The cycle of muscle-tone loss and restoration coinciding with periods of deep and light sleep repeats throughout the patients period of sleep. The number of apnoea and hypopnoea episodes during any given hour is counted and given a score. If a patient has an average of five or more episodes per hour, mild OSA may be confirmed. An average of 30 or more episodes per hour indicates severe OSA. Pathophysiological models
The causes of spontaneous upper-airway blockage are strongly debated by clinical professionals. The areas of thought are divided mostly into three medical groups. Some pulmonologists and neurologists believe the risk factors to be: 

Advanced age, although OSA occurs in neonates, as with Pierre Robin syndrome, and in all age groups of people. Brain injury (temporary or permanent), although this does not account for the 99% of OSA patients who have normal brains and normal lives. Decreased muscle tone caused by drugs or alcohol, or caused by neurological disorders. This also would not account for the majority of people with OSA. Long-term snoring, which is postulated to potentially induce local nerve lesions in the soft tissues of the pharynx. Snoring may produce traumatic vibrations that may give rise to nerve injuries in the upper airway muscles, further contributing to OSA.
This sleep interruption in Stage 3 (also called slow-wave sleep), and in REM sleep, can interfere with normal growth patterns, healing and immune response, especially in children and young adults. The fundamental cause of OSA is a blocked upper airway, usually behind the tongue and epiglottis, whereby the otherwise patent airway, in an erect and awake patient, collapses when the patient is lying on his or her back and loses muscle tone upon entering deep sleep. At the beginning of sleep, a patient is in light sleep and there is no tone loss of throat muscles. Airflow is laminar and soundless. As the upper airway collapse progresses, the obstruction becomes increasingly apparent by the initiation of noisy breathing as air turbulence increases, followed by gradually louder snoring as a Venturi effect forms through the ever-narrowing air passage. The patients blood-oxygen saturation gradually falls until cessation of sleep noises, signifying total airway obstruction of airflow, which may last for several minutes. Eventually, the patient must at least partially awaken from deep sleep into light sleep, automatically regaining general muscle tone. This switch from deep to light to deep sleep can be recorded using ECT monitors. In light sleep, muscle tone is near normal, the airway spontaneously opens, normal noiseless breathing resumes and blood-oxygen saturation rises. Eventually, the patient reenters deep sleep, upper airway tone is again lost, the patient enters the various levels of noisy breathing and the airway blockage returns.