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Advances in our understanding of the physiological basis of locomotion enable us to optimize the neurorehabilitation of patients with lesions to the central nervous system, such as stroke or spinal cord injury (SCI). It is generally accepted, based on work in animal models, that spinal neuronal machinery can produce a stepping-like output. In both incomplete and complete SCI subjects spinal locomotor circuitries can be activated by functional training which provides appropriate afferent feedback. In motor complete SCI subjects, however, motor functions caudal to the spinal cord lesion are no longer used resulting in neuronal dysfunction. In contrast, in subjects with an incomplete SCI such training paradigms can lead to improved locomotor ability. Appropriate functional training involves the facilitation and assistance of stepping-like movements with the subjects' legs and body weight support as far as is required. In severely affected subjects standardized assisted locomotor training is provided by body weight supported treadmill training with leg movements either manually assisted or moved by a driven gait orthosis. Load- and hip-joint related afferent input is of crucial importance during locomotor training as it leads to appropriate leg muscle activation and thus increases the efficacy of the rehabilitative training. Successful recovery of locomotion after SCI relies on the ability of spinal locomotor circuitries to utilize specific multisensory information to generate a locomotor pattern. It seems that a critical combination of sensory cues is required to generate and improve locomotor patterns after SCI. In addition to functional locomotor training there are number of other promising experimental approaches, such as tonic epidural electrical or magnetic stimulation of the spinal cord, which both promote locomotor permissive states that lead to a coordinated locomotor output. Therefore, a combination of functional training and activation of spinal locomotor cir

Objectives: Motor evoked potential (MEP) amplitudes have the disadvantage of a high variability when repeatedly assessed. This affects the reliability of MEP amplitude measurements taken during the course of motor incomplete spinal cord injury (iSCI). The study investigated the reliability of anterior tibial (TA) MEP measures controlled for dorsal flexion torque and motor task. Methods: TA MEPs were recorded at 10, 20, 40 and 60% of maximal voluntary contraction (MVC) during a static and dynamic (isometric increase of dorsal flexion torque) motor task. To determine reliability, 20 healthy and five chronic iSCI subjects were tested twice (≥7 days) by the same investigator. Intraclass correlation coefficients (ICCs) were calculated. MEP amplitudes and latencies were compared between 20 healthy and 29 iSCI subjects. Results: The reliability of MEP amplitude was in general good (ICC ≥ 0.52) and was highest during the static task at 40% MVC (ICC = 0.77). The increased facilitation by the dynamic motor task showed the best reliability at 20% MVC (ICC = 0.48). The reliability was good to excellent for MEP latency (0.46 ≥ ICC ≥ 0.81), MVC (ICC ≥ 0.90) and for the TMS threshold required to evoke a MEP response (ICC ≥ 0.77). The torque generated by the MEP response ()0.02 ≥ ICC ≥ 0.55) and the duration of the silent period (0.07 ≥ ICC ≥ 0.50) were not reliable. Both MEP amplitudes and latencies differed significantly between healthy and iSCI subjects. Conclusions: Controlling for torque generation and motor task establishes a reliability of TA MEP amplitudes that is sufficient for longitudinal assessments in motor incomplete SCI

In healthy subjects, functionally appropriate modulation of short latency leg muscle reflexes occurs during gait. This modulation has been ascribed, in part, to changes in presynaptic inhibition of Ia afferents. The changes in modulation of quadriceps tendon jerk reflexes during gait of healthy subjects were compared with those of hemi- or paraparetic spastic patients. The spasticity was due to unilateral cerebral infarction or traumatic spinal cord injury, respectively. The modulation of the quadriceps femoris tendon jerk reflex at 16 phases of the step cycle was studied. The reflex responses obtained during treadmill walking were compared with control values obtained during gait-mimicking standing postures with corresponding levels of voluntary muscle contraction and knee angles. In healthy subjects the size of the reflexes was profoundly modulated and was generally depressed throughout the step cycle. In patients with spinal lesion the reflex depression during gait was almost removed and was associated with weak or no modulation during the step cycle. In patients with cerebral lesion there was less depression of the reflex size associated with a reduced reflex modulation on the affected side compared with healthy subjects. On the 'sunaffected' side of these patients reflex modulation was similar to that of healthy subjects, but the reflex size during gait was not significantly different from standing control values. These observations suggest that the mechanisms responsible for the depression of reflex size and the modulation normally seen during gait in healthy subjects are impaired to different extents in spasticity of spinal or cerebral origin, possibly due to the unilateral preservation of fibre tracts in hemiparesis