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

ObjectiveModulation 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.MethodsElbow 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.ResultsLLR 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.ConclusionModulation of the LLR is altered in the paretic and non-paretic arms after stroke.SignificanceOur 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.

► Stroke survivors are unable to adapt their long-latency stretch reflex amplitude during tasks that require increased stability. ► Impaired regulation of the long-latency reflex is evident in both the paretic and non-paretic limbs. ► The inability to regulate long-latency stretch reflexes to account for the mechanical properties of the environment may contribute to bilateral deficits in tasks that require proprioceptive feedback and rapid changes in muscle activity to maintain stability.