4 research outputs found
Using Wearable Sensor Technology to Measure Motion Complexity in Infants at High Familial Risk for Autism Spectrum Disorder
Background: Motor dysfunction has been reported as one of the first signs of atypical development in infants at high familial risk for autism spectrum disorder (ASD) (HR infants). However, studies have shown inconsistent results regarding the nature of motor dysfunction and whether it can be predictive of later ASD diagnosis. This is likely because current standardized motor assessments may not identify subtle and specific motor impairments that precede clinically observable motor dysfunction. Quantitative measures of motor development may address these limitations by providing objective evaluation of subtle motor differences in infancy. Methods: We used Opal wearable sensors to longitudinally evaluate full day motor activity in HR infants, and develop a measure of motion complexity. We focus on complexity of motion because optimal motion complexity is crucial to normal motor development and less complex behaviors might represent repetitive motor behaviors, a core diagnostic symptom of ASD. As proof of concept, the relationship of the motion complexity measure to developmental outcomes was examined in a small set of HR infants. Results: HR infants with a later diagnosis of ASD show lower motion complexity compared to those that do not. There is a stronger correlation between motion complexity and ASD outcome compared to outcomes of cognitive ability and adaptive skills. Conclusions: Objective measures of motor development are needed to identify characteristics of atypical infant motor function that are sensitive and specific markers of later ASD risk. Motion complexity could be used to track early infant motor development and to discriminate HR infants that go on to develop ASD
Quantitative Gait Analysis in Duplication 15q Syndrome and Nonsyndromic ASD
International audienceMotor impairments occur frequently in genetic syndromes highly penetrant for autism spectrum disorder (syndromic ASD) and in individuals with ASD without a genetic diagnosis (nonsyndromic ASD). In particular, abnormalities in gait in ASD have been linked to language delay, ASD severity, and likelihood of having a genetic disorder. Quantitative measures of motor function can improve our ability to evaluate motor differences in individuals with syndromic and nonsyndromic ASD with varying levels of intellectual disability and adaptive skills. To evaluate this methodology, we chose to use quantitative gait analysis to study duplication 15q syndrome (dup15q syndrome), a genetic disorder highly penetrant for motor delays, intellectual disability, and ASD. We evaluated quantitative gait variables in individuals with dup15q syndrome (n = 39) and nonsyndromic ASD (n = 21) and compared these data to a reference typically developing cohort. We found a gait pattern of slow pace, poor postural control, and large gait variability in dup15q syndrome. Our findings improve characterization of motor function in dup15q syndrome and nonsyndromic ASD. Quantitative gait analysis can be used as a translational method and can improve our identification of clinical endpoints to be used in treatment trials for these syndromes
Quantitative Gait Analysis in Duplication 15q
International audienceMotor impairments occur frequently in genetic syndromes highly penetrant for autism spectrum disorder (syndromic ASD) and in individuals with ASD without a genetic diagnosis (nonsyndromic ASD). In particular, abnormalities in gait in ASD have been linked to language delay, ASD severity, and likelihood of having a genetic disorder. Quantitative measures of motor function can improve our ability to evaluate motor differences in individuals with syndromic and nonsyndromic ASD with varying levels of intellectual disability and adaptive skills. To evaluate this methodology, we chose to use quantitative gait analysis to study duplication 15q syndrome (dup15q syndrome), a genetic disorder highly penetrant for motor delays, intellectual disability, and ASD. We evaluated quantitative gait variables in individuals with dup15q syndrome (n = 39) and nonsyndromic ASD (n = 21) and compared these data to a reference typically developing cohort. We found a gait pattern of slow pace, poor postural control, and large gait variability in dup15q syndrome. Our findings improve characterization of motor function in dup15q syndrome and nonsyndromic ASD. Quantitative gait analysis can be used as a translational method and can improve our identification of clinical endpoints to be used in treatment trials for these syndromes