http://journal.frontiersin.org/Journal/10.3389/fnhum.2014.00864/full?
S. Jayne Garland1*, Courtney L. Pollock2 and Tanya D. Ivanova1
- 1Department of Physical Therapy, University of British Columbia, Vancouver, BC, Canada
- 2Graduate Program in Rehabilitation Sciences, Department of Physical Therapy, University of British Columbia, Vancouver, BC, Canada
Introduction
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.
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), particularly those that innervate type II MUs (Lukacs et al., 2008).
It has been suggested that chronically paretic muscle is made up of
fewer, but larger, MUs due to collateral sprouting of the remaining
motoneurons to innervate a greater number of muscle fibers (Lukacs, 2005; Kallenberg and Hermens, 2011; Li et al., 2011) and this process could result in a mismatch of muscle fiber type and motoneuron characteristics (Young and Mayer, 1982; Dattola et al., 1993).
Ultimately both of these changes may result in muscle contractions with
slower rates of force development and decreased levels of force
production (Garland et al., 2009).
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Concluding Remarks
There is no doubt that there are changes in the MU
discharge characteristics after stroke. But the AHP and common drive
data suggest that residual motor control strategies may remain after
stroke, albeit diminished, and may reveal a need to consider functional
task-dependency in future research to explore MU impairment and
adaptation post-stroke. It remains to be seen whether treatments that
challenge the neuromuscular system could prevent the muscle remodeling
and any compensatory MU control adaptations.