**4.4 Nocturnal panic attacks**

*Psychopathology - An International and Interdisciplinary Perspective*

plays a central role in the maintenance of insomnia.

**4.3 Why is sleep altered in PD?**

stage 1 and stage 2 sleep do not differ between patients with PD and controls. For

A recent literature review highlighted the need for studies to go beyond mere descriptions of sleep disturbances and to investigate the role of sleep disturbances in the development and maintenance of PD [3]. Research on the impact of cognitive activity on sleep yielded important insights into the onset of insomnia in PD. Studies of the possible links between repetitive thought (e.g., worry or rumination) and various sleep characteristics in college students indicated that repetitive thoughts impact sleep [49]. Since patients with PD often worry about having panic attacks, it is possible that reported sleep alterations could be associated with repetitive worry about future panic. This hypothesis is consistent with Harvey's [14] cognitive model of insomnia, which proposes that excess negative cognitive activity

In patients with PD, the content of repetitive thinking often relates to possible panic attacks and their consequences. Patients develop a fear of anxiety itself, i.e., anxiety sensitivity [18, 50]. Researchers have found that, in patients with PD, anxiety sensitivity is linked to insomnia and, in particular, to longer sleep latency [18]. Authors hypothesized that anxiety sensitivity makes patients monitor their anxiety signs and symptoms and could increase levels of cognitive, emotional, and physiological activation [18]. This state of activation could disrupt the healthy course of

Sleep impairment caused by activation could be the beginning of a cycle where anxiety and insomnia mutually feed each other. Evidence suggests that sleep deprivation induces activation and anxiety in the general population [12] and increases the risk of panic in patients with PD [13]. Therefore, it is hypothesized that a sleep deficit could increase the risk of panic by inducing activation and anxiety. Indeed, since patients with PD fear signs of anxiety, the activation and anxiety caused by the sleep deficit trigger more anxiety that can culminate into panic attacks. These panic attacks could further disrupt sleep because of the activation state they caused and apprehensiveness. Future research should aim at verifying the hypothesis of the vicious cycle between panic and insomnia in order to better understand the cognitive, behavioral, and emotional mechanisms behind the sleep disturbances identi-

The majority of the results issued from objective data were consistent with cognitive models of insomnia and PD. In contrast, the finding that patients with PD have shorter stage 2 sleep is not intuitive. One possible explanation for this result is the inclusion of patients with NPA. Since NPA usually occur between stage 2 and stage 3 sleep, there may be a relationship between the presence of NPA and decreased stage 2 sleep. An alternative explanation is that shorter stage 2 sleep is an artifact of overall shorter sleep time. Since stage 2 sleep is the longest stage over the course of a night's sleep (i.e., 45–55% of total sleep time; [51]), the changes in sleep continuity observed in our study (longer sleep latency, lower sleep efficiency, and shorter total sleep time) may be attributable to shorter sleep in all three stages. Since stage 2 occupies the majority of the night, it may be the only stage for which the change can be statistically detected. Indeed, the fact that the percentage of stage 2 sleep observed in patients with PD does not differ significantly from that observed

Gathering detailed data on the nature of subjective and objective insomnia is a first step toward a greater understanding of the mechanisms (e.g., cognitions, anxiety sensitivity, repetitive thinking, etc.) through which insomnia could

other variables, further research is required to confirm existing results.

**106**

sleep [18].

fied in the present study.

in control subjects supports this hypothesis.

This study's secondary aim was to estimate the prevalence rate of NPA. Results indicated that, among patients with PD, 52.1% (95% CI [46.4, 57.7]) experienced at least one lifetime NPA and 27.0% (95% CI [17.9, 38.6]) experienced at least one panic attack in the past month. Furthermore, 40.9% (95% CI [18.1, 68.5]) of patients with PD reported recurrent NPA (at least 1–2/month in the past 6 months) with apprehensiveness about possible future nocturnal attacks. Of the three estimates, the lifetime prevalence obtained here is the most precise and reliable, with a confidence interval ranging from 46.4 to 57.7%. This represents an improvement compared to previously reported estimates: 44–71% in Lee and Douglass [38], 18–69% in Mellman [39], and 33–71% in Papadimitriou and Linkowski [40]. The two other NPA prevalence estimates calculated in our meta-analysis have wider confidence intervals, indicating poorer reliability. The poorer reliability may explain why the prevalence rate is higher using a more restrictive criterion (1/month or/2 months, with apprehensiveness, present since 6 months; 40.9%) than using a less restrictive criterion (one NPA in the past month; 27.0%). These results may be attributable to measurement error rather than to real differences in prevalence.

Some authors have proposed that NPA could be linked to abnormalities in breathing regulation and patterns [52]. Previous research has suggested that patients with PD have chronic hyperventilation [53], which would cause CO2 depletion in the blood [54]. The metabolism would then adapt and become more sensitive to small increases of CO2 in the blood [52]. Since non-REM sleep stages imply a reduced breathing rate and, therefore, a rise in CO2, authors propose that they could be sufficient to induce the physiological reactions and physical sensations that are feared by people with PD [54, 55]. Considering that there have been reports linking nocturnal panic to sleep apnea [56], we could hypothesize that sleep apnea could induce even stronger physiological sensations in people with CO2 hypersensitivity. Therefore, they would be more at risk of having NPA. However, the abnormalities in breathing regulation cannot totally explain the presence of NPA. Cognitive components such as beliefs about physiological sensations and interoceptive conditioning still have to be present in order for NPA to occur.
