Disturbances of motor unit rate modulation are prevalent in muscles of spastic-paretic stroke survivors.

Stroke survivors often exhibit abnormally low motor unit firing rates during voluntary muscle activation. Our purpose was to assess the prevalence of saturation in motor unit firing rates in the spastic-paretic biceps brachii muscle of stroke survivors. To achieve this objective, we recorded the incidence and duration of impaired lower- and higher-threshold motor unit firing rate modulation in spastic-paretic, contralateral, and healthy control muscle during increases in isometric force generated by the elbow flexor muscles. Impaired firing was considered to have occurred when firing rate became constant (i.e., saturated), despite increasing force. The duration of impaired firing rate modulation in the lower-threshold unit was longer for spastic-paretic (3.9 ± 2.2 s) than for contralateral (1.4 ± 0.9 s; P < 0.001) and control (1.1 ± 1.0 s; P = 0.005) muscles. The duration of impaired firing rate modulation in the higher-threshold unit was also longer for the spastic-paretic (1.7 ± 1.6 s) than contralateral (0.3 ± 0.3 s; P = 0.007) and control (0.1 ± 0.2 s; P = 0.009) muscles. This impaired firing rate of the lower-threshold unit arose, despite an increase in the overall descending command, as shown by the recruitment of the higher-threshold unit during the time that the lower-threshold unit was saturating, and by the continuous increase in averages of the rectified EMG of the biceps brachii muscle throughout the rising phase of the contraction. These results suggest that impairments in firing rate modulation are prevalent in motor units of spastic-paretic muscle, even when the overall descending command to the muscle is increasing.

Origins of spontaneous firing of motor units in the spastic-paretic biceps brachii muscle of stroke survivors.

One potential expression of altered motoneuron excitability following a hemispheric stroke is the spontaneous unit firing (SUF) of motor units at rest. The elements contributing to this altered excitability could be spinal descending pathways, spinal interneuronal networks, afferent feedback, or intrinsic motoneuron properties. Our purpose was to examine the characteristics of spontaneous discharge in spastic-paretic and contralateral muscles of hemiparetic stroke survivors, to determine which of these mechanisms might contribute. To achieve this objective, we examined the statistics of spontaneous discharge of individual motor units and we conducted a coherence analyses on spontaneously firing motor unit pairs. The presence of significant coherence between units might indicate a common driving source of excitation to multiple motoneurons from descending pathways or regional interneurons, whereas a consistent lack of coherence might favor an intrinsic cellular mechanism of hyperexcitability. Spontaneous firing of motor units (i.e., ongoing discharge in the absence of an ongoing stimulus) was observed to a greater degree in spastic-paretic muscles (following 83.2 ± 16.7% of ramp contractions) than that in contralateral muscles (following just 14.1 ± 10.5% of ramp contractions; P < 0.001) and was not observed at all in healthy control muscle. The average firing rates of the spontaneously firing units were 8.4 ± 1.8 pulses/s (pps) in spastic-paretic muscle and 9.6 ± 2.2 pps in contralateral muscle (P < 0.001). In 37 instances (n = 63 pairs), we observed spontaneous discharge of two or more motor units simultaneously in spastic-paretic muscle. Seventy percent of the dually firing motor unit pairs exhibited significant coherence (P < 0.001) in the 0- to 4-Hz bandwidth (average peak coherence: 0.14 ± 0.13; range: 0.01-0.75) and 22% of pairs exhibited significant coherence (P < 0.001) in the 15- to 30-Hz bandwidth (average peak coherence: 0.07 ± 0.06; range: 0.01-0.31). We suggest that the spontaneous firing was likely not attributable solely to enhanced intrinsic motoneuron activation, but attributable, at least in part, to a low-level excitatory synaptic input to the resting spastic-paretic motoneuron pool, possibly from regional or supraspinal centers.