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The title of this Special Issue is: “Underlying Mechanisms and Neurorehabilitation of Gait after Stroke” [...]

The central nervous system (CNS) control of human gait is complex, including descending cortical control, affective ascending neural pathways, interhemispheric communication, whole brain networks of functional connectivity, and neural interactions between the brain and spinal cord. Many important studies were conducted in the past, which administered gait training using externally targeted methods such as treadmill, weight support, over-ground gait coordination training, functional electrical stimulation, bracing, and walking aids. Though the phenomenon of CNS activity-dependent plasticity has served as a basis for more recently developed gait training methods, neurorehabilitation gait training has yet to be precisely focused and quantified according to the CNS source of gait control. Therefore, we offer the following hypotheses to the field: Hypothesis 1. Gait neurorehabilitation after stroke will move forward in important ways if research studies include brain structural and functional characteristics as measures of response to treatment. Hypothesis 2. Individuals with persistent gait dyscoordination after stroke will achieve greater recovery in response to interventions that incorporate the current and emerging knowledge of CNS function by directly engaging CNS plasticity and pairing it with peripherally directed, plasticity-based motor learning interventions. These hypotheses are justified by the increase in the study of neural control of motor function, with emerging research beginning to elucidate neural factors that drive recovery. Some are developing new measures of brain function. A number of groups have developed and are sharing sophisticated, curated databases containing brain images and brain signal data, as well as other types of measures and signal processing methods for data analysis. It will be to the great advantage of stroke survivors if the results of the current state-of-the-art and emerging neural function research can be applied to the development of new gait training interventions.

With discoveries of brain and spinal cord mechanisms that control gait, and disrupt gait coordination after disease or injury, and that respond to motor training for those with neurological disease or injury, there is greater ability to construct more efficacious gait coordination training paradigms. Therefore, it is critical in these contemporary times, to use the most precise, sensitive, homogeneous (i.e., domain-specific), and comprehensive measures available to assess gait coordination, dyscoordination, and changes in response to treatment. Gait coordination is defined as the simultaneous performance of the spatial and temporal components of gait. While kinematic gait measures are considered the gold standard, the equipment and analysis cost and time preclude their use in most clinics. At the same time, observational gait coordination scales can be considered. Two independent groups identified the Gait Assessment and Intervention Tool (G.A.I.T.) as the most suitable scale for both research and clinical practice, compared to other observational gait scales, since it has been proven to be valid, reliable, sensitive to change, homogeneous, and comprehensive. The G.A.I.T. has shown strong reliability, validity, and sensitive precision for those with stroke or multiple sclerosis (MS). The G.A.I.T. has been translated into four languages (English, Spanish, Taiwanese, and Portuguese (translation is complete, but not yet published)), and is in use in at least 10 countries. As a contribution to the field, and in view of the evidence for continued usefulness and international use for the G.A.I.T. measure, we have provided this update, as well as an open access copy of the measure for use in clinical practice and research, as well as directions for administering the G.A.I.T.

Background/Problem: Standard neurorehabilitation and gait training has not proved effective in restoring normal gait coordination for many stroke survivors. Rather, persistent gait dyscoordination occurs, with associated poor function, and progressively deteriorating quality of life. One difficulty is the array of symptoms exhibited by stroke survivors with gait deficits. Some researchers have addressed lower limb weakness following stroke with exercises designed to strengthen muscles, with the expectation of improving gait. However, gait dyscoordination in many stroke survivors appears to result from more than straightforward muscle weakness. Purpose: Thus, the purpose of this case study is to report results of long-duration gait coordination training in an individual with initial good strength, but poor gait swing phase hip/knee and ankle coordination. Methods: Mr. X was enrolled at >6 months after a left hemisphere ischemic stroke. Gait deficits included a ‘stiff-legged gait’ characterized by the absence of hip and knee flexion during right mid-swing, despite the fact that he showed good initial strength in right lower limb quadriceps, hamstrings, and ankle dorsiflexors. Treatment was provided 4 times/week for 1.5 h, for 12 weeks. The combined treatment included the following: motor learning exercises designed for coordination training of the lower limb; functional electrical stimulation (FES) assisted practice; weight-supported coordination practice; and over-ground and treadmill walking. The FES was used as an adjunct to enhance muscle response during motor learning and prior to volitional recovery of motor control. Weight-supported treadmill training was administered to titrate weight and pressure applied at the joints and to the plantar foot surface during stance phase and pre-swing phase of the involved limb. Later in the protocol, treadmill training was administered to improve speed of movement during the gait cycle. Response to treatment was assessed through an array of impairment, functional mobility, and life role participation measures. Results: At post-treatment, Mr. X exhibited some recovery of hip, knee, and ankle coordination during swing phase according to kinematic measures, and the stiff-legged gait was resolved. Muscle strength measures remained essentially constant throughout the study. The modified Ashworth scale showed improved knee extensor tone from baseline of 1 to normal (0) at post-treatment. Gait coordination overall improved by 12 points according to the Gait Assessment and Intervention Tool, Six Minute Walk Test improved by 532′, and the Stroke Impact Scale improved by 12 points, including changes in daily activities; mobility; and meaningful activities. Discussion: Through the combined use of motor learning exercises, FES, weight-support, and treadmill training, coordination of the right lower limb improved sufficiently to exhibit a more normal swing phase, reducing the probability of falls, and subsequent downwardly spiraling dysfunction. The recovery of lower limb coordination during swing phase illustrates what is possible when strength is sufficient and when coordination training is targeted in a carefully titrated, highly incrementalized manner. Conclusions/Contribution to the Field: This case study contributes to the literature in several ways: (1) illustrates combined interventions for gait training and response to treatment; (2) provides supporting case evidence of relationships among knee flexion coordination, swing phase coordination, functional mobility, and quality of life; (3) illustrates that strength is necessary, but not sufficient to restore coordinated gait swing phase after stroke in some stroke survivors; and (4) provides details regarding coordination training and progression of gait training treatment for stroke survivors.