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Background. Development of motor pathways is modulated by activity in these pathways, when they are maturing (ie, critical period). Perinatal stroke injures motor pathways, including the corticospinal tracts, reducing their activity and impairing motor function. Current intervention for the lower limb emphasizes passive approaches (stretching, braces, botulinum toxin injections). The study hypothesis was that intensive, early, child-initiated activity during the critical period will enhance connectivity of motor pathways to the legs and improve motor function. Objective. The study objective was to determine whether early intervention with intensive activity is better than standard care, intervention delivered during the proposed critical period is better than after, and the outcomes are different when the intervention is delivered by a physical therapist in an institution vs. a parent at home. Design. A prospective, delay-group, single-blind, randomized controlled trial (RCT) and a parallel, cohort study of children living beyond commuting distance and receiving an intervention delivered by their parent. Setting. The RCT intervention was provided in university laboratories, and parent training was provided in the childs home. Participants. Children 8 months to 3 years old with MRI-confirmed perinatal ischemic stroke and early signs of hemiparesis. Intervention. Intensive, play-based leg activity with weights for the affected leg and foot, 1 hour/day, 4 days/week for 12 weeks. Measurements. The primary outcome was the Gross Motor Function Measure-66 score. Secondary outcomes were motion analysis of walking, full-day step counts, motor evoked potentials from transcranial magnetic stimulation, and patellar tendon reflexes. Limitations. Inter-individual heterogeneity in the severity of the stroke and behavioral differences are substantial but measurable. Differences in intervention delivery and assessment scoring are minimized by standardization and training. Conclusions. The intervention, contrary to current practice, could change physical therapy interventions for children with perinatal stroke. [ABSTRACT FROM AUTHOR]

Background. It is unclear which individuals with incomplete spinal cord injury best respond to body-weight-supported treadmill training. Objective. The purpose of this study was to determine the factors that predict whether a person with motor incomplete spinal cord injury will respond to bodyweight- supported treadmill training. Design. This was a prognostic study with a one-group pretest-posttest design. Methods. Demographic, clinical, and electrophysiological measurements taken prior to training were examined to determine which measures best predicted improvements in walking speed in 19 individuals with chronic (>7 months postinjury), motor-incomplete spinal cord injuries (ASIA Impairment Scale categories C and D, levels C1-L1). Results. Two initial measures correlated significantly with improvements in walking speed: (1) the ability to volitionally contract a muscle, as measured by the lower-extremity manual muscle test (LE MMT) (r=.72), and (2) the peak locomotor electromyographic (EMG) amplitude in the legs (r=.56). None of the demographics (time since injury, age, body mass index) were significantly related to improvements in walking speed, nor was the clinical measure of balance (Berg Balance Scale). Further analysis of LE MMT scores showed 4 key muscle groups were significantly related to improvements in walking speed: knee extensors, knee flexors, ankle plantar flexors, and hip abductors (r=.82). Prediction using the summed MMT scores from those muscles and peak EMG amplitude in a multivariable regression indicated that peak locomotor EMG amplitude did not add significantly to the prediction provided by the LE MMT alone. Change in total LE MMT scores from the beginning to the end of training was not correlated with a change in walking speed over the same period. Limitations. The sample size was limited, so the results should be considered exploratory. Conclusions. The results suggest that preserved muscle strength in the legs after incomplete spinal cord injury, as measured by MMT, allows for improvements in walking speed induced by locomotor training. INSET: The Bottom Line. [ABSTRACT FROM AUTHOR]

Following spinal cord injury (SCI), prolonged muscle spasms are readily triggered by brief sensory stimuli. Animal and indirect human studies have shown that a substantial portion of the depolarization of motoneurons during a muscle spasm comes from the activation of persistent inward currents (PICs). The brief (single pulse) sensory stimuli that trigger the PICs and muscle spasms in chronically spinalized animals evoke excitatory post-synaptic potentials (EPSPs) that are broadened to more than 500 ms, the duration of depolarization required to activate a PIC in the motoneuron. Thus, in humans, we investigated if post-synaptic potentials (PSPs) evoked from brief (<20 ms) sensory stimulation are changed after SCI and if they are broadened to > or =500 ms to more readily activate motoneuron PICs and muscle spasms. To estimate both the shape and duration of PSPs in human subjects we used peristimulus frequencygrams (PSFs), which are plots of the instantaneous firing frequency of tonically active single motor units that are time-locked to the occurrence of the sensory stimulus. PSFs in response to cutaneomuscular stimulation of the medial arch or toe of the foot, a sensory stimulus that readily triggers muscle spasms, were compared between non-injured control subjects and in spastic subjects with chronic (>1 year), incomplete SCI. In non-injured controls, a single shock or brief (<20 ms) train of cutaneomuscular stimulation produced PSFs consisting of a 300 ms increase in firing rate above baseline with an interposed period of reduced firing. Parallel intracellular experiments in motoneurons of adult rats revealed that a 300 ms EPSP with a fast intervening inhibitory PSP (IPSP) reproduced the PSF recorded in non-injured subjects. In contrast, the same brief sensory stimulation in subjects with chronic SCI produced PSFs of comparatively long duration (1200 ms) with no evidence for IPSP activation, as reflected by a lack of reduced firing rates after the onset of the PSF. Thus, unlike non-injured controls, the motoneurons of subjects with chronic SCI are activated by very long periods of pure depolarization from brief sensory activation. It is likely that these second-long EPSPs securely recruit slowly activating PICs in motoneurons that are known to mediate, in large part, the many seconds-long activation of motoneurons during involuntary muscle spasms. [ABSTRACT FROM AUTHOR]