Introduction Mobius syndrome is a complex bilateral congenital facial paralysis involving different cranial nerves, including the extra-ocular motor and facial nerves. In 1880, von Graef described a patient with congenital facial paralysis and inability to abduct the eyes. (1) However, Mobius was the first to suggest that the association of paralysis of the VI and VII nerves constituted an independent pathological entity.(2) Classically, the facial paralysis is bilateral, but incomplete with less compromise of the marginal mandibular and cervical branches. Patients present with incomplete eyelid closure during sleep, excessive drooling, and feeding difficulties in infancy. The most remarkable feature is the inability to smile and the lack of expression when crying, giving the face a mask-like appearance. At times, paralysis of the VI nerve may go unnoticed as the child compensates for the inability to abduct the eyes by turning the head to track objects. Other cranial nerves, specially the III, V, IX, and XII, may be affected to a variable degree. Additionally, Mobius syndrome is often associated with lower limb abnormalities and Poland syndrome. Although the etiology of this facial paralysis is unknown, the proximity of the nuclei of the VI and VII nerves suggests a lesion at that level. Different procedures have been tried to improve the lack of facial musculature. Microsurgery, specially the gracilis muscle transfer with the use of nerve grafts, improved the possibilities to reconstruct facial palsy.(3, 4, 5, 6) Based on the study by Zuker et al. we present our experience in segmental gracilis muscle transplant using facial or temporal vessels for revascularization and the motor nerve to the masseter for reinnervation. (7, 8, 9, 10)
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