Normal eye transient is an ocular nerve reflex, so that the tear film destroyed by environmental pollution and water evaporation when opening the eyes is rebuilt, and the tears are evenly distributed on the eye surface, which has an ocular surface protection function. The general transient frequency is 10-15 times per minute. Children with abnormal transient eyes blink frequently, more than 15 times per minute, up to 30 times per minute, and even close their eyes briefly. Traditionally, infection is thought to be the main cause of transient blinking in children with transient eye disease, but clinical observations have shown that most children have insufficient evidence of infection, no relief or even worsening of symptoms after anti-infective treatment. Transient eyes are a very brief unconscious opening and closing of the eyelids, lasting 0.3-0.4s, with one transient within 5s being frequent. Frequent blinking is the most common clinical complaint in children. Currently, the following causes are recognized in children: (1) eye rubbing by dirty hands; (2) eye fatigue due to improper eye hygiene and eye habits; (3) nutritional deficiencies due to partial eating; (4) trachoma (rare nowadays) and conjunctivitis; (5) tics and intestinal parasites. Treatment is mainly etiological. It is noteworthy that many patients, although cured of eye disease but abnormal transient disorder for a long time. The main reason for this is the lack of understanding of the underlying mechanism of the abnormal transients caused by the above mentioned etiology. Recent studies have shown that transient movements carry tears that are evenly coated in front of the cornea and conjunctiva to form a tear film that moistens the cornea and conjunctiva and provides nutrients to prevent cell damage. As time increases, the tear film thins locally, surface tension decreases, tear film stability decreases, and subsequently ruptures, exposing the cornea and conjunctiva to air, and its receptors sense and conduct stimuli through the trigeminal nerve to one side of the cerebral cortex to the nerve and eyelid muscle to complete a transient, forming a new tear film, and so on. This suggests that the direct cause of abnormal transients may be: (1) decreased stability of the tear film and shortening of the BUT; (2) inflammatory factors that stimulate the corneoconjunctival receptors and cause the transient reflex. It has been shown that inflammatory factors are an important factor in the decreased stability of the tear film and shortened BUT. It can be seen that abnormal transient eyes are closely related to decreased tear film stability.