{"@context":{"@language":"en","Affiliation":"http:\/\/vivoweb.org\/ontology\/core#departmentOrSchool","AggregatedSourceRepository":"http:\/\/www.europeana.eu\/schemas\/edm\/dataProvider","Campus":"https:\/\/open.library.ubc.ca\/terms#degreeCampus","Creator":"http:\/\/purl.org\/dc\/terms\/creator","DateAvailable":"http:\/\/purl.org\/dc\/terms\/issued","DateIssued":"http:\/\/purl.org\/dc\/terms\/issued","Degree":"http:\/\/vivoweb.org\/ontology\/core#relatedDegree","DegreeGrantor":"https:\/\/open.library.ubc.ca\/terms#degreeGrantor","Description":"http:\/\/purl.org\/dc\/terms\/description","DigitalResourceOriginalRecord":"http:\/\/www.europeana.eu\/schemas\/edm\/aggregatedCHO","Extent":"http:\/\/purl.org\/dc\/terms\/extent","FileFormat":"http:\/\/purl.org\/dc\/elements\/1.1\/format","FullText":"http:\/\/www.w3.org\/2009\/08\/skos-reference\/skos.html#note","Genre":"http:\/\/www.europeana.eu\/schemas\/edm\/hasType","GraduationDate":"http:\/\/vivoweb.org\/ontology\/core#dateIssued","IsShownAt":"http:\/\/www.europeana.eu\/schemas\/edm\/isShownAt","Language":"http:\/\/purl.org\/dc\/terms\/language","Program":"https:\/\/open.library.ubc.ca\/terms#degreeDiscipline","Provider":"http:\/\/www.europeana.eu\/schemas\/edm\/provider","Publisher":"http:\/\/purl.org\/dc\/terms\/publisher","Rights":"http:\/\/purl.org\/dc\/terms\/rights","RightsURI":"https:\/\/open.library.ubc.ca\/terms#rightsURI","ScholarlyLevel":"https:\/\/open.library.ubc.ca\/terms#scholarLevel","Title":"http:\/\/purl.org\/dc\/terms\/title","Type":"http:\/\/purl.org\/dc\/terms\/type","URI":"https:\/\/open.library.ubc.ca\/terms#identifierURI","SortDate":"http:\/\/purl.org\/dc\/terms\/date"},"Affiliation":[{"@value":"Education, Faculty of","@language":"en"},{"@value":"Kinesiology, School of","@language":"en"}],"AggregatedSourceRepository":[{"@value":"DSpace","@language":"en"}],"Campus":[{"@value":"UBCV","@language":"en"}],"Creator":[{"@value":"Pauhl, Katherine Elizabeth","@language":"en"}],"DateAvailable":[{"@value":"2008-08-01T14:58:48Z","@language":"en"}],"DateIssued":[{"@value":"2008","@language":"en"}],"Degree":[{"@value":"Master of Science - MSc","@language":"en"}],"DegreeGrantor":[{"@value":"University of British Columbia","@language":"en"}],"Description":[{"@value":"A common symptom of Idiopathic Parkinson\u2019s disease (IPD) is decreased trunk and balance control. These deficits in patients with IPD are not treatable, and their underlying mechanisms are not well understood. Additionally, it is not known to what extent decreased trunk control contributes to postural instability in patients with IPD. Previous work by Martin (1965) observed that patients with post-encephalitatic Parkinson\u2019s disease would fall in the direction of the tilt when perturbed while seated. In order to better understand the underlying causes of these observed trunk deficits and attempt to replicate Martins findings, this study investigated postural corrective movement of the trunk while seated in patients with IPD and age-matched healthy controls. Participants\u2019 range of motion (ROM) was tested actively and passively while lying supine, following which, bilateral electromyography (EMG) (rectus abdominis (RA), external oblique (EO), and erector spinae (EST9, L3)) and 3-D kinematic measures were recorded while participants were seated on a modified chair and received unexpected perturbations, 7\u00b0 at 40\u00b0\/sec, in four different directions (forward, backward, left, and right). EMG responses were normalized to participant\u2019s maximum voluntary contractions. We observed patients with IPD to have decreased active and passive ROM only in the frontal plane relative to controls. Patterning of muscle responses to rotational perturbations did not vary between groups in any direction, except backward, and trends toward significantly greater EST9 activity were observed during backward and left tilts in patients with IPD. Despite this both patients with IPD and controls were able to make appropriate trunk corrective movements opposite the direction of the tilt. However, two patients, who were most severely affected, did make incorrect trunk movements in the direction of the tilt during left and right tilting perturbations which, upon visual inspection, appear to be due to improperly modulated and timed muscle responses. Thus, our data counters the findings of Martin, and suggests the trunk is posturally stable in IPD. Therefore, balance instabilities during stance are likely due to improper responses of the lower limbs. However, as disease severity increases, the contributing influence of an improperly responding trunk may add to their postural deficits.","@language":"en"}],"DigitalResourceOriginalRecord":[{"@value":"https:\/\/circle.library.ubc.ca\/rest\/handle\/2429\/1242?expand=metadata","@language":"en"}],"Extent":[{"@value":"13996246 bytes","@language":"en"}],"FileFormat":[{"@value":"application\/pdf","@language":"en"}],"FullText":[{"@value":"THE EFFECT OF IDIOPATHIC PARKINSON\u2019S DISEASE ON SEATED TRUNK REACTIONS by KATHERINE ELIZABETH PAUHL B.Sc., University of Waterloo, 2005 A THESIS SUBMITTED IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF MASTER OF SCIENCE in THE FACULTY OF GRADUATE STUDIES (Human Kinetics) THE UNIVERSITY OF BRITISH COLUMBIA (Vancouver) July 2008 \u00a9 Katherine Elizabeth Pauhl, 2008 ii ABSTRACT A common symptom of Idiopathic Parkinson\u2019s disease (IPD) is decreased trunk and balance control. These deficits in patients with IPD are not treatable, and their underlying mechanisms are not well understood. Additionally, it is not known to what extent decreased trunk control contributes to postural instability in patients with IPD. Previous work by Martin (1965) observed that patients with post-encephalitatic Parkinson\u2019s disease would fall in the direction of the tilt when perturbed while seated. In order to better understand the underlying causes of these observed trunk deficits and attempt to replicate Martins findings, this study investigated postural corrective movement of the trunk while seated in patients with IPD and age-matched healthy controls. Participants\u2019 range of motion (ROM) was tested actively and passively while lying supine, following which, bilateral electromyography (EMG) (rectus abdominis (RA), external oblique (EO), and erector spinae (EST9, L3)) and 3-D kinematic measures were recorded while participants were seated on a modified chair and received unexpected perturbations, 7\u00b0 at 40\u00b0\/sec, in four different directions (forward, backward, left, and right). EMG responses were normalized to participant\u2019s maximum voluntary contractions. We observed patients with IPD to have decreased active and passive ROM only in the frontal plane relative to controls. Patterning of muscle responses to rotational perturbations did not vary between groups in any direction, except backward, and trends toward significantly greater EST9 activity were observed during backward and left tilts in patients with IPD. Despite this both patients with IPD and controls were able to make appropriate trunk corrective movements opposite the direction of the tilt. However, two patients, who were most severely affected, did make incorrect trunk movements in the iii direction of the tilt during left and right tilting perturbations which, upon visual inspection, appear to be due to improperly modulated and timed muscle responses. Thus, our data counters the findings of Martin, and suggests the trunk is posturally stable in IPD. Therefore, balance instabilities during stance are likely due to improper responses of the lower limbs. However, as disease severity increases, the contributing influence of an improperly responding trunk may add to their postural deficits. iv TABLE OF CONTENTS Abstract ............................................................................................................................... ii Table of Contents ............................................................................................................... iv List of Tables .................................................................................................................... vii List of Figures .................................................................................................................. viii Acknowledgements ............................................................................................................ ix 1. BACKGROUND .............................................................................................................1 1.1 Quiet standing ....................................................................................................5 1.2 Anticipatory postural adjustments (APAs) ........................................................7 1.3 Standing reactive postural responses in a healthy age matched control population ....................................................................................................8 1.4 Standing reactive postural responses in an IPD patient population .................10 1.5 Seated postural responses in a healthy age matched control population .........13 1.6 Seated postural responses in an IPD patient population ..................................19 1.7 Influences on postural responses .....................................................................23 1.8 Hypotheses .......................................................................................................24 2. METHODS ...................................................................................................................25 2.1 Subjects ............................................................................................................25 2.2 Active and passive ranges of motion (ROM) ..................................................26 2.2.1 Setup .................................................................................................26 2.2.2 Procedure ..........................................................................................27 2.2.3 Measures and data analysis ...............................................................29 2.2.4 Statistical analysis .............................................................................30 v 2.3 Tilting perturbations .........................................................................................30 2.3.1 Setup .................................................................................................30 2.3.2 Measures ...........................................................................................32 2.3.3 Procedure ..........................................................................................33 2.3.4 Data analysis .....................................................................................34 2.3.5 Statistical analysis .............................................................................36 3. RESULTS ......................................................................................................................37 3.1 ROM kinematics ..............................................................................................37 3.1.1 Sagittal plane trunk flexion and extension ........................................37 3.1.2 Frontal plane trunk flexion (left and right) .......................................39 3.2 Tilting perturbations .........................................................................................39 3.2.1 Sagittal plane perturbations ...............................................................39 3.2.2 Frontal plane perturbations ...............................................................46 3.3 Case studies ......................................................................................................47 4. DISCUSSION ................................................................................................................51 4.1 Lateral range of motion (ROM) of the trunk was not influenced by IPD ........51 4.2 Timing and amplitude of corrective trunk movements in the sagittal plane are not influence by IPD ....................................................................................................53 4.3 Timing, but not amplitude of corrective trunk movements in the frontal plane are influenced by IPD ..................................................................................................54 4.4 Evidence for lateral trunk instability was observed in most severely affected patients with IPD....................................................................................................56 vi 4.5 Patients with IPD have altered patterns of muscle responses to backward perturbations ..........................................................................................................57 4.6 Larger muscle response magnitudes were observed in patients with IPD when responding to backward and leftward tilting perturbations ...................................58 4.7 Possible mechanisms for muscle co-contraction and improperly modulated muscle responses in patients with IPD ...............................................................................59 4.8 The role of the trunk in postural stability.........................................................61 4.9 Strengths and limitations..................................................................................64 5. CONCLUSION ..............................................................................................................67 5.1 Future research .................................................................................................67 REFERENCES ..................................................................................................................69 APPENDIX A ....................................................................................................................83 APPENDIX B ....................................................................................................................85 vii LIST OF TABLES Table 1 Demographic and disease characteristics of controls and patients with IPD .................................................................................25 Table 2 Normalized MVC % and raw group 100 ms area averages for rectus abdominis (RA), external oblique (EO), erector spinae (EST9, ESL3)........44 viii LIST OF FIGURES Figure 1 Tilting reactions from Martin (1965).\u2026\u2026\u2026\u2026\u2026\u2026\u2026\u2026\u2026\u2026\u2026\u2026\u2026\u2026.........20 Figure 2 Range of motion (ROM) apparatus ............................................................27 Figure 3 Passive range of motion apparatus .............................................................28 Figure 4 Tilting perturbations apparatus ..................................................................31 Figure 5 Group averages of active and passive ranges of motion, and stiffness graphs . ......................................................................................................38 Figure 6 Average group traces of trunk corrective movements from the T3 rigid body . ...........................................................................................40 Figure 7 Patterns of muscle activation during forward and rightward tilts ..............42 Figure 8 Normalized EST9 MVC %, 100 ms area data during forward and backward tilting perturbations. ...................................................................................45 Figure 9 Case studies: Tilting kinematics from T3 rigid body of incorrect corrective trunk movements. ......................................................................49 Figure 10 Case study: Muscle response characteristics of an incorrect and correct trunk response to a left tilt. ........................................................................50 ix ACKNOWLEDGEMENTS I would firstly like to thank my supervisor Dr. Mark Carpenter. Mark, I would like to thank you for your patience and encouragement throughout my Masters. I deeply appreciate all you have done for me, and can not thank you enough for taking me on as your first graduate student. Your unwavering support and guidance throughout the past three years has shaped and influenced not only who I am as a researcher but has directly impacted me personally. I am proud to say I am leaving UBC with not only a Masters degree and the accredited qualities that are associated with it, but also a new found outlook at life and personal expectations. I only hope that I am able to bring as much devotion to my future endeavors as you bring to your research and students. To my committee members Dr. Timothy Inglis and Dr. Romeo Chua, I would like to express my gratitude for all your support, encouragement and guidance during my time at UBC. Your informative suggestions and knowledge helped increase the depth of my project. While your caring, friendly natures made it easy to approach both of you with questions no matter how big or small and helped to make this a truly enjoyable experience. I would also like to thank Dr. Inglis for welcoming me and allowing me to be apart of his lab during my first year. To my lab members Adam Campbell, Justin Davis, Chantelle Murnaghan, Brian Horslen and Katie Fukushima, I could have asked for no one better to have shared this experience with and I would like to thank all of you for taking the time to review and edit my thesis, providing helpful suggestions and supporting me. I would also like to thank Melanie x Lam for her friendship and the time she committed to editing and providing feedback on my thesis. This project would not have been possible without the help and support of the recruiting staff at the Pacific Parkinson\u2019s Research Centre. Thank you for all your hard work to ensure we had participants and for seeing the value and importance of this research. To my fellow graduate students, whose names are too many to list, thank you for your support, friendships and many laughs. I would like to thank all my friends and family back in Ontario for their support and kind words, and would specifically like to thank my parents. Their untiring support now and throughout my life has been essential for battling life obstacles and has been the backbone of my success. Thank you for all you have sacrificed and all you have given me. Lastly I would like to thank my husband Andrew Pauhl who selflessly put on hold his academic pursuits so that I could follow mine. His support, love and encouragement were my crutch in times of weakness and were what saw me through to the end. You are a blessing in my life and inspire me to be a stronger person. 1 1. BACKGROUND Idiopathic Parkinson\u2019s disease (IPD) was classically described in 1817 by James Parkinson. An English physician, and paleontologist, James Parkinson described and depicted the classic symptoms of Parkinson\u2019s disease in his book, \u201cAn Essay on Shaking Palsy\u201d. However, it was not until the 1830\u2019s when Wilhelm von Humboldt (1767-1835) self documented, in a series of letters, the progression and development of the disease that it became well known and accepted in the medical profession. However, it still took until the end of the 19th century to be accepted as a special disease (Horowski et al., 1995). Today, the human population is anything but unaware of Parkinson\u2019s disease. With major Hollywood celebrities, such as Michael J Fox, presenting with the disease an increased amount of attention and research has been focused on it; and for good reason. Presently, 10% of the American population is now over the age of 65yrs, and over a million of those individuals are believed to have IPD (Morris, 2000). It is thought that by the year 2020 more than an estimated total of 40 million people world wide will have this disease (Morris, 2000). Though no set cause has been pinpointed as of yet, current thoughts regarding the cause of the disease are extensive and can include; mitochondrial dysfunction and oxidative metabolism, excitotoxins or neurotrophic factors (Lang & Lozano, 1998). Idiopathic nature of Parkinson\u2019s disease Idiopathic Parkinson\u2019s disease (IPD) is known foremost as a progressive movement disorder, resulting from degeneration of dopaminergic cells within the basal ganglia (BG). The BG itself is made up of four main nuclei: (1) striatum (putamen, and caudate); (2) globus pallidus (internal and external segments); (3) subthalamic nucleus and (4) substantia nigra (pars reticulata, and compacta parts). The degeneration of dopaminergic cells, in IPD, has 2 been found to be localized to the substantia nigra pars compacta (SNpc). The major input nuclei of the BG is believed to be the striatum, which receives projections from the frontal cortex and limbic areas. In contrast, the major output nuclei of the BG is the globus pallidus internus (GPi). There are two different pathways within the BG nuclei, the output of which influences the level of cortical excitation in motor control areas via the thalamus. Both pathways originate in the putamen, the main input nuclei in the BG. The \u2018direct\u2019 pathway involves the putamen, and GPi and has a net excitatory effect on the thalamus. The indirect pathway involves the putamen, GPe, sub-thalamic nucleus and GPi, and has a net inhibitory effect on the thalamus. One analogy is to think of these pathways as the \u2018accelerator\u2019 and \u2018decelerator\u2019 respectively. These pathways work in parallel and are regulated by dopaminergic inputs originating from the SNpc to facilitate voluntary movement. In healthy individuals dopamine has an excitatory effect on the direct pathway and an inhibitory effect on the indirect pathway. In this way movements are properly facilitated and can be performed with ease. Conversely, diseases involving dopamine deficiencies, such as IPD, result in decreased activity of the direct pathway enabling the indirect pathway to over activate the GPi due to overly active STN projections (Ferrarin et al., 2004). Degeneration of dopaminergic cells results in motor control deficits. These deficits can range, but are not limited to, shuffling gait, bradykinetic movements, tremors, akinesia, postural instability and increased occurrences of falls (for review see (Jankovic, 2008). In addition to the above stated symptoms of IPD, clinical symptoms present such as reduced flexibility (range of motion \u2013 ROM) (Pedersen et al., 1997) and impaired axial control (such as turning in bed) in IPD patients (Stack & Ashburn, 2006; Steiger et al., 1996). In many 3 cases, patients with IPD present with inconsistent sleep patterns in conjunction with fatigue due to restless night\u2019s sleep (Stack & Ashburn, 2006), and must fully sit up to turn themselves in bed because they lack the ability to rotate their trunk (Stack & Ashburn, 2006). Supplementary Balance Disorders In addition to IPD, there are a number of supplementary balance disorders that despite their IPD symptomatic commonalities (such as those listed above) are quite different in terms of their mechanistic causes. Some of the current parkinsonism movement disorders include corticobasal degeneration, diffuse lewy body disease, encephalitis, vascular parkinsonism, progressive supranuclear palsy (PSP) and Wilson's disease (Lang & Lozano, 1998). For instance, PSP involves the deterioration and death of cells in selected areas of the brain and is not isolated to the BG. Therefore, the possibility exists that balance control deficits seen with PSP may not be directly related to specific BG dysfunction because additional areas of the brain may be affected. Advances in imaging techniques and quality now enable researchers to better understand the neuroanatomical differences that occur with PSP pathology. For instance through magnetic resonance imaging (MRI) researchers have found that PSP patients have an enlarged third ventricle, lower midbrain diameter and a smaller\/thinning quadrigeminal plate compared to patients with IPD (Barsottini et al., 2007). Similarly, post encephalitic parkinsonism symptoms are caused by swelling of the entire brain and the death of cells as the brain is forced into the side of skull. This again speaks to the point that cell death is not localized to the same brain regions in these parallel disorders and concurrent damage in additional cortical sites may be occurring. 4 Treatment Common treatment for IPD can come in two forms; pharmaceutical or through surgical means such as deep brain stimulation (DBS). During early stages of IPD most patients are very receptive to drug therapy, such as levodopa (L-dopa) or other dopamine agonists. These drugs provide relief from the most established symptoms such as bradykinesia, akinesia, tremor and deficits in gait (Ferrarin et al., 2004; Loher et al., 2002; Steiger et al., 1996). However, both trunk and postural control deficits do not benefit from this treatment (Bonnet et al., 1987; Koller et al., 1989; Maurer et al., 2003; Vaugoyeau et al., 2007). Although some studies have observed IPD patients to have a short term benefit from L-dopa treatment on clinical axial measures such as turning in bed (Steiger et al., 1996), over time, as the disease progresses, the effect of L-dopa diminishes and improvements are not as noticeable (Ferrarin et al., 2004; Maurer et al., 2003). As IPD progresses and reaches its more advanced stages and when drug treatment efficacy declines, DBS can be used as a supplement therapy (Hallett & Litvan, 1999) to aid in managing symptoms (Bejjani et al., 2000; Shivitz et al., 2006). DBS involves surgically implanting a stimulating electrode into the GPi or STN. A wire is then passed from the electrode under the skin to a control unit placed subcutaneously below the clavicle. Patients are then capable of triggering the stimulation by placing an additional magnet over the termination unit under the skin. Once triggered DBS results in a decrease in the over active indirect pathway by removing inhibitory output from the GPi to the thalamus, resulting in an improvement in motor performance (Ferrarin et al., 2004; Maurer et al., 2003). However, postural stability does not appear to benefit from DBS and postural responses are slower compared to controls (Shivitz et al., 2006). 5 The current lack of an effective treatment for postural instability and trunk control deficits in patients with IPD, results in patients suffering from an increased risk of falling (Grimbergen et al., 2004). In addition IPD patients adopt inefficient and improper response strategies to balance perturbations. These responses include stiffening their trunk and pelvis through increased co-contraction (Carpenter et al., 2004), narrowing their base of support (Dimitrova et al., 2004b) and limiting and or altering their protective arm movements (Carpenter et al., 2004). When all these factors are combined, IPD patients become severely prone to falls. The importance of better understanding the postural deficits that exist within the IPD patient population is clearly demonstrated by Bloem et al., (2001). In their six month study, 50% of IPD patients reported a fall. Of these individuals 35% suffered a serious injury from the fall or experienced more than one fall over the six month course. Based on these findings it is clear that patients with IPD are prone to falling. Although we are aware of these features of IPD, we do not understand what is causing these deficits to develop, or to what degree these deficits affect balance control. One question that arises from this base level knowledge is whether there is a relationship between decreased trunk control and postural stability in patients with IPD? The following section will review current literature on postural instability of IPD, with the aim to identify potential relationships between postural control and trunk control deficits in IPD. 1.1 Quiet standing Characteristics of standing postural control in a healthy and IPD patient populations For most healthy individuals standing quietly is not a demanding task. As participants maintain a straight upright posture, changes in body position are constantly 6 occurring. Humans continuously sway and change their centre of pressure (COP) as they stand as a means to preserve balance. Such an assumed \u201csimple\u201d task becomes challenging for individuals with balance deficits such as IPD. During the initial stages of the disease patients present with a more backward tilt to their posture. However, as the disease progresses increased muscle rigidity and decreases in ROM begin to set in and patients are observed to have more of a forward lean to their posture (Vaugoyeau et al., 2007). The forward lean is a classical characteristic of IPD known as stooped posture or camptocornia (Umapathi et al., 2002). However, it has also been postulated that camptocornia may be a strategy used by patients to bring themselves away from the direction in which they most often experience falls, backward (Jacobs et al., 2005). Research has found that if asked to close their eyes while standing, patients with IPD will actually move back toward their more feared position, backward. This finding suggests that IPD patients may be consciously maintaining a more forward lean of their trunk (Kitamura et al., 1993) and that camptocornia is more of a postural strategy than it is a direct symptom of the disease. It has also been postulated that myopathy may be a mechanistic cause of camptocornia. The effects of improperly functioning muscle fibers within the trunk and neck extensors, compounded by fat stores replacing depleted muscle and altered motor unit potentials, none of which are common with aging, could possibly account for changes in IPD posture (Schabitz et al., 2003). Not only are there changes in IPD patient\u2019s postural angle, but there are also marked changes in their ability to maintain quiet standing. This is evident from increased COP oscillations and decreased postural limit boundaries (Schieppati et al., 1994). Despite these changes, it is thought that patients with IPD are fairly stable while standing and problems 7 arise when IPD patients attempt to move from a static position to a more demanding motor control scenario. For instance, when asked to perform a \u201csimple\u201d task, such as rising onto their toes, patients have difficulty generating the necessary amount of torque and have delayed centre of mass (COM) responses (Frank, Horak, & Nutt, 2000). 1.2 Anticipatory postural adjustments (APAs) APA characteristics; control population In order for the body to generate a discrete movement or move from a static position such as quiet stance to walking, changes within the body\u2019s centre of gravity are required. These movements result in a disequilibrium of balance (Cuisinier et al., 2005; van der Fits et al., 1998). In anticipation of this upcoming movement, a strategy of activating trunk musculature in the opposing direction of the upcoming events occurs to counteract the expected mechanical affects of the perturbation (Cuisinier et al., 2005; Massion, 1992). The activity seen in the postural muscles has been termed an anticipatory postural adjustment (APA). APAs are temporally and spatially adaptable depending on the speed, displacement, load, symmetry and postural support used during the movement (van der Fits et al., 1998). Research examining APA activity when participants perform various upper limb movements while standing, has been documented in a control population (Lee et al., 1995; van der Fits et al., 1998). In most cases, APA activity while standing is seen in both the leg musculature (rectus femoris, biceps femoris, tibialis anterior, soleus) and trunk superficial musculature (rectus abdominis, and erector spinae) and are direction specific to the upcoming movement (Aruin & Shiratori, 2003; P. Hodges et al., 1999). 8 APA characteristics; IPD population Patients with IPD demonstrate abnormalities when attempting to generate anticipatory muscle action prior to a self generated movement (Frank, Horak, & Nutt, 2000; Lee et al., 1995). Research examining the activity of APAs in a Parkinson population while standing and performing upper limb movements suggests that APA activity is rarely present, approximately 5% of time, compared to 100% of time in otherwise healthy controls (Bazalgette et al., 1987). Similar changes in APAs with IPD are observed during voluntary leg movements (Lee et al., 1995) gait initiation (Martin et al., 2002) and rising to the toes (Frank, Horak, & Nutt, 2000). However, postural adjustments made by patients with Parkinson\u2019s disease appear to be subject to change and depend on the magnitude of the perturbation used to trigger the activity (Aruin et al., 1996). 1.3 Standing reactive postural responses in a healthy age matched control population Biomechanics When we compare self generated movements to standing reactive postural control, a clearer understanding of the balance deficits seen in IPD patients emerges. As would be expected, humans are posturally more stable when self triggering a movement in comparison to having to reactively respond to a perturbation (Nougier et al., 1999). In a laboratory setting, standing reactive perturbations can be generated through either translational or rotational perturbations. Responses to rotational or translational perturbations are typically directionally specific. Current literature regarding the order of muscle activation of these postural responses to a dynamic disturbance is divided. While some believe muscle onsets and balance correcting responses ascend in a distal to proximal fashion (Horak et al., 1996), 9 others have found a more proximal to distal activation order (Allum et al., 2002; McIlroy & Maki, 1995). During anterior-posterior translations or pitch plane rotations, plantar or dorsi flexor torques within the ankle are required to maintain stability. Typically speaking, regardless of perturbation direction, the required torque is generated within the first 150- 200ms following platform movement (Carpenter et al., 2004; Horak et al., 1996). In control participants, the generation of torque is adaptable to both velocity and perturbation amplitude (Horak et al., 1996). Depending on perturbation direction, changes in trunk position are seen. For instance, fast backward perturbations cause a forward inclination of the body (Dietz et al., 1993); whereas a forward, or anterior perturbation, cause the body to become more erect (Dietz et al., 1993). In most cases, trunk responses are seen approximately 100ms following the perturbation (Allum & Honegger, 1992; Carpenter et al., 2004). Quick responses observed in trunk activity stress its importance and contribution to balance correcting activity. As the trunk is a key factor in maintaining postural stability, it can also limit an individual\u2019s ability to respond to a perturbation. This may be due to intersegmental caudo-rostral spinal motion and anatomical restrictions (Preuss & Fung, 2007). The spinal column is designed to have a greater ROM in the sagittal plane. Ligaments, muscle attachments and spinous processes all contribute to stabilizing the spine and in doing so limit it\u2019s ROM in the posterior direction. This makes it more difficult to respond as efficiently to perturbations such as anterior translations. Such anatomical restraints, as well as those associated with other joints such as the ankle; also make it more challenging to respond to perturbations in the medial-lateral direction. Due to limitations in ROM quick movements, such as quick backward movements, cause the CoM to fall outside the base of support and are difficult to recover from. 10 Muscle responses As previously stated, muscle responses to reactive perturbations are typically direction specific and act to oppose the upcoming perturbation. Muscle responses to a backward or posterior perturbation elicit activity in GAS, hamstrings and paraspinals (Horak et al., 1996). Anterior perturbations tend to cause activity in TIB, soleus and biceps femoris (Dietz et al., 1993; Dimitrova et al., 2004b). In comparison to healthy young controls, elderly participants generate atypical responses when the velocity of the posterior perturbation is increased. In instances such as these, elderly participants generate activity in the quadriceps with reciprocal activity occurring between hamstrings and GAS (Horak et al., 1996). 1.4 Standing reactive postural responses in an IPD patient population Biomechanics When perturbed, patients with IPD tend not to produce sufficient amounts of torque in response to the perturbation (Carpenter et al., 2004; Horak et al., 1996). Similar to the negligible effect anti-parkinson medication has on balance control, torque generation is not enhanced nor does it greatly improve while participants are ON anti-parkinsonian medication (Horak et al., 1996). However, patients are capable of scaling torque production to various velocities and small changes in amplitude; although, these changes are not as adequately scaled as those observed in controls (Horak et al., 1996). The limited ability to accurately generate torque is a major concern for IPD patients as this deficit has been found to correlate with a patient\u2019s degree of postural instability (Frank, Horak, & Nutt, 2000), which also declines with disease progression. When IPD patients are required to respond to translational perturbations alternating 11 between a wide and narrow base of support, they are unable to adapt their postural responses correctly (Dimitrova et al., 2004a; Dimitrova et al., 2004b). During instances such as these, IPD patients are most unstable when standing with a narrow base of support (Dimitrova et al., 2004b). This finding is most perplexing considering the fact that patients with IPD naturally adopt a narrower base of support with disease onset and progression. Such an unstable base of support could be one of the factors that contribute to their postural instability. Of great interest is the fact that patients with IPD also respond to perturbations with fewer corrections and modulations in the upper body or trunk compared to controls and when trunk corrections are present they are delayed in onset (Dietz et al., 1993). Their inability to accurately control and modulate trunk activity may be a key factor in explaining and better understanding their postural deficits. These inabilities may be a causal factor to their increased susceptibility to falls. Muscle responses The ability to finely control and modulate postural responses is accomplished by reciprocal asymmetric muscle activation based on multi-sensory afferent information. The inability to effectively incorporate these two aspects of balance control can cause an individual to become prone to postural imbalances and falls. This inability is one of the fundamental deficits that persist in patients with IPD. Although their muscle onsets to reactive perturbations are similar to those of healthy age matched elderly controls (Horak et al., 1996), patients with IPD react to dynamic perturbations with symmetrical co-activation of both agonist and antagonist muscles (Carpenter et al., 2004; Dietz et al., 1993; Dimitrova et al., 2004a; Dimitrova et al., 2004b; Horak et al., 1996). Additionally, they have tendencies 12 to activate antagonist muscles earlier than agonists especially when perturbed at higher velocities (Dietz et al., 1993; Dimitrova et al., 2004a; Dimitrova et al., 2004b; Horak et al., 1996). These tendencies are not only seen in the lower musculature, but also in the trunk (Dimitrova et al., 2004b; Horak et al., 1996). These unfavorable postural responses create a situation where postural modulation is not feasible as the trunk becomes more rigid. This stiffening strategy is exacerbated as the magnitude of the response is increased beyond typical balance limits (Carpenter et al., 2004; Dimitrova et al., 2004a; Dimitrova et al., 2004b). Atypical muscle responses are common among all perturbation directions indicating that the greater instability observed in lateral and backward perturbations could in part be due to biomechanical limitations (Dimitrova et al., 2004b). The importance and impact of sensory information on postural responses, especially for patients with IPD, becomes clear when a given sensory system is removed. When required to respond to perturbations with no vision, IPD patients lose the ability to make a reactive counter movement. The dependency these individuals place on the visual system is evident and could possibly aid in explaining their overactive use of antagonist flexor muscle activity versus agonist extensors. Flexor muscles have been found to be directly affected and modulated by visual information in comparison to extensors (Dietz et al., 1989; Dietz et al., 1992; Dietz et al., 1993). Although this evidence supports the improper and detrimental balance correcting strategies employed by patients with IPD, it is difficult to isolate where the deficits are originating. It is also unclear whether the body as a whole is improperly responding or whether one segment is the main contributor to postural deficits. Literature to date has 13 focused on the contributions and reactions made by the lower limbs to dynamic perturbations, while little emphasis has been placed on the relative contributions made by the trunk. Because there is such a dominant bias and focus on dynamic balance control research on the lower limbs, it is not known how the trunk alone, irrespective of the lower limbs, responds to dynamic balance disturbances especially in a patient population such as IPD. Furthermore, it is not known how atypical muscle activity in the trunk could be contributing to an overall decreased ability to maintain balance. The following section reviews the limited research of trunk control during dynamic perturbations in both control and patient populations. 1.5 Seated postural responses in a healthy age matched control population Seated postural responses in a control population Completely isolating the trunk is not an easy task. In different seated paradigms participants may sit with their feet resting on either the apparatus surface itself (Forssberg & Hirschfeld, 1994), on low friction surface (Zedka et al., 1998), or secured to a chair (Preuss & Fung, 2007). It is also common for participants to sit self supported with their legs free to hang from the support surface (Martin, 1965). Despite the differences in apparatus set up, each paradigm directly assesses one\u2019s ability to dynamically control their balance with almost complete isolation of the trunk. Feedforward and feedback reactions An additional way to gain insight into the relative contributions of the trunk in postural control is to have participants perform dynamic balance tasks such as maintaining 14 balance on a wobble board. In contrast to reactive perturbations, such as those mentioned above, this paradigm requires participants to use both feedforward and feedback control methods to maintain postural stability and balance. The balance aspect of this task is different in that the participant must actually balance\/stabilize the support surface instead of their body position relative to the support surface. During acts of dynamic balance control, an increased difficulty in maintaining balance in the medial-lateral direction during sitting (Cholewicki et al., 2000) could reflect inadequate feedback processing to modulate phasic muscle activation patterns. Important factors that contribute to an individual\u2019s ability to maintain postural control, especially in this scenario, are trunk length and body weight. Individuals who are longer in the trunk and are greater in weight have an increased difficulty stabilizing themselves during such challenging feedforward feedback balance scenarios (Cholewicki et al., 2000). A raised COM combined with a greater body weight to support requires increased muscular force to overcome the torque generated at the hip joint. Unsuccessful force or muscle pattern generation would otherwise provide ample freedom for the COM to deviate from outside of the base of support and a less stable and unsuccessful trial could occur. Biomechanics of seated postural adjustments in a control population Whether translational or rotational perturbations are given, one of the cardinal characteristics observed across subjects is rotation of the pelvis following a flexion or extension of the hip joint respectively. Backward or forward tilts of the pelvis, seen during forward translations or legs up rotations and backward translations or leg down rotations respectively, are consistently observed within milliseconds of platform movement (Forssberg 15 & Hirschfeld, 1994; Hirschfeld & Forssberg, 1994; Preuss & Fung, 2007). Based on what little research there is, it is hypothesized this pelvic activity triggers the pattern of postural response required to compensate for rotational perturbations (Forssberg & Hirschfeld, 1994; Hirschfeld & Forssberg, 1994). The initial trigger is thought to act in a manner similar to that of a central pattern generator (CPG) as seen with gait. Further shaping of the response occurs based on previous experience (ie internal models) and the integration of sensory information arising from changes in such as head orientation\/position (Forssberg & Hirschfeld, 1994; Hirschfeld & Forssberg, 1994). Changes in trunk position, as seen through changes in thorax positioning, occur following rotations of the pelvis (60-70ms) (Forssberg & Hirschfeld, 1994). Those responses described above for toe up rotations or forward translations are also accompanied with a downward acceleration, then backward rotation of the head. Toe up and backward translations are subject to greater response variability (Forssberg & Hirschfeld, 1994). Though sequences of body segment responses are somewhat similar between rotational and translational perturbations there are a few variations. For instance, changes in hip responses are seen depending on perturbation type. Forward translations of a platform cause an extension of the hip joint, while leg up rotations cause a flexion of the hip joint. Similarly, movements of the head and thorax are in the backward direction during a forward translation, but are in a forward direction during a leg down rotation (Forssberg & Hirschfeld, 1994). Changes in biomechanical characteristics between these two perturbation types should not be unexpected as each possesses different restraints on the responding muscles. That is, translation perturbations cause stretch reflexive responses in the same muscles that are required to counteract the perturbation, whereas rotational perturbations do not stretch those 16 muscles required to maintain stability and balance. The advantage of using rotational perturbations is that there is a clear onset of muscle activity indicative of the actual balance correcting response. In contrast, muscle response onsets during translation perturbations have onsets that are intermixed with stretch reflexive activity. Directional activity of seated postural muscles and muscle characteristics Seated participants have a greater degree of background, or tonic, activity in the dorsal muscles (erector spinae (ES), latisimus dorsi (LD)) compared to ventral muscles such as external and internal oblique and rectus abdominis (Zedka et al., 1998). Similar to what would be expected during standing (Preuss & Fung, 2007), seated postural muscle activity is dependent on the direction of the perturbation. When participants are seated and translated quickly forward or given a legs up rotational perturbation, activity of more ventral muscles (ie. rectus abdominis (RA) and internal and external obliques (IEO) are seen while dorsal muscles (ie ES or paraspinal muscles) relax (Forssberg & Hirschfeld, 1994; Zedka et al., 1998). Following the perturbation a gradual increase in dorsal muscle activity is representative of postural correcting or long latency muscle responses. In some instances, activity of rectus femoris (RF) has been found to precede activity in ventral muscles in response to a quick leg up rotation. The trigger for this activity may originate from fast flexion of the hip created by the perturbation (Forssberg & Hirschfeld, 1994). Early onset of this muscle activity may also be indicative of a stabilizing strategy used to limit rotation of the pelvis. The similar directional sensitivity seen during fast leg up rotations is additionally seen during legs down. However, the decrease in muscle activity seen in the ventral muscles 17 during a forward rotation (legs down) is not as great as that seen in dorsal muscles during backward (leg up) perturbations (Zedka et al., 1998). As well, stretch reflexive activity is not as apparent, nor is a consistent muscle pattern maintained (Forssberg & Hirschfeld, 1994). With respect to fast rotational perturbations in the frontal plane, muscle activity increases in those muscles contralateral to the perturbation while ipsilateral muscles become more relaxed (Zedka et al., 1998). That is, if a leftward perturbation were to be given, left ES (antagonist) activity would decrease while the right ES (agonist) activity would increase. In conjunction, after the initial perturbation, phasic muscle activity occurs between these two agonist and antagonist muscles (Zedka et al., 1998). The directional specificity that is seen with respect to activation patterns of these muscles is not unexpected. A tilt to the left would not be well compensated for with increased left ES activity as this would further destabilize the participant and pull them in the direction of the perturbation instead of counteracting it. Also, modulation of such a quick response in a phasic manner is advantageous as a more accurate and specific response can be generated to countermand the perturbation. Unlike dorsal muscles, ventral muscle activity (RA) during frontal plane perturbations do not demonstrate phasic muscle activation patterns (Zedka et al., 1998). The uncharacteristic responses seen in the ventral muscles could be related to their role in ventilation (Hodges et al., 2007). For the most part a similar pattern of direction specific muscle activation is seen during translational seated perturbations (Forssberg & Hirschfeld, 1994). However, there are small differences in muscle responses between rotations and translation perturbations. For instance, rotational perturbations elicit some dorsal muscle activity first (RF) during legs up rotations prior to ventral muscles, translated perturbations generate initial responses in the 18 ventral muscles as a whole prior to dorsal muscle activity (Forssberg & Hirschfeld, 1994). Variations in neck muscle onsets also occur. Neck flexors have an early onset time during forward translations (Forssberg & Hirschfeld, 1994). In contrast, legs up rotations elicit early onset times in neck extensors. In general neck muscle activity and the changes seen with it, correspond well to opposing the movement generated from the trunk and head (Forssberg & Hirschfeld, 1994). Influences on seated postural responses The speed of a perturbation does appear to impact muscle activation patterns. Slow backward perturbations (legs up rotation) induce stretch reflexive muscle activity in the dorsal muscles, while a more gradual increase in ventral or abdominal muscles are seen. This is in contrast to what is seen during the quick large bursts of muscle activity during a fast perturbation. Forward rotations (legs down) at this slower speed cause parallel and gradual increases in both dorsal and ventral muscle activations. A phasic muscle activation response in the frontal plane diminishes while the directionally specific pattern of muscle activity remains constant (Zedka et al., 1998). In contrast, the impact manipulations to vision and expectancy of a perturbation do not seem to influence muscle activation patterns while seated in a control population (Zedka et al., 1998). An additional factor that does not appear to influence muscle activation patterns during seated rotational perturbations is participant\u2019s body position relative to the axis of rotation. Changing participants seated position relative to the axis of rotation does not alter muscle activation patterns despite changes in head acceleration that this causes (Forssberg & 19 Hirschfeld, 1994). Because of this, the relative contribution of the vestibular system in coordinating a postural adjustment in these paradigms remains unclear. Although we appear to have some understanding regarding seated postural control, when we compare this to what is documented in the field of standing balance, relatively speaking, little is actually known. As this field advances the importance of trunk control in maintaining balance and postural stability is becoming more apparent. Especially when looking at populations with balance deficits such as patients with Parkinson\u2019s disease. With that stated, it is necessary to point out the fact that even less is known regarding trunk control in this clinical population. The following sections outline what information is currently available with respect to seated trunk control in an IPD patient population. 1.6 Seated postural responses in an IPD patient population Feedforward and feedback reactions Previous research by van der Burg (2006) observed IPD patients changes in COP measures during a postural feedforward and feedback task. From these data a general understanding of how muscle activation may be coordinated to maintain dynamic seated balance can be formulated. When required to balance using the wobble board paradigm, van der Burg et al (2006) observed that patients demonstrated increased COP excursions in combination with increased medial-lateral (ML) root mean square (RMS) values and decreased mean power frequency (MPF) values. These data demonstrate the large variability and lack of trunk control in IPD patients. As previously mentioned delays in balance correcting adjustments and greater COP excursions may be reflective of decreased asymmetrical muscle activation. As much as this study demonstrates IPD patient\u2019s inability 20 to properly maintain balance and trunk control, it does not reflect their ability to reactively respond to an external perturbation because this task requires both feedforward and feedback information processing while a reactive perturbation task does not. Biomechanics of seated postural adjustments in an IPD patient population Martin (1965) investigated postural responses in patients with post encephalitic Parkinson\u2019s (PEP) disease, among other patient groups, while patients were seated on a manually tilted bed (Figure 1). Following the perturbation in the seated condition, patients appeared to have no postural response and would fall or tip in the direction of the tilt (Figure 1B). In contrast, a healthy control participant would have a balance correcting response in the opposing direction of the tilt (Figure 1C). Directional activity of seated postural muscles and muscle characteristics Despite the need to gain an increased understanding of muscle activity in the trunk within this patient group, research to date is limited. With this stated, when attempting to better understand the muscle responses during a seated paradigm, one could make sound Figure 1: Tilting reactions from Martin (1965) These figures illustrate the trunk responses of subjects with; (A) complete loss of labyrinthine function, (B) a post-encephalitic Parkinsonian patient and (C) control participant as observed by Martin (1965). A B C 21 hypotheses based on our knowledge of muscle activation patterns during standing reactive perturbations. However, these data are neither specific nor detailed enough to truly understand the deficits that may exist within the trunk and how balance responses vary depending on the postural condition (ie standing or sitting) (Preuss & Fung, 2007). Although there have been studies investigating the relationship between bimanual limb coordination, trunk control (Tunik et al., 2004) and functional reaching tasks (Poizner et al., 2000; Stack et al., 2005) in patients with IPD. This research does not directly isolate reactive trunk responses, but provides insight, more so, into the degree of stability that is required in the trunk in order to have a stable base from which to execute such movements. Although no direct measures of EMG activity are available, one could draw from the previous work of Martin (1965) to predict the patterns of muscle activations that may occur during a seated reactive perturbation. Based on the responses made during the perturbation, falling in the direction of the tilt, one could hypothesize that patients with IPD may have responded with a similar muscle activation pattern as seen in response to perturbations while standing. These muscle activation patterns may include co-contraction (symmetrical muscle activation) and or insufficient muscle modulation (Carpenter et al., 2004). These factors, coupled with the decreased ROM and increased resting tonic muscle activity observed in patients with IPD, could have caused the trunk to stiffen. Therefore, this stiffening may have facilitated falling in the direction of the tilt. Such an explanation for the observed responses may more accurately account for the documented postural responses than those proposed by the author. Martin (1965) suggests that the lack of postural response witnessed in PEP patients was due more to a complete lack of labyrinthine function than basal gangliar dysfunction, and as such, tilting reactions would be an efficient means by which to test 22 pallida integrity. Martin\u2019s (1965) interpretations of his results were based on the fact that PEP patient responses simulated those of patients tested with complete loss of labyrinthine function (Figure 1A). In either case, the fact that an anecdotal hypothesis is required to currently explain trunk activity and its contribution to balance control in patients with IPD highlights the need to further expand our understanding in this field of research. Limitations of current seated perturbation research in both control and patient populations Not only is research investigating seated postural responses in patients with IPD limited in the amount of information available, but much of the current literature is limited in their design consistency. Perturbing and isolating the trunk specifically is challenging. To do so requires a machine or technique that is able to perturb a participant with a consistent velocity and amplitude. In attempts to substitute or make due with limited equipment, perturbations have been elicited manually by an experimenter. In the study by Martin (1965) patients sat on a bed while a researcher would hold onto the corner and pull the bed upward or downward. Inconsistencies in force generation could have greatly influenced both the degree and type of postural response elicited by all participants within the study. A similar limitation has also been observed in control research (Zedka et al., 1998). As mentioned previously, when recruiting clinical populations, especially IPD, distinguishing between disorders that present with similar symptoms as IPD and true IPD is required. During Martin\u2019s study post encephalitic Parkinson\u2019s patients were tested instead of IPD patients. As stated in the clinical section, the issue with generalizing the Parkinsonian symptoms, as caused by an ailment, is that it\u2019s effects are not isolated specifically to the basal ganglia and additional neurological deficits may be present. 23 1.7 Influences on postural responses Effects of fear Besides the aforementioned influences on seated postural control, fear of falling can also greatly impact a patient\u2019s ability to maintain balance. The effect of fear of falling and or anxiety on postural control has not only been documented during seated responses in an IPD patient population (van der Burg et al., 2006), but also during standing (Adkin et al., 2003). During seated balance tasks, patients with IPD demonstrate an increased fear of falling not only through increases in COP excursions, but decreases in MPF when compared to \u201cnon-fearful\u201d patients and controls (van der Burg et al., 2006). If seated balance performance as measured by COP and MPF data are compared to what is currently known with respect to standing balance literature in a healthy population an inconsistent result is seen. During times of higher anxiety (or increased fear of falling) while standing, control participants COP excursions decrease, and their MPF increases creating a quickly gyrating inverted pendulum (Adkin et al., 2000; Carpenter et al., 1999; Carpenter et al., 2001). Similarly, a reduction in COM displacement is observed even when responding to tilt during high threat\/anxious situations (Carpenter, Frank et al., 2004). The inconsistent findings between patients and controls may be related to their response characteristic of increased symmetric muscle activation. This would limit their ability to make fast corrective movements, and could result in the larger COP traces seen. Better understanding postural stability and trunk control as it relates to falls is important not only to IPD patients but to healthy elderly populations as well. During 2001 an estimated 15,000 individuals died due to fall related injuries. The cost of falls alone in the USA reached 20 billion dollars in 2001 and is only expected to rise over the years to come 24 (Bloem et al., 2003). The importance of better understanding the contributing factors to falls and developing ways to prevent them is not just important economically for our health care system, but is also important for ensuring and maintaining overall quality of life. The lack of supporting data, specific to trunk muscles, in a reactive paradigm in an IPD patient population and its contributing role in balance control and fall prevalence is clear. In an attempt to further this field of research and replicate or refute previous findings, such as those by Martin (1965), the study proposed here aims to investigate trunk muscle responses in an idiopathic Parkinson\u2019s disease population and healthy age matched controls while seated. 1.8 Hypotheses On the basis of previous literature we hypothesize that during seated tilting perturbations: (1) Relative muscle response patterning in patients with IPD will be similar to that of controls. (2) The magnitude of IPD patients postural muscle activity will be modulated incorrectly, and over amplified. (3) Patients with IPD will have a greater degree of postural instability in the medial-lateral (left, right), and backward directions. (4) Lastly, IPD patient\u2019s range of motion will be decreased in both sagittal and frontal planes. 25 2. METHODS 2.1 Subjects Seven individuals diagnosed with Idopathic Parkinson\u2019s disease (IPD) according to the UK Brain Bank criteria (Hughes et al, 1992) and 10 otherwise healthy age-matched controls, recruited from a local community program, volunteered to participate in this study (Table 1). Disease severity was assessed using the Unified Parkinson\u2019s Disease Rating Scale (UPDRS) and Hoehn and Yahr scale. Inclusion criteria for both control and patient groups were the following: 1) being able to stand and sit independently without external support, and 2) be free from any additional confounding neurological impairments such as vestibular imbalance or orthopedic pathologies of the hip or spine. Furthermore, patients with IPD had to have been classed Table 1: Demographic and disease characteristics of controls and patients with IPD The numbers associated with each medication represent the number of patients that were on that medication at the time of testing. Significant differences between groups are represented by (**). Values in parenthesis represent the standard deviations, with the exception of No. women whose value in parenthesis represents the percentage of women that participated in that group. Patients Controls (n = 7) (n = 10) Age (years) 70.4 (7.59) 68.4 (6.0) No. of women 3 (42%) 5 (55%) Height (m) 1.7 (0.09) 1.7 (0.09) Weight (lbs) 172 (44.5) 149.6 (33.7) Trunk length (cm) 50.4 (6.0) 49.35 (4.1) Duration of disease (years) 8.0 (3.2) - No. of falls in the past 6 months 4.7 (9.6) 0.1 (0.3) Fear of falling (%) 22.1 (23.8) 7.8 (11.7) UPDRS score 35 (9.0) - Hoehn and Yahr stage 2.5 (0.41) - Medication Sinemat 4 (57%) - Sinemat CR 3 (43%) - Mirapex 3 (43%) - Synthroid 1 (14%) - Hydrozine 1 (14%) - Propranolol 1 (14%) - Comtan 1 (14%) - 26 between 1.5 \u2013 3.0 on the Hoehn and Yahr scale. IPD participants were asked to take their normal anti-Parkinson medications one hour prior to arriving for their testing session to ensure an optimal \u201cON medication\u201d state was achieved during the testing session. All procedures were approved by the University of British Columbia ethics review board and participants provided their informed consent prior to participating in the study. Prior to the experiment, participants fear of falling and fall histories were assessed using a series of verbal questions including: \u201c1) Have you ever fallen? 2) If yes, can you recall how many times you have fallen in the past 6 months?; and 3) Rate your fear of falling on an incremental scale from zero to one hundred, where zero is not fearful and one hundred is very fearful.\u201d In addition, we recorded participants\u2019 height, weight, age and trunk length measured from the first thoracic vertebra (T1) to the top of the sacrum (Table 1). 2.2 Active and passive ranges of motion (ROM) 2.2.1 Setup Participants were positioned atop a customized swivel table with foam support on either their back (to test frontal plane ROM) or on their right side (to test sagittal plane ROM). Their hips were positioned at the most superior edge of the fixed portion of the table while their trunk was positioned onto a trunk support table (21.5\" x 16\"). As shown in Figure 2, the trunk support board moved freely around a base table (61.5\"x 49\") covered with nylon balls, 1\/2\" in diameter, to create a nearly frictionless surface (Parkinson, 2004). The trunk support board was positioned so that its inferior edge was aligned with the eleventh thoracic vertebra (T11), ensuring similar placement across participants. Stabilizing straps were placed across participants\u2019 hips, thighs and chest. A rigid body was mounted onto a 27 wooden dowel at the upper right hand corner of the trunk support (Figure 2), and an Optotrak Certus motion sensor (Northern Digital Inc, Waterloo) was positioned behind the swivel table. The trunk support could translate freely (for active ROM) or be pulled by a cable attached at one end to the upper right or left hand corner of the trunk support for passive ROM. This cable was attached to a weighted pulley system that could be lowered manually. 2.2.2 Procedure Once positioned on the swivel table, participants completed all of the required ROM tests in one plane (frontal; left and right lateral trunk flexion) before continuing in the second plane (sagittal; on their right side; for trunk flexion and extension). Measures of active and passive ROM as well as corresponding measures of relative trunk stiffness were performed in each test direction. Movement direction and task (active\/passive) were counterbalanced across subjects. Active ROM tests were performed 3 times in each direction and required participants to voluntarily bend their trunk to their perceived end ROM. To help relax Figure 2: Range of motion (ROM) apparatus (A) Depiction of swivel table apparatus for measuring ROM and trunk stiffness. The freely moving trunk support is shown on top the white base support square table. Images (B) and (C) are depictions of participant positioning during frontal and sagittal plane movements, respectively. As illustrated in (B) and (C) support straps were placed across participants chest, pelvis and tigh. C B A 28 participants prior to the initiation of each trial, they were instructed to inhale and slowly release their breath (Mak et al., 2007). During passive ROM testing, participants were additionally instructed not to aid or resist the movement. To calculate passive ROM and relative trunk stiffness, incremental weights, applied from lightest to heaviest (2.5lbs, 5lbs, 7.5lbs, 10lbs, 17.5lbs) were secured to the pulley system, and slowly lowered manually by the researcher. A baseline pull angle, relative to the trunk support board and cable, of 45\u00b0 was used while pulling participants in the frontal plane during left and right lateral trunk flexion and sagittal backward extension. During passive sagittal forward trunk flexion tasks, a baseline pull angle of 25\u00b0 was used (Figure 3). (A) Figure 3: Passive range of motion apparatus (A) Depiction of experimental setup during passive left frontal plane ROM. (B) Depiction of experimental setup during passive backward extension ROM in the sagittal plane. Similar to active ROM testing, support straps were placed over the participants\u2019 chest, hips, and thighs. The white arrow in each image indicates the cable that was attached to pulley system and trunk support and has been outlined in white as well. In both (A) and (B) the cable is attached to the upper left hand corner of the trunk support. For both right frontal plane and forward sagittal plane flexion the cable was attached to the upper right hand corner of the trunk support. The red arrows point to the weights which were attached to the pulley system and lowered by a researcher. (B) 29 Baseline angles of pull were chosen based on pilot testing and were the most accurate representation of participants\u2019 active path of motion. The first four weights were lowered to a point where they were able to hang freely (if the 5th weight was too heavy, it was slightly supported by the researcher) and the position was held for three seconds. The weight was then lifted slowly upward, removed and the subsequent weight added. If the participant reached their end ROM during implementation of one of the lower weights, as confirmed through their verbal report, subsequent weights were not added. The greatest weight combination was used to determine the participants end ROM. If end ROM was not achieved with the maximum weight (17.5lbs) a manual pull trial was performed. 2.2.3 Measures and data analysis Peak active and passive ROM (deg) values were determined from the positional data collected from the mounted rigid body placed on the dowel on the trunk support. The rigid body consisted of four infra-red light emitting diodes that were recorded by an Optotrak Certus motion sensor with a sampling frequency of 50Hz. Before each task, a resting 3 sec control trial was collected with the participant lying as straight and relaxed as possible. The maximum active and passive ROM was calculated by subtracting the resting mean from the maximum angular displacement recorded for each trial, and then averaged across trials for each subject. Incremented passive stiffness values were measured as the slope of the force (N) versus displacement (deg) curve (Panjabi, 2003) as determined from the last three maximum weights applied during passive ROM. 30 2.2.4 Statistical analysis Non-parametric statistical analysis was used to account for small and uneven sample sizes and non-normally distributed data. Maximum ROM and stiffness values were ranked then analyzed using a 2x2 (group x direction) analysis of variance (ANOVA) for frontal and sagittal planes independently with a p-value of 0.05. Significant trends were considered for 0.05