Modulation of soleus stretch reflexes during walking in people with chronic incomplete spinal cord injury

Abstract

In people with spasticity due to chronic incomplete spinal cord injury (SCI), it has been presumed that the abnormal stretch reflex activity impairs gait. However, locomotor stretch reflexes across all phases of walking have not been investigated in people with SCI. Thus, to understand modulation of stretch reflex excitability during spastic gait, we investigated soleus stretch reflexes across the entire gait cycle in nine neurologically normal participants and nine participants with spasticity due to chronic incomplete SCI (2.5–11 year post-injury). While the participant walked on the treadmill at his/her preferred speed, unexpected ankle dorsiflexion perturbations (6° at 250°/s) were imposed every 4–6 steps. The soleus H-reflex was also examined. In participants without SCI, spinal short-latency “M1”, spinal medium latency “M2”, and long-latency “M3” were clearly modulated throughout the step cycle; the responses were largest in the mid-stance and almost completely suppressed during the stance-swing transition and swing phases. In participants with SCI, M1 and M2 were abnormally large in the mid–late-swing phase, while M3 modulation was similar to that in participants without SCI. The H-reflex was also large in the mid–late-swing phase. Elicitation of H-reflex and stretch reflexes in the late swing often triggered clonus and affected the soleus activity in the following stance. In individuals without SCI, moderate positive correlation was found between H-reflex and stretch reflex sizes across the step cycle, whereas in participants with SCI, such correlation was weak to non-existing, suggesting that H-reflex investigation would not substitute for stretch reflex investigation in individuals after SCI.

H‐reflex conditioning during locomotion in people with spinal cord injury

“…We studied people with spastic hyperreflexia and moderately impaired locomotion as a result of chronic spinal cord injury. They comprised an appropriate study population because hyperreflexia during the swing-phase probably contributed to their impairment (Yang et al 1991;Fung & Barbeau, 1994;Thompson et al 2019) and because they walked sufficiently well to be able to attend to the conditioning protocol when walking on a treadmill. ) in whom the late-swing phase H-reflex decreased significantly.…”

“…In humans, SCI often increases the excitability of spinal stretch reflexes and H-reflexes and impairs their normal modulation over the step cycle (Yang et al 1991;Stein et al 1993;Fung & Barbeau, 1994;Boorman et al 1996;Little et al 1999;Hiersemenzel et al 2000;Crone et al 2003;Nakazawa et al 2006;Dietz & Sinkjaer, 2007;Nielsen et al 2007;Thompson et al 2009b; Thompson et al 2019). These abnormalities contribute to locomotor impairments in people with spasticity as a result of SCI (Corcos et al 1986;Fung & Barbeau, 1989;Hidler & Rymer, 1999Khan et al 2016).…”

An Adeno-Associated Viral vector encoding Neurotrophin 3 injected into affected forelimb muscles modestly improves sensorimotor function after contusive mid-cervical spinal cord injury

“…Despite being only one component of the spasticity syndrome, hyperreflexia of the stretch reflex is a well-studied phenomenon in both patients and numerous preclinical models of CNS injury [16][17][18] . The stretch reflex arc acts to contract the stretching muscle and comprises muscle spindles, Ia afferents, the monosynaptic connection between Ia afferents and homonymous α-motor neuron, and finally the α-motor neuron itself which innervates the muscle at the motor end plate 19,20 .…”

Ground Walking in Chronic Complete Spinal Cord Injury

“…A “spastic crutch” may be helpful in fostering some form of functional stepping and may even foster the enhancement of the supraspinal drive. 20 However, enhanced muscle stretching (hence, enhanced spasticity) could have been made possible by the new standing and walking performances. Let us accept that the emerging muscle activation was the effect of the stimulation; however, the suggestion that “… suprasegmental excitation of spinal networks is entrained for walking after cord injury by the technique we describe” 1 (p1250) still remains unsubstantiated.…”

“…With the data at hand, there is no way to disentangle the “peripheral stimulation first” versus the “volitional drive first” interpretation. Neither tendon reflexes nor the H-reflex, 20 nor measures of corticospinal drive (eg, motor evoked potentials), and the central muscle activation through the interpolated twitch technique 21 were provided in the article. A more substantial investigation on neurophysiology and the spinal cord anatomy would have been beneficial.…”