Slow Potentials of the Sensorimotor Cortex during Rhythmic Movements of the Ankle

The objective of this dissertation was to more fully understand the role of the human brain in the production of lower extremity rhythmic movements. Throughout the last century, evidence from animal models has demonstrated that spinal reflexes and networks alone are sufficient to propagate ambulation. However, observations after neural trauma, such as a spinal cord injury, demonstrate that humans require supraspinal drive to facilitate locomotion. To investigate the unique nature of lower extremity rhythmic movements, electroencephalography was used to record neural signals from the sensorimotor cortex during three cyclic ankle movement experiments. First, we characterized the differences in slow movement-related cortical potentials during rhythmic and discrete movements. During the experiment, motion analysis and electromyography were used characterize lower leg kinematics and muscle activation patterns. Second, a custom robotic device was built to assist in passive and active ankle movements. These movement conditions were used to examine the sensory and motor cortical contributions to rhythmic ankle movement. Lastly, we explored the differences in sensory and motor contributions to bilateral, rhythmic ankle movements. Experimental results from all three studies suggest that the brain is continuously involved in rhythmic movements of the lower extremities. We observed temporal characteristics of the cortical slow potentials that were time-locked to the movement. The amplitude of these potentials, localized over the sensorimotor cortex, revealed a reduction in neural activity during rhythmic movements when compared to discrete movements. Moreover, unilateral ankle movements produced unique sensory potentials that tracked the position of the movement and motor potentials that were only present during active dorsiflexion. In addition, the spatiotemporal patterns of slow potentials during bilateral ankle movements suggest similar cortical mechanisms for both unilateral and bilateral movement. Lastly, beta frequency modulations were correlated to the movement-related slow potentials within medial sensorimotor cortex, which may indicate they are of similar cortical origin. From these results, we concluded that the brain is continuously involved in the production of lower extremity rhythmic movements, and that the sensory and motor cortices provide unique contributions to both unilateral and bilateral movemen

Measuring the Plasticity of Social Approach: A Randomized Controlled Trial of the Effects of the PEERS Intervention on EEG Asymmetry in Adolescents with Autism Spectrum Disorders

This study examined whether the Program for the Education and Enrichment of Relational Skills (PEERS: Social skills for teenagers with developmental and autism spectrum disorders: The PEERS treatment manual, Routledge, New York, 2010a) affected neural function, via EEG asymmetry, in a randomized controlled trial of adolescents with Autism spectrum disorders (ASD) and a group of typically developing adolescents. Adolescents with ASD in PEERS shifted from right-hemisphere gamma-band EEG asymmetry before PEERS to left-hemisphere EEG asymmetry after PEERS, versus a waitlist ASD group. Left-hemisphere EEG asymmetry was associated with more social contacts and knowledge, and fewer symptoms of autism. Adolescents with ASD in PEERS no longer differed from typically developing adolescents in left-dominant EEG asymmetry at post-test. These findings are discussed via the Modifier Model of Autism (Mundy et al. in Res Pract Persons Severe Disabl 32(2):124, 2007), with emphasis on remediating isolation/withdrawal in ASD

Event-Related Potentials, Inhibition, and Risk for Alzheimer’s Disease Among Cognitively Intact Elders

Background: Despite advances in understanding Alzheimer’s disease (AD), prediction of AD prior to symptom onset remains severely limited, even when primary risk factors such as the apolipoprotein E (APOE) ɛ4 allele are known. Objective: Although executive dysfunction is highly prevalent and is a primary contributor to loss of independence in those with AD, few studies have examined neural differences underlying executive functioning as indicators of risk for AD prior to symptom onset, when intervention might be effective. Methods: This study examined event-related potential (ERP) differences during inhibitory control in 44 cognitively intact older adults (20 ɛ4+, 24 ɛ4-), relative to 41 young adults. All participants completed go/no-go and stop-signal tasks. Results: Overall, both older adult groups exhibited slower reaction times and longer ERP latencies compared to young adults. Older adults also had generally smaller N200 and P300 amplitudes, except at frontal electrodes and for N200 stop-signal amplitudes, which were larger in older adults. Considered with intact task accuracy, these findings suggest age-related neural compensation. Although ɛ4 did not distinguish elders during go or no-go tasks, this study uniquely showed that the more demanding stop-signal task was sensitive to ɛ4 differences, despite comparable task and neuropsychological performance with non-carriers. Specifically, ɛ4+ elders had slower frontal N200 latency and larger N200 amplitude, which was most robust at frontal sites, compared with ɛ4-. Conclusion: N200 during a stop-signal task is sensitive to AD risk, prior to any evidence of cognitive dysfunction, suggesting that stop-signal ERPs may be an important protocol addition to neuropsychological testing