Moving forward

The review highlights the effectiveness of SRT for primary sleep diary measures in insomnia but questions remain regarding the use and the impact of SRT on sleep and daytime functioning outcomes. Further testing is required to elucidate the effectiveness of this therapy in relation to subjective daytime and, objective measures of sleep as well as physiological functioning. The next chapter will describe the methodology for the assessment of sleep and set the scene for the subsequent experimental chapters.

In chapter four an ecological momentary assessment is used to evaluate subjective point-in-time alterations to daypoint-in-time cognition in those with insomnia through SRT. This new approach hypothesises that daytime levels of cognition and mood will initially deteriorate (acute restriction of sleep) but will then improve beyond baseline levels through SRT. In chapter five, salivary cortisol concentrations are assessed throughout therapy to inform potential changes to hypothalamic-pituitary-adrenal-axis functioning with SRT. A further hypothesis relates to a reduction in salivary cortisol concentrations compared to baseline levels after effective SRT.

The results of these initial studies were used to substantiate the overall assessment of the data in chapter six. Chapter six evaluates the role of objective sleep, temperature and night time plasma cortisol concentrations in response to effective SRT. It was hypothesised that objectively defined sleep would improve, and measures of physiological arousal would reduce (cortisol & core body temperature). Chapter seven is a case control study which evaluates the differences in cerebral metabolism between those with insomnia and healthy good sleeping controls. This was undertaken to: 1. assess whether brain metabolites in individuals with insomnia are different from good sleeping controls and 2. to provide further objective potential markers of insomnia. It was hypothesised that concentrations of brain metabolites would display increased arousal across the brain in line with the hyperarousal theory of insomnia.

81

Chapter 3: Methodology for the assessment of sleep

The contents of this chapter have been accepted for publication as follows:

‘Methodology for the assessment of sleep’, Christopher B. Miller, Simon D. Kyle, Kerri L. Melehan &

Delwyn J. Bartlett, (In Press). In K.A. Babson & M.T. Feldner (Eds.), Sleep and affect: Assessment, Theory, and Clinical Implications. San Diego: Elsevier Academic Press Inc, accepted 23/04/2014.

82

3.1 Abstract

This chapter provides an overview of the assessments and methodology applied in this thesis. The chapter initially focuses on the tools and techniques that are commonly used to diagnose insomnia and other sleep disorders. A number of methods will be covered in this chapter including:

polysomnography, actigraphy, cortisol assessment, magnetic resonance spectroscopy, and subjective measures including self-report questionnaires and sleep diaries. The chapter ends with an overview of the procedures of sleep restriction therapy, participant recruitment and the statistical analysis employed in this thesis.

83

3.2 Introduction

As this chapter has been accepted for publication as an overview of the assessments used in sleep research, the format of this chapter is different to the rest of the thesis. Compared to the accepted version, the chapter has also been modified to provide a specific overview of the assessments and methods employed directly in this thesis. The chapter begins with an overview of sleep and the measurement of sleep (including polysomnography, actigraphy, clinical interviews &

sleep diaries) and then moves on to address subjective assessments of sleepiness and insomnia. The chapter then covers objective measures of cortisol and cerebral metabolism and ends with an overview of sleep restriction therapy for insomnia, the recruitment procedures and statistical analyses used in the data chapters.

Sleep is a complex behaviour that has been described as: “a reversible state of perceptual disengagement and unresponsiveness from the environment” (Carskadon and Dement (2011), p.

16). In addition to perceptual disengagement, normal sleep also consists of closed eyes, postural recumbency, and relative stillness (Carskadon & Dement, 2011; Hirshkowitz, 2004). Although the primary function for sleep is currently unknown many theories exist. Sleep is thought to be necessary for repair of bodily ‘wear and tear’, memory encoding, and learning processes (Colrain, 2011). However, measuring sleep is difficult. The aim and focus of this chapter is to provide an overview of the measures and techniques used in this thesis (see Table 10 for an overview).

Two main processes interact to regulate sleep and wakefulness. The first is the homeostatic drive for sleep, which is commonly referred to as sleep propensity or ‘sleep need/debt’ (Borbély, 1982). Sleep homeostasis is dependent upon the amount of time spent awake and can be quantified physiologically by the main objective measure of sleep, electroencephalography (EEG) (Achermann, Dijk, Brunner, & Borbely, 1993). Cognitive performance and specifically alertness is known to be sensitive to accumulating sleep pressure during the day (Van Dongen & Dinges, 2005). Homeostatic sleep pressure can only be reset through sleep. Secondly, sleep is also governed by the circadian

84

rhythm. Internal biological rhythms have evolved to revolve around the Earth’s solar period of roughly 24 hours (Hirshkowitz, 2004). Such rhythms are endogenously produced and therefore can operate without external time cues (Czeisler et al., 1999). Photic and non-photic cues are used by the body to synchronise the internal clock to the light-dark environment (Czeisler et al., 1999).

Internal circadian timing is known to be controlled by the suprachiasmatic nucleus (SCN). The SCN is the master clock and is located in the hypothalamus, directly above the optic chiasm (Dibner, Schibler, & Albrecht, 2010). Exposure to light synchronises the SCN with the external light dark cycle and serves as the primary circadian time giver for mammals (Czeisler et al., 1999; Stephan & Nunez, 1977).