Less common symptoms are morning headaches; insomnia; trouble concentrating; mood changes such as irritability, anxiety, and depression; forgetfulness; increased heart rate or blood pressure; decreased sex drive; unexplained weight gain; increased urinary frequency or nocturia; frequent heartburn or gastroesophageal reflux; and heavy night sweats.Many people experience episodes of OSA for only a short period. This can be the result of an upper respiratory infection that causes nasal congestion, along with swelling of the throat, or tonsillitis that temporarily produces very enlarged tonsils. The Epstein-Barr virus, for example, is known to be able to dramatically increase the size of lymphoid tissue during acute infection, and OSA is fairly common in acute cases of severe infectious mononucleosis. Temporary spells of OSA syndrome may also occur in individuals who are under the influence of a drug (such as alcohol) that may relax their body tone excessively and interfere with normal arousal from sleep mechanisms. Adults
The hallmark symptom of OSA syndrome in adults is excessive daytime sleepiness. Typically, an adult or adolescent with severe long-standing OSA will fall asleep for very brief periods in the course of usual daytime activities if given an opportunity to sit or rest. This behavior may be quite dramatic, sometimes occurring during conversations with others at social gatherings.The hypoxia (absence of oxygen supply) related to OSA may cause changes in the neurons of the hippocampus and the right frontal cortex. Research using neuro-imaging revealed evidence of hippocampal atrophy in people with 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.