Brainstem-Originating Neuromodulatory Inputs to Spinal Motoneurons May Facilitate Motor Impairments in Chronic Stroke

Accumulating evidence points to the role that brainstem-originating monoaminergic (i.e., norepinephrine, serotonin) drive plays in the manifestation of multiple motor impairments in chronic hemiparetic stroke. Monoamines increase spinal motoneuron excitability and, therefore, could yield hyperexcitable motoneurons that contribute to hypertonicity/spasticity while also amplifying weak and indirect motor pathways that generate flexion synergy expression. To investigate these potential monoaminergic contributions, we used high-density surface electromyography and decomposed biceps brachii motor units during a volitional elbow flexion contraction and a non-volitional contraction generated during flexion synergy expression. We then used outcome metrics developed from realistic motoneuron models to predict alterations in motor commands. Across eleven individuals, we found significant changes in metrics during the flexion synergy task that indicate greater monoaminergic drive and increased inhibitory synaptic inputs to motoneurons. These changes illuminate the dependence of flexion synergy expression on monoaminergic output and the use of indirect motor pathways (e.g., reticulospinal).