postural responses and to compare them with older healthy adults (Badke and Duncan 1983; Badke et al. 1987; Berger et al. 1988; Dietz and Berger 1984; Di Fabio et al. 1986; Di Fabio 1987; Jiang et , al. 1998). Individuals with chronic stroke suffer from similar problems as healthy older adults ; although usually on a much larger scale. The additional presence of hemiparetic upper and lower extremities and a tendency for asymmetrical weight bearing results in decreased stability and greater challenges for the postural control system. Further, damage to supraspinal centers ' may limit cognitive resources and sensory integration ability for maintaining postural stability (unpublished observations). Individuals with stroke who undergo platform perturbations show frequent co-contraction of muscles surrounding the ankle and knee joint (Badke and Duncan 1983; Berger et al. 1988; Di Fabio et al. 1986; Di Fabio 1987; Hocherman et al. 1988), no clear muscle sequencing and greater variability of muscle activity (Badke and Duncan 1983), and frequent occurrences of zero-onset responses (absent postural muscle response bursts) (Di Fabio et al. 1986; D i Fabio 1987). Moreover, individuals with stroke exhibit delayed paretic muscle onset latencies compared to the non-paretic limb and healthy older adults (Berger et al. 1988; Dietz and Berger 1984; Di Fabio and Badke 1988; Di Fabio et al. 1986; Di Fabio 1987) and delayed paretic limb ankle muscle torque response compared to healthy older adults (Al-Zamil 1998; Ikai et al. 2003) in response to platform perturbations. Interestingly, prior knowledge of the direction of perturbation reduces the frequency of zero-onset responses and shortens the muscle onset latencies in the paretic limb (Badke et al. 1987). Recent evidence also suggests that individuals with chronic stroke have a greater tendency to use multiple steps to recover balance (majority of who step first with their loaded non-paretic limb) and/or use grasping strategies following perturbed stance (Jiang et al. 1998). In this thesis, sudden horizontal platform translations (i.e. platform perturbations) were used to generate postural reflexes in individuals with chronic stroke and to provide a measure of their reactive postural control system. 9 1.5 Research Questions Several research questions were posed in order to address the purpose of this thesis. We conducted three experiments using individuals with chronic stroke to answer these questions. Experiments II and m were from the same sample of participants (i.e. data for Experiment II came from baseline data of Experiment m). The following are the research questions, which guided this thesis along with a brief statement of how they contribute to the overall thesis and/or our research knowledge base: 1.5.1 Research Question #1 (Chapter 2) Does weight-bearing load on lower extremities affect postural reflexes in individuals with chronic stroke? Hypothesis: muscle onset latencies will be faster and the magnitude of postural reflexes wil l increase as weight-bearing load is increased for both ankle dorsiflexors and extensors. ; Since individuals with stroke often adopt an asymmetrical weight-bearing posture (i.e. ' greater weight-bearing on the non-paretic lower extremity) and exercise may alter this strategy,, it is important to determine whether loading on a limb affects postural reflexes. If weight-bearing load does influence the latency of postural reflexes then weight-bearing load during post-intervention testing following the exercise intervention study would need to be matched to baseline values. This experiment also determines whether individuals with stroke can still modulate postural reflexes. In order to determine whether an exercise intervention is capable of modifying postural reflexes, we must first establish test re-test reliability to ensure that the change can be attributed to the intervention rather than a learning effect over time. Thus, this experiment was repeated a second time within a few days. Intraclass Correlation Coefficients (Shrout and Fleiss 1979) were determined along with Standard Error of Measurement. Results of the test re-test reliability are in Chapter 4 and in Appendix IV. 10 1.5.2 Research Question #2 (Chapter 3) What are the primary neural mechanisms for falls during unexpected platform translations; that challenge the reactive postural control system in individuals with chronic stroke? Hypothesis: individuals with stroke who fall will have delayed muscle onset latencies in response to unexpected platform translations and demonstrate reduced ankle muscle strength during clinical testing. It is important to understand why some individuals with stroke fall and others do not so that rehabilitation strategies can be developed to target the appropriate aspects contributing to these falls. Postural reflexes are evoked by a translating platform upon which participants are standing. 1.5.3 Research Question #3 (Chapter 4 - primary study) i What are the effects of two different exercise interventions (a fast-paced, multi-sensory, agility exercise program versus a slow-paced, stretching/weight-shifting exercise program) on the timing of standing postural reflexes, functional balance and mobility, reaction time, falls, health-related quality of life, and balance confidence in individuals with chronic stroke? Hypothesis: the two exercise programs will improve these measures as demonstrated by (a) faster standing postural reflexes, (b) increased Berg Balance (see Appendix V) scores, (c) decreased time for the Timed Up and Go Test, (d) faster step reaction time (e) decreased Nottingham Health Profile (see Appendix VI) scores, (f) increased Activity-specific Balance ~ Confidence (see Appendix VII) scores, (g) and reduced 12-month prospective number of falls in the community. It is hypothesized that the Agility exercise intervention wil l show greater improvements than the Stretching/weight-shifting program for all measures. The knowledge obtained from this study will help guide clinicians with developing effective interventions for improving postural control following stroke. Further, i f changes with exercise are demonstrated, this might suggest neural plasticity in the chronic stage of injury following stroke. 11 CHAPTER 2 - Experiment I Modulation of Ankle Muscle Postural Reflexes in Stroke: Implications For Falls i (In review with Journal of Physiology) 2.1 Abstract Background and Purpose - Falls are common among individuals with stroke. Postural reflexes are essential reactive control mechanisms to prevent falls when an unexpected destabilizing force is applied to the body. Given the known sensorimotor deficits and asymmetrical weight-bearing posture in stroke, the aim of this study was to determine whether stroke affects the modulation of standing postural reflexes with varying weight-bearing load. Methods - Ten individuals with chronic stroke and 10 healthy older adult controls were exposed to unexpected forward and backward platform translations while standing. Three , different stance conditions were imposed: increased weight-bearing load, decreased weight-bearing load, and self-selected stance. Surface E M G from bilateral ankle dorsiflexors (tibialis anterior) and extensors (gastrocnemius) were recorded and the magnitude of background muscle activity (prior to the platform translation), magnitude of a postural reflex (75 msec following reflex onset), and postural reflex muscle onset latency were determined. Results - Load-dependent modulation of ankle extensors was found in controls and individuals with stroke. In contrast, load did not change the onset latency of postural reflexes of the individuals with stroke. Although controls demonstrated modulation of ankle dorsiflexors to different loads, individuals with stroke did not show this modulation and falls were most frequent when participants were required to utilize the ankle dorsiflexors. Conclusions - Delayed paretic muscle onset latencies in conjunction with impaired modulation of ankle dorsiflexor postural reflexes may contribute to the instability and frequent falls observed among persons with stroke. 2.2 Introduction The incidence of falls for community-dwelling individuals with stroke has been reported to be as high as 73% (Forster and Young 1995). Thus, an understanding of postural control in stroke is of importance to facilitate the reduction of falls in this population. Reactive postural 12 control entails a response, mediated by postural muscle reflexes, to a sudden unexpected perturbation applied to the body and relies on the central nervous system's (CNS) ability to interpret afferent information to ensure that the centre of mass (COM) stays within the base of support. Proprioceptive afferents from extensor muscles in the legs and exteroceptive afferents from mechanoreceptors in the foot are among the available inputs to the CNS to modulate standing or locomotor postural reflexes (Duysens et al. 2000). It has been suggested that these afferent inputs can provide information regarding load, and thus, have been referred to as load receptors and are particularly useful in signalling C O M position (Dietz et al. 1992). Load receptor input for the regulation of stance in humans has been demonstrated in studies which found an increase in the magnitude of postural reflexes with increasing body load (via lead vests) in response to a translation of a platform upon which participants were standing | : under water (Dietz et al. 1989; Horstmann and Dietz 1990). Furthermore, greater load applied to the body during standing platform translations on land was associated with an increase in the magnitude of extensor muscle postural reflexes in healthy individuals (Dietz et al. 1992). It is believed that lb afferents from golgi tendon organs (GTOs) provide load information to the spinal cord (Dietz et al. 1992; Duysens et al. 2000). In addition to lb afferents from GTOs, cutaneous mechanoreceptors in the sole of the foot are in an optimal location to sense limb load and have been recently shown to be important in standing balance (Kavounoudias et al. 2001). Understanding the postural responses under varying weight-bearing load is of interest since individuals with stroke tend to bear greater weight on the non-paretic limb (Eng and Chu 2002). Whether load-dependent modulation remains intact following stroke is unknown. Hassid et al. (1997) and Trueblood (2001) have studied the use of body-weight supported (BWS) treadmill training in stroke, which inherently altered limb loading and have shown improvements in gait and balance. Albeit few, studies on postural reflexes in stroke have demonstrated delayed e muscle onset latencies and abnormal recovery strategies in response to external perturbations while standing (Berger et al. 1988; Dietz and Berger 1984; Di Fabio et al. 1986; D i Fabio 1987). The objective of this study was to determine whether stroke affects the modulation of postural reflexes with weight-bearing load. Assessing the contribution of postural reflexes from weight-bearing load will determine whether the asymmetrical posture in individuals with stroke (i.e., reduced loading on the paretic limb) contributes to these altered reflexes and wil l quantify the extent that afferent information from the lower extremities can be utilized for modulation of postural reflexes in stroke. 13 2.3 Method 2.3.1 Participants Ten individuals with hemiparesis (4 right and 6 left) due to stroke and ten healthy older adult controls were recruited from the community. Participant characteristics are described in Table 2.1. The inclusion criteria for the individuals with stroke were: (1) over 50 years of age, (2) only one stroke, (3) at least one year post stroke onset, (4) able to stand independently for at least 5 minutes without an assistive device, and (5) able to follow two-step commands. Persons with musculoskeletal or neurological disorders in addition to their stroke were excluded. Healthy older adults with musculoskeletal or neurological disorders were also excluded. Limb dominance of the healthy older adults was determined by asking which leg they used to kick a soccer ball.- Following university and hospital ethics approval, informed consent was received from all participants prior to their participation (see Appendix VTfi). Table 2.1: Mean (SD) of participant characteristics. Stroke (N = 10) Controls (N = 10) Age,yrs 61.3(8.9) 60.6(5.5) Mass, kg 76.2(17.6) 76.7(10.2) Height, cm 166.5 (18.2) 174.6(10.0) Stroke Duration, yrs 4.1(2.9) N / A Affected Side 4 Right / 6 Left N / A Berg Balance, max. 56 44.9 (8.3) N / A Type of Stroke 5 Ischemic, 4 Hemorrhagic, N / A 1 unknown 14 2.3.2 Protocol Participants stood on two force plates (Bertec Corp.), one limb on each force plate, embedded in a platform and forward or backward translations of the platform were applied during three stance conditions: increased weight-bearing load (Increased Load), decreased weight-bearing load (Decreased Load), and self-selected stance (Neutral). Participants wore a: full-body harness that was attached to a beam in the ceiling via a dynamic climbing rope to prevent the occurrence of a fall and at least one spotter was present. Participants were instructed to maintain their normal standing posture or shift their weight onto either the right or left leg (depending on the condition) and sustain the standing position. For the Increased or Decreased Load conditions, the experimenter visually monitored the force plate vertical forces in order to ensure that participants maintained the appropriate amount of weight-bearing (target of approximately 70% weight-bearing on one limb) prior to triggering the platform translation. A total of 15 backward and 15 forward platform translations (8 cm displacement, 30 cm/s velocity, and 300 cm/s acceleration) were induced in three blocks (Increased Load, Decreased Load, and Neutral) of 5 trials separated by 15-30 second intervals (see Appendix IX for experimental protocol). Participants were told that the platform could move at any time prior to triggering the perturbation but the onset and direction of translation were unexpected in nature. The blocks of trials were randomly ordered for both platform directions and weight-bearing load conditions. Surface electromyography (EMG) (Bortec) from bilateral tibialis anterior (TA) and the medial head of gastrocnemius (MG) were recorded at 600 Hz for 6 seconds (2 seconds prior to platform movement and 4 seconds after) along with force plate data (see Appendix X for E M G placement protocol). The M G muscle was used for analysis in the backward translations and the T A muscle was used in the forward translations due to their role as primary recovery muscles for these movements (Horak and Nashner 1986). 2.3.3 Data Analysis For each condition in both directions, trials 2-5 were averaged. The first trial in response to a perturbation has been shown to be clearly different from subsequent ones (Marigold and Patla 2002). Custom M A T L A B software was used to calibrate the force plate data and subsequently, 15 the mean vertical forces were calculated one second prior to platform onset to determine the amount of weight-bearing for each limb for each trial. E M G was full-wave rectified and low-pass filtered at 100 Hz. A l l E M G data processing used a custom written M A T L A B program. The mean E M G signal for one second prior to the : onset of platform movement was determined along with the standard deviation. Muscle onset latency, representing a postural reflex, was defined as an increase in muscle activity that : exceeded + 2 standard deviations (SD) or fell below - 2 SD (depending on whether the burst was excitatory or inhibitory) for at least 30 msec and was determined by a combination of visual inspection and computer algorithm via an interactive program (Marigold and Patla 2002). Background muscle activity was calculated as the area under the curve (trapezoid rule) for one second prior to the onset of the platform movement. The magnitude of muscle activity for 75 msec following the onset of a postural reflex was also calculated as the area under the curve (see Figure 2.1a). For each individual trial, the magnitude was obtained after removal of each muscle's background activity from the E M G signal (on a single trial basis) so that the reflex magnitude was not masked by any changes in background activity. Data from the dominant and non-dominant limbs of controls were collapsed over each load condition because there was no significant difference between them using paired t-tests. Three-separate repeated measures analyses of variance (ANOVA) determined the effect of weight-bearing load conditions (Decreased Load, Neutral, Increased Load) on the background muscle activity of the (1) paretic limb of the stroke group, (2) non-paretic limb of the stroke group, and (3) controls. Post-hoc analysis consisted of Duncan's test. These statistical procedures were ' also performed for the dependent variables of the postural reflex magnitude and muscle onset latency. For graphical presentation, both background muscle activity and magnitude of postural reflexes were normalized to the Neutral condition (Figure 2.2 and 2.3); however, statistical analyses were performed on the non-normalized data. Paired t-tests compared the muscle onset latencies between the paretic and non-paretic limbs of the individuals with stroke and independent t-tests compared the stroke and control groups. A l l statistical analyses (alpha = \ 0.05) were performed with SPSS, version 11.0 for Windows. ' 16 2.4 Results Three individuals with stroke fell (i.e. were caught by the rope and harness system or ? required the assistance of the spotter) during the platform translations, of which all falls occurred during the forward translations (i.e. backward induced sway that required T A activity). No control participants experienced a fall. Table 2.2 shows the amount of weight-bearing on the paretic and non-dominant limb for the individuals with stroke and controls, respectively. In the Neutral condition the individuals with stroke had approximately 10% greater weight-bearing on their non-paretic limb while controls were nearly symmetrical. Table 2.2: Weight-bearing load in percent body-weight Neutral 49.0(1.9) 41.9(10.4) Increased Load 77.3 (8) 61.3 (17.5) Forward Decreased Load 23.0 (4.8) 24.0 (6.1) Neutral 49.0 (2.4) 40.8 (10.3) Increased Load 74.8 (7.3) 61.3 (17.8) 17 sop 200 0 0 20 40 W 80 100 120 140 Tin* (msec) ?PlatfbmPrtset . . . Deere as toadi ?Neiitrall*>ad 800i 800i 180 200 800 i IacMas«d:Load 800 goo; 4005 .ft iSOO »:600 iob: 300 -500 0 -1*000 -500' J -ftOO -500 ,0 Time (msec) Time (msec) Time (msec) Figure 2.1: (A) Diagrammatic definitions of the onset latency and postural reflex magnitude (hatched is the postural reflex magnitude calculated from a 75 msec area from the onset latency). Typical postural reflex responses of the (B) paretic M G and (C) non-paretic M G under the three load conditions for one individual with stroke. 800; 400 100 n 18 2.4.1 The effect of weight-bearing load on the magnitude ofpostural reflexes In response to the backward platform translations, the magnitude of M G postural reflexes (i.e. after removal of background activity) increased with increasing weight-bearing load for the controls and both limbs of the individuals with stroke (Figure 2.1 and 2.2). Post-hoc analysis revealed a difference between the Increased Load and Decreased Load conditions for both groups (p < 0.05). Furthermore, there was a greater magnitude postural reflex in the Increased Load condition compared to the Neutral condition and in the Neutral condition compared to the Decreased Load condition for the controls (p < 0.05). Background muscle activity of the M G demonstrated identical results to the magnitude of M G postural reflexes for both individuals with stroke and controls (Figure 2.3). The T A postural reflex magnitude (in response to forward platform translations) was greater in the Increased Load and Neutral conditions versus the Decreased Load condition in the control group (p < 0.05); however, T A changes were small (i.e. 20% increase in the Increased Load compared to Decreased Load versus a 90% change with the extensor muscles in controls) k (Figure 2.2). In contrast, there was no difference in magnitude of T A postural reflexes among the three load conditions for both limbs in the individuals with stroke. In fact, there was a trend (p = 0.09) of increasing magnitude of postural reflexes in the non-paretic T A in the Decreased Load condition compared to the Neutral condition. The T A background muscle activity produced similar findings to the magnitude of the postural reflex (Figure 2.3). Specifically, post-hoc analysis indicated greater (p < 0.05) background muscle activity in the Increased Load condition compared to both the Neutral and Decreased Load conditions for the controls. In contrast, non-paretic T A background muscle ' activity in the individuals with stroke was greater in the Decreased Load condition compared to both the Neutral and Increased Load conditions (p < 0.05). 19 Magnitude of MG postural reflex in response to backward translations Controls Stroke Decreased Load Neutral Increased Load Decreased Load Neutral Increased Load Magnitude of TA postural reflex in response to forward translations Controls Stroke • Paretic TA • Non-paretic TA Decreased Load Neutral Increased Load Decreased Load Neutral Increased Load Figure 2.2: Postural reflex magnitude from M G and T A for the stroke and control groups. Values normalized to the Neutral condition are shown, although statistical analyses were performed on the non-normalized data. Note that background muscle activity was removed prior to calculating the magnitude. 20 Background MG activity prior to backward translations Controls Stroke • Paretic MG • Non-paretic MG Decreased Load Neutral Increased Load Decreased Load Neutral Increased Load Background TA activity prior to forward translations Controls Stroke • Paretic TA • Non-paretic TA Decreased Load Neutral Increased Load Decreased Load Neutral Increased Load Figure 2.3: Background muscle activity from M G and T A for the stroke and control groups. ,( Values normalized to the Neutral condition are shown. 2.4.2 The effect of weight-bearing load on muscle onset latency In response to the backward platform translations, the controls demonstrated differences in M G muscle onset latency among the three weight-bearing conditions (p < 0.05). M G postural reflexes were faster as weight-bearing load increased with the Increased Load condition approximately 13 msec faster than the Decreased Load condition (Table 2.3). In contrast, no differences in M G muscle onset latency among the weight-bearing conditions were found for the individuals with stroke for either the paretic or non-paretic limb. Furthermore, there was no difference in onset latency (means less than 5 msec apart) among the three weight-bearing 21 conditions for the T A in the stroke and control groups during the forward platform translations (Table 2.3). In the individuals with stroke, the paretic limb T A and M G were significantly delayed up to 15 msec and 26 msec, respectively, compared to the non-paretic T A and M G (p < 0.05). The paretic limb T A and M G latencies were also delayed compared to the control T A and M G , respectively (p < 0.05). In contrast, there was no difference for the T A or M G latencies between the non-paretic limb of the individuals with stroke and the controls. Table 2.3: Mean (SD) onset latencies (msec) for backward & forward platform translations. Controls Stroke Condition Paretic Non-paretic MG onset latency in response to backward translations Decreased Load 115.4 (20.7)* 141.1 (25.3) 115.9(12.4) Neutral 107.1 (10.1) 139.3 (22.7) 113.5 (20.1) Increased Load 102.5 (17.1) 136.8 (28.1) 118.9(21.8) TA onset latency in response to forward translations Decreased Load 105.7(16.5) 123.6 (22.8) 111.3 (13.2) Neutral 102.4 (9.7) 122.8 (23.1) 107.8(13) Increased Load 101.3 (7.5) 124.5 (22) 109.3 (13.1) * Increased Load different from Decreased Load condition for M G , p < 0.05. 2.5 Discussion The major findings of this study suggest that: (1) load-dependent modulation of ankle extensor postural reflex magnitude remains intact following stroke, (2) load does not affect 22 muscle onset latencies in individuals with stroke, and (3) individuals with stroke are unable to modulate ankle dorsiflexor postural reflex magnitude under different load conditions. 2.5.1 Modulation of ankle muscle postural reflex magnitude following stroke Following stroke, individuals demonstrated load-dependent modulation of the magnitude of ankle extensor muscle postural reflexes to varying levels of weight-bearing load. Dietz and colleagues (Dietz et al. 1989; Dietz et al. 1992; Horstmann and Dietz 1990) have demonstrated that the magnitude of human postural reflexes of ankle extensors is sensitive to load in healthy individuals. Thus, load modulation may not require intact supraspinal input (e.g. from corticospinal tract fibres) but rather, has substantial integration within the spinal cord. Weight-bearing load has been shown to modulate lower limb muscle activity in individuals with spinal cord injury (Harkema et al. 1997). The fact that individuals with stroke still utilize load information supports recent body-weight supported treadmill-training studies (Hassid et al. 1997; Trueblood 2001) and substantiates the rationale for their implementation for stroke rehabilitation. For the ankle muscles of the control group and the extensor muscles of the stroke group, the concept of 'automatic gain compensation' was demonstrated where the muscle response (after removal of background activity) increased with increasing background activity (Matthews 1986). This phenomenon may be of benefit during perturbed stance in that a larger reflex could be used to stabilize balance through an ankle strategy that is potentially compromised in asymmetrical posture. For example, the larger reflex evoked in the loaded limb would allow i f to overcome the biomechanical constraint imposed by the extra load and subsequently step forward or backward. Older adults in response to sudden platform translations often utilize compensatory steps (Maki and Mcllroy 1997). Although the T A does not directly sense load (it is non weight-bearing), the modulation of the magnitude of T A postural reflexes under different loads for the controls was likely from a combination of foot mechanoreceptors, joints receptors, and antagonistic extensor muscle feedback regarding load. Why was modulation of the ankle dorsiflexor, but not extensor postural reflex magnitude disrupted from stroke? Clinically, individuals with stroke often present with weakness of the u paretic ankle dorsiflexors. It is possible that a decreased number of motor units (Dietz et al. 1986), disturbed motor unit recruitment (Gemperline et al. 1995), and decreased motor unit 23 firing rates (Dietz et al. 1986; Rosenfalck and Andreassen 1980) contributed to the lack of modulation in the ankle dorsiflexor muscles. Further, Brouwer and Ashby (1992) reported that there are stronger connections of supraspinal motor centres (i.e. corticospinal tract fibres) to the distal leg flexors than the extensors as evident from transcranial magnetic stimulation studies. Given our observations of an increased incidence of falling when the condition required T A activity and the inability to modulate the magnitude of T A postural reflexes with load, we performed post-hoc analyses to examine the T A impairment. Based on ankle dorsiflexor isokinetic strength data and Chedoke-McMaster Foot scores, six of the 10 individuals with stroke had severe T A impairment (i.e. dorsiflexor torque < 0.06 Nm/kg and/or Chedoke-McMaster Foot score < 3/7). Of these six individuals, five were unable to modulate T A reflex magnitude to load and three fell. The remaining four individuals had minimal T A impairment (dorsiflexors torque > 0.13 Nm/kg and/or Chedoke-McMaster Foot score of 7/7), demonstrated modulation of T A reflex magnitude, and did not fall. It is apparent that the ankle dorsiflexors ' are essential for the recovery from falls. In Figure 2.2, the non-paretic T A postural reflex was not modulated and in fact, a trend toward an increased magnitude in the Decreased Load condition when it would be expected to be the reverse was found. We postulate due to the inability of the paretic limb T A to modulate magnitude in addition to its delayed muscle onset latency, a compensatory strategy results in an increase in the postural reflex magnitude of the non-paretic T A muscle. This interlimb response would serve to initiate a rapid step with the non-paretic limb i f need be during a time when the paretic limb is being loaded and compromising stability. 2.5.2 Altered supraspinal control due to stroke affects timing of postural reflexes 1 independent of load Regardless of the group (i.e. controls or stroke), the timing of the observed postural reflexes in response to platform translations suggests long-latency reflexes that receive supraspinal input. Although others (Berger et al. 1988; Dietz and Berger 1984; Di Fabio et al. 1986; D i Fabio 1987) have reported slower postural onset latencies on the paretic side, our study is the first to;V-control for the load taken through the limbs during the perturbation. The finding that postural reflex muscle onset latencies are independent of weight-bearing load in stroke suggests that the typical asymmetric stance adopted by individuals with stroke does not explain the delay in 24 muscle onset latencies observed following an external perturbation. Thus, deficits in the latency of paretic lower limb muscles can be attributed to the loss of supraspinal control and/or .i alterations in muscle properties resulting from the stroke. Interestingly, M G muscle onset latency demonstrated load-dependent modulation in that •, postural reflexes were elicited faster when limb load was increased in the healthy, but not stroke participants. However, the functional consequences of the 13 msec faster response in controls from the Decreased to Increased Load conditions needs further exploration. In conclusion, delayed paretic limb muscle onset latencies in conjunction with impaired modulation of dorsiflexor muscle postural reflex magnitude may contribute to the instability and frequent falls observed among individuals with stroke. 2.6 Bridging Summary The first study found that individuals with stroke could still utilize sensory feedback regarding weight-bearing load to modulate the magnitude of postural reflexes. In addition, weV identified a potential cause of falls in this population in that ankle dorsiflexor modulation is impaired following stroke. Our study has confirmed the results of others that report delayed paretic limb postural reflex muscle onset latency compared to the non-paretic lower limb and lower limbs of healthy older adults in response to standing perturbations. However, it is i : unknown whether delays in postural reflex onset latency and/or the magnitude of the reflex contribute to falls in individuals with stroke. Therefore, the second study sought to identify the underlying neural mechanisms contributing to falls in individuals with stroke. Evoking standing perturbations and identifying those individuals who fell accomplished this objective. This .( enabled us to separate out falling trials so that postural reflex muscle onset latency and magnitude could be compared. 25 CHAPTER 3 - Experiment II Neural Mechanisms Contributing to Falls in Individuals with Chronic Stroke (In review with Journal of Neurophysiology) 3.1 Abstract Falling is a major concern in individuals with stroke. The mechanisms contributing to falls are largely unknown. The purpose of this study was twofold: (1) to determine whether the latency and magnitude of postural reflexes utilized for recovery from standing platform translations could discriminate individuals who fell in response to the translations and (2) to determine whether a clinical assessment of a stroke-related impairment, lower extremity muscle strength, could differentiate individuals who fell in response to platform translations versus those who did not. Fifty-six individuals with chronic stroke underwent unexpected forward and backward standing platform translations in which postural reflex muscle onset latency and magnitude were determined and clinical testing of isokinetic joint torque of the lower extremities. Those who fell during the standing platform translations (N = 14) and those who did not (N = 42) were compared to determine the contributors of falling in this population. Eighty-nine percent of falls occurred during the forward translations. Results demonstrated that paretic tibialis anterior postural reflex magnitude was reduced in those trials in which Fallers fell compared to the trials in which Fallers did not fall during platform translations. Furthermore, Fallers had delayed non-paretic rectus femoris postural reflex onset latency compared to Non-fallers. The altered long-latency postural reflexes suggest supraspinal c involvement. In addition, the non-paretic rectus femoris response may be a strategy to compensate for the deficits in the paretic tibialis anterior. Studies using animal and human-based models are required to identify which pathways and structures may contribute to these altered reflexes and subsequent falls. 26 3.2 Introduction Falls and fall-related injuries occur frequently among community-dwelling stroke survivors with many of these individuals falling multiple times within a year (Forster and Young 1995; Hyndman et al. 2002; Kanis et al. 2001). Whether injury occurs or not, fear of falling may result (Friedman et al. 2002), which could lead to activity restriction and/or further sedentary -lifestyle (Murphy et al. 2002). The primary mechanisms behind a falling episode in individuals with stroke are not clear. To date, the few studies on falls in individuals with chronic stroke have focussed on predictors (Forster and Young 1995; Jorgensen et al. 2002; Lamb et al. 2003), which can identify those individuals at high risk for falls, but do not delineate the specific motor strategies which are necessary to prevent the occurrence of a fall. A n understanding of strategies which prevent falls are essential in designing effective rehabilitation programs that may lead to improved quality of life and a reduced burden on the health care system. Following an unexpected balance-threatening event (i.e. perturbation), reactive and protective strategies are initiated by postural reflexes to prevent the occurrence of a fall. The central nervous system (CNS) must utilize and integrate the available sensory and environmental information and an appropriate strategy is generated quickly with sufficient <> muscle strength and coordination. Studies have shown that individuals with stroke have delayed paretic limb muscle onset latencies following perturbations while standing on a moveable platform compared to their non-paretic limb and to healthy older adults (Berger et al. 1988; Dietz and Berger 1984; Di Fabio and Badke 1988; Di Fabio et al. 1986; Di Fabio 1987). This is in combination with decreased paretic ankle torque responses following platform translations (Ikai et al. 2003). Whether delays in postural reflex muscle onset latency and magnitude contribute to falls in individuals with stroke is unknown. Falls generated in a laboratory setting can be induced in such a way that every individual is exposed to the same destabilizing force. Consequently, the neurophysiological mechanisms associated with falls can be quantified. Thus, the first objective of this study was to determine whether the latency and magnitude of postural reflexes utilized for recovery from standing platform translations are different in those' individuals with stroke who fall during this task versus those who do not. Reduced lower extremity muscle strength has been found to predict falls in healthy older adults (Lord et al. 1994; Whipple et al., 1987). Lower extremity muscle strength is further reduced in individuals with stroke compared to healthy older adults, particularly in the paretic limb (Adams et al. 1990; Eng et al. 2002). In addition, both the time to initiate a muscle 27 contraction and time to generate torque are delayed in individuals with stroke (Chae et al. 2002; McCrea et al. 2003). Therefore, the second objective of this study was to determine whether clinical assessments of a stroke-related impairment, lower extremity muscle strength, could discriminate individuals who fell in response to standing platform translations versus those who did not. 3.3 Methods 3.3.1 Participants "i Fifty-six individuals with hemiparesis due to stroke were recruited from the community. Participant characteristics are described in Table 3.1. Information on the type and location of the participants' stroke was collected through medical records and/or physician notes. The American Heart Association Stroke Functional Classification (AHASFC) was used to provide ' an indication of the level of impairment of the participants (see Appendix XI). The A H A S F C is based on the level of independence of an individual where level I represents complete independence in basic and instrumental daily activities of living and level V represents complete dependence (Kelly-Hayes et al. 1998). The inclusion criteria for the individuals with stroke were: (1) over 50 years of age, (2) only one stroke, (3) at least one year post stroke onset (i.e. chronic stroke), (4) able to stand independently for at least 5 minutes without an assistive device, and (5) able to follow two-step commands. Persons with musculoskeletal or neurological disorders in addition to their stroke were excluded. Following university and hospital ethics approval, informed consent was received from all participants prior to their participation in the study (see Appendix XII). Table 3.1: Participant characteristics of the non-fallers (N = 42) and fallers (N = 14). 28 Non-fallers Mean (SD) or n Fallers Mean (SD) or n Gender, M/F 32/10 Age,yrs 66.9(8.1) Height, cm 171.5(8.7) Mass, kg 81.0(16.8) Stroke Duration, yrs 4.0 (3.3) Hemiparetic Side, R/L/NA 15/27/0 AHASFC, 1 - 5 2.2 (0.9) 7/7 69.9 (7.1) 165.8 (9.3) 77.7(13.5) 3.1 (2.0) 5/8/1 2.9(1.1) Type of Stroke 20 ischemic 8 ischemic 15 hemorrhagic 2 hemorrhagic 2 subarachnoid hemorrhage 1 subarachnoid hemorrhage 3 lacunar 1 lacunar 2 unknown 2 unknown Stroke Location 10 cortical 15 subcortical 8 brainstem/cerebellum 1 cortical/subcortical 8 unknown 6 cortical 2 subcortical 3 brainstem/cerebellum 3 unknown Abbreviations: M = male; F = female; R = right; L = left; N A = not applicable; A H A S F C = American Heart Association Stroke Functional Classification 3.3.2 Protocol Participants were tested over two occasions separated by one to seven days to minimize fatigue. For assessing postural reflexes, a total of 20 platform translations (8 cm displacement, 29 30 cm/s velocity, and 300 cm/s2 acceleration), separated by 15-30 second intervals, were induced while participants stood on two force plates (Bertec Corp.), one limb on each force plate, embedded in a custom built platform (see Appendix XHI for experimental protocol). To prevent the occurrence of a fall to the ground, participants wore a full-body harness that was attached to a beam in the ceiling via a dynamic rock-climbing rope and at least one spotter stood beside them. Participants were told that the platform could move at any time but the onset and direction of the translation were unexpected in nature. The direction of the translation was counterbalanced across participants so that either 10 consecutive backward translations followed 10 consecutive forward translations or vice versa. Surface electromyography (EMG) (Bortec) from bilateral tibialis anterior (TA), medial head of gastrocnemius (MG), rectus femoris (RF), and biceps femoris (BF) were recorded at 600 Hz for 6 seconds (2 seconds prior to platform movement and 4 seconds after) along with force plate data (see Appendix X for E M G placement protocol). Muscle strength (i.e. isokinetic, concentric joint torque) of the ankle, knee, and hip flexors and extensors was collected using a Kin-Corn Isokinetic Dynamometer (Chattanooga Group Inc). Muscle strength tested by this apparatus has been shown to be reliable in individuals with chronic stroke (Eng et al., 2002). A detailed description of participant positioning during testing can be found in Eng et al. (2002). A n angular velocity of 30-degrees per second for the ankle and 60-degrees per second for the knee and hip were used. One sub-maximal and one maximal trial for each joint and direction were completed as practice. During the maximal practice trial and subsequent three test trials, participants were instructed to "push or pull as hard as possible" throughout their range of motion. Rests were given as needed. 3.3.3 Data Analyses Each trial during the platform translations was classified as a fall or no-fall. A fall was defined as applying weight to the rope (i.e. caught by the rope and harness system) or requiring I the assistance of the spotter to prevent a loss of balance. E M G of the postural reflexes was full-wave rectified and low-pass filtered at 100 Hz (single-pass, second-order Butterworth algorithm). A l l E M G data processing used a custom written M A T L A B program. The mean E M G signal for one second prior to the onset of platform movement was determined along with the standard deviation (SD). Muscle onset latency, representing a postural reflex, was defined i as an increase in muscle activity that exceeded + 2 SD or fell below - 2 SD (depending on 30 whether the burst was excitatory or inhibitory) for at least 30 msec and was determined by a combination of visual inspection and computer algorithm via an interactive program (Marigold et al. 2003). One second of background muscle activity prior to platform movement was calculated as the area under the curve (trapezoid rule). The magnitude of muscle activity for 75 msec following the onset of a postural reflex was also calculated as the area under the curve after removal of each muscle's background activity from the E M G signal (on a single trial basis) so that the reflex magnitude was not masked by any changes in background activity. For each movement tested using the Kin-Corn isokinetic dynamometer, a single ensemble-averaged torque-angle curve was calculated from three maximal repetitions. Subsequently, the1 mean torques calculated over the torque-angle curve were normalized to the participant's body mass. 3.3.4 Statistical Analyses f Falls occurred predominantly in response to the forward platform translations (58 falls in response to forward translations compared to only seven in response to backward translations). Thus, only the responses to forward platform translations were assessed as sufficient Fallers and Non-fallers could be identified for this condition. Consequently, only ankle dorsiflexor, knee extensor, and hip flexor strength data and the T A and RF E M G activity were analyzed since these muscles would be utilized in the primary recovery response to forward platform translations (Horak and Nashner 1986). Those who fell at least once during the forward translations were identified as Fallers. Among the Fallers, those trials where a fall occurred (i.e. fall trial) and those trials in which a fall didn't occur (i.e. no-fall trial) were compared using paired t-tests for the following variables: T A onset latency and magnitude and RF onset latency and magnitude for both the paretic and non-paretic limbs. To compare the Fallers (fall trials only) with the Non-fallers, independent t-tests were used for the following variables: T A onset latency and RF onset latency for the paretic and non-paretic limbs. E M G magnitude was not compared between thef Non-fallers and Fallers due to methodological constraints associated with E M G collection. Paretic limb joint torques were entered into a one-way analysis of variance (ANOVA) (ankle dorsiflexion, knee extension, and hip flexion together) to compare overall muscle strength between groups (Fallers and Non-fallers). An A N O V A for the non-paretic limb was also performed. 31 A l l statistical analyses were performed using SPSS, version 11.5, for Windows, with an alpha level set at 0.05. 3.4 Results Figure 3.1 shows a sample of the postural reflexes evoked from the forward platform translations from a Non-faller (3.1 A) and Faller (3.IB). Fourteen (25%) individuals with stroke fell during forward platform translations for a total of 58 falls. 3.4.1 Muscle postural reflexes Individuals in both groups initiated their recovery response from a forward platform translation with the T A prior to RF (i.e. an ankle strategy) and with the non-paretic T A prior to the paretic TA. The mean muscle onset latencies of the postural reflexes for the Fallers (N = 14) and Non-fallers (N = 42) are shown in Table 3.2. The paretic limb onset latencies were delayed compared to the non-paretic limb for both groups. When comparing the fall trials (n = 58) with the no-fall trials (n = 68) within the group of individuals with stroke who fell (Table 3.2), the results demonstrated a reduced paretic T A '• postural reflex magnitude in the fall trials (p = 0.03). Further, there was a trend (p = 0.08) for a reduced non-paretic T A postural reflex magnitude in the fall trials compared to the no-fall trials within the individuals who fell at least once. The latency of the postural reflexes of each muscle was not different between the fall and no-fall trials for the Faller group (p > 0.05). When comparing the postural reflex latencies of the Fallers (fall trials) versus the Non-fallers, all muscle group means were slower for the Fallers; however, only the non-paretic RF onset latency was significantly slower in the Fallers (fall trials) compared to the Non-fallers (p = 0.007; Table 3.2). . 1 32 Paretic TA Hon-paretic TA Non-paretic RF toooi -400^200 0 200 :;;MQO^200 0 200 400-200 0 200 400-200 0 200 B l o p o -800 i# ,$00 '400 200 0 -400-200 0 .200 Time (msec) 1000 800 600 400 200 d c4;oo-2oo; o 200^  400-200 0 200- ." 400-200 p 200 Tine; (msec): :Timei!J&ec) TMesCjrrisee} Figure 3.1: Sample paretic limb postural reflexes evoked from a forward platform translation for (A) a Non-faller and (B) a Faller. Time zero represents the onset of the platform movement. 3.4.2 Muscle strength Paretic isokinetic joint torque was reduced in individuals who fell at least once versus those who did not (p = 0.02; Figure 3.2A), with the greatest difference between groups for the ankle ; dorsiflexors (50% reduction) and knee extensors (34% reduction). Non-paretic isokinetic joint torque was greater than the paretic side for all muscle groups for both individuals who fell and those who did not fall. In addition, non-paretic limb joint torque was reduced in the individuals who fell compared to those who did not (p = 0.05; Figure 3.2B), with the greatest difference between groups for the ankle dorsiflexors (33% reduction). Table 3.2: Postural reflex differences between Fallers and Non-fallers Fallers (N = 14) Non-fallers Fall Trials No Fall Trials (N = 42) Measure (n = 58) (n = 68) Muscle Onset Latency (msec) Paretic T A 126.8 (17.9) 121.6(22.5) 119.4(19.5) Paretic RF 170.6(48.6) 171.7(41.0) 149.6(30.0) Non-paretic T A 110.8 (15.2) 105.8 (10.3) 107.6(14.7) Non-paretic RF 163.5 (36.3) 155.9(33.5) 136.7(28.6)** Postural Reflex Magnitude (uV-s) Paretic T A 8.86(4.29) 10.95 (4.81)* Paretic RF 3.22 (2.67) 3.88 (3.74) Non-paretic T A 13.92(6.43) 14.83 (7.01) Non-paretic RF 4.66 (3.06) 4.44 (3.21) Note: Mean (SD) * Fallers (Fall trials) different than Fallers (No-Fall trials), p < 0.05 **Non-fallers different than Fallers (Fall trials), p < 0.05 34 A 1 i Dorsiflexors Knee Extensors Hip Flexors B 1 n Dorsiflexors Knee Extensors Hip Flexors Figure 3.2: Isokinetic joint torques normalized to body mass for the ankle dorsiflexors, knee extensors, and hip flexors. (A) Paretic limb joint torque for the Non-fallers and Fallers. (B) Non-paretic limb joint torque for the Non-fallers and Fallers. 35 3.5 Discussion The purpose of this study was to determine the neural mechanisms which contribute to falls among individuals with chronic stroke. Two limitations of the study were (1) the smaller number of individuals who fell compared to individuals who did not fall and (2) the falls were generated in a laboratory. We felt it was preferable to use the entire sample rather than match the number of Non-fallers to Fallers. The proportion of fallers (i.e. 25%) within the entire sample agrees with proportions of fallers from other studies, which examine prospective community-based falls in individuals with chronic stroke (Jorgensen et al. 2002). Additionally, laboratory-generated falls provide more constant and reproducible perturbations, which allow for controlled comparisons across groups (i.e. Fallers versus Non-fallers). Future research needs to determine the relationship of laboratory-generated falls compared to those occurring in the community. While rotational perturbations in healthy older adults have not been able to differentiate individuals who fall from those who do not using retrospective fall data (Smith et al. 1996), translational perturbations have demonstrated delayed T A postural reflex onset latency in older adults who have fallen at least once in the past year (Studenski et al. 1991). Injury to the CNS from cerebrovascular accident often has devastating consequences to sensorimotor function. Thus, characteristics of postural reflexes may be particularly important in the recovery responses for preventing a fall following an upper motoneuron lesion, as these individuals are inherently more unstable and closer to a threshold at which a fall is inevitable. Our study suggests that the magnitude and onset latency of some lower extremity muscles in response to a forward platform translation while standing are neural mechanisms which discriminate as to whether a fall occurs or not during this perturbation. In addition, these neural mechanisms could even discriminate successful recovery and falls within consecutive trials within the same subject. Furthermore, the clinical impairment of decreased paretic and non-paretic lower extremity muscle strength increased the risk of falling in response to a platform translation. 3.5.1 Postural reflexes evoked from forward platform translations: contribution to falls The present study has identified aspects of postural reflex magnitude and latency, which lead to falls in individuals with chronic stroke. Although others have reported delays in paretic 36 limb onset latency in response to platform perturbations (Berger et al. 1988; Dietz and Berger 1984; D i Fabio and Badke 1988; Di Fabio et al. 1986; Di Fabio 1987), none have attempted to relate this to falls. One of the major differences between successful recovery and falls was the paretic T A postural reflex magnitude. Individuals with stroke often present with weak paretic ankle dorsiflexors resulting in 'foot-drop' during gait. Stroke typically affects the corticospinal tract fibres, which innervate and control predominantly distal lower limb muscles (Brouwer and Ashby 1992). Accordingly, in this study muscle strength assessment revealed severely reduced paretic limb ankle dorsiflexion strength in those who fell. We believe that stroke-specific impairments such as the poor T A postural response of the paretic limb contributes to the necessity of compensatory mechanisms such as that observed in the non-paretic hip. Di Fabio et al. (1986) have suggested that the non-paretic hip most likely compensates for paretic ankle muscle impairments in response to standing perturbations. Proximal muscle activation of the non-paretic hip (i.e. RF) likely compensated for the poor paretic T A activation. The importance of this compensation was evident by the Fallers who demonstrated a significant delay in non-paretic RF onset latency compared to Non-fallers. It is then possible that once the centre of mass goes beyond the base of support (imminent fall), the individual attempts to recover with a late non-paretic hip response to enhance an ankle strategy, albeit too late. This compensatory strategy would be an a priori compensation due to past daily experiences or an interlimb coordination (Dietz and Berger 1984; Eng et al. 1994; Marigold et al. 2003) mediated by propriospinal pathways when an impaired ankle muscle response occurs. ! There was no difference in onset latency for the non-paretic RF between fall trials and no-fall trials among the individuals who fell; however, this may be due to slight differences in the kinematic strategies employed on a trial-to-trial basis or may be due to Type II error associated : with the large variability in the measure in this population. The propensity to fall could potentially be related to the location of the stroke. For example, it has been suggested that vestibulospinal pathways regulate anterior leg (i.e. RF and TA) muscle postural reflexes (Allum et al. 1995) while corticospinal tract fibres have a greater influence over distal leg muscles such as T A (Brouwer and Ashby 1992). Additionally, extrapyramidal tract pathways such as the reticulospinal tract have differential control over leg muscles, which may be altered following stroke due to injury to the CNS and/or CNS plasticity during the acute recovery phase. Hemispheric side and location of stroke (cortical versus 37 subcortical) did not appear to be different between the Faller and Non-Faller group of this study (Table 3.1). However, larger samples of both groups are likely required, in addition to information regarding the integrity of individual tracts and infarct volume. Therefore, there is a need to identify the specific neural pathways and supraspinal centres responsible for postural control following stroke. Specifically, do different neural pathways contribute to the compensatory strategies, such as the earlier non-paretic RF onset latency, or do individuals activate similar connections as prior to their stroke? Further, is the integrity of the tract used for these strategies differentially affected in those more prone to falls? Where are the residual deficits within the neural pathways (e.g. cortical, brainstem, spinal cord, peripheral nerve, neuromuscular junction, or muscle) that contribute to falls? Techniques such as transcranial magnetic stimulation to investigate motor output from the cortex or H-reflex testing to examine the integrity of the spinal reflex arc and spinal motoneuron excitability over the v course of recovery and/or after an exercise intervention may provide clues to the answers to these questions. In addition, it may be useful during these investigations to separate individuals based on fall history and/or whether they utilize compensatory strategies for postural control. Subsequently, rehabilitation clinicians would then be able to target these areas with specific exercises that require the neuronal connections associated with these pathways and centres. For example, agility-training programs may be beneficial to help elicit quick reflexive responses (Eng et al. 2003). Thus, collaborative efforts between basic and clinical scientists must be fostered to further advance our understanding of the underlying mechanisms associated with falling after an upper motoneuron lesion. 3.5.2 Muscle weakness contributes to falls Both paretic and non-paretic muscle strength, particularly the ankle dorsiflexors and paretic-knee extensors, contributed to falls with severe muscle weakness in the Faller group. Whipple et al. (1987) have shown that ankle dorsiflexor strength is particularly reduced in older adult fallers compared to non-fallers. While ankle strength is decreased in older age, the greater impairment in individuals with stroke compared to healthy older adults (Adams et al. 1990) may explain the increased risk of falling in this population. The reduction in muscle strength in individuals with stroke may be attributed to the changes in muscle properties that follow brain injury. Studies in stroke have reported decreased type II muscle fibres (Dietz et al. 1986; McComas et al. 1973), decreased motor unit firing rates (Dietz 38 et al. 1986; Rosenfalck and Andreassen 1980), and decreased motor unit recruitment (Gemperline et al. 1995). Thus, individuals at risk for falls may have greater residual muscle impairments following their stroke than those with lower risk. However, a recent study by Landau and Sahrmann (2002) suggests that muscle weakness may not be due to the muscle tissue but rather a central mechanism, as maximal force of the tibialis anterior muscle elicited by electrical stimulation was similar between individuals with stroke and healthy controls. 3.5.3 Future directions and implications In contrast to the older adult literature, balance, motor function, cognition, muscle strength, and activities of daily living impairment have not been able to predict falls in individuals with • chronic stroke (Jorgensen et al. 2002; Forster and Young 1995; Lamb et al. 2003). Thus, identifying the neural mechanisms contributing to lab-induced falls is an alternative and promising approach to understanding falls in people with chronic stroke. The next step will be to examine the relationship of lab-induced falls to actual falls in the community. The results of this study suggest that rehabilitation programs designed to reduce falls in individuals with stroke may benefit from including functional exercises to improve muscle strength (particularly ankle dorsiflexors) and exercises that evoke postural reflexes (particularly the paretic and non-paretic ankle and non-paretic hip muscles). This in turn may improve the latency and magnitude of postural responses involved in recovery strategies. Ultimately, the identification of pathways utilized following brain injury may provide the necessary link for improving function and reducing falls in individuals with chronic stroke. 3.6 Bridging Summary The results from the first and second studies demonstrate the importance of ankle dorsiflexor postural reflex magnitude for preventing falls in individuals with chronic stroke. Experiment II also demonstrated the importance of the postural reflex muscle onset latency and of volitional muscle strength, particularly with the paretic lower limb, for preventing falls. The question then becomes whether some type of intervention can alter postural reflexes. Additionally, can interventions in individuals with chronic stroke reduce falls and/or improve postural control? .! 39 Exercise interventions in individuals with chronic stroke have demonstrated improvements in physical function including balance (Bastien et al. 1998; Eng et al. 2003; Mudge et al. 2003;1 Tangeman et al. 1990; Weiss et al. 2000). None have investigated falls-reduction, nor are the types of exercises that are most effective known. Based on the early findings of our experiments, the known deficits in postural control and frequency of falls following stroke, and I' literature in healthy older adults, we designed two types of exercise interventions for individuals with chronic stroke. The following experiment was a randomized clinical trial to determine which exercise intervention was more effective in improving postural control and reducing falls. 40 CHAPTER 4 - Experiment III Exercise Leads to Faster Standing Postural Reflexes and Better Functional Balance and Mobility in Persons with Chronic Stroke: A Randomized Clinical Trial (In preparation for submission) 4.1 Summary Background: Although falls and fall-related injuries in persons with chronic stroke are an enormous burden on both the individual and the health care system, the types of exercise programs that are most effective are unknown. Further, it is unknown whether interventions like exercise can alter neural circuitry, such as postural reflexes, which may be important for preventing falls. We aimed to determine the effect of two different community-based group exercise programs on functional balance, mobility, and standing postural reflexes in persons with chronic stroke. Methods: We screened 109 persons with chronic stroke, of which 61 were randomized into one of two exercise groups (Agility or Stretching/weight-shifting). Persons were assessed prior to, immediately after, and one-month following a 10-week exercise intervention for clinical outcome measures including Berg Balance (primary outcome measure), Timed Up and Go, step reaction time, Activities-specific Balance Confidence, and Nottingham Health Profile. In addition, neurophysiological testing of standing postural reflexes evoked by a translating platform was also performed. Analyses were by intention-to-treat. Findings: For both groups, exercise led to improvements in all clinical outcome measures. In addition, this was the first time it has been shown that exercise leads to faster paretic lower extremity postural reflexes. The Agility group demonstrated greater improvement in step reaction time and paretic rectus femoris postural reflex onset latency compared to the Stretching/weight-shifting group. Although there was no difference in the number of fallers between groups when the entire sample was included, a sub-analysis of those with a history falls demonstrated a reduction in the number of fallers in the Agility exercise group. 41 Interpretation: Community-based group exercise programs are effective in improving functional balance and mobility and lead to faster standing postural reflexes in persons with chronic stroke. 4.2 Introduction One of the most devastating consequences of having a stroke is the increased risk of falling and consequent fall-related injuries. Twenty-three to 73% of community-dwelling persons with chronic stroke have been reported to fall over a 4-12 month period with approximately half falling repeatedly (Forster and Young 1995; Hyndman et al. 2002; Jorgensen et al. 2002) and there is a greater than seven-fold increase in hip fracture risk in this population (Kanis et al. 2001). Stroke-related impairments such as muscle weakness, sensorimotor dysfunction, and balance problems presumably contribute to the large number of falls. One potential way of improving balance and reducing falls is through exercise interventions. A number of recent studies have demonstrated that exercise can improve mobility (Ada et al. 2003; Dean et al. 2000; Rodriquez et al. 1996; Silver et al. 2000; Sullivan et al. 2002; Teixeira-Salmela et al. 1999) and functional balance (Eng et al. 2003; Tangeman et al. 1990) in persons with chronic stroke. However, it is unclear what are the advantages to different types of exercise programs (i.e. specific exercises) and the mechanisms, which underlie their improvements. Postural reflexes, in the form of coordinated muscle activity, are the first line of defence against falling subsequent to an unexpected destabilizing force (i.e. perturbation) applied to the body (e.g. collision, slip, and trip) or from self-induced movements (e.g. reaching, transferring). Persons with stroke have delayed paretic limb postural reflex muscle onset latencies compared to healthy older adults in response to unexpected perturbations during standing (Berger et al. 1988; Di Fabio et al. 1986). It is unknown whether exercise can alter the latency of postural reflexes, which could lead to improved postural control and a reduction in falls. Such a concept would support an emerging idea of the brain's ability to adapt in terms of structural/neural changes (i.e. brain plasticity) in persons with chronic stroke (Nudo et al. 2001). Therefore, the purpose of this study was to determine the effect of two different community-based group exercise programs (a fast-paced, multi-sensory, agility versus a slow-paced, 42 stretching/weight-shifting program) on functional balance, mobility, and standing postural reflexes in persons with chronic stroke. 4.3 Methods 4.3.1 Participants Participants living in the community were recruited over a two-month period from the GF Strong Rehab Centre database, community stroke groups, and via advertisements in local community centres, newspapers and television (see Appendix XIV). Inclusion criteria to participate in the study included (1) age > 50 years, (2) single stroke at least one year previously, (3) able to follow two-step commands, (4) able to walk, with or without an assistive device, for a minimum of 10 meters and have an activity tolerance of 60 minutes with rest intervals, and (5) not participating in any formal therapy programs. Exclusion criteria were (1) not medically stable (e.g. congestive heart failure, uncontrolled hypertension), (2) significant , musculoskeletal or other neurological conditions not related to stroke, (3) a score of < 22 (unless language was a problem in which lower scores were re-evaluated) on the Mini-Mental State exam (see Appendix X V ) (Folstein et al. 1975), and (4) a Berg Balance score over 52/56, as this indicates minimal balance deficits. Following university and hospital ethics approval, written informed consent was received from all participants prior to their participation (see Appendix XII). The participant's physician confirmed the presence of stroke and the inclusion/exclusion criteria (see Appendix XVI). In addition, type, location, and onset of stroke were collected through medical records and/or physician information where available. 4.3.2 Study design This study was a randomized-stratified, clinical intervention trial. Participants completed ah initial screening assessment prior to participation in the intervention, which assessed six-month fall history, balance (Berg Balance), and cognition/dementia (Mini-Mental State exam). Participants were then randomly assigned alphanumeric codes through a random number generator program that allowed an unbiased randomization/stratification process. Participants 43 were stratified (Tate et al. 1999) into groups for factors of (1) functional balance (Berg Balance score < 40 or > 40) and (2) number of falls (< 2 falls or > 2 falls recalled over the past six months). Subsequently, a person independent (and blinded) of the study randomly assigned participants (using their alphanumeric codes) such that there were equal numbers of participants for each level of stratum in the two exercise groups. Participants knew they were in one of two exercise groups but were unaware of the differences between them. Exercise instructors were not aware of the outcome measures of the study. A l l testers of the clinical measures were blinded to the group assignment, study design, and purpose. Some of the spotters during the standing postural reflex assessment were aware of the group assignment, but not the purpose or outcome measures, and in addition, the data collection was driven by a computer system. 4.3.3 Intervention The two exercise programs consisted of 1 hour sessions, 3x/week for 10-weeks held at a local community centre. Three instructors (physical therapist, kinesiologist, and recreation f; therapist) supervised the exercise programs. There were six classes (three for each of the ' exercise programs) with an approximate 1:3 instructor to participant ratio. The Agility exercise program consisted of dynamic functional movement tasks (see Appendix XVII) with emphasis on multi-sensory training including standing on foam (with eyes open and closed and with one foot or both feet), sit-to-stand movements, rapid stepping, tandem walking, walking on foam, obstacle courses, standing perturbations (i.e. instructor pushing participant in a controlled manner or vice versa), and other exercises to challenge functional balance. Exercises in this program were designed so that tasks were progressively increased in difficulty on an individual basis. The Stretching/weight-shifting exercise program consisted of slow movement tasks (see Appendix XVII) including Tai Chi-like movements, standing weight-shifting tasks, and stretching both while standing or sitting and while on mats on the floor. 4.3.4 Outcome measures Participants were evaluated three times: before the intervention (baseline), at the end of the intervention (post-intervention), and one-month following (retention). For each of these time 44 periods, participants were assessed on two occasions separated by approximately two days. In. one session, clinical measures including functional balance and mobility were assessed along ; with balance-confidence and health-related quality of life. In the other session, standing postural reflexes and step reaction time were assessed. The Berg Balance Scale (Berg et al. 1989, 1992) was used to assess functional balance and has established validity and reliability in several different populations including stroke. It consists of 14 balance-related tasks (such as stepping, reaching, and turning) each scored on a 4-point scale (max. 56 points) (see Appendix V). The Timed Up and Go test (Ppdsiadlo and Richardson 1991) was used to assess functional mobility and measures the time to stand up from an arm chair, walk a distance of 3 m, turn, and walk back to the chair and sit down again. Balance confidence and health-related quality of life were measured using the Activities-specific Balance Confidence (ABC) Scale (Powell and Myers 1995) and Nottingham Health Profile (NHP), respectively. The A B C (see Appendix VII) is a 16-item self-report questionnaire that asks individuals to rate their balance confidence in performing specific functional activities on a scale (where 100 represents complete confidence). The NHP (see Appendix VI) is a 38-item questionnaire (low scores represent higher quality of life) that has demonstrated reliability in persons with stroke (Visser et al. 1995). To assess standing postural reflexes, a total of 20 platform translations (8 cm displacement, 30 cm/s velocity, and 300 cm/s acceleration), separated by 15-30 second intervals, were induced while participants stood on two force plates (Bertec Corp.) embedded in a custom built platform (see Appendix Xm for experimental protocol). Participants wore a full-body harness attached to a ceiling beam via a dynamic rock-climbing rope to prevent the occurrence of a fall to the ground with at least one spotter present. Participants were told that the platform could move at any time but the onset and direction of the translation were unexpected in nature. The1 direction of the translation was counterbalanced across participants so that either 10 consecutive backward translations followed 10 consecutive forward translations or vice versa. The first trial from each direction was discarded from the analysis, as the first trial to an unexpected perturbation is different than subsequent ones (Marigold and Patla 2002). Surface electromyography (EMG) (Bortec) from bilateral tibialis anterior (TA), medial head of gastrocnemius (MG), rectus femoris (RF), and biceps femoris (BF) were recorded at 600 Hz for 6 seconds (2 seconds prior to platform movement and 4 seconds after) along with force plate data (see Appendix X for E M G placement protocol). The T A and RF muscles were analyzed for the forward platform translations while M G and BF were analyzed for the backward 45 translations due to their roles in the primary recovery response to those translation directions (Horak and Nashner 1986). A l l E M G data processing used custom written software. E M G was full-wave rectified and low-pass filtered at 100 Hz and the mean signal for one second prior to the onset of platform movement was determined along with the SD. Muscle onset latency, representing a postural reflex, was defined as an increase in muscle activity that exceeded + 2 SD for at least 30 msec and was determined by a combination of computer algorithm and visual inspection via an interactive program. In order to determine whether muscle onset latencies could be reliably measured, test re-test reliability was assessed (using Intraclass Correlation Coefficients [ICC] and standard error of measurement [SEM]) using ten persons with stroke (tested on two separate occasions within seven days). ICCs ± SEMs (msec) for the paretic TA, RF, and M G demonstrated moderate to high reliability (0.92 ± 9.2, 0.87 ± 11.2, 0.79 ± 9.9, respectively), as did the non-paretic TA, RF, and M G (0.79 ± 4.3, 0.79 ±14 .1 , and 0.67 ± 4.4, respectively). In addition, no learning effect was observed as evident from non-significant F-tests over the two days (see Appendix IV). Reaction time was assessed using a simple step reaction time task. Participants stood on the platform looking forward and were instructed to step forward with the specified lower limb as fast as possible following an auditory cue. A total of five trials were performed for this task, ; ' where the first two trials and the last two trials were with the non-paretic limb while the middle trial was with the paretic limb in order to prevent any standing postural bias adopted throughout the repeated trials. Only data from the non-paretic limb was recorded because initial pilot work uncovered a tendency for individuals with stroke to step with this particular limb in recovery responses to platform translations. Reaction time, averaged over the four non-paretic limb trials, was defined as the time between the auditory cue and the time when the vertical force from the force plate reached zero due to the foot lifted off the ground. A self-report falls diary was kept by participants and returned via mail to our research lab on a monthly basis over one year from the start of the intervention. If participants did not return ! the monthly diary, an experimenter phoned to remind them. Falls were recorded on a weekly basis (excluding any in the exercise classes) during the 10-week intervention period. A fall was defined as unintentionally coming to rest on the floor or another lower level but not due to seizure, stroke/myocardial infarction, or an overwhelming displacing force (e.g. earthquake). 4.3.5 Statistical analysis 46 Based on an average Berg Balance score (primary outcome measure) of 45.3 with a SD of 5.65 (Eng et al. 2003) and a desired 5-point change, a sample size of 21 persons per exercise group would have 80% power with a p < 0.05. Thus, thirty persons per group were sought to account for dropouts. Data were analyzed on an intention-to-treat basis. Baseline descriptive j variables between the exercise groups were compared using chi-square (gender, affected limb), Mann-Whitney U (age, stroke duration), Median (AHASFC), or independent t (height, mass) tests. Outcome measures were tested for normality and, when applicable, were either log (Berg Balance, Timed Up and Go, step reaction time) or rank (NHP) transformed for subsequent analysis. Baseline outcome measures between the exercise groups were compared using independent t-tests. Three separate repeated measures multivariate analyses of variance ( M A N O V A ) were performed to compare the outcome measures of the two exercise groups (Group: Agility versus Stretching/weight-shifting) and at the three assessment times (Time: baseline, post-intervention, retention) to control for Type I error associated with multiple statistical tests. The first M A N O V A included the clinical outcome measures: (1) Berg Balance, (2) Timed Up and Go, 1 (3) step reaction time, (4) A B C , and (5) NHP. The second M A N O V A included the paretic limb postural reflex muscle onset latencies for the: (1) TA, (2) RF, (3) M G , and (4) BF, and the third M A N O V A included the non-paretic limb postural reflex muscle onset latencies for the: (1) TA, (2) RF, (3) M G , and (4) BF. Following a significant M A N O V A , a two-way (Group and Time) repeated measures analysis of variance (RM ANOVAs) and, i f applicable, Duncan's post-hoc ; tests for a Time effect were also performed (SAS 8.2, SAS Institute Inc.). A covariate (baseline scores) was included in the R M A N O V A s when baseline differences were significant for a particular variable. The number of falls for each participant was normalized to the number of months over which information was collected. Subsequently, the number of falls/month over the course of one year from the start of the intervention (excluding any falls during the exercise classes) for each group was compared using a Mann-Whitney U test. Additionally, the number of fallers ' and number of repeat fallers (> 2 falls) over the same time period were compared between the two groups using Chi-square tests. A significance level of p < 0.05 was selected for all statistical analyses. 47 4.4 Results 4.4.1 Participant characteristics We identified 109 potential participants between July and September 2002. We excluded 48 participants: 35 did not meet the inclusion/exclusion criteria, 2 refused to participate, and 11 could not obtain physician approval, make the exercise class times, or were planning an extended vacation during the assessment times and/or intervention. Thus, 61 persons with stroke were recruited and underwent stratification/randomization to be placed into one of the two exercise programs: 31 into the Stretching/weight-shifting and 30 into the Agility program. Two individuals discontinued the study due to time commitment issues from the Agility program prior to baseline assessment. A total of 11 individuals discontinued the intervention or were unable to attend post-intervention assessment due to time commitment reasons (n = 2), hip fracture (n = 1, during a non-challenging task in the Agility program), illness (n = 5), or personal reasons (n = 3). Six participants were lost at retention testing due to illness (n = 2), vacation (n = 3), or personal reasons (n = 1). Figure 4.1 summarizes the trial profile. The mean (SD) percent of exercise classes attended for the Stretching/weight-shifting and Agility groups were 94.4 % (5.5) and 92.6 % (10.4), respectively. Table 4.1 describes the participant characteristics for both exercise programs. There were no differences between exercise groups for baseline descriptive variables (p > 0.2). 4.4.2 Clinical outcome measures With the exception of step reaction time (p = 0.01), there were no baseline differences in the clinical outcome measures (p > 0.2, except A B C p = 0.09). Thus, baseline values for step reaction time were entered as a covariate. The M A N O V A demonstrated an overall Group by Time interaction (Wilk's X = 0.76, p = 0.04), Time main effect (Wilk's X = 0.33, p < 0.0001), ! i but no Group main effect (Wilk's X = 0.83, p = 0.18). Step reaction time was decreased in the Agility exercise group to a greater extent than the Stretching/weight-shifting group following the intervention (Table 4.2). There was also a trend for a Group by Time effect for the Timed Up and Go test (Table 4.2). A l l clinical measures showed improvements after the intervention,' which with the exception of step reaction, were retained at follow-up (Table 4.2). 48 109 persons screened for eligibility 48 persons were excluded 61 persons were randomly assigned to one the two exercise groups 30 persons assigned to Agility exercise program 31 persons assigned to Stretching/weight-shifting exercise program 2 persons declined to participate 28 persons assessed at baseline 31 persons assessed at baseline 6 withdrew 22 persons assessed post-intervention 3 withdrew 19 persons assessed for one-month retention 5 withdrew 26 persons assessed post-intervention 3 withdrew 23 persons assessed for one-month retention Figure 4.1: Trial profile. 49 Table 4.1: Participant characteristics. Stretching/weight-shifting Agility (n = 26) (n = 22) Dropouts (n = l l ) Gender, M/F Age, yrs Height, cm Mass, kg Stroke Duration, yrs 18 (69)/8 (31) 67.5 (7.2) 168.9 (8.9) 78.4(15.9) 3.8 (2.4) 17 (77)/5 (23) 68.1 (9.0) 171.0 (9.4) 83.5 (17.7) 3.6(1.8) 6(55)/5(45) 69.6 (10.8) 169.7 (12.9) 76.3 (16.3) 4.1 (5.7) Affected Side, R/L/NA 8 (31) / 18 (69) / 0 (0) 10 (45) / 11 (50) / 1 (5) 3 (27) / 7 (64) / 1 (9) AHASFC, 1 - 5 # of Fallers (retrosp.) Stroke Location Cortical Subcortical Brainstem/cerebellum Cortical-subcortical Unknown 2.5 (2 - 3) 15 (58) 2.0 (1 - 3) 15(68) 3.0 (2.5 - 3)-6(55) 10 (39) 8(31) 4(15) 4(15) 4(18) 7(32) 6(27) 0 5(23) 2(18) 2(18) 3 (27) 1(9) 3 (27) Values are (1) mean (SD) for age, height, and mass, (2) are number (%) for gender, affected side, and # of Fallers, and (3) are median (IQR) for AHASFC. Abbreviations: R = right; L = left; N A = not applicable; A H A S F C = American Heart Association Stroke Functional Classification; retrosp. = 6-month retrospective data 50 4.4.3 Muscle onset latencies The paretic RF and non-paretic M G demonstrated baseline differences between exercise groups (p = 0.03 and 0.04, respectively) while the remaining muscles' baseline measures were not different (p > 0.2, except non-paretic BF p = 0.08). Thus baseline values for the paretic RF and non-paretic M G were entered as a covariate for their respective analyses. The M A N O V A for the paretic limb muscle onset latencies demonstrated an overall Group by Time interaction (Wilk's X = 0.68, p = 0.05), Time main effect (Wilk's X = 0.50, p = 0.0004), but no Group main effect (Wilk's X = 0.87, p = 0.31). The paretic RF onset latency was significantly faster by 27.5 msec following the Agility exercise program compared to 11 msec following the Stretching/weight-shifting exercise program. Onset latencies were faster in all paretic muscles ranging between 4.7 and 27.5 msec (Figure 4.2). Changes in latency were not due to different • recovery strategies employed, as muscle sequencing was similar in all test sessions. Table 4.3 , summarizes the results of the interventions on the standing postural reflex muscle onset latencies. The M A N O V A for the non-paretic limb did not show a Group by Time interaction (Wilk's X = 0.84, p = 0.21) or Group main effect (Wilk's X = 0.86, p = 0.20), but did show a Time main effect (Wilk's X = 0.64, p = 0.0008). Of the non-paretic musculature, only the RF showed faster onset latency over time. 4.4.4 Falls Table 4.4 illustrates the number of falls and fallers in the two exercise groups over one year following the start of the intervention. No significant differences were observed (p > 0.05). A sub-analysis on those who fell prior to the intervention (15 in each exercise group) using a Chi-square test revealed that only eight continued to fall in the Agility group compared to 13 in the Stretching/weight-shifting group (p = 0.046). 51 BOO 400 2§0 800 600 ,400 o 0 50 100 150 200 250 Time (msec) >:PmtfcMG 0 50 100 150 200 250 Time (msec) 800 600 m 200 50 100 150 200 250 Time (msec) 0 ' 50 100 150 200 250; Time.(msec) Figure 4.2: Changes in paretic limb postural reflex muscle onset latencies following the exercise intervention. A typical filtered E M G profile (sample from one participant within the Agility group) demonstrating the faster postural reflexes with exercise training. The solid thick line represents the postural reflex during baseline testing and the dashed line represents the postural reflex during post-intervention testing. Table 4.2: Changes over time with clinical measures for both exercise groups. Stretching/weight-shifting Group (N = 26) Agility Group (N = 22) P-value Outcome Measure Baseline Post-intervention Retention Baseline Post-intervention Retention Time Group X Time Berg Balance, max. 56 44.8(7.1) 48.1 (5.7) 47.5 (6.0) 44.7 (6.5) 49.1 (5.0) 49.0 (5.4) <0.0001f 0.63 Timed Up & Go, sec 18.4(13.1) 17.0(10.7) 17.5(11.0) 20.2 (10.8) 16.7 (9.6) 16.9(10.5) 0.0004f 0.08 Step Reaction Time, msec* 590(171) 540 (144) 659(175) 721 (170) 608 (124) 633 (130) 0.005* 0.01 ABC, % 58.0(21.2) 68.3 (19.4) 64.8 (20.0) 68.1 (18.6) 74.0(18.3) 76.0 (17.2) <0.0001f 0.39 NHP, max. 38 10 (6.4) 7.9 (8.0) 8.7 (7.8) 7.7 (6.2) 6.6 (6.5) 6.1 (6.0) o.ooo^ 0.34 Data are mean (SD). * Baseline differences between exercise groups, p < 0.05. f Post-intervention and retention different than baseline assessment * Post-intervention different than baseline and retention assessment Table 4.3: Effects of the exercise interventions on postural reflex muscle onset latencies. Stretching/weight-shifting Group (N = 26) Agility Group (N = 22) P-value Muscle Baseline Post-intervention Retention Baseline Post-intervention Retention Time Group X Time Paretic TA 115.7(18.8) 109.5(15.9) 115.9(18.4) 122 8(19.5) 118 1 (19.9) 124.7 (27.8) 0.05f 0.94 Paretic RF* 140.3 (32.2) 129.3 (26.6) 1.38.0 (28.4) 164 7(33.6) 137 2 (22.5) 146.9 (23.1) O.OOOl* 0.04 Paretic M G 130.0 (33.7) 117.7(18.0) 120.2(18.3) 131 6(19.1) 126 4(21.1) 132.1 (31.1) 0.004§ 0.47 Paretic BF 170.9 (37.8) 164.6 (21.5) 156.7 (33.6) 185 7 (27.5) 167 4 (13.4) 156.6(24.9) 0.0111 0.49 Non-paretic TA 107.1 (13.0) 105.1 (11.3) 106.5 (14.5) 109 1 (16.8) 111 7 (20.4) 106.7(18.4) 0.52 0.57 Non-paretic RF 139.6 (33.0) 134.5 (26.5) 129.0(23.4) 148 2 (35.5) 141 2 (24.5) 133.1 (29.2) 0.0111 0.61 Non-paretic M G * 109.1 (15.3) 109.2 (20.5) 107.6(14.0) 120 1 (20.5) 113 2(17.6) 113.5(18.3) 0.15 0.22 Non-paretic BF 149.9 (30.7) 145.7 (22.7) 152.7(31.5) 171 4 (22.2) 162 6(31.5) 153.5 (33.8) 0.09 0.68 Data are mean (SD) in msec. Baseline differences between exercise groups, p < 0.05. Post-intervention different than baseline and retention assessments Three time periods different than each other Post-intervention different than baseline assessment Retention different than baseline assessment Retention different than baseline and post-intervention assessments 54 Table 4.4: Fall data over one year from the start of the exercise interventions for the Stretching/weight-shifting and Agility groups. Fall Measure Stretching/weight-shifting (N = 26) Agility (N = 22) # of Total Falls 75 25 # of Falls/Month/Person 0.26 0.10 # of Fallers 16 11 # of Repeat Fallers 11 7 4.5 Discussion Regardless of the type, exercise training improved functional balance and mobility, led to faster standing paretic limb postural reflex muscle onset latencies, and resulted in greater balance confidence and health-related quality of life in persons with chronic stroke. In addition, this study showed that a fast-paced, multi-sensory, agility exercise program results in greater improvements in step reaction time and paretic RF postural reflex onset latency in persons with chronic stroke compared to a slow-paced, stretching/weight-shifting exercise program. This was only the second study to examine the retention effects of a community-based group exercise program: our results and those of Eng et al. (2003) suggest that the exercise effects are maintained for at least one month. It is imperative to develop effective community-based exercise programs to offset earlier acute care discharge. The group aspect of the programs enhances social contact, which is important considering 20% of this population suffers from depression (Jorgensen et al. 2002). The task-specific nature of the Agility exercise program may have contributed to the greater improvements in postural control. For example, the vestibular stimulation in this multi-sensory program may have contributed to the faster paretic RF onset latency as it strengthened those descending pathways responsible for proximal limb control (Allum et al. 1995). However, the weight-shifting components of the Stretching/weight-shifting program may have aided in the improvements of many of the clinical outcome measures. Further, for many individuals getting' 55 to the floor for mat exercises was a major challenge, as it was the first time they had performed this task since their injury. This is the first time postural reflex muscle onset latency has been shown to change with exercise. For example, the postural reflex onset latency of the paretic RF was over 27 msec ' faster post-intervention in the Agility exercise group and this magnitude is well outside the S E M on a repeated test. Further, this is approximately the latency of the monosynaptic stretch reflex for this muscle (Bergui et al. 1992) and is highly suggestive of functional significance when coupled with the concomitant increase in functional balance. The behavioural and neurophysiological changes in this study are most likely the result of neuronal circuitry remodelling. Exercise has been suggested to promote this brain plasticity through mechanisms such as increased expression of brain-derived neurotrophic factor (Cotman and Berchtold 2002; Gomez-Pinilla et al. 2001). Additionally, exposure to enriched rehabilitative training has demonstrated that increased dendritic arborisation accompanies increased motor performance in rats (Biernaskie and Corbett 2001). In humans, forced-use of the paretic limb in persons with chronic stroke has shown cortical reorganization and improved motor performance (Liepert et al. 2000). It has been suggested that disinhibition of gamma-aminobutyric acid neuron activity with a concomitant enhancement of N-methyl-D-aspartate receptor activation may allow plastic changes within the human brain (Butefisch et al. 2000; Ziemann et al. 2001). Given our results, we suggest that exercise programs in persons with chronic stroke should include balance training, with emphasis on multi-sensory tasks. The reduced number of falls following the Agility exercise program compared to the Stretching/weight-shifting program is ^ encouraging, although larger studies are required to investigate this finding, as this trial was powered for balance rather than falls. In addition, the relationship of faster standing postural reflexes to falls-reduction warrants further study. 4.6 Platform-induced falls Falls that occurred during the platform translations for baseline, post-intervention, and retention testing were recorded. The results are shown in Appendix XVIII; however, no statistical analyses were performed. , CHAPTER 5 - Conclusions and General Discussion 56 5.1 General Findings The purpose of this thesis was (1) to understand how individuals with chronic stroke modulate postural control and determine the underlying neural mechanisms contributing to falls and (2) to determine the effects of two different exercise interventions on postural control and physical function. The results of the three studies collectively contributed to four main conclusions. First, the control of the paretic ankle dorsiflexors (i.e. tibialis anterior) is severely impaired in individuals with chronic stroke, which along with delayed non-paretic rectus femoris postural reflex onset latency contributes to falls in this population. We propose that deficits in supraspinal control are responsible for these findings. Second, an Agility exercise program is more beneficial than a Stretching/weight-shifting program, although both demonstrate improvements. Third, community-based group exercise programs for individuals with chronic stroke are effective and methods should be explored for their implementation within the community. And fourth, exercise in individuals with chronic stroke induces neural plasticity. The discussion to follow expands on these conclusions. 5.2 Evidence of altered supraspinal control contributing to impaired postural control in stroke Reactive postural control entails a rapid coordinated muscular response (i.e. postural reflexes), which is evoked following an unexpected destabilizing event (or perturbation) such as a slip, trip, or collision,(Marigold and Patla 2002; Patla 2003). If the central nervous system , (CNS) does not react with sufficient speed or strength a fall may occur. In our experiments we ', utilized a servomotor driven translating platform to elicit standing postural reflexes. Postural control is clearly impaired following brain injury, such as stroke, and we have shown that this is a contributing factor for falls in this population. For example, we demonstrate in all three experiments that the latency of paretic lower limb postural reflexes is delayed in individuals with chronic stroke following unexpected perturbations while standing. 57 We propose central mechanisms are responsible for the impaired postural control observed;, following stroke. Specifically, deficits in supraspinal control contribute, in large part, to postural control dysfunction in stroke survivors. Postural control mechanisms require (1) the detection of external stimuli and (2) transmission of this afferent input to spinal cord, brainstem, subcortical, and cortical regions through neuronal circuits. Supraspinal centres can then contribute to the response by, for example, modulating reflex gain or selecting an appropriate muscle synergy. Stroke may affect the detection or transmission of afferent information or alternatively, disrupt cognitive processing centres. Several converging lines of research lend support that the latter is more detrimental and responsible for impaired postural control. 5.2.1 Peripheral mechanisms contribute minimally to the impaired postural control following stroke Our first experiment demonstrated load-dependent modulation of ankle extensor muscles (i.e. gastrocnemius) in response to backward platform translations during different standing weight-bearing load conditions. Dietz and colleagues (Dietz et al. 1992) argue what has already been suggested in cats (Duysens and Pearson 1980; Pearson and Collins 1993) that golgi tendon organs (GTO) within extensor muscles contribute to load-dependent modulation. Thus, GTO function appears to be intact following stroke. In addition, Wilson et al. (1999) have recently shown muscle spindle activity in individuals with stroke is similar to healthy controls suggesting that muscle spindle function remains intact after stroke as well. Muscle spindle function is important for recovering after platform translations, as these perturbations are thought to be somatosensory-triggered (Inglis et al. 1994) and the stretch of ankle musculature in response to' the translations would evoke spindle activity. Several muscle property changes have been observed following stroke including a decreased number of motor units (Dietz et al. 1986), disturbed motor unit recruitment (Gemperline et al. 1995), decreased motor unit firing rates (Dietz et al. 1986; Rosenfalck and Andreassen 1980), and delayed time to generate peak torque (McCrea et al. 2003). Furthermore, motor conduction velocities to paretic leg muscles are slower, albeit in the range of approximately 3-4 msec, than non-paretic motor conduction velocities (Cruz-Martinez 1983). However, a recent investigation in individuals with stroke (Landau and Sahrmann 2002) demonstrated that maximal voluntary muscle contraction elicited by electrical stimulation was no different than healthy age-matched controls, which led these authors to suggest that muscle weakness may stem from central 58 impairments (such as corticospinal tract involvement) rather than a problem with the muscle tissue itself. Additionally, Chae et al. (2002) have recently shown in individuals with chronic stroke that the time to initiate a muscle contraction in the paretic limb following an auditory cue (a task which would require cortical processing) is delayed compared to the non-paretic limb. 5.2.2 Supraspinal deficits are responsible for the impaired postural control following stroke In order to initiate a postural response, the CNS integrates incoming sensory and environmental information. This process requires sufficient cognitive processing resources and thus, is attention demanding (Redfern et al. 2001). Attention relies on a complex interaction of many cortical, subcortical, and brainstem areas (Banich 1997). Our hypothesis that deficits in supraspinal control contribute to the impairment in postural control following stroke is supported by several recent findings in studies dealing with cognitive processing. First, individuals with chronic stroke do suffer from permanent cognitive impairments (Hochstenbach et al. 2003). Second, Hyndman and Ashburn (2003) have recently reported that attention deficits correlate with falls in individuals with chronic stroke. Third, using a dual-task paradigm in individuals with chronic stroke, Brown et al. (2002) demonstrated increased reaction time (verbal response to a visual stimulus) during various postural tasks compared to healthy older adults. Fourth, individuals in the acute phase of stroke who demonstrate slower reaction time of finger tapping following a visual stimulus are at higher risk for falls than those individuals with1 acute stroke who have faster reaction time (Mayo et al. 1990). Fifth, step reaction time is delayed in individuals who fall in response to platform perturbations versus those who do not (unpublished observations). Sixth, sensory integration is impaired following stroke compared to healthy older adults, as demonstrated by increased postural sway and falls during manipulation:' of ankle proprioception and visual cues while standing (unpublished observations). Lastly, premotor time but not mean motor time for an ankle dorsiflexion task with the paretic leg was delayed compared to that in the non-paretic limb, supporting the notion that stroke affects central, premotor time processing centres rather than peripheral deficits (Smith et al. 1998a). The lack of cognitive resources for postural control duties may be the result of increased attention to the hemiparetic side. In other words, in order to function, individuals with stroke 0 devote a large amount of conscious effort in ensuring stability in the face of sensorimotor ! 59 dysfunction on one side of their body. In particular, the compensatory strategies adopted over the course of recovery from brain injury may require extra resources. Therefore, deficits in the supraspinal control over postural reflexes following stroke likely contributed to the results observed in Experiment U. Specifically, these deficits likely contributed to the delay in non-paretic rectus femoris latency, attenuated tibialis anterior postural reflex magnitude, and reduced volitional muscle strength (assessed through an isokinetic dynamometer) in individuals with stroke who fell in response to platform translations. 5.2.3 Implications for rehabilitation What then does this mean for rehabilitation? Clinicians treating individuals with stroke and those involved in developing exercise protocols must ensure that supraspinal centres are stimulated. This may be accomplished through multi-sensory training (as performed in Experiment JR with great success) whereby the brain would be required to integrate multiple sources of sensory information. This concept is discussed in more depth in later sections. Additionally, the use of dual-task paradigms may be beneficial. Here, two tasks are performed simultaneously, competing for attention and processing resources. This may include walking or standing in various challenging postures while counting or performing arithmetic, ? object recognition during challenging balance tasks, or even having individuals perform a circuit in which obstacle avoidance is required. The results of obstacle course training in exercise programs for individuals with chronic stroke are promising (Ada et al. 2003; Bassile et al. 2003). 5.3 Exercise interventions for individuals with chronic stroke There is an urgent need to develop safe and effective community-based group exercise programs for individuals with chronic stroke to offset earlier discharge from a rehabilitation setting and to maintain and/or improve functional balance and mobility. Further, these programs can help reduce sedentary lifestyle and secondary complications as well as improve 11 quality of life. Barnett et al. (2003) have recently shown that a community-based group exercise program in healthy older adults results in improved balance and a reduction in falls over one year. The benefits of a community-based group exercise program in individuals with chronic 60 stroke have also been reported (Ada et al. 2003; Bassile et al. 2003; Batien et al. 1996; Dean et al. 2000; Eng et al. 2003; Rimmer et al. 2000; Teixeira-Salmela et al. 1999, 2001). 5.3.1 Program adherence, safety, and exercise instructors Although the attrition rate for the exercise intervention (Experiment III) was 18.6%, the average attendance for the Agility exercise group was 92.6 % (range 51.7 - 100%) and for the Stretching/weight-shifting exercise group was 94.4 % (range 82.8 - 100%). Thus, program adherence was excellent for those who remained in the interventions. The most common reason for discontinuing the intervention was illness. These results are encouraging as the Stretching/weight-shifting program was minimally challenging and although it was difficult to keep the high functioning individuals challenged our instructors did an excellent job to keep them entertained. In addition, the Agility program was highly challenging and low functioning individuals still attended and gave their best. This latter aspect may have been facilitated by the fact that exercise difficulty was graded on an individual basis. Adherence in both exercise programs may also have been due to the collegiality that developed among participants. The programs were an excellent way for the participants to interact with one another and connect with individuals with similar impairments. The finding that perceived health-related quality of life, assessed by the Nottingham Health Profile, was improved for both exercise groups supports this. Therefore, both exercise programs appear to be feasible for maintaining participation and improving quality of life, presumably from a combination of social interaction and the perception of improved physical function. The class length (one hour sessions) and frequency (3x/wk) seemed to have worked out well. Bastien et al. (1998) investigated class length and frequency of exercise programs and found that moderate improvements were noticeable even with a 90-minute class once per week' or two 60-minute classes per week. However, to show meaningful improvement in balance we recommended that the length and frequency be maintained as in Experiment in . Safety is a major concern when running an exercise program, particularly with individuals at high risk for falls and fall-related injuries. The 3:1 instructor-to-client ratio was chosen based on a previous study by Eng et al. (2003). This ratio proved to be sufficient for both exercise groups. We do not recommend this ratio being adjusted especially i f agility exercises are being performed. Since exercises were implemented in a graded fashion on an individual basis for the Agility program, a large number of clients did not perform all types of exercises. For example, very few utilized the tilt-board or the most difficult piece of foam in the Agility program. Instructors spotted those individuals at higher risk for falls and during exercises that were particularly challenging regardless of the client's functional level. There was one injury related to the Agility exercise intervention group (i.e. a hip fracture). However, it must be emphasized that this adverse event was unavoidable. The client involved had a very high Berg Balance score and did not typically require spotting. Furthermore, the event occurred during a non-challenging task (i.e. standing balloon toss). Only one hip fracture out of the 59 individuals who started the exercise intervention represents less than 2% of the sample, which is well within the percent of individuals with stroke that fracture their hip in a given year (Dennis et al. 2002; Kanis et al. 2001). In the future, it may be beneficial to have clients utilize hip protectors as a precaution and/or have high absorbent flooring in the exercise classroom to minimize the chance of serious injury. The exercise instructor team consisted of a physiotherapist (head instructor), kinesiologist, and recreation therapist. The combination worked exceptionally well, with each instructor providing a different level and kind of expertise. Of particular benefit was the presence of a recreation therapist. A recreation therapist provides expertise on using leisure and recreation for achieving optimal health and quality of life. They not only focus on the exercises to improve function but also on adapting the program based on the goals and interests of each individual (e.g. social interaction, making exercises fun and meaningful, instilling confidence). In an ideal situation, future community-based group exercise programs would utilize all three of these professionals. 5.3.2 Types of exercises used in the intervention and their effectiveness The selection of appropriate exercises for the Agility exercise group were based, in large part, on the work of Fitzgerald et al. (2002), Gardner et al. (2001), and Hu and Woollacott (1994a, b) in healthy older adults and modifying them to suit a lower functioning population. The major foci for this exercise program were the multi-sensory and agility components (see Appendix XVTI). A variety of densities of foam were used to alter somatosensation, thereby enhancing afferent input from the visual and vestibular systems. Removing visual input by closing the eyes was also used to further emphasize the need for vestibular regulation of postural control. 62 Agility training has been shown to be effective in older adults (Fitzgerald et al. 2002). Rapid forward and backward stepping was a major task in our program, as compensatory stepping is a common strategy employed in response to standing perturbations in older adults (Maki and Mcllroy 1997). Standing perturbation training was also utilized. In this task, the instructor would attempt to knock the client off balance to force them to step (in a highly controlled and safe manner). Additionally, clients were given the chance to attempt to knock the instructor off balance (a self-induced perturbation). This, not surprisingly, was one of the more enjoyable tasks for the clients. Both the rapid stepping and standing perturbation tasks may have contributed to the faster standing postural reflexes and step reaction time outcome measures. The braiding and tandem walking were also very effective, as demonstrated by the improved functional mobility seen after the intervention. It is recommended that clients be % carefully spotted during the braiding task because of the risk of tripping on their feet. The major foci of the Stretching/weight-shifting exercise program were, as the name implies, stretching and weight-shifting (see Appendix XVII). Stretching of major muscle groups was performed during standing, sitting, and while on mats on the floor. This latter location was particular important for this exercise program as getting down to and up from mats on the floor proved to be a challenge for many of the clients. In fact, several clients told us that they had not been down on the floor since their injury. Although none of the instructors involved in the exercise intervention were trained in the art of Tai Chi, similar weight-shifting movements were incorporated and provided a constant driving force for this program. Increasing the ability to take load through the paretic limb is important for many activities of daily living, such as standing up from a chair and reaching forward, and for postural stability (Cheng et al. 1998; Eng and Chu 2002; Sackley 1990). Although the Agility exercise group demonstrated additional benefits over the Stretching/weight-shifting exercise group, a combination of the two programs is likely important. We recommend that mat exercises be incorporated into the Agility exercise program. Further, group discussions (and even educational sessions) would also be of benefit to this program. The results of this thesis should facilitate the design of rehabilitation programs for individuals with chronic stroke. It is clear from Experiments I and II that clinicians need to focus on the ankle dorsiflexors, particularly on the paretic limb, to improve muscle strength. This in turn may then help reduce the incidence of falling in this population. Furthermore, it is important to incorporate exercises that evoke postural reflexes, such as standing perturbation training, and exercises that require fast movements, such as rapid stepping. Multi-sensory 63 training would also be effective as this type of training might improve cognitive processing and may have contributed to some of our clinical trial (Experiment HI) results (see neural plasticity section below). Balance training has not been extensively studied in individuals with chronic stroke. Exercise tasks that have been used include reaching tasks while seated or standing with feet together or in tandem (Dean et al. 2000), stepping onto blocks or steppers (Dean et al. 2000; Eng et al. 2003), walking over obstacles (Ada et al. 2003; Bassile et al. 2003; Dean et al. 2000), walking on different surface terrain (Ada et al. 2003; Dean et al. 2000; Eng et al. 2003), and varying step length or speed during walking (Ada et al. 2003; Eng et al. 2003). Unfortunately, Tangeman et al. (1990) did not report the type of functional balance exercises performed during their intervention, although they did mention weight-shifting tasks. Foam (walking task) was used in only one study (Eng et al. 2003); however, not to the extent of this clinical trial. Furthermore, no other study in individuals with chronic stroke has utilized standing perturbation tasks. We have demonstrated that these tasks are not only feasible, but may also have contributed to the better performance of the Agility exercise group. , Overall, both exercise programs were highly effective in improving functional balance and mobility among other measures. The cost of equipment used was minimal and readily available in most communities. We argue that it is time to implement community-based group exercise '' programs for individuals with chronic stroke. 5.4 Exercise-induced Neural Plasticity Neural plasticity refers to a persistent nervous system modification (whether it be structural, molecular, or cellular) that results from past experience and affects future behaviour (Wolpaw and Tennissen 2002). How the brain adapts to recovery from injury is one form of plasticity. In addition, motor learning, which is a set of internal processes associated with practice or experience leading to relatively permanent changes in the capability for motor skill (Schmidt 1 and Lee 1999), is another form of plasticity. Until recently, it was believed that functional recovery of individuals with stroke plateaus after about 6-months following injury (Duncan and Lai 1997; Jorgensen et al. 1999; Wade et al. 1985). However, recent studies of exercise training and constraint-induced therapy in individuals with chronic stroke (i.e. greater than 6-months post-stroke) suggest that improvements in function are still possible (Liepert et al. 1998, 2000a). 64 We showed that functional balance and mobility were improved following our exercise interventions (Experiment III). Further, we demonstrate for the first time that paretic limb postural reflexes become faster following exercise, particularly following an Agility intervention (e.g. approx. 28 msec change in latency of the paretic rectus femoris). We argue ;. that the faster standing postural reflexes are functionally significant as there was a concomitant i improvement in functional balance and mobility. Moreover, we argue that the investigation of postural reflexes provide a means to speculate on whether plastic changes occur within the nervous system and the faster postural reflexes represent neural plasticity. The faster step reaction time for the Agility exercise group also supports the notion of neural plasticity. This : task requires individuals to process the auditory cue for initiating the step forward and integrate this afferent information within multiple cortical association areas so that a motor command can be generated and subsequently sent through descending pathways to the muscle itself. The onset latency of the postural reflexes (> 100 msec) and especially the time to initiate a step (> 500 msec) for the step reaction task are highly suggestive of cortical involvement (Di Fabio et , al. 1992). Although the small changes in the paretic tibialis anterior, gastrocnemius, and biceps femoris may have occurred through spinal cord plasticity and/or alterations in peripheral nerve\ conduction velocity and muscle fibre type, the larger change with the paretic rectus femoris is too great not to have been from plasticity within cortical neuronal networks. This is especially true for the change in step reaction time (> 100 msec faster for the Agility exercise group post-intervention). Further support comes from the fact that the changes are not from spontaneous recovery, as this would have occurred well before entry into the intervention. In terms of postural reflex onset latency, the change is not due to an alteration in muscle sequencing or recovery strategy as individuals continued to demonstrate the same responses before and after the intervention. In addition, the faster postural reflexes are not the result of learning as we demonstrated that postural reflex muscle onset latencies have moderate to high test re-test reliability (without improvement) (see Appendix IV). Thus, it appears as though exercise induces neural plasticity in individuals with chronic stroke. 5.4.1 Reasons for exercise-induced neural plasticity Why might these changes have occurred? The faster step reaction time and paretic rectus femoris postural reflex onset latency occurred in the Agility exercise group, which might be 65 explained by the task-specific training involved in this program. Task-specific training is thought to drive neuronal reorganization (Shepherd 2001). The use of the rectus femoris muscle to step forward during the rapid stepping tasks and the standing perturbations performed in the Agility exercise program may have facilitated the faster paretic limb rectus femoris onset latency and faster non-paretic limb step reaction time. Strengthening of redundant or alternative pathways could be responsible for the faster onset latency of the paretic rectus femoris and step reaction time in the Agility exercise group. Several studies using transcranial magnetic stimulation (TMS) or functional magnetic resonance imaging (fMRI) in individuals with stroke during recovery have demonstrated that activation of the unaffected hemisphere (which would stimulate ipsilateral pathways) occurs during thumb or hand movements; although whether this correlates with functional recovery is still under debate (Caramia et al. 2000; Cramer et al. 1997; Cramer and Bastings 2000; Feydy et al. 2002; Netz et al. 1997). Lee and van Donkelaar (1995) have reported that after gradual improvement over several years from a left hemispheric stroke resulting in right-sided hemiparesis, a patient experienced a second stroke in the opposite hemisphere in almost the identical location. The result was a mild sensorimotor deficit in the left arm but a marked worsening of the original right hemiparesis. The authors argue that the most plausible explanation is that the original unaffected hemisphere was responsible for the improved right hemiparesis following the first stroke. Animal studies have also demonstrated neural plasticity in both the affected and unaffected hemispheres (Frost et al. 2003; Jones et al. 1996; Kozlowski and Schallert 1998; x Stroemer et al. 1995). 11 The exercise tasks encompassing the Agility program, for example, the use of multi-sensory tasks, enhanced vestibular stimulation and hence, the vestibulospinal tract. It is believed that the vestibulospinal tract, particularly the lateral vestibulospinal tract, has a large influence on proximal leg muscles (e.g. rectus femoris) for postural control (Allum et al. 1995). The lateral: vestibulospinal tract remains uncrossed and thus, is stimulated by the unaffected hemisphere (Fredericks 1996). Uncrossed pontine reticulospinal tract fibres, which receive ipsilateral cortical projections, also have a large influence on proximal leg muscles (Fredericks 1996). It is possible that a combination of neural plasticity in these pathways contributed to the faster paretic rectus femoris postural reflex. Since all paretic limb muscles exhibited faster postural reflexes, albeit to different amounts, these pathways may have influenced these other muscles. ' Alternatively, ipsilateral corticospinal tract fibres may have been the driving force; particularly 66 with the paretic tibialis anterior and gastrocnemius as corticospinal tract fibres have strong influences over distal leg muscles (Brouwer and Ashby 1992). The Agility exercise program presumably stimulated proprioceptive pathways as well. Thus, improvements in functional balance and mobility as well as the faster postural reflexes and step reaction time may have been facilitated by neural pathways and supraspinal centres associated with this sensory system. 5.4.2 Potential mechanisms for exercise-induced neural plasticity The question then arises as to what are the underlying mechanisms involved in the neural plasticity induced through exercise training? Exercise can activate the molecular and cellular cascades involved in neural plasticity (Cotman and Berchtold 2002). Wheel running or treadmill exercise in rats for multiple days leads to an increase in brain-derived neurotrophic factor (BDNF) expression within the soleus muscle, spinal cord, hippocampus, and cerebral cortex (Cotman and Berchtold 2002; Gomez-Pinilla et al. 2001; Neeper et al. 1996). BDNF has many characteristics that make it suitable for neural plasticity: its expression is activity-dependent (Black 1999; Cotman and Berchtold 2002; Kohara et al. 2001), it can be transported to a post-synaptic neuron from a pre-synaptic neuron (Kohara et al. 2001), it enhances synaptic transmission (Black 1999; Cotman and Berchtold 2002), and stimulates synaptophysin for synaptogenesis (Cotman and Berchtold 2002). Recently, Kwon et al. (2002) discovered that rubrospinal neurons do not die in spinal cord injured rats but rather they are in a state of severe atrophy, which can be reversed with BDNF treatment one-year post-injury. It is possible that following stroke, rubrospinal tract neurons as well as additional pathways such as corticospinal tract neurons are also severely atrophied and exercise-induced BDNF expression reverses this process and contributes to the observed neural plasticity. Exercise also increases nerve growth factor (NGF) expression in wheel running rats ; (Cotman and Berchtold 2002; Neeper et al. 1996) and increases neurotrophin-3 (NT-3) expression in treadmill exercising rats (Gomez-Pinilla et al. 2001). Kolb et al. (1996) has f shown that NGF treatment prevents dendritic atrophy and promotes dendritic arborisation and increases spine density following unilateral lesions in rats. In addition, van Praag et al. (1999a, 1999b) have reported enhanced neurogenesis in conjunction with better performance on the Morris water maze task following wheel running in mice. 67 Plastic changes to neurons must be accompanied by local increases in oxygen and glucose (Kleim et al. 2002). This may be accomplished by increased growth of capillaries (angiogenesis) within regions undergoing plasticity. Kleim et al. (2002) and Swain et al. (2003) have recently shown exercise (wheel running) induces angiogenesis in the motor cortex of rats. Thus, BDNF, NGF, and NT-3 expression along with angiogenesis may facilitate exercise-induced neural plasticity. Few studies have investigated neural plasticity in individuals with chronic stroke. The cortical reorganization seen in animal models has also been demonstrated in individuals with chronic stroke following forced-use of the paretic arm through constraint-induced (CI) therapy (Liepert et al. 1998, 2000a). Individuals with chronic stroke experienced two-weeks of CI therapy and motor function was improved with a concomitant increase in motor output area size of the affected hemisphere, which was retained up to 6-months (Liepert et al. 1998, 2000a). Cortical reorganization and changes in cortical excitability may stem from several processes including long-term potentiation (LTP), changes in N-methyl-D-aspartate (NMDA) receptor activity, changes in gamma-aminobutyric acid ( G A B A ) A receptor activity, through intracortical connections, or unmasking silent synapses. LTP refers to a brief high-frequency train (or tetanus) stimulus causing a prolonged increase in amplitude and excitatory potential in a connecting neuron (Bliss and Lomo 1973). The activity-dependent induction of LTP, its longevity, and property of associativity (which is the ability of a strong LTP inducing stimulation to cause a non-LTP inducing stimulation with which it is paired to exhibit LTP) remain compelling reasons why LTP may be one mechanism of neural plasticity (Martinez et al. 1998). LTP is also involved in motor learning (Martinez et al. 1998) and exercise in rats has shown enhanced LTP (van Praag et al. 1999a). Following stroke, changes in excitatory receptor activity (i.e. up-regulation of N M D A receptors) and inhibitory receptor activity (i.e. down-regulation of G A B A A receptors) occur (Qu etal. 1998). The intracortical connections, which are supposed to modulate cortical ' representation (i.e. regions within the cortex responsible for specific movements) area sizes, are mainly GABAergic (Jones 1993). Early studies in rat brains by Donoghue and colleagues support the notion of unmasking latent intracortical (horizontal) connections for reorganizing cortical representations (Hess and Donoghue 1994; Hess et al. 1996; Jacobs and Donoghue 1991). After application of bicuculline methobromide, a G A B A antagonist, to a remote region in the primary motor cortex from the electrical stimulations site, forelimb movements could be evoked (Jacobs and Donoghue 1991). In rat primary motor cortex slice preparations, LTP could 68 be produced with theta burst stimulation only after application of the G A B A A receptor antagonist, bicuculline methiodide, in layer JUTS, horizontal projections (Hess and Donoghue 1994; Hess et al. 1996). Furthermore, application of 2-amino-5-phosphonovaleric acid, a N M D A receptor antagonist, blocked LTP in these connections (Hess et al. 1996). Recent experiments in human subjects have confirmed the plausibility of G A B A A and N M D A receptor mediated neural plasticity. In a study by Biitefisch et al. (2000), TMS was used to evoke thumb movements in one direction. Subsequently, participants practiced for 30-minutes thumb movements in the opposite direction, which TMS post-training then induced thumb movements in the practiced direction. This process was repeated over several days in which oral doses of lorazepam, a G A B A receptor agonist, or dextromethorphan, a N M D A receptor blocker, were given to participants prior to testing. The results demonstrated both these drugs decreased thumb movements in the practiced direction evoked by TMS post-training. More recently, Ziemann et al. (2001) found that motor practice of ballistic contractions of the biceps brachii during ischemic nerve block (to decrease G A B A inhibition) increased motor evoked potentials assessed by TMS whereas motor practice after an oral dose of lorazepam decreased motor evoked potentials. Thus, neural plasticity appears to involve an increase in N M D A receptor density and/or efficiency with a concomitant decrease in inhibitory G A B A A receptor density and/or efficiency. The knowledge gained from studies on the effects of rehabilitative training following j ischemic infarct to the sensorimotor cortex may also serve to be fruitful in providing potential mechanisms for plasticity in the chronic stage of injury. Environmental enrichment and task-specific rehabilitation in rats following unilateral middle cerebral artery occlusion improved b motor function and increased dendritic arborisation of layer V pyramidal cells within the undamaged motor cortex (Biernaskie and Corbett 2001). Jones and colleagues (Chu and Jones 2000; Jones et al. 1999) have shown that an acrobat task (i.e. obstacle course) following unilateral forelimb sensorimotor lesion in rats increases dendritic growth and synaptogenesis . compared to rats undergoing repetitive task training and those who received the lesion but no intervention. Our Agility exercise program may be the human equivalent to enhanced rehabilitative training in animals. In monkeys, a lesion to the motor cortex hand area with subsequent behavioural rehabilitation training (food pellet retrieval task) increased performance and cortical reorganization (Nudo et al. 1996). This form of 'rehab' prevented the loss of spared hand cortical representations in adjacent, intact cortex. In humans, a single physiotherapy session 69 during the subacute phase of rehabilitation in individuals with stroke resulted in an increased cortical representation (i.e. motor output map) of the paretic hand muscle in the affected hemisphere one-hour after therapy as assessed by TMS (Liepert et al. 2000b). Thus, increased dendritic arborisation, dendritic spine density, synaptogenesis, and on a larger scale, cortical reorganization, may contribute to the exercise-induced neural plasticity. It would be interesting to utilize TMS or fMRI to investigate neural plasticity in individuals with chronic stroke during the course of an exercise intervention similar to ours. 5.5 Limitations This was the first study to investigate falls-reduction following a community-based group exercise program in individuals with chronic stroke. There were three times as many falls in the Stretching/weight-shifting group than the Agility group over the one-year follow-up; however, this did not reach statistical significance. Further, the number of fallers was not different between exercise groups. A limitation of the clinical trial was that it was not powered for falls. However, following a sub-analysis on just the individuals who fell prior to the intervention, the number of fallers was significantly lower in the Agility group versus the Stretching/weight-shifting group. There is an obvious need to examine strategies for falls-reduction in individuals with chronic stroke. The results from our clinical trial are encouraging; however, multi-centre clinical trials with a larger sample size are required to firmly establish whether an exercise intervention can reduce falls in this population. Several additional limitations to this thesis exist. First, data for Experiment II was obtained from the baseline assessment of the clinical trial (Experiment IJf). Hence, the knowledge gained on the neural mechanisms of falling from Experiment II was not used in the development of the exercise interventions. Although this information may have been useful, the exercises still targeted the aspects associated with falls that we identified. Exercises were based on previous studies in individuals with chronic stroke, from knowledge of the clinical presentation of individuals with chronic stroke, and studies in healthy older adults. We would not have altered the exercise interventions in any way had we run Experiment II before designing the clinical trial. Second, we were unable to obtain information regarding the location of the stroke for approximately 20% of our sample. Further, we did not have information on the volume of the 70 stroke. Thus, we could not determine which specifics areas within the brain were damaged and responsible for our observations. It would be fruitful to have future studies obtain this information. Third, changes in the latency of postural reflexes but not the magnitude following exercise were investigated in Experiment m. Unfortunately, this is due to methodological constraints • associated with E M G collection (e.g. skin impendence) that may influence magnitude from one day to the other. Changes in kinematics during perturbations following exercise interventions : would also be interesting and warrants further study. Fourth, we restricted our perturbations to the anterior-posterior direction. Individuals with stroke often load their non-paretic lower limb to a greater extent. Further, falls do occur to a large extent in the medial-lateral direction, thereby increasing the chance for hip fracture. Unfortunately, no study has used medial-lateral surface translations in individuals with chronic stroke and thus, little is known about how these individuals react in this direction. Fifth, screening and recruitment were limited. Not every person screened for our clinical trial was eligible. Cognitive deficits and the inability to ambulate were among the reasons for exclusion. Since we required participants to ambulate, this might have excluded those with -severe motor impairments, sensory impairments, or spasticity. Fortunately, the majority of : individuals with stroke do become ambulatory after their injury (Jorgensen et al. 1999; Wade et al. 1985) and thus, a large portion would be able to participate in community-based exercise programs. Due to the amount of questionnaires and testing which required several instructions, we excluded individuals with cognitive deficits. However, these individuals may still be able to participate (possibly with an extra assistant present during the exercise classes) in exercise programs in the community where laboratory testing is not required. In addition, we recruited participants on a voluntary basis. Thus, the fact that these people wanted to get better may have influenced our results. And sixth, the difficulty in transportation to the community centre for the exercise classes made it impossible for those living outside the Vancouver area (such as Powell River) to participate. Since a portion of the population does live in these areas, methods for including these individuals must be explored. Fortunately, transportation in Vancouver for individuals :l with impairments, such as stroke, is available and effective. A final concern must be addressed regarding the lack of a true control group in Experiment in. Although we cannot exclude the possibility that the simple act of attending the exercise classes (i.e. getting to and from the classes) may have contributed to the changes, there are 71 several reasons why the exercise interventions were the primary cause of the observations. First, test re-test reliability was established (and learning was not evident) for the standing postural reflexes and the changes (particular the rectus femoris muscle of the paretic limb) were outside the S E M range. Second, Eng et al. (2003) report that Berg Balance scores are stable over time and also found improvements with exercise. And third, the Agility exercise group demonstrated additional improvements in some outcome measures over the Stretching/weight-shifting group. In addition, the changes were not due to recovery over time as a plateau of recovery is reached within 6 months post-stroke (Duncan and Lai 1997; Jorgensen et al. 1999; Wade et al. 1985). Thus, the changes observed in Experiment in were in fact due to the exercise interventions. 5.6 Future directions We propose a three-tier community-based group exercise program system be implemented:'! in the community for individuals with chronic stroke. This exercise program should follow the tasks outlined in the Agility exercise program with the addition of (1) the task of getting down to and up from the floor, (2) group discussions, and (3) educational sessions such as fall prevention and cardiovascular health. Additional social events and/or outings may also be included. Each of the three tiers would represent a separate exercise class/program held for one-hour, three times per week throughout the year. In terms of the exercise instructor team, a 3:1 instructor-to-client ratio should be maintained. In addition, we recommend the team consist of a physiotherapist, kinesiologist, and recreation therapist; although a physiotherapist could act as a consultant and be replaced as an instructor by another kinesiologist or rehab assistant trained to deal with individuals with stroke. The difficulty of tasks in each tier would be progressively more challenging. Tier one would be tailored to clients predominantly wheelchair bound and/or very low functioning. Tier two would be tailored to clients of medium functioning. And tier three would be tailored to high functioning clients. This last and final tier would also be considered an exercise class for maintaining any improvements in functional balance and mobility. Thus, multiple classes may be required to accommodate the larger amount of individuals that wil l eventually be at a tier ' three level. 72 Participation in this recreation/exercise program would be voluntary. However, prior to entry all individuals would be required to undergo an assessment to determine which tier is most suitable for them and to determine any goals of the individual. A composite score based on clinical testing of Berg Balance, Timed Up and Go, and step reaction time is recommended due to the speed and ease in which these tests can be administered as well as their relevance to the purpose of the program. At certain points throughout the year (for example, every two months) clients would be re-evaluated to determine whether they could graduate to the next tier level. This assessment period would also serve as a point in which new clients could enter the program. 5.7 Final thoughts In conclusion, we have identified aspects of impaired postural control and the neural mechanisms contributing to falls in individuals with chronic stroke. Further, we have shown the benefits of exercise in this population. 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To establish the N=2696 Followed - Falls - 4% 2002 rate of fracture strokes; x=68 stroke patients Fractures experienced after stroke and yrs old; admitted between fracture (30% of DSM510 compare that rate 1426M, 1990-1998 and hip and 75% due with that of the 1270F referred to a clinic to a fall) for general between 1994-1998 hospital referred population Followed up at 6 months and 1 and 2 years Calculated risk of admission with hip fracture to hospital after stroke patients Hospital discharge data ->• 2% had fracture by 1 year and 10.6% by 10 years 1.2 times the rate of hip fracture compared to general population and 2.3 times compared to patients with MI Forster and To undertake a N=108 Community- - Falls - 73% fell Young 1995 systematic stroke; 57M, dwelling stroke Motor club within six months inquiry into the 5 IF; 46 right, survivors recruited assessment after discharge DSM 172 incidence and 57 left hemi; - Barthel Index from hospital for a consequences of x=70 yrs old; Frenchay total of 270 falls falls in a cohort activities index reported of elderly - NHP Fallers were patients with less socially active stroke after at six months and discharge from more had • hospital depressed mood • Patients who fell in hospital were more like to fall after discharge Hyndman To describe N = 48 - Fall Berg Balance Attention and levels of chronic information - ADL deficits in stroke Ashburn attention deficits stroke; 30M, collected from Attention common 2003 and explore 18F; 21 right, retrospective (12 (sustained Balance was. relationships 26 left hemi; months) data attention, auditory correlated with between x=68.4 yrs Performed selective, visual ADL (r=0.83), DSM 1079 attention, ADL old; x=46 measures of selective, visual elevator counting ability, balance, months post- attention, ADL, and inattention) (r=0.4), telephone and falls in stroke; balance - Falls searching while chronic stroke counting (r=0.51), and fall status (r=-0.42) Fall status also correlated with ADL (r=-0.38), elevator counting (r=-0.37), and telephone search 95 while counting (r=-0.41) Those with normal scores on sustained and divided attention > tests had significantly better balance and ADL ability Repeat fallers had lower balance scores and ADL than non-fallers with no near-falls and non-fallers with near-falls Hyndman et To determine N=41 strokes; Fall -> defined - Falls - 50% were al. 2002 whether 26M, 15F; as "an event that - ADL classified as fallers circumstances of x=69.7 yrs results in a person (Nottingham and approx. 80% DSM 509 falls and fall risk old; x=50.4 corning to rest extended ADL) had experienced a differ among a months post; unintentionally on Rivermead near fall community 16 right, 23 the ground or other Mobility Index Repeat fallers sample of stroke left hemi and lower level, not as a (RMI) had significantly patients whose 2 brainstem result of a major Rivermead reduced arm time since stroke intrinsic event or Motor assessment function and ADL varies and to overwhelming upper limb scale ability compare hazard" (quoted (RMA) - Trend of RMI characteristics of from another Hospital for repeat fallers to fallers and non- article) anxiety and be lower than noji-fallers Classified as depression (HAD) fallers with no near fallers if fell in past scale falls 12 months - 62.8% of Falls had to fallers landed occur outside sideways toward hospital their affected side - Used Fall - In 50% of ' Events near-fall questionnaire descriptions, patients recovered their balance by using arm movements Jorgensen et To compare the N=ll l Recruited from Risk of first Depression al. 2002 incidence of falls stroke; community fall predicted falls in^ among non- 57%M; x=68 froml 994-1995. - Risk of stroke institutionalized yrs old; x=10 Descriptive recurrent falls - 23%> of stroke DSM 316 long-term stroke yrs post- collected Type and fell during a 4-survivors with stroke; 4-month characteristics of month period healthy older N=143 prospective fall falls while living in the, adults controls; history community (50%" 57%M; x=67 of fallers fell yrs old; multiple times) - 77% of falls were during walking Kanis et al. To examine N=273,288 Followed - - After 2001 whether stroke strokes; subjects from time hospitalization for 96 might be 136,800M of stroke until 1996 stroke, there was,a associated with a (x=71.5 yrs (1987-1996 >7-fold increase in DSM 365 transient increase old), hospital admissions fracture risk within in risk after the 136,488F used) the first year >\. acute event and (x=75.5 yrs Used Poison Younger aged to determine the old) model to determine groups showed L; time course of absolute risk of greater risk any increase in subsequent Declined with fracture risk after fractures and risk time post stroke stroke compared with that but still over 2-3-of general fold more risk after population 6-months Mean duration of follow-up was 2.54 yrs old with max. of 10 yrs Lamb et al. To investigate N=94 stroke; Recruited - Falls - 48% fell 2003 the relevance of all women; women from - ADL during 1 year known x=76 yrs old; community of - BMI follow-up predisposing risk x=48 months which people with Depression - 29% of DSM 833 factors for falling post-stroke; stroke included Cognition sample fell more-and stroke- (N=124 started Balance than once j specific factors study) Visual acuity Frequent \ in a population 12-month Knee balance problems of women with a prospective fall extensor strength while dressing was history of stroke history Pinch grip the strongest risk' strength factor for falls (OR Walking = 7) speed Residual Chair rising balance, dizziness, or spinning stroke symptoms were also a strong risk. factor for falling (OR = 5.2) Nyberg and To investigate N=161 stroke Falls were Frequencies - 39% of Gustafson the incidence, patients; recorded while in and incidence patients fell and 1995 characteristics, x=23 days rehab setting (x=48 rates of falling 24% of entire and post-stroke; days in study) sample fell more DSM 586 consequences of 84M, 77F; Descriptive than once patient falls in a x=75.2 yrs collected Most frequent stroke old; location for falls •: rehabilitation was patients room setting Transferring! (37%>) was the y most frequent activity being performed when fall occurred. - 28% of falls resulted in injury Ugur et al. To investigate N=131 (44% Patients were Barthel Index Falling . 2000 the incidence o of all followed in stroke Depression occurred most falling, to patients) unit between 1992- scale often in the oldest DSM 762 identify the risk stroke fallers; 1996 Risk factors age group factors for falling x=62.5 yrs Stroke - Right CVA after stroke, and old; 70M, location (i.e. left hemi) to evaluate the 61F, 48 left Affected side were more likely 97 relationship hemi, 38 right - Falls to fall } between lesion hemi; Fallers were localization and N=162 non- more depressed falling faller stroke and lower Barthel patients; Index scores x=59.88 yrs old; 78F, 84M; 39 left hemi, 57 right hemi Yates et al. To examine the N=280 stroke Follow-ups Stroke 51% patients 2002 relationship patients; were completed 1, severity fell while in the between x=68.3 yrs 3, & 6 months post- Motor community accumulated old; 50%M; stroke impairment (Fugl- - 35% of those DSM 898 neurological Meyer) fell multiple times impairments Sensory and Risk of falling following stroke visual in stroke was > and the increased impairments increased 2x when risk of falling in - Falls motor impairment community- present and 3x 'f dwelling stroke when motor and survivors sensor impairments were present compared to stroke fallers with no impairments 98 Appendix II: Literature table - Exercise in individuals with stroke Table n. 1: Persons with Chronic Stroke ARTICLE PURPOSE SUBJECTS PROTOCOL OUTCOME MEASURES RESULTS Ada et al. To determine N = 13 stroke Experimental Walking Walking speed 2003 whether 4 weeks in group intervention speed and walking ;' of treadmill and experimental -> 3x/wk, 45- 6-rnin walk capacity (6-min overground group; x=66 minute sessions test walk test) were DSM 1026 walking yrs old; x=28 over 4-weeks Handicap increased in .'" increases speed months post- Intervention measure (SA- experimental group and capacity of stroke; 9M, was treadmill SIP30) at post-test and walking, 4F; 8 right, 5 training Step length, retention improve quality left hemi; (decreasing by cadence, and step Step length for of walking, and N = 14 stroke 10% each week width both legs increased decrease in control from 80%) and by post-test in handicap and are group; x=66 overground experimental group these changes yrs old; x=26 walking; walking and remained at maintained 3 months post- speed was varied retention testing ., months after stroke; 10M, 4F; 6 right, 8 left hemi; and dual cognitive task was introduced; overground walking was done forward, backward, or sideways, and up and down stairs and had target stepping involved; in addition, A '!; overground walking involved an outdoor circuit of curbs, slopes, stairs and rough terrain Intervention was community-based (2 people trained together) but individual attention from PT Control group was given a home exercise program { carried out 3x/wk over 4-weeks consisting of lengthening and strengthening exercises and balance and coordination training but not in 1 sufficient number 99 or intensity or structure to discredit them as a sham program Tested pre-, post-, and 3-months following intervention Badics et To examine the N = 56 stroke; Exercise Muscle No increase in al. 2002 effects of 3wks-10 program was a strength tone sequential yrs post- residential rehab Muscle tone Muscle exercising on stroke; 34M, program of 4 strength increased DSM 1073 muscle tone and 22F; x=61 yrs weeks of upper and in all patients strength in old lower limb Intensity and stroke strengthening number of (exercise units -> exercising units 30-50% of max., 3- positively 5 series of 20 reps) correlated with strength gain Bassile et To develop an N=5 chronic Pre-, post-, 1- Motor 6-min walk test al. 2003 obstacle training stroke; 41-88 month retention assessment scale and walking program for yrs old; 0.5-6 testing (MAS) velocity improved DSM 757 people with yrs post- 4-week - SF-36 Only walking stroke and stroke; 4 training (group) 6-min walk velocity showed assess its effects right, 1 left program of test retention hemi walking over Walking - MAS time obstacles velocity improved and was; retained 5 - SF-36 improved but not significant Bastien et To determine (1) N=24 Multi-location Berg Balance Berg Balance al. 1998 acceptability of chronic trial Get Up and improved by 4-various stroke; 17M Community- Go test points DSM 1071 exercises, (x=64.2 yrs based group Grip strength Get Up and Go activities, old), 7F exercise program - RNL improved by about games, (2) (x=67.4 yrs Intervention -> Fall events 4 sec. optimal class old); greater N = 14, 2x/wk, 60- during classes time, (3) than 9-months min over 6 wks, 2 Falls self-instructor/client post-stroke; instructors; N = 4, efficacy ratio, (4) lx/wk, 90-min over Social and outcome Only 15 had 8 wks, 1 instructor leisure measures, (5) post-test and 1 assistant; N = involvement compliance, and assessment 6, same as previous (6) cost or but with 2 running an instructors exercise Warm-up, program for balance and it individuals with coordination stroke exercises (dance and T'ai Chi), resistive strengthening of upper and lower limbs, relaxation, group discussions, health promotion and education 100 Carr and To investigate N = 40 stroke; Baseline V 0 2 max A&ST group Jones 2003 the long-term 22M, 18F; testing of V 0 2 and Peak torque increased V 0 2 max effects of greater than blood testing on knee Knee flexion moderate 6-months Randomly flexion/ extension increased in both DSM 1074 exercise training post-stroke assigned into one and shoulder groups on physiological of two groups after extension/flexion Shoulder and metabolic baseline testing: Cholesterol extension increased outcomes for aerobic training High-density in both groups and stroke survivors (ATO) and aerobic lipoprotein (HDL) flexion in A&ST and strength levels group training (A&ST) Glucose Cholesterol 1 16-week levels (fasting) decreased for program A&ST group Pre- and post-testing Individual lab-based training f 3x/wk ATO group did training on upper and lower limb ergometer; Phase 1 (5 wks) -40-50% of original test wattage (from V 0 2 testing) for 20-min; Phase 2 (5 wks) - 50-60% for 30-min; Phase 3 (6 wks) - 60-70% for 40-min; also did flexibility A&ST group did same protocol but also strength training (2 sets of 10 reps for upper and lower limbs using free weights and machines); weight progressively increased Dean and To examine the N=20 stroke; Randomly Max. reaching Increased max. Shepherd effect of a Exp. (n=10) assigned into difference reaching distance 1997 training program -> x=68.2 yrs experimental or Ground and shorter time designed to old; 7M, 3F; control group reaction force after framing and DSM 3 improve the 5 right, 5 left 10 sessions - EMG of vs. controls ability to hemi; x=6.7 over two weeks in- anterior deltoid Increased balance in yrs post; home (non-paretic) and vertical GRF sitting after Control Experimental bilateral lateral through affected stroke (n=10) -» -> designed to vastus, TA, and limb after framing x=66.9 yrs improve sitting soleus and vs. controls old; 7M, 3F; balance, loading Experimental x=5.9 yrs affected leg while group could post; 6 left, 4 reaching, etc. activate affected leg right hemi - Control -> muscles more after cognitive- training than 101 manipulative tasks controls while seated at a Increased peak table vertical GRF Reaching tests through affected -> reached with foot during sit-to-unaffected hand stand in forward, 45° experimental group toward unaffected side, and 45° across body Dean et al. To investigate N=12 chronic 4-week Walking Significant & 2000 the feasibility stroke training program speed and retained and efficacy of -> 3x/wk endurance improvement for /' DSM 6 an exercise class Experimental 6-min walk experimental group aimed at group -> focused test vs. control in improving on strengthening Step test walking speed and performance of the affected lower (repetitions of 6-min walk test, locomotor- limb & practicing stepping onto 7.5 force production related tasks in functional tasks cm block in 15 through affected individuals with involving the lower seconds) limb during sit-to-stroke limbs (sit-to-stand, Timed Up and stand, and # of walking, reaching Go repetitions of step sitting & standing, Peak vertical test stair ascent & GRF through descent) affected foot Control group during sit-to-stand -> upper limb tasks and the step test 2 month follow-up Eng et al. To evaluate a N=25 chronic 2 baseline test Berg balance - BBS, gait 2003 community- stroke; sessions (BBS) speed, 12-minwalk based exercise x=63.13 yrs 8-week 12-rninwalk test, stair climbing, DSM 918 intervention on old; x=4.24 exercise program test and COPM A both balance and yrs post- (lhr, 3x/wk) of Self-paced improved with functional stroke; 13 balance training, and fast-paced gait exercise capacity in right, 12 left walking, and speed - RNL did not " stroke. Also, to hemi strength Self-paced improve evaluate the 1 post-test and and fast-paced Improvements effect of the 1 one-month stair climbing demonstrated intervention on retention test speed retention measures of - RNL health-related - COPM quality of life Engardt et To investigate N= 10 stroke Two strength Integrated After training, al. 1995 the effect of in eccentric groups: eccentric EMG knee extensor isokinetic group; x=62.2 training and Concentric strength increased DSM 1051 maximal yrs old; 7M, concentric training and eccentric in eccentric and voluntary knee 3F; 7 left, 3 Trained paretic muscle strength concentric actions extensions in right hemi; leg for 6-weeks (joint torque) of in both groups persons with x=26.5 (2x/wk) with Kin- knee extensors and Eccentric and •, chronic stroke months post- Com isokinetic flexors concentric strength stroke; dynamometer Body-weight in the paretic limb N= 10 stroke distribution on the relative to the non-' in concentric legs while rising paretic increased in group; x=64.6 and sitting down eccentric but not yrs old; 8M, Gait speed concentrically 2F; 5 left, 5 (self-selected and trained group right hemi; fast-paced) Antagonist 102 x=27.8 Swing to muscles increased months post- stride ratio of activity in stroke paretic leg concentric actions for concentrically but not eccentrically trained groups {{ Nearly perfect symmetrical body^  weight distribution on the legs in the? eccentric but not concentric group ; No change in gait speed between groups Eccentric training has some advantages over concentric training in persons with stroke Hesse et al. To investigate N = 7 stroke Treadmill Functional Treadmill 1995 the efficiency of inpatients; training phase, Ambulation training was more treadmill 6M, IF; regular PT based Category (FAC) effective with training with x=60.3 yrs Bobath phase, Rivermead regard to gait ' DSM 306 partial body- old; x=176.8 another treadmill Motor Assessment ability and gait weight support days post- phase each lasting Motricity speed (PBW) stroke (range 3-weeks (15 Index Other measures compared with 91-362 sessions, 30-minute Modified improved over time gait training days...4 of 7 for treadmill and Ashworth within regular seven in 45-min for Spasticity scale physiotherapy in chronic stage) physiotherapy) Gait speed nonambulatory patients with chronic hemiparesis Kim et al. To determine N=20 chronic Pre and post- Lower Trend for 2001 the effect of a 6- stroke (10 per test measures extremity muscle intervention group, week maximal group) Intervention strength to increase strength DSM 708 isokinetic Exp./ x=60.4 (3x/wk, 45-min) (composite score) vs. controls strength yrs old; x=4.9 for 6 weeks on Walking No differences program on the yrs post- strength training velocity (slow and between groups for paretic lower stroke; 7M, with Kin Com fast-paced) other measures extremity 3F; 4 right, 6 Isokinetic Health-related left hemi; Dynamometer quality of life (SF-Control/ Control group 36) x=61.9 yrs did same but no Stair climbing old; x=3.2 yrs resistance on Kin speed post-stroke; Com 7M, 3F; 7 right, 3 left hemi Macko et To investigate N=9 stroke; Stress test - V02 Significant al. 1997 the safety and x=67 yrs old; 6 month low- - HR decrease in energy efficacy of 0.7-6.7 yrs intensity aerobic Energy expenditure, HR, DSM 227 graded treadmill post; exercise training expenditure and V02 after as an aerobic program -> 3x/wk, training ; ) 103 exercise training 40min/session at modality in 50-60% heart rate older stroke reserve patients Pre, after 3 months, & post-testing >.£ Macko et To determine N=23 stroke; Training Gait economy 21 completed al. 2001 whether x=67 yrs old; consisted of 3, 40 - V02 3-month & 19 the treadmill 6-81 (x=28) min sessions - RER 6-month DSM 502 training will months post; weekly of treadmill Economy of improve peak 19M, 4F walking at 60% gait decreased & fitness while HRR for 6 months peakV02& lowering energy Treadmill fractional cost of exercise testing at utilization increased hemiparetic gait sub-max with open after training in chronic stroke circuit spirometry used to measure economy of gait at baseline, after 3 & 6 months of training Miller 2001 To determine if N = 1 female, Baseline Orpington Berg Balance} combined body- 71 yrs old, testing, treatment Prognostic Scale MAS, Gait speed : weight right hemi, 19 intervention (OPS) improved and \Z retained DSM 389 supported months post- introduced and - FIM (BWS) treadmill stroke removed, second Berg Balance and overground baseline test, and Step lengths training was one-month Motor feasible and retention test Assessment Scale effective in 3 sessions per (MAS) improving the day -> BWS Gait speed functional treadmill (10-m walk test capabilities of a ambulation, and 6-min walk patient with overground test) chronic stroke ambulation with BWS, and overground ambulation without BWS Each session was between 5 and 10 minutes BWS percent was decreased over time 3x/wk for 8 weeks of training Miller et al. To report the N = 2 chronic - BWS Berg Balance One patient 2002 feasibility and stroke; 87 yrs ambulation 2- Tinetti Gait improved in Berg patient tolerance old female, 10 3x/wk for 6-7 and balance balance and 10-m for using body- yrs post- weeks assessment walk time while the DSM 429 weight stroke; 93-yrs 4 bouts of 10-m timed other improved in supported old female, 14 ambulation per walk step length and 10-(BWS) treadmill yrs post- session -> first 3 Step length m walk time and overground stroke consisted of Step length ambulation ambulation on the ratio training and to treadmill with measure the BWS and the 104 function before fourth with and after overground training ambulation with BWS. Monger et To investigate N = 6 chronic 3-week home- Sit-to-stand Improved MAS al. 2002 the feasibility stroke; x=65 based exercise (STS) item of score of STS, gait and efficacy of a yrs old; 4M, program under Motor Assessment speed, and time-tor task-specific and 2F; x=3.6 yrs supervision Scale (MAS) peak VGRF at post-DSM 1072 home-based post-stroke; 3 (3x/wk, 20 min) Gait speed test exercise left, 3 right Exercises -> Grip strength protocol for hemi sit-to-stand, step- Mean vertical improving sit- ups, and calf ground reaction to-stand in stretches force (VGRF) stroke Also told to practice 20-min. a day on own Pre-, post-test measured through limbs during STS task Mudge et To investigate N = 1 chronic No treatment Gait velocity Berg Balance al. 2003 the influence of stroke; Male, during initial 4- Trunk control increased during -a period of 48 yrs old, weeks, then body- (Trunk control and at follow-up DSM 945 body-weight left hemi, 30 weight supported test) Lateral reach supported months post- treadmill training Berg Balance for both arms treadmill stroke for 4-weeks Functional improved during training in a (3x/wk), then no Independence intervention (right single subject training for 4- Measure (FIM) also at follow-up) . with stroke on weeks Lateral reach Trunk control' gait, balance, Tested before, test and FIM didn't trunk control during, and after change and general intervention function Potempa et To describe the N=42 chronic Experimental - HR Experimental al. 1995 responses of stroke (n=19 group = 10-week - BP group increased in stroke patients in aerobic exercise - V02, VC02, V02, workload, DSM 955 to intense experimental program VE, RER and exercise time . exercise and to group and Control group Exercise time and decreased SBP determine the n=23 in = 10-week passive Sensorimotor at sub-max f-effect on control ROM exercises function (Fugl- X cardiovascular group); 43-72 - 3x/wk, 30- Meyer) and functional yrs old; at min. over 10-weeks Workload outcome least 6-monts for both groups measures post-stroke; Pre- and post-testing Rimmer et To determine N=35 strokes; Screened - Peak V02 Increase in al. 2000 the effects of a 9M, 26F; blood, performed - 10RM for absolute and 12-week x=53.2 yrs graded exercise test bench press and relative peak V02 exercise training old; 31 and fitness testing leg press after framing and DSM 532 program in a African- - PeakV02 Flexibility decrease for predominantly Americans recorded - Body controls African- electronically via a composition Increase in American group braked upright gains of time to of stroke stationary cycle exhaustion and survivors with Strength tested max. workload post multiple co- on LifeFitness training morbidities bench press and seated leg press machine Increase in ^ bench and leg press post training -105 Pre/post test Increase in lag control group gains in hamstring design and low back i Exercise flexibility program -> Decrease in lhr/session, 3x/wk body weight, BMI, for 12 wks; and total skin folds cardiovascular - Suggest endurance (30min), education on signs muscle strength of stopping are -and endurance (20 important min) and flexibility (lOmin); during 1st 2 wks, participants went through educational program; 70% 10RM for one set of 15-20 reps than increased 10% 10RM later Rodriquez 1) Further N=18 stroke; Training - WGS -> see Intra- & interr et al. 1996 substantiate the 31-78 (x=54) program -> 3-5 paper for tasks rater reliability of benefits of post- yrs old; 12M, days of in-home Falls Efficacy WGS was shown DSM 5 acute gait 6F; 2.2 yrs training (mean of Scale (FES) and Average WGS training, (2) post 5.7 times HSQ test score increased evaluate the throughout Cost after training -> efficacy of a program) to several parameters home-based gait establish home- (see paper) training model based program; PT improved (Wisconsin Gait contact average 35 FES decreased Scale, WGS), hrs & training after training i (3) assess the extended over a HSQ increased relation of mean of 22 months after training improved gait to (10-65 range) - $4200/patient patients' Training was US dollars at 35 hrs perceptions of individualized and of PT therapy their health consisted of status and well normalizing lower-being, (4) extremity passive characterize ROM, balance which factors skills in transitional i associated with movements, weight stroke & rehab shifts, balance on are predictors of the involved leg, outcome, & (5) feedback via EMG determine cost of home-based training Sharp and To determine N= 15 Tested Muscle Paretic muscle Brouwer whether persons chronic baseline, post- strength strength improved' 1997 with chronic stroke; 10M, intervention, and 4 Spasticity after fraining while hemiparesis due 5F; x=67 yrs weeks after (pendulum test) tone remained to stroke can old; 0.9-18 training Gait speed consistent but only DSM 262 improve yrs post- Intervention Timed Up and quadriceps torque function and stroke; 8 left, 3x/wk over 6- Go test was still increased muscle strength 7 right hemi weeks consisting of Timed stair at follow-up at an isolated a warm-up, climbing Gait velocity 106 joint of the strength training of Human increased after 'affected' lower reciprocal knee Activity Profile framing and at extremity extension and scores follow-up following a flexion movements Stair climbing training program on an isokinetic and Timed Up and and whether machine Go were not ; gains are performing three different associated with sets of 6-8 reps at Paretic j.;<„ alterations in max. for three spasticity remained muscle speeds (only constant ; spasticity affected knee musculature) Silver et al. To determine N=5 stroke; Aerobic Timed Up & - TUG & SAW 2000 whether task- 5M; x=60.4 exercise on Go (TUG): arise decrease with oriented aerobic yrs. old; x=26 treadmill 3x/wk, from chair, walk training DSM 173 exercise months post progressed to 40 3.1m in line & sit Decrease mean improves gait stroke; 4 rnin/session at 60- again stance & swing ability and right, 1 left 70% max HRR for Sit-to-stand times for both limbs quality in hemi 3 months (STS) times with framing chronic stroke Pre- and post- Straight-away Symmetry patients testing walk (SAW) times unchanged: intra Asymmetry limb stance/swing Swing/stance ratios trend ; times towards normal Smith et al. To investigate N= 14 Exercise Reflexive Increase in :: 1998b the effects of 3- chronic consisted of (passive) & mean eccentric months of stroke; 12M, progressive low to volitional torque generation"; progressive 2F; x=66 yrs moderate intensity (concentric & following the ;( DSM 1069 treadmill old;x=19 aerobic exercise eccentric) torque exercise training on months post- treadmill training from bilateral intervention of 50% volitional and stroke; 6 left, -> 40-min/day, quadriceps and 25% for the reflexive 7 right hemi, 3x/wk, for 3- obtained using paretic and non-quadriceps 1 bilateral months at 60-70% isokinetic paretic limb, femoris torque HRR dynamometer with respectively generation Pre- and post- torque measured at Increase in testing 30°, 60°,90°, & mean concentric . 120°/s angular torque following velocity intervention of 38% Torque was and 17% for the determined paretic and non-between 35° and paretic limb, 45° of knee respectively flexion Reflexive torque decreased in both limbs but ' didn't reach significance " Eccentric ' torque higher at ' each angular velocity than concentric torque - "Task-oriented" treadmill training good for individuals with chronic stroke Smith et al. To determine N=14 stroke; Exercise Reflexive With exception 107 1999 whether a 12- 12M, 2F; intervention -> (passive) & of reflexive torque, week program x=66 yrs old; treadmill walking volitional gradual decrease in DSM 225 of "task- greater than 6 3x/wk, progressed (concentric & absolute torque as-oriented" months post; to 40 min/session eccentric) torque angular velocity treadmill 7 right, 6 left, for 3 months (i.e. from bilateral increased exercise would 1 bilateral 12 weeks) at 60- hamstrings Concentric increase muscle 70% heart rate obtained using torques -> strength and reserve isokinetic increased torque for decrease spastic Pre- and post- dynamometer with affected less than reflexes in testing torque measured at for non-affected chronic 30°, 60°,90°, & Eccentric ! hemiparetic 120°/s angular torques -> same patients velocity Reflexive torques affected greater than non-affected decrease in torque after training Increase in volitional torque, : decrease in reflexive torque, & increase T/T (spinal motor recruitment& sustainability) after 3 months training Smith et al. To investigate N=ll stroke; Exercise Reaction No change pre-2000 the effect of a 10M, IF; protocol 3 times (RXT) -» to post in all treadmill x=23.7 months (i.e. 12 initial loss of measures (RXT, DSM 97 exercise training months post weeks), 3x/wk, contact after RXT, MVT) paradigm on progressively perturbation When compare equilibrium graded treadmill Recovery fast and slow reactions and aerobic exercise times (RCT) -> responders -> no recovery times (AEX) training post-perturbation change in RXT, after program; 5 min time at which full main effect for standardized warm-up and cool- foot contact is RXT showing translational down at 30% heart reestablished increased RXTs to, balance rate reserve (HRR); bilaterally for at posterior perturbations limited to 40% least 300 msec perturbations, RCT HRR for 10-20 min Movement and MVT improved at onset of study to times -> (RXT- in slow group 60-70% HRR for RCT) M 40 min later ft Balance testing protocol horizontal perturbations on 1.2mx 1.5m platform; practice trials at 10cm displacement, 10 cm/s, 50 cm/s2 perturbation; collection perturbation at 40 cm/s 150 cm/s2 perturbation; 7 'l directionally randomized 108 practice trials followed by 3 randomized collection trials Sullivan et al. 2002 DSM 505 To determine whether faster treadmill training speeds would result in better transfer to overground walking in stroke patients N = 24 stroke; 5F, 19M; 34-81 (x=67) yrs.; 6-62 (x=25.8) months post; 16 left, 8 right hemi Stratified into a category by locomotor severity based on self-selected gait speed Groups: slow, variable, and fast velocity Training program: 12 sessions over 4-5 wks, 20 min/session Pre-, post-, and 3-month retention testing No orthosis allowed - Total Fugl-Meyer motor score (TFM) Lower extremity Fugl-Meyer (LEFM) - SF-36 Self-selected overground walking speed over 10m (SSV) All groups showed increases in SSV over framing & retention No group effect although trend for greatest "! improvement in fast framing group When slow & variable groups S combined, increase in SSV for fast vs.< combined Increased gains for less severe strokes - Change in SSV correlated with LEFM (r=0.46), re-fraining group (r=0.39), & locomotor severity (r=-0.47) Tangeman et al. 1990 DSM 8 To investigate the changes in functional level that would occur after intensive rehabilitation therapy for stroke patients who were at least one year post stroke N=40 stroke; 13M, 27F; 27-77 (x=65.6) yrs old; 1-23 (x=3.09) yrs post; 4-week training program -> 2 hrs/session, 4x/wk individual treatment by PT & OT 1 month pre (to serve as control period), pre-, post-, & 3 months post-testing Therapy program focused on weight shift to the affected side, balance, and functional activities Balance -> using a 10-point scale - Weight shift -> # of objects moved in 20 seconds - ADL Increase in weight shift >•, between pre & post & between pre & retention Increase in •Im-balance between .u. pre & post and „ between 1-month pre & post & retention Increase in ADL between pre & post and between pre & retention ,, Correlations between balance & weight shift (1=0.768), ADL & weight shift (r=0.695), & ADL & balance ^ (r=0.763) H Teixeira-Salmela et al. 1999 DSM 4 To evaluate the impact of a combined program of physical conditioning & muscle N=13 stroke; 1-34 yrs post; 7 left, 6 right hemi; 7M, 6F Randomly assigned into experimental or control group Pre- & post testing 10-week Gait speed (22m) Human activity profile (HAP) -> adjusted using metabolic energy Gait speed increased after training - Adjusted HAP & NHP increased' after training Increase in 109 strengthening on training program consumption strength (mean peak reducing -» 3x/wk, 60-90 Quality of life torque generated by impairments and min/session by Nottingham muscle groups of disability in Control group Health Profile affected leg) subjects with no intervention and (NHP) Muscle tone • • chronic stroke then did training Lower- showed no change: protocol after extremity muscle Training strength using program -> 5-10 Cybex II '•S min warm-up, isokinetic y> aerobic exercises dynamometer consisting of Muscle tone graded walking plus stepping or cycling at 70% max HR, strength training, cool-down for 5-10 min • - Strength training -> isometric, concentric & eccentric contractions; body weight, sandbag weights, and elastic bands Teixeira- To evaluate the N= 13 Pre- and post- Gait speed Gait speed ! Salmela et impact of a chronic testing Gait kinetics improved al. 2001 combined stroke; 6F, Intervention and kinematics Gait improved program of 7M; x=67.7 3x/wk, 60-90 min, Able to muscle yrs old; x=7.7 over 10-weeks generate higher DSM 408 strengthening yrs post- Were given a levels of powers and physical stroke; 7 left, list of exercises to during gait conditioning on 6 right hemi do at home and Demonstrated gait told to do them at increases in positive performance in least 3x/wk work performed by individuals with Community- ankle plantar ' 1 chronic stroke based group flexors and hip program of warm- flexor/extensor up, aerobic muscles exercise, strength training, and cool-down Aerobic exercise -> 1st 5 wks at 50-70% of aerobic capacity for 10-20 minutes 'A and increased to 70% capacity for 2nd 5 wks; consisted of graded walking plus stepping or cycling Strength training progressive u p resistance training for 30-min for hip, -knee, and ankle joint Trueblood To examine the Series of pilot Compared gait Symmetry of Symmetry in 2001 effects of partial studies with characteristics stance/swing times stance/swing times body-weight chronic stroke during 3 modes of and EMG of pre- and EMG improved (PBW) -> see article walking: level tibialis and during PBW either DSM 436 ambulation in for details ground ambulation, quadriceps over level ground people with level ground Tinetti or on the treadmill chronic stroke ambulation with Balance Increased PBW, and single limb and ., treadmill decreased double ambulation with limb support PBW improved over all Examined gait symmetry effects of repeated during level ground (6-8 weeks) PBW ambulation treadmill training following 6-8 ; during level ground weeks of repeated ambulation PBW treadmill See article for training details Tinetti Balance score improved "; Weiss et al. To evaluate the N=7 stroke; Baseline - 1RM Only knee & 2000 effects of a high x=70 yrs old; testing twice Gait velocity hip ext. strength on intensity x=2.3 yrs. separated by 5 days Chair rise affected side DSM 274 resistance post; 5 right, Exercise time decreased vs. non-strength training 2 left hemi training program: Stair climb affected side intervention on 12 wks, 2x/wk Unilateral leg Affected leg bilateral lower Standing hip stance knee ext. vs. 1 RM limb strength, flexion, abduction, Motor correlated (r=-performance, & and extension with assessment scale 0.783) at baseline clinical outcome machines, sitting (MAS) Affected leg measures in knee extension and Berg Balance press, hip flexion & individuals with press, 3 sets of 8- Scale (BBS) non affected hip stroke 10 reps at 70% 1 Quality of ext. correlated at rep max (1RM) life, depression, & r=-0.857 - 1RM ADL assessments - BBS vs. measured every 2 affected leg press wks. correlated at r=0.875 ,;c All muscle ~i strength improved with training except hip ext. using leg press Chair stand time decreased, improved MAS, & increased BBS with training I l l Table n.2: Persons with Acute Stroke - relevant and important articles only ARTICLE PURPOSE SUBJECTS PROTOCOL OUTCOME RESULTS MEASURES Barbeau and To identify N = 50 stroke Both groups - Berg - BWS group Visintin stroke patients patients (43 trained 4x/wk for 6- Balance scored 2003 who are most finished) in weeks (max. 3 Motor significantly likely to benefit BWS group; walking trials for recovery higher in all DSM 1027 from locomotor x=66.5 yrs old; no more than 20- (STREAM) clinical measures training with 19F, 31M; 20 min) Walking - When body-weight right hemi, 30 - BWS group speed stratified support (BWS), left;x=68.1 trained with BWS Walking according to initial to determine the days post- on treadmill endurance (10- walking speed, • extent of stroke; - BWS m walk) endurance, : carryover from N = 50 stroke progressively balance, and treadmill patients (36 decreased over time motor recovery, training to finished) in no- Tested pre-, more severely overground BWS group; post-, and 3-months impaired stroke in-locomotion, and x=66.7 yrs old; retention patients showed' to determine the 22F, 28M; 29 Time effect variables that right, 21 left Older adults are most likely hemi; 78.4 days in BWS group to influence the post-stroke increased walking recovery of speed more than locomotion older adults in no-BWS group !! Duncan et al. 1) To develop N=20 stroke; After baseline 6 min walk Increase in 1998 an exercise 30-90 days assessments, the - BBS lower-extremity intervention post; 11 left, 8 subjects were Jebson test Fugl-Meyer motor DSM 7 based on right hemi randomly assigned of hand function score for principles of to experimental or Barthel and experimental exercise control group Lawton ADL group physiology & Intervention -> scales Gait speed motor learning exercise program 10 meter increased more for and to deliver it for 12 weeks, walk experimental in the home to 3x/wk, 1.5 Fugl-Meyer group individuals with hrs/session that was motor score ADL showed mild or home-based no differences -moderate stroke, (supervised for first (2) evaluate the 8 weeks - all feasibility and 3x/week); 10 min (3) assess the warm-up, assistive effects or resistive exercises using PNF patterns or theraband, balance exercises, upper extremity functional activities, progressive walking or bicycle ergometer - Control -> 2x/wk visit to home for assessment of activity & exercise level only 112 Duncan et al. To determine N=50 acute Pre- and 3- Gait speed Both groups' 2003 the effect of a stroke months following Berg improved but structured, (intervention); intervention testing Balance (BBS) control no in DSM 956 reproducible, x=68.5 yrs old Intervention = Fugl-Meyer endurance physiologically N=50 acute home-based for 36 Motor score Intervention based exercise stroke (control); sessions of 90-min. Isokinetic group improved.. program on x=70 yrs old; over 12-14 weeks strength more in V02, , strength, - focusing on balance - V02 BBS, 6-min walk balance, Approximately and strength 6-min walk distance, and gait endurance, and 75 days post- test speed upper limb stroke function in persons with stroke Hocherman To train N=24 stroke; Platform Average MMA change etal. 1984 hemiparetic anterior cerebral moved at 0.5 Hz integrated EMG in treatment group individuals to circulation; 10- within a range of 1- ofTA was larger than DSM 481 sustain posture 21 days post; 16 cm - Body control (i.e. better by using x=72.7 yrs old Treatment weight stability) v platform -> Treatment group underwent 15 distribution (i.e. Patients with movements group = N=13; training sessions asymmetry) lowest initial 6F, 7M; 8 right over 3 wks Maximal ability showed and 5 left CVA consisting of two 5 movement better -» Control min parts (one with amplitude improvements group = N=l 1; patients standing (MMA) - IEMGofTA 5F, 6M; 6 right, parallel to axis of was similar in 5 left CVA movement and one with patients perpendicular) - AP and ML perturbations both legs during;, training but , affected limb TA was rninimal during quiet standing ;i Improved weight distribution on the feet in both groups (more in treatment group) Moreland et To investigate N = 68 stroke in Tested at 4- Disability - N o i, al. 2003 whether lower- experimental weeks, discharge, Inventory differences extremity group; 39M, and 6-months Change score between groups DSM 1025 strength-training 29F; 27 left, 35 following 2-rnin walk exercises plus right, 5 Intervention -> test (walking conventional bilateral, 1NA 3x/wk, 30-minutes velocity) physiotherapy is hemi; x=69.1 for duration of Muscle more effective yrs old; x=36.8 rehab stay; tone change than months post- progressive score (MAS) conventional stroke; resistance exercises therapy alone N = 65 stroke in control group; 42M, 23F;31 left, 27 right, 6 bilateral, 1 NA hemi; x=72 yrs old;x=38.1 months post-stroke with weights Control group exercises same but with no resistance Richards et To determine N = 27 acute Randomly Fugl-Meyer - PTtime ; 113 al. 1993 whether early stroke patients assigned to one of Balance, arm, highest in and intensive three treatment and leg scores experimental DSM 379 physiotherapy groups after - Barthel group that emphasized stratified for Ambulation Gait velocity gait training Barthel Index Berg similar between promoted a gait scores Balance two control groups outcome and an One control - Gait after 6-weeks but early return of group (N = 8), PT velocity faster in functional started early and experimental mobility that was intensive as for group (thus timing was superior to the experimental not important) that obtained group but contained Effects not following either more traditional retained at } early and approaches retention testing of intensive Second control . 3 and 6 months conventional group (N= 6), PT as physiotherapy usual (started later that did not and not as intense focus on as other control ambulation or group) conventional Experimental physiotherapy group (N = 9), started early as possible and provided an intensive and focused approach to therapy that incorporated use of tilt-table, resisted exercises, and a treadmill Tested at baseline, after 6-weeks, and after 3 and 6 months Suzuki et al. To investigate N=34 stroke; Received Max. - MWS & 1999 biomechanical 34M; 19 right, computer-assisted walking speed LR% significantly determinants 15 left hemi; gait training (MWS) improved after DSM 361 and predictors of x=8.6 wks post (CAGT) for 8 wks, Muscle training walking speed in 4-5x/wk strength during - MWS related early gait Pre- & post- knee extension to sway path (r=-training after testing (isokinetic) of 0.501), LR% stroke Testing after 4 both limbs (r=0.674), non-wks as well - COP (10 affected limb -i' sec, eyes open, strength (r=0.417), feet 10cm & affected limb apart): change strength (r=0.644) in COP while At 8 wks shift to right & training, the left (LR%) and determinant of back & forth MWS was the (FB%) affected limb * strength & predictors were initial MWS & affected limb strength 114 Appendix III: Literature table - Postural control following stroke Table HI. 1: Postural control following stroke ARTICLE PURPOSE SUBJECTS PROTOCOL OUTCOME RESULTS MEASURES Al-Zamil To identify N=24 stroke; Motor control Onset latency Latencies were 1998 posturographic 13M, 11F; test using dynamic of response, abnormal in 75% methods that x=63 yrs old; posturography strength (force of patients DSM 364 can be used to x=2.9 weeks platform (Equitest, relative to rate of Non-affected quantify post; Neurocom Int.) increase in ankle limb had normal symptoms N=25 age- - 9 forward & 9 torque over 150 latencies but associated with matched backward msec), and affected limb postural deficit controls; movements of 3 symmetry (force latencies were x=62.4 yrs old magnitudes (1.25, exerted by each significantly 3.15, and 5.7 cm) leg against force delayed and of in 250, 300, and plates) of limb decreased 400 msec response amplitude if present at all Badke & To describe the N=10 Platform on Fugl-Meyer Hemiparetics Duncan patterns of normals; 3M, wheels that -> used to group showed frequent 1983 postural 7F; x=35 yrs displaced 15 cm in patients co-contraction of adjustments old; AP at constant EMG onset, all 4 muscles in DSM 214 during induced N=10 stroke; acceleration amplitude and both perturbation body sway in 6M, 4F; right - EMG -» MG, sequencing directions healthy and hemi; x=54 TA, Hams, Quads Sway and Inconsistent lt hemiparetic yrs old; 8 of Sway recorded weight ratios of subjects 10 -> 6 Stood on distribution intermuscular months (<1 platform barefoot activation in yr) post; 2 of Perturbation hemiparetics 1 0 - » > l y r order for all Distal to post subjects: 1) 2 trials proximal sequence forward in normals displacement, 2) 1 No clearly trial backward, 3) defined sequence 1 trial forward, 4) in hemiparetics 2 trials backward Large variability with "; hemiparetics Lower the lower-extremity Fugl-Meyer, the more abnormal findings of postural adjustments -Badke et al. To determine N=10 stroke; 3 phases: (1) Bilateral Hemiparetics' 1987 whether prior 6M, 4F; x=56 voluntary AP EMG of TA, had longer and knowledge of yrs old; right sways, (2) Quads, Gastrocs, more variable DSM 213 the direction of hemi; 3-29 balancing during and Hamstrings onsets in the the balance months post; unexpected for latency, paretic limb during perturbation N=5 normals; support surface sequencing and voluntary AP sway improved 2M, 3F; x=47 displacements, & amplitude Prior neuromuscular yrs old; (3) support surface knowledge had no sequencing displacements with effect on responses during postural prior knowledge of in normals adjustments direction Prior 6-12 practice knowledge showed 115 trials shorter onsets in „ Phases paretic limb randomized - Default Phase 1: 6 responses (no clear trials where onsets) in both verbally told to groups less with rapidly shift prior knowledge posture anteriorly Proximal-or posteriorly distal for paretic - Phase 2: 12 limb even with •'; trials of 5 cm/s AP knowledge whereas perturbations reverse for normals - Phase 3: 12 trials with warning tone and prior knowledge of which 8 were told correct info Berger et al. To analyze the N=15 spastic Treadmill - TA and MG Mean 1984 activity and hemiparesis walking (1.5-2.5 activity amplitude of functional (11 from km/hr) Ankle joint spastic side ankle DSM 497 significance of stroke); 39-74 Gauge fixed angle joint movement mono- and (x=54) yrs old laterally near Tension in was half of that of poly-synaptic Achilles tendon Achilles tendon unaffected side reflexes during 3 patients Reduction of normal and randomly EMG strength was disturbed gait, displaced at correlated with the and to evaluate distinct step cycle severity of paresis their phases (increase to - When -, contributions to 7.5 km/hr in perturbation .,, the development 100ms) induced to „ j of tension in the Comparison unaffected limb, _ triceps surae to using acceleration strong MG compensate for during standing on response (65-75 ms body load after treadmill onset with respect impact to ankle joint movement) but when induced to spastic limb, small biphasic potentials appeared with 40.. ms onset Reciprocal modulation of mono- and poly-synaptic EMG responses during '•: gait -> normals have reduced mono but not spastic hemiparetics ! No connection between |. exaggerated monosynaptic reflexes and hypertonia -> may be due to change in 116 mechanical muscle fibre properties , Berger et al. To evaluate the N= 11 Forward and - TA and MG Delayed MG': 1988 extent to which patients; backward treadmill muscle activity response of spastic reflexes and the x=52.1 yrs accelerations side :| programmed old; 8 had during standing Steepness of, DSM 899 pattern are vascular (random order) increase in activity impaired in lesion 4 ramp depended on spastic paresis accelerations -> acceleration for TA following 5.5 m/s2, 4cm; and MG for treadmill 11.1 m/s2, 7 cm; respective perturbations 16.6 m/s2, 10.5 cm; 22 m/s2, 15 cm directions Co-activation with higher accelerations . Two parts to compensatory response to stance perturbations: functionally directed early EMG response ' mediated by stretch reflexes which are impaired in spastic paresis, followed:.' by a triggered ->> complex ,j component which is unchanged in patients (motor programs are intact) Chaudhuri & To determine N=10 stroke; Used EquiTest Weight Lifts improved Aruin 2000 whether a lift 7M, 3F; 68.7 system with symmetry scores symmetry of . applied to the yrs old; 8.2 medium = (RF + RR / LF weight bearing DSM 149 nonparetic limb wks post; 7 (0.026m/deg) and + LR + RF + RR) - No lifts -» would result in right, 3 left large (0.048m/deg) *200, where right faster onset latency improved hemi; perturbations and left frontal and stronger symmetry of Stood on force and rear load cells response for non-weight bearing plates used paretic limb to during dynamic 1st series-> no Latency of perturbations postural lifts response -> onset Tendency for; perturbations in 2-4 series -> of active response small lift to { decreased latency hemiparetic stood with lifts Strength of patients under non-affected limb 4 translations for no lift and each of the 3 lifts (0.6, 0.9, & 1.2cm) and was repeated 3x with order of lifts, random response -> active force generated in paretic limb Tendency for lifts to increase V strength of response of paretic limb Di Fabio & To examine the N=4 stroke; Stood on - TA and MG Normals Badke 1988 effects of a right hemi; moveable platform EMG -> onset, agonist-antagonist rapid length 3M, IF; 43-71 that moved zero onset burst onset DSM 212 change in the yrs old unexpectedly in a frequency, separated by -10 to 117 elongated and N=4 normals; horizontal amplitude -15 msec <}$ shortened ankle 1M, 3F; 39-45 direction at 5 cm/s Strokes were,: muscles of yrs old - 12 separated by -200 standing perturbations at msec •'' patients with random intervals - Right and left hemiplegia posterior limb difference during forward direction only was scores significant body sway recorded for strokes and greater than normals Longer burst latencies for agonists in paretic limb and antagonist responses in paretic limb were significantly delayed with ,', respect to non- ' paretic limb antagonistic f{. response attenuated or absent Greater disassociation between MG and TA than healthy Non-paretic « agonist amplitude was increased compared to normals and earlier onset To examine the N=8 stroke; See Di Fabio Muscle onset Initial long-interaction of 31-73 yrs old; et al. 1986 latency and latency response supraspinal and 4M, 4F; 4-31 sequencing (LLR) in muscle segmental months post; Integrated stretched by mechanisms right hemi; EMG amplitude perturbation and related to N=5 normals; over 100 msec subsequent amplitude and x=46.4 yrs antagonist response phasing of old; 2M, 3F (AR) in opposing* opposing muscle shortened muscles in a in normals stroke AR was population symmetrically activated in normals Hemiplegics;: show early activation of AR w/rt initial LLR only when gastrocnemius shortened (Forward displacement and toes down rotation) Frequent co- ; 118 activation of distal and proximal synergists noted for both initial LLR j and AR for hemiplegics Longer latencies for paretic limb Significant ,{ delay in AR in paretic vs. non- ;-; paretic limb More frequent AR defaults (zero muscle onset latency) compared to normals Normals suggest AR could be a polysynaptic spinal stretch reflex induced by the LLR but strokes refute the segmental pathology Cortical modulation appears to control amplitude and latency and LLR--" AR coupling rather than segmental of vestibular :>" pathology - Difficulty recruiting proximal synergists To evaluate the N = 4 stroke; Simple - Default Stroke had consistency of x=54 yrs old; reaction time task response (i.e. no higher number of postural muscle right of visual tracking EMG activity) default or zero recruitment in hemiparesis target via body Postural onset responses ;• several different N = ?? sway reaction time Normals got directions of healthy Measured (time between faster with practice volitional body controls; x=52 EMG from visual target and but stroke got sway in a non- yrs old bilateral TA and change in force slower choice reaction MG for body sway) Stroke tended time task EMG onset to recruit muscles in an all-or-none fashion Tonic rather „ than phasic burst patterns dominated in stroke Suggest stroke have to rely more on conscious Di Fabio and Badke 1989 DSM 716 119 volitional control for sway than automatic control Di Fabio et To study N=4 stroke; Participants Integrated Tendency for. al. 1986 symmetry and x=60 yrs old; stood on platform EMG amplitudes strokes to initiate adaptability of a 3M, IF; 5-30 and had 6-12 over 100 ms from non-paretic o. DSM 95 postural months post; practice trials EMG onsets limb (proximal response lower 3 horizontal and activation muscles) .: following stroke extremity displacements patterns Latency Jf Fugl-Meyer (5cm/s) given at modulation score = 78-98; random intervals appeared to be -f.i: right hemi; within 2 min with organized in a N=5 normals; 3 rotational diagonal fashion x=46.4 yrs perturbations (8°/s) Significantly old; 2M, 3F; randomly delayed non-paretic interspersed distal limb - EMG of activation bilateral TA, Non-paretic Quads, Gastrocs, proximal limb and hamstrings latencies were shorter Latencies ranged from 124-187 ms Normal attenuation of synergistic muscle activity to rotations in strokes ";' Distal to [,'• proximal activation (i.e. inverted pendulum) in both groups Greater onset difference between distal and proximal muscles for non-' paretic limb indicating co-contraction for paretic Normal paretic proximal onset and non-paretic distal onset Delayed ;i: paretic distal onset with compensation via early non- J paretic proximal onset Di Fabio et To determine N = 5 stroke; Backward Thenar Although not al. 1992 how the onset of x=58 yrs old; platform muscle and MG significant, there postural reflexes 3F, 2M; 1-24 displacements activity was a delay in RT compared to the month post- 1-9 cm Zero (default) for stroke ... DSM 715 conscious stroke displacement, 5-45 responses No difference identification of N = 5 female cm/s velocity, 80- Reaction time between groups for 120 body sway in controls; x=58 360 msec duration (RT) of thenar ANR stroke yrs old Some trials activation No correlation had foam placed under feet Using hand-held response key, told to press when sensed movement Automatic neuromuscular response (ANR) -> MG onset Response time (muscle onset and platform movement) between RT and; ANR 'p Dickstein et Assess the N=10 strokes; - AP Modulatory Hemiplegics al. 1989a effect of weight 5M, 5F; x=61 perturbations at 0.5 Index (MI) -» have asymmetric;! shift over the yrs old; 7 Hz level and with ratio between weight distribution DSM 434 affected leg of right, 3 left one leg elevated on IEMG (area under both on level and hemiparetic hemi a step monitoring curve) of each elevated positions patients on two N=9 healthy MG and TA muscle during the with the latter attributes of adults: 4M, time showing increased postural 5F; x=55 yrs corresponding to lateral sway responses old forward half cycle Healthy group during of movement and showed no change continuous AP the total IEMG in MI between sinusoidal during the whole loading conditions movements of cycle No change in1 the base of MI with support: (1) hemiplegics as well adaptation of Loading by the activation this technique pattern of the made no (+) MG and TA contributions to muscles to the posture responses imposed Most movements and adaptation took ' (2) relative place in sound limb amount of integrated EMG activity of these muscles Dickstein et To examine the N=17 stroke; Subjects stood - Bilateral TA Descriptive j,' al. 1989b effect of motor x=71.8yrs on moveable and MG EMG responses mainly. set on the old; x=2.4 platform -» AP responses Anticipatory , DSM 496 postural months post; translations Maximal responses in n.; adjustments 11 left hemi, 6 (sinusoidal) fixed movement normals ^ required to right hemi; at 0.5 Hz, 1-11 cm amplitude (MMA) MMA was J' maintain 11M, 6F; amplitude, 3.22- -> max amplitude 3cm for cortical .'l balance during N=42 35.42 cm/s could withstand stroke and 1.25 cm continuous normals; 20- velocity, 10.37- for vertebral artery displacements 84 yrs old; 114.07 cm/s2 stroke of the base of 21M, 21F; acceleration Affected limb support and to cyclic reciprocal compared these pattern was lost in adjustments to strokes -> hemiplegic complete (or patients nearly) silence of TA and variable amounts of cyclicity of MG; : low amplitude co-" contraction of 121 antagonists Dietz & To analyze the N=15 normals Stood eyes - EMG of TA - 4-5 Hz Berger 1984 impairment of N=12 spastic open for 90 andMG balancing interlimb hemiparetics seconds on see- bilaterally oscillations on DSM 428 coordination in due to stroke saw and then Force unaffected side and patients with a (7) or other single changes on force under 1 Hz for -supraspinal causes(5) supramaximal plate spastic side lesion of the N=12 spastic electrical stimuli Twitch Less activity in motor system to paraparetics (2msec) were contraction of affected side obtain due to randomly applied triceps surae - Healthy information as cervical to tibial nerve in showed to the influence spondylotic either spastic or simultaneous of higher motor myelopathy healthy leg bilateral responses centers on the (6) or myelitis 5 patients also and same spinal (3) or had see-saw amplitude to coordinating unknown apparatus they unilateral mechanisms Age for were standing on displacement for patients 30-65 move suddenly both stimulation j. (x=46 yrs old) that mimicked the and see-saw displacement triggered caused by movements electrical Reduced stimulation amplitude and delayed responses in spastic side (20-30 msec) V regardless of side : perturbed - Not simultaneous activation when stimulated or triggered for hemiparetics Latency of H t reflex not different between sides (i.e; nerve conduction! velocities same) Reduced amplitude and delayed onset for paraparetics Twitch amplitude same but delayed for spastic side Impaired responses in spasticity due to a. dysfunction of a spinal interneuronal system from a loss of supraspinal control Hocherman To train N=24 stroke; Platform Average MMA change et al. 1984 hemiparetic anterior moved at 0.5 Hz integrated EMG in treatment group 122 individuals to cerebral within a range of ofTA was larger than DSM 481 sustain posture circulation; 1-16 cm Body weight control (i.e. better by using 10-21 days Treatment distribution (i.e. stability) platform post; x=72.7 group underwent asymmetry) Patients with movements yrs old 15 training Maximal lowest initial -> Treatment sessions over 3 movement ability showed group = wks consisting of amplitude (MMA) better N=13; 6F, two 5 min parts improvements 7M; 8 right (one with patients - IEMG of TA and 5 left standing parallel to was similar in both CVA axis of movement legs during teaming -> Control and one with but affected limbA group = patients TA was minimal x N=ll; 5F, perpendicular) during quiet -: 6M; 6 right, 5 - AP and ML standing left CVA perturbations Improved weight distribution on the feet in both groups (more in treatment group):!, Hocherman To see whether N=21 elderly; Stood on - TA and MG Anticipatory et al. 1988 anticipatory x=68 yrs old; platform for 5 min activity -> onsets, reactions from TA adjustments N=15 stroke; that moved at 0.5 average EMG, and MG were seen DSM 492 (and strategies 9 right, 6 left Hz area under curve, in the elderly used) occur hemi; 5-12 Collected modulation index Subjects with repetitive weeks post; EMG for 60 sec (ratio between adapted a leaning reciprocal after 2 min into backwards and strategy perturbations time (thus allowed forwards Stroke differed during stance practice time) displacements) from elderly in that and is the tonic contractions^  inability of were present in hemiplegic MG or TA, co- * patients to contractions were; withstand these seen perturbations Stroke had due to a abnormal stance reduction in the strategies effectiveness of postural responses or a change in the strategy Holt et al. To compare N=21 (13 Lateral 10 m timed Stroke swayed 2000 balance used) strokes; perturbations walk more when pushed responses of right hemi; applied via a waist Functional to hemi side and DSM 257 stroke vs. range 22-77 belt by a machine reach with compared to controls to yrs old; Alternate unaffected hand controls ,. external x=86.4 wks blocks of 5 pushes Pelvic - GRF onset ], perturbations to post; (left, right, etc.) displacement increased for stroke the lateral side N=15 until 20 pushes (sway) compared to ! > : of the pelvis controls; each direction Ground controls -range 17-80 - 3% body reaction force - N o yrs. weight force applied - 27-30 cm apart at 5th toes and 10 cm at heel onset correlations between measures and functional assessments Message: latency of GRF 123 onset after a push at the hips is related to sway ; Ikai et al. To evaluate N = 59 stroke; EquiTest Weight Symmetry was 2003 dynamic 39M, 20F; system used and symmetry during deviated toward / postural control x=61.5 yrs motor control and perturbations non-paretic limb in in patients with old; 32 right, adaptation tests during motor left hemi patients • DSM 928 hemiparesis and 27 left hemi; used control test but same in right,,; in normal x=11.3 Motor control Latency and hemi and controls subjects months post- test consisted of 3 amplitude Strength of matched for age stroke trials of small (5 (strength) of response more in cm/s, 250 msec), response based on non-paretic limb medium (10 cm/s, force plate for both right and 300 msec), and measures during left hemi patients large (15 cm/s, 400 motor control test Latency of ;• msec) forward and Sway response delayed in backward response scores paretic limb for perturbations during adaptation both right and left Adaptation test hemi patients test consisted of 5 Strength of toes-up and toes- response reduced down rotation in paretic limb of perturbations at right and left herrii 87s for 400 msec patients £ Longer '-k adaptation in stroke with toes-down .i rotation Sway response greater in stroke than controls for toes-down rotation Jiang et al. To examine the N=8 stroke; Healthy Step timing Both groups, 1998 influence of 20-72 months subjects instructed - COM relied on chronic post to weight bear at - Arm EMG compensatory DSM 315 hemiparesis on N=8 healthy 70% on dominant stepping but the control of older adult leg to mimic strokes stepped compensatory controls hemiparetics with loaded (non-stepping and Stepping and paretic) leg (68%) grasping grasping reactions Stroke had reactions in were evoked by greater tendency to stroke patients unpredictable use multiple steps j platform and/or grasp -\ translations handrail \ Handrails - APAs in MLj: were at the direction also perimeter observed in stroke Random order but led to delayed perturbations in step and increased AP direction A P C O M Light-cued displacement voluntary grasping reactions also tested First set of 10 trials, compensatory stepping elicited 124 with no instructions In grasping trials, told to grasp handrail in front Kirker et al. To describe the N=13 stroke; Subjects stood Rivermead 4 patterns 2000a different range 33-75 on force plate and mobility Index found: (1) no patterns of yrs old; 7M, received up to 30 (RMI) response in any hip DSM 392 activation in 8F; 8 right, 5 3% body weight 10m walk muscle after push stroke subjects left hemi sideways pushes time to either direction, and changes N=18 via a computer- Motricity (2) little or no during recovery controls; x= controlled linear Index response in 46 yrs old motor in blocks of - EMG ofGM hemiparetic GM 5 alternating left and adductor after push to weak and right bilaterally side but minimal or Tracked observing onset increased activity" subjects over and presence of in unaffected course of recovery response and adductor. Pushtq, Received magnitude and strong side showed physiotherapy in patterns normal activation-hospital over of unaffected GM recovery 5 but no response in days/wk and 1-2 hemiparetic times after adductor, (3) push discharge to weak side -normal hemiparetic GM, increase or normal unaffected adductor; push to strong side — normal unaffected GM, no response in hemiparetic adductor, (4) push to weak side - ; normal hemiparetic GM, increase or r normal unaffected-, adductor; push to,; strong side -normal unaffected GM, normal hemiparetic adductor 8 strokes showed change towards normal recruitment with recovery Kirker et al. To compare the N=17 stroke; Stood on force - EMG Push to 2000b pattern of pelvic x=54 yrs old; plate and received amplitude (area hemiparetic side girdle muscle 12M, 5F; 13 sideways push via under curve) showed smaller DSM 273 activation in right, 4 left waist belt in blocks EMG onsets and later increase , normal subjects hemi; of 5 alternating in activity vs. '.• and hemiparetic median=74 sides up to 20 each controls in GM patients while wks post; Gait initiation Hemiparetic < stepping and N=16 controls -> 40 total, blocks GM and adductor^ mamtaining of 5 alternating recruitment smaller 125 standing starting foot in standing balance balance and Measure GM than stepping receiving a and adductors compared to \ sideways push bilaterally controls and unaffected adductor recruited more than in controls Standing balance and gait \ initiation are k distinct and may be good to train gait: 1st via supported'^  treadmill walking' Leonard et To determine N = 4CP - While H- H-reflex - Healthy al. 1998 whether or not N = 6 chronic reflex of soleus - EMG onset subjects soleus H- stroke and EMG ofTA demonstrated reflexes were N= 12 was being inhibition of soleus DSM 13 reciprocally healthy recorded, a (assessed through inhibited during controls forward platform H-reflex) during TA muscle translation of 15 both voluntary f contractions cm at 88.9 cm/s dorsiflexion and in elicited by a was evoked (350 response to balance to 889 cm/s2 perturbation platform- random requiring TA induced postural accelerations) activation perturbation 15 trials - CVA and CP.i. collected patients did not , Voluntary demonstrate soleus dorsiflexion trials inhibition '.• also collected (reciprocal inhibition) for either task Wing et al. To describe the N=ll stroke; Perturbation Functional No differences 1993 effects of x=65 yrs old; applied via an impairment of in offsets applying left- greater than actuator attached balance and Larger peak DSM 261 right direction 12 months to waist belt correlations displacements on horizontal post; 4M, 7F; providing up to +/- between other push and release forces to the 5 right, 6 left 100 N over 400 ms measures for stroke vs. hips in stroke hemi and max speed of - Peak controls patients N=12 elderly 350 mm/s displacement Release of controls; x=67 Feet slightly Stabilization push towards yrs old apart with hips times involved side the centered Offsets (on peak displacement Force push and release) (i.e. sway over the determined based noninvolved side), on Vi force subject was less than on could exert on release from a push machine; control towards the subjects all got noninvolved side, j; 31.7N force Release and P compared to 26.4N push (only on 1st average in strokes session) 13 sec trials; 6 stabilization times trials in a block increase in stroke alternating force Correlations Keep feet in longer 126 place and not move them stabilization time from push to noninvolved side; decreases activity rating for reach i| (noninvolved) and reach involved Appendix IV: Test re-test reliability for standing postural reflexes 127 Table TV. l : Test re-test reliability Muscle Condition Mean 1 (msec) Mean 2 (msec) SD1 SD2 ICC F-test SEM (3,1) P-value (msec) P_MG Backward 139.63 124.90 24.08 19.11 0.79 0.05 9.90 NPJV1G Backward 107.59 106.15 7.65 7.66 0.67 0.46 4.40 P_TA Forward 125.83 105.83 22.33 43.04 0.92 0.25 9.24 P_RF Forward 151.09 155.83 28.04 33.92 0.87 0.68 11.17 N P T A Forward 104.55 109.17 8.17 10.67 0.79 0.12 4.32 NP RF Forward 140.55 134.96 32.24 29.17 0.79 0.53 14.07 Abbreviations: P M G = paretic gastrocnemius N P M G = non-paretic gastrocnemius P T A = paretic tibialis anterior NP_TA = non-paretic tibialis anterior P_RF = paretic rectus femoris NP_RF = non-paretic rectus femoris SD = standard deviation ICC = Intraclass Correlation Coefficient (ICC3,i) S E M = Standard Error of Measurement Formula -» S E M ' s m + S D 2 \ ^ 7 c c 128 Appendix V: Berg Balance Scale 1. Sitting to Standing Instruction: Please stand up. Try not to use your hands for support. Grading: 4: Able to stand no hands and stabilize independently 3: Able to stand independently using hands 2: Able to stand using hands after several tries 1: Needs minimal assist to stand or to stabilize 0: Needs moderate or maximal assist to stand 2. Standing Unsupported Instruction: Stand for two minutes without holding. Grading: 4: Able to stand safely 2 minutes 3: Able to stand 2 minutes with supervision 2: Able to stand 30 seconds unsupported 1: Needs several tries to stand 30 seconds unsupported 0: Unable to stand 30 seconds unassisted If subject able to stand 2 minutes safely, score full marks for sitting unsupported. Proceed to position change standing to sitting. 3. Sitting Unsupported Feet on Floor Instruction: Sit with arms folded for two minutes. Grading: 4: Able to sit safely and securely 2 minutes 3: Able to sit 2 minutes under supervision 2: Able to sit 30 seconds 1: Able to sit 10 seconds 0: Unable to sit without support 10 seconds 4. Standing to sitting Instructions: Please sit down. Grading: 4: Sits safely with minimal use of hands 3: Controls descent by using hands 2: Uses back of legs against chair to control descent 1: Sits independently but has uncontrolled descent 0: Needs assistance to sit 129 5. Transfers Instructions: Please move from chair to bed and back again. One way toward a seat with armrests and one way toward a seat without armrests. Grading: 4: Able to transfer safely with minor use of hands 3: Able to transfer safely definite use of hands 2: Able to transfer with verbal cuing and/or supervision 1: Needs one person to assist 0: Needs two people to assist or supervise to be safe 6. Standing Unsupported with Eyes Closed Instructions: Close your eyes and stand still for 10 seconds. Grading: 4: Able to stand 10 seconds safely 3: Able to stand 10 seconds with supervision 2: Able to stand 3 seconds 1: Unable to keep eyes closed 3 seconds but stays steady 0: Needs help to keep from falling 7. Standing Unsupported with Feet Together Instructions: Place your feet together and stand without holding. Grading: 4: Able to place feet together independently and stand for 1 minute safely 3: Able to place feet together independently and stand for 1 minute with supervision 2: Able to place feet together independently but unable to hold for 30 seconds 1: Needs help to attain position but able to stand 15 seconds feet together 0: Needs help to attain position and unable to hold for 15 seconds 8. Reaching Forward with Outstretched arm. Instructions: Lift arm to 90 degrees. Stretch out your fingers and reach forward as far as you can. (Examiner places a ruler at end of fingertips when arm is at 90 degrees. Fingers should not touch the ruler while reaching forward. The recorded measure is the distance forward that the fingers reach while the subject is in the most forward lean position.) Grading: 4: Can reach forward confidently more than 10 inches 3: Can reach forward more than 5 inches safely 2: Can reach forward more than 2 inches safely 1: Reaches forward but needs supervision 0: Needs help to keep from falling 130 9. Pick Up Object from the Floor Instructions: Pick up the shoe/slipper, which is placed in front of your feet. Grading: 4: Able to pick up slipper safely and easily 3: Able to pick up slipper but needs supervision 2: Unable to pick up but reaches 1 to 2 inches from slipper and keeps balance independently 1: Unable to pick up and needs supervision while trying 0: Unable to try/needs assistance to keep from falling 10. Turning to Look Behind Over Left and Right Shoulders Instructions: Turn to look behind you over toward left shoulder. Repeat to the right. Grading: 4: Looks behind form both sides and weight shifts well 3: Looks behind one side only; other side shows less weight shift 2: Turns sideways only but maintains balance 1: Needs supervision when turning 0: Needs assist to keep from falling 11. Turn 360 Degrees Instructions: Turn completely around in a full circle. Pause. Then turn a full circle in the other direction. Grading: 4: Able to turn 360 degrees safely in less than 4 seconds each side 3: Able to turn 360 degrees safely one side only - less than 4 seconds 2: Able to turn 360 degrees safely but slowly 1: Needs close supervision or verbal cuing 0: Needs assistance while turning 12. Count Number of Times Step Touch Measured Stool Instructions: Place each foot alternately on the stool. Continue until each foot has touched the stool four times. Grading: 4: Able to stand independently and safely and complete 8 steps in 20 seconds 3: Able to stand independently and complete 8 steps in more than 20 seconds 2: Able to complete 4 steps without aid with supervision ^ 1: Able to complete more than 2 steps - needs minimal assist 0: Needs assistance to keep from falling - unable to try 131 13. Standing Unsupported One Foot in Front Instructions: (DEMONSTRATE to subject.) Place one foot directly in front of the other. If you feel that you cannot place your foot directly in front, try to step far enough ahead that the heel of your forward foot is ahead of the toes of the other foot. Grading: 4: Able to place foot tandem independently and hold 30 seconds 3: Able to place foot ahead of the other independently and hold 30 seconds 2: Able to take small step independently and hold 30 seconds 1: Needs help to step but can hold 15 seconds 0: Loses balance while stepping or standing 14. Standing on One Leg Instructions: Stand on one leg as long as you can without holding. Grading: 4: Able to lift leg independently and hold more than 10 seconds 3: Able to lift leg independently and hold 5 to 10 seconds 2: Able to lift leg independently and hold at least 3 seconds 1: Tries to lift leg, unable to hold 3 seconds but remains standing independently 0: Unable to try or needs assist to prevent fall Additional Instructions A l l questions should be scored in the lowest category that applies. A l l furniture or chairs should be normal height, not very low sofas or easy chairs. A l l questions after #5 are performed standing unsupported. Subjects may be permitted a rest between items as required. 4. The instructions do not specify that the subject refrain from using hands. It would not have been consistent with the clinical training given most patients. ••. 5. This item tests how well the subjects are able to transfer from and towards seats with and without arm rests. The purpose is not to test the strength of either side. Therefore, persons with a definite side preference may be positioned so as to go in the same direction twice. 11. The subject is awarded 3 points if he or she can turn 360 degrees independently and safely in both directions but one side took longer than 4 seconds. 12. This item can be performed using the bottom step of a staircase or a stool of comparable height. 132 Appendix VI: Nottingham Health Profile (NHP) Please check the appropriate box ("Yes" or "No") to each question. Table VI. 1: NHP YES NO I'm tired all the time. I have pain at night. Things are getting me down. I have unbearable pain. I take pills to help me sleep. I've forgotten what it's like to enjoy myself. I'm feeling on edge. I find it painful to change position. I feel lonely. I sleep badly at night. I'm finding it hard to get along with people. I need help to walk about outside (e.g. a walking aid or someone to support me). I'm in pain when going up or down stairs. 133 I wake up feeling depressed. I'm in pain when I'm sitting. I can walk about only indoors I find it hard to bend. Everything is an effort. I'm waking up in the early hours of the morning. I'm unable to walk at all. I'm finding it hard to make contact with people. The days seem to drag. I have trouble getting up and down stairs and steps. I find it hard to reach for things. I'm in pain when I walk. I lose my temper easily these days. I feel there is nobody that I am close to. I lie awake for most of the night. 134 I feel as i f I'm losing control. I'm in pain when I'm standing. I find it hard to get dressed by myself. I soon run out of energy. I find it hard to stand for long (e.g. at the kitchen sink, waiting in line.) I'm in constant pain. It takes me a long time to get to sleep. I feel I am a burden to people. Worry is keeping me awake at night. I feel that life is not worth living. 'Yes' responses summated for total score out of 38. Lower scores represent better health-related quality of life. Appendix VII: Activities-specific Balance Confidence (ABC) Scale 135 For each of the following activities, please indicate your level of self-confidence by choosing a corresponding number from the following rating scale. Answer all items even i f there are activities you would not do or are unsure about. 0%10% 20% 30% 40% 50% 60% 70% 80% 90% 100% Not Completely Confident Confident How confident are you that you will not lose your balance or become unsteady when you. A) walk around the house? % B) walk up and down stairs? % C) pick up a slipper from the floor? % D) reach at eye level? % E) reach while standing on your tiptoes? % F) stand on a chair to reach? % G) sweep the floor? % H) walk outside to nearby car? % I) get in and out of a car? % J) walk across a parking lot? % K) walk up and down a ramp? % L) walk in a crowded mall? % M) walk in a crowd or get bumped? % N) ride an escalator holding the rail? % O) ride an escalator not holding the rail? % P) walk on icy sidewalks? % Appendix VIII: Informed consent for Experiment I 136 Informed Consent Form Posture and Locomotion Database Principal Investigator: Dr. Janice Eng School of Rehabilitation Sciences University of British Columbia (604) 714-4105 Purpose: I understand that I am being invited to participate in this study so that my balance, walking patterns, and strength can be evaluated and entered into a posture and locomotion database. This database will be used to provide information as to the effects of aging, neurological conditions and musculoskeletal conditions on posture and locomotion. Study Procedures: I may be asked to stand for one minute, stand and balance on a moveable platform, and/or raise my arms while standing. Electrodes will be attached to the surface of my limbs and trunk with double-sided tape to record the activity of my muscles. Small markers will also be attached to my limbs and trunk with double-sided tape so that cameras can record my movements. The whole evaluation procedure will take approximately 2.0 hours. Rest breaks can be taken at any time. Exclusions: Subjects who are not able to rise from a chair and stand for 10 seconds with minimal assistance from one person wil l be excluded from this study. Confidentiality: Any information resulting from this research study will be kept strictly confidential. A l l documents will be identified only be a code number and kept in a locked filing cabinet. I wil l not be identified by name in any reports of the completed study. M y medical record may, however, be inspected by the Health Protection Branch HPB Canada) in the presence of the Investigator or her designate. Copies of relevant data which identify me only by code number may be required by the HPB, but I will not be identified by name, initials or date of birth. Contact: I understand that i f I have any questions or desire further information with respect to this study, or i f I experience any adverse effects, I should contact Dr. Janice Eng or one of her associates at (604) 714-4105. If I have any concerns about my treatment or rights as a research subject I may 137 contact the Director of Research Services at the University of British Columbia at (604) 822-8598. Patient Consent: I understand that participation in this study is entirely voluntary and I may refuse to participate or I may withdraw from the study at any time without any consequences. I have received a copy of this consent from for my own records. I consent to participate in this study. Subject Signature Date Witness Signature Date :, Investigator Signature Date 138 Appendix IX: Platform translation protocol for Experiment I Table IX. 1: Experiment I protocol Increased WtBr = 30% on non-paretic leg, 70% on paretic leg Decreased WtBr = 70% on non-paretic leg, 30% on paretic leg Neutral = 50% on each leg **lnterval between perturbations (random) = 30 seconds to 1 minute Perturbation Displacement Velocity Acceleration Magnitude: 8 cm 30 cm/s 300 cm/s2 Perturbation # Trial # Condition Platform Direction 1 Neutral Forward 2 Neutral Forward 3 Neutral Forward 4 Neutral Forward 5 Neutral Forward 6 Increased WtBr Backward 7 Increased WtBr Backward 8 Increased WtBr Backward 9 Increased WtBr Backward 10 Increased WtBr Backward 11 Increased WtBr Forward 12 Increased WtBr Forward 13 Increased WtBr Forward 14 Increased WtBr Forward 15 Increased WtBr Forward 16 Decreased WtBr Forward 17 Decreased WtBr Forward 18 Decreased WtBr Forward 19 Decreased WtBr Forward 20 Decreased WtBr Forward 21 Neutral Backward 22 Neutral Backward 23 Neutral Backward 24 Neutral Backward 25 Neutral Backward 26 Decreased WtBr Backward 27 Decreased WtBr Backward 28 Decreased WtBr Backward 29 Decreased WtBr Backward 30 Decreased WtBr Backward 139 Appendix X: E M G electrode placement guidelines Table X . 1: Electrode placement Study: Subject Code: Date: Muscle Group Placement Guidelines Segment Measurements (electrodes should be placed on either side of central measurement point) Tibialis Anterior (TA) Over the greatest muscle bulk just lateral to tibial crest; most proximal half of the shank Right leg: cm down from inferior border of patella Left leg: cm down from inferior border of patella Medial Gastrocnemius (MG) Over greatest muscle bulk on medial side of calf (proximal posterior shank)-> line from the popliteal fossa to the heel: 1/3 down from popliteal fossa Right leg: line cm 1/3 = cm Left leg: line cm 1/3 = cm Biceps Femoris (BF) On lateral posterior distal thigh: line from 2 cm lateral to the spinal cord at the level of iliac crests to the head of the fibula -> 1/3 up from the head of the fibula Right leg: line cm 1/3 = cm Left leg: line cm 1/3 = cm Rectus Femoris (RF) Midway between a line from the ASIS to the superior border of the patella Right leg: line cm 1/2 = cm Left leg: line cm 1/2 = cm 140 Appendix XI: American Heart Association Stroke Functional Classification; (AHASFC) Function Level I -> Independent in B A D L and IADL activities and tasks required of roles of patient had before stroke. Patient is able to live alone, maintain a household, and access the community for leisure and/or productive activities such as shopping, employment, or volunteer work. II -> Independent in B A D L but partially dependent in routine IADL. Patient is able to live alone but requires assistance/supervision to access the community for shopping and leisure activities. Patient may require occasional assistance with meal preparation, household tasks, and taking medication. HI -> Partially dependent in B A D L (<3 areas) and IADL. Patient is able to live alone with substantial daily help from family or community resources for more difficult B A D L tasks such as dressing lower extremities, bathing, or climbing stairs. Patient requires assistance with such IADL tasks as meal preparation, home maintenance, community access, shopping, handling finances, and/or taking medications. IV -> Partially dependent in B A D L (> 3 areas). Patient is unable to live alone safely and requires assistance with IADL except for simple tasks such as answering the telephone. V -> Completely dependent in B A D L (> 5 areas) and IADL. Patient is unable to live alone safely and requires full-time care. B A D L indicates Basic Activities of Daily Living: feeding and swallowing, grooming, dressing, bathing, continence, toileting, and mobility. IADL indicates Instrumental Activities of Daily Living: using the telephone, handling money, shopping, using transportation, maintaining a household, working, participating in leisure activities, etc. 141 Appendix XII: Informed consent for Experiment II and III Informed Consent Postural Control in Individuals with Stroke Principle Investigator: Dr. Janice Eng, PhD, PT/OT, School of Rehabilitation Sciences, Contact: (604) 714-4105 Co-investigators: Daniel Marigold, BSc. Kin , Graduate Program in Neuroscience Dr. Tim Inglis, PhD, Human Kinetics Dr. Drew Dawson, M D , FRCPC, Acquired Brain Injury Dr. Heather McKay, PhD, Human Kinetics Jocelyn Harris, B A , OT, School of Rehabilitation Sciences j . Background: You are being invited to participate in this study because the exercise programs involved in this study may improve your physical function, which has been affected by a stroke. Purpose: The purpose of this study is to determine whether exercise interventions affect physical function in individuals with chronic stroke. Study Procedures: Should you choose to participate in this study, you will be assigned by chance (i.e. like flipping a coin with a 50% chance of being assigned to a particular group) to one of two exercise groups: 1) balance-based exercise group or 2) posture-based exercise group. Physical therapists, occupational therapists, and/or kinesiologists will supervise the exercise programs. Your involvement in the study means that you will participate in your assigned exercise program (1 hour/session, 3 sessions/week for 10 weeks) aimed at improving physical function. Your primary care physician must consent to your participation in this study before you are officially accepted into the study. Your primary care physician will also release to the principle investigator the type (e.g. ischemic versus hemorrhagic stroke) and the location in the brain of your stroke i f this information is known. You will be provided with a release-of-information form to give to your physician. Both exercise programs will consist of a warm-up, stretching, exercises that challenge posture and balance, and a cool-down. Rest breaks can be taken at any time. I You wil l be asked to come for assessments at three different weeks (prior to the exercise program, immediately following the exercise program, and one month after the end of the exercise program). At each of these weeks, there will be 3 test sessions separated by one or two days. Each test session will last 2 hours. One session will have you perform standing tasks for 60 seconds with eyes open and eyes closed, standing and raising your arms to the side, and maintaining standing balance on a platform that will suddenly move horizontally. During these tasks, you will be fitted with a harness for safety and have markers attached to your body segments to monitor your movement and surface electrodes on leg and trunk muscles 142 to measure their muscle activity. The second session will assess your functional balance, walking speed and muscle strength and have you answer questionnaires on balance confidence and quality of life. The third session will measure your bone density and structure using a bone densitometer and computerized tomography system. You will also maintain a diary in which you will record any time you experience a fall and the circumstances surrounding the incident and return by mail to the GF Strong Rehab Centre every month for the following year. Exclusions: Individuals who have had their stroke for less than 1 year or who have had more than 1 stroke wil l be excluded from the study. In addition, individuals will be excluded i f they are not medically stable (e.g. have congestive heart failure, unstable cardiovascular status, uncontrolled hypertension, atrial fibrillation, or left ventricular failure), and have significant musculo-skeletal problems (e.g. active inflammatory arthritis) due to conditions other than stroke. Risks: There is a chance that you may feel tired or experience some muscle soreness after the exercise and/or testing sessions. These symptoms should disappear within a few days. These symptoms can be minimized with stretching following the testing and exercise sessions. In addition, there is a slight chance that the electrodes used to monitor muscle activity and/or the tape used to secure infrared emitting diodes to monitor movement during the testing sessions may cause some minor skin irritation. Although the bone measurements are X-ray based, the total effective dose per session wil l be approximately 10 millirem. This is less than you receive on an airplane flight across the country. Benefits: ,4 The balance-based and posture-based exercise programs may have the potential to improve your physical function. ; Confidentiality: Any information resulting from this research study will be kept strictly confidential. A l l documents will be identified only by a code number and kept in a locked filing cabinet. You wil l not be identified by name in any reports of the completed study. Your medical records may be inspected by the Health Protected Branch (HPB Canada) in the presence of the investigator or her designate. Copies of relevant data, which identify you only by code number, may be required by the HPB, but name, initials, or date of birth will not identify yourself. Remuneration/Compensation: You wil l be reimbursed for bus or parking charges to attend the sessions. Compensation for Injury: Signing this consent form in no way limits your legal rights against the sponsor, investigators, or anyone else. !• Contact: If you have any questions or desire further information with respect to this study or experience any adverse effects, please contact Dr. Janice Eng or one of her associates at (604) 714-4105. If 143 you have any concerns about your treatment or rights as a research participant you may contact the Director of Research Services at the University of British Columbia at (604) 822-8598. Participant Consent: I understand that participation in this study is entirely voluntary and I may refuse to participate or I may withdraw from the study at any time without any consequences to my continuing u medical care. I have received a copy of this consent form for my own records. I consent to participate in this study. Participant Signature Date Witness Signature Date Investigator Signature Date Appendix XIII: Platform translation protocol for Experiment II and III Table X m . l : Experiment II and m protocol TR Protocol Subject Code: ** Interval between perturbations (random) = 15-30 seconds Perturbation Magnitude Displacement Velocity Acceleration 8 cm 30 cm/s 300 cm/s2 Perturbation Trial # Platform Step Limb Direction Fall Comments # Direction 1 Backward 2 Backward 3 Backward 4 Backward 5 Backward 6 Backward 7 Backward 8 Backward 9 Backward 10 Backward 11 Forward 12 Forward 13 Forward 14 Forward 15 Forward 16 Forward 17 Forward 18 Forward 19 Forward 20 Forward Appendix XIV: Recruitment for Experiment II and III 145 Newspaper Advertisement Persons with stroke are invited to take part in a study undertaken by the School of Rehabilitation Sciences, University of British Columbia in conjunction with the GF Strong Rehab Centre. This study wil l examine the effect of 10-week balance-based and posture-based exercise programs on physical function. Physical therapists, occupational therapists, recreational therapists and/or kinesiologists will supervise the exercise programs. For more information or to participate in this study, contact: Daniel Marigold (Kinesiologist) at the GF Strong Rehab Centre at (604) 714-4109. Flyer * * * R E S E A R C H S T U D Y * * * Exercise Program for Individuals with Stroke Persons with stroke are invited to take part in a study undertaken by the School of Rehabilitation Sciences, University of British Columbia in conjunction with the GF Strong Rehab Centre. This study wil l examine the effect of 10-week balance-based and posture-based exercise programs on physical function. Physical therapists, occupational therapists, and/or kinesiologists will supervise the exercise programs. Participants will be assigned by chance to either the balance-. based or posture-based exercise program groups. Participants will be assessed at three difference weeks (prior to the exercise programs, immediately following the exercise programs, and again one month after the programs). During each of these weeks, there will be three test sessions separated by one or two days. During the tests sessions, you wil l be asked to perform various standing tasks, undergo muscle strength, balance testing and bone density testing. In addition, you will be asked to complete questionnaires about your balance ability and quality of life. Both exercise programs will last 10 weeks and consist of 3 sessions/week, maximum of 1 3 hr/session. Transportation can be arranged. ! i For more information or to participate in this study, contact: Daniel Marigold (Kinesiologist) at the GF Strong Rehab Centre at (604) 714-4109. 146 Appendix XV: Mini-Mental State Exam Score 1 for every correct answer: 1. What year is it? u 2. What season are we in? 3. What month are we in? 4. What is today's date? 5. What day of the week is it? 6. What country are we in? r 7. What province are we in? 8. What city are we in? 9. What hospital are we in? 10. What floor of the hospital are we on? Name three objects ("Ball," "Car," "Man"). Take a second to pronounce each word. Then ask the patient to repeat all 3 words. Take into account only correct answers given on the first try. Repeat these steps until the subject learns all the words. 11. Ball? 12. Car? 13. Man? Either "please spell the word WORLD and now spell it backwards" or "Please count from 100 subtracting 7 every time" 14. " D " or 93 15. " L " or 86 16. "R" or 79 17. "O" or 72 18. " W " or 65 147 What were the 3 words I asked you to remember earlier? 19. Ball? 20. Car? a 21. Man? Show the subject a pen and ask: "Could you name this object?" 22. Pen. Show the subject your watch and ask: "Could you name this object?" 23. Watch Listen and repeat after me: 24. "Noifs, ands, orbuts." Put a sheet of paper on the desk and show it while saying: "Listen carefully and do as I say." 25. Take the sheet with your left/right (unaffected) hand. 26. Fold it in half. 27. Put in on the floor. Show the patient the visual instruction page directing him/her to "CLOSE Y O U R E Y E S " and say: 28. Do what is written on this page. Give the subject a blank sheet and a pen and ask: 29. Write a sentence, whatever you want, but a complete sentence. Give the patient the geometric design page and ask: 30. Could you please copy this drawing? Total Score: (/30) 148 Appendix XVI: Experiment II and III physician consent Physician's Consent Dear Doctor: Your patient has expressed interest in participating in our Postural Control in Individuals with Stroke study examining the effectiveness of a 10-week exercise program focused on improving balance, posture, and functional mobility in stroke survivors. This study is being undertaken at the G.F. Strong Rehab Centre in collaboration with the School of Rehabilitation Sciences at the University of British Columbia and has been approved by the U B C and hospital ethics committees. A l l participants will undergo assessments at three different weeks (prior to the exercise program, immediately following the exercise program, and one month after the completion of , the exercise program). At each of these weeks, there wil l be 3 test sessions separated by one or two days with each session lasting approximately 2 hours. One session wil l have your patient perform standing tasks that challenge their balance. Another session will assess your patient's function and muscle strength and have them answer questionnaires on balance confidence and quality of life. The other session will measure your patient's bone density and structure using a bone densitometer and computerized tomography system. Your patient will be assigned by chance (i.e. like flipping a coin with a 50% chance of being assigned to a particular group) to either a balance-based or posture-based exercise program group. Both exercise programs will last 10 weeks (3 sessions/week, lhr/session) and consist of a warm-up, stretching, moderate intensity exercises that challenge posture and balance (e.g. rapid stepping, muscle strength training, and brisk walking), and a cool-down. Individuals with stroke who have residual weakness on one side of the body and can walk independently shall be included in the study. Theses individuals must have had their stroke for greater than one year and have only suffered from one stroke. However, those with uncontrolled hypertension, congestive heart failure, unstable cardiovascular status, atrial fibrillation, left ventricular failure, or significant musculo-skeletal problems (e.g. active . inflammatory arthritis) due to conditions other than stroke wil l be E X C L U D E D . We would be grateful i f you would decide whether your patient would be suitable to participate in this exercise research study and complete the relevant medical information regarding the type and location of their stroke. Sincerely, Dr. Drew Dawson, M D , FRCPC Dr. Janice Eng, Ph.D, PT/OT Acquired Brain Injury Research Scientist, GF Strong Rehab Centre G.F. Strong Rehab Centre Assistant Professor, University of BC Daniel Marigold, BSc. K in MSc. Candidate Graduate Program in Neuroscience, University of BC 149 Patient Release I agree to the release of the following medical information to the Postural Control in Individuals with Stroke Study conducted by the School of Rehabilitation Sciences, U B C and G.F. Strong Rehab Centre. Relevant Medical Information of Patient (Physician Please fill out this information) Type of Stroke (e.g. ischemic versus hemorrhagic stroke): Location in Brain of Stroke (e.g. middle, aneterior, or posterior cerebral artery): Signed: Patient Signature Please print patient's full name Date: Physician's Assessment The above patient is suitable for the Postural Control in Individuals with Stroke Study described on page 1 of this letter and I have filled out the above information related to the type and location of the patient's stroke. Signed: Physician's Signature Please print Physician's full name Address of Physician's Office Date: Appendix XVII: Exercise interventions 150 Exercise Interventions (*major component) Agility Exercise Group Exercises for many of the components were performed in stations (1 instructor to approximately 3 clients) Stations allowed for more challenging exercises to be performed since small group easier to handle for instructor and since groups could be assigned in such a way to have a low functioning client with a high functioning client or a group of high functioning clients could be formed -> Warm-up (5 min) Walking (little steps, big steps, side steps, knee high steps) Weight-shifting while standing -> Multi-sensory Component* Walking on foam (little steps, big steps, tandem, backwards)* Standing on foam (separate or combination of: eyes open, eyes closed, weight-shifting, head turning, head back, feet together, feet staggered, feet parallel, one foot)* Rapid stepping onto foam - Note: several different types of foam were used with various densities -> Strength Component (functional) Sit-to-stand (repetitions of 10) Ankle strengthening (heel raises and toe raises while supported by chair) - Rapid knee raises (hip and knee flexion) with ankle weights -> Agility Component* Rapid stepping forward and backward* Side stepping across room - Braiding (alternating front and back crossover steps during side stepping) across room - Tandem walking (heel-to-toe walking) across room Figure-8 eight (drawn in chalk on floor) walking (tandem, regular, and backward) Stepping onto and over steppers Target stepping (into circles of varying size and distance) across room Standing balloon toss games Standing on tilt-board Standing perturbations (instructor pushing client or vice versa)* 151 Cool-down (5 min) Light stretching Stretching/weight-shifting Exercise Group Small group discussions were also done at the beginning of class occasionally -> Warm-up (5 min) - Walking (little steps, big steps, and side steps) -> Weight-shifting* Side-to-side weight-shifting* Reaching up and down tasks Tai Chi-like movements* Seated balloon toss -> Mat exercises* - On all fours (shifting side-to-side, superman stretch - opposite arm and leg raised) Arm weight exercises Stretching various muscle groups -> Cool-down (5-10 min) Relaxation Appendix XVIII: Platform-induced falls for Experiment III 152 Table X V m . 1: Falls on platform Stretching/weight-shifting Group Agility Group Measure Baseline Post-intervention Retention Baseline Post-intervention Retention # of Falls 19 # of 0.76 Falls/person # of Fallers 6 # of Repeat 3 Fallers 30 1.20 8 6 18 0.90 5 3 36 1.64 6 5 22 1.00 5 4 18 1.06 6 4 

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