Identifier

etd-0730103-102957

Degree

Doctor of Philosophy (PhD)

Department

Psychology

Document Type

Dissertation

Abstract

Obstructive sleep apnea syndrome (OSAS) is a sleep-disordered breathing condition that causes disrupted sleep. Although OSAS is most often associated with daytime hypersomnolence, a number of OSAS patients complain of insomnia, i.e., disorders of initiating or maintaining sleep. If the insomnia in patients with OSAS is secondary to the medical condition, then it would be expected to abate with the successful treatment of OSAS. If, however, the insomnia is primarily of a psychological nature, thus considered primary or psychophysiological insomnia, little to no change in insomnia symptoms would be expected after the treatment of OSAS. The present study examined the relations between OSAS and insomnia and attempted to determine if insomnia is secondary to OSAS by studying changes in insomnia over the course of treatment for OSAS with continuous positive airway pressure (CPAP). Forty-one individuals participated in the baseline assessment and a smaller sample of participants (n = 15) were followed over the course of OSAS treatment. All participants underwent a nocturnal diagnostic polysomnography (PSG) and self-monitored insomnia, daily functioning, sleep hygiene practices, and somatic and cognitive pre-sleep arousal for a one-week period prior to, and after, CPAP treatment. Baseline and post-treatment analyses provided evidence suggesting that OSAS and insomnia are independent sleep disorders. There was no association between sleep apnea severity and any self-reported measure of insomnia. Furthermore, there were no significant changes in insomnia after successful treatment of OSAS with CPAP. There were however, significant reductions in both somatic and cognitive arousal, constructs known to be closely associated with insomnia, after CPAP treatment. It is possible that somatic and cognitive arousal decreased as a function of decreased worry and anxiety about the sleep disruption typically caused by OSAS. Another potential explanation of why insomnia did not improve after CPAP treatment involves the significant correlation (r = .59) between CPAP interference and sleep-onset insomnia. These results suggest that a longer adjustment time to the CPAP stimulus might be necessary before definitive conclusions are reached regarding the proposed lack of association between OSAS and insomnia. Implications for the assessment and treatment of comorbid OSAS and insomnia are discussed.

Date

2003

Document Availability at the Time of Submission

Release the entire work immediately for access worldwide.

Committee Chair

William F. Waters

DOI

10.31390/gradschool_dissertations.903

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Psychology Commons

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