146 CHAPTER 7 was not focused on cerebral motor control in a large proportion of patients (11/27, 6 of whom received no formal treatment at all), suggests that some natural recovery of visuomotor adaptations occurs. This observation opens an array of interesting directions to pursue to help improve our understanding of the underlying cerebral mechanisms and how to optimally target them with rehabilitation. First, we need to improve our understanding of the natural progression of cerebral adaptations in NA. Ideally, brain activity should be measured at regular intervals throughout the recovery process, starting right after NA onset, up to when peripheral nerve recovery plateaus (e.g. 2 years later). Once we better understand how cerebral adaptations develop over time, we may be able to identify the ‘window of opportunity’ of when to apply interventions targeting cerebral motor control. More specifically, it would be important to determine whether early intervention could prevent cerebral adaptions all together, or whether reduced visuomotor activity actually benefits patients at an early stage. In other words, would it be beneficial to start with rehabilitation as soon as possible, or would waiting until natural recovery has reached a certain level lead to a more favorable outcome? Some patients may not need any specific rehabilitation to return to pre-injury cerebral activity levels, although it will remain challenging to determine when natural recovery suffices without extra treatment. This brings us to the second direction to pursue. Although it appears that cerebral adaptations in NA can recover naturally to some extent, it is not clear whether cerebral recovery is complete and occurs in all patients. Clinically, some patients show great (natural) recovery, whereas others suffer from persistent motor dysfunction. These clinical differences may be related to differences in how the brain responds to peripheral nerve injury in NA and how well cerebral adaptations recover towards normality with time. Our current sample size did not allow us to look into differences between treatment responders and nonresponders. Identifying the ‘brain signature’ of persistence of clinical symptoms could be an important next step to better understand these cerebral mechanisms and their link to clinical outcome. Future work should therefore focus on discerning differences in cerebral processes between patients that show good vs. poor clinical recovery. This may also help to identify which sub-groups of patients may benefit from different treatment strategies: some patients may require specific training of central motor control, whereas others may not. Due to the heterogeneity of the NA patient population, it is important to also investigate the influence of other patients’ characteristics, such as age, sex, occurrence of recurrent attacks, unilateral vs. bilateral involvement, hand dominance, and the extent and distribution of nerve injury and sensory and motor symptoms. As recovery and optimal treatment strategies may vary depending on these factors, this could bring us closer to more personalized care. Although cerebral (mal)adaptations may play a bigger role in certain groups of patients, targeting cerebral processes could also offer opportunities for patients that do show good clinical outcome. It may be possible to accelerate and facilitate natural recovery, which could lead to a faster return to activities of daily life and increased quality of life for the patient. This is especially important for the young NA patient population, whose active lives are often disrupted by the acute NA attack and its consequences. It is clear that much remains to be uncovered about the role cerebral mechanisms play in NA patients recovering from peripheral nerve injury. Nevertheless, we can already