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Slow-Wave Activity in Sleep Apnea Patients Before and After Continuous Positive Airway Pressure Treatment: Materials and Methods

Ten men (mean age, 42.7 ± 1.87 years; age range, 36 to 57 years; mean body mass index [BMI], 37.54 ± 1.98 kg/m2) with a diagnosis of severe SAS who showed a good clinical and polysomnography (PSG) response to CPAP after 9 ± 0.7 months of treatment were included in the study. Inclusion criteria were as follows: (1) an apnea plus hypopnea index (AHI) of > 30 events/h during the diagnosis night; (2) a good response to CPAP treatment, defined as an AHI of < 10 events/h; and (3) an index of periodic limb movements during sleep of < 10 movements/h of sleep. Exclusion criteria were the presence of any other sleep disorder or pulmonary disease and the use of any medication likely to affect sleep, EEG, or respiratory functions in the month prior to entering the study. Ten normal male subjects (mean age, 43.9 ± 2.2 years; age range, 36 to 55 years; mean BMI, 26.9 ± 1.15 kg/m2) were used as control subjects and were studied with the same procedure. None of the control subjects had a AHI > 5 events/h. Exclusion criteria were the same as those of the SAS group. All subjects signed a consent form prior to starting the experiment, and the study was approved by the ethics committee of the hospital and university. COPD
Nocturnal Sleep Studies
All subjects underwent 1 night of PSG, followed by a modified MSLT the next day; for the SAS patients, the same procedure was repeated after 9 ± 0.7 months of CPAP treatment (Tranquility Plus 7100; Healthdyne; Marietta, GA). Sleep was monitored using two EEG leads (C3-A2, O2-A1), right and left electrooculogram, chin electromyogram, and ECG. To assess apneas and hypopneas, nasal and oral airflow were recorded with thermistors, and respiratory movements with abdominal and thoracic strain gauges. An apnea was defined as a cessation of the respiratory airflow of at least 10-s duration, and an hypopnea as reduction of the airflow > 50% (lasting > 10 s). The AHI represents the number of apneas and hypopneas per hour of sleep. Arterial oxygen saturation (Sao2) was measured continuously with a finger oximeter (Biox III; Ohmeda; Boulder CO); both time < 90% and minimum Sao2 were calculated. Surface electromyogram of anterior tibialis muscles was recorded to quantify periodic leg movements during sleep.
Sleep was recorded and scored manually according to the criteria of Rechtschaffen and Kales using 20-s epochs. The use of the 20-s epoch is essential when performing all-night quantitative EEG analysis on signals recorded at 128 Hz (analysis window of 4 s), to keep the time course of sleep staging and quantitative EEG values aligned. The following variables were calculated: total sleep time; sleep efficiency; number and index of microarousals; percentage of stages 1,2,3 and 4; and REM sleep, and mean and lowest oxygen saturation levels. Sleep efficiency was defined as the percentage of time spent asleep over the total recording time from sleep onset to the last awakening. A microarousal was defined as a return to a or 0 frequency well differentiated from the background EEG activity lasting at least 3 s but < 10 s.