Analysis of the oral dyskinesia by using experimental animals.

1.实验一分析了口吃这一言语产生障碍的生理功能，探讨了气流感觉输入对腭帆提肌运动的影响。结果表明，喉上和喉下气流输入均促进了LVP的活动。结果表明，口吃是由于上呼吸道气流敏感性增高引起的发音器官之一软腭运动障碍所致。2.口腔感觉障碍可能是口腔运动障碍的原因。观察硬腭浸润麻醉对D1、D2激动剂（Quinpirole，SKF38393）诱发的口腔运动障碍大鼠舌不自主运动的影响。腭部麻醉可明显减少不自主运动量。3.猴下颌骨和舌的不自主运动可由不适当的假体组引起。然而，在另一方面，通过长期剂量的氟哌啶醇，它没有被诱导。因此，很明显，口腔感觉障碍引起的口腔运动障碍。

1.In the first experiment, the physiological function of the stuttering, which is one of the disturbance of speech production, was analyzed, effect of airflow sensory inputs to the airway on the levator veli palatini muscle activity was investigated. As a result, both of supralaryngeal and sublaryngeal airflow inputs facilitated the LVP activity. These result revealed that stuttering is based on the disorder of movement in the soft palate (one of the articulatory organs) which is elicited by hyper sensitivity of airflow through the upper airway.2.It is supposed that the oral sensory disorder caused oral dyskinesia. In the seconds, the effect of infiltration anesthesia of the hard palate on the involuntary movement of the tongue in the oral dyskinesia rat induced by the D1,D2 agonist (Quinpirole,SKF38393) injection were observed. It is clear that the amount of involuntary movements decreased by the anesthesia of the palate.3.In monkey, the involuntary movement of mandible and tongue were induced by the set of inadeqate prosthesis. In the other hands, however, by the chronic dosage of haloperidol, it was not induced. Therefore,it is clear that the oral sensory disorder caused the oral dyskinesia.