Neural Control Of Gait Research Articles

Children With Unilateral Cerebral Palsy Utilize More Cortical Resources for Similar Motor Output During Treadmill Gait.

Children with unilateral cerebral palsy (CP) walk independently although with an asymmetrical, more poorly coordinated pattern compared to their peers. While gait biomechanics in unilateral CP and their alteration from those without CP have been well documented, cortical mechanisms underlying gait remain inadequately understood. To the best of our knowledge, this is the first study utilizing electroencephalography (EEG) during treadmill gait in older children with and without CP. Lower limb surface electromyographic (EMG) data were collected and muscle synergy analyses performed to quantify motor output. Our primary goal was to evaluate the relationships between cortical and muscle activation within and across groups and hemispheres to provide novel insights into neural control of gait and how it may be disrupted by an early unilateral brain injury. Participants included 9 children with unilateral CP, mean age 16.0 ± 2.7 years, and 12 with typical development (TD), mean age 14.8 ± 3.0 years. EEG data were collected during a standing baseline and treadmill walking at self-selected speed. EMG of 16 lower limb muscles were also collected bilaterally and synchronized with EEG. No significant group differences were found in synergy number or structure across groups. Six cortical clusters were identified as having gait-related activation and all contained participants from both CP and TD groups; however, the percent of individuals per group appearing in different clusters varied. Notably, the cluster least represented in CP was the non-dominant motor region. Both groups showed mu-band ERD in the motor clusters during gait although sustained beta-band ERD was not evident in TD. The CP group showed greater cortical activation than TD during walking as measured by mu- and beta-ERD in the dominant and non-dominant motor and parietal regions and elevated low gamma-activity in the frontal and parietal areas, a unique finding in CP. CP showed greater bilateral motor EEG-EMG coherence in the gamma-band with the hallucis longus compared to TD. In summary, individuals with CP display increased cortical activation during gait possibly relating to differences in distal motor control of the more affected side. Strategies that iteratively reduce cortical activation while improving selective motor control are needed in CP.

Neural predictors of gait stability when walking freely in the real-world

BackgroundGait impairments during real-world locomotion are common in neurological diseases. However, very little is currently known about the neural correlates of walking in the real world and on which regions of the brain are involved in regulating gait stability and performance. As a first step to understanding how neural control of gait may be impaired in neurological conditions such as Parkinson’s disease, we investigated how regional brain activation might predict walking performance in the urban environment and whilst engaging with secondary tasks in healthy subjects.MethodsWe recorded gait characteristics including trunk acceleration and brain activation in 14 healthy young subjects whilst they walked around the university campus freely (single task), while conversing with the experimenter and while texting with their smartphone. Neural spectral power density (PSD) was evaluated in three brain regions of interest, namely the pre-frontal cortex (PFC) and bilateral posterior parietal cortex (right/left PPC). We hypothesized that specific regional neural activation would predict trunk acceleration data obtained during the different walking conditions.ResultsVertical trunk acceleration was predicted by gait velocity and left PPC theta (4–7 Hz) band PSD in single-task walking (R-squared = 0.725, p = 0.001) and by gait velocity and left PPC alpha (8–12 Hz) band PSD in walking while conversing (R-squared = 0.727, p = 0.001). Medio-lateral trunk acceleration was predicted by left PPC beta (15–25 Hz) band PSD when walking while texting (R-squared = 0.434, p = 0.010).ConclusionsWe suggest that the left PPC may be involved in the processes of sensorimotor integration and gait control during walking in real-world conditions. Frequency-specific coding was operative in different dual tasks and may be developed as biomarkers of gait deficits in neurological conditions during performance of these types of, now commonly undertaken, dual tasks.

Part 2: Adaptation of Gait Kinematics in Unilateral Cerebral Palsy Demonstrates Preserved Independent Neural Control of Each Limb.

Motor adaptation, or alteration of neural control in response to a perturbation, is a potential mechanism to facilitate motor learning for rehabilitation. Central nervous system deficits are known to affect locomotor adaptation; yet we demonstrated that similar to adults following stroke, children with unilateral brain injuries can adapt step length in response to unilateral leg weighting. Here, we extend our analysis to explore kinematic strategies underlying step length adaptation and utilize dynamical systems approaches to elucidate how neural control may differ in those with hemiplegic CP across legs and compared to typically developing controls. Ten participants with hemiplegic CP and ten age-matched controls participated in this study. Knee and hip joint kinematics were analyzed during unilateral weighting of each leg in treadmill walking to assess adaptation and presence and persistence of after-effects. Peak joint angle displacement was used to represent changes in joint angles during walking. We examined baseline and task-specific variability and local dynamic stability to evaluate neuromuscular control across groups and legs. In contrast to controls, children with unilateral CP had asymmetries in joint angle variability and local dynamic stability at baseline, showing increased variability and reduced stability in the dominant limb. Kinematic variability increased and local stability decreased during weighting of ipsilateral and contralateral limbs in both groups compared to baseline. After weight removal both measures returned to baseline. Analogous to the temporal-spatial results, children with unilateral CP demonstrated similar capability as controls to adapt kinematics to unilateral leg weighting, however, the group with CP differed across sides after weight removal with dominant limb after-effects fading more quickly than in controls. The change in kinematics did not completely return to baseline in the non-dominant limb of the CP group, producing a transient improvement in joint angle symmetry. Recent studies demonstrate that neural control of gait is multi-layered with distinct circuits for different types of walking and for each leg. Remarkably, our results demonstrate that children with unilateral brain injury retain these separate circuits for each leg during walking and, importantly, that those networks can be adapted independently from one another to improve symmetry in the short term.

Regional Gray Matter Volume Loss Is Associated with Gait Impairments in Young Brain-Injured Individuals.

Traumatic brain injury (TBI) often leads to impairments in gait performance. However, the underlying neurostructural pathology of these gait deficits is poorly understood. We aimed to investigate regional gray matter (GM) volume in young moderate-to-severe TBI participants (n = 19; age 13 years 11 months ±3 years 1 month), compared with typically developing (TD) participants (n = 30; 14 years 10 months ±2 years 2 months), and assess whether reduced volume was related to impaired gait performance in TBI participants. Cortical and subcortical GM structures involved in the neural control of gait were selected as regions of interest (ROIs) and their volume was extracted using Freesurfer. Moreover, established spatiotemporal markers of gait impairments in TBI participants, including step length asymmetry, step length variability, and double support time, were obtained using an electronic walkway. Compared with TD participants, TBI participants showed increased double support time, step length asymmetry, and step length variability, suggesting a reduced gait control. Secondly, in TBI participants, reduced volumes were demonstrated in overall subcortical GM and individual subcortical ROIs, including the hippocampus, cerebellar cortex, putamen, and thalamus. Moreover, in the TBI group, volume losses in subcortical ROIs were highly inter-correlated, indicating that atrophy tends to occur in combined subcortical structures. Finally, it was demonstrated, for the first time, that gait abnormalities in TBI subjects were associated with reduced volume in specific GM structures, including the hippocampus, thalamus, and the cerebellar, superior frontal, paracentral, posterior cingulate, and superior parietal cortices. The present study is an important first step in the understanding of the neurostructural pathology underlying impaired gait in TBI patients.

Toward new sensitive measures to evaluate gait stability in focal cerebellar lesion patients

The evident ataxic characteristics of gait in patients with cerebellar damage suggest that the cerebellum plays an important role in the neural control of gait. Ataxic features, such as increased gait variability and increased step width, are often related to gait stability. However, the link between these measures and gait stability is not straightforward. Therefore, to gain more insights into relations between gait stability, gait variability and gait ataxia, we quantified gait stability using the short-term maximum Lyapunov exponent. This is a more valid measure of gait stability, derived from dynamical systems theory. Eighteen patients with focal cerebellar lesions after tumor resection walked on an instrumented treadmill at 1.0m/s for 3min. The patients displayed relatively mild functional deficits (ICARS=6.9±6.4, range 0–20) and had a lower overground walking speed as compared to healthy controls (1.12m/s versus 1.31m/s). During treadmill walking, the short-term maximum Lyapunov exponent was higher in cerebellar patients, indicating reduced gait stability. Furthermore, step width was increased in the patient group while other spatio-temporal gait parameters were similar. Patients with the largest lesions in the vermis displayed the least stable gait pattern. These observations imply that the short-term maximum Lyapunov exponent is a sensitive measure of gait deficits in mildly ataxic cerebellar patients.

Dynamic knee stability: current theory and implications for clinicians and scientists.

We will discuss the mechanisms by which dynamic knee stability may be achieved and relate this to issues that interest clinicians and scientists concerned with dynamic knee stability. Emphasis is placed on the neurophysiologic evidence and theory related to neuromuscular control. Specific topics discussed include the ensemble firing of peripheral mechanoreceptors, the potential for muscle stiffness modulation via force and length feedback, postural control synergies, motor programs, and the neural control of gait. Factors related to answering the difficult question of whether or not knee ligament injuries can be prevented during athletic activities are discussed. Prevention programs that train athletes to perform their sport skills in a safe fashion are put forth as the most promising prospect for injury prevention. Methods of assessing neuromuscular function are reviewed critically and the need for future research in this area is emphasized. We conclude with a brief review of the literature regarding neuromuscular training programs.

Neural control of gait: clinical neurophysiological aspects.

From the three essential mechanisms in locomotion, the antigravity, equilibrium and stepping mechanisms, only the latter is specific for gait. The spinal cord is considered to be a central pattern generator in experimental animals and is under the influence of different afferent sources and descending impulses. In clinical practice locomotor mechanisms can be modified at peripheral levels, as with functional electrical stimulation of peripheral nerves, and at the spinal cord, as in spinal cord stimulation, and theoretically also at midbrain and subthalamic locomotor areas. The importance of the spinal cord pattern generator in spinal cord injured patients is discussed. The role of postural mechanisms in locomotion is emphasized.