51 ALTERED SENSORIMOTOR REPRESENTATIONS IN NA 3 Introduction Plasticity is a key feature of our nervous system, allowing humans to recover from injury.12, 13 When parts of the motor system are damaged, motor function can be regained by recruiting compensatory brain circuits. 60, 65, 66 However, plastic reorganization of the motor system is not always advantageous: it may actually worsen motor dysfunction, in which case it is referred to as “maladaptive neuroplasticity”. 12, 15 The occurrence of maladaptive plasticity has been described in several central nervous system disorders. 18, 67 There are also clinical examples of maladaptive plasticity occurring after damage to the peripheral nervous system. One example is obstetric brachial plexus palsy, where developmental apraxia – i.e. clinical motor dysfunction despite peripheral reinnervation – is thought to result from maladaptive central motor programming after birth-related brachial plexus damage. 42 Accordingly, adults with this disorder have altered motor-related brain activity compared to healthy controls. 68 Here we focus on changes in sensorimotor processes occurring in neuralgic amyotrophy (NA), which is a common and disabling peripheral nervous disorder characterized by auto-immune inflammation of the brachial plexus. 3, 6 NA is typically asymmetric and most often affects one upper limb. 7 Paresis of muscles that are innervated by the damaged nerves leads to motor dysfunction. Many patients subsequently develop compensatory, but atypical movement patterns of the affected limb. Several clinical clues link these abnormal patterns to changes in central sensorimotor processes. First, many NA patients show a lack of functional recovery, even after reinnervation of the affected muscles and return of muscle strength. 6, 8, 10 Second, motor dysfunction of the affected upper limb is more severe when patients perform well-trained movements that rely on existing motor programs, as compared to the situation where they perform novel movements requiring ad hoc formation of a new motor plan. 6 Third, some NA patients develop abnormal and involuntary movements that phenotypically resemble dystonia – a symptom commonly associated with central changes. 4 Finally, patients can regain normal motor function by relearning correct movement patterns through rehabilitation, even years after onset. 1 This latter finding indicates the clinical importance of distinguishing between peripheral and central causes for motor dysfunction in peripheral nervous system disorders, since they require different treatments. However, the hypothesis that central sensorimotor processes become deficient in NA has never been tested. Here we tested this hypothesis by using a hand laterality judgment task, which involves mental rotation of one’s upper limb, without overt motor expression. Laterality judgment relies on the same sensorimotor representations and similar brain regions as motor planning and execution, 21, 24 and controls for possible disease-related peripheral changes in motor execution or associated afferent feedback.29, 30 Some posit that these sensorimotor representations reflect “motor imagery”, the mental simulation of movement without motor expression. 25, 29 We used a validated task in which subjects are presented with pictures of hands and are asked to indicate their laterality (left or right). Behavioral responses during this hand laterality judgment task follow the same biomechanical and motor constraints as the execution of movements bringing a participant’s hand into the same orientation of the hand pictures. 25, 29 Responses are also influenced by the position of the subjects’ own arms, which indicates that subjects
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