A cognitive model of insomnia

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Abstract

Insomnia is one of the most prevalent psychological disorders, causing sufferers severe distress as well as social, interpersonal, and occupational impairment. Drawing on well-validated cognitive models of the anxiety disorders as well as on theoretical and empirical work highlighting the contribution of cognitive processes to insomnia, this paper presents a new cognitive model of the maintenance of insomnia. It is suggested that individuals who suffer from insomnia tend to be overly worried about their sleep and about the daytime consequences of not getting enough sleep. This excessive negatively toned cognitive activity triggers both autonomic arousal and emotional distress. It is proposed that this anxious state triggers selective attention towards and monitoring of internal and external sleep-related threat cues. Together, the anxious state and the attentional processes triggered by it tricks the individual into overestimating the extent of the perceived deficit in sleep and daytime performance. It is suggested that the excessive negatively toned cognitive activity will be fuelled if a sleep-related threat is detected or a deficit perceived. Counterproductive safety behaviours (including thought control, imagery control, emotional inhibition, and difficulty problem solving) and erroneous beliefs about sleep and the benefits of worry are highlighted as exacerbating factors. The unfortunate consequence of this sequence of events is that the excessive and escalating anxiety may culminate in a real deficit in sleep and daytime functioning. The literature providing preliminary support for the model is reviewed and the clinical implications and limitations discussed.

Introduction

The National Sleep Foundation reported the prevalence of insomnia in the United States to be 33% with 9% of participants reporting insomnia on a regular nightly basis and 24% reporting that it occurs occasionally, especially during stressful life events (Ancoli-Israel & Roth, 1999). Insomnia has been linked to daytime fatigue, greater medical service utilisation, self-medication with alcohol or over-the-counter medication, greater functional impairment, greater work absenteeism, impaired concentration and memory, decreased enjoyment of interpersonal relationships, and increased risk of serious medical illness and traffic and work accidents (American Psychiatric Association, 1994; Edinger & Wohlgemuth, 1999; Roth & Ancoli-Israel, 1999). There is high comorbidity between insomnia and a range of psychological disorders, especially depression, anxiety, and substance abuse (Morin & Ware, 1996; Ohayon, Caulet, & Lemoine, 1998). Insomnia is often trivialised and attributed to these ‘psychiatric’ causes. However, the evidence suggests that insomnia is unlikely to be merely consequential to these disorders, but rather is a risk factor for and may even be causal in their development (for review see Harvey, 2001a, Lichstein, 2000).

Insomnia is a complex disorder of heterogeneous aetiology that may include physical disorders, substances, circadian rhythm disturbances, psychological factors, and poor sleep habits (Bootzin, Mauber, Perlis, Salvio, & Wyatt, 1993). Deciphering the complexities has been hampered by a lack of agreement on standard criteria to diagnose insomnia. The Diagnostic and Statistical Manual of Mental Disorders, 4th Edition (DSM-IV; American Psychiatric Association, 1994), the International Classification of Sleep Disorders — Revised (ICSD-R; American Sleep Disorders Association, 1997), and the International Classification of Diseases, 10th Edition (ICD-10; World Health Organization, 1992) all present vastly differing diagnostic criteria. Further, the unwieldy and under-researched 38 different insomnia subtypes defined by the ICSD-R have generated controversy as to the correct inclusion/exclusion criteria for research and the appropriate assessment procedures. Despite these obstacles, a range of coherent contributions have been made to the understanding and treatment of insomnia. Perspectives taken have included physiological (Bonnet & Arand, 1997), behavioural (Bootzin, 1972; Spielman, Saskin, & Thorpy, 1987), cognitive behavioural (Espie, 1991, Morin, 1993), chronobiological (Campbell, Murphy, van den Heuvel, Roberts, & Stauble, 1999), and biochemical (Doble, 1999, Haefely, 1990, Vogel, 1992). The purpose of this paper is to introduce a cognitive model of the maintenance of insomnia. The cognitive perspective was chosen as the ‘cognitive revolution’ which has lead to vast improvements in theoretical models and treatments for several psychological disorders (Clark & Fairburn, 1997), advances that to date have been minimally applied to insomnia. Indeed, in a recent review of the efficacy of psychological treatments for insomnia the American Academy of Sleep Medicine concluded that the cognitive approach has received insufficient evaluation (Chesson et al., 1999, Morin et al., 1999). At the outset it must be emphasised that the model focuses on delineating processes involved in the maintenance of the disorder rather than the original cause. Two key benefits of specifying a theoretical model of the maintenance of a disorder are: (1) to delineate specific testable predictions and (2) to allow the development of interventions to reverse the maintaining processes (Clark, 1997). The former is specified throughout the body of the paper and a section toward the end of the paper is devoted to the latter.

This model has primarily been developed to explain the maintenance of DSM-IV defined primary insomnia. In order to meet criteria for primary insomnia: (1) the predominant complaint must be a difficulty with initiating or maintaining sleep or nonrestorative sleep for at least one month (Cluster A); (2) the complaint must cause clinically significant distress or impairment (Cluster B); and (3) it must not occur exclusively as a result of another sleep or mental disorder (Clusters C and D) nor as a result of the effects of substance or illness (Cluster E). A tentative proposal requiring empirical validation, is that while the original cause of the insomnia may be psychiatric, circadian, medical or drug-induced, cognitive processes contribute to maintenance.

The model draws heavily from and owes much to theorising relating to a range of psychological disorders (Barlow, 1988, Beck, 1976; Clark & Fairburn, 1997; Ehlers & Clark, 1999; Fairburn, Shafran, & Cooper, 1999; Rapee & Heimberg, 1997; Salkovskis, 1996) as well as to psychological theories of insomnia (Borkovec, 1979, Borkovec, 1982, Espie, 1991, Lundh, 1998, Morin, 1993; Perlis, Giles, Menselson, Bootzin, & Wyatt, 1997). In particular, a central notion in recent work relating to anxiety is the identification of processes that prevent automatic correction of distorted beliefs and perceptions (Clark & Fairburn, 1997; Salkovskis, 1996). Many people develop clinically significant anxiety throughout their lives but most recover without intervention (Clark, 1999). Similarly, nearly everyone at one time or other has had a bout of insomnia. What sets apart those who recover without treatment from those who do not recover and need treatment? Clark (1999) proposed six processes that impede natural self-correction of anxiety; safety-seeking behaviours, attentional deployment, spontaneous imagery, emotional reasoning, memory processes, and the nature of the threat representation. Throughout this paper it will be argued that several of these processes are helpful in explaining what sets apart those who have a few sporadic nights of insomnia from those who develop a chronic problem.

Section snippets

Overview of the model

People with insomnia suffer unpleasant intrusive thoughts and excessive and uncontrollable worry during the pre-sleep period (Borkovec, 1979, Borkovec, 1982, Morin, 1993). During wakefulness insomniacs have been similarly characterised. Common descriptors of the daytime state include proneness to anxiety, worry, neuroticism, obsessionality, dysphoria, hypervigilance, and tension (Edinger, Stout, & Hoelscher, 1988; Hauri & Fisher, 1986; Kales & Kales, 1984; Morin, 1993). Accordingly, the entry

Processes operating during the night

In opening this section relating to processes operating during the night, it is important to note that these processes are proposed to be equally relevant to the initial sleep-onset period as to episodes of awakening (as awakenings involve another sleep onset period). As such, the model provides an account of problems with sleep-onset and sleep-maintenance.

Processes operating during the day

A novel feature of the model is that daytime processes are assumed to be of equal importance to the processes that operate during the night. Unfortunately, the role of daytime processes has received minimal attention within the insomnia literature. Accordingly, most of the predictions relating to the day remain to be empirically validated.

Preliminary clinical implications

One implication of the model is that treatment should not aim to increase total sleep time and reduce sleep onset latency. Instead, treatment should aim to: (1) reduce selective attention and monitoring for sleep-related threat cues; (2) correct distorted perception of sleep and daytime deficits; (3) correct erroneous beliefs about sleep; and (4) eliminate the use of counterproductive safety behaviours. Although not yet evaluated in isolation, approaches designed to correct erroneous beliefs

Limitations

A model of the maintenance of insomnia has been proposed. As such, predisposing and precipitating factors have not been covered. Common predisposing factors are likely to include an innate higher arousal setpoint (Bonnet and Arand, 1995, Bonnet and Arand, 1997), tendency to internalise conflicts (Kales et al., 1976), and emotional reactivity and vulnerability to worry (Spielman & Glovinsky, 1997). Likely precipitants to insomnia include life stress (Healey et al., 1981), accident, illness, and

Conclusions

A conceptual model of the way in which cognitive processes may be involved in the maintenance of insomnia has been presented. The central maintaining processes according to the model are selective attention and monitoring, distorted perception of sleep and daytime deficits, erroneous beliefs, and counterproductive safety behaviours. It is proposed that these processes cause an escalation of excessive and increasingly catastrophic worry along with the associated physiological arousal and

Acknowledgements

I am grateful to Dick Bootzin, David M. Clark, Colin Espie, Warren Mansell, Julia Nelson, Ron Rapee, Christina Neitzert Semler, and Nicole Tang for helpful discussions relating to insomnia and for their comments on this paper.

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