Affiliations: University of Hong Kong Hong Kong SAR, China,
Correspondence to: Ka-Fai Chung, MBBS, MRCPsych Assistant Professor, Department of Psychiatry, University of Hong Kong, Pokfulam Rd, Hong Kong SAR, China; e-mail: email@example.com
I read with interest the article by Krakow et al (December 2001)1 on the prevalence of insomnia symptoms (ISs) in patients with sleep-disordered breathing (SDB). The study showed that insomnia complaints were common in SDB patients, but it remained unclear why some patients with repeated apneas had insomnia whereas others did not. I report here the prevalence of different subtypes of insomnia in SDB patients. The finding is useful in understanding the relationship between SDB and insomnia.
I analyzed the data of 150 consecutive patients referred to our laboratory because of suspected obstructive sleep apnea (OSA).2 ISs were reported using a Likert-scale to four statements: “difficulty getting to sleep” (IS-1); “wake up during the night and have a hard time getting back to sleep” (IS-2); “wake up repeatedly during the night” (IS-3); and “wake up too early in the morning and can’t get back to sleep” (IS-4). Responses of “often” and “almost always” were considered presence of insomnia complaints.
OSA according to the international classification of sleep disorders was diagnosed in 119 patients3 who had an apnea-hypopnea index (AHI) ≥ 5 events per hour. The 119 subjects were predominately male (105 male and 14 female patients) and 44.6 ± 10.4 years of age (mean ± SD). The mean body mass index was 27.8 ± 5.0 and AHI was 37.3 ± 26.5. The most frequent IS was IS-3 (33%), followed by IS-4 (21%), IS-2 (16%), and IS-1 (9%). Subjects with and without ISs were similar in demographics, daytime sleepiness, and AHI. However, patients with difficulty initiating sleep (IS-1, IS-2, or IS-4) had significantly lower AHI (26.7 ± 24.6) than subjects with frequent awakenings (IS-3 only) [45.0 ± 26.1] and those with no insomnia (40.4 ± 26.3) [F = 4.5; degrees of freedom = 2, 116; p = 0.01].
The most common IS in SDB patients was frequent awakening, while a significant proportion of subjects had difficulty initiating sleep. It appears that repeated apnea is not the single factor that can account for the ISs in SDB patients, particularly in those with difficulty initiating sleep. Individual vulnerability to develop insomnia needs to be addressed.1,4–5
We concur with Chung’s conclusion, “Individual vulnerability to insomnia [in patients with sleep-disordered breathing (SDB)] needs to be addressed,” and our data also showed a statistically significant higher apnea-hypopnea index (AHI) in those without insomnia compared to those with insomnia.1A tempting explanation, then, for SDB plus insomnia (“complex insomnia”2) in our sample would be their greater self-reported psychiatric distress and ruminations and anxiety about sleep1 in contrast to SDB-induced respiratory compromise and resultant sleep fragmentation. We believe this conclusion has validity but is also an incomplete model for several reasons.
First, conclusions drawn from polysomnography using AHI may be undermined by the lack of advanced respiratory monitoring3(eg, esophageal manometry [EM],4 nasal cannula pressure transducer [NCPT]5–), which detects subtle breathing disturbances such as respiratory effort-related arousals (RERAs)6 that fragment sleep in ways similar to apneas and hypopneas. In our study or in the study by Chung, it may be misleading to suggest that one group has more apneas or hypopneas without accounting for a broader respiratory disturbance index (apnea plus hypopnea plus RERAs) that might more accurately reflect pathology.3 In fact, we reported that RERAs may be the predominant type of respiratory event among insomniacs with comorbid SDB.2 Therefore, we speculate that meaningful statistical analyses cannot be conducted from these studies with the use of AHI as it is currently configured.
Second, in our clinical practice and research experience, approximately 80% of patients reporting insomnia for > 6 months also have SDB, which has led us to assume that the disorders termed psychophysiologic insomnia (PPI) and SDB reflect two overlapping pathophysiologies of sleep fragmentation. However, when these two disorders occur together, resultant sleep fragmentation may produce an impairment continuum, comprising symptoms of pathologic sleepiness (hypersomnia) on one end and pathologic sleeplessness (insomnia) on the other end (Fig. 1
). A typical SDB presentation with recurrent awakenings but no true sleeplessness manifests as hypersomnia, day or night, whereas an atypical SDB presentation might manifest at any point along this continuum in a complex insomnia patient; that is, sleep fragmentation ought to produce sleepiness but instead manifests paradoxical complaints of sleepiness and sleeplessness,7 each symptom highly dependent on the time of day and behavioral contexts for the individual patient. A patient in the middle of the continuum has comparable problems with daytime sleepiness and nighttime insomnia. This construct suggests that the symptom of insomnia lies dormant within SDB and then “awakens” in certain patients depending on their “individual vulnerability.”
Third, factors and interactions to explain this vulnerability are likely to be exceedingly complex because of the mediating effects of SDB itself. SDB is frequently associated with symptoms of depression,8 and we observed greater severity of posttraumatic stress, depression, anxiety, suicidality, and worse quality of life impairment in trauma survivors with PPI and SDB compared to trauma survivors with PPI and no SDB.7,9–10 Thus, an interaction may occur between SDB and psychiatric distress, which further contributes to individual vulnerability. We believe testing this hypothesis will prove to be especially informative to the fields of sleep medicine and psychiatry.
Finally, counterintuitive reasoning might be needed to study complex insomnia because we speculate that PPI may have as much influence in causing or promoting SDB as SDB might in the reverse role. We developed this hypothesis because of research findings on 451 trauma survivors seeking treatment for insomnia in the past 7 years, of which 93% met American Academy of Sleep Medicine subjective research criteria for SDB.11Of 174 objectively assessed with polysomnography (n = 82) or portable monitoring devices (n = 92) with built-in NCPT (Autoset Portable II Plus; Resmed; North Ryde, Australia), 87% tested or screened positive for SDB. Although some trauma survivors reported life-long sleep complaints, a much larger proportion alleged that sleep problems developed after the trauma. As sleep is known to worsen with posttraumatic stress and its cardinal hyperarousal symptoms, we speculate that these psychophysiologic processes impact respiration. In this model (Fig 1), PPI produces stress-related sleep fragmentation in the form of arousals or increased time spent in stage 1 non-rapid eye movement (NREM) sleep, both of which might lead to greater instability of the upper airway13 and subsequent incursion of SDB events, perhaps RERAs. The dual elements of insomnia and RERAs could fuel a vicious cycle in which insomnia creates a breeding ground for sporadic or regular airway collapse, which leads to RERAs that promote more arousal activity that feeds the insomnia. Over time, perhaps some RERAs progress to hypopneas or apneas in patients with other risks for SDB.14–16
Continuous positive airway pressure (CPAP) can interrupt this cycle, but “CPAP for insomnia” is not likely to resonate with chronic insomniacs. Nonetheless, we observed resolution or improvement in sleep maintenance or sleep-onset insomnia in patients treated with CPAP or oral appliances without intercurrent interventions,17as well as in those receiving combined SDB treatment and cognitive-behavioral therapy.18Thus, the recommendations of our institute for standard of care in chronic insomnia (minimum 6 months’ duration) include diagnostic polysomnography with EM or NCPT, followed by CPAP titration to document reversal of arousal activity. Still, it cannot go without saying that treatment of SDB in an insomniac might be very challenging. To enhance treatment outcomes in complex insomnia, we are currently exploring two questions: (1) Will hierarchical CPAP desensitization combined with cognitive-imagery therapy reduce patients’ anxieties or other unpleasant or stigmatizing feelings about the mask and pressurized airflow? (2) Will improved nasal airflow with Breathe Right nasal strips (CNS; Minneapolis, MN) diminish sleep maintenance problems? In our view, much more research is urgently needed to determine the prevalence and pathophysiology of complex insomnia and how to treat it effectively.19
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