%0 Journal Article
%T Role of Sensory Stimulation in Amelioration of Obstructive Sleep Apnea
%A Mak Adam Daulatzai
%J Sleep Disorders
%D 2011
%I Hindawi Publishing Corporation
%R 10.1155/2011/596879
%X Obstructive sleep apnea (OSA), characterized by recurrent upper airway (UA) collapse during sleep, is associated with significant morbidity and disorders. Polysomnogram is employed in the evaluation of OSA and apnea-hypopnea number per hour reflects severity. For normal breathing, it is essential that the collapsible UA is patent. However, obstruction of the UA is quite common in adults and infants. Normally, important reflex mechanisms defend against the UA collapse. The muscle activity of UA dilators, including the genioglossus, tensor palatini (TP), and pharyngeal constrictors, is due to the integrated mechanism of afferent sensory input to motor function. Snoring is harsh breathing to prevent UA obstruction. Unfortunately, snoring vibrations, pharyngeal suction collapse, negative pressure, and hypoxia cause pathological perturbations including dysfunctional UA afferent sensory activity. The current paper posits that peripheral sensory stimulation paradigm, which has been shown to be efficacious in improving several neurological conditions, could be an important therapeutic strategy in OSA also. 1. Introduction Obstructive sleep apnea (OSA) is characterized by recurrent upper airway (UA) obstruction, hypoventilation, hypoxia, and hypoxemia. Two cardinal features of OSA are (1) decrease in UA dilator muscles¡¯ force during sleep and (2) narrowed cross-sectional pharyngeal lumen that presents a significant mechanical constraint to normal ventilation. During UA collapse, ventilation is compromised (hypopnea) or absent (apnea), and hypoxia and hypercapnia develop. These blood gas changes increase respiratory drive until the UA reopens, at which time ventilation increases to reverse the blood gas abnormalities. This scenario reflects a dysfunctional genioglossus (a major UA dilator muscle) activity during sleep, in conjunction with a hypotonic pharynx that collapses. OSA affects ~4% of men and ~2% of women and is strongly linked to obesity. Owing to recurrent UA obstruction and hypoventilation, clinical consequences due to OSA (in most if not all sufferers) are several, ranging from¡ªcardiovascular disease (hypertension, myocardial infarction, heart failure), stroke, metabolic derangement, respiratory failure, and cognitive dysfunction (see [1, 2]). Recent Australian and American studies have documented OSA to be an important risk factor from all-cause death-being as high as 33% in patients with severe OSA. The untreated OSA patients are at even greater risk, being 3.8 times more likely to die from any cause and 5.2 times more likely to die from
%U http://www.hindawi.com/journals/sd/2011/596879/