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Force Modulation Deficits in Chronic Stroke

Permanent Link: http://ufdc.ufl.edu/UFE0041222/00001

Material Information

Title: Force Modulation Deficits in Chronic Stroke Grip Formation and Grip Release Phases
Physical Description: 1 online resource (110 p.)
Language: english
Creator: Naik, Sagar
Publisher: University of Florida
Place of Publication: Gainesville, Fla.
Publication Date: 2009

Subjects

Subjects / Keywords: grip, hand, severity, stroke
Applied Physiology and Kinesiology -- Dissertations, Academic -- UF
Genre: Applied Physiology and Kinesiology thesis, M.S.
bibliography   ( marcgt )
theses   ( marcgt )
government publication (state, provincial, terriorial, dependent)   ( marcgt )
born-digital   ( sobekcm )
Electronic Thesis or Dissertation

Notes

Abstract: The aim of the present study was to elucidate force modulation deficits in various grip phases in chronic stroke and to develop an algorithm to quantify stair-stepping phenomenon. Nine chronic stroke participants (age = 66.39 plus or minus 9.84 years), nine age-matched healthy adults (age = 66.38 plus or minus 8.31 years), and 10 young adults (age = 22.65 plus or minus 2.94 years) performed a submaximal isometric power grip tracking task. The task consisted of ramp up and down at 5% MVC/s, 10% MVC/s and 20% MVC/s rates. The peak force was set at 35% MVC for all rate trials. Analyses of root mean square error, standard deviation, number of steps, and number of steps with larger step widths revealed three critical findings 1) stroke leads to force modulation deficits for the grip release phase of both hands (affected and less-affected), 2) developed novel approach in quantifying stair-stepping phenomenon while explore possible mechanisms responsible for force modulation deficits in various grip phases, and 3) high functioning stroke survivors showed greater deficits in the grip release phase, whereas low functioning stroke survivors showed greater deficits in grip formation phase. Collectively, these findings carry significant implications for stroke rehabilitation by differentiating low functioning and high functioning stroke individuals with impairments in different grip phases. Further, potential mechanisms that account for the impairments in the grip phases were discussed and these increased our understanding of stair-stepping phenomenon in aging and stroke.
General Note: In the series University of Florida Digital Collections.
General Note: Includes vita.
Bibliography: Includes bibliographical references.
Source of Description: Description based on online resource; title from PDF title page.
Source of Description: This bibliographic record is available under the Creative Commons CC0 public domain dedication. The University of Florida Libraries, as creator of this bibliographic record, has waived all rights to it worldwide under copyright law, including all related and neighboring rights, to the extent allowed by law.
Statement of Responsibility: by Sagar Naik.
Thesis: Thesis (M.S.)--University of Florida, 2009.
Local: Adviser: Cauraugh, James H.

Record Information

Source Institution: UFRGP
Rights Management: Applicable rights reserved.
Classification: lcc - LD1780 2009
System ID: UFE0041222:00001

Permanent Link: http://ufdc.ufl.edu/UFE0041222/00001

Material Information

Title: Force Modulation Deficits in Chronic Stroke Grip Formation and Grip Release Phases
Physical Description: 1 online resource (110 p.)
Language: english
Creator: Naik, Sagar
Publisher: University of Florida
Place of Publication: Gainesville, Fla.
Publication Date: 2009

Subjects

Subjects / Keywords: grip, hand, severity, stroke
Applied Physiology and Kinesiology -- Dissertations, Academic -- UF
Genre: Applied Physiology and Kinesiology thesis, M.S.
bibliography   ( marcgt )
theses   ( marcgt )
government publication (state, provincial, terriorial, dependent)   ( marcgt )
born-digital   ( sobekcm )
Electronic Thesis or Dissertation

Notes

Abstract: The aim of the present study was to elucidate force modulation deficits in various grip phases in chronic stroke and to develop an algorithm to quantify stair-stepping phenomenon. Nine chronic stroke participants (age = 66.39 plus or minus 9.84 years), nine age-matched healthy adults (age = 66.38 plus or minus 8.31 years), and 10 young adults (age = 22.65 plus or minus 2.94 years) performed a submaximal isometric power grip tracking task. The task consisted of ramp up and down at 5% MVC/s, 10% MVC/s and 20% MVC/s rates. The peak force was set at 35% MVC for all rate trials. Analyses of root mean square error, standard deviation, number of steps, and number of steps with larger step widths revealed three critical findings 1) stroke leads to force modulation deficits for the grip release phase of both hands (affected and less-affected), 2) developed novel approach in quantifying stair-stepping phenomenon while explore possible mechanisms responsible for force modulation deficits in various grip phases, and 3) high functioning stroke survivors showed greater deficits in the grip release phase, whereas low functioning stroke survivors showed greater deficits in grip formation phase. Collectively, these findings carry significant implications for stroke rehabilitation by differentiating low functioning and high functioning stroke individuals with impairments in different grip phases. Further, potential mechanisms that account for the impairments in the grip phases were discussed and these increased our understanding of stair-stepping phenomenon in aging and stroke.
General Note: In the series University of Florida Digital Collections.
General Note: Includes vita.
Bibliography: Includes bibliographical references.
Source of Description: Description based on online resource; title from PDF title page.
Source of Description: This bibliographic record is available under the Creative Commons CC0 public domain dedication. The University of Florida Libraries, as creator of this bibliographic record, has waived all rights to it worldwide under copyright law, including all related and neighboring rights, to the extent allowed by law.
Statement of Responsibility: by Sagar Naik.
Thesis: Thesis (M.S.)--University of Florida, 2009.
Local: Adviser: Cauraugh, James H.

Record Information

Source Institution: UFRGP
Rights Management: Applicable rights reserved.
Classification: lcc - LD1780 2009
System ID: UFE0041222:00001


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1 FORCE MODULATION DEFICITS IN CHRONIC STROKE: GRIP FORMATION & GRIP RELEASE PHASES By SAGAR K. NAIK A THESIS PRESENTED TO THE GRADUATE SCHOOL OF THE UNIVERSITY OF FLORIDA IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR T HE DEGREE OF MASTER OF SCIENCE UNIVERSITY OF FLORIDA 2009

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2 2009 Sagar K. Naik

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3 To my Parents and Sister

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4 ACKNOWLEDGMENTS I have had the opportunity to work with well renowned researchers in their respective fields ove r the past two years. These individuals with their constant guidance have helped me to grow, and develop into a person I am today. This journey would not have been completed without the support of following people. I would like to express my sincere gratit ude to my advisor, Dr. James H. Cauraugh for his patience, motivation, encouragement during my graduate school training and financial support in completing this research project. Dr. Cauraugh has been abundantly helpful, and assisted me in developing writi ng skills and recruiting participants for the project. I have also had the pleasure of working with Dr. Carolynn Patten during this process and I am eternally grateful for her contribution in the entire project. The inception of the project from the raw th ought began from her invaluable inputs, and she has shown full enthusiasm about the project from the beginning to end. Her ability to explore beneath the text is a true gift, and her insights have strengthened this project significantly. Along the journey, Dr. Patten allowed me to join her laboratory meetings and now to Neural Motor Laboratory to develop new skills, which helped me to understand importance of clinical reasoning and mechanisms of stroke rehabilitation. I would also like to thank Dr. Christopher Janelle, for his encouragement and feedback throughout my time as a graduate student. I am highly thankful to Dr. Stephen Coombes at University of Illinois at Chicago, for allowing me to work on his study, which laid the foundation of all most important qualitative research skills in me. H is enthusiasm for his work and compassion for others has been inspiring. I thank Dr. Coombes for his incredible support, confidence and guidance throughout my project. Occasionally, we shared good memories of cricket ( the

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5 game, we both loved) during our journey. I would like to share this joyfulness with my colleague, Neha Lodha, for always helping and providing valuable inputs for my research project. I am very grateful to Neha and her husband, Gaurav Mishra, for their genuine care and assistance when I thought I did not need any. I want to thank Foi and Fhuvaji, Mrs. Smita and Mr. Shamir Desai and their daughter Shruti, who helped me with their love and kind support to get settled in United States after leaving my home country, I ndia for first time after 24 long years. I truly think I would not have completed the journey successfully without their presence I also want to recognize Amit Verma, who helped me in developing excel skills for data analysis. I would also lik e to thank Dr. Saravanan and Dr. Prerana (The Sarvajanik College of Physiotherapy, India), who showed unconditional support and encouraged me to pursue thesis based masters degree in motor control and learning and influenced my decision to come to the Uni versity of Florida. Without their confidence in my abilities, I am sure I would not be where I am today. My family has been the backbone of my life. I thank my mummy and papa, Kalpanaben and Kiritbhai Naik, for their patience and understanding as I pursued a dream to learn more about the body and mind. Many thanks goes to my lovely sister and brother in law, Rima and Jwalant Naik; my aunty and uncle, Jayshreeben and Janakbhai Naik; my cousins, Chintan, Bhargav, Durva, Vidhi, Chandni and Deep; my both Masi and Masaji; my evergreen grandfather, Nanubhai Naik; and my grandmother, Rekhaben Naik, whom I miss. I would like to whole heartily thank Kina Chanasana and her family, for their patience and believing in me, since we met six years ago. My parents, sister R ima and Kina have always supported my decisions and walked along

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6 side me during my entire journey. At times, it has been good to know they have just been a video call away, thanks to Skype. With all their love and encouragement, I complete this journey and begin another. Lastly, but by no means least, I wish to thank all my participants for their time and commitment to this project. I truly believe I learn from everyone I meet, and I know I will continue my journey of enhancing knowledge throughout the res t of my life.

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7 TABLE OF CONTENTS page ACKNOWLEDGMENTS .................................................................................................. 4 LIST OF TABLES ............................................................................................................ 9 LIST OF FIGURES ........................................................................................................ 10 LIST OF ABBREVIATIONS ........................................................................................... 12 ABSTRACT ................................................................................................................... 13 CHAPTER 1 INTRODUCTION .................................................................................................... 15 Stroke and Upper Extremity Function Post Stroke ................................................. 15 Grasping/Gripping Function and Stroke .................................................................. 16 Force Control in Aging and Stroke .......................................................................... 18 Aim, Hypothesis and Significance ........................................................................... 23 Aim ................................................................................................................... 23 Hypothesis ........................................................................................................ 24 Significance ...................................................................................................... 24 2 METHODS .............................................................................................................. 25 Participants ............................................................................................................. 25 Clinical Assessment Tools ...................................................................................... 26 Modified Ashworth Scale .................................................................................. 26 Box and Block Test .......................................................................................... 26 Upper Extremity subset of the Fugl Meyer Motor Function Assessment .......... 26 Mini Mental State Examination ......................................................................... 26 Instrumentation ....................................................................................................... 27 Experimental Protocol ............................................................................................. 27 Participants Position ........................................................................................ 27 Maximal Voluntary Contraction ......................................................................... 28 Force Tracking Task ......................................................................................... 28 Procedure ............................................................................................................... 29 Data Reduction ....................................................................................................... 30 Root Mean Square Error .................................................................................. 31 Standard Deviation ........................................................................................... 31 Stair Stepping Phenomenon ............................................................................. 31 Stair Stepping with Larger Step Widths ............................................................ 32 Statistical Analysis .................................................................................................. 33 3 RESULTS ............................................................................................................... 40

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8 Maximal Voluntary Contraction Force and Fat igue ................................................. 40 Root Mean Square Error ......................................................................................... 40 Affected Hand of Stroke and Non dominant Hand of AgeMatched and Young Adults ................................................................................................. 40 5% MVC/s rate ........................................................................................... 40 10% MVC/s rate ......................................................................................... 41 20% MVC/s rate ......................................................................................... 41 Less Affected Hand of Stroke and Dominant Hand of AgeMatched and Young Adults ................................................................................................. 42 Low Functioning versus High Functioning Stroke Participants ......................... 42 Standard Deviation ................................................................................................. 43 Affected Hand of Stroke and Non Dominant Hand of AgeMatched and Young Adults ................................................................................................. 43 Less Affected Hand of Stroke and Dominant Hand of AgeMatched and Young Adults ................................................................................................. 44 Total Number of Steps ............................................................................................ 44 Low Functioning versus High Functioning Stroke Participants ......................... 45 Correlation with Disease Severity ..................................................................... 45 Stair Steps with Larger Step Widths ....................................................................... 46 Low Functioning versus High Functioning Stroke Participants ......................... 46 Correlation with Disease Severity ..................................................................... 47 4 DISCUSSION ......................................................................................................... 77 Motor Learning Deficits after Stroke ....................................................................... 79 Co Contraction of Agonist and Antagonist Muscles ................................................ 80 Motor Unit Recruitment and Derecruitment Patterns .............................................. 81 Visual Perceptual Deficits Post Strok e .................................................................... 82 Lesion Location ....................................................................................................... 83 Less Affected Hand Motor Deficits and Stroke ....................................................... 84 Low Functioning versus High Functioning Stroke Participants ............................... 84 Summary ................................................................................................................ 86 APPENDIX A FUGL MEYER MOTOR AND SENSORY SCALE .................................................. 89 B MODIFIED ASHWORTH SCALE ............................................................................ 94 C DEMOGRAPHICS .................................................................................................. 95 LIST OF REFER ENCES ............................................................................................... 96 BIOGRAPHICAL SKETCH .......................................................................................... 110

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9 LIST OF TABLES Table page 2 1 Inclusion criteria .................................................................................................. 35 2 2 Stroke participants clinical characteristics .......................................................... 36 2 3 Total number of trials removed from analysis ..................................................... 37 3 1 Standard deviation across groups and rates of a ffected hand ............................ 48 3 2 Standard deviation across groups and rates of l ess affected ............................. 49 3 3 Mean number of steps as a function of group, grip phases and rates of l ess affected ............................................................................................................... 50

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10 LIST OF FIGURES Figure page 2 1 Tracking task ...................................................................................................... 38 2 2 Grip phases in a tracking trajectory .................................................................... 39 3 1 Pre MVC and post MVC across groups and hands ............................................ 51 3 2 Root mean square error across groups at 5% MVC/s rate of affected hand ...... 52 3 3 Root mean square error bias score across groups and rates of affected hand .. 53 3 4 Root mean square error across groups at 10% MVC/s rate of affected hand .... 54 3 5 20% MVC /s Rate r oot mean square error across groups of affected hand ..... 55 3 6 Root mean square error at 5% MVC/s r ate of l ess affected hand ...................... 56 3 7 Root mean square error at 10% MVC/s rate of l ess affected hand .................... 57 3 8 Root mean square error at 20% MVC/s rate of l ess affected hand .................... 58 3 9 Normalized root mean square error across rates of a ffected hand of low functioning versus high functioning stroke participants ....................................... 59 3 10 Total number of steps at 5% MVC/s rate of a ffected hand ................................. 60 3 11 Total number of steps at 10% MVC/s rate of a ffected hand ............................... 61 3 12 Total number of steps at 20% MVC /s rate of a ffected hand ............................... 62 3 13 Total number of steps across rates of a ffected hand of low functioning versus high functioning stroke participants .................................................................... 63 3 14 Correlation of total number of steps with Fugl Meyer Assessment scores of stroke group ........................................................................................................ 64 3 15 Number of steps with larger step widths at 5% MVC/s r ate of a ffected hand ..... 67 3 16 Number of steps with larger step widths at 10% MVC/s r ate of a ffected hand ... 68 3 17 Number of steps with larger step widths at 20% MVC/s r ate of a ffected hand ... 69 3 18 Number of steps with larger step widths at 5% MVC/s r ate of l ess affected hand ................................................................................................................... 70

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11 3 19 Number of steps with larger step widths at 10% MVC/s r ate of l ess affected hand ................................................................................................................... 71 3 20 Number of steps with larger step widths at 20% MVC/s r ate of l ess affected hand ................................................................................................................... 72 3 21 Number of steps with larger step widths across rates of a ffected hand of low functioning versus high functioning stroke participants ....................................... 73 3 22 Correlation of total number of steps with larger step widths with Fugl Meyer Assessment Scores of stroke group ................................................................... 74 4 1 Sample force trace of one participant from each group at 5% MVC/s r ate ......... 88

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12 LIST OF ABBREVIATIONS ANCOVA Analysis of Covariance ANOVA Analysis of Variance BBT Box and Block Test CE Constant Error F Female FMA Fugl Meyer Assessment MAS Modified Ashworth Scale H Hemorrhagic I Ischemic L Left M Male MMSE Mini Mental State Examination MVC Maximal Voluntary Contraction N Newton O Age Matched Older Adults R Right RMSE Root Mean Square Error SA Stroke Affected Hand SD Standard Deviation SU Stroke Less Affected Hand Y Younger Adults

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13 Abstract of Thesis Presented to the Graduate School of the University of Florida in Partial Fulfillment of the Requirements for the Degree of Master of Science FORCE MODULATION DEFICITS IN CHRONIC STROKE: GRIP FORMATION & GRIP RELEASE PHASES By Sagar K. Naik D ecember 2009 Chair: James H. Cauraugh Major: A pplied Physiology and Kinesiology The aim of the present study was to elucidate force modulation deficits in various grip phases in chronic stroke and to develop an algorithm to quantify stair stepping phenomenon. Nine chronic stroke participants (age = 66.39 9.84 years) nine agematched healthy adults (age = 66.38 8.31 years) and 10 young adults (age = 22.65 2.94 years) performed a submaximal isometric power grip tracking task. The task consisted of ramp up and down at 5% MVC/s, 10% MVC/s and 20% MVC/s rates. The peak force was set at 35% MVC for all rate trials. Analyses of root mean square error, standar d deviation, number of steps, and number of steps with larger step widths revealed three critical fin dings 1) stroke leads to force modulation deficits for the grip release phase of both hands (affected and less affected), 2) developed novel approach in quantify ing stair stepping phenomenon while explore possible mechanisms responsible for force modulation deficits in various grip phases, and 3) high functioning stroke survivors showed greater deficits in the grip release phase, whereas low functioning stroke survivors showed greater deficits in grip formation phase. Collectively, these findings carry significant implications for stroke rehabilitation by differentiating low functioning and high functioning stroke individuals with impairments in

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14 different grip phases. Further, potential mechanisms that account for the impairments in the grip phases were disc ussed and these increased our understanding of stair stepping phenomenon in aging and stroke.

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15 CHAPTER 1 INTRODUCTION Stroke and Upper Extremity Function Post Stroke Stroke is a neurological deficit characterized by rapidly developing signs of focal or g lobal disturbance of cerebral functions (World Health Organization, 1978). More than 795,000 people in United States suffer from a new or recurrent stroke each year imposing immense rehabilitation cost demands on the economy, amounting to $ 68.9 billion in 2009 (Lloyd Jones, et al., 2009) Motor deficits post stroke are highly conspicuous on the side contralateral to the most affected hemisphere. These deficits arise because of multifactorial reasons, including weakness of specific groups of muscles (Colebatch & Gandevia, 1989; Patten, Lexell, & Brown, 2004) abnormal muscle tone or hypertonia (Bruke, 1988; Katz, Rovai, Brait, & Rymer, 1992; Lance, 1980; Wiesendanger, 1990) abnormal muscle synergies (Bobath, 1990; Brunnstrom, 1970; Twitchell, 1951) and loss of coordination (Levin, 1996) Most survivors after initi al stroke insult regain their walking ability, but about 30 to 66% of them are not able to use the upper extremity (G. Kwakkel, Kollen, B.J., Wagenaar, R.C., 1999; Sunderland, Tinson, Bradley, & Hewer, 1989; Wade, LangtonHewer, Wood, Skilbeck, & Ismail, 1983) Similar findings were reported by Gowland and colleagues in that 69% of stroke survivors that were admitted to a rehabilitation unit recover from motor deficits had mild to severe upper extremity disability (Gowland, deBruin, Basmajian, Plews, & Burcea, 1992) Of this population only 14% 16% with initial upper extremity hemiparesis recover complete or near complete motor functions (Hendricks, van Limbeek, Geurts, & Zwarts, 2002) In addition, the recovery process of

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16 upper extremity motor deficits is often slower than the lower extremity motor deficits (G. Kwakkel, Wagenaar, Kollen, & Lankhorst, 1996; Wagenaar, 1990) A simple task of grasping and holding a glass of water requires fine motor coordination and control of the entire upper extremity muscles, including shoulder girdle, elbow, and hand muscles (Ghez, 2000) A loss of hand function accounts for about 90% loss of upper extremity function (Hume, 1990) Moreover, a hand recovery post stroke often plateaus in about one year leaving impaired daily living activities such as feeding, dressing, holding delicate objects (Andrews, Brocklehurst, Richards, & Laycock, 1981; Ford & Katz, 1966; Jorgensen, et al., 1999) writing and sensation (Fearnhead, 1999; Tubiana, 1981) After 18 months post stroke, 45% of participants had limited hand functions (Welmer, Holmqvist, & Sommerfeld, 2008) Upper arm functions are less impaired than hand functions post stroke (Saladin, 1996; Twitchell, 1951) however, loss of hand functions result in marked disrupti on in performance of fine and gross motor skills such as reaching, grasping, and manipulating objects, which requires motor planning, control, skill, and coordination. Grasping/Gripping Function and Stroke Grasping is one of the most important and complex motor skills. Jeannerod first described two phases of grasping: 1) transport phase for reaching the object by hand activating proximal muscles and 2) grasp phase during which distal muscles of hand make contact with the object for making force adjustments (manipulation) (Jeannerod, 1984, 1986) While lifting an object during the grasp phase, force is exerted by prime movers (agonists) of the hand and modulations occur according to the load force and load characteris tics (Johansson, 1998; Johansson & Cole, 1992, 1994; Johansson & Westling, 1988) Frequently, a primary goal of grasping is to maintain a stable grip of an

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17 object by manipulating finger forces (MacKenzie, 1994) In stroke survivors, the neuromuscular system involved in grasping is adversely affected due to disruption of some percentage of the corticospinal system (HeppReymond & Wiesendanger, 1972; Pineiro, et al., 2000; Stinear, et al., 2007; Wenzelburger, et al., 2005) thus, resulting in impaired upper extremity functions (Fugl Meyer, Jaasko, Leyman, Olsson, & Steglind, 1975; Hermsdorfer, Hagl, Nowak, & Marquardt, 2003) The corticospinal system is distributed in a proximal to distal gradient to the cervical spinal cord with greater motoneuron pools for the dis tal hand than the proximal arm (Clough, 1968; Colebatch, Rothwell, Day, Thompson, & Marsden, 1990; Fetz & Cheney, 1980; Palmer & Ashby, 1992; Porter, 1993) Therefore, in chronic stroke, insult to this system leads to more severe hemiparesis of the distal muscles than the proximal muscles of the upper extremity (Colebatch & Gandevia, 1989) However, recent findings showed that in acute stroke participants, loss of hand function was caused by loss of movements of many upper extremity segments. These data suggest that the acute phase is an exception to the proximal to distal gradient of motor deficits (Beebe & Lang, 2008) Despite these contrasting anatomical st ructural and functional differences, gripp ing and manipulating objects requires movement control of all segments of upper extremity to modulate goal directed amounts of grip force to complete tasks (Beebe & Lang, 2008; Lang & Beebe, 2007) Gri p ping an object is a component of grasping, that includes interaction of hand with the object for manipulation skills (Prodoehl, Corcos, & Vaillancourt, 2009) and can be div ided into four phases: 1) opening of the hand, 2) positioning and closing of the fingers and thumb to stabilize an object, 3) exerting force to grasp an object and 4)

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18 releasing the object by the opening hand (Landsmeer, 1962; Magee, 2007) To understand these phases clearly, we used the following three terminologies in this paper: 1) Grip Formation Phase positioning and closing of the fingers and thumb to grasp an object; 2) Sustained Grip Phase exerting force to stabilize an object; and 3) Grip Release Phase both opening of hand and releasing the object. An i ncapability of opening the hand leads to impaired formation and release phase s. The im portance of the release phase of grasp in upper extremity function has been defined in normal healthy children (Lewis, Duff, & Gordon, 2002) children with cerebral palsy (Eliasson & G ordon, 2000) and older adults with stroke (Hines, 1995; Perdan, et al., 2008) However, c urrent grip assessment methods based on these stages are subjective and lack quantifiable measures. Moreover the liter ature based on quantifiable measures lack s a definitive understanding how grip phases are differentially altered in healthy subjects and a neurologically impaired stroke population. Force Control in Aging and Stroke Force control is the ability of muscles to produce force steadily, accurately, and temporally matched to the target goal (Patten, 2000) Force control is termed as steadiness when referred to isometric force regulation (R. M. Enoka, 1997) The functional significance of steadiness of force involves the ability of an individual to produce precise force and to perform required movement trajectories. To accomplish daily living activities like walking, manipul ating objects, writing, and playing sports require control of muscle forces at different levels. These various ranges of forces can be produced by modulating firing properties and the recruitment order of motor units (Freund, Budingen, & Dietz, 1975) Modulations within the properties of motor units can occur in two different strategies: a) rate coding or making adjust ments of motor unit

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19 firing frequency and b) recruiting motor units in an orderly manner with increased force levels (Clamann, 1993) Recruitment of motor units and their modulation in firing rates are used in combination normally to produce muscle forces. A relative contribution of either strategy depends on the level of force and the muscles required to accomplish task (Floeter, 2003) Deficits in force control in an elderly population is substantially documented in aging literature, and is often reported as increased force variability, slowness of movement and decreased accuracy of movement compromising execution of motor performance (Doherty, Vandervoort, Taylor, & Brown, 1993; R. M. Enoka, Christou, E.A., Hunter, S.K., Kornatz. W.K., Semmler, J.G., Taylor, A.M., Tracy, B.L., 2003; Galganski, Fuglevand, & Enoka, 1993; Keen, 1994; Laidlaw, Bilodeau, & Enoka, 2000) These deficits in force control may arise because of agerelated changes at the motor unit, structural changes such as loss of motor neurons (McComas, Galea, & de Bruin, 1993) increased motor unit innervati ons ratios, or increased motor unit forces (Doherty & Brown, 1997) In addition to these structural changes, aging leads to disturbances in neural mechanisms causing reduced motor unit discharge rates (Connelly, Rice, Roos, & Vandervoort, 1999) altered recruitment and der ecruitment patterns of motor units (Spiegel, Stratton, Burke, Glendinning, & Enoka, 1996) and increased motor unit discharge variability (Laidlaw, et al., 2000) Aging literature also suggests that lengthening contractions (eccentric) are more variable than shortening contractions (concentric) (Burke, Hagbarth, & Lofs tedt, 1978; Christou & Carlton, 2002a, 2002b; Fang, Siemionow, Sahgal, Xiong, & Yue, 2001) Further, aging literature suggests that older adults produce a stair stepping phenomenon especially during force

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20 release phase of an isometric ramp contractions, during movement transitions and also during lengthening cont ractions (Patten, 2000) However, quantitative differences in force control and stair stepping phenomenon during formation and release phases of an isometric contraction in young and older adults has yet to be explored extensively. Moreover, there is no evidence on stair stepping patterns in force control of chronic stroke participants. Thus, we developed a novel approach to quantify stair stepping phenomenon. Additionally, aging leads to reduction in rate of force development, which might arise from a) physiological changes like muscle atrophy and slowness of muscle contracti le properties (Hook, Sriramoju, & Larsson, 2001; Larsson, Li, & Frontera, 1997) or b) alterations in neural control of muscles (Barry, Riek, & Carson, 2005; Barry, Warman, & C arson, 2005; Darling, Cooke, & Brown, 1989; Morgan, et al., 1994; Seidler, Alberts, & Stelmach, 2002) These force control differences across various rates of grip formation and release during isometric contraction has not been studied in any population. Therefore, we looked at isometric grip phases at different rates of force production in normal, aging, and stroke populations. S troke leads to increased tone in the flexor muscles along with weakness of an extensor group of muscles of elbow, wrist and fingers (T rombly, 2007; Twitchell, 1951) This increased tone of finger muscul ature commonly causes impaired motor control of the voluntary opening of hand (Cruz, Waldinger, & Kamper, 2005; Hines, 1995; Kamper & Rymer, 2001; Popovic, 2005) Stroke participants with sensorimotor deficits produced excessive force while lifting, holding and moving handheld objects (Blennerhassett, Carey, & Matyas, 2006; Hermsdorfer & Mai, 1996; Nowak, Her msdorfer, & Topka, 2003;

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21 Wenzelburger, et al., 2005) and also to prevent slipping of an object during precision grip (Hermsdorfer, et al., 2003) Excessive grip force production is a compensatory strategy adopted by stroke participants to deal with their sensorimotor deficits (Johansson & Westling, 1984) Additionally, stroke participants wi th a subcortical lesion in the left cerebral hemisphere show deficits in scaling the peak load and grip force rates suggesting the presence of motor planning deficits (Raghavan, Krakauer, & Gordon, 2006) Analysis of aperture path ratios in stroke survivors with severe hemiparesis has shown deficits in opening the fingers accurately when approaching an object to be grasped (Lang, et al., 2005) Similar results were reported by Wenzelburg and associates in that movement time was increased during terminal reaching and gr asping phases in reach to grasp and grasp to lift tasks (Wenzelburger, et al., 2005) In addition, previous studies have described movement init iation and termination problems in various upper and lower extremity motor activities (Chae, et al., 2006; Chae, Yang, Park, & Labatia, 2002a; Howes & Boller, 1975; R. D. Jones, Donaldson, & Parkin, 1989) Recently, Soe and colleagues showed that grip initiation and termination was delayed on affected hand with greatest deficits found for the grip termination phase (Seo, Rymer, & Kamper, 2009) This study examined delays in gr ip initiation and termination phases in a maximal voluntary contraction task. Because of the timing nature of the experimental protocol, force control deficits during these phases were not explored at submaximal everyday activity force levels, which might have given better insight regarding these phases. Moreover, stroke participants even after successfully reaching grip target force level, have problems maintaining constant force while performing sustained isometric grip task (Blennerhassett, et al., 2006; Hermsdorfer &

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22 Mai, 1996) Thus, the current stroke literature shows some evidence of deficits in various grip phases in terms of either delayed grip initiation or termination or deficits in force control during sus tained phase, which requires better understanding using force control paradigms. In particular, evidence concerning force control in grip release phase is completely nonexistent. Thus, the development of quantifiable outcome measures evaluating grip phase s in stroke survivors will contribute to a better understanding of the capabilities required to execute various grip phases. Moreover, quantifying the gripping phases involved in tracking motor impairments will provide sound empirical evidence for designing r ehabilitation protocols to improve grip function post stroke. Therefore, this study tests how force control is impaired across different power grip phases in chronic stroke participants. In clinical settings, physical and occupational therapists typical ly assesses range of motion of fingers and wrist, maximal voluntary grip strength and hand dexterity by various methods (Fugl Meyer, et al., 1975; Innes, 1999; Jebsen, Taylor, Trieschmann, Trotter, & Howard, 1969; Wolf, et al., 2001) However, these standard measures based on subjective evaluation give only partial information of hand functionality (Marx, Bombardier, & Wright, 1999; McPhee, 1987) Frequently, daily living acti vities require submaximal force control of fingers; therefore, assessment of maximal voluntary grip force explains only a small part of the hand functionality (Marshall & Armstrong, 2004; McPhee, 1987) Additionally fine dexterous hand activities require dynamic control of grasping movements due to task constraints and movement of the object in space (Flanagan & Wing, 1993; Wing, 1996) A force tracking task allows understanding of

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23 force control during various phases of grip, i.e., grip formation and grip release. For example, the ability to lift an object (grip formation) followed by accurately placing an object on a surface (grip release) can be studied using force tracking systems. Past research has shown that grip control in participants with neuromuscular disease, showed larger tracking errors in comparison to healthy subjects in a precision grip (Kurillo, Zupan, & Bajd, 2004) Recently, investigators have shown that grip functions are altered with age (Kurillo, Bajd, & Tercelj, 2004; Lindberg, Ody, Feydy, & Maier, 2009; Sosnoff & Newell, 2006; Vaillancourt & Newell, 2003; Voelcker Rehage & Alberts, 2005) Additionally, brain damaged participants showed improvements in grip force control after feedback based tracking training (Kriz, Hermsdorfer, Marquardt, & Mai, 1995) Similarly, chronic stroke subjects reduced tracking error when a for ce tracking system was used to rehabilitate their hand functions (Kurillo, Gregoric, Goljar, & Bajd, 2005; Perdan, et al., 2008) In summary, evidence supporting tracking systems is accumulating as a rehabilitation task assisting stroke participants. Thus, the current force tracking system used to study grip phases across different populations will provide valuable quantitative measures. A im, Hypothesis and Significance Aim The aim of this study is to quantify forc e control capabilities and deficits using a force tracking system in chronic stroke, agematched elderly and college participants during a power grip using kinetic measures of force control.

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24 Hypothesis The primary hypothesis is that in power grip chronic stroke subjects will display greater force control deficits (root mean square error) during the grip release phase than during the grip formation phase. To control for a potential aging effect, force control data was collected and compared during power gri p formation and release phase in healthy young and elderly adults. In addition, relative to healthy elderly and young adults, our secondary hypothesis predicted that stroke will show 1) increased variability of force control (standard deviation) during the release phase, 2) greater number of steps during the release phase, and 3) larger error (root mean square error), variability (standard deviation) and number of steps in grip release phases with higher force rate levels. Significance The significance of this study is that quantifying different phases of grip in three populations at three different force rates will help rehabilitation professionals to translate findings to clinical settings for both evaluation and intervention purposes. In addition, furthe r quantifying the stair stepping phenomenon across grip formation and release phases and populations will provide information about the potential mechanisms underlying this phenomenon.

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25 CHAPTER 2 METHODS Participants Participants in the present study were nine chronic stroke (age = 66.39 9.84 years), nine agematched healthy participants (age = 66.38 8.31 years), and ten healthy young adults (age = 22.65 2.94 years). Two stroke participants were not able to meet inclusion criteria and were not included in our nine stroke participants. Stroke participants were recruited from North Central Florida stroke population, agematched controls from Living Well, and healthy college students from the University of Florida. Admission criteria for stroke participants, agematched healthy controls and college st udents are summarized in Table 21 For chronic stroke participants, functional ability of the affected upper arm was assessed using the upper extremity subset of the Fugl Meyer Motor Function Assessment (F MA) before the force tracking protocol (Fugl Meyer, et al., 1975) The Box and Block tes t was used to evaluate upper extremity motor function (Mathiowetz, Volland, Kashman, & Weber, 1985) In addition, muscle tone at the wrist and finger joint s was assessed in sitting position by the Modified Ashworth Scale. Wrist range of motion was measured with a universal goniometer and finger thumb range of movements with finger goniometer. Demographic characteristics and clinical data of stroke participants are reported in Table 22 All procedures in the study were approved by University of Floridas Institutional Review Board. All participants provided written informed consent prior to participation in the study.

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26 Clinical Assessment Tools Modified Ashworth Scale The Modified Ashworth Scale is a clinical test used for the neurologic assessment of muscle tone. Assessment involves application of rapid passive stretch to specific group of muscles by moving limb rapidly through the full range of movement. On a 6 point ordinal scale grades, a minimum score of z ero represents no increase in muscle tone and a maximum score of four represents a rigid affected part (severe hypertonia spasticity). Box and Block Test Box and block test is a standardized, timed, quick, simple and inexpensive test for assessing upper extremity manual dexterity and gross motor function. Test involves transferring of individual wooden blocks (2.54 cm cube) within a partitioned box using the unimpaired hand first in 60 s and followed by the impaired hand. Performance for each hand is the number of blocks transferred successfully in 60 s. Upper Extremity subset of the Fugl Meyer Motor Function Assessment FMA is a stroke specific, performance based impairment index used to assess motor recovery, balance, sensation, and joint positioning and range of movement. Each item is scored on a threepoint scale: 0 = cannot perform; 1 = can perform partially; 2 = fully performed. Score of upper extremity subset of FMA ranges from 0 to 66 with score of 66 represents nearly normal function. Mini Mental St ate Examination MMSE (Folstein, Folstein, & McHugh, 1975) is a tool to assess the cognitive mental status. Eleven questions measure five areas of cognition: orientation,

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27 registration, attention and calculation, reca ll, and language. Maximum score is 30 and a score of 23 or lower indicates cognitive impairment. Instrumentation The power grip force measuring device were designed using four force transducers (2 MLP 50; range 50 lbs and 2 MLP 200; range 200 lbs). The transducers (Transducer Techniques, 4.16 1.27 1.90 cm, 0.1% sensitivity) were embedded in cushioned wooden platforms. The shape and size of the force measuring units were developed based on objects used in daily living activities (e.g., holding a cup). The power grip force customized design allowed assessment of functional gripping forces. The output from each force transducer was amplified using a 15LT Grass Technologies Physio data Amplifier System (Astro Med Inc.) with an excitation voltage of 10V and a gain of 200. The analog signal from each force transducer was digitized by a 16bit analogto digital converter (A/D; NI cDAQ9172 + NI 9215, National Instruments) and sampled at 100 Hz. The least amount of force detectable by the A/D converter was 0.00016 N. The force trace was displayed on a computer screen (1024 768 resolutions, 100 Hz refresh rate) with a visual gain of 15 pixels/N. Trial onset, trial offset, and visual stimulus presentation (tracking task) were controlled by a custom Lab VIEW program (8.1; National Instruments). Experimental Protocol Participants Position Participants were seated in a chair with back support in front of computer screen (17 inches) at 1 m distance. A standardized upper extremity testing position was defined by 5 to 10 of shoulder forward flexion with 10 to 15 abduction, elbow in a 90 forearm in mid prone position supported on the table and wrist in slight extension to

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28 augment maximal performance of power grip. Participants were instructed to maintain consistent posture during the power grip task and were not allowed to use any compensatory movements (e.g., changing arm or forearm orientation to alter power grip force). Maximal Voluntary Contraction (MVC) Prior to starting the experimental protocol, all participant s completed a MVC for each hand independently in accordance with a previously established and accepted method (Morrison, 1998; Vaillancourt, Slifkin, & Newell, 2002) Participants were instructed on hearing an auditory beep to squeeze the power grip device as hard as possible followed by relaxation on the second beep MVC of each 6 s trial was determined as the average of 10 greatest force samples. Three trials of MVC were performed with 60 s rest between each trial to avoid fatigue (Bigland Ritchie, Johansson, Lippold, Smith, & Woods, 1983) The computed mean value of three MVC trials was used to calculate each participants 35% peak force level for further experimental protocol (Coombes, Gamble, Cauraugh, & Janelle, 2008; Vaillancourt & Newell, 2003) Additionally, three MVC trials were recorded as previously stated after completion of the experiment to examine the level of fatigue (Chri stou, Poston, Enoka, & Enoka, 2007; Ryan, Beck, et al., 2008; Ryan, Cramer, Egan, Hartman, & Herda, 2008) Force Tracking Task Following MVC measurement and calculations a submaximal white stationary force tracing trajectory with peak force of 35% MVC wa s displayed on the computer screen. This represented trial onset. Participants were instructed to t rack the stationary force trace as accurately as possible by modulating appropriate power grip force s.

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29 Figure 1 1A shows the actual representation of the tri al. Real time feedback was provided with a blue trace that plotted the force produced by participant s. A t rial involved rest at 1 % MVC for 1 s followed by gradual modulation of power grip force from 1 % MVC to 35% MVC peak force, maintaining 35% MVC contrac tion for 3 s and then gradually returning to baseline (1 % MVC) Ramp up and ramp down rates were manipulated at 5% MVC/s, 10% MVC/s and 20% MVC/s to determine the effect of force rate change on force control Durations of ramp up and ramp down during each trial were 6.6 s, 3.3 s, and 1.7 s for 5% MVC/s, 10% MVC/s and 20% MVC/s trials respectively. Characteristics of a single force trace are described in figure 1 1 B. Procedure Before proceeding with the experimental protocol, participants signed the informed consent. Once participants were seated comfortably in the required testing position, the experimenter explained entire experimental procedure to participants. Participants then completed three MVC trials as described previously. Following MVC trials, part icipants performed 15 practice trials to get accustomed to the novel force control task and temporal pattern of the force trajectory along with visual feedback. Additional feedback was provided at the end of each practice trial with the display of root mean square error (RMSE), (i.e., difference between the target force trace and the participants performed force trajectory in blue line). RMSE feedback was not given during the experimental trials. After completion of practice session 10 experimental trials for each hand at different force rate levels were performed. Hence, each participant completed a total of 30 trials for each hand with 15 s rest interval between trials and 5 min between two hand conditions to avoid fatigue. Force rate conditions were randomized to avoid a test order effect. Hand conditions were fixed in the order of less affected hand practice

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30 block, more affected practice block, less affected experiment block and more affected experiment block. Similarly, young controls and agematched el derly controls performed dominant hand blocks first during practice and experimental trials. This paradigm was used to enhance learning of the novel task for the more affected hand in stroke and nondominant hand for controls. After completion of experimental trials with both hands, three more MVC trials were measured. The experimenter remained in the testing room for entire duration to ensure that the participants performed the force tracking task as instructed without compensatory movements. Data Reduction Force signals were digitally filtered at a cut off frequency of 20 Hz using a fourthorder Butterworth filter. Raw force time series was broken down into five phases based on the algorithm (Figure 22 ): 1) phase 1 onset of trial till onset of ramp up phase (point A to B); 2) grip formation phase onset of ramp up phase to the peak of the trial (point B to C); 3) sustained grip phase peak of the trial to onset of ramp down phase (point C to D); 4) grip release phase onset of ramp down phase to basel ine (point D to E); and 5) phase 2 baseline to end of trial (point E to F). Three force variables, Root Mean Square Error (RMSE), Standard Deviation (SD), and Constant Error (CE) were calculated for grip formation phase, constant grip phase, and grip rel ease phase for each trial. Phases 1 and 2 were not included in the analysis. These two phases were included in the trial to ensure that participants completed entire duration of grip formation and release phases accurately. Table 2 3 shows numbers of trial s removed from the analysis as participants were not able to complete trial successfully. Calculations for root mean square error, standard deviation and constant error were done online using a custom built Lab VIEW program and number of steps was

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31 quantifi ed using Microsoft Excel. Each measure is reported as the mean score for each grip phase of the 10 trials at each force rate condition. Measures for each trial are calculated using the following methods. Root Mean Square Error (RMSE) Performance error was defined by RMSE. RMSE was calculated as the square of the vertical distance between the target force and amount of force produced. The following formula was used to calculate RMSE for each grip phase. Where t = target force, xi = ith force sample and N = number of samples Standard Deviation (SD) The linear trend in the force signal was removed and the amount of total force variability for each grip phase within each trial was determined by standard deviation. Stair Stepping Phenomenon During grip formatio n there is a sequential increase in force production while during grip release; there is a continuous decrease in force at each required force rate. However, these two phases can intermittently be presented with steps, where there is no change in force. S uch duration of constant force production is defined as step. This constant force production duration can range from 20 ms to more than 1 s. Hence, to quantify the stair stepping phenomenon in tracking, we used the following algorithm to define step widt h based on rate of force production for both grip phases. Defining step width for different rate of change of force: Force data were sampled at 100 Hz: 100 samples in 1 second; 1 sample = 10 millisecond.

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32 5% MVC/s Rate Change of 5% MVC force requires 100 samples Therefore, a change of 1% MVC force requires 100 samples 1% MVC / 5 % MVC = 20 samples If 10 or more consecutive force samples increased (grip formation) / decreased (grip release) less than 2% of the first force sample in the 10 or more successi ve force samples, then a step was defined. In other words, if the force trace remained constant (increased / decreased less than 2%) for more than half of the duration required to change force of 1% MVC (more than 100 ms) at 5% MVC/s rate, then it was cons idered as a step. Similarly, for 10% MVC/s rate, 10 samples are required to change 1% MVC force. Therefore, if the force trace increased / decreased less than 2% for more than 50 ms, then it was defined as a step. At 20% MVC/s rate, 5 samples are required to change 1% MVC force. The above criterion defined a step to be 25 ms (i.e., 2.5 samples). However, the precision of our analysis program was not able to capture 2.5 samples. Thus, we adopted conservative approach by using 3 samples. Hence, if more than 30 ms of force trace remained constant (increased / decreased less than 2%), then a step occurred. Stair Stepping with Larger Step Widths Larger step widths were defined if the duration of constant step was five times or more than the criterion duration for step. Hence, for 5% MVC/s rate, larger step widths was define as 5 100 ms (criterion duration for step) = 500 ms and above. Similarly, larger step widths were 250 ms or above and 150 ms or above for 10% MVC/s and 20% MVC/s rates.

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33 Statistical Analysis T o examine differences for root mean square error, standard deviation, total number of steps and steps with greater step widths at different rates of force production, separate twoway ANOVAs were conducted; 3 Groups (stroke, older adults, and young) 3 Gr ip Phases (grip formation, sustained phase, and grip release) with repeated measures on grip phases. In the previous analysis for total number of steps and steps with larger step widths, only grip formation and grip release phases were used as we didnt ex pect any steps during sustained grip phase. Separate analyses were conducted for each rate and for each hand condition. In addition, threeway ANOVAs were conducted, 3 Groups (stroke, older adults, and young) 2 Hand (affected/nondominant hand, and less affected/dominant hand) 2 Sessions (pre MVC, and Post MVC) to delineate differences among groups in testing the fatigue effect on pre MVC (before experiment) and post MVC (after experiment). Further, to minimize the effect of fatigue and to test motor learning effect, we divided 10 trials at each rate into two trial blocks: a) 1st block first five trials and b) 2nd block last five trials. Analysis was conducted using threeway repeated measures ANOVA, 3 Groups (stroke, older adults, and young) 2 Tri al Blocks (1st block, and 2nd trial block) 3 Grip Phases (grip formation, sustained force, and grip release). Post hoc analysis included Tukeys HSD test. Further, when the sphericity assumption was violated, we adopted the GreenhouseGeisser correction method (Greenhouse, 1959) Additionally, independent t tests for each grip phase were used to tes t if low functioning stroke participants performed task differently than high functioning participants. t tests were preferred for secondary analysis due to small sample size of low and high functioning stroke participants. To test the relationship between the number of steps and steps with larger

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34 widths to stroke severity, a regression analysis was conducted. T his analysis included disease severity (FMA, MAS, and BBT) as independent variables and total number of steps and steps with larger step widths as dependent variables. The alpha level for all statistical procedures was set at P

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35 Table 2 1. Inclusion c riteria Stroke participants: 1) Single, unilateral, focal cerebrovascular accident 2) At least 6 months post stroke 3) Minimum of 15 4) Minimum of 10 5) Actively able to open fingers 6) Modified Ashworth Scale Score 7) Absence of other neurological deficits such as proprioceptive and sensory deficits of upper extremity Stroke participants, agematched healthy participants and college students 1) No cognitive impairment (Mini Mental State Examination Score 2) Absence of neurological deficits 3) No marked visual or hearing deficits 4) No severe medical problems such as shoulder pain or any other orthopedic condi tion affecting the upper extremity.

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36 Table 2 2. Stroke p articipants c linical c haracteristics Subject No. Age (Years) Sex Dominant Limb Stroke Type Affected Hemisphere Disease Duration (Months) FMA MAS BBT 1 78.42 M R I L 123 30 2 20 2 65.00 M L H R 155 34 3 18 3 59.92 M R I R 18 50 1 40 4 70.50 F R I L 74 61 0 70 5 71.00 M L H R 26 32 3 25 6 63.08 M R I L 25 59 0 52 7 76.92 M R I R 15 55 0 23 8 56.17 M R I R 15 22 3 1 9 56.42 M R N/A R 148 16 3 1 M Male, F Female, L Left, R Right, I Ischemic, H Hemorrhagic FMA Upper Extremity Fugl Meyer Assessment MAS Modified Ashworth Scale (Average of Wrist and Long Finger Flexors) BBT Box and Block Test

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37 Table 2 3 Total number of t ri als r emoved from a nalysis Groups 5 % MVC/s 10% MVC/s 20% MVC/s Young 4 (200) 8 (200) 10 (200) Age Matched 6 (180) 7 (180) 30 (180) Stroke 4 (180) 7 (180) 24 (180) Number in parenthesis indicate total number of trials collapsed across hand conditions

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38 Figure 21 Tracking task A) Presentation on the screen during the experiment B) Characteristics of a tracking task Participants Response Trace Target Stationary Trace A B

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39 Figure 22. Grip phases in a tracking trajectory F A B C D E Phase Grip Formation Phase Grip Release Phase Constant Grip Phase Phase

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40 CHAPTER 3 RESULTS Maximal Voluntary Contraction Force and Fatigue Threeway ANOVA revealed no differences in MVC force before beginning the experimental protocol across groups (P > 0.40). Also, pre MVC and post MVC revealed no significant differences (Figure 31 ). However, pre MVC of stroke group on affected hand (less affected hand) varied from 65.48N to 459.08N (244.17N 508.33N), similarly non dominant hand (dominant hand) of agematched ranged from 164.44N 451.72N (159.65N 486.78N) and young adults from 143.96N 498.91N (149.87N 573.17N) Hence, we used analysis of covariance (ANCOVA) for all outcome measures to account for high amount of variability in pre MVC scores within subjects and these values were used as the covariate. In addition, trial block analysis for each outcome measure (f irst 5 trials 1st trial block and last 5 trials 2nd trial block) also showed no differences. Based on our results, we concluded that fatigue was not the contributing factor for the differences in all outcome measures with minimal to no motor learning e ffect. Root Mean Square Error Affected H and of S troke and N ondominant H and of A geM atched and Y oung A dults 5% MVC/s rate (Figure 32 ) The 3 3 (Group Grip Phases) mixed design ANCOVA with repeated measures on grip phases, revealed a main effect of group (F(2,24) = 11.955; P < 0.001) and grip phases (F(2,48) = 5.455; P = 0.007) Across grip phases, stroke participants produced greatest error (5.576 0.368) compared to agematched old (3.573 0.371) and young adults (3.245 0.338). Also, grip release phase produced greatest error (5.095 0.307)

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41 than grip formation (3.825 0.165) and sustained force (3.475 0.263). We also found significant Group Grip Phases interaction (F(4,48) = 3.770; P = 0.020). Follow up analysis revealed that, stroke group sh owed greater tracking error on grip release phase compared to agematched and young adults. In addition, stroke participants produced greatest tracking deficits on grip release phase compared to grip formation and sustained phases. To delineate differences between grip phases, bias score analysis (Grip Release Grip Formation) showed that stroke participants produced greatest error on grip release phase compared to young (P = 0.011) and agematched adults (P = 0.05) (Figure 33 ) 10% MVC/s r ate As shown i n Figure 34 the 3 3 (Group Grip Phases) mixed design ANCOVA, showed a main effect of group (F(2,24) = 12.368; P < 0.001) and grip phases (F(2,48) = 5.699; P = 0.010) Stroke participants showed greatest error (7.022 0.429) compared to agematched old (4.939 0.431) and young adults (4.176 0.393). In addition, tracking performance was more impaired on grip release phase (7.107 0.462) compared to grip formation (5.301 0.210) and sustained force (3.730 0.232) phases. Significant Group Grip P hases interaction (F(4,48) = 3.472; P = 0.022) revealed that, stroke group reported greatest error on grip formation and release phases compared to agematched and young adults. Stroke participants showed greater impairment on grip release phase compared t o grip formation and sustained phases. Bias score analysis (Grip Release Grip Formation) showed no differences among groups. 20% MVC/s r ate (Figure 35 ) In line with 5% MVC/s and 10% MVC/s rates, a significant twoway interaction was found (F(4,48) = 4. 575; P = 0.007) for 20% MVC/s rate. Stroke participants showed

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42 greatest error on grip formation and release phases compared to agematched and young adults. Also, stroke participants were more impaired on grip release phase compared to grip formation and s ustained force phases. As shown in figure 33 bias score analysis was significant (P = 0.020) with stroke participants producing greater error on grip release phase than young adults. Less A ffected H and of S troke and D ominant H and of A geM atched and Y oung A dults At 5% MVC/s rate (Figure 3 6 ), consistent with affected/nondominant hand results, we found significant group main effect, F(2,24) = 3.712; P = 0.039 and Group Grip Phases interaction (F(4,48) = 2.571; P = 0.050). Follow up analysis revealed that stroke participants significantly produced greater error on grip release phase than young adults. Within stroke group analysis revealed greater error scores on grip release phase compared to grip formation and sustained force phases. For 10% MVC/s (Figur e 37 ) and 20% MVC/s (Figure 3 8 ) rates, we found significant effects of group, grip phases and Group Grip Phases interaction. Interaction finding represented greater error on grip release phase in stroke group compared to young adults. In addition, for both rates within stroke group analysis showed similar results as seen for 5% MVC/s rate. Hence, we conclude that irrespective of rate, stroke participants show tracking error differences on grip release phase even on less affected hand compared to young adults. Low F unctioning versus H igh F unctioning S troke P articipants As shown in figure 3 9 Independent t test analysis between low functioning and high functioning stroke participants revealed that high functioning participants showed

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43 significant reduction in error on grip formation phase at 5% MVC/s and 10% MVC/s rates. However, there was no significant difference on grip release phase at all rates. These results suggested that high functioning stroke participants improve on grip formation but on grip rel ease phase there is no significant improvement compared to low functioning individuals. Standard Deviation Affected H and of S troke and N onD ominant H and of A geM atched and Y oung A dults ( Table 3 1 ) The variability outcome measure showed consistent results w ith our tracking performance further strengthening our results. The 3 3 (Group Grip Phases) mixed design ANCOVA. At 5% MVC.s rate, we found main effects of group (F(2,24) = 6.485; P = 0.006) and grip phases (F(2,48) = 14.530; P < 0.001). Post hoc analy sis showed that grip release phase (4.699 0.227) was most variable and sustained force phase (2.375 0.218) was least variable. Intermediate variability was found for grip formation phase (4.224 0.163). In addition, stroke participants showed greater variability on sustained and grip release phase compared to young adults. Finally, strong trend was seen with agematched adults on grip release phase. Additionally at 10% MVC/s and 20% MVC/s rates, comparable results were evident for main effects as seen for 5% MVC/s rate. Further at 10% MVC/s rate, stroke group produced greater variability than healthy young adults on sustained and grip release phases. At 20% MVC/s rate, we also reported high amount of variability in stroke group compared to young adults but only on sustained grip phase.

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44 Less A ffected H and of S troke and D ominant H and of A geM atched and Y oung A dults Table 3 2 reveals consistent findings with affected hand results, stroke participants showed greater variability compared to young adults on gr ip release phase at 5% MVC/s (P = 0.028) and 10% MVC/s rates (P = 0.010). Further, at 20% MVC/s rate, we found significant differences between stroke and young groups for sustained grip phase. Therefore, we concluded that stroke participants exhibits greater variability on grip release phase compared to younger adults at 5% MVC/s and 10% MVC/s rates even with less affected hand. Total Number of Steps At 5% MVC/s rate, the 3 2 (Group Grip Phases) mixed design ANCOVA with repeated measures on grip phases showed strong trend of grip phases (F(1,24) = 3.478; P = 0.074). Collapsed across other conditions, there were fewer steps on grip release phase (14.744 0.507) compared to grip formation phase (16.231 0.555). As shown in figure 3 10, stroke participants on more affected hand produced fewer steps on grip release phase compared to healthy agematched and young adults. In addition, stroke group also showed less number of steps compared to agematched and young adults on grip formation phase. Similar find ings were obtained at 10% MVC/s (Figure 3 1 1 ) and 20% MVC/s (Figure 3 12) rates for all groups when participants performed tracking task with their affected hand (stroke) and nondominant hand (elderly and young adults). Table 33 shows noticeable differences in number of steps during tracking task with the less affected hand (stroke) and dominant hand (elderly and young adults).

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45 Thus, across all rates, stroke participants produced fewer steps on both grip formation and release phases when they performed t racking task with either hands. Low Functioning versus High Functioning Stroke Participants For the secondary analysis on the number of steps based on severity, one low functioning stroke participant was excluded for grip formation (P9) and grip release (P 1) because of extreme scores. The analysis indicated that both low functioning and high functioning stroke individuals showed that on grip formation phase stroke participants produced fewer steps compared to high functioning participants at 5% MVC/s (P = 0 .097), 10% MVC/s (P = 0.040) and 20% MVC/s (P = 0.008). Contrasting findings were observed for the grip release phase. The low functioning group accumulated a higher number of steps in comparison to the high functioni ng group at all rates (Figure 3 13) Co rrelation with Disease Severity A linear regression analysis was computed to assess the relationship between disease severity (as measured with FMA, MAS and BBT) and the total number of steps produced during the tracking task. There was a positive and significant correlation between FMA and the total number of steps produced on grip formation phase at 5% MVC/s (r2 = 0.499, n = 8, P = 0.050), 10% MVC/s (r2 = 0.642, n = 8, P = 0.017), and 20% MVC/s (r2 = 0.775, n = 8, P = 0.004). Similarly, we found negative correlation between FMA and the total number of steps on grip release phase with r2 = 0.569, n = 8, P = 0.030 at 5% MVC/s rate and r2 = 0.422, n = 8, P = 0.081 at 10% MVC/s rate. A similar trend was seen at 20% MVC/s rate but, was not reached significance. The scatterplots summarizes the results (Figures 3 1 4 A, B, and C). Overall, across all rates, there was positive correlation between the two variables on grip formation and contrast was seen for grip release phase. Increase in functional capacity of stroke participants

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46 resulted into greater number of steps on grip formation and reduced number of steps on grip release phase. Similar relationships were evident on total number of steps and other clinical severity measures (MAS and BBT). Stair Steps with Larger Step Widths At 5% MVC/s rate, we found main effects of group (F(2,24) = 12.356; P < 0.001) and a strong trend of grip phases (F(1,24) = 4.041; P = 0.056) for steps with greater steps widths. In addition, the grip release phase had greater number steps of larger step width than the grip formation phase. Finally, comparisons between groups and grip phases revealed that stroke participants showed more number of steps with larger step widths compared to agematched and young adults on grip formation and release phases. In addition, stroke participants showed greater number of steps on grip release phase compared to grip formation phase (Figure 315) Similar significant patterns remained the same across 10% MVC/s (Figure 316) and 20% MVC/s (Figure 3 1 7 ) rat es. Further, similar results were reported for t he unaffected hand as shown in f igures 3 18, 31 9 and 3 20. Low Functioning versus High Functioning Stroke Participants One low functioning stroke participant was again excluded from the analysis for grip formation (P9) and grip release (P1) done for number of steps analysis because of extreme scores. Independent t tests showed that low functioning participants produced a higher number of steps with larger step widths on grip formation compared to high functi oning participants at 5% MVC/s (P = 0.099), 10% MVC/s (P = 0.046) and 20% MVC/s (P = 0.087). However, the low functioning group showed less number of steps with larger step widths on grip release phase compared to high functioning group but failed to reach significance level across all rates (Figure 3. 21)

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47 Correlation with Disease Severity Linear regression analysis on total number of steps with greater step widths is in line with above results of low functioning versus high functioning stroke participants There was a negative correlation between clinical severity measures (FMA and BBT) and the total number of steps with larger step widths on grip formation phase at all rates. Similarly, we found positive correlation between MAS and the total number of ste ps with larger step widths across all rates. No significant correlation was found between total number of steps with larger step widths and severity measures on grip release phase. The scatterplots summarizes the results correlation with FM A (Figures 3 22A B, and C)

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48 Table 3 1. Standard de viation across groups and rates of a ffected hand of stroke and non dominant hand of c ontrols Group 5% MVC/s 10% MVC/s 20%MVC/s Formation Sustained Release Formation Sustained Release Formation Sustained Release Young 3.85 (0.27) 1.86 (0.37) 3.83 (0.38) 6.35 (0.22) 2.16 (0.29) 6.19 (0.39) 9.11 (0.45) 2.66 (0.39) 9.37 (0.56) Age Matched 4.02 (0.30) 1.98 (0.40) 4.36 (0.42) 6.74 (0.24) 2.43 (0.31) 6.78 (0.42) 11.31 (0.50) 2.87 (0.43) 11.14 (0.62) Stroke 4.80 (0.30) 3.2 8 (0.40)* 5.91 (0.41)* 7.18 (0.24) 3.33 (0.31) 7.81 (0.42) 10.40 (0.49) 4.36 (0.43) 11.07 (0.61) stroke is different from young and age matched controls stroke is different from young controls

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49 Table 3 2. Standard de viation across groups a nd rates of l ess affected hand of stroke and dominant hand of c ontrols Group 5% MVC/s 10% MVC/s 20%MVC/s Formation Sustained Release Formation Sustained Release Formation Sustained Release Young 4.28 (0.80) 1.89 (0.24) 4.40 (0.47) 7.29 (0.30) 2.17 (0.26) 7.03 (0.44) 10.98 (0.57) 2.88 (0.39) 11.36 (0.66) Age Matched 4.632 (0.29) 2.32 (0.25) 5.28 (0.49) 7.27 (0.31) 2.62 (0.27) 7.63 (0.46) 11.66 (0.59) 3.87 (0.40) 11.75 (0.68) Stroke 4.69 (0.29) 2.54 (0.25) 6.33 (0.49) 7.33 (0.31) 3.10 (0.28) 9.15 (0.46 )* 10.97 (0.59) 4.71 (0.40) 12.78 (0.69) stroke is different from young and age matched controls stroke is different from young controls

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50 Table 3 3. Mean number of steps as a function of group, grip phases and rates of l ess affected of stroke a nd dominant hand of elderly and young adults Groups 5% MVC/s 10% MVC/s 20% MVC/s Formation Release Formation Release Formation Release Stroke 20.10 (0.67) 15.71 (0.86) 20.43 (0.95) 14.71 (1.00)* 16.47 (0.76) 13.70 (1.17)* Age Matched 18.52 (0.67) 16.54 (0.85) 20.98 (0.95) 16.81 (1.00) 16.37 (0.76) 15.74 (1.16) Young 17.63 (0.65) 15.72 (0.82) 21.29 (0.99) 19.99 (0.95) 18.56 (0.73) 20.64 (1.12) stroke is different from young controls grip formation is different from grip release

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51 Figure 31 Pre MVC and post MVC across groups and h ands

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52 Figure 32. Root mean square error across groups at 5% MVC/s rate of affected hand of stroke group and nondominant hand of controls

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53 Figure 33. Root mean square error bias score across groups and rates of affected hand of stroke group and nondominant hand of controls

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54 Figure 34. Root mean square error across groups at 10% MVC/s rate of affected hand of stroke group and nondominant hand of controls

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55 Figure 35. 20% MVC/s Rate Root mean square error across groups of affected hand of stroke group and nondominant hand of controls

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56 Figure 36. Root mean square error at 5% MVC/s Rate of l ess affected hand of stroke group and dominant hand of controls

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57 Figure 37. Root mean square error at 10% MVC/s rate of l ess affected hand of stroke group and dominant hand of controls

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58 Figure 38. Root mean square error at 20% MVC/s rate of l ess affected hand of stroke group and dominant h and of controls

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59 Figure 39. Normalized root mean square error across rates of affected hand of low functioning versus high functioning stroke participants

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60 Figure 310. Total number of steps at 5% MVC/s rate of a ffected hand of stroke group and nondominant hand of controls

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61 Figure 311. Total number of steps at 10% MVC/s rate of affected hand of stroke group and nondominant hand of controls

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62 Figure 312. Total number of steps at 20% MVC/s rate of a ffected hand of stroke group and nondominant hand of controls

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63 Figure 313. Total number of steps across rates of a ffected hand of low functioning versus high functioning stroke participants

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64 Figure 314. Correlation of total number of steps with Fugl Meyer Assessment scores of stroke group at A) 5% MVC/s Rate B) 10% MVC/s Rate. C) 20% MVC/s Rat e. A

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65 Figure 314. Continued B

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66 Figure 314. Continued C

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67 Figure 315. Number of steps with larger step widths at 5% MVC/s rate of a ffected hand of stroke and nondominant of controls

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68 Figure 316. Number of steps with l arger step widths at 10% MVC/s r ate of a ffected hand of stroke and nondominant of controls

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69 Figure 317. Number of steps with larger step widths at 20% MVC/s rate of a ffected hand of stroke and nondominant of controls

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70 Figure 318. Number of steps with larger step widths at 5% MVC/s r ate of l ess affected hand of stroke and dominant of controls

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71 Figure 319. Number of steps with l arger step widths at 10% MVC/s r at e of l ess affected hand of stroke and dominant of controls

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72 Figure 320. Number of steps wi th larger step widths at 20% MVC/s rate of l ess affected hand of stroke and dominant of controls

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73 Figure 321. Number of steps with larger step w idths across r at es of a ffected hand of low f unctioning versus h igh f unctioning stroke participants

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74 Fig ure 322. Correlation of t otal n umber of s teps with l arger step w idths with Fugl Meyer Assessment Scores of stroke group at A) 5 % MVC/s Rate B) 10% MVC/s Rate. C) 20% MVC/s Rate. A

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75 Figure 322. Continued B

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76 Figure 322. Continued C

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77 CHAPTER 4 DISCUSSION The primary finding of the present study supports our hypothesis of tracking performance that chronic stroke participants produce greater force control deficits as measured with root mean square error on the affected hand during the grip release phase than the grip formation and sustained grip phases. Moreover across groups, the root mean square error results revealed that stroke participants have greater tracking deficits on both grip formation and grip release phases compared to young and agematched heal thy adults. Further, chronic stroke survivors are more variable on affected hand than the control groups on sustained and release phases. Similar findings were found for less affected hand. Therefore, we conclude that stroke leads to force control deficits in both hands during both grip phases with greater deficits seen on the release phase. To examine a stair stepping phenomenon, we developed a novel approach to quantify the grip release phase. Applying the algorithm to both grip formation and grip releas e phases indicated stair stepping evidence. Across all groups there are a greater number of steps during grip formation phase than grip release phase. This finding contradicts our hypothesis and unpublished reports on stepping phenomenon. A discrepancy in our results from the aging literature may account for our methodology adopted for defining step widths based on the rate of force. To understand this novel finding, we investigated steps with larger step widths and found that the grip release phase produce d stair stepping phenomenon which was consistent with the aging literature on visual inspection. Therefore, our results of a higher number of steps with larger steps widths further explains, the visually inspected stair stepping phenomenon.

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78 In addition, st roke participants had the least number of steps and larger steps compared to healthy elderly and young adults. The above root mean square error and standard deviation results of tracking performance and number of steps with different step widths can be at tributed to five potential mechanisms. First, as it was a tracking task, stroke participants might have problem learning the new task causing greater performance deficits in terms of accuracy and number of steps. Second, stroke participants might not be able to modulate the firing of agonist (flexor) and antagonist (extensor) muscles leading to co contraction of these muscles. We know that, the power grip task requires some amount of co contraction to stabilize wrist joint. Further, initial phase of learning a new motor task causes co contraction. Thus, co contraction may be one of the potential mechanisms that can explain our findings. Third, there might be a mismatch between motor unit recruitment (grip formation phase) or derecruitment (grip release phase) patterns and motor unit firing leading to stair stepping phenomenon and declined performance. Fourth, visual and perceptual deficits after stroke might have account for some of the deficits observed in force control as the protocol challenged visuomotor system continuously. Fifth, these findings might be because of involvement of higher centers which might have caused motor planning or activation and inhibition deficits. In addition, fatigue might have contributed to reduced performance during grip phas es but our secondary analysis on pre MVC post MVC and trial block disproves fatigue as the potential factor. Moreover, this study was not designed to define or identify the exact mechanism involved in grip formation or grip release phases. Our focus in thi s first study was to investigate grip phases and rates of

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79 force production for three different types of participants as well as quantify stair stepping and step widths. We tentatively conclude that combination of these mechanisms lead to greater deficits i n grip phases in stroke participants. Hence, further research is required to validate the novel approach to quantifying stair stepping phenomenon and understand underlying mechanisms. Motor Learning Deficits after Stroke Motor learning involves skill acqu isition, motor adaptation, and decision making to accomplish goal directed tasks successfully. Motor learning studies have focused on the effects of various motor learning approaches after stroke (Butefisch, Hummelsh eim, Denzler, & Mauritz, 1995; Hanlon, 1996; Platz, Denzler, Kaden, & Mauritz, 1994; Sunderland, et al., 1992) There have been few studies on motor learning deficits (Krakauer, 2006; Takahashi & Reinkensmeyer, 2003; Winstein, Merians, & Sullivan, 1999) Takahashi and colleagues reported that stroke participants have impaired adaptation capabilities on the affected side, attributed to slowness of movement because of weakness and not due to motor learning deficits (Takahashi & Reinkensmeyer, 2003) Based on these motor learning and stroke studies, we conducted a secondary analysis on trial blocks (first 5 trials 1st trial block and last 5 trials 2nd trial block) to test if motor learning contributed in gripping deficits. We found no differences across two trial blocks for all grip phases across all rates. Our findings are in line with a recent study which reported that motor learning is preserved post stroke and is related to proprioceptive deficits (Vidoni & Boyd, 2009) None of our stroke participants reported any proprioceptive deficits as measured by proprioceptive component of FMA. In addition, the current procedure consisted of 15 practice trials (five trials at each rate) for each hand, which might have allowed for initial learning of

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80 the novel tas k. Further, our method tested hand conditions in a blocked order: a) less affected hand practice block, b) affected hand practice block, c) less affected hand experiment block and d) affected hand experiment block. Hence, based on our secondary analysis, experimental procedures, and motor learning literature, we conclude that our findings of deficits on grip phases after stroke are most likely not due to motor learning deficits. However, the present secondary analysis had only five trials per block, so furt her studies explicitly testing motor learning during grip phases is required before making definitive conclusions. Co Contraction of Agonist and Antagonist Muscles Current findings of tracking performance and number of steps might be attributed to co cont raction phenomenon; activation of the agonist and antagonist muscles, simultaneously. Cocontraction has been reported during early stages of learning a novel skilled task (Franklin, Osu, Burdet, Kawato, & Milner, 2003; Smith, 1981; Thoroughman & Shadmehr, 1999) Also, isometric power grip task itself produces some level of co contraction among forearm and wrist musculatures to provide stabilization (Basmajian, 1978; Long, 1970; Rasch, 1993) Thus, some level of co contraction was expected because of the novel power grip task. This might have been accounted with young and agematched healthy adults as the baseline groups along with practice session. However, Kamper and colleagues reported abnormal EMG activity patterns in the stroke group during isometric flexion and extension torques about the metacarpophalangeal joints of all four fingers (Kamper & Rymer, 2001) In addition, they found decreased EMG activity of extensor mus cles of fingers (Kamper & Rymer, 2001) as reported in the wrist, elbow and shoulder muscles (Chae, Yang, Park, & Labatia, 2002b; Dewald, Pope, Given, Buchanan, & Rymer, 1995; el Abd, Ibrahim, & Dietz,

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81 1993; Gowland, et al., 1992; Hammond, et al., 1988; Hu, et al., 2007; Stoeckmann, Sullivan, & Scheidt, 2009) Comparing these findings with our results might explain possible mechanism for impaired grip phases after stroke. Abnormal co contraction patterns of forearm flexors and extensors in the stroke group might have caused greater number of steps but in turn decreased number of steps with larger step widths on grip formation phase. One possible reason for this might be increased abnormal activation of extensor muscles with normal flexor activation pattern of forearm during grip formation (predominantly flexion task), which might have caused a greater number of steps with smaller step widths. However, opposite results were found for the grip release phase. A greater number of steps with larger steps widths were found perhaps because of in creased flexor activation with diminished extensor activity during the grip release phase (extension task). This explanation needs additional evidence confirming the role of co contraction during various grip phases. Studies with electromyography and H ref lex techniques combined with kinetic data will advance our understanding. Motor Unit Recruitment and Derecruitment Patterns In addition to the above mentioned mechanisms, deficits in motor unit recruitment and derecruitment patterns in stroke participants may have influenced our findings of the total number of steps seen during the tracking task. Control of motor units in normal and aging populations has been studied extensively but, advanced understanding of various motor unit mechanisms in neurological populations like stroke is limited. Stroke leads to changes in the motor unit physiological properties (Young & Mayer, 1982) suc h as degeneration of motor units in type II (fast twitch) muscle fibers (Brooke & Engel, 1969; Dattola, et al., 1993; Dietz, Ketelsen, Berger, & Quintern, 1986) because of disuse atrophy and these changes may start as early as 2 weeks post stroke (Hara,

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82 Masakado, & Chino, 2004) Recent surface EMG study of stroke groups showed that recruitment threshold was smaller on affected hand compared to less affected hand suggesting inc reased activity of low threshold motor units due to degeneration of high threshold motor units (Kallenberg & Hermens, 2009) .In addition, according to orderly recruitment of the motor unit principle (size principle), low threshold motor units will be recruited first followed by activation of high threshold motor units. Further, reverse will occur while deactivation of motor units, high threshold motor units will be derecruited first followed by low threshold motor units (Henneman, Somjen, & Carpenter, 1965a, 1965b) Also, orderly recruitment of motor units leads to smooth generation of force which is proportional to the level of f orce required to recruit the motor unit (Henneman & Olson, 1965; Zajac & Faden, 1985) These two phenomena acting together might explain our findings of total number of steps. During the grip formation phase, the low threshold motor units might have been activated after stroke leading to a smooth increment in force producing greater number of steps with smaller step widths. However, during the release phase, as high threshold motor units are degenerated, we see a greater number of steps with larger step widths causing intermittent type of relaxation of force. The present study did not test this mechanism, therefore, future studies are required to confirm if differences in grip phases is attributed to abnormal motor re cruitment or derecruitment patterns. Visual Perceptual Deficits Post Stroke Stroke leads to many visual problems such as low vision, visual field loss, ocular motility disorders and visual perceptual disorders (Dutt on, 2003; Falke, et al., 1991; Gilhotra, Mitchell, Healey, Cumming, & Currie, 2002; S. A. Jones & Shinton, 2006; Lotery, et al., 2000; Stone, Halligan, & Greenwood, 1993; Sunderland, Wade, &

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83 Langton Hewer, 1987) A recent multi center study conducted at 14 acute trust hospitals, revealed that 92% of stroke participants had visual impairment out of 323 stroke participants suspected of having visual deficits (Rowe, et al., 2009) However, stroke participants in the present study didnt report any visual perceptual disturbances on verbal questioning; but no clinical assessment tool was used to confirm visual perceptual deficits. Therefore, we were not able to certainly alleviate a possible contribution of visual perceptual deficits on our tracking results. Lesion Location Deficits in grip formation and release phases in stroke group found in this study might be because of differences in brain areas activated during these two phases. Spraker and colleagues using fMRI in normal right handed young adults reported that during grip formation, left primary motor cortex and bilateral caudate nucleus had greater activity than during grip relaxation. Further, they found that during controlled grip release, there was greater activ ation of right dorsolateral prefrontal cortex and bilateral anterior cingulate cortex (Spraker, Corcos, & Vaillancourt, 2009) These differential activation patterns during grip phases might have caused differences in the two grip phases of the stroke group because of involvement of these areas. In addition, visually guided grasping m ovement is controlled by parietofrontal circuits (Grol, et al., 2007) Also, posterior parietal cortex is involved in spatial perception (Rizzolatti & Matelli, 2003; Ungerl eider, 1982) vision for action (Milner, 1995; Rizzolatti & Matelli, 2003) and visuospatial attention (Corbetta & Shulman, 2002; Malhotra, Coulthard, & Husain, 2009) Thus damage to any of these circuits might have lead to different performance deficits which might have influenced our results. However, specific lesion location data was not available from all stroke participants in our study; hence studies exploring these

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84 d ifferent circuits in stroke participants are required in future to better understand grip deficits. LessAffected Hand Motor Deficits and Stroke In the stroke literature, there is growing evidence in support of unilateral brain damage leading to significant motor deficits on the less unaffected hand (Carey, Baxter, & Di Fabio, 1998; Colebatch & Gandevia, 1989; Desrosiers, Bourbonnais, Bravo, Roy, & Guay, 1996; Fisk & Goodale, 1988; Haaland & Harrington, 1989; Halaney & Carey, 1989; Hermsdorfer, Laimgruber, Kerkhoff, Mai, & Goldenberg, 1999; Pohl & Winstein, 1999; Winstein & Pohl, 1995) With this current study, we extended our understanding of the less affected hand motor function deficits to different grip phases. We found consistent results across all rates that our stroke participants showed greatest deficits on grip release phase compared to young adult s. Thus, we concluded that stroke leads to bilateral motor deficits. Hence, rehabilitation protocols should emphas ize bilateral arm use to improve motor deficits on both hands (Cauraugh, In Press; McCombe Waller & Whitall, 2008) Low Functioning versus High Functioning Stroke Participants Our correlation analysis of the total number of steps with clinical measures (FMA, MAS and BBT) suggests three major findings: a) total number of steps on less affected hand on both grip formation and release phases approaches normal values (young and agematched group means) as the severity of motor deficits reduces, b) similarly, on grip formation phase, as the disease severity improved stroke participants reached normative values, and c) on grip release phase, stroke participants behaved differently as the severity of stroke improved. High functioning participants showed less number of steps compared to low functioning stroke participants, young, and agematched healthy

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85 adults. Combining all three results, we conclude that on less affected hand low functioning stroke participants have greater impairment on both grip formation and release phases but high functioning participants have normal function. In addition, low functioning participants have impaired grip formation function but high functioning individuals display higher capabilities. Howev er, on grip release phase, low functioning stroke group have near normal function but, release phase shows lesser number of steps in high functioning stroke survivors. Figure 4 1 represents one trial for an individual participant force trace at 5% MVC/s r ate from all groups, which explain above mentioned novel findings. Emerging stroke evidence suggests that weakness of agonist muscles post stroke leads to compromised motor function (R.W. Bohannon, 1989; R. W. Bohannon, 2007; Canning, Ada, & O'Dwyer, 2000; Nadeau, Arsenault, Gravel, & Bourbonnais, 1999; Patten, et al., 2004) Post stroke muscle weakness may arise because of a) loss of muscle mass or motor units (Brooke & Engel 1969; Dattola, et al., 1993; Dietz, et al., 1986) b) force velocity relationship of muscles, and c) capacity of nervous control to activate motor units (Chae, et al., 2002a, 2002b; Kallenberg & Hermens, 2009; Pat ten, et al., 2004) Our low functioning stroke participants also showed weakness with MVC of 123.16N 54.48N compared to our high functioning group (MVC 322.03N 97.68N). Thus, muscle weakness or activation deficits evident from stroke literature and our data lead to impaired grip formation phase in low functioning stroke group and near normal grip formation function in high functioning group. Further, we found that grip release phase was impaired more in high functioning group compared to low functioning stroke participants. Deficits in the grip release phase in high functioning individuals

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86 might be because of lack of inhibitory control from higher centers. However, further investigations are required with larger sample size to confirm these novel find ings, which will help us answer a few of the most awaited questions in rehabilitation concerning type of intervention for wide variety of stroke population. In conclusion, this study developed a novel approach to quantify stair stepping phenomenon in grip formation and release phases during an isometric force tracking task. As discussed above, evidence suggested possible mechanisms. Along with the correlational data of stroke clinical assessment scales, we have speculated possible mechanisms which might be involved in gripping function deficits as supported by our findings. Moreover, combing the low and highfunctioning preliminary evidence with gripping deficits post stroke and correlation findings, rehabilitation professionals might be able to design trea tment protocols based on level of severity to improve hand function post stroke. Summary The present study establishes that stroke leads to force modulation deficits for grip release phase of both hands (affected and less affected). Further, we developed a novel approach to quantify stair stepping phenomenon to explore possible mechanisms responsible for force modulation deficits in various grip phases. Lastly, this study differentiates stroke population based on the severity of the disease. High functioning stroke survivors showed greater deficits in the grip release phase, which might be because of abnormal derecruitment or inhibition of motor unit patterns. However, force modulation during the grip formation phase was more impaired in low functioning stroke individuals, perhaps because of lack of recruitment or activation of motor units. To further confirm these novel findings and explore possible mechanisms involved in these

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87 force modulation deficits in grip phases post stroke additional studies are requi red, which are in preparation for future studies.

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88 Figure 41. Sample force trace of one participant from each group at 5% MVC/s r ate Formation: Abnormal Release: Abn ormal Formation: Normal Release: Abnormal

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89 APPENDIX A FUGL MEYER MOTOR AND SENSORY SCALE Participant ID Date Affected Arm A. Shoulder /Elbow/ Forearm 1. Reflexes No reflex elicited Reflex elicited a. Biceps or finger flexors b. Triceps 2. Flexor Synergy (forearm pronated and crossed over contralateral thigh, bring affected arm to ipsilateral ear) 3. Extensor Synergy (forearm supinated and resting on ipsilateral thigh, bring hand to contr alateral knee Cannot perform at all Perform partly Perform faultlessly a. Retraction b. Elevation c. Abduction d. External Rotation e. Elbow Flexion f. Forearm Supination Cannot perform at all Perform partly Perform faultlessly a. Adduction and Internal rotation b. Elbow extension c. Forearm supination

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90 4. Mixed Synergy Patterns 5. Isol ated Movements w ithout Synergy Cannot perform at all Perform partly Perform faultlessly a. Hand to lumbar spine Synergy components begin with onset of movement Synergy components begin later in movement No Synergy components b. Shoulder flexion to 90, elbow at 0, forearm neutral or pronated c. Forearm pronation supination, shoulder at 0 elbow flesed at 90 Synergy components begin with onset of movement Synergy components begin later in movement No Synergy components a. Shoulder adduction to 90, elbow at 0, forearm pronated c. Shoulder flexion 90 to 150, elbow at0 forearm neutral Cannot perform at all Perform partly Perform faultlessly c. Forearm pronation supination, shoulder flexion 30 elbow at 0

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91 6. Normal Reflex Activity (complete only if all tasks in question 5 were performed faultlessly): B. Wrist (all tests with forearm pronated) : 2 or 3 reflexes are markedly Hyperactive 1 reflex is hyperactive or 2 are lively No more than 1 re f lex i s lively. None are hyperactive Biceps, Finger Flexion Triceps No volitional movement Wrist flexion/extension through partial range Controlled movement through full range 1. Wrist Flexion/extension with elbow at 90, shoulder at 0 2. Wrist Flexion/extension with elbow at 90, shoulder at 30 Unable to extend wrist to 15 Wrist Extension to 15 unable to take resistance Able to maintain wrist extension to 15 against minimal resistance 3. Wrist stability with elbow at 90, shoulder at 0 3. Wrist stability with elbow at 90, shoulder at 30 Unable Incomplete or uncontrolled motion Complete controlled motion 5. W r i st circumduction with elbow at 90, shoulder at 0

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92 C. Han d D. Coordination / Spe ed (Finger to Nose 5 X with eye closed) Time (sec) Less affected Arm: Time (sec) Affected Arm: Cannot perform at all Perform partly Perform faultlessly 1. Fingers mass flexion 2. Fingers mass extension Unable to perform Performed weakly without resistance Performed with great resistance 3. Pip DIP hook grasp : MP joints extended and P ips +DIPs are flexed 4. Thumb adduction with paper : all other joints at 0 Unable Able to hold Hold firmly with tug 5. Pincer grasp with pencil 6. Cylinder grasp with small can 7. Spherical grasp with tennis ball Marked Tremor or dysmetria Slight tremor or dysmetria No tremor or dysmetria 1. Tremor 2. Dysmetria > 6 seconds differ b/w hands 2 5 seconds differ b/w hands < 2 seconds differ b/w hands 3. Time

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93 E. Sensation Scale F. Proprioception Scale: Upper extremity Fugl Meyer Score Anesthesia Hyperesthesia or Dyesthesia Normal Upper Arm Affected Unaffected Palm of Hand Affected Unaffected No Sensation answers Corre ct Normal 1. Shoulder 2. Elbow 3. Wrist 4. Thumb

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94 APPENDIX B MODIFIED ASHWORTH SCALE Participant ID Date Affected Arm Left / Right Muscle under stretch Score The modified Ashworth scale Score Ashworth Scale (1964) Modified Ashworth Scale Bohannon & Smith (1987) 0 (0) No increase in tone No increase in muscle tone 1 (1) Slight increase in tone giving a catch when the limb was moved in flexion or extension Sli ght increase in muscle tone, manifested by a catch and release or by minimal resistance at the end of the range of motion when the affected part(s) is moved in flexion or extension. 1+ (2) Slight increase in muscle tone, manifested by a catch, followed by minimal resistance throughout the reminder (less than half) of the ROM (range of movement). 2 (3) More marked increase in tone but limb easily flexed. More marked increase in muscle tone through most of the ROM, but affected part(s) easily moved. 3 (4) Considerable increase in tone passive movement difficult. Considerable increase in muscle tone passive, movement difficult. 4 (5) Limb rigid in flexion or extension. Affected part(s) rigid in flexion or extension.

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95 APPENDIX C DEMOGRAPHICS Subject ID____________ Date_________________ 1 ) Date of Birth: 2) Sex: 3) Dominant Limb : 4 ) Affected Side (Left or Right): 5) Date of first Cerebro Vascular Accident: 6) Type of Stroke (Ischemic /Hemorrhage): 7) # of incidence of Stroke (Date of last incidence if more than 1): 8 ) Medication : 9) Any other condition: 10) Mini mental state Examination score : 1 1 ) Box and Block: 12) Modified Ashworth Score: 1 3 ) Fugl Meyer (Upper extremity) : 14) Contact Address and email: 15) Phone

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96 LIST OF REFERENCES Andrews, K., Brocklehurst, J. C., Richards, B., & Laycock, P. J. (1981). The rate of recovery from stroke and its measurement. Int Rehabil M ed, 3(3), 155 161. Barry, B. K., Riek, S., & Carson, R. G. (2005). Muscle coordination during rapid force production by young and older adults. J Gerontol A Biol Sci Med Sci, 60 (2), 232 240. Barry, B. K., Warman, G. E., & Carson, R. G. (2005). Age related differences in rapid muscle activation after rate of force development training of the elbow flexors. Exp Brain Res, 162(1), 122132. Basmajian, J. V. (1978). Muscle Alive. Their function revealed by electromyography. (Fourth ed.). Baltimore: Williams & Wi lkins. Beebe, J. A., & Lang, C. E. (2008). Absence of a proximal to distal gradient of motor deficits in the upper extremity early after stroke. Clin Neurophysiol, 119(9), 20742085. BiglandRitchie, B., Johansson, R., Lippold, O. C., Smith, S., & Woods, J J. (1983). Changes in motoneurone firing rates during sustained maximal voluntary contractions. J Physiol, 340, 335346. Blennerhassett, J. M., Carey, L. M., & Matyas, T. A. (2006). Grip force regulation during pinch grip lifts under somatosensory guidan ce: comparison between people with stroke and healthy controls. Arch Phys Med Rehabil, 87 (3), 418429. Bobath, B. (1990). Adult Hemiplegia: Evaluation and Treatment Oxford: Heinemann Medical. Bohannon, R. W. (1989). Selected determinants of ambulatory capacity in patients with hemiplegia. Clin Rehabil. (3), 47 53. Bohannon, R. W. (2007). Muscle strength and muscle training after stroke. J Rehabil Med, 39(1), 1420. Brooke, M. H., & Engel, W. K. (1969). The histographic analysis of human muscle biopsies with regard to fiber types. 2. Diseases of the upper and lower motor neuron. Neurology, 19 (4), 378393. Bruke, D. (1988). Spasticity as an adaptation to pyramidal tract injury. Advanced Neurology, 47, 401423. Brunnstrom, S. (1970). Movement Therapy in Hemiplegia: A Neurophysiological Approach New York: Harper & Row.

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110 BIOGRAPHICAL SKETCH Sagar Naik was born in Navsari, a small town in the state of Gujarat, India. He received the Bachelor of Science in Physical Therapy from The Sarvajanik College of Physiotherapy, Surat, India in 2007. During the same year, he started the Master of Science program at the Applied Physiology and Kinesiology Department of University of Florida, Gainesville. Sagar received his Master of Science from the University of Florida in the fall of 2009 with concentration in motor learning and control under the guidance of Dr. James Cauraugh. He intends to continue pursuing research in stroke rehabilitation.