60 CHAPTER 3 and primary motor cortex despite peripheral regeneration after peripheral nerve injury in monkeys99-103 and rats,104-106 respectively. In humans, examples include phantom pain and phantom movements after upper limb amputation,107-109 paresthesia, pain and functional deficits in carpal tunnel syndrome43, 110, 111 and focal hand dystonia in response to (over) use.16. 17 Maladaptive motor representations have also been linked to developmental apraxia and muscle weakness in individuals with birth-related brachial plexus injury.42, 68 The main finding of this study, i.e. abnormal sensorimotor representations in NA patients, confirms our clinical impression that many NA patients have persistent motor deficits despite clinical signs of peripheral nerve recovery. It is therefore possible that cerebral (mal)adaptations also play a role in persistent motor dysfunction in NA. This notion may have important implications for treatment. Behavioral therapies that target cerebral plasticity, such as sensory and motor re-education, show promising results in other peripheral disorders with documented cerebral (mal)adaptations.12, 112 In our outpatient clinic, NA patients are able to regain normal motor function through relearning correct movement patterns. 1 It remains to be investigated whether markers of central dysfunction can predict the response of NA patients to these therapies. Strengths and Interpretational issues Mechanical factors related to the disorder did not underlie the selectivity of the reported deficit, as participants responded with their feet, instead of with their finger(s), which is the typical method of response in this task. The lower extremities were not affected in the NA patients that participated in this study,6. 7 ensuring that the physical button press was not influenced by peripheral factors related to the disorder, which may have been the case if finger button presses were used. As performance was only decreased for the affected limb, our findings cannot be explained by general group differences in cognitive factors such as working memory, attention or motivation, which may also affect performance on this task.113-116 Our findings are also not explained by group differences in speed-accuracy trade-off, as evidenced by the analysis on efficiency scores. Thus, we conclude that the deficit we found is task-induced and likely to be caused by NA itself. We did not find a significant correlation between performance on the hand laterality judgment task and any of our clinical outcome measures. Although some studies have found that clinical measures such as pain duration, predicted pain, pain medication intake and general activities are associated with performance on this task in other upperlimb disorders,117-119 others have not found such associations.45, 120 The lack of significant correlations in our study could mean that clinical measures are only indirectly related to, or are not sensitive enough to the sensorimotor representations deficit we found evidence for in NA. There may also be lasting peripheral changes that could contribute to persistent motor problems in NA. 6 However, peripheral changes cannot explain the current findings: our experimental design eliminates the influence of peripheral factors (such as nerve damage and altered motor execution), and instead relies on central sensorimotor processes.
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