The subjects for this study were 39 patients (mean age, 50.1 ± [SDJ11.57; nine women and 30 men) given the diagnosis of OSAS at the Henry Ford Hospital Sleep Center. All patients presented with complaints of EDS and loud, habitual snoring during a clinical sleep history and physical examination.
All patients underwent a CPSG and a MSLT. The standard nocturnal polysomnogram consisted of a continuous monitoring of the central and occipital EEGs, EOGs, and a submental EMG at the conventional placements. The recording instrument was a Grass 78D polygraph calibrated at 50 jjlV equal to 7.5 mm with standard amplifier settings. Respiratory airflow was measured by nasal/oral thermistors and respiratory effort by mercury-filled strain gauges placed on the abdomen. Oxygenation was monitored by a Biox 3 ear oximeter and heart rate by a V5 placement. naturalbreastenhancementpill.com
On the day immediately following the nocturnal recording, a MSLT was performed. At 1,000,1,200,1,400, and 1,600 h, patients were instructed to lie in bed in a quiet, darkened room and to try to fall asleep. The standard EEGs, EMG, and EOGs for sleep stages were recorded. Each MSLT ran for 20 min if no sleep occurred. If sleep occurred, the MSLT was terminated 15 min after sleep onset. Patients were directed not to nap between MSLTs and were monitored for compliance.
All sleep recordings were scored for sleep stages using the Rechtschaffen and Kales criteria. Respiratory channels were scored for presence of apnea (cessation of airflow for 10 s) and type (obstructive, mixed, or central) and for hypopnea (50 percent decrease in airflow compared to baseline for 10 s with an associated 3 percent fall in oxygenation and EEG/EMG arousal). Oximetry data were scored for the number of times and total minutes that oxygen saturation descended below 85 percent during the recording.
All patients received a diagnosis of OSAS and were included in the study based on two polysomnographic criteria, (1) a respiratory index (apnea+hypopnea/h of total sleep time) greater than 20, and (2) a mean latency to sleep onset of less than 7 min. All patients were obese but generally were free of waking lung disease as determined by a standard pulmonary evaluation. The subjects were randomly assigned to one of three conditions, 13 in each group. The first condition consisted of a CPSG with CPAP treatment followed the next day by a MSLT. The two remaining conditions returned subjects for a CPSG with CPAP and MSLT after 14 and 42 nights of continuous nightly treatment.
The introductory CPSG with the CPAP therapy provided the sleep laboratory with an opportunity to set the minimum pressure necessary to prevent airway obstruction. Patients in the 14- and 42-night groups were instructed in the use of the apparatus and sent home with it to use until their return CPSG and MSLT. Compliance was monitored by daily logs. A two-factor multivariate analysis of variance using the general linear models procedure of SAS (SAS Institute) was performed on the nocturnal and daytime sleep parameters. The first factor is treatment with two levels, pretreatment night and posttreatment night. The second factor is duration of treatment with three levels, one-, 14-, or 42-nights. Significant omnibus F test results were followed by Duncan post hoc comparisons.