In 88% of the subjects, there is a history of early extraction or absence of wisdom teeth. There is an increased prevalence of UARS in east Asians. Pathophysiology
Upper airway resistance syndrome is caused when the upper airway narrows without closing. Consequently, airflow is either reduced or compensated for through an increase in inspiratory efforts. This increased activity in inspiratory muscles leads to the arousals during sleep which patients may or may not be aware of.A typical UARS patient is not obese and possesses small jaws, which can result in a smaller amount of space in the nasal airway and behind the base of the tongue. Patients may have other anatomical abnormalities that can cause UARS such as deviated septum, inferior turbinate hypertrophy, a narrow hard palate that reduces nasal volume, enlarged tonsils, or nasal valve collapse. UARS affects equal numbers of males and females.Why some patients with airway obstruction present with UARS and not OSA is thought to be caused by alterations in nerves located in the palatal mucosa. UARS patients have largely intact and responsive nerves, while OSA patients show clear impairment and nerve damage. Functioning nerves in the palatal mucosa allow UARS patients to more effectively detect and respond to flow limitations before apneas and hypopneas can occur. Patients with intact nerves are able to dilate the genioglossus muscle, a key compensatory mechanism utilized in the presence of airway obstruction.
Long-term use of sedative-hypnotics for insomnia lacks an evidence base and has traditionally been discouraged for reasons that include concerns about such potential adverse drug effects as cognitive impairment (anterograde amnesia), daytime sedation, motor incoordination, and increased risk of motor vehicle accidents and falls. In addition, the effectiveness and safety of long-term use of these agents remain to be determined. It was concluded that more research is needed to evaluate the long-term effects of treatment and the most appropriate management strategy for elderly persons with chronic insomnia. Pharmacology
Estazolam is classed as a "triazolo" benzodiazepine drug. Estazolam exerts its therapeutic effects via its benzodiazepines receptor agonist properties. Estazolam at high doses decreases histamine turnover via its action at the benzodiazepine-GABA receptor complex in mouse brains. Pharmacokinetics
Peak plasma levels are achieved within 1–6 hours. Estazolam is an intermediate acting benzodiazepine. The elimination half life of estazolam is an average of 19 hours, with a range of 8–31 hours. The major metabolite of estazolam is 4-hydroxyestazolam. Other identified metabolites include 1-oxo-estazolam, 4-hydroxy-estazolam, and benzophenone. Interactions
Alcohol enhances the sedative hypnotic properties of estazolam. In package inserts, the manufacturer clearly warns about an interaction with Ritonavir, and although clinical interactions of Ritonavir with estazolam have not yet been described, the lack of clinical descriptions of the interactions does not negate the seriousness of the interaction.