Changes in reflex spinal pathways after stroke have been shown to affect motor activity in agonist and antagonist muscles acting at the same joint. However, only a few studies have evaluated the heteronymous reflex pathways modulating motoneuronal activity at different joints. This study investigates whether there are changes in the spinal facilitatory and inhibitory pathways linking knee to ankle extensors and if such changes may be related to motor deficits after stroke. The early facilitation and later inhibition of soleus H reflex evoked by the stimulation of femoral nerve at 2 times the motor threshold of the quadriceps were assessed in 15 healthy participants and on the paretic and the non-paretic sides of 15 stroke participants. The relationships between this reflex modulation and the levels of motor recovery, coordination and spasticity were then studied. Results show a significant (Mann-Whitney U; P<0.05) increase in both the peak amplitude (mean±SEM: 80±22% enhancement of the control H reflex) and duration (4.2±0.5 ms) of the facilitation on the paretic side of the stroke individuals compared to their non-paretic side (36±6% and 2.9±0.4 ms) and to the values of the control subjects (33±4% and 2.8±0.4 ms, respectively). Moreover, the later strong inhibition observed in all control subjects was decreased in the stroke subjects. Both the peak amplitude and the duration of the increased facilitation were inversely correlated (Spearman r = −0.65; P = 0.009 and r = −0.67; P = 0.007, respectively) with the level of coordination (LEMOCOT) of the paretic leg. Duration of this facilitation was also correlated (r = −0.58, P = 0.024) with the level of motor recovery (CMSA). These results confirm changes in transmission in heteronymous spinal pathways that are related to motor deficits after stroke.
BackgroundAbnormal coactivation of leg extensors is often observed on the paretic side of stroke patients while they attempt to move. The mechanisms underlying this coactivation are not well understood. This study (1) compares the coactivation of leg extensors during static contractions in stroke and healthy individuals, and (2) assesses whether this coactivation is related to changes in intersegmental pathways between quadriceps and soleus (Sol) muscles after stroke.MethodsThirteen stroke patients and ten healthy individuals participated in the study. Levels of coactivation of knee extensors and ankle extensors were measured in sitting position, during two tasks: maximal isometric voluntary contractions in knee extension and in plantarflexion. The early facilitation and later inhibition of soleus voluntary EMG evoked by femoral nerve stimulation were assessed in the paretic leg of stroke participants and in one leg of healthy participants.ResultsCoactivation levels of ankle extensors (mean ± SEM: 56 ± 7% of Sol EMG max) and of knee extensors (52 ± 10% of vastus lateralis (VL) EMG max) during the knee extension and the ankle extension tasks respectively were significantly higher in the paretic leg of stroke participants than in healthy participants (26 ± 5% of Sol EMG max and 10 ± 3% of VL EMG max, respectively). Early heteronymous facilitation of Sol voluntary EMG in stroke participants (340 ± 62% of Sol unconditioned EMG) was significantly higher than in healthy participants (98 ± 34%). The later inhibition observed in all control participants was decreased in the paretic leg. Levels of coactivation of ankle extensors during the knee extension task were significantly correlated with both the increased facilitation (Pearson r = 0.59) and the reduced inhibition (r = 0.56) in the paretic leg. Measures of motor impairment were more consistently correlated with the levels of coactivation of biarticular muscles than those of monoarticular muscles.ConclusionThese results suggest that the heteronymous pathways linking quadriceps to soleus may participate in the abnormal coactivation of knee and ankle extensors on the paretic side of stroke patients. The motor impairment of the paretic leg is strongly associated with the abnormal coactivation of biarticular muscles.
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