The transition from wakefulness to sleep (either REM sleep or NREM sleep) is associated with a reduction in upper-airway muscle tone. During REM sleep, muscle tone of the throat and neck, as well as that of the vast majority of skeletal muscles, is almost completely attenuated. This allows the tongue and soft palate/oropharynx to relax, reducing airway patency and potentially impeding or completely obstructing the flow of air into the lungs during inspiration, resulting in reduced respiratory ventilation. If reductions in ventilation are associated with sufficiently low blood-oxygen levels or with sufficiently high breathing efforts against an obstructed airway, neurological mechanisms may trigger a sudden interruption of sleep, called a neurological arousal. This arousal can cause an individual to gasp for air and awaken. These arousals rarely result in complete awakening but can have a significant negative effect on the restorative quality of sleep. In significant cases of<unk> , one consequence is sleep deprivation resulting from the repetitive disruption and recovery of sleep activity. 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<unk>  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 patient's 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. The cycle of muscle-tone loss and restoration coinciding with periods of deep and light sleep repeats throughout the patient's period of sleep. The number of<unk>  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<unk>  may be confirmed. An average of 30 or more episodes per hour indicates severe<unk> . 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<unk>  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<unk>  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<unk> . * 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<unk> . * Increased soft tissue around the airway, often resulting from obesity, though not seen in all patients with<unk> . Some otorhinolaryngologists believe the risk factors to be structural features that give rise to a narrowed airway, such as enlarged tonsils, an enlarged posterior tongue or fat deposits in the neck. Further factors leading to<unk>  can be impaired nasal breathing, floppy soft palate or a collapsible epiglottis. Some oral and maxillofacial surgeons believe the risk factors to be a number of primary forms of mandibular hypoplasia, which offers a primary anatomical basis to the development of<unk>  through glossoptosis. Some maxillofacial surgeons who offer orthognathic surgery for treatment of<unk>  believe that their treatments offer superior guarantees of cure of<unk> .
Obstructive sleep apnea
Sleep apnea
Central sleep apnea
Obesity hypoventilation syndrome
Hyperventilation syndrome
Sleep-related breathing disorder
Central hypoventilation syndrome
Reactive airway disease