The purpose of this article is to provide a brief review of the principles of motor control and learning. Different models of motor control from historical to contemporary are presented with emphasis on the systems model. Concepts of motor learning including skill acquisition, measurement of learning, and methods to promote skill acquisition by examining the many facets of practice scheduling and use of feedback are provided. A fictional client case is introduced and threaded throughout the article to facilitate understanding of these concepts and how they can be applied to clinical practice.
The study of dual task interference has gained increasing attention in the literature for the past 35 years, with six MEDLINE citations in 1979 growing to 351 citations indexed in 2014 and a peak of 454 cited papers in 2013. Increasingly, researchers are examining dual task cost in individuals with pathology, including those with neurodegenerative diseases. While the influence of these papers has extended from the laboratory to the clinic, the field has evolved without clear definitions of commonly used terms and with extreme variations in experimental procedures. As a result, it is difficult to examine the interference literature as a single body of work. In this paper we present a new taxonomy for classifying cognitive-motor and motor-motor interference within the study of dual task behaviors that connects traditional concepts of learning and principles of motor control with current issues of multitasking analysis. As a first step in the process we provide an operational definition of dual task, distinguishing it from a complex single task. We present this new taxonomy, inclusive of both cognitive and motor modalities, as a working model; one that we hope will generate discussion and create a framework from which one can view previous studies and develop questions of interest.
The purpose of this study was to quantify gait impairments in presymptomatic and symptomatic Huntington's disease (HD) subjects, and examine sensitivity of gait measures. Our sample (n = 65) included presymptomatic mutation carriers (PMC) (n = 15), symptomatic HD subjects (SHD) (n = 30) and healthy controls (n = 20). Participants were requested to walk at their preferred speed on a computerized walkway that recorded spatiotemporal variables. We administered the Unified HD Rating Scale (UHDRS) for PMC and SHD. PMC demonstrated decreased gait velocity (P < 0.01), stride length (P < 0.008), and increased time in double support (P < 0.001); and demonstrated higher variability in stride length (P < 0.01) and step time (P < 0.004) compared with controls. These impairments worsened with increasing disease severity for SHD. Gait impairments were correlated with predicted years to onset in PMC (velocity = -0.65; cadence = -0.70, step time = 0.71) and demonstrated high sensitivity and specificity in distinguishing between controls and mutation carriers. In contrast, UHDRS scores did not reveal impairments in gait and balance. Gait bradykinesia and dynamic balance impairments begin in the presymptomatic stage of HD and continue to worsen in the symptomatic stages. Gait measures are sensitive in differentiating between mutation positive and negative individuals even when impairments were not detected by clinical neurological examination. (c) 2008 Movement Disorder Society.
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