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What determines the effectiveness of neurorehabilitation approaches on the outcome of function in stroke or spinal cord injured subjects? Many studies claim that an improvement of function is based on the intensity of training, while some actual studies indicate no additional gain in function by a more intensive training after a stroke. Inherent factors seem to determine outcome, such as damage of specific tracts in stroke and level of lesion in spinal cord injured subjects, while the improvement of function achieved by an intensive training is small in relation to the spontaneous recovery. It is argued that an individual capacity of recovery exists depending on such factors. This capacity can be exploited by a repetitive execution of functional movements (supported as far as required), irrespective of the intensity and technology applied. Elderly subjects have difficulties to translate the recovery of motor deficit into function. Alternative, non-training approaches to restore motor function, such as epidural or deep brain stimulation as well as CNS repair are still in an early clinical or in a translational stage., (© The Author(s) (2021). Published by Oxford University Press on behalf of the Guarantors of Brain.)

The neural control of "cooperative" hand movements reflecting "opening a bottle" was explored in human subjects by electromyographic (EMG) and functional magnetic resonance imaging (fMRI) recordings. EMG responses to unilateral nonnoxious ulnar nerve stimulation were analyzed in the forearm muscles of both sides during dynamic movements against a torque applied by the right hand to a device which was compensated for by the left hand. For control, stimuli were applied while task was performed in a static/isometric mode and during bilateral synchronous pro-/supination movements. During the dynamic cooperative task, EMG responses to stimulations appeared in the right extensor and left flexor muscles, regardless of which side was stimulated. Under the control conditions, responses appeared only on the stimulated side. fMRI recordings showed a bilateral extra-activation and functional coupling of the secondary somatosensory cortex (S2) during the dynamic cooperative, but not during the control, tasks. This activation might reflect processing of shared cutaneous input during the cooperative task. Correspondingly, it is assumed that stimulation-induced unilateral volleys are processed in S2, leading to a release of EMG responses to both forearms. This indicates a task-specific neural coupling during cooperative hand movements, which has consequences for the rehabilitation of hand function in poststroke patients., (© The Author 2013. Published by Oxford University Press. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.)

The purpose of this review is to discuss the achievements and perspectives regarding rehabilitation of sensorimotor functions after spinal cord injury. In the first part we discuss clinical approaches based on neuroplasticity, a term referring to all adaptive and maladaptive changes within the sensorimotor systems triggered by a spinal cord injury. Neuroplasticity can be facilitated through the training of movements with assistance as needed, and/or by electrical stimulation techniques. The success of such training in individuals with incomplete spinal cord injury critically depends on the presence of physiological proprioceptive input to the spinal cord leading to meaningful muscle activations during movement performances. The addition of rehabilitation technology, such as robotic devices allows for longer training times and provision of feedback information regarding changes in movement performance. Nevertheless, the improvement of function by such approaches for rehabilitation is limited. In the second part, we discuss preclinical approaches to restore function by compensating for the loss of descending input to spinal networks following complete spinal cord injury. This can be achieved with stimulation of spinal networks or approaches to restore their descending input. Electrical and pharmacological stimulation of spinal neural networks is still in an experimental stage; and despite promising repair studies in animal models, translations to humans up to now have not been convincing. It is likely that combinations of techniques targeting the promotion of axonal regeneration and meaningful plasticity are necessary to advance the restoration of function. In the future, refinement of animal studies may contribute to greater translational success.

Severe spinal cord injury in humans leads to a progressive neuronal dysfunction in the chronic stage of the injury. This dysfunction is characterized by premature exhaustion of muscle activity during assisted locomotion, which is associated with the emergence of abnormal reflex responses. Here, we hypothesize that undirected compensatory plasticity within neural systems caudal to a severe spinal cord injury contributes to the development of neuronal dysfunction in the chronic stage of the injury. We evaluated alterations in functional, electrophysiological and neuromorphological properties of lumbosacral circuitries in adult rats with a staggered thoracic hemisection injury. In the chronic stage of the injury, rats exhibited significant neuronal dysfunction, which was characterized by co-activation of antagonistic muscles, exhaustion of locomotor muscle activity, and deterioration of electrochemically-enabled gait patterns. As observed in humans, neuronal dysfunction was associated with the emergence of abnormal, long-latency reflex responses in leg muscles. Analyses of circuit, fibre and synapse density in segments caudal to the spinal cord injury revealed an extensive, lamina-specific remodelling of neuronal networks in response to the interruption of supraspinal input. These plastic changes restored a near-normal level of synaptic input within denervated spinal segments in the chronic stage of injury. Syndromic analysis uncovered significant correlations between the development of neuronal dysfunction, emergence of abnormal reflexes, and anatomical remodelling of lumbosacral circuitries. Together, these results suggest that spinal neurons deprived of supraspinal input strive to re-establish their synaptic environment. However, this undirected compensatory plasticity forms aberrant neuronal circuits, which may engage inappropriate combinations of sensorimotor networks during gait execution.

The aim of this study was to evaluate the sensorimotor interactions between unaffected and affected sides of post-stroke subjects during locomotion. In healthy subjects, stimulation of the tibial nerve during the mid-stance phase is followed by electromyography responses not only in the ipsilateral tibialis anterior, but also in the proximal arm muscles of both sides, with larger amplitudes prior to swing over an obstacle compared with normal swing. In post-stroke subjects, the electromyography responses were stronger on both sides when the tibial nerve of the unaffected leg was stimulated compared with stimulation of the affected leg. This difference was more pronounced when stimuli were applied prior to swing over an obstacle than prior to normal swing. This indicates an impaired processing of afferent input from the affected leg resulting in attenuated and little task-modulated reflex responses in the arm muscles on both sides. In contrast, an afferent volley from the unaffected leg resulted in larger electromyography responses, even in the muscles of the affected arm. Arm muscle activations were stronger during swing over an obstacle than during normal swing, with no difference in electromyography amplitudes between the unaffected and affected sides. It is concluded that the deficits of the affected arm are compensated for by influences from the unaffected side. These observations indicate strong mutual influences between unaffected and affected sides during locomotion of post-stroke subjects, which might be used to optimize rehabilitation approaches.

The aim of this study was to evaluate the course of spinal neuronal activity following spinal cord injury (SCI). In patients with a complete SCI, the leg muscle EMG activity early and up to 33 years after an SCI was analysed during locomotor movements induced and assisted by a driven gait orthosis (DGO). Only in chronic SCI patients did a premature exhaustion of neuronal activity occur. This was reflected in a reduced density and fading of leg muscle EMG activity. The early exhaustion of EMG activity was more pronounced in the leg flexor (e.g. biceps femoris) than extensor (e.g. gastrocnemius) muscles. The timing of the leg muscle pattern remained unchanged in the chronic patients. A preserved amplitude of motor action potentials following repetitive peripheral nerve stimulation and during spasms indicated an interneuronal site of impairment. In patients who participated in a locomotor training programme lasting up to 13 weeks, no positive effect on the slope of exhaustion was seen. It is concluded that a degradation of spinal neuronal activity takes place following an SCI. If in the future regeneration of spinal tract fibres becomes feasible in patients with complete SCI, such an approach can only become functionally successful if neuronal activity below the level of the lesion is maintained. This might be achieved by a continuous training approach starting early after injury.

The aim of this study was to differentiate the effects of body load and joint movements on the leg muscle activation pattern during assisted locomotion in spinal man. Stepping movements were induced by a driven gait orthosis (DGO) on a treadmill in patients with complete para-/tetraplegia and, for comparison, in healthy subjects. All subjects were unloaded by 70% of their body weight. EMG of upper and lower leg muscles and joint movements of the DGO of both legs were recorded. In the patients, normal stepping movements and those mainly restricted to the hips (blocked knees) were associated with a pattern of leg muscle EMG activity that corresponded to that of the healthy subjects, but the amplitude was smaller. Locomotor movements restricted to imposed ankle joint movements were followed by no, or only focal EMG responses in the stretched muscles. Unilateral locomotion in the patients was associated with a normal pattern of leg muscle EMG activity restricted to the moving side, while in the healthy subjects a bilateral activation occurred. This indicates that interlimb coordination depends on a supraspinal input. During locomotion with 100% body unloading in healthy subjects and patients, no EMG activity was present. Thus, it can be concluded that afferent input from hip joints, in combination with that from load receptors, plays a crucial role in the generation of locomotor activity in the isolated human spinal cord. This is in line with observations from infant stepping experiments and experiments in cats. Afferent feedback from knee and ankle joints may be involved largely in the control of focal movements.