Elsevier

Sleep Medicine Reviews

Volume 10, Issue 4, August 2006, Pages 215-245
Sleep Medicine Reviews

Theoretical review
The attention–intention–effort pathway in the development of psychophysiologic insomnia: A theoretical review

https://doi.org/10.1016/j.smrv.2006.03.002Get rights and content

Summary

Psychophysiologic insomnia (PI) is the most common form of persistent primary insomnia. Its ‘behavioral phenotype’, comprising elements such as conditioned arousal, sleep-incompatible behavior and sleep preoccupation, has not changed markedly across several generations of diagnostic nosology. Moreover, a substantial outcome literature demonstrates that PI can be treated effectively using a range of psychological interventions. It seems evident that behavioral and cognitive factors play a part. What is less clear is exactly how PI develops and what are its crucial maintaining factors. This paper proposes an explanatory model, that we call the attention–intention–effort pathway. The argument is that sleep normalcy is a relatively automatic process. Consequently, it is vulnerable, and may be inhibited, by focused attention and by direct attempts to control its expression. Drawing upon parallels in the literature on adult psychopathology, and upon recent clinical and experimental studies on insomnia, the evidence for this pathway is considered and a research agenda is outlined. In particular, computerized tests of cognitive bias are seen as offering an objective means of appraising mental processes in insomnia. These may be applied concurrently with somatic measurements in future studies to better understand this common psycho-physiologic condition.

‘Sleep (is like) a dove which has landed near one's hand and stays there as long as one does not pay any attention to it; if one attempts to grab it, it quickly flies away’

(Viktor E. Frankl (1965, p. 253): [Frankl VE. The Doctor and the soul. 2nd ed. New York: Knopf; 1965.] cited in Ansfield, Wegner and Bowser (1996) [Ansfield ME, Wegner DM, Bowser R. Ironic effects of sleep urgency. Behav Res Ther 1996;34:523–31.]

Introduction

In this paper, we propose a possible pathway for the development and maintenance of persistent psychophysiologic insomnia. Our thinking is guided by predictions from recently described insomnia models, by the relevant literature, including work undertaken in other disorders, and by recent experimental data.

Section snippets

Psychophysiologic insomnia

Psychophysiologic insomnia (PI) is the most common insomnia sub-type, found in 1–2% of the general population, and in 12–15% of all patients seen at sleep centers. According to clinical nosologies3, 4, 5 and research diagnostic criteria,6 the central pillars of PI are heightened arousal and learned sleep-preventing associations, with patients exhibiting an excessive focus upon and anxiety about sleep. A number of models has been proposed, each placing somewhat differing emphases upon these

The attention–intention–effort pathway

This idea has its origins in the psychobiological inhibition model of insomnia (Espie, 2002),13 which differs from most other conceptualisations in that it takes as its starting point a perspective upon normalcy rather than pathology. The model considers what it takes to upset the course of normal good sleep, and to prevent (inhibit) its recovery. Lundh and Broman (2000)14 similarly reflected on the importance in insomnia research of having “a sufficiently adequate understanding of how the

Discussion

In this paper, we have argued for an expansion of experimental cognitive research on insomnia, and have focused upon evidence relevant to the appraisal of what we believe may represent (for Psychophysiologic Insomnia at least) one critically important sleep inhibitory process: the attention–intention–effort pathway. Consistent with our starting point of understanding how PI differs from sleep normalcy,13 we have suggested that the involuntary and automatic nature of the ‘two process’ sleep

Acknowledgements

Supported by research grants from the Chief Scientist Office, Scottish Executive (CZH/4/Z), Cancer Research UK (C8265/A3036), The Wellcome Trust (070969/Z/03/Z) and support from the Mortimer and Theresa Sackler Foundation. The authors are grateful to Dr Allison G. Harvey (University of Berkeley, CA) for her helpful comments and suggestions during the preparation of this paper.

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