JOURNAL ARTICLE
REVIEW

To breathe, perchance to sleep: sleep-disordered breathing and chronic insomnia among trauma survivors

Barry Krakow, Dominic Melendrez, Teddy D Warner, Richard Dorin, Ronald Harper, Michael Hollifield
Sleep & Breathing 2002, 6 (4): 189-202
12524572
Standard psychiatric classification (DSM-IV-TR) traditionally attributes post-traumatic sleep disturbance to a secondary or symptomatic feature of a primary psychiatric disorder. The DSM-IV-TR paradigm, however, has not been validated with objective sleep assessment technology, incorporated nosological constructs from the field of sleep disorders medicine, or adequately addressed the potential for post-traumatic stress disorder (PTSD) sleep problems to manifest as primary, physical disorders, requiring independent medical assessments and therapies. This paradigm may limit understanding of sleep problems in PTSD by promulgating such terms as "insomnia related to another mental disorder," a.k.a. "psychiatric insomnia." Emerging evidence invites a broader comorbidity perspective, based on recent findings that post-traumatic sleep disturbance frequently manifests with the combination of insomnia and a higher-than-expected prevalence of sleep-disordered breathing (SDB). In this model of complex sleep disturbance, the underlying sleep pathophysiology interacts with PTSD and related psychiatric distress; and this relationship appears very important as demonstrated by improvement in insomnia, nightmares, and post-traumatic stress with successful SDB treatment, independent of psychiatric interventions. Continuous positive airway pressure treatment in PTSD patients with SDB reduced electroencephalographic arousals and sleep fragmentation, which are usually attributed to central nervous system or psychophysiological processes. Related findings and clinical experience suggest that other types of chronic insomnia may also be related to SDB. We hypothesize that an arousal-based mechanism, perhaps initiated by post-traumatic stress and/or chronic insomnia, may promote the development of SDB in a trauma survivor and perhaps other patients with chronic insomnia. We discuss potential neurohormonal pathways and neuroanatomatical sites that may be involved in this proposed interaction between insomnia and SDB.

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