![]() Soft synergies resulting purely from functional co-activation are therefore potentially more dynamic and context-dependent than hard synergies. These “anatomical synergies” would be “hard,” in the sense that the combinations of muscles involved will be relatively fixed. Alternatively, synergies may be constructed in synergy-specific anatomical structures and then at some subsequent point in the motor pathway that information would have to diverge to the different muscles. For example, the spatiotemporal dynamics of upper limb movement change markedly in the context of bimanual tasks, even though the anatomical substrate (for a single side) is identical between unimanual and bimanual conditions ( Kelso et al., 1979). These functional synergies could be considered “soft” in the sense there are not dedicated anatomical structures existing to subserve them. ![]() Some synergies may arise purely from functional coordination of high-dimensional structures (“functional synergies”). Abstractly, synergies represent low-dimensional movement information expressed in a higher dimensional space of possible activations. To make sense of the ways in which stroke can alter muscle synergies, we need first to appreciate the relationship between the anatomical and physiological basis for synergy formation, and the deficit caused by the stroke, remembering that both acute and chronic changes occur. In the present article, we adopt the general definition of the term synergy given above, although reference will also be made to clinically abnormal synergies as well as synergies identified by matrix factorization, and the caveats with regard to the definitions of each should be borne in mind. This phrasing stems from the fact that pathological synergies are “lower dimensional” than in healthy individuals, hence there are more co-dependencies (synergies) present. Another usage of synergy arises in clinical settings, where the term “abnormal muscle synergies” may refer only to the pathological patterns of muscle co-activation that emerge after disruption of the motor system, such as stroke ( Brunnström, 1970). For example, non-negative matrix factorization (NNMF) does not capture inhibitory relationships, which may be a limitation of the method. The details of the mathematical operation determine specific properties of the synergy estimates extracted. In recent experiments, the term “muscle synergy” has been used to label estimates of synergies derived from quantitative matrix factorization methods applied to simultaneous electromyographic (EMG) measurements ( Tresch et al., 2006). Natural motor behaviors may result from the additive effect of several synergies. Conversely, activity in one muscle may coincide with quiescence in another due to reciprocal inhibition. If motor neurons of two muscles are excited simultaneously, the muscles are coactivated. Descending neural activity may result in a net excitation or inhibition of the alpha motor neurons innervating each muscle. As a biological phenomenon, a commonly accepted general definition of muscle synergy is simply a stable spatiotemporal pattern of activity across muscles simultaneously involved in the performance of a movement. “Muscle synergy” can mean subtly different things, creating the opportunity for confusion. A consideration of the integrity of remaining descending motor pathways may aid in the design of new rehabilitation therapies. The location of the stroke lesion and properties of the secondary descending pathways and their regulation are then critical for shaping the synergies in the remaining motor behavior. The contribution of these pathways may emerge as new synergies take shape at the chronic stage after stroke, as a result of plasticity along the neuroaxis. When the CST is damaged after stroke, other descending pathways may be up-regulated to compensate. ![]() In healthy individuals, motor cortical activity, descending via the corticospinal tract (CST) is the predominant driver of voluntary behavior. The time course of abnormal synergy formation seems to lag spontaneous recovery that occurs in the initial weeks after stroke. The mechanism underlying this change reflects damage to key motor pathways as a result of the stroke lesion, and the subsequent reorganization along the neuroaxis, which may be further detrimental or restorative to motor function. ![]() After stroke, these synergies change, often in stereotypical ways. Muscle synergies describe common patterns of co- or reciprocal activation that occur during movement.
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