Human gait is a complex process in the central nervous system that results from the integrity of various mechanisms, including different cortical and subcortical structures. In the present study, we investigated cortical activity during lower limb movement using EEG. Assisted by a dynamic tilt table, all subjects performed standardized stepping movements in an upright position. Source localization of the movement-related potential in relation to spontaneous EEG showed activity in brain regions classically associated with human gait such as the primary motor cortex, the premotor cortex, the supplementary motor cortex, the cingulate cortex, the primary somatosensory cortex and the somatosensory association cortex. Further, we observed a task-related power decrease in the alpha and beta frequency band at electrodes overlying the leg motor area. A temporal activation and deactivation of the involved brain regions as well as the chronological sequence of the movement-related potential could be mapped to specific phases of the gait-like leg movement. We showed that most cortical capacity is needed for changing the direction between the flexion and extension phase. An enhanced understanding of the human gait will provide a basis to improve applications in the field of neurorehabilitation and brain-computer interfaces.

This study investigated the interactions of supraspinal with spinal neuronal circuits during obstacle steps by recordings of electroencephalography (EEG), reflex activity and limb muscle electromyography (EMG). Subjects walking with reduced vision on a treadmill were acoustically informed about an approaching obstacle and received feedback about task performance. Only following a task-relevant acoustic signal, spinal reflex responses, evoked by tibial nerve stimulation during mid-stance, were enhanced in proximal arm and leg flexor muscles prior to obstacle compared to normal swing, reflecting the neuronal preparation of the task. During swing over the obstacle, limb muscle EMG activity was greater than in normal swing. Both the preparation and the performance (i.e. ascending movement slope of the obstacle-crossing leg) were associated with an enhanced EEG signal mainly in the prefrontal cortex of the right hemisphere. Adaptational changes in performance, reflex activity and muscle activation during repetitive obstacle stepping were not reflected in the EEG activity, probably due to an insufficient resolution of the EEG. The observations suggest that drive from supraspinal centers initiates and maintains spinal neuronal activity underlying obstacle task preparation and performance.

The development of a non-human primate (NHP) model of spinal cord injury (SCI) based on mechanical and computational modeling is described. We scaled up from a rodent model to a larger primate model using a highly controllable, friction-free, electronically-driven actuator to generate unilateral C6-C7 spinal cord injuries. Graded contusion lesions with varying degrees of functional recovery, depending upon pre-set impact parameters, were produced in nine NHPs. Protocols and pre-operative magnetic resonance imaging (MRI) were used to optimize the predictability of outcomes by matching impact protocols to the size of each animal's spinal canal, cord, and cerebrospinal fluid space. Post-operative MRI confirmed lesion placement and provided information on lesion volume and spread for comparison with histological measures. We evaluated the relationships between impact parameters, lesion measures, and behavioral outcomes, and confirmed that these relationships were consistent with our previous studies in the rat. In addition to providing multiple univariate outcome measures, we also developed an integrated outcome metric describing the multivariate cervical SCI syndrome. Impacts at the higher ranges of peak force produced highly lateralized and enduring deficits in multiple measures of forelimb and hand function, while lower energy impacts produced early weakness followed by substantial recovery but enduring deficits in fine digital control (e.g., pincer grasp). This model provides a clinically relevant system in which to evaluate the safety and, potentially, the efficacy of candidate translational therapies.

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Following nociceptive heat or laser stimulation, an early contralateral and later vertex potential can be recorded. Although more indicative of the nociceptive input, the acquisition of the contralateral N1 after contact heat stimulation (contact heat-evoked potentials [CHEPs]) remains difficult. An advantage of contact heat is that the baseline skin temperature preceding peak stimulation can be controlled. Increasing the baseline temperature may represent a novel strategy to improve the acquisition of CHEPs without resulting in more subjective pain to stimulation. A study was undertaken in 23 healthy subjects to examine the effects of increasing the baseline temperature but not the perceived intensity of contact heat stimulation. A combined standard averaging and single-trial analysis was performed to disclose how changes in averaged waveforms related to latency jitter and individual trial amplitudes. By increasing the baseline temperature, the acquisition of N1 was improved among subjects with a low-amplitude response (greater than -4μV) following 35°C baseline temperature stimulation (P<.05). Based on standard averaging, N2/P2 amplitudes were also significantly increased with and without an accompanying change in the rating of perceived pain when the baseline temperature was increased (P<.05). In contrast, automated single-trial averaging revealed no significant difference in N2 amplitude when the baseline temperature was increased to 42°C and the peak temperature reduced. These findings suggest that 2 mechanisms underlie the improved acquisition of CHEPs: increased synchronization of afferent volley, yielding larger-amplitude evoked potentials in response to the same rating of intensity; and reduced inter-trial variability.