Modulation of presynaptic inhibition and disynaptic reciprocal Ia inhibition during voluntary movement in spasticity

Abstract

The aim of the study was to investigate whether impaired control of transmission in spinal inhibitory pathways contributes to the functional disability of patients with spasticity. To this end, transmission in the pathways mediating disynaptic reciprocal Ia inhibition and presynaptic inhibition was investigated in 23 healthy subjects and 20 patients with spastic multiple sclerosis during ankle dorsiflexion and plantar flexion. In healthy subjects, but not in spastic patients, the soleus H reflex was depressed at the onset of dorsiflexion (300 ms rise time, 20% of maximal voluntary effort). At the onset of plantar flexion, the soleus H reflex was more facilitated in the healthy subjects than in the patients. The H reflex increased more with increasing level of tonic plantar flexion and decreased more with dorsiflexion in the healthy subjects than in the spastic patients. Transmission in the disynaptic Ia reciprocal inhibitory pathway from ankle dorsiflexors to plantar flexors was investigated by conditioning the soleus H reflex by previous stimulation of the common peroneal nerve (conditioning-test interval 2-3 ms; stimulation intensity 1.05 times the motor response threshold). At the onset of dorsiflexion, stimulation of the common peroneal nerve evoked a significantly larger inhibition than at rest in the healthy subjects but not in the spastic patients. At the onset of plantar flexion the inhibition decreased in the healthy subjects, but because only weak inhibition was observed at rest in the patients it was not possible to determine whether a similar decrease occurred in this group. There were no differences in the modulation of inhibition during tonic plantar flexion and dorsiflexion in the two populations. Presynaptic inhibition of Ia afferents terminating on soleus motor neurones was evaluated from the monosynaptic Ia facilitation of the soleus H reflex evoked by femoral nerve stimulation. Femoral nerve facilitation was decreased at the onset of dorsiflexion and increased at the onset of plantar flexion in the healthy subjects and patients, but the changes were significantly greater in the healthy subjects. There was no difference between the two populations in the modulation of presynaptic inhibition during tonic plantar flexion and dorsiflexion. It is suggested that the abnormal regulation of disynaptic reciprocal inhibition and presynaptic inhibition in patients with spasticity is responsible for the abnormal modulation of stretch reflexes in relation to voluntary movement in these patients. Lack of an increase in reciprocal inhibition and presynaptic inhibition at the onset of dorsiflexion may be responsible for the tendency to elicitation of unwanted stretch reflex activity and co-contraction of antagonistic muscles in patients with spasticity.

Effects of hip joint angle changes on intersegmental spinal coupling in human spinal cord injury

“…These effects are mediated via the muscle spindle of the flexor group Ia afferents, and the pathway involved is known as reciprocal Ia inhibition (Tanaka 1974;Crone et al 1987;see review in Crone 1993). This reflex inhibition is reported to decrease considerably, and be eliminated during voluntary movement in individuals with established SCI (Boorman et al 1996a;Morita et al 2001;Crone et al 2003), contributing to spasticity and to poor movement performance.…”

“…This reflex depression is attributed to presynaptic inhibition of soleus Ia afferents (reviewed in Katz 1999). In human SCI, modulation of Ia input is diminished under both static (Faist et al 1994;Morita et al 2001) and dynamic (Yang and Whelan 1993) conditions, suggesting that the timely regulation of presynaptic inhibition at the onset of stretch or movement in these patients might be lost.…”

Effects of sustained stimulation on the excitability of motoneurons innervating paralyzed and control muscles

“…The balance between the excitatory and inhibitory synaptic inputs may be altered as a result of the removal of descending drive to the motoneurons, interneurons, and presynaptic terminals (e.g., Refs. 3,26). The motoneurons of paralyzed muscles may receive new inputs from axons that have sprouted from neighboring cells (for reviews see Refs.…”

rTMS modulates reciprocal inhibition in patients with traumatic spinal cord injury

“…Impairment of rTMS modulates reciprocal inhibition in SCI patients R Nardone et al reciprocal inhibition has been suggested to have a causal role in the development of spasticity, 6,14-17 and a decreased excitability in the disynaptic reciprocal inhibitory pathway has indeed been demonstrated in patients with spasticity of different origin. 14,17,18 TMS studies in awake humans have already demonstrated cortical control of spinal reflex circuits. In fact, subthreshold TMS produces a short-latency inhibition on the soleus H-reflex followed by a period of facilitation, [19][20][21] whereas the TA H-reflex is facilitated at an early conditioning-test interval.…”