Infants born extremely prematurely (ie. &lt29 weeks gestation) or with extremely low birth weight (ie. &lt1000 grams) are at high-risk of major and minor motor sequelae that persist into the school years. Most of the research on the outcome of these high-risk infants has concentrated on the prevalence of major disability. The majority of high-risk children at school age have normal intelligence and no sensorineural disability. Despite this, these ???apparently normal??? high-risk children have a higher incidence of minor morbidities. Motor coordination problems are frequently reported, yet further investigation into the emergence of minor motor dysfunction, or its impact on academic achievement and everyday activities is seldom explored. The aim of this thesis was to provide a comprehensive investigation into motor dysfunction, which is commonly found in ???apparently normal??? high-risk children. This was addressed in a series of five studies that intended to provide insight into the emergence, prevalence, nature, and prediction of motor dysfunction in otherwise ???normal??? high-risk children. Study 1 examined the development of gross and fine motor skills from infancy to school age using a longitudinal cohort study design. ???Apparently normal??? high-risk children (n=58) were assessed with the Peabody Developmental Motor Scales at 18 months corrected age, 3 and 5 years. A significant proportion continued to have fine motor deficits to school age (64%), reflecting a persistent problem with fine motor skills throughout this period. The proportion of infants with gross motor deficits significantly increased from 18 months to 5 years (81.1%), particularly for the ???micropreemies???. Whilst there was no gender difference found, the development of gross and fine motor skills appeared to be influenced differently by the home environment. Study 2 examined the impact of motor dysfunction on performance at school age. The prevalence of Developmental Coordination Disorder (DCD) in ???apparently normal??? high-risk children was determined using a controlled cohort study design. In addition, the nature of DCD in this population was explored by testing sensorimotor abilities that possibly underlie the motor dysfunction. Fifty (50) high-risk children with IQ&lt85 and no identified sensorineural disability were assessed at 8 years of age along with a matched control from their respective class at school. The Movement Assessment Battery for Children and a battery of sensorimotor tests were administered. Results indicated a significantly higher prevalence of DCD (42%) in the high-risk group in comparison to the control group (8%). In relation to sensorimotor abilities that may influence motor performance, the high-risk group scored significantly lower on most of tests, however it was neurological ???soft signs???, postural praxis, and sequencing praxis that contributed to DCD in the high-risk group. Study 3 was designed to investigate the impact of motor dysfunction on a motor-based task performed within the school setting. Specifically, this study described handwriting skills in ???apparently normal??? high-risk children, determined the prevalence of handwriting dysfunction, and investigated sensorimotor abilities that may be associated with problematic handwriting. The high-risk cohort and matched controls described in study 2 were also administered a number of handwriting tests. High-risk children were found to have poorer handwriting legibility and speed in comparison to their classmates. The prevalence of handwriting dysfunction in the high-risk group was 46%, significantly higher than controls (18%). Hand preference, pencil grasp used, and pain whilst writing were comparable to the control group. The contribution of underlying sensorimotor abilities to handwriting dysfunction in the high-risk population however was not evident. By using the same subjects in studies 2 and 3, the co-morbidity of handwriting dysfunction with DCD could be determined. Of those high-risk children identified with DCD, 43% had co-morbid handwriting dysfunction. Study 4 explored the relationship between perinatal and environmental variables to Developmental Coordination Disorder and handwriting dysfunction in high-risk children. Perinatal and environmental variables of the 50 ???apparently normal??? high-risk children that participated in the previous study were analysed. Results indicated prolonged rupture of membranes (PROM) and retinopathy of prematurity (ROP) were significantly and independently associated with DCD, perhaps reflecting the impact of the antenatal infection process and visual development related to ROP on motor outcome in high-risk children. Perinatal variables were not associated with handwriting dysfunction, but high-risk males were more likely to have handwriting dysfunction. Maternal education and paternal occupation were associated with aspects of handwriting. Whilst handwriting is a motor-based activity, it appears to be influenced by environmental variables, similar to other academic areas for the high-risk population. Study 5 sought to determine whether a motor assessment at an earlier age could predict DCD in the ???apparently normal??? high-risk population at school age. Motor assessment at 12 months, 3 and 5 years for the high-risk subjects who participated in study 2 were analysed using Receiver Operator Curves (ROC curves). The 3 year assessment with the Peabody Developmental Motor Scales was the best predictor of DCD at 8 years, with the Griffiths Locomotor Scale at 3 years yielding a similar result. Findings suggest that high-risk children who scored below the specified cut-off points on 3 year motor assessments and who had a history of PROM or ROP were at greater risk of having motor-based problems that had the potential to interfere with functioning at school.

This thesis investigates the processes of human postural control. How do we keep still? In any action, the force required changes with limb position. This force-position relationship is elastic stiffness. Holding a desired posture requires muscle activation that accounts for this load property. The studies here examine the physiological processes of postural control as elastic stiffness changes. Psychophysical studies show that thresholds for detecting differences in load stiffness are large relative to those normally encountered. To discriminate stiffness, subjects made consistent movements and judged the force required and detection thresholds followed rules for force perception. For the purposes of postural control, stiffness per se is not a variable of primary interest. The effects of load stiffness on postural stability were investigated using a pendulum that allowed independent control of load force and stiffness. Postural stability varied with load stiffness and this effect was independent of load force. Performance deteriorated as load stiffness became more negative. Load-dependent changes were at low frequencies only, suggesting neural processes operating at long latency, and perhaps ???volitional??? tracking, are the key to postural control. Imposed perturbations evoke patterns of muscle activation reflecting the state of the neural pathways of postural control. Stretch responses obtained while subjects held different loads show that the short-latency spinal reflex and the long-latency functional reflex in the active flexor muscle are unaffected by load stiffness. However, a stereotyped response observed after stretch-reflex latency varied systematically with load stiffness, as did reciprocal activation of the antagonist extensor muscle. The long-latency reflex appears to be a part of a coordinated reciprocal response of antagonist muscle pairs. Adapting to load properties involves modulating these later neural responses. A method was developed, based on ultrasound, to track changes in muscle and tendon length associated with small postural movements. The relationship between wrist angle and muscle and tendon length in the active muscle changed with load stiffness. Particularly with negative-stiffness loads, the wrist moves on the end of a compliant tendon without corresponding changes in muscle length. Thus, compensation of postural performance by neural modulation is limited by the properties of muscle and tendon.

This thesis investigates the processes of human postural control. How do we keep still? In any action, the force required changes with limb position. This force-position relationship is elastic stiffness. Holding a desired posture requires muscle activation that accounts for this load property. The studies here examine the physiological processes of postural control as elastic stiffness changes. Psychophysical studies show that thresholds for detecting differences in load stiffness are large relative to those normally encountered. To discriminate stiffness, subjects made consistent movements and judged the force required and detection thresholds followed rules for force perception. For the purposes of postural control, stiffness per se is not a variable of primary interest. The effects of load stiffness on postural stability were investigated using a pendulum that allowed independent control of load force and stiffness. Postural stability varied with load stiffness and this effect was independent of load force. Performance deteriorated as load stiffness became more negative. Load-dependent changes were at low frequencies only, suggesting neural processes operating at long latency, and perhaps ???volitional??? tracking, are the key to postural control. Imposed perturbations evoke patterns of muscle activation reflecting the state of the neural pathways of postural control. Stretch responses obtained while subjects held different loads show that the short-latency spinal reflex and the long-latency functional reflex in the active flexor muscle are unaffected by load stiffness. However, a stereotyped response observed after stretch-reflex latency varied systematically with load stiffness, as did reciprocal activation of the antagonist extensor muscle. The long-latency reflex appears to be a part of a coordinated reciprocal response of antagonist muscle pairs. Adapting to load properties involves modulating these later neural responses. A method was developed, based on ultrasound, to track changes in muscle and tendon length associated with small postural movements. The relationship between wrist angle and muscle and tendon length in the active muscle changed with load stiffness. Particularly with negative-stiffness loads, the wrist moves on the end of a compliant tendon without corresponding changes in muscle length. Thus, compensation of postural performance by neural modulation is limited by the properties of muscle and tendon.

This thesis investigates the processes of human postural control. How do we keep still? In any action, the force required changes with limb position. This force-position relationship is elastic stiffness. Holding a desired posture requires muscle activation that accounts for this load property. The studies here examine the physiological processes of postural control as elastic stiffness changes. Psychophysical studies show that thresholds for detecting differences in load stiffness are large relative to those normally encountered. To discriminate stiffness, subjects made consistent movements and judged the force required and detection thresholds followed rules for force perception. For the purposes of postural control, stiffness per se is not a variable of primary interest. The effects of load stiffness on postural stability were investigated using a pendulum that allowed independent control of load force and stiffness. Postural stability varied with load stiffness and this effect was independent of load force. Performance deteriorated as load stiffness became more negative. Load-dependent changes were at low frequencies only, suggesting neural processes operating at long latency, and perhaps ???volitional??? tracking, are the key to postural control. Imposed perturbations evoke patterns of muscle activation reflecting the state of the neural pathways of postural control. Stretch responses obtained while subjects held different loads show that the short-latency spinal reflex and the long-latency functional reflex in the active flexor muscle are unaffected by load stiffness. However, a stereotyped response observed after stretch-reflex latency varied systematically with load stiffness, as did reciprocal activation of the antagonist extensor muscle. The long-latency reflex appears to be a part of a coordinated reciprocal response of antagonist muscle pairs. Adapting to load properties involves modulating these later neural responses. A method was developed, based on ultrasound, to track changes in muscle and tendon length associated with small postural movements. The relationship between wrist angle and muscle and tendon length in the active muscle changed with load stiffness. Particularly with negative-stiffness loads, the wrist moves on the end of a compliant tendon without corresponding changes in muscle length. Thus, compensation of postural performance by neural modulation is limited by the properties of muscle and tendon.

Thesis (M.S.)--Wisconsin State University (La Crosse), 1967. / Includes bibliographical references (leaves [74]-75).

Thesis (Ph. D.)--Georgia State University, 2007. / Title from file title page. Rose A. Sevcik, committee chair; MaryAnn Romski, Rihana Williams-Smith, Robin D. Morris, committee members. Electronic text (99 p. : ill.) : digital, PDF file. Description based on contents viewed Jan. 28, 2008. Includes bibliographical references (p. 90-99).

Thesis (M.S.)--University of Nevada, Reno, 2007. / "May, 2007." Includes bibliographical references. Online version available on the World Wide Web. Library also has microfilm. Ann Arbor, Mich. : ProQuest Information and Learning Company, [2007]. 1 microfilm reel ; 35 mm.

Diss. (sammanfattning) Umeå : Univ., 2004. / Härtill 4 uppsatser.

Thesis (MHSc--Health Science) -- Auckland University of Technology, 2004. / Also held in print (199 leaves, col. ill., 30 cm.) in Akoranga Theses Collection. (T 615.82 SIM)

Thesis (M.Sc.). / Written for the Dept. of Kinesiology and Physical Education. Title from title page of PDF (viewed 2008/05/13). Includes bibliographical references.