139 SUMMARY & GENERAL DISCUSSION 7 Although chapter 3 provided the first empirical evidence that the brain adapts to peripheral nerve damage in NA, based on the behavioural findings alone, the nature of the underlying cerebral processes and brain regions involved remained unclear. Chapter 4 addressed that issue in an independent sample of NA patients (again with right-lateralized persistent motor dysfunction) and matched healthy volunteers, with task-based fMRI during performance of the same hand laterality judgement task. We expected to find similar upper extremity-specific behavioural deficits, as well as cerebral group differences specific to the affected upper extremity in key (somato)motor/sensory brain regions, visuomotor brain regions, or both. Behavioural and cerebral task responses confirmed that the task activated embodied sensorimotor processes in both somatomotor and visuomotor brain regions. NA patients were overall slower than healthy volunteers, but did not have the upper extremity-specific behavioural deficits found in chapter 3. Interestingly, the cerebral findings were specific to the affected upper extremity, as NA patients showed decreased brain activity when imagining movement with their affected upper extremity. These decreases occurred in two visuomotor brain regions involved in sensorimotor integration: the right extrastriate cortex and the parieto-occipital sulcus. We additionally found links between brain, behaviour and clinical outcome: across patients, extrastriate activity specific to the affected upper extremity decreased as persistent pain increased, and parieto-occipital activity decreased as imagery performance of the affected upper extremity became slower. Chapter 4 thus provided neuroimaging evidence that the brain indeed adapts to peripheral nerve injury in NA, it localized alterations to occipito-parietal brain areas involved in visuomotor processing, and it established possible links with clinical outcome. Concluding part 1, we confirmed the clinical intuition that maladaptive neuroplasticity plays a role in NA and persistent motor dysfunction. We showed that the brain adapts to peripheral nerve damage in NA by altering sensorimotor representations of the affected upper extremity, specifically in visuomotor brain areas. Having gained new insights into the cerebral mechanisms at play in NA in part 1 of this thesis, part 2 focussed on how specific rehabilitation targeting the central motor system can aid recovery. Part 2 – How rehabilitation can aid recovery in NA Despite the fact that residual motor dysfunction is prevalent in NA, there was no validated treatment option for the residual complaints experienced by a large proportion of NA patients when the NA-CONTROL study was designed. Usual care is often ineffective and can even worsen symptoms. Although approaches vary, usual care commonly involves conventional physical therapy focused on regaining strength and endurance. The Radboudumc Neuromuscular Center in Nijmegen, the Netherlands, hosts the (inter) national expert clinic for NA, and has developed a specific multidisciplinary outpatient rehabilitation program. The program combines occupational and physical therapy. Occupational therapy focuses on improving self-management. Physical therapy employs coordinative training to regain motor control, which aims to target the central motor system. This multidisciplinary approach has shown promising results, both in clinical experience and in a small pilot study, but had never been formally tested in a clinical trial in a large sample of patients. Chapter 5 of this thesis described the first RCT on residual complaints after NA, comparing clinical outcome after 17 weeks of specific
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