Bilateral impairments in task-dependent modulation of the long-latency stretch reflex following stroke

Abstract

Objective Modulation of the long-latency reflex (LLR) is important for sensorimotor control during interaction with different mechanical loads. Transcortical pathways usually contribute to LLR modulation, but the integrity of pathways projecting to the paretic and non-paretic arms of stroke survivors is compromised. We hypothesize that disruption of transcortical reflex pathways reduces the capacity for stroke survivors to appropriately regulate the LLR bilaterally. Methods Elbow perturbations were applied to the paretic and non-paretic arms of persons with stroke, and the dominant arm of age-matched controls as subjects interacted with Stiff or Compliant environments rendered by a linear actuator. Reflexes were quantified using surface electromyograms, recorded from biceps. Results LLR amplitude was significantly larger during interaction with the Compliant load compared to the Stiff load in controls. However, there was no significant change in LLR amplitude for the paretic or non-paretic arm of stroke survivors. Conclusions Modulation of the LLR is altered in the paretic and non-paretic arms after stroke. Significance Our results are indicative of bilateral sensorimotor impairments following stroke. The inability to regulate the LLR may contribute to bilateral deficits in tasks that require precise control of limb mechanics and stability.

Common muscle synergies for balance and walking

“…In Parkinson's disease (PD), a reduced number of muscle synergies has been identified during walking (Rodriguez et al, 2013), but the relationship to postural instability, a cardinal sign of PD, is unknown. Further, degradation in upper limb function after stroke may be a result of changes in the modular organization of long-latency responses (Trumbower et al, 2010, 2013). These initial studies suggest that muscle synergy analysis may be a powerful tool for distinguishing specific deficits in muscle coordination leading to functional impairments that may be generalized across different motor behaviors.…”

“…Remaining variability in muscle activity may reflect sensorimotor noise, or other neural mechanisms such as short-latency reflex responses and may not be accounted for by recruitment of muscle synergies (Ting, 2007). In particular, heterogenic reflex responses (Nichols, 1994) may have different organization than muscle synergies for long-latency responses and voluntary movements (Trumbower et al, 2013). Further, motoneuron excitability may vary with joint angle (Hyngstrom et al, 2007), causing differences in apparent muscle synergy composition across postures.…”

Deficits in startle-evoked arm movements increase with impairment following stroke

“…It is well-established that following stroke individuals have important deficits resisting perturbations of the arm and ankle (Dietz and Berger, 1984, Dietz, Trippel, 1991, Finley et al, 2008, Lum et al, 2004, Sangani et al, 2007, Trumbower et al, 2013, Trumbower et al, 2010). Perturbation-specific, short and long latency stretch reflexes, are significantly impaired following stroke disrupting their ability to resist arm perturbation (Dietz and Berger, 1984, Dietz, Trippel, 1991, Lum, Patten, 2004, Trumbower, Finley, 2013, Trumbower, Ravichandran, 2010) leading to a reduced torque capacity. Recent evidence demonstrates that this ability is driven not only by perturbation-specific stretch reflexes but also by task-specific early release of planned movement (Hammond, 1956, Lewis et al, 2006, Ravichandran, Honeycutt, 2013).…”

The ipsilateral motor cortex does not contribute to long‐latency stretch reflex amplitude at the wrist

“…2013). As the ipsilateral motor cortex is not involved in generation or modulation of the LLSR in healthy nervous systems, it is difficult to explain why the arm ipsilateral to a stroke lesion displays impairments of reflex modulation almost as severe as the paretic arm.…”