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Humans with spinal cord injury (SCI) show deficits in associating motor commands and sensory feedback. Do these deficits affect their ability to adapt movements to new demands? To address this question, we used a robotic exoskeleton to examine learning of a sensorimotor adaptation task during reaching movements by distorting the relationship between hand movement and visual feedback in 22 individuals with chronic incomplete cervical SCI and 22 age-matched control subjects. We found that SCI individuals showed a reduced ability to learn from movement errors compared with control subjects. Sensorimotor areas in anterior and posterior cerebellar lobules contribute to learning of movement errors in intact humans. Structural brain imaging showed that sensorimotor areas in the cerebellum, including lobules I–VI, were reduced in size in SCI compared with control subjects and cerebellar atrophy increased with increasing time post injury. Notably, the degree of spared tissue in the cerebellum was positively correlated with learning rates, indicating participants with lesser atrophy showed higher learning rates. These results suggest that the reduced ability to learn from movement errors during reaching movements in humans with SCI involves abnormalities in the spinocerebellar structures. We argue that this information might help in the rehabilitation of people with SCI. [ABSTRACT FROM AUTHOR]

Human and animal studies have documented that neural circuitries in the spinal cord show adaptive changes caused by altered supraspinal and/or afferent input to the spinal circuitry in relation to learning, immobilization, injury and neurorehabilitation. Reversible adaptations following, e.g. the acquisition or refinement of a motor skill rely heavily on the functional integration between supraspinal and sensory inputs to the spinal cord networks. Accordingly, what is frequently conceived as a change in the spinal circuitry may be a change in either descending or afferent input or in the relative integration of these, i.e. a change in the neuronal weighting. This is evident from findings documenting only task-specific functional changes after periods of altered inputs whereas resting responses remain unaffected. In fact, the proximity of the spinal circuitry to the outer world may demand a more rigid organization compared to the highly flexible cortical circuits. The understanding of all of this is important for the planning and execution of neurorehabilitation. [ABSTRACT FROM AUTHOR]

Repetitive transcranial magnetic stimulation (rTMS) has been shown to induce adaptations in cortical neuronal circuitries. In the present study we investigated whether rTMS, through its effect on corticospinal pathways, also produces adaptations at the spinal level, and what the neuronal mechanisms involved in such changes are. rTMS (15 trains of 20 pulses at 5 Hz) was applied over the leg motor cortical area in ten healthy human subjects. At rest motor evoked potentials (MEPs) in the soleus and tibialis anterior muscles were facilitated by rTMS (at 1.2×MEP threshold). In contrast, the soleus H-reflex was depressed for 1 s at stimulus intensities from 0.92 to 1.2×MEP threshold. rTMS increased the size of the long-latency depression of the soleus H-reflex evoked by common peroneal nerve stimulation and decreased the femoral nerve facilitation of the soleus H-reflex. These observations suggest that the depression of the H-reflex by rTMS can be explained, at least partly, by an increased presynaptic inhibition of soleus Ia afferents. In contrast, rTMS had no effect on disynaptic reciprocal Ia inhibition from ankle dorsiflexors to plantarflexors. We conclude that a train of rTMS may modulate transmission in specific spinal circuitries through changes in corticospinal drive. This may be of relevance for future therapeutic strategies in patients with spasticity. [ABSTRACT FROM AUTHOR]

Training-induced changes in cortical excitability may play an important role in rehabilitation of gait ability in patients with neurological disorders. In this study, we investigated the effect of a 32-min period of motor skill, non-skill and passive training involving the ankle muscles on leg motor cortical excitability in healthy humans. Transcranial magnetic stimulation (TMS) at a range of intensities was applied to obtain a recruitment curve of the motor evoked potentials (MEPs) in the tibialis anterior (TA) muscle before and after training. We also explored the effect of training on inhibitory and facilitatory cortical circuits by using a paired-pulse TMS technique at intervals of 2.5 ms (short-interval intracortical inhibition, SICI) and 8 ms (intracortical facilitation, ICF). During motor skill training, subjects were instructed to make a cursor follow a series of target lines on a computer screen by performing voluntary ankle dorsi- and plantarflexion movements. Non-skill and passive training consisted of repeated voluntary and assisted dorsi- and plantarflexion movements, respectively. Recruitment curves increased significantly after 32 min of motor skill training but not after non-skill and passive training, suggesting that only skill motor training increases motor cortical excitability. Motor skill training was not accompanied by any changes in the recruitment curves of TA MEPs evoked by transcranial electrical stimulation, suggesting that the increased MEPs to TMS was likely caused by changes in excitability at a cortical site. SICI was decreased after 32 min of motor skill training but no changes were observed in ICF. We conclude that similar plastic changes as have previously been reported for the hand motor following motor skill training may also be observed for the leg motor area. The observed plastic changes appeared to be related to the degree of difficulty in the motor task, and may be of relevance for rehabilitation of gait disorders. [ABSTRACT FROM AUTHOR]

A putative spinal circuit with convergent inputs facilitating human wrist flexors has been recently described. This study investigated how central nervous system lesions may affect this pathway. We measured the flexor carpi radialis H-reflex conditioned with stimulation above motor threshold to the extensor carpi radialis at different intervals in fifteen patients with stroke and nine with spinal cord injury. Measurements after stroke revealed a prolonged facilitation of the H-reflex, which replaced the later suppression seen in healthy subjects at longer intervals (30-60 ms). Measurements in patients with incomplete spinal cord injury at cervical level revealed heterogeneous responses. Results from patients with stroke could represent either an excessive facilitation or a loss of inhibition, which may reflect the development of spasticity. Spinal cord injury results possibly reflect damage to the segmental interneuron pathways. We report a straightforward method to assess changes to spinal circuits controlling wrist flexors after central nervous system lesion. [ABSTRACT FROM AUTHOR]