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Roeder, L.

Publications and source records attributed to Roeder, L..

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Dynamics of corticospinal motor control during overground and treadmill walking in humans

Increasing evidence suggests cortical involvement in the control of human gait. However, the nature of corticospinal interactions remains poorly understood. We performed time-frequency analysis of electrophysiological activity acquired during treadmill and overground walking in 22 healthy, young adults. Participants walked at their preferred speed (4.2, SD 0.4 km h-1), which was matched across both gait conditions. Event-related power, corticomuscular coherence (CMC) and inter-trial coherence (ITC) were assessed for EEG from bilateral sensorimotor cortices and EMG from the bilateral tibialis anterior (TA) muscles. Cortical power, CMC and ITC at theta, alpha, beta and gamma frequencies (4-45 Hz) increased during the double support phase of the gait cycle for both overground and treadmill walking. High beta (21-30 Hz) CMC and ITC of EMG was significantly increased during overground compared to treadmill walking, as well as EEG power in theta band (4-7 Hz). The phase spectra revealed positive time lags at alpha, beta and gamma frequencies, indicating that the EEG response preceded the EMG response. The parallel increases in power, CMC and ITC during double support suggest evoked responses at spinal and cortical populations rather than a modulation of ongoing corticospinal oscillatory interactions. The evoked responses are not consistent with the idea of synchronization of ongoing corticospinal oscillations, but instead suggest coordinated cortical and spinal inputs during the double support phase. Frequency-band dependent differences in power, CMC and ITC between overground and treadmill walking suggest differing neural control for the two gait modalities, emphasizing the task-dependent nature of neural processes during human walking.\n\nNew & NoteworthyWe investigated cortical and spinal activity during overground and treadmill walking in healthy adults. Parallel increases in power, CMC and ITC during double support suggest evoked responses at spinal and cortical populations rather than a modulation of ongoing corticospinal oscillatory interactions. These findings identify neurophysiological mechanisms that are important for understanding cortical control of human gait in health and disease.

physiology

Intrinsically photosensitive retinal ganglion cell mediated pupil function is impaired in Parkinson’s disease

Parkinsons disease is characterised by non-motor symptoms including sleep and circadian disruption, but the underlying aetiology is not well understood. Melanopsin-expressing intrinsically photosensitive Retinal Ganglion Cells (ipRGC) transmit light signals from the eye to brain areas controlling circadian rhythms and the pupil light reflex. Here we evaluate the hypothesis that these non-motor symptoms in people with Parkinsons disease may be linked to ipRGC dysfunction. Using chromatic pupillometry, we measured intrinsic (melanopsin-mediated) ipRGC and extrinsic (rod/cone photoreceptor-mediated) inputs to the pupil control pathway in a group of optimally medicated participants with a diagnosis of Parkinsons disease (PD, n = 17) compared to controls (n = 12). Autonomic tone was evaluated by measuring pupillary unrest in darkness. The PD participants underwent additional clinical assessments using the Unified Parkinsons disease Rating Scale (UPDRS) and the Hoehn and Yahr scale (H&Y).\n\nCompared to controls, the PD group demonstrated an attenuated pupil constriction amplitude in response to long wavelength pulsed stimulation, and reduced post-illumination pupil response (PIPR) amplitude in response to both short wavelength pulsed and sinusoidal stimulation. In the PD group, PIPR amplitude did not correlate with measures of sleep quality, retinal nerve fibre layer thickness, UPDRS or H&Y score, or medication dosage. Both groups exhibited similar pupillary unrest in darkness.\n\nWe show that melanopsin and the rod/cone-photoreceptor contributions to the pupil control pathway are impaired in people with early-stage Parkinsons disease. Given that the deficits are independent of clinical assessment severity and are observed despite optimal medication, the melanopsin-mediated PIPR may be a biomarker for the detection of Parkinsons disease and its continued monitoring in both medicated and unmedicated individuals.

neuroscience