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  • Title: Experimental studies on the recovery processes from severe facial palsy and the development of its sequelae.
    Author: Takeda T, Takeda S, Okada T, Kakigi A, Yamasoba T.
    Journal: Otol Neurotol; 2015 Jun; 36(5):896-903. PubMed ID: 25871969.
    Abstract:
    OBJECTIVE: To experimentally elucidate the pathogenesis of inappropriate co-contraction of facially innervated muscles after severe facial palsy. METHODS: Twenty-two guinea pigs with severe facial palsy induced by the interruption of the petrosal artery were used to follow up behavioral facial movement, including the degree of facial palsy and abnormal hyperkinetic facial movement of synkinesis and mass contracture. At the end of the follow-up, the evoked facial compound muscle action potential (evoked FCMP) and antidromically evoked facial nerve response (AFNR) were examined in a few typical cases with complete recovery and with incomplete recovery accompanied by synkinesis. After the follow-up, all animals were sacrificed for morphological studies, which consisted of a light-microscopic study (by Luxol fast blue and hematoxylin and eosin staining or toluidine blue staining) and/or an electron-microscopic study. RESULTS: The initial sign of recovery was mass contracture or spasm. This condition continued for 2 weeks or more. As voluntary facial movement recovered, the mass contracture became unnoticeable. It could not be distinguished when the so-called synkinesis developed. Synkinesis usually developed during the recovery process from severe to moderate palsy, and synkinesis persisted or progressed once it appeared. Histologically, unmyelinated fibers were intermingled with myelinated fibers in an early stage of recovery with mass contracture. In the late stage with the development of synkinesis, however, such an intermingling of unmyelinated and myelinated axons was not observed. In this stage, axons became well myelinated, but they were irregular in shape in cases with synkinesis. Especially, axons irregularly ran at the level of the G1 (at the region of the second genu) segment, and bifurcated axons were sporadically found. The axon count had a tendency to increase toward the periphery. AFNR was not detected, although evoked FCMP could be clearly detected in cases with synkinesis. CONCLUSION: Misguidance of regenerated axons is an important cause of facial synkinesis in the ischemia-induced facial palsy model. Ephaptic transmission between unmyelinated and myelinated axons is also likely to be responsible for mass contracture manifested in the early stage of the recovery process.
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