14 CHAPTER 1 thebraincontrolsmovement. 6 Tounderstandhowdamage toperipheral nervesmay lead to changes in the brain, I will first introduce the concept of plasticity before circling back toNA. Our brains are able to adapt to a changing environment, by adjusting their structural or functional organization to meet the new environmental requirements. This plasticity enables us to learn a new skill, or to recover function after injury. 11-13 An example of the latter is how when one brain area is damaged through stroke, patients are able to retain some level of function through compensation in related, uninjured, regions of the brain. 14 Although plasticity is essential to our survival, such reorganization of the system is not always beneficial, and can even have detrimental consequences. 12, 15 A striking example of such consequences is focal hand dystonia. Individuals that frequently perform highly skilled movements, such as musicians and writers, may develop task-specific involuntary muscle contractions, which impair hand use. This phenomenon is related to an excess of plasticity in response to intensive training. 16, 17 While the occurrence of (mal)adaptive cerebral plasticity and its potential down sides are recognized in disorders that directly affect the brain, such as stroke, 15, 18 cerebral (mal)adaptations may also occur in peripheral nerve disorders where cerebral structures are intact, such as NA. As established at the start of this section, the fact that peripheral nerve recovery does not always translate directly into clinical recovery, is a strong indicator that maladaptive cerebral plasticity may be involved in residual complaints and variable recovery in NA. Moreover, some NA patients develop abnormal and involuntary postures and movements that resemble dystonia, 4 which is linked to cerebral maladaptations. 12, 16, 17, 19 Finally, with specific rehabilitation that focusses on relearning correct movement patterns through coordinative training, NA patients can regainmotor function, even after years of persistent scapular dyskinesia following an NA episode. 1 This thesis introduces and examines the interplay between peripheral nerve damage, motor dysfunction, and the brain in recovery in NA. This hypothesized interplay is depicted in Figure 1: A. auto-immune inflammation of nerves in the brachial plexus territory causes peripheral nerve damage in NA, which leads to muscle weakness and subsequent scapular dyskinesia; B. scapular dyskinesia may induce cerebral maladaptations through plasticity; C. these cerebral maladaptations may contribute to perpetuation of scapular dyskinesia, despite peripheral nerve recovery; D. specific rehabilitation, focused on regaining motor control, may alleviate scapular dyskinesia and related residual complaints by influencing these cerebral maladaptations. Figure 1 The hypothesized interplay between peripheral nerve damage, scapular dyskinesia and cerebral mechanisms in neuralgic amyotrophy
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