Insomnia

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Theories and Models of Insomnia

Insomnia’s development and maintenance has been conceptualized in various theoretical models. These models can assist in providing a rationale for a specific treatment formulation. This chapter will briefly describe early behavioral models of insomnia and then present newer models that have refined the earlier theories by incorporating cognitive perspectives. Early biological perspectives explaining insomnia that focus on physiological hyperarousal will also be described. These initial models serve as the foundation for a discussion of more recent neurobiological models of insomnia that are being proposed as advances in neuroimaging technology permit us to better understand brain function. Finally, a framework that integrates these multiple approaches to understanding insomnia will be presented. Before discussing the insomnia models, a brief description of the normal sleep–wake process will be presented.

2.1 Fundamentals of Sleep–Wake Regulation

Behavioral interventions often incorporate a psychoeducational module that provides a rationale for treatment to facilitate patients’ acceptance of, and adherence to, treatment. Similarly, CBT-I integrates a psychoeducational component that incorporates concepts associated with the sleep process. The most widely used model of sleep–wake regulation, called the two-process model, is presented here to facilitate a basic understanding of the sleep process and factors that can impede normal sleep.

Borbély (1982) originally described a model that considers the effect of homeostatic processes and circadian influences on sleep and wakefulness. While the two separate processes independently contribute to sleepiness and wakefulness, they occur simultaneously and interact to produce regularity in the sleep–wake cycle.

2.1.1 Homeostatic Process

The homeostatic process (called Process S by Borbely) is a mechanism by which a “sleep drive” or a propensity to fall asleep gradually develops. The longer an individual is awake, the greater is the drive to fall asleep. In turn, once a sleep period is initiated, the sleep drive gradually dissipates. In this context, an increase in the drive to sleep occurs as we spend more time awake. |11|This homeostatic process is driven by sleep-regulating substances, of which adenosine is the most widely studied. Adenosine is a by-product produced as energy is utilized by an active, waking brain. The longer an individual is awake, the more pronounced is the buildup of adenosine and other sleep-regulating substances. Eventually the drive to sleep is overwhelming, and under normal circumstances and without any external influences that might hinder this process, an individual falls asleep.

2.1.2 Circadian Process

The second process described by Borbely is the circadian process (referred to as Process C) that maintains the sleep–wake cycle occurring regularly in an overall period that lasts approximately 24 hrs. This process is driven by an internal clock residing in the suprachiasmatic nucleus of the hypothalamus. This internal clock drives many biological functions that oscillate in 24-hr cycles – for example, internal body temperature, level of arousal, and the release of cortisol. Daily synchronization or entrainment of this internal clock helps to ensure that this 24-hr regularity is maintained. This entrainment process occurs via exposure to sunlight and other cues that can provide synchronization (such as alarm clocks or meal times). Under normal circumstances, the circadian process influences sleep by synchronizing the sleep period to occur at approximately the same time every day.

2.1.3 Interaction of Homeostatic and Circadian Processes

Homeostatic and circadian processes interact with each other to either maintain wakefulness or induce sleep (Figure 1). As the homeostatic drive builds up throughout the day, the propensity to sleep increases. However, arousal level – driven by circadian influence – is also building up during the day, counterbalancing the sleep drive and helping to maintain wakefulness. Into the evening hours, the alertness provided by circadian factors begins to wane, and concomitantly with the increasing sleepiness fostered by the homeostatic sleep drive, sleep eventually is induced. Over the nighttime period as sleep progresses, the sleep drive associated with homeostatic factors diminishes and the rhythmicity of the circadian process begins to build up once more to facilitate wakefulness.

While these two biological processes work automatically to maintain a regular sleep–wake cycle, many behaviors or activities can disrupt each process. For example, in the case of homeostatic sleep drive, consumption of caffeine can inhibit the effects of adenosine on the sleep system, and napping late in the day can reduce the buildup of sleep drive. Both of these actions can, in turn, delay the onset of sleep. In turn, the circadian process can be affected by significant daily schedule changes that routinely alter bedtimes and waketimes and, in turn, negatively affect the ability to get sleepy at the same time every night. Dysregulation of these underlying sleep–wake processes may interfere with the ability to fall asleep and stay asleep, and ultimately precipitate insomnia.

2.2 Behavioral Model of Insomnia

The popularity of behaviorism in the 1960s and 1970s influenced thinking about the development of insomnia symptoms. Bootzin (1972) proposed a model of insomnia based on principles of learning theory, and more specifically, operant conditioning. His conceptualization proposed that falling asleep is an instrumental act designed to yield reinforcement – that is, sleep. Any stimulus associated with sleep (e.g., bedroom, bed), therefore, can become a discriminative stimulus for sleep. Bootzin proposed that in insomnia, the stimulus control for sleep is lacking, or alternatively, there are discriminative stimuli present that are not compatible with sleep behavior. In essence, the environment and stimuli that are traditionally associated with sleep are no longer discriminative stimuli for sleep behaviors and instead are associated with wakefulness. For individuals experiencing insomnia, being awake in bed increases arousal and frustration which, in turn, leads to greater concern and anxiety about falling asleep and/or staying asleep. Moreover, behaviors such as tossing and turning in bed, watching the clock constantly, and catastrophizing about lack of sleep occur frequently. During this process, the surrounding environment begins to be associated with the unpleasant experience of being awake, and stimuli that normally should be discriminative for sleep (such as the bed or bedroom) are no longer soporific and become discriminative cues for wakefulness. Often individuals with insomnia will report feeling sleepy |13|in the moments leading up to bedtime only to find themselves wide awake once in bed. Their sleep environment becomes associated with cues associated with wakefulness. This is often referred to as conditioned arousal. It is not uncommon for these individuals to report much better sleep when they find themselves sleeping outside of their habitual sleep environment (e.g., a different room, in a hotel), as these other settings do not contain the conditioned stimuli for wakefulness that exist in their normal sleeping environment. This model is widely accepted by sleep specialists, and CBT-I generally incorporates stimulus control techniques to extinguish the arousal experienced in the normal sleep environment.

2.3 Cognitive Models of Insomnia

Various cognitive models have been proposed to explain underlying cognitive processes that may predispose an individual to insomnia or perpetuate its symptoms. In parallel with psychology’s recognition of the importance of the role cognitions play in influencing behavior, Morin (1993) described the role of sleep-related dysfunctional beliefs and...