Reply: Facial Symmetry Enhancement and Brain Network Modifications in Facial Palsy Patients after Botulinum Toxin Type A Treatment

We thank Dr. Salles and Dr. Mota1 for their comments on our article.2 It has been observed that botulinum toxin type A (BTX-A) can produce long-lasting benefits in the treatment of facial palsy. The facial motor system is organized hierarchically into 3 levels: the facial motor cortex, the facial nucleus, and the extracranial branches of the facial nerve. This structure parallels that of the skeletal motor system, which comprises the primary motor cortex, the anterior horn of the spinal cord, and the spinal nerves. Before our studies on facial palsy, a central question guiding our research is whether mechanisms of neural plasticity observed in peripheral nerve injury also apply to facial nerve injury. Functional reorganization following nerve injury can induce structural changes in the brain, with significant therapeutic implications.3 In patients with facial palsy, the brain continuously adapts to changes induced by BTX-A therapy. The temporary suppression of aberrant muscle activity through BTX-A–induced motor de-efferentation provides a critical window for the central nervous system to reorganize and establish healthier patterns of motor control. We propose that this neural reorganization underlies the sustained therapeutic effect of BTX-A. A primary aim of our research is to characterize these neuroplastic changes in greater detail and to identify key regions or neural events that facilitate the restoration of normal facial motor control.2 Such findings are essential for developing more effective and efficient therapies leveraging the long-term benefits of BTX-A. We further posit that early intervention with BTX-A seeks to inhibit abnormal muscle contractions and counteract maladaptive plasticity that reinforces pathological motor patterns. The strategy of partially limiting movement on the unaffected side during the initial phase of nerve injury represents an innovative approach to modulating cortical reorganization. Although this may prolong the overall recovery timeline, it is expected to substantially reduce maladaptive plasticity and improve functional outcomes. In patients with synkinesis, recovery of muscle strength may take precedence over symmetry or reduction in co-contraction. Improving motor control through the restoration of myodynamic capacity not only supports functional recovery but also aligns with ethical considerations in patient care. DISCLOSURE The authors have no conflicts of interest to declare.