Early scholars interpreted lingual muscle atrophy as a result of decreased trophic function of the motor nerve, damaging single, multiple, or all motor endplates or neuromuscular synapses, based on pathological changes of neurogenic origin of the lingual muscle and the absence of abnormalities in the motor nucleus of the sublingual nerve of the brainstem. Pathogenesis: Because the motor nerve has the function of transmitting nerve impulses and nutritional endplates, its nutritional function is impaired in the presence of defective neuromuscular junction transmission and muscle atrophy occurs. In recent years, it is believed that antibodies to the neuromuscular junction transmission receptors cause degradation and destruction of the receptors after blockade, producing functional denervation-like changes and muscle fiber-type grouping. The lingual muscles contain supraglossal and infraglossal longitudinal muscles, transverse lingual muscles and rectus lingual muscles. The direction, fiber type composition and function of the muscle fibers are very complex to ensure flexible flexibility in multiple positions and directions. The anterior part of the tongue is composed of type II fibers, which are fast moving and related to articulation and phonemes, and the posterior part of the tongue is composed of I and IM and IIc fibers, which are related to swallowing and respiratory functions, so this structural and compositional complexity may become the basis of vulnerability to damage.