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Review reveals potential cellular mechanisms of synkinesis following facial nerve injury, highlighting aberrant axonal sprouting and nuclear scarring as drivers of faulty reinnervation.
When the facial nerve is injured, changes occur in muscle, proximal nerve, distal nerve, and the cell body in the nucleus. All of these changes contribute to the quality of regeneration and repair. This paper describes the usual processes of neuronal regeneration with the objective of a better understanding of why some injuries inevitably result in poor return of motion and synkinesis, while others recover completely. The possible mechanisms of synkinesis include: imperfect regeneration due to axonal misdirection, demyelination, microglial scarring in the facial nucleus, neuron depopulation, multiple axon sprouting, and misdirection of regenerating axons via vertical anastomotic filaments.
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Roger L. Crumley (1979) studied this question.
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