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Static and Dynamic Balance Control in Children with Autism Spectrum Disorders

Permanent Link: http://ufdc.ufl.edu/UFE0022093/00001

Material Information

Title: Static and Dynamic Balance Control in Children with Autism Spectrum Disorders
Physical Description: 1 online resource (74 p.)
Language: english
Publisher: University of Florida
Place of Publication: Gainesville, Fla.
Publication Date: 2008

Subjects

Subjects / Keywords: autism, balance, center, disorders, dynamic, forces, gait, ground, initiation, mass, of, posture, pressure, quiet, reaction, spectrum, stance, static
Applied Physiology and Kinesiology -- Dissertations, Academic -- UF
Genre: Health and Human Performance thesis, Ph.D.
bibliography   ( marcgt )
theses   ( marcgt )
government publication (state, provincial, terriorial, dependent)   ( marcgt )
born-digital   ( sobekcm )
Electronic Thesis or Dissertation

Notes

Abstract: Children with Autism Spectrum Disorders (ASD) typically exhibit impairments in three core symptom areas (deficits in communication, abnormal social interactions and restricted and/or repetitive behaviors). Within the third core category, symptoms related to stereotyped body movements and abnormalities in posture have been observed. Research suggests the postural control system in individuals with autistic disorder is immature and may never reach adult levels. Functional independence requires a postural control system that provides both postural stability during quiet stance and also dynamic stability as the body?s center of mass (COM) moves away from its base of support. The purpose of this study was to identify postural control deficiencies associated with ASD during both static and dynamic postural challenges. Using functional tasks with increasing postural challenge, we investigated postural sway (movement of the center of pressure, COP) and separation of the COM from the base of support during quiet standing and displacements of the COP during gait initiation. The hypothesis that children with ASD would have impaired postural control was supported. Statistical differences were detected between groups in all but one measure of postural sway. Further, the maximum separation between the COP and COM was on average 100% greater and more variable in children with ASD. These results seem to indicate an immature control of posture during quiet standing. The hypothesis that children with ASD would have difficulty uncoupling the COP and COM during gait initiation was only partially supported. No statistical differences in posterior COP shift were detected between the groups, suggesting the COP shift mechanism for generating forward momentum is intact in children with ASD. However, significantly smaller lateral COP shifts were observed in children with ASD and may indicate instability or an alternative strategy for generating stance side momentum or lateral weight shifting.
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.
Thesis: Thesis (Ph.D.)--University of Florida, 2008.
Local: Adviser: Hass, Christopher J.
Electronic Access: RESTRICTED TO UF STUDENTS, STAFF, FACULTY, AND ON-CAMPUS USE UNTIL 2010-05-31

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Source Institution: UFRGP
Rights Management: Applicable rights reserved.
Classification: lcc - LD1780 2008
System ID: UFE0022093:00001

Permanent Link: http://ufdc.ufl.edu/UFE0022093/00001

Material Information

Title: Static and Dynamic Balance Control in Children with Autism Spectrum Disorders
Physical Description: 1 online resource (74 p.)
Language: english
Publisher: University of Florida
Place of Publication: Gainesville, Fla.
Publication Date: 2008

Subjects

Subjects / Keywords: autism, balance, center, disorders, dynamic, forces, gait, ground, initiation, mass, of, posture, pressure, quiet, reaction, spectrum, stance, static
Applied Physiology and Kinesiology -- Dissertations, Academic -- UF
Genre: Health and Human Performance thesis, Ph.D.
bibliography   ( marcgt )
theses   ( marcgt )
government publication (state, provincial, terriorial, dependent)   ( marcgt )
born-digital   ( sobekcm )
Electronic Thesis or Dissertation

Notes

Abstract: Children with Autism Spectrum Disorders (ASD) typically exhibit impairments in three core symptom areas (deficits in communication, abnormal social interactions and restricted and/or repetitive behaviors). Within the third core category, symptoms related to stereotyped body movements and abnormalities in posture have been observed. Research suggests the postural control system in individuals with autistic disorder is immature and may never reach adult levels. Functional independence requires a postural control system that provides both postural stability during quiet stance and also dynamic stability as the body?s center of mass (COM) moves away from its base of support. The purpose of this study was to identify postural control deficiencies associated with ASD during both static and dynamic postural challenges. Using functional tasks with increasing postural challenge, we investigated postural sway (movement of the center of pressure, COP) and separation of the COM from the base of support during quiet standing and displacements of the COP during gait initiation. The hypothesis that children with ASD would have impaired postural control was supported. Statistical differences were detected between groups in all but one measure of postural sway. Further, the maximum separation between the COP and COM was on average 100% greater and more variable in children with ASD. These results seem to indicate an immature control of posture during quiet standing. The hypothesis that children with ASD would have difficulty uncoupling the COP and COM during gait initiation was only partially supported. No statistical differences in posterior COP shift were detected between the groups, suggesting the COP shift mechanism for generating forward momentum is intact in children with ASD. However, significantly smaller lateral COP shifts were observed in children with ASD and may indicate instability or an alternative strategy for generating stance side momentum or lateral weight shifting.
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.
Thesis: Thesis (Ph.D.)--University of Florida, 2008.
Local: Adviser: Hass, Christopher J.
Electronic Access: RESTRICTED TO UF STUDENTS, STAFF, FACULTY, AND ON-CAMPUS USE UNTIL 2010-05-31

Record Information

Source Institution: UFRGP
Rights Management: Applicable rights reserved.
Classification: lcc - LD1780 2008
System ID: UFE0022093:00001


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1 STATIC AND DYNAMIC BALANCE CONT ROL IN CHILDREN WITH AUTISM SPECTRUM DISORDERS By KIMBERLY ANN FOURNIER A DISSERTATION PRESENTED TO THE GRADUATE SCHOOL OF THE UNIVERSITY OF FLOR IDA IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF DOCTOR OF PHILOSOPHY UNIVERSITY OF FLORIDA 2008

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2 2008 Kimberly Ann Fournier

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3 To my loving parents Jud ith and George Fournier

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4 ACKNOWLEDGMENTS I wish to thank Dr. Chris Hass for providi ng me with invaluable insight, support and mentorship in the areas of biomechanics and pos tural control. In a ddition, I would like to sincerely thank him for mainta ining a challenging learning environment necessary for the development of skills and confidence that wi ll no doubt contribute to my success as an independent researcher. I wish to offer my sincerest gratitude to my internal supervisory committee members Dr. Mark Tillman and Dr Erik Wikstrom for their expe rtise and invaluable contributions to my specific area of study as well as my academic growth. I would also like to extend my genuine appreciation to my external supervisory committee members Dr. Krestin Radonovich and Dr. Mark Lewis for their experi ence and guidance in helping me learn an extensive amount about autism spectrum disorders. I would like to thank the faculty members in Applied Physiology and Kinesiology for openi ng many doors to my academic future. Their broad range of expertise has provided me with a solid f oundation on which to build my continuing academic career. My experience at th e University of Florid a would most certainly have been lacking without the challenging demands put forth by the faculty members. I would especially like to thank Cara Kimberg for her expertise, her support, and her willingness to help at all costs. She is a dear friend and was absolutely instrumental in the completion of this project. I would also like to acknowledge th e support provided by my colleagues in the Biomechanics Laboratory. I w ould like to thank Dana Otzel for being a very reliable assistant for data collection, and al so Kari Mader and Steven Albrechta for being enthusiastic and competent worker bees. I w ould also like to acknowledge all the hard work and support offered by Michelle Benjamin and th e volunteer students in the Neurodevelopmental lab.

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5 I absolutely must also thank my family Ga ston, Nicole, Greg, Kerry Michelle, Isabelle, Annika, Leila and my dear friend Lori for s upporting me, loving me, and providing me with the much needed support required to endure this leng thy and challenging process. A special thank you to the Bourke family for their friendship an d for allowing me to shamelessly use their images in presentations and flyers distributed in the community in order to recruit participants for this study.

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6 TABLE OF CONTENTS page ACKNOWLEDGMENTS...............................................................................................................4 LIST OF TABLES................................................................................................................. ..........8 LIST OF FIGURES.........................................................................................................................9 ABSTRACT...................................................................................................................................10 CHAP TER 1 IN TRODUCTION..................................................................................................................12 Purpose of the Study........................................................................................................... ....14 Significance of the Study........................................................................................................15 Research Goals and Hypotheses............................................................................................. 15 Specific Aim 1.................................................................................................................15 Hypothesis 1................................................................................................................... .15 Specific Aim 2.................................................................................................................16 Hypothesis 2................................................................................................................... .16 Specific Aim 3.................................................................................................................16 Hypothesis 3................................................................................................................... .16 2 MATER IALS AND METHODS...........................................................................................17 Participants.............................................................................................................................17 Inclusion/Exclusion Criteria for Children with ASD...................................................... 17 Inclusion/Exclusion Criteria for Typically Developing Children ...................................17 Experimental Setup............................................................................................................. ....18 Testing Protocol......................................................................................................................18 Static Balance (Quiet Stance)..........................................................................................18 Dynamic Balance (Gait Initiation).................................................................................. 18 Data Reduction.......................................................................................................................18 Outcome Measures: Static Balance (Quiet Stance)......................................................... 19 Outcome Measures: Dynamic Balance (Gait Initiation)................................................. 20 Data Analysis..........................................................................................................................20 Static Balance (Quiet Stance)..........................................................................................20 Dynamic Balance (Gait Initiation).................................................................................. 21 3 LITERATURE REVIEW.......................................................................................................27 Autism and Autism Spectrum Disorders (ASD).................................................................... 27 Etiology of Autism............................................................................................................. ....28 Development of Postural Control........................................................................................... 32 Motor Deficits and Autism.....................................................................................................35

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7 Static Balance (Quiet Stance) and Autism.............................................................................. 35 Dynamic Balance (Gait Initiation).......................................................................................... 39 4 RESULTS ...............................................................................................................................45 Static Balance (Quiet Stance).................................................................................................45 Dynamic Balance (Gait Initiation).......................................................................................... 46 5 DISCUSSION.........................................................................................................................53 Static Balance (Quiet Stance).................................................................................................53 Dynamic Balance (Gait Initiation).......................................................................................... 56 Limitations and Future Directions.......................................................................................... 58 6 CONCLUSIONS.................................................................................................................... 61 APPENDIX CENTER OF PRESSURE (COP) & CEN TER OF MASS ( COM) CALCULATIONS............... 63 Calculating COP for One Forceplate...................................................................................... 63 Calculating COPnet for Two Forceplates................................................................................ 63 Calculating COM via Integration........................................................................................... 63 Trapezoidal Method of Nu m erical Integration................................................................ 63 Estimating COM Displacement....................................................................................... 64 LIST OF REFERENCES...............................................................................................................65 BIOGRAPHICAL SKETCH.........................................................................................................74

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8 LIST OF TABLES Table page 2-1 Descriptive statistics (means and SD) for age, height and m ass........................................ 22 2-2 Leiter International Performance ScaleRev ised (Leiter-R) means and ranges for all participants.........................................................................................................................23 2-3 Repetitive Behavior Scales-Revised (RBS -R) m eans and ranges for all participants....... 24 2-4 Adaptive Behavior Assessment System (ABAS-II) means and ranges for all participants. ........................................................................................................................25 2-5 Brief Rating Inventory of Executive F unctioning-Parent Form (BRIEF) m eans and ranges for all participants...................................................................................................26

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9 LIST OF FIGURES Figure page 4-1 Means and SD for normalized COP measures (COPML, COPAP, and COPSWAY) during quiet stance (* p<0.05)...........................................................................................47 4-2 Scatter of normalized mean COP measures during quiet stance for each participant. A) COP movement in mediolateral directi on. B) COP movement in anteroposterior direction. C) COP sway area............................................................................................. 48 4-3 Means and SD for normalized peak COPCOM mom ent arms (COPCOMmaxML, COPCOMmaxAP and COPCOMmaxR) during quiet stance (* p<0.05).................. 49 4-4 Scatter of normalized mean, peak CO PCOM m oment arms during quiet stance for each participant. A) COPCOM moment ar m in mediolateral direction. B) COP COM moment arm in anteroposterior dire ction. C) COPCOM resultant moment arm.....................................................................................................................................50 4-5 Means and SD for normalized COP di splacem ents (S1_ML and S1_AP) during gait initiation for ASD (* p<0.05)............................................................................................51 4-6 Scatter of normalized mean COP disp lacem ents during gait initiation. A) COP displacement in mediolateral direction. B) COP displacement in anteroposterior direction.............................................................................................................................52

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10 Abstract of Dissertation Pres ented to the Graduate School of the University of Florida in Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy STATIC AND DYNAMIC BALANCE CONT ROL IN CHILDREN WITH AUTISM SPECTRUM DISORDERS By Kimberly Ann Fournier May 2008 Chair: Christopher J. Hass Major: Health and Human Performance Children with Autism Spectrum Disorders (ASD ) typically exhibit impairments in three core symptom areas (deficits in communication, abnormal social interactions and restricted and/or repetitive behaviors). Within the third core category, symptoms related to stereotyped body movements and abnormalities in posture have been observed. Research suggests the postural control system in indivi duals with autistic disorder is immature and may never reach adult levels. Functional indepe ndence requires a postural contro l system that provides both postural stability during quiet stance and also dynamic stability as the bodys center of mass (COM) moves away from its base of support. The purpose of this study was to identify postural control deficiencies associated with ASD during both static and dynamic postural challenges. Using functional tasks with incr easing postural challenge, we investigated postural sway (movement of the center of pressure, COP) and separation of the COM from the base of support during quiet standing and displacements of the COP during gait initiation. The hypothesis that children with ASD woul d have impaired postural control was supported. Statistical differences were detected between groups in all but one measure of postural sway. Further, the maximum separati on between the COP and COM was on average 100% greater and more variable in children with ASD. These results seem to indicate an

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11 immature control of posture during quiet sta nding. The hypothesis that children with ASD would have difficulty uncoupling the COP and COM during gait initiatio n was only partially supported. No statistical differences in posterior COP shift we re detected between the groups, suggesting the COP shift mechanism for generating forward momentum is in tact in children with ASD. However, significantly smaller lateral CO P shifts were observed in children with ASD and may indicate instability or an alternative strategy for genera ting stance side momentum or lateral weight sh ifting.

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12 CHAPTER 1 INTRODUCTION Autism is a neurodevelopmental disorder dia gnosed according to specific impairments in the areas of communication, reci procal interaction and stereotypic behavior (DSM-IV., 2000). Autism Spectrum Disorders (ASD) is an inclusive te rm for individuals with autistic disorder and those diagnosed with Pervasive Developmental DisorderNot Otherwise Specified (PDDNOS) and Aspergers Syndrome (DSM-IV., 2000; Tanguay, Robertson, & Derrick, 1998). The primary impairments observed in children with ASD span across three broad categories: social interactions, communication and repe titive and restrictive behaviors. Associated features include diagnosis of mental retardation (~75%), uneven impairments in the development of cognitive skills, behavioral symptoms, altered responses to sensory stimuli, abnormalities in eating and mood and various nonspecific neurological sympto ms (primitive reflexes, delayed development of hand dominance and seizures) (DSM-IV., 2000). Within the third main category of symptoms (repetitive and restricted behavi ors), previous research in th e area of motor development has suggested that movement disturbances may be pr esent during infancy and may be considered one of the earliest signs of autism (Teitelbaum, Teitelbaum, Nye, Fryman, & Maurer, 1998). Furthermore, motor problems have been the mo st frequently reported nonverbal deficits in children with autism (Noterdaeme, Mildenberger, Minow, & Amorosa, 2002). An immature postural control system can be a limiting factor on the emergence of other motor skills (such as coordinated hand/head movements and inhibition of reflexes), may constrain the ability to develop mobility and manipulatory skills (S humway-Cook & Woollacott, 2001), and is of significant importance to quality of life. Therefor e, systematically evaluating postural control in this population may be a first step towards dete rmining the best approach for improving postural stability and related skills (mobility and manipulation).

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13 With the etiology of ASD not being clearly defined, the specific pattern and source of motor deficits in this populati on remain unclear (Noterdaeme et al., 2002). However, the early onset of abnormal movements (within the first ye ar of life) (Teitelbaum et al., 1998), perhaps even before communicative or social deficits manifest, suggests that motor deficits may be partially linked to some core characteristic of ASD (Leary & Hill, 1996; Nayate, Bradshaw, & Rinehart, 2005). Unfortunately, li ttle attention has been given to motor deficits in the ASD population and have been referred to simply as a less important or a cooccurring syndrome (Noterdaeme et al., 2002). Leary & Hill (1996) in their review, however, suggest motor deficits likely impair the development of sufficient comm unicative and interactive skills (Leary & Hill, 1996). Indeed, Noterdaeme et al. (2002) suggested that motor disturbances in children with autism put an additional strain on the childrens development; resulting in difficulty mastering daily activities such as eating with a knife and fork, stair climbing, writing, ball games and bicycling. Therefore, it appears that the occurr ence of neuromotor deficits in autism may be a partial indication of the biological factors in the etio logy of the disorder (Jones & Prior, 1985; Leary & Hill, 1996). The ability to maintain an upright posture is a fundamental skill necessary for typical motor development in humans. Research suggests that individuals with autistic disorder have developmental delays in postural control with sy stems that never fully mature to adult levels (Kohen-Raz, Volkmar, & Cohen, 1992). The vestib ular, somatosensory and visual systems are the afferent inputs involved in maintaining an upright posture. A deficit in any one of these systems or in the integration of information provided from these systems could affect the ability to maintain balance. Postural patterns employe d by children with autistic disorder over the age of 6 years have been observed to differ from typically developing children, mentally retarded

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14 children and adults with vestibular disorders. In addition, these olde r children with autistic disorder, when compared to typically developing children (ages 4 to 11 years), exhibited more variable and less stable postural control, particularly in the medi olateral direction (Kohen-Raz et al., 1992). Both children and adults with ASD ha ve been observed to have impaired postural stability when compared to individuals with typical neuromotor development under conditions where one or more sensory inputs had been rem oved or modified. However, when afferent inputs were not modified, differe nces in postural sway are not as apparent (Gepner, Mestre, Masson, & de Schonen, 1995; Minshew, Sung, J ones, & Furman, 2004; Molloy, Dietrich, & Bhattacharya, 2003). In addition, when investigating age effects, data indicated a delayed development of the postural system in subjects with autistic disorder, which only began to improve at the age of 12 years, and never reach ed adult levels (Kohen-Raz et al., 1992; Minshew et al., 2004). These authors have therefore suggested that there is an involvement of the neural circuitry beyond the neural systems for soci al behavior, communication and reasoning. Furthermore, despite this informa tion, there is still is a paucity of research investigating a wider range of functional tasks challenging both the static and dynamic postural control of this population. Purpose of the Study Functional independence require s a postural control system that provides both postural stability during quiet stance a nd also dynamic stability as the bodys center of mass (COM) moves away from its base of support. The primary purpose of this study was to identify postural control deficiencies associated with ASD during both static and dynamic postural challenges. Using functional tasks with increasing postural ch allenge, we investigated postural sway and the separation of the COM from the base of support ( center of pressure, COP) during quiet standing and manipulation of the COP during gait initiation.

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15 Significance of the Study The source and type of motor impairments in children with ASD remain unclear. The early onset of motor impairments suggests that moto r deficits may indeed be related to some core characteristic of ASD. Delayed or abnormal balance control may cons train the ability for children with ASD to develop related stability or mobility skills. To date, limited research has focused on static balance in the ASD population. Furthermore, to the best of our knowledge, research in the area of dynamic balance in this population is nonexistent. Using quantifiable measures of postural control that have been us ed successfully in othe r populations (elders, stroke, Parkinsons disease); findings from this investigation have the potential to provide important insight into static a nd dynamic control of children with ASD. Furthermore, by better characterizing these impairments, we can assist in the design of treatments that address postural instabilities early in development, which may he lp minimize or prevent subsequent emergence of deficits in other motor abilities. Research Goals and Hypotheses Specific Aim 1 To determine whether children with ASD ha ve impaired postural control by quantifying COP measures during quiet stance. Hypothesis 1 Based on previous research, we hypothesized that children with ASD would have increased postural sway. As a result, we believed the COP ranges (mediolateral and anteroposterior) and sway areas observed in children with ASD woul d differ from those observed in typically developing, agedmatched children. Specifically, we believed COP ranges and sway areas would be greate r in children with ASD, indica ting static balance instability.

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16 Specific Aim 2 To determine whether children with ASD ha ve impaired postural control by quantifying COPCOM distances during quiet stance. Hypothesis 2 Based on previous research, we hypothesized that children with ASD would have increased postural sway. As a result, we believed the peak COPCOM distances observed in children with ASD would differ from those obs erved in typically developing, agedmatched children. Specifically, we believed peak COPCO M distances would be gr eater in children with ASD, indicating static balance instability. Specific Aim 3 To determine whether children with ASD have impaired dynamic postural stability as the body transitions from a static to a cha nging base of support (gait initiation). Hypothesis 3 We hypothesized that during gait initiation, children with ASD would have impaired abilities to uncouple the COP and COM, essential for propulsion in the forward and lateral directions. Specifically, we belie ved displacements of the COP would be decreased in children with ASD compared to typically developing, age matched children, as seen in older individuals and those with disability.

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17 CHAPTER 2 MATERIALS AND METHODS Participants Thirteen children with ASD (ages 8) we re recruited from the Child & Adolescent Psychiatry Clinic at the Univer sity of Florida. Thirteen ty pically developing, chronologically agedmatched children (within one year) were recruited from the community and served as controls. We chose the age range of 8 years to ensure a relatively mature postural system in typically developing children, which in turn serv ed as benchmarks for comparisons with children with ASD (Table 2). Descriptive data for ch ildren diagnosed with ASD (Leiter International Performance Scale-Revised (Leiter-R), Repetitive Behaviors Scales-Revised (RBS-R), Adaptive Behavior Assessment System (ABAS-II), and Br ief Rating Inventory of Executive FunctioningParent Form (BRIEF)) are presented in Ta bles 2-2, 2-3, 2-4 and 2-5 respectively. Inclusion/Exclusion Criteria for Children with ASD Clinical diagnoses of ASD from a licensed professional (psychologist or physician) and confirmed with one of three scales (Autism Diagnostic Observation Schedule (ADOS; Lord, Rutter, Dilavore, & Risi, 1999), Soci al Communication Questionnaire (Rutter, Bailey, & Lord, 2003), Childhood Autism Rating Scale (Schopler, Reichler, & Renner, 1988)). No known genetic/medical conditions (fragile X syndrome, tuberous sclerosis, seizures) as confirmed by medical records/examinations. No known sensory deficits (not blind or deaf) Ambulatory with no signifi cant physical impairments Inclusion/Exclusion Criteria for Typically Developing Children No known sensory deficits (not blind or deaf) Ambulatory with no signifi cant physical impairments No medical chart diagnoses of psychiatri c (e.g. ADHD) or neurologi cal (e.g. Tourettes Syndrome) disorders

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18 Experimental Setup All biomechanical testing was performed in the Biomechanics Laboratory, Center for Exercise Science at the University of Florida, Gainesville, Florida. Using a two adjacent forceplates (Type 4060, Bertec Corp., Columbus, OH), ground reaction forces (GRF) were recorded (360 Hz). Testing Protocol Static Balance (Quiet Stance) All participants were asked to stand with thei r feet comfortably apart with one foot on each of the adjacent forceplates w ith a selfselected stance width. Foot positioning was marked on the initial trial and used for all subsequent trials Participants were asked to stand as still as possible for 20 seconds with their arms comfortably at their side Participants performed four experimental trials. Trials where voluntary movements were observed were rejected and additional trials were performed. Dynamic Balance (Gait Initiation) Participants were asked to stand on the adja cent forceplates as pr eviously described. Participants began from a quiet stance position, and were gi ven a verbal cue to initiate movement. Once the cue was given, particip ants were asked to take a short pause (approximately 2 sec) and then start walking with their preferred foot, at a selfselected speed, in the forward direction. Data colle ction began with the verbal cue and continued for several steps after both feet had left the forceplates. Particip ants were allowed several practice trials and data from 4 experimental trials were collected and used in subsequent analyses. Data Reduction Ground reaction forces and moments collected fro m the two forceplates were processed and the location of the COP for each forceplate was calculated (Appendix A). The location of the

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19 COPnet from the two forceplates, in both the mediolat eral (ML) or anteroposterior (AP) directions was calculated according to previously reported literature (Winter, Patla, Ishac, & Gage, 2003) (Appendix A). Once the COP was computed, the p eak displacements in the mediolateral and anteroposterior directions were determined and the sway area was calculated. Because differences in stance width can influence postura l control, specifically in the mediolateral direction (Rocchi et al., 2006), displacements duri ng quiet stance and gait initiation trials were normalized to the individuals stance width and foot length. Typically the position of the COM is calculate d from positional data. This technique uses a weighted sum to estimate the COM for each pa rticipant using the 3D positional data from markers and anthropometric data. It is important to note however, that this technique requires that reflective markers (stickers) be affixed to an individuals skin in order to define body segments. This procedure was problematic in the ASD population, where most individuals did not like the sensations of stickers being affixed to their skin or clothing. As a result, segmental data could not be collected without markers pr esent. The COM for the whole body was therefore determined via an alternative method. The accel erations obtained from ground reaction forces were doubly integrated using the trapezoidal method (Appendix A). Assuming the position of COP will coincide with that of the COM during quiet stance (Winter, Patla, Prince, Ishac, & Gielo-Perczak, 1998), estimates for COM displacement were obtained using the methodology described in the literatu re (Chan, 1999). Both methods (marker and integration) yield equivalent approximations of the whole body COM and can be used interchangeab ly (Chan, 1999; Lafond, Duarte, & Prince, 2004; Zatsiorsky & King, 1998). Outcome Measures: Static Balance (Quiet Stance) Characteristics of the individual s postural sway were assessed using traditional COP analyses including the range of anteroposte rior and mediolateral sway and the overall sway area for each

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20 of the quiet stance trials. Furthe rmore, the distance between the COM and COP in the transverse plane, defined as the COPCOM moment arm, was also calculated. As a result, peak moment arms (COPCOMmax) in the mediolateral and anteroposterior directions and s ubsequent resultant moment arms were also identified and analy zed for each of the quiet stance trials. Outcome Measures: Dynamic Balance (Gait Initiation) The COP trajectory during gait initiation wa s divided into 3 phases (S1, S2, S3) by identifying 2 landmark events previously described in the literature (Hass et al., 2004). Because the S1 phase represents the pur poseful uncoupling of the COP and COM and thus is the initial balance challenge, peak disp lacement of the COP in the mediolateral (S1_ML) and anteroposterior (S1_AP) directions were calculated and analyzed for each of the gait initiation trials. Data Analysis Descriptive statistics (Mean a nd SD) were calculated for age, height, and weight (Table 2). Measures of central tendency and variability were calculated for the variables of interest. An individuals data from the four experimental trials in each condition were then averaged to provide one representative datum for each depe ndent variable. The representative datum was then submitted for statistical analyses. Static Balance (Quiet Stance) The primary hypotheses were that children w ith ASD would posses more postural sway during quiet stance than age matched controls. Initial exploration of the data revealed heterogeneity of variance between groups. Mu ltivariate analyses of variance (MANOVA) have been reported to lack robustness in accurate ly testing for overall group differences when the assumption of homoscedasticity has been violat ed (Finch, 2005). As a result, non parametric MannWhitney U tests were used to test for group differences on COP trajectories and COP

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21 COM interactions during quiet stance. An prio ri alpha level of 0.05 was set for all statistical tests. All statistical tests were performed using SPSS 16.0 fo r Windows (Chicago, Illinois). Dynamic Balance (Gait Initiation) The primary hypothesis was that children w ith ASD would possess altered anticipatory postural adjustments resulting in reduced displa cements of the center of pressure during gait initiation. Similarly to quiet stance data, the depe ndent variables of interest were submitted for MannWhitney U Tests to evaluate overall group differences. An priori alpha level of 0.05 was set for all statistical tests. All statistical tests were pe rformed using SPSS 16.0 for Windows (Chicago, Illinois).

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22 Table 2-1. Descriptive statistics (mean s and SD) for age, height and mass. Group Age (years) Height (m) Mass (Kg) ASD (n=13) Mean 11.1 1.45 50.2 SD 2.3 0.17 21.8 TD (n=13) Mean 13.1 1.57 48.2 SD 2.2 0.12 10.3

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23 Table 2-2. Leiter International Performance Scale-Revised (Leiter-R) means and ranges for all participants. (Roid & Miller, 1997) ASD (N=13) Mean (range) Control (N=13) Mean (range) Leiter-RBrief IQ 80.2 ( 36-124) 104.9 (67-129)

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24 Table 2-3. Repetitive Behavior Scales-Revised (RBS-R) means and ranges for all participants. (Bodfish, Symons, & Lewis, 1999; Bodfis h, Symons, Parker, & Lewis, 2000) ASD (N=13) Mean (range) Control (N=13) Mean (range) RBS-R*overall 20.6 (11-36) 0.9 (0-8) RBS-R subscale 1 (stereotyped behavior) 3.8 (2-6) 0.2 (0-2) RBS-R subscale 2 (self-injurious behavior) 1.5 (0-6) 0.0 RBS-R subscale 3 (compulsive behavior) 3.3 (0-6) 0.2 (0-1) RBS-R subscale 4 (ritualistic behavior) 4.2 (1-6) 0.2 (0-1) RBS-R subscale 5 (insistence on sameness) 5.2 (2-10) 0.4 (0-5) RBS-R subscale 6 (restricted behavior) 3.6 (0-20) 0.1 (0-1)

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25 Table 2-4. Adaptive Behavior Assessment System (ABAS-II) means and ranges for all participants. (Harrison & Oakland, 2003) ASD (N=13) Mean (range) Control (N=13) Mean (range) Communication 3.9 (1-9) 11.1 (7-14) Community Use 3.7 (1-8) 11.3 (8-16) Functional Academics 5.9 (1-15) 12.0 (5-16) Home Living 4.3 (1-11) 11.5 (6-17) Health and Safety 4.3 (1-13) 11.3 (3-16) Leisure 3.7 (1-9) 11.4 (7-15) Self-Care 3.4 (1-11) 10.8 (5-15) Self-Direction 2.1 (1-9) 10.6 (5-16) Social 1.5 (1-4) 11.4 (7-14)

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26 Table 2-5. Brief Rating Invent ory of Executive Functioning-Par ent Form (BRIEF) means and ranges for all participants. (Gioia, Isquith, Guy, & Kenworthy, 2000) ASD (N=13) Mean (range) Control (N=13) Mean (range) Inhibit 68.2 (42-91) 47.6 (37-68) Shift 75.4 (59-95) 44.8 (36-70) Emotional Control 67.3 (45-91) 43.8 (37-80) Behavioral Regulation Index 73.2 (53-99) 44.7 (36-76) Initiate 64.3 (46-83) 50.8 (35-76) Working Memory 65.2 (45-86) 52.5 (38-71) Plan/Organize 63.2 (44-90) 48.6 (35-61) Organization of Materials 55.3 (37-71) 47.6 (33-60) Monitor 69.3 (50-84) 46.8 (33-70) Metacognition Index 65.7 (49-87) 48.2 (34-63) Global Executive Composite 70.2 (55-92) 47.0 (33-66)

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27 CHAPTER 3 LITERATURE REVIEW Autism and Autism Spectrum Disorders (ASD) Five childhood disorders (autistic disorder pervasive developmental disorder not otherwise specified (PDDNOS ), Aspergers disorder, Retts disorder and childhood disintegrative disorder) are all grouped under the pervasive de velopmental disorders umbrella according to The Diagnostic and Statistical Manual for Mental Disorders (DSMIV). Three of these disorders (autisti c disorder, PDDNOS and Aspergers syndrome) are often referred to as Autism Spectrum Disorders (ASD). These disorders are lifelong neurologi cal conditions that can affect an individuals ability to communicate, und erstand language, play and socially interact with others and are often accomp anied by restricted, repetitive and stereotyped patterns of behavior, interests and activities. Although the classical form of autism, (autistic disorder) which typically manifests itself in developmental delays before the age of 3, can be differentiated from other forms of ASD, the terms autism and ASD are often used interchangeably. Although ASD affect functioning of the brain, th eir specific causes remain unknown. It is widely believed that their etiology are multifactor ial with each factor possibly leading to the expression of different phenotypes within ASD. As a result, individuals with ASD vary widely in ability and functioning. Although individu als with ASD are typically characterized by developmental delays in verbal and nonverbal communication, social re latedness and leisure and play activities, these i ndividuals also exhibit unusual, repetitive and perseverative movements. It is estimated that 1 in ever y 150 individuals is diagnosed with ASD, making it more prevalent than pediatric cancer, diabet es, and AIDS combined. It is not bound by any racial or social groups but is more likely to be diagnosed in boys than girls. Approximately 67 children are diagnosed with ASD each day with an estimated health care cost of 90 billion

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28 dollars per year. With no medical detection or cure for ASD, rese arch aimed at providing further insight into the etiology, early detection and treatment are of the utmost importance (Autism Society of America, Retrieved December 11, 2007). Etiology of Autism Autism spectrum disorders are some of the most heritable neuropsychiatric syndromes with a highly variable phenotype (Sykes & Lamb, 2007).Wholegenome linkage scans have implicated nearly every chromosome, although none have been consis tently identified as contributory (Sykes & Lamb, 2007). There is growing evidence to suggest that as many as 3 genes are associated with ASD (Pickles et al ., 1995; Risch et al., 1999) Although several loci have been identified in multiple studies (2q, 7q and 17q), lack of conclusive linkage results suggests the etiology of ASD is more complex a nd heterogeneous than original supposed (Sykes & Lamb, 2007). Many of these genes of interest have only accounted for a small fraction of the genetic variation in the disorder and knowledge of most of the genes rema ins incomplete (Sykes & Lamb, 2007). Other factors such as prenatal environmental exposures and gender are thought to exacerbate the matter further by increasing the likeli hood of presenting with the disorders and influencing their severity (DiCicco-B loom et al., 2006; Sykes & Lamb, 2007). Given that ASD is primarily a genetic disord er involving multiple genes, understanding the underlying mechanisms will likely require a collaboration of multiple disciplines. Assessment of the earliest signs of ASD has helped guide th is multidisciplinary research in the areas of abnormal brain growth, development and functio n (DiCicco-Bloom et al., 2006). Although ASD are neurodevelopmental disorders w ith a clinical onset between the ages of 2 and 4 years, very few studies have investigated th e anatomical development of the brain during this critical age range (Courchesne et al., 2007), This period (2 years) is a crucial period in development as neural wiring patterns begin to lay the foundatio n for the development of higher order social,

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29 emotional and communication functions (Courchesne et al., 2007). Unfortunately, most of the anatomical studies have focused on the older child, adolescent or adult with ASD (Cody, Pelphrey, & Piven, 2002). As a result, the abnormal brain growth responsible for the dysfunction in social, emotiona l and communication networks re mains unclear (Courchesne et al., 2007). Movement coordination is believ ed to be controlled by three important structures including the motor cortex, basal ganglia and the cerebellum. Although the cerebellum is integral in the coordination, it is not a significan t contributor in either sensor y or motor functioning (ShumwayCook & Woollacott, 2001). Ev en if the cerebellum is de stroyed, sensation and motor functioning are not lost. However, the quality of movement may be drastically altered (Shumway-Cook & Woollacott, 2001). Similarly, lesions of the basal ganglia do not result in paralysis; however, problems in coordinated movements emerge. The motor cortex interacts with the cerebellum and basal ganglia in order to identity the intended movement, the plan necessary for movement and the execution of the movement (Kandel et al., 2000). The most consistent brain abnormalities re lated to ASD have been observed in the cerebellum (Bauman & Kemper, 2005). Regardless of age, sex or cognitive abilities, significant decreases in the number of Purkinje cells a ffecting the cerebellar hemispheres have been consistently observed (Arin, Bauman, & Kemper, 1991). Though the cerebellum only constitutes 10% of the total volume of the brain, it contains over half of all its neurons. The cerebellum functions as a relay station between intent ion and action by adjusting motor output in the cortex and brain stem during movement (Kandel, Schwartz, & Jessell, 2000). The cerebellum compares internal feedback signals which define the intended movement and the external feedback signals which define the actu al movement. When the movement is repeated,

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30 the cerebellum is able to perform corrections and gradually reduce error and therefore plays a key role in motor learning and adaptation (Kande l et al., 2000). Damage to the cerebellum may not necessarily affect the basic elements of perception and movement, but temporospatial coordination of movement is affected. Subseque ntly certain cognitive functions, motor learning and posture may be impaired (Kandel et al., 2000). In addition to the cerebellum being implicated as a site of possibl e dysfunction in ASD, studies of locomotion have also suggested the involvement of the basa l ganglia (Hughes, 1996; Minshew, Sung, Jones, & Furman, 2004; Vilens ky, Damasio, & Maurer, 1981). It has been suggested that the basal ganglia are involved in the control of movement and movement disorders such as diminished movement in Pa rkinsons disease and excessive movement in Huntingtons disease (Kandel et al., 2000). It is believed that the basal ganglia contribute to postural changes in the mediolat eral direction during gait initiation and the maintenance of locomotion, which are necessary for providing stability during these movements (Bachevalier, 1994; Bronstein, Brandt, Woollacott, & Nutt, 1996; Ebersbach et al., 1999). Thus, it should not seem too surprising, that based on the role of the cerebellum and basal ganglia in coordinating movement, that children with ASD may posses altered postural control during both static and dynamic challenges. Much of the morphological findings observed in mature individuals with ASD are in stark contrast to those observed in th e relatively few studies that have investigated the developing brain in very young children with ASD (Courchesne et al., 2007). It is however important to note that much of the developing brain literatu re is based on single ca se studies and studies investigating larger samples are st ill necessary. Briefly, brain volum es have been reported to be 5% greater in very young children with ASD (2 years) relative to co ntrols, where only an

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31 average of 1% increase has been observed in adol escents or adults with ASD (Courchesne et al., 2001; Hazlett et al., 2005; Redcay & Courchesne 2005; Sparks et al., 2002). Similarly, the amygdala has been observed to be larger in ve ry young children with ASD relative to controls (Sparks et al., 2002), whereas decreased neuron numbers have been observed in the amygdalas of adults with ASD (Schumann & Amaral, 2006). Very young children with ASD have been reported to have average minicolumn size rela tive to controls (Cour chesne et al., 2007). Conversely, older individuals with ASD present with reduced minicolumn size (Buxhoeveden et al., 2006). And finally, there does not appear to be cerebellar Purkinje cell loss in very young children with ASD relative to controls (Bailey et al., 1998), whereas a cons istent loss has been observed in older individuals with ASD (Baile y et al., 1998; Kemper & Bauman, 1998; Lee et al., 2002; Vargas, Nascimbene, Krishnan, Zimmerman, & Pardo, 2005). Preliminary studies in very young children with ASD suggest the brai n displays areas of overgrowth early in development but then shows dege neration, loss and size reduction in these very same areas later in life (Courchesne et al., 2007). These findi ngs have resulted in a new hypothesis for brain growth pathology in ASD. This new hypothesi s postulates two distin ct phases, one of overgrowth during infancy and then one of a rrest of growth during early childhood with a possible third phase of degeneration later in life (Courchesne et al., 2007). It is hypo thesized that these areas of early abnormal overgrowth may display abnormal function later in development. However, it remains unclear whether the neural systems that fail to provide essential language, social, emotional and attention skills in childre n with ASD are also the same ones affected by overgrowth (Courchesne et al., 2007). The three core symptoms associated with ASD (deficits in communication, abnormal social interactions and restricted and/or repetitive behaviors) are believed to involve widespread

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32 neural systems. It appears that neural structures subserving per ception of facial expression, joint attention, empathy and social cognition in ASD ar e compromised, as indicated by reduced neural activity in regions that govern these functions (Baron-Cohen et al., 1999; Critchley et al., 2000; DiCicco-Bloom et al., 2006; Pe lphrey, Morris, & Mc Carthy, 2005; Pierce, Muller, Ambrose, Allen, & Courchesne, 2001). However, given that some skills such as basic perceptual skills and overall intelligence may be unaffect ed, it is thought that not all br ain systems are affected equally (DiCicco-Bloom et al., 2006). It is theorized th at excess neuron numbers resulting form the early overgrowth during infancy may profoundly disrupt circuit formation and thereby hinder the emergence of higher order behavioral skills (C ourchesne et al., 2007). As a result, mapping of the networks may appear to be normal, however the long distance interact ions of the networks would be weakened and possible noisy. Development of Postural Control The development of postural control is tradi tionally defined as a series of predictable motor behaviors: crawling, sitting, creeping, pulltostand, inde pendent stance and walking. These behaviors are generally referred to as motor milestones (Gesell, 1946; McGraw, 1931). Postural control theories descri be these milestone behaviors and relate them to underlying neural structures (Shumway-Cook & Woo llacott, 2001). Classic theories define postural control in terms of the emergence and integration of re flexes (Shaltenbrand, 1928). Reflexhierarchy theory suggests that the inhibition and integration of reflexes is indicative of maturity within the lower levels of the CNS, allowing for more functional voluntary movements (Shumway-Cook & Woollacott, 2001; Woollacott & Shumway-Cook 1990). Recent theories however, have alternatively suggested that the postural control system is a mo re complex interaction between musculoskeletal and neural systems, with contro l of movement being determined by both task and environment (Shumway-Cook & Woollacott, 2001).

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33 The progression to bipedal stan ce is one of the major milest ones of motor development and typically occurs during the first year of life, and continues to become refined throughout the course of development (Assaiante & Amblard, 1995) Given that the development of postural control is a complex process, i nvolving much more than matura tion of reflexes; new behaviors and skills are believed to emerge from an interaction between the maturing neural and musculoskeletal systems and the surrounding envi ronment. Important milestones in the development of the neural and musculoskeletal systems are: 1) the development of muscle strength and changes relative to the differe nt body segments, 2) the development of neuromuscular response synergies used to mainta in balance, 3) the maturation of individual sensory systems, 4) the formation of sensory strategies to organize redundant inputs, 5) the development of internal representation important in the mapping of perception to action, and 6) the development of anticipatory postural adjustments (APA) mechanisms to allow modification in postural control (Shumway-Cook & Woollacott, 2001). Although children appear to be smaller version of adults, they are proportionally different. Due to the relative size of the head compared to the body, the COM of a child is located roughly around the T12 vertebrae rather than the L5S1 loca tion seen in adults. The shifted location of the COM causes children to be top heavy and as a result, makes the task of static balance more challenging (Zeller, 1964). Under normal se nsory conditions, children produce larger, more variable and oscillatory postural responses than adults (Forssbe rg & Nashner, 1982). As such, postural control has been found to be less effici ent in children and onl y becomes essentially adultlike between the ages of 7 and 10, where amplitude, frequency and variability of sway begin to decrease (Figura, Cama, Capranica, Guid etti, & Pulejo, 1991; Hatz itaki, Zisi, Kollias, &

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34 Kioumourtzoglou, 2002; Odenrick & Sandstedt, 1984; Rival, Ceyt e, & Olivier, 2005; ShumwayCook & Woollacott, 2001). There is an extensive amount of literature in the area of postural cont rol in children and according to Nougier (1998), the three main observa tions that emerge from these investigations are: a) children are less efficient at controlling static or dynamic balance, b) the contribution of vision in postural control appears to be less important in children than in adults and c) the development of balance and locomotion is nonm onotonic, that is, there is a transition phase around 7 to 8 years in the development of the se nsorymotor processes (Hay, 1984). Children 4 6 years have generally slower pos tural responses and more variable than those of children aged 7 yrs. Further, changes in body segment compos ition as a result of maturation are thought to contribute to the variability (Kugler, Kelso, & Turvey, 1982). Young children under the ag e of 7 years have been shown to have difficulty controlling posture when somatosensory and visual inputs were altered (Forssberg & Nashner, 1982). However, children 6 years in age have been show n to maintain postural stability similarly to children 10 years in age (Nougier, Bard, Fleury, & Teasdale, 1998). In contrast, children 7 to 8 years old display increased sway due to an in ability to minimize the magnitude of the COP displacements (Hay & Redon, 2001; Riach & Starke s, 1994) and begin to adopt more adultlike balance control strategies (Kirsh enbaum, Riach, & Starkes, 2001). These results suggest that the ability to reorganize basic postural control under altered somatose nsory information conditions is already present at the age of 6 years. Thes e observations related to the use of sensory information during postural control are believed to support the existence of a critical phase, particularly around the age of 7 to 8 years, where there is a reweighting of the different sensory systems involved in controlling balance.

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35 Motor Deficits and Autism Restricted, repetitive, and st ereotyped patterns of behavior interests and activities are among the core features of autistic disorder. Of these, stereotype d body movements (clapping, finger flicking, rocking, dipping, and swaying) and abnormalities in posture (walking on tiptoe, odd hand movements and body postures) are of particul ar interest However, the specific pattern and source of these motor deficits remain unclear (Noterdaeme et al., 2002). This is likely due to feelings that motor deficits ma y be a less important side effect rather than a concomitant symptom (Noterdaeme et al., 2002). Leary & Hill (1996) in their review however, suggest that motor deficits likely impair the development of sufficient communicative and interactive skills. Indeed, motor disturbances have been reporte d to affect daily activ ities (playing, writing, drawing, games) and social integr ation (Kalverboer, 1993). In a ddition, children with fine motor and coordination disturbances have been reported to a have hi gher risk of developing learning and behavioral problems (Hadders-Algra & Touw en, 1992; Losse et al., 1991). In children with ASD, motor deficits have been reported to furt her tax development; resulting in difficulty with the full acquisition of functional skills related to manipulation, mobility and play (Noterdaeme et al., 2002). Therefore, it appears that the occurrence of neuromot or deficits in ASD may be a partial indication of the biological factors in the etio logy of the disorder (Jones & Prior, 1985; Leary & Hill, 1996). Static Balance (Quiet Stance) and Autism The vestibular, somatosensory and visual systems are the afferent inputs involved in maintaining an upright posture. A deficit in any one of these sy stems or in the integration of information provided from these systems could aff ect the ability to maintain balance. Limited research has focused on the postural system in individuals with ASD during quiet stance. Postural patterns employed by children with autistic disorder over the age of 6 years have been

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36 observed to differ from typically developing children, mentally reta rded children and adults with vestibular disorders. Children with autistic disorder were observed to have a paradoxical postural stress response with equa l or better stability under seem ingly more difficult conditions, had an unusual distribution of body weight over their heels and toes, and tended to employ a more primary somatosensory, postural control system (even when visual cues were available). In addition, these older children with autistic diso rder exhibited more variable and less stable postural control, particularly in the mediolat eral direction when compared to typically developing children (ages 4 to 11 ye ars) (Kohen-Raz et al., 1992). Both children and adults with ASD have been observed to have greater impairme nts in postural stability during times of altered sensory inputs when compared to individuals wi th typical neuromotor development. However, when afferent inputs were not modified, there app ears to be conflicting resu lts in the literature. Some research has detected differences in pos tural sway between the groups (Gepner et al., 1995; Kohen-Raz et al., 1992; Mi nshew et al., 2004), while one study detected no such difference (Molloy et al., 2003). In addition, when investigating age effects, results reveal a delayed development of the postural system in s ubjects with ASD, which appears to improve at the age of 12 years, however never reaches adul t levels (Kohen-Raz et al ., 1992; Minshew et al., 2004). These authors have, therefore, highlighted an involvement of th e neural circuitry beyond the neural systems for social behavior, comm unication and reasoning. However, despite this information, there is still is a pa ucity of research investigating a wider range of functional tasks challenging both the static and dynamic postural control of this population. Postural instability has often been analyzed through the assessment of COP movements only. It has been suggested, however, that ther e are inherent limitations to relying solely on traditional COP measures to quantify postural stabili ty. During upright stance, with side by side

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37 foot placement, the body has often been simplifie d to a 2 dimensional inverted pendulum with movement confined to the ankle joint (Winte r et al., 1998). The basic assumption when using COP measures to evaluate postural control is th at the shifting of weight and muscular control (measured by changes in COP) provides an estimate of body position or sway of the COM. Research suggest however, this may not be a valid assumption under al l conditions (Panzer, Bandinelli, & Hallett, 1995). Although the COP is known to be controlled by ankle plantarflexors and dorsiflexors in the anteroposterior direction and hip abductors and adductors in the mediolateral direction, th is simplification to a simple inverted pendulum has provided further insight into the dynamic relationship betw een the COP and COM. In order to keep the COM in a stable position, the COP must oscillate a bout the COM and as such, must have a larger dynamic range by comparison (Winter et al., 1998). Differences detected by the central nervous system (CNS) between the COP and the COM must then be corrected. As result, the difference between these two measures is often referred to as an error signal with in the postural control system where the COM is the variable being co ntrolled by the COP for the purposes of meeting the mechanical criterion for st ability (Winter et al., 1998). The mechanical criterion for stability duri ng quiet stance is maintenance of the COM within the base of support (BOS). This criterion is generally be lieved to be achieved through the CNSs manipulation of the COP (Martin et al ., 2002; Riley, Mann, & Hodge, 1990). Changes in the COP reflect forces that must be produced to return the COM to a more stable position (Martin et al., 2002). Consequently, an increase in COP sway has traditionally been believed to indicate increased COM sway. However, it has been suggested that an increase in COP sway may also indicate the adoption of a different pos tural control strategy (P anzer et al., 1995). According to these authors, an inverted pe ndulum model may be inadequate in describing

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38 multilink systems such as the human body. Results from their investigation suggest that increases in COP sway do not have to coinci de with increases in COM sway. During quiet stance, significant movements were observed in participants indivi dual body segments, indicating that not all movement s were confined to the ankle. As a result, segmental accelerations associated with th ese movements were reflected in the COP as increased sway. However, no simultaneous changes in COM sway were detected. Therefore, the authors concluded that even with increased COP sw ay, the sum of the segmental accelerations successfully achieved their goal of stabilizing th e COM. As a result, the observed increased sway in the COP was likely representative of an alternative strategy rather than instability. In addition, even though there may be some underlying dysfunction in postural control, it still may be possible for the COP movements to successfu lly stabilize the COM movements (Corriveau, Hebert, Prince, & Raiche, 2001). Given that the COP and COM may yield different information and that measurements based solely on COP sway may be inadequate u nder certain conditions, researchers have become increasingly interested in the combined error measure of COP and COM separation (Corriveau et al., 2001; Corriveau, Hebert, Raiche, Duboi s, & Prince, 2004; Hass, Waddell, Fleming, Juncos, & Gregor, 2005). This combined measure, defined as the distance at any given time between the COP and COM, is believed to prov ide better insight into postural control and efficacy than either measure taken separately (W inter et al., 1998). During quiet stance, the COP and COM should more or less coincide (Chang & Kr ebs, 1999; Jian, Winter, Ishac, & Gilchrist, 1993) in the transverse plane. This condition re presents the individuals most stable standing position (Martin et al., 2002). Wh en the body deviates from this position, the distance between the COP and COM increases and introduces an instability requiring active control by the

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39 individual to return the COM to a more stable position within the BOS. The greater the COP COM distance, the more inherently unstable the individual is and the more active postural control is needed. In taki ng both the COP and COM into acc ount, this combined COPCOM distance has successfully identified small cha nges in postural control in other populations (stroke, elderly, diabetes with distal neuropathy) with know inst ability (Corriveau et al., 2001; Corriveau et al., 2004). Therefore, by combin ing the COP and COM measures and widening the range of task complexity to those including tran sition, we may be able to emphasize and clarify some of the more subtle and conflicting results currently reported in th e literature focusing on postural control in ASD. Dynamic Balance (Gait Initiation) An intact postural control system is necessary to tolerate larger separations that occur between the COP and COM when movements transiti on from static conditions to ones that are more dynamic in nature. Gait in itiation is a prerequisite to locomotion and has received considerable attention in the literature as a scr eening tool for dynamic balance control in elders and individuals with Parkinsons disease (Chang & Krebs, 1999; Ha ss et al., 2005; Martin et al., 2002). Gait initiation is defined as the transition phase between static balance in an upright position and the start of steady state walking (Burleigh, Horak, & Malouin, 1994; Jian et al., 1993; Mann, Hagy, White, & Liddell, 1979) and can therefore be considered a dynamic balance skill. It has been suggested that individuals with less effective postural control systems are inclined to reduce the separation between the COP and COM, particularly during transition movements, in an effort to reduce the amount of active control needed (M artin et al., 2002). In order for gait to be initia ted, there must be a separation of COP and COM (Jian et al., 1993). This separation represen ts a natural but deliberate destabilization during which momentum is generated and must be combined with a simultaneous maintenance of balance

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40 (Breniere, Do, & Bouisset, 1987). These requ irements however, are in conflict because momentum generation requires moving the COM outsi de of the BOS thereby creating instability (Polcyn, Lipsitz, Kerrigan, & Collins, 1998). Th e interaction between the COP and the COM therefore provides insight into how postura l and intentional movement components are coordinated during locomotion (C hang & Krebs, 1999). As menti oned, gait initiation has been shown to be a sensitive indicator of balance dysfunction (Chang & Krebs, 1999) and is believed to be ideal for identifying changes in the postural and locomotor systems, including those less apparent deficits not typically identified with less sensitive m easures taken during quiet stance and steady state walking (Hass et al., 2004). The path traveled by the COP during gait initiation also discriminates between healthy adults, elders and elders with disability (Halliday, Winter, Fr ank, Patla, & Prince, 1998; Hass et al., 2004). The COP path can be divided into thr ee phases (S1, S2, S3), with S1 being the initial phase beginning with the start command and endi ng with the most posterolateral position of the COP towards the initial swing leg. According to inverted pendulum theory, this combined displacement in the posterior and lateral directio ns (defined as the COP shift mechanism) will propel the COM in the forward and lateral direct ions respectively (Ha ss et al., 2004; Winter, 1995). S1 represents the purposeful uncoupli ng of the COP and COM and decreased COP displacements in either direction may be indica tive of instability (Martin et al., 2002; Zettel, McIlroy, & Maki, 2002) or perhaps the use of an a lternative, possibly less efficient strategy for generating momentum (Hass et al., 2004; Polcyn et al., 1998). S2 begins with the shifting of the COP towards the initial stance limb and ending with the point at which the COP begins to move anteriorly under the initial stance foot. During this phase, the COM continues to accelerate in the forward direction while the body weight and as a result COP, are shifted towards the stance limb.

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41 Transferring the COP laterally allows for loading of the stance limb while simultaneously unloading of the swing limb, a process critical for initiating a step (Martin et al., 2002). Finally, S3 begins with the anterior movement of the CO P under the stance foot and ends with toe off of the stance foot. The magnitudes of temporospatial parameters such as COP displacement and average velocity reported during the different phases of gait initiation have, as a result, defined a continuum between stability and instability. W ith increasing age and disability, values are reported to be smaller, slower and more variab le in both the anteroposterior and mediolateral directions (Hass et al., 2004; Martin et al., 2002). Even with deficits in speed and forcefulness, older individuals are still able control gait with similar muscle activation patterns and kinematic and kinetic patterns when compared to healthy, young individuals. Thes e results suggest that quality or efficiency of movement is being sacr ificed for stability and safety (Halliday et al., 1998). Although there appears to be a deterioration of the COP shift mechanism with increasing age and disorder, it seems this deterioration is no t the only means by which insight into the control of dynamic balance can be achieved. Th ere has also been a concurrent interest in research focusing of the emergence of this COP shift mechanism or basic anticipatory behavior prior to gait initiation. The development of internal anticipatory postural adjustments (APA) related to gait initiation has been investigated in young child ren. Although APA are generally believed to safeguard against instability re sulting from the impending movement, they may also serve as a necessary condition required fo r the intended movement (Ledebt, Bril, & Breniere, 1998). During gait initiation, uncoupling of the COP and COM is necessary to create propulsive forces required to reach intended gait speed (Breniere et al., 1987). Shifting of the COP prior to

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42 movement is therefore necessary to accelerate th e COM and ultimately generate the velocity of the subsequent steps. Understanding how thes e APA emerge and how they are refined during development may provide further insight into the maturation of neuromuscular systems in children with ASD. The development of APA may be dependent on neural maturation, mastering of the task, or a combination of both (Ledebt et al., 1998). When compared to adul ts, observed differences in anticipatory behavior in children have been reported to be the result of immature neural functioning (peripheral nerve c onduction and central processi ng) (Hirschfeld & Forssberg, 1994). Alternatively, having observed anticipatory behavior in ch ildren as young as 4 years of age, researchers suggest children will develop a feedforward control of posture as soon as they are able to sufficiently maintain posture thr ough feedback control (H aas & Diener, 1988). Therefore, although general anticipatory behaviors appear in a less mature form at a very early age, these APA will then continue to be refine d through experience. As a result Haas & Diener (1988) believe APA to be more taskdependent rather than age dependent. This ability to anticipate upcoming instabilities and/or adjust current movements to facilitate future actions is an element essential to motor contro l (Ledebt et al., 1998). For this reason, the COP shift prior to gait initiation in children is of considerable interest, because it provides information on how feedforward control of moveme nt is developed. The COP shift mechanism prior to gait initiation has been reported in children as young as 4 years of age; however when compared to adults, appears to be less consistent and less refined (Ledebt et al., 1998; Malouin & Richards, 2000; Stackhouse et al., 2007). Although Malouin & Richards (2000) reported the pres ence of a COP shift in typically developing children 4 years, the magnitudes of the displacements were smaller in the posterior direction and larger in the

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43 lateral direction when compared to adults (50 years). Ledebt et al. (1998) similarly observed anticipatory shifting of the COP prior to gait initiation in child ren 2 years. These authors reported an increase in shift magnitude with in creasing age, suggesting the youngest participants (2.5 years) were the least eff ective at generating forward mome ntum. Anticipatory behavior prior to gait initiation has also been reported in children with cerebral palsy (CP) (Stackhouse et al., 2007). These authors reported that although the APA of child ren with CP were similar to those of typically developing ch ildren, children with CP appear ed to demonstr ate alternative strategies for developing forw ard momentum. Due to a decrea sed lateral shift of the COP towards the stance limb, Stackhouse et al. (2007) suggested there was an increased dependency on the stance limb to create the posterior shif t of the COP necessary to generate forward momentum. Research suggests the development of APA prio r to gait initiation follows a progression of increased muscle activity and posterior displacemen t of the COP with increasing age, resulting in increased gait velocity (Stackhous e et al., 2007). An inabilit y to fully develop or refine anticipatory movements associated with gait initia tion may as a result, be indicative of delay or dysfunction. Ledebt et al. ( 1998) have suggested that the i mmature anticipatory behavior observed in very young children (2.5 years) during gait initiation may be the result of a less stable initial posture and/or a l ack of cognitive control of moveme nt. According to these authors, children may indeed have the ab ility to produce anticipatory move ments at the muscular level, however, any effects of these movements on a global scale, may be obscured by postural instabilities. Further, as children acquire knowle dge of new skills, they must develop cognitive structures and representations that allow them to negotiate new environmen ts while attempting to

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44 execute purposeful action. Therefore, in order fo r APA associated with ga it initiation to emerge, young children must have a representation of their forthcoming velocity (Ledebt et al., 1998). Evaluating the APA or COP shift mechanism dur ing gait initiation may therefore be used as a means of quantifying motor coordination (Stackhouse et al., 2007). Analysis of the destabilizing movements may provide new insight into the dynamic control of posture in children with ASD. Further, by simultaneously evaluating static postural c ontrol, the results of this investigation have the potential to delineat e subtle movement disturbances over a spectrum of tasks with increasing demands on postural cont rol. The use of measures aimed at evaluating the relationship between the COP and the CO M during both static and dynamic tasks may provide much needed information for interventi ons aimed and improving balance and subsequent movement coordination in chil dren diagnosed with ASD.

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45 CHAPTER 4 RESULTS Static Balance (Quiet Stance) Significant differences between groups were identified for all three traditional COP measures of postural control during quiet stan ce (Figure 4-1). Childre n with ASD produced significantly greater (>%400 greater, U =48, NASD=13, NTYP=13, p=0.032) normalized mediolateral sway (COPML) than their agematched controls Similarly, the magnitude of the anteroposterior sway (COPAP) was >100% greater in the ASD group ( U =18, NASD=13, NTYP=13, p<0.001). Consequently, sway area (COPSWAY) was also significantly greater in the group with ASD ( U =25.5, NASD=13, NTYP=13, p =0.010, onetailed). Furthermore, children with ASD had significantly greater variability from trial to tria l when compared to typi cally developing children in the anteroposterior direction ( t =-2.83, df=23, p=0.007) and sway area ( t =-1.89, df=23, p=0.043). However, only a trend toward significance was detected for the mediolateral direction ( t =-1.63, df=23, p=0.066) (Figure 4-2). Significant differences between groups were also identified in two of the three COP COMmax moment arms during quiet stance (Figure 4-3). The max separation between the COP and COM was significantly greater for the group with ASD in the anteroposterior (COP COMmaxAP, > 90% greater, U =37, NASD=13, NTYP=13, p=0.007) direction as we ll as the resultant (COPCOMmaxR, >100% greater, U =47.5, NASD=13, NTYP=13, p=0.029). No significant difference between groups was observed in the mediolateral direction (COPCOMmaxML, U =58.5, NASD=13, NTYP=13, p=0.093), in spite of the >100 % gr eater separation detected in children with ASD. Independent sample t -tests also revealed that children with ASD had significantly greater variability from trial to tria l when compared to typi cally developing children

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46 in the mediolateral ( t =-2.12, df=24, p=0.028), anteroposterior ( t =-3.03, df=24, p=0.005) and resultant directions ( t =-2.24, df=24, p=0.023) (Figure 4-4). Dynamic Balance (Gait Initiation) While no differences were observed in the posterior direction (S1_AP, U =30, NASD=13, NTYP=13, p=0.447), children diagnosed with ASD displa ced their COP significantly less towards the swing leg (mediolateral direction) dur ing gait initiation (S1_ML, >40 % less, U =75, NASD=13, NTYP=13, p=0.004) (Figure 4-5). Children with ASD performed with significantly greater variability from trial to trial when co mpared to typically de veloping children in the anteroposterior direction only ( t =-2.22, df=23, p=0.018) (Figure 4-6).

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47 Quiet Stance (COP)0.00 0.10 0.20 0.30 0.40 0.50 0.60 0.70 0.80 0.90 1.00 MLAPSway ASD TD Figure 4-1. Means and SD for normalized COP measures (COPML, COPAP, and COPSWAY) during quiet stance (* p<0.05). *

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48 A COP ML 0.0 0.2 0.4 0.6 0.8 1.0 1.2 1.4 1.6 1.8 Individual Participants ASD (Leiter>70) ASD (Leiter<70) TD B COP AP 0.0 0.2 0.4 0.6 0.8 1.0 1.2 1.4 1.6 1.8 Individual Participants ASD (Leiter>70) ASD (Leiter<70) TD C COP SWAY 0.0 0.2 0.4 0.6 0.8 1.0 1.2 1.4 1.6 1.8 Individual Participants ASD (Leiter>70) ASD (Leiter<70) TD Figure 4-2. Scatter of normalized mean COP measur es during quiet stance for each participant. A) COP movement in mediolateral directi on. B) COP movement in anteroposterior direction. C) COP sway area.

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49 Quiet Stance (COP-COMmax)0.00 0.01 0.02 0.03 0.04 0.05 0.06 0.07 0.08 MLAPR ASD TD Figure 4-3. Means and SD for normalized peak COPCOM moment arms (COPCOMmax ML, COPCOMmaxAP and COPCOMm axR) during quiet stance (* p<0.05). *

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50 A COP-COM ML 0.00 0.02 0.04 0.06 0.08 0.10 0.12 Individual Participants ASD (Leiter>70) ASD (Leiter<70) TD B COP-COM AP 0.00 0.02 0.04 0.06 0.08 0.10 0.12 Individual Participants ASD (Leiter>70) ASD (Leiter<70) TD C COP-COM R 0.00 0.02 0.04 0.06 0.08 0.10 0.12 Individual Participants ASD (Leiter>70) ASD (Leiter<70) TD Figure 4-4. Scatter of normalized mean, peak COPCOM moment arms during quiet stance for each participant. A) COPCOM moment ar m in mediolateral direction. B) COP COM moment arm in anteroposterior dire ction. C) COPCOM resultant moment arm.

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51 Gait Initiation (COP)0.00 0.05 0.10 0.15 0.20 0.25 0.30 ML AP ASD TD Figure 4-5. Means and SD for normalized COP displacements (S1_ML and S1_AP) during gait initiation for ASD (* p<0.05). *

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52 A S1_ML 0.00 0.05 0.10 0.15 0.20 0.25 0.30 Individual Participants ASD (Leiter>70) ASD (Leiter<70) TD B S1_AP 0.00 0.05 0.10 0.15 0.20 0.25 0.30 Individual Participants ASD (Leiter>70) ASD (Leiter<70) TD Figure 4-6. Scatter of normalized mean COP displacements during gait initiation. A) COP displacement in mediolateral direction. B) COP displacement in anteroposterior direction.

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53 CHAPTER 5 DISCUSSION An effective postural control system is a ne cessary foundation for individuals to acquire skills inherent to functional independence. Initi ally, there must be an ability to maintain equilibrium during static conditi ons where the COM remains within BOS such as during quiet stance; however, that ability must be further developed to include stabili ty during dynamic conditions where the COM moves away from th e BOS, such as duri ng gait initiation. The current investigation has highlighted systematic postural instabilities in children with ASD using functional tasks representative of two different categories of postural challenges. Our hypothesis that children with ASD would have increased postural sway, indi cated by larger traditional COP measures and greater separation of the COP a nd COM was supported by the data. Children with ASD exhibited significantly greater sway in the mediolateral and anteroposterior directions and subsequent sway area. Further, larger p eak anteroposterior COPCOM moment arms and resultant COPCOM moment arms were observe d in children with ASD. However, no differences were detected between the groups for the peak mediolateral separation. Furthermore, children with ASD shifted their COP significantly less in the mediolateral direction but not the anteroposterior direction duri ng gait initiation. Thus, it appe ars that the sequella of ASD includes a retarded development or deterioration of postural control abili ties during quiet stance. Static Balance (Quiet Stance) Using traditional measures of postural sway (COP) and a measure believed to provide further insight into postural efficacy (COPCOM moment arm), we were able to identify differences in postural stability between childr en with ASD and typica lly developing children during quiet stance. Although the outcome m easures of COP sway and COPCOM moment arms were normalized to stance width in the me diolateral direction and foot length in the

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54 anteroposterior direction for statistical analysis in the present investigat ion, the absolute values for these measures appear to be consistent wi th values reported elsewhere for various young adolescent populations. As a re sult, our findings appear to support prevailing reports that children with ASD have increased postural instability under conditions where sensory information has not been modified or remove d (Gepner et al., 1995; Kohen-Raz et al., 1992; Minshew et al., 2004). Sway area is a commonly reported outcome measure in the postural stabi lity literature. It is a useful measure because it combines the postural sway in both th e anteroposterior and mediolateral directions. In the present i nvestigation, mean sway areas were 35.54 49.70 cm2 for children with ASD and 2.46 1.80 cm2 for TD children. These values are similar to those reported in children with pos tural deficits (2.74 to 10.1cm2 ) and TD children (1.9 to 8.2 cm2) (Bhattacharya, Shukla, Bornschein, Dietrich, & Keith, 1990; Geuze, 2003; Nault et al., 2002). Furthermore, median sway areas in the present investigation were 4.88 cm2 for children with ASD and 1.83 cm2 for TD children. These values are also similar to those repor ted previously in children with ASD (4.7 cm2) and TD children (3.30 cm2). When combining the findings of the current crosssectional investigation with those of previously observed in ASD, it appears postural sway, as indicated by medi an sway area, decreases as age increases for TD children, but remains relatively unchanged for children with ASD. Although the currently investigation was not a longitudinal study, these observations appear to lend support to previous finding that the development of the postural system in children with ASD is delayed, and may never reach adult levels (Kohen-Raz et al., 1992; Mins hew et al., 2004). Furthermore, in the current investigation, postural sway was observed to be over 400% greate r in the mediolateral direction compared to a

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55 100% increase in the anteropos terior direction for childre n with ASD, supporting the directionally inconsistent and sporadic late ral sway observed by KohenRaz et al. (1992). The combined measure of COPCOM moment ar m is believed to prov ide better insight into postural control and efficacy than either meas ure taken separately (Winter et al., 1998). The greater the COPCOM distance, th e more inherently unstable the individual is and the more active postural control is needed. Children with ASD had larger peak COPCOM moment arms in the anteroposterior and resu ltant directions (0.31 0.17 cm and 0.72 0.61 cm respectively) when compared to TD children (0.16 0.06 cm, and 0.27 0.12 cm respectively). COPCOM moment arms in TD children and children with scoliosis have been reported to range from 0.06 to 0.09 cm in the mediolateral direction, 0.08 to 0.10 cm in the anteroposterior direction and 0.1 to 0.13 cm in the resultant dir ection (Nault et al., 2002). Furt hermore, COPCOM peak moment arms of 0.98cm have been reported for healt hy adults 21 years of ag e (Panzer et al., 1995) during quiet stance. Peak COP COM moment arms observed in the current inves tigation appear to be consistent with those previously publishe d in various populations. Therefore, increased peak COPCOM moment arms observed in the cu rrent investigation furt her suggest postural instability in children with ASD under static cond itions, particularly in the anteroposterior and resultant directions. Although no differences be tween groups were detect ed for peak COPCOM moment arms in the mediolateral direction, ch ildren with ASD were observed to have over 100% larger moment arms in this direction when co mpared to the TD children. Given the significant difference in COP sway but a non significant difference in peak COPCOM moment arms during quiet stance, it is speculate d that the COM and COP may move together more consistently in the mediolateral direction in children with ASD.

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56 Dynamic Balance (Gait Initiation) The hypothesis that children with ASD woul d have difficulty uncoupling the COP and COM during gait initiation, indi cated by decreased COP displacements was only partially supported by the data. The ability to uncouple the COP and COM is essen tial for initiating gait; however it simultaneously requires active postural control to counteract the instabil ity created by the uncoupling (Hass et al., 2005). This activ e uncoupling creates momentum in both the anterior and stance side directi ons. Decreased COP displacement s in either direction may be indicative of instability (Martin et al., 2002; Zettel et al., 2002) or the perhaps the use of an alternative, possibly less efficient strategy for generating momentum (Hass et al., 2004; Polcyn et al., 1998). S1_AP distances have been repor ted to range between 2.14 and 4.70 cm for young adults, 3.54.69 cm for older adults and 2.02.07 cm for individuals with Parkinsons disease (Halliday et al., 1998; Hass et al., 2004; Martin et al., 2002). Although absolute displacements in the posterior direction (S1_AP) did not di ffer significantly betwee n TD children (2.77 1.00 cm) and children with ASD (2.75 1.50 cm), magn itudes for S1_AP in the present study appear to be similar to those reported elsewhere for various populations for children with ASD. The posterior shift mechanism creates an increased moment arm, a llowing the ground reaction forces to accelerate the COM anteriorly. The nons ignificant results between groups for S1_AP indicate that the COP shift mechanism for genera ting forward momentum appears to be intact in children with ASD. Stance side momentum is generated when the COP moves laterally towards the swing limb. This mediolateral momentum is believed to contribute to lateral stability during gait initiation. Stackhouse et al. (2007) observed decreased S1_ML distances in children with hemiplegic CP. According to th ese authors, children with hemi plegic CP had a tendency not to load their affected limb, resulti ng in decreased latera l displacements. St ackhouse et al. (2007)

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57 further suggest this decreased lateral displa cement characterized an alternative method for creating momentum. According to these authors, there was an increased reliance on the initial stance limb to create the posterior COP shift n ecessary for generating forward momentum. In the current investigation, S1_ML values were observed to be signifi cantly smaller (2.18 1.50 cm) for children with ASD when compared to typically developing children (3.72 1.38cm). Decreased S1_ML distances have been observed in older adults with disability and those transitioning to frailty and have been reported to be the result of decreased hip muscle functions (Hass et al., 2004; Hass et al., 2005; Martin et al., 2002). Re ported S1_ML distances have ranged between 3.63 and 4.38 cm for young adul ts, 2.19.12 cm for older adults and 2.02.30 cm for individuals with Parkinsons disease (H alliday et al., 1998; Hass et al., 2004; Martin et al., 2002). Just as posterior shift of the COP will propel the COM in th e anterior direction, shifting of the COP in the lateral direction allo ws for the COM to move towards the stance limb. Thus, decreases in S1_ML observed in children with ASD will limit the extent to which the COM shifts towards the stance limb. As a result, when they transition from double limb support to single limb support, their COM will be further away from the base of support, resulting in less stable positioning during gait initia tion. It therefore seems plausibl e that the significantly shorter S1_ML distances in the current i nvestigation may indeed impart a dynamic postural instability. In addition to further defining motor deficits in the ASD population, re search investigating movement disturbances attempt to indirectly iden tify areas of the brain that may be responsible for these disturbances. Neuroanatomical and beha vioral studies have imp licated numerous areas of the brain responsible for impairments in this population, with an emphasis on the cerebellum (Courchesne, 1997; Courchesne et al., 1994; Pi erce & Courchesne, 2001; Pierce et al., 2001; Ritvo et al., 1986) and the basa l ganglia (Lewis, Tanimura, L ee, & Bodfish, 2007; McAlonan et

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58 al., 2002; Nayate et al., 2005; Ri nehart, Bradshaw, Brereton, & Tonge, 2001; Sears et al., 1999) for impairments observed in posture and gait. Both of these areas contribute to the tasks collected in the current investig ation. The cerebellum is believed to integrate sensory information for balance control and the coordination of body movements (Kandel et al., 2000) whereas basal ganglia, although not as clearly defined, are reported to play an important role in normal voluntary movement and postural changes required for gait initiation and the maintaining of locomotion (Ebersbach et al., 1999; Kandel et al ., 2000; Patchay, Gahery, & Serratrice, 2002) Somatosensory (70%), vision (10 %) and vestibular (20%) sensory information are the three main inputs in the control of posture (Horak, 2006). Several interconn ected structures in the brain play a role in integrating this information, including the cerebellum and basal ganglia. The ability to reweight sensory information is necessary for maintaining stability under changing environmental conditions (Horak, 2006). Limited studies of postural cont rol and gait in ASD have lead to the belief that postural impairments observed in this population may be due to a dysfunction in sensory input inte gration occurring in the cerebe llum (Hallett et al., 1993; KohenRaz et al., 1992). However, other findings suggest generalized pos tural dysfunction, gait initiation and gait patterns in ASD may be similar to those seen in Parkinsons disease, thereby implicating dysfunction in the basal ganglia (Hughes, 1996; Minshew et al., 2004; Vilensky, Damasio, & Maurer, 1981). While results from this investigation are unable to pinpoint specifically which anatomical structure or combin ation of structures are responsible for postural instabilities observed in children with ASD, these results do help confirm involvement of the cerebellum and/or basal ganglia. Limitations and Future Directions The current work has some limitations. Only two representative tasks were used in the current investigation to challe nge postural control under static and dynamic conditions. A more

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59 thoroughly defined spectrum of f unctional tasks with varying degr ees of demands on the postural control system (including arm rais e, sit to stand and sit to walk), is warranted. Tasks used in the current investigation are not dir ectly related to one underlying control system (somatosensory, vision, and vestibular). Investigation of more tasks aimed at syst ematically manipulating each of these systems individually is needed to furt her identify the underlyi ng causes of the postural deficits observed in this population. It has been reported that an es timated 75% of children diagnose d with autistic disorder also possess mental retardation (MR). Of the limited literature investigating posture in the ASD population, some have controlled for MR (Minsh ew et al., 2004; Mollo y et al., 2003) while others have not (Gepner et al., 1995; Kohen-Raz et al., 1992). Investigations containing individuals diagnosed with ASD and MR together, only ASD and onl y MR have reported that all of these have increased postural instability wh en compared to controls (Gepner et al., 1995; Kohen-Raz et al., 1992; Minshe w et al., 2004; Molloy et al., 2003; Suomi & Koceja, 1994). It appears that both ASD and MR contribute to postural instabi lity, but the extent of each individual contribution remain s unclear. Evidence suggests however, that occurrence of abnormal repetitive behaviors is elevated in AS D when compared to MR (Bodfish et al., 2000). The distribution of the data in Figures 4-2, 4-4 an d 4-6 appear to indicate that children with ASD and Leiter-R IQ scores of less than 70 (indicatin g MR), had larger values for the quiet stance variables measured and smaller values for the gait initiation variables measured, when compared to children with ASD and Leiter-R scores of gr eater than 70. These observations would suggest that MR contributed to the ove rall increased variabil ity of the ASD group and as a result, may have contributing to the diffe rences detected between groups Therefore, it seems any

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60 contribution the associated feature of MR has on postural instability in individuals with ASD should not be neglected. Using one measure over a range of tasks is the inherent appeal in using the COPCOM moment arm for biomechanical analyses of pos tural control. Having one measure, not only allows comparisons across tasks, but also allows for comparison across ages, genders, disorders, and treatments. In order to compare COPCOM moment arms, the COP and COM must be collected. Although the COP is relatively easy to obtain in a laboratory and clinical settings via forceplates, the COM has traditionally been more cumbersome to obt ain. Typically, motion analysis systems make use of marker data (defining body se gments) to estimate the bodys COM. It is a process that can be time consuming and re quires expensive equipment and software. There are various methods for estim ating the COM mathematically, however methods specific to gait initiation (as opposed to steadystate velocity) are still lim ited. As a result, the COPCOM moment could not be obtained for ga it initiation trials. Therefore, choosing functional tasks where the COM ha s previously been obtained ma thematically is suggested. Alternatively, for tasks where the COM cannot be obtained mathematically, it may be worth developing a plan aimed at increasing marker tolerance is this population.

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61 CHAPTER 6 CONCLUSIONS The findings of the current investigation suggest that motor differences in postural control are present in children diagnosed with ASD unde r both static and dynamic postural challenges. Larger COP movements in the medi olateral and anteroposterior di rections and subsequent sway areas and larger peak COPCOM moment arms in the anteroposterior and resultant directions under static conditions ( quiet stance) observed in children wi th ASD suggest increased postural sway and as result, increased postural instabi lity. The development of anticipatory behavior characterized by the COP shift mechanism during ga it initiation is not necessary for walking, but is required for efficient walking. Subtle differe nces in the ability to generate momentum while simultaneously maintaining balance under dynamic conditions (gait initiation) were observed between the two groups of children. Children with ASD shifted their COP significantly less towards the swing limb during gait initiation, suggesting instability in the mediolateral direction or possibly a less efficient strategy for generati ng momentum. No differences were detected between groups for posterior displacement of the COP, suggesting their ability to generate forward momentum during gait initiation is intact. The results of the current investigation ha ve systematically highlighted postural instabilities in children with ASD using functional tasks representative of two different categories of postural challenges. These finding s have helped clarify some of the existing literature, indicating that children with ASD (8 16 years) ha ve postural instabilities, even under the most basic of conditions when no afferent or sensory information has been removed or modified. By further quantifying postural abilities over a wider ra nge of tasks in this population, the extent to which deficits in motor control underl ie core characteristics of the disorder will be further delineated. Given that moto r control is mediated by brain st ructures that are consistently

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62 reported to be compromised in this population, investigations into pos tural control provide a unique avenue for accessing altered functioning in these structures associated with ASD. Furthermore, by better characterizing the impairment associated with these disorders, behavioral treatments that include balance training, early in development, may help to prevent subsequent emergence of deficits in other motor abilities.

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63 APPENDIX CENTER OF PRESSURE (COP) & CENTER OF MASS (COM) CALCULATIONS Calculating COP for One Forceplate COPi(x) = -Myi/Fzi (1) COPi(y) = Mxi/Fzi (2) Calculating COPnet for Two Forceplates Method for calculating combined COP. COPnet (x) = [(COP(x1)*Fz1)/(Fz1+Fz2)] + [(COP(x2)*Fz1)/(Fz1+Fz2)] (3) COPnet (y) = [(COP(y1)*Fz1)/(Fz1+Fz2)] + [(COP(y2)*Fz1)/(Fz1+Fz2)] (4) Where, i = forceplate of interest COP (x) = COP location in the x direction COP (y) = COP location in the y direction x = M/L direction y = A/P direction My = moment about the yaxis Mx = moment about the xaxis Fz = ground reaction force in the vertical direction (Winter et al., 2003) Calculating COM via Integration Trapezoidal Method of Numerical Integration Ii = Ii-1 + [(yi+1 yi)/2] *(xi+1 xi) (5) Where, i = point of interest or ith point Ii = Integral of interest yi = y coordinate a ith point xi = x coordinate at ith point Note: i-1 term is required for even the first point. This is considered the initial condition for the integration.

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64 Estimating COM Displacement Method for estimating COM displacement described in Chan, 1999. a(t) = (g/W) f(t) horizontal acceleration (6) v(t) = [a(t) a0] dt integrated velocity (7) s(t) = [v(t) v0] dt integrated position (8) r(t) = s(t) [u(t) p(t)] estimated COM (9) Where, f(t) = horizontal ground reaction force W= body weight g = acceleration due to gravity a0 = mean of a(t) v0 = mean of v(t) u(t) = moving average of s(t) p(t) = moving average of COP r(t) = estimated COM displacement Note: moving averages are taken with a window of 4 seconds. (Chan, 19 99)

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65 LIST OF REFERENCES Autism Society of America, (Retrieved D ecember 11, 2007). What is Autism (Facts and Statistics)?, from http://www.autismsociety.org/site/PageServer? pa gename=about_whatis_factstats Arin, D. M., Bauman, M. L., & Kemper, T. L. (1991). The distribution of Purkinje cell loss in the cerebellum in autism. Neurology, 41 (Suppl.), 307. Assaiante, C., & Amblard, B. (1995). An ontogenetic model for the sensorimotor organization of balance control in humans. Human Movement Science, 14 13-43. Bailey, A., Luthert, P., Dean, A., Harding, B ., Janota, I., Montgomery, M., et al. (1998). A clinicopathological study of autism. Brain, 121 ( Pt 5) 889-905. Baron-Cohen, S., Ring, H. A., Wheelwright, S., Bullmore, E. T., Brammer, M. J., Simmons, A., et al. (1999). Social intelligence in the normal and autistic brain: an fMRI study. The European Journal of Neuroscience, 11 (6), 1891-1898. Bhattacharya, A., Shukla, R., Bornschein, R. L., Dietrich, K. N., & Keith, R. (1990). Lead effects on postural balance of children. Environmental Health Perspectives, 89 35-42. Bodfish, J. W., Symons, F. J., & Lewis, M. H. (1999). The Repetitive Behavior Scales (RBS) : Western Carolina Center Research Reports. Bodfish, J. W., Symons, F. J., Parker, D. E., & Lewis, M. H. (2000). Varieties of repetitive behavior in autism: comparis ons to mental retardation. Journal of Autism and Developmental Disorders, 30(3), 237-243. Breniere, Y., Do, M. C., & Bouisset. (1987). Are dynamic phenomena prior to stepping essential to walking? Journal of Motor Behavior, 19 62-76. Burleigh, A. L., Horak, F. B., & Malouin, F. (19 94). Modification of postural responses and step initiation: evidence for goal-directed postural interactions. Journal of Neurophysiology, 72(6), 2892-2902. Buxhoeveden, D. P., Semendeferi, K., Buckwalter, J., Schenker, N., Switzer, R., & Courchesne, E. (2006). Reduced minicolumns in the front al cortex of patients with autism. Neuropathology and Applied Neurobiology, 32 (5), 483-491. Chan, R. B. (1999). A method of estimating center of mass from forceplate data during quiet standing. Paper presented at the BMES/EMBS Serving Humanity, Advancing Technology, GA, USA. Chang, H., & Krebs, D. E. (1999). Dynamic balan ce control in elders: ga it initiation assessment as a screening tool. Archives of Physical Medicine and Rehabilitation, 80 (5), 490-494.

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74 BIOGRAPHICAL SKETCH Kimberly Ann Fournier was born on A ugust 31, 1973 in Moncton, New Brunswick, Canada. The second of three children, she grew up in Montreal, Canada where she graduated from Pierrefonds Comprehensive High School in 1990. She earned her B.S. in Athletic Training at Concordia University, Montreal, Canada in 1999 and her M.H.K. in Biomechanics at the University of Windsor, Windsor, Ontario, Cana da. Upon completion of her Ph.D. program, Kimberly will be continuing her research in the area of autism, as a postdoctoral fellow with the support of funding obtained by Dr. Chris Ha ss and Dr. Krestin Radonovich through Autism Speaks.