Abstract
There is considerable evidence on the impairments that a cerebral stroke will have down-stream of the stroke, i.e., in the spinal motoneuron and the muscle. Motor impairment following stroke has been documented as force production that is slow, weak, and lacking in precision (Garland et al., 2009) and is associated with difficulty in fully activating the muscle (Klein et al., 2013). Furthermore, in functional tasks such as standing balance and gait, there is evidence of deficits in intra-limb coordination of muscles even on the non-paretic side (Marigold and Eng, 2006; Raja et al., 2012). In this opinion paper, we will first briefly review the changes observed at the level of the motor unit (MU) after stroke and second reflect upon whether some changes in the intrinsic properties of motoneurons, typically considered to be maladaptive, might also reflect a positive adaptation that could assist in force production. Lastly, this paper will explore the control of MUs between limbs during standing balance and suggest that, while some impairment may exist, there remains the possibility of a preservation of fundamental motor control strategies after stroke that might be a target for rehabilitation.
Highlights
There is considerable evidence on the impairments that a cerebral stroke will have down-stream of the stroke, i.e., in the spinal motoneuron and the muscle
Could the motoneuron be adapting to the remodeling at the level of the muscle? No studies have yet been performed to determine if the time-course of the AHP and the muscle unit remain matched after stroke
We examined the common drive in people after stroke in the medial gastrocnemius muscle during an external perturbation task in standing
Summary
There is considerable evidence on the impairments that a cerebral stroke will have down-stream of the stroke, i.e., in the spinal motoneuron and the muscle. MOTOR UNIT/MUSCLE CHARACTERISTICS At the level of the MU, studies have demonstrated a loss of spinal motoneurons following stroke (McComas et al, 1973; Hara et al, 2004; Lukacs, 2005; Li et al, 2011), those that innervate type II MUs (Lukacs et al, 2008). A systematic review and meta-analysis performed by English et al (2010) demonstrated that lean paretic muscle mass was significantly less than that of non-paretic muscle, in both upper and lower extremities, in people at least 6 months post-stroke.
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