23 NA-CONTROL STUDY PROTOCOL 2 Background Plasticity is a feature of the central motor system that allows change in the system organisation. It enables the development of new motor strategies in a changing environment, which can be advantageous when learning a new skill, or when recovering from injury by adapting with a compensatory strategy. When elements of the motor system are damaged, for example in neurological disorders, neuroplasticity enables patients to regain (part of their) motor function. 40, 41 However, the plasticity is maladaptive when changes in the central motor system are not beneficial to functioning. Maladaptive neuroplasticity can have detrimental consequences, resulting in impaired motor function. There are indications that maladaptive motor strategies can occur not only in central, but also in peripheral nervous system disorders. 42-45 Neuralgic amyotrophy (NA) is a peripheral nervous system disorder in which (mal) adaptive central neuroplasticity might be important. There are several indications from clinical experience that (mal)adaptive central neuroplasticity is involved in this disorder. 6 However, little is currently known about the central mechanisms in this peripheral nervous system disorder. NA is a distinct peripheral nervous system disorder of the brachial plexus, with a yearly incidence ratio of 1/1000. 3, 6 It can also be described as an asymmetric, autoimmune inflammation of the brachial plexus and peripheral nerves. In the acute phase, the inflammation causes damage to the affected nerves, leading to the characteristic acute severe upper extremity pain, multifocal paresis (i.e. muscle weakness) with functional impairments, and patchy areas of sensory loss. The long thoracic nerve that innervates the serratus anterior muscle, is affected in about 70% of patients with NA. 7 In a substantial subset of patients (>50%), weakness of the serratus anterior muscle in the acute phase leads to compensatory, abnormal positioning and movement patterns of the scapula in the chronic phase. These patients develop chronic musculoskeletal pain in the paretic and compensating muscles, which leads to residual complaints of decreased functional capability of the affected upper extremity. 8 Many patients additionally suffer from impairment of activities of daily living, fatigue and decreased participation in daily occupations. 6, 8 The abnormal posture and movement patterns of the scapula are referred to as scapular dyskinesia. The concept of persisting shoulder complaints in NA is that through its plasticity, the motor system adapts to retain motor control of the shoulder region by forming compensatory movement patterns in the acute phase. After the acute phase, most of the damaged nerves recover over time and with this recovery, the strength of affected muscles, including the stabilising serratus anterior muscle, can return. However, recovery often does not lead to improved function because of dysfunctional coordination and instability of the scapula. Although some patients with NA recover well after 2–3 years, recovery is complicated in many. 5-8, 10 Residual complaints in NA are strongly correlated with persisting scapular dyskinesia. 8 There is currently no proven effective causative treatment for NA9 and the usual care given, mostly standard physical therapy, is ineffective and may even worsen complaints in more than half of patients with NA. 8 The fact that scapular dyskinesia persists even when the peripheral nerves and strength of the stabilising scapula muscle recover implies that other, cerebral factors may play a role in explaining the residual symptoms and variable recovery in patients with NA. We introduce the concept that peripheral nerve damage in NA may lead to adaptations in motor planning and representations that are compensatory in the acute phase, but lead
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