In this chapter, we aim to discuss the neurophysiological basis of the brain reorganization (also called plasticity) that associates with a traumatic brachial plexus injury (TBPI), as well as following the brachial plexus surgical reconstruction and its physical rehabilitation. We start by reviewing core aspects of plasticity following peripheral injuries such as amputation and TBPI as well as those associated with chronic pain conditions. Then, we present recent results collected by our team centered on physiological measurements of plasticity after TBPI. Finally, we discuss that an important limitation in the field is the lack of systematic measurement of TBPI clinical features. We finish by proposing possible future venues in the domain of brain plasticity following a TBPI.

Background: Traumatic brachial plexus injury (TBPI) is a potentially debilitating event, that usually affects young men following car or motorbike accidents. TBPI interferes with hand sensorimotor function, is associated with chronic pain, and causes cortical reorganization. Interactions between the somatosensory and motor cortices are of fundamental importance for motor control. The hands and face stand out as regions of high functionality with a privileged interaction existing between them, as reflected by the proximity and extension of their representations. Face-hand sensorimotor interactions have been demonstrated in healthy subjects. Objective: The aim of this study was to investigate changes in the sensorimotor interaction in the hand and between the face and the hand in TBPI patients in order to better understand the plasticity of face-hand sensorimotor circuits following TBPI. Method: The experimental design consisted of activating the representation of a hand muscle using transcranial magnetic stimulation (TMS) preceded by an electrical stimulation (ES) applied to the hand or face, which allows the investigation of the cortical reorganization resulting from TBPI. In the paradigm called afferent inhibition (AI), the motor evoked potential (MEP) in a target muscle is significantly reduced by a previous peripheral ES. AI can be evoked in short-latency (SAI) or long-latency (LAI) interstimulus intervals. Nine TBPI patients participated: five had partial sensorimotor function in their hands and were evaluated on the injured side (TBPI-I group) and four had complete loss of sensorimotor function in their hands and were evaluated on the uninjured side (TBPI-UI group). A control group (CG) included 18 healthy adults. A detailed clinical evaluation complemented the analysis. Results: The results showed preserved hand sensorimotor integration for TBPI patients at SAI intervals, but not at LAI intervals. For the face-to-hand sensorimotor integration, the results showed no inhibition at SAI intervals for the TBPI patients. For LAI intervals, a facilitation effect was observed for the TBPI patients, an effect we termed long afferent facilitation or LAF. LAF positively correlated with results in the Central Sensitization Inventory and in the Disabilities Arm, Shoulder, and Hand questionnaire. Conclusion: These results point to the existence of an inhibitory regulation system between the representations of the face and the hand that seems to be suppressed in TBPI and correlates with pain. Moreover, brain changes arising from TBPI are not restricted to the hemisphere contralateral to the injured limb, but extend to both hemispheres.

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