So you described a problem, offered no solution. Useless. Do your mentors and senior researchers know that the only goal in stroke is 100% recovery? This does nothing for that.
Changes in activation timing of knee and ankle extensors during gait are related to changes in heteronymous spinal pathways after stroke
Journal of NeuroEngineering and Rehabilitation volume 11, Article number: 148 (2014)
Abstract
Background
Extensor synergy is often observed in the paretic leg of stroke patients. Extensor synergy consists of an abnormal stereotyped co-activation of the leg extensors as patients attempt to move. As a component of this synergy, the simultaneous activation of knee and ankle extensors in the paretic leg during stance often affects gait pattern after stroke. The mechanisms involved in extensor synergy are still unclear. The first objective of this study is to compare the co-activation of knee and ankle extensors during the stance phase of gait between stroke and healthy individuals. The second objective is to explore whether this co-activation is related to changes in heteronymous spinal modulations between quadriceps and soleus muscles on the paretic side in post-stroke individuals.
Methods
Thirteen stroke patients and ten healthy individuals participated in gait and heteronymous spinal modulation evaluations. Co-activation was measured using peak EMG activation intervals (PAI) and co-activation amplitude indexes (CAI) between knee and ankle extensors during the stance phase of gait in both groups. The evaluation of heteronymous spinal modulations was performed on the paretic leg in stroke participants and on one leg in healthy participants. This evaluation involved assessing the early facilitation and later inhibition of soleus voluntary EMG induced by femoral nerve stimulation.
Results
All PAI were lower and most CAI were higher on the paretic side of stroke participants compared with the co-activation indexes among control participants. CAI and PAI were moderately correlated with increased heteronymous facilitation of soleus on the paretic side in stroke individuals.
Conclusions
Increased co-activation of knee and ankle extensors during gait is related to changes in intersegmental facilitative pathways linking quadriceps to soleus on the paretic side in stroke individuals. Malfunction of intersegmental pathways could contribute to abnormal timing of leg extensors during the stance phase of gait in hemiparetic individuals.
Introduction
Following stroke, impaired coordination is frequently observed and manifests by the incapacity to activate muscles selectively[1]. This lack of voluntary control produces abnormal coupling of joint movements on the paretic side that can hamper motor task performance[1–3]. Altered motor coordination in the paretic leg among stroke patients is associated with functional deficits[4]. As a result of this lack of coordination, these patients often produce stereotypical co-activation of several muscles on the paretic side as they voluntarily attempt to move[1, 5]. These co-activations, which are commonly referred to as abnormal synergies, are defined as the simultaneous recruitment of muscles at multiple joints resulting in a stereotypical pattern of movement[6]. In the paretic leg of stroke patients, prevalent extensor synergy consisting of the co-contraction (i.e., co-activation) of the majority of the leg extensor muscles is often present throughout most of the stance phase of gait[7, 8]. This co-activation can be observed in EMG tracings showing the simultaneous activation of leg extensors during stance[6]. In the present study, the term “co-activation” will be used to describe the simultaneous EMG activity in knee and ankle extensor muscles[9]. This co-activation is a key component of extensor synergy[7] since it can produce abnormal coupling of knee and ankle extension, often resulting in an altered gait pattern after stroke[7, 10].
Since knee and ankle extensors are both anti-gravity muscles with out-of-phase activation during healthy gait, their abnormal co-activation could contribute to hemiparetic gait disabilities. The quadriceps muscle normally reaches its peak activation during the early stance phase in order to support body weight[11]. In turn, calf muscles demonstrate maximal activity during the late stance phase in order to control ankle dorsiflexion and produce push off[12]. In hemiparetic gait, prolonged activation of the quadriceps at the end of the stance phase[8, 13] may impede knee flexion in preparation for the swing phase. Premature activation of ankle extensors early in the stance phase[14, 15] could hamper body weight support upon initial foot contact[7]. These changes are consistent with abnormal co-activation of leg extensors on the paretic side during the stance phase of gait[14, 16].
Although the co-activation of leg extensors has been widely described in clinical literature, few studies have quantified its extent in the paretic leg during gait. The paucity of studies assessing muscular co-activation via EMG approaches may stem from limitations related to the normalization of EMG signals[17] and the determination of the timing of muscular activation[18], variables which allow inter-subject comparisons to be made. Analyses of EMG activity by factorization procedures have been used to objectively identify shared patterns of activation among different muscle groups in the paretic lower limb during gait[19, 20]. Through the use of a factorization procedure, it has been shown that the number of EMG modules required to describe muscle activation patterns in the paretic leg correlates with walking performance measures in post-stroke individuals[19].
Furthermore, the underlying mechanisms of leg extensor co-activation after stroke are not fully understood. Supraspinal and spinal mechanisms may both contribute to motor deficits in the paretic leg[21–23]. Spinal interneuronal systems are basic sensorimotor mechanisms that can integrate influences from sensory and descending pathways to modulate the activity of motoneurones (MNs)[9, 21]. Intersegmental or propriospinal pathways can regulate the activity of muscles acting at different joints[21, 24]. In humans, these pathways are assessed with electrophysiological methods, whereby conditioning stimulation is used to modulate the activity of a heteronymous muscle[25–27]. For example, intersegmental excitatory and inhibitory pathways linking quadriceps (Quads) to soleus (Sol) can be assessed by measuring the effects of femoral nerve (FN) stimulation on Sol activity[9, 21]. More precisely, FN stimulation induces early, short-term facilitation and later longer-lasting inhibition of both Sol H reflex and voluntary EMG, which have been attributed to projections from Quads to Sol group excitation and recurrent inhibition, respectively[28, 29]. An increase in early heteronymous facilitation and a decrease in later inhibition of Sol activity after FN stimulation have been found in stroke subjects[21]. Moreover, based on the results of this study, increased facilitation was correlated with level of motor coordination of the paretic leg[21]. This raises the question of whether co-activation of knee and ankle extensors in the paretic leg during gait is related to transmission changes in intersegmental pathways linking Quads to Sol. This study aims to (1) compare co-activation of knee and ankle extensors during gait between stroke and healthy individuals, (2) assess whether this co-activation is related to clinical measures of motor deficits after stroke, and (3) determine whether it is related to changes in heteronymous modulations of Sol voluntary EMG after FN stimulation in the paretic leg.
No comments:
Post a Comment