The affinity of AChR at end plates and different number of AChR per unit fiber cross-sectional area may be the mechanisms for differential sensitivities to neuromuscular blockers between facial nerve-innervated muscles and somatic nerve-innervated muscles. The lower EEMG responses in the impaired facial nerve-innervated muscles may result from the lower AChR density at end plates compared with the normal facial nerve-innervated muscles.
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