“…The RF muscle was highly implicated in quadriceps spasticity, doubling the peak spastic torque with the hip extended compared with the hip flexed, at both velocities. Even so, hip sensory afferent feedback from the ipsilateral and contralateral hip is known to adjust the ipsilateral soleus H-reflex, 30 and heteronymous muscle afferents also could have increased quadriceps spasticity in the hip extended position.…”
BoNT A appeared to delay the stretch-reflex angle at peak torque, whereas the voluntary torque decreased. After strict patient selection, BoNT A injection into the RF muscle led to improvements in impairment, activity, and discomfort.
“…The RF muscle was highly implicated in quadriceps spasticity, doubling the peak spastic torque with the hip extended compared with the hip flexed, at both velocities. Even so, hip sensory afferent feedback from the ipsilateral and contralateral hip is known to adjust the ipsilateral soleus H-reflex, 30 and heteronymous muscle afferents also could have increased quadriceps spasticity in the hip extended position.…”
BoNT A appeared to delay the stretch-reflex angle at peak torque, whereas the voluntary torque decreased. After strict patient selection, BoNT A injection into the RF muscle led to improvements in impairment, activity, and discomfort.
“…Crossed postsynaptic inhibition in contralateral soleus motoneurons from ipsilateral groups I and II afferents at short latencies (3–7 ms), similar to those reported for the feline spinal cord, has recently been described for humans [ 168 ]. Further, activation of contralateral hip proprioceptors results in ipsilateral soleus H-reflex depression [ 169 ]. Taken altogether, differences between right-left leg H-reflex changes during the stance phase may thus represent plastic changes of commissural interneurons, but it is evident that there is a need for in-depth exploration of the physiological changes of commissural interneurons in people with SCI after locomotor training.…”
Section: Pathways and Circuits Underlying Neuronal And Motor Plastmentioning
Locomotor training is a classic rehabilitation approach utilized with the aim of improving sensorimotor function and walking ability in people with spinal cord injury (SCI). Recent studies have provided strong evidence that locomotor training of persons with clinically complete, motor complete, or motor incomplete SCI induces functional reorganization of spinal neuronal networks at multisegmental levels at rest and during assisted stepping. This neuronal reorganization coincides with improvements in motor function and decreased muscle cocontractions. In this review, we will discuss the manner in which spinal neuronal circuits are impaired and the evidence surrounding plasticity of neuronal activity after locomotor training in people with SCI. We conclude that we need to better understand the physiological changes underlying locomotor training, use physiological signals to probe recovery over the course of training, and utilize established and contemporary interventions simultaneously in larger scale research studies. Furthermore, the focus of our research questions needs to change from feasibility and efficacy to the following: what are the physiological mechanisms that make it work and for whom? The aforementioned will enable the scientific and clinical community to develop more effective rehabilitation protocols maximizing sensorimotor function recovery in people with SCI.
“…For example, passive rhythmic movement of one leg suppressed the contralateral soleus H-reflex at rest (McIllroy et al, 1992 ; Collins et al, 1993 ; Cheng et al, 1998 ; Misiaszek et al, 1998 ). Either in-phase or anti-phase rhythmic passive movement of both hips or unilateral rhythmic passive movement of the hip contralateral to the tested side suppressed the soleus H-reflex (Stanislaus et al, 2010 ). During passive movement, the descending motor drive is absent, but the somatosensation induced by the movement is present.…”
The activity of the left and right central pattern generators (CPGs) is efficiently coordinated during locomotion. To achieve this coordination, the interplay between the CPG controlling one leg and that controlling another must be present. Previous findings in aquatic vertebrates and mammalians suggest that the alternate activation of the left and right CPGs is mediated by the commissural interneurons crossing the midline of the spinal cord. Especially, V0 commissural interneurons mediate crossed inhibition during the alternative activity of the left and right CPGs. Even in humans, phase-dependent modulation of the crossed afferent inhibition during gait has been reported. Based on those previous findings, crossed inhibition of the CPG in one leg side caused by the activation of the contralateral CPG is a possible mechanism underlying the coordination of the anti-phase rhythmic movement of the legs. It has been hypothesized that the activity of the flexor half center in the CPG inhibits the contralateral flexor half center, but crossed inhibition of the extensor half center is not present because of the existence of the double limb support during gait. Nevertheless, previous findings on the phase-dependent crossed inhibition during anti-phase bilateral movement of the legs are not in line with this hypothesis. For example, extensor activity caused crossed inhibition of the flexor half center during bilateral cycling of the legs. In another study, the ankle extensor was inhibited at the period switching from extension to flexion during anti-phase rhythmic movement of the ankles. In this review article, I provide a critical discussion about crossed inhibition mediating the coordination of the anti-phase bilateral rhythmic movement of the legs.
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