These results show that there was a statistically significant reduction in GHS in standing compared to sitting, suggesting that a reduction in the BOS also reduced the amount of GHS in participants after stroke.
There were several limitations to this study, most notably the small sample size. Nonetheless, the results support the practice of considering BOS of the patient when treating individuals following stroke [12, 16], as in standing there appears to be a greater potential for muscle recruitment and thus reduced GHS. However, these findings require verification in a larger study before clinical recommendations can be developed and therapists should balance the safety implications when reducing an individual’s BOS against any possible benefits in muscle activity.
This small study was unable to demonstrate the cause of the reduced subluxation seen on standing, but it is likely that the changes observed are as a result of greater activity within the rotator cuff. These muscles, with some deltoid activity provide the main component of control at the GH joint [17-19, 20]. Indeed, paralysis of the supraspinatus muscle in particular has been suggested to be a predictor of a greater risk of GHS by some . Marieb (2004)  describes the rotator cuff tendons as being kept taut by the resting tone within the muscle and Edwards (2002)  suggests that local stabilisers, comprising slow oxidative (tonic) fibres, are largely fatigue resistant with long lasting but weak contractions. The findings of the current study lend some support to the notion that the rotator cuff muscles appear to act as postural muscles. The results also suggest that they increase their activity on standing and thereby reduce GHS.
The effect of postural control on GHS has not been explored within the literature. The mechanical factors relating to aetiology and treatment have been outlined but few studies have considered the effect of changing the base of support upon muscle activity and GHS and so we can only hypothesise the mechanisms by which these changes have occurred . It is possible that the activation of the rotator cuff and subsequent reduction in GHS within the standing position may occur because different neurological pathways are activated, for example, the medial reticulospinal tract [18, 19]. In comparison to sitting, standing elicits greater sensory input from the lower limbs, particularly the soles of the feet which can increase extensor muscle activity via synergistic muscle patterns . This process is likely to utilise propriospinal neurons which are located within the spinal cord. The longest of axons of these nerve cells lie within the medial pathways and can innervate both proximal and axial muscles creating co-activation, even in the presence of a damaged central nervous system .
Another potential contributor to a reduction in GHS on standing is that some tracts which can influence muscle activity at the shoulder may originate on the ipsilateral side of the brain and so would maintain innervations to the affected side after stroke. Such tracts include the medial reticulospinal pathway which creates activity within the postural muscles and limb extensors and the lateral vestibulospinal tract which is activated by changes in response to gravity [18, 19].
An alternative explanation of why GHS may reduce as BOS and COM rises could be that it is purely the effect of the effort required to overcome the inertia of sitting to achieve standing. During movements that require effort it is normal to have a generalised increase in activity elsewhere in the body . It is therefore a limitation of this study that the reason for the reduction in GHS cannot be determined; this could be further examined in future work by asking participants to stand for longer to determine if an initial increase in muscular activity reduces.
Further research could also seek to identify if muscular activity is related to shoulder pain in GHS  and to see which muscles increase their activity on standing, to determine the mechanism by which GHS was observed to decrease . It is now also necessary to evaluate if treatment with a smaller BOS has lasting benefits to upper limb function in individuals who have GHS after a stroke.