Motoneurons of Spastic-Paretic Stroke Survivors

30 Stroke survivors often exhibit abnormal motoneuron excitability, manifested clinically 31 as spasticity with exaggerated stretch reflexes in resting muscles. We examined whether this 32 abnormal excitability is a result of increased activation of intrinsic voltage-dependent 33 persistent inward currents (PICs), or whether it is due to enhanced synaptic inputs to the 34 motoneuron. This distinction was made by recording firing rate profiles of pairs of motor units 35 during isometric contractions of elbow flexor muscles. 36 To estimate PIC amplitude, the discharge of the lower-threshold (reporter) motor unit 37 of the pair was used to estimate the synaptic input to the higher-threshold (test) motor unit. The 38 estimated synaptic input required to recruit the test unit was compared to the synaptic input 39 when the test unit was de-recruited (∆F), and this served as an estimate of the intrinsic (PIC) 40 contribution to motoneuron firing. We found that PIC estimates were not larger in spastic41 paretic motoneurons (∆F = 4.0 ± 1.6 pps) compared with contralateral (4.6 ± 1.4 pps) and age42 matched healthy control motoneurons (3.8 ± 1.7, all P > 0.1). 43 Instead, following the voluntary contractions, the majority of lower-threshold motor 44 units in spastic-paretic muscles (83%) exhibited spontaneous discharge, compared with 14% of 45 contralateral and 0% of control motor units. Furthermore, there was strong co-modulation of 46 simultaneously active units in spastic muscle. The presence of ongoing, correlated unit activity 47 at “rest”, coupled with firing behavior at recruitment unique to lower-threshold motor units in 48 spastic muscles, suggested that firing changes are likely a result of a low-level depolarizing 49 synaptic drive to the resting motoneuron pool. 50