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The Conceptual Framework for CBT-I
While nearly everyone refers to the nonpharmacologic treatment of insom- nia as “cognitive behavioral therapy,” the guiding perspective and princi- ples that govern treatment (and in fact the primary treatments themselves) are behavioral.
The Behavioral Model of Insomnia, put forward by Spielman and Col- leagues in 1987 (17), is the first, most articulated, and most widely cited theory regarding the etiology of chronic insomnia. The perspective provides a powerful point of view: one which is inclusive and allows for explanation, prediction and control. At the heart of the behavioral model is a diathesis- stress perspective which, by taking into account behavioral factors, allows one to (1) conceptualize how acute insomnia develops into a chronic con- dition and (2) conceive of what factors should be targeted for treatment. A schematic representation of the model is presented in Figure 2.1.
In brief, this three factor diathesis-stress model posits that insomnia occurs acutely in relation to both predisposing and precipitating factors and that the chronic form of the disorder is maintained by maladaptive coping behaviors (perpetuating factors). Thus, an individual may be prone to insomnia due to trait characteristics, experiences acute episodes because of precipitating factors, and suffer from a chronic form of the disorder because of behavioral factors.
Interestingly, patients often describe their insomnia in precisely these terms.
Dialogue #1: Patient Description of Insomnia
Patient: I started having trouble sleeping three months ago when I had a job interview. I’ve always been high-strung and a bit of a worrier, but the stress of that interview really did me in. What I don’t under- stand is that I got the job and things have been great ever since, but I still can’t sleep. Its as if the insomnia has a life of its own.
Predisposing factors extend across the entire biopsychosocial spectrum.
Biological factors include hyperarousal/hyperreactivity and/or an inher-
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ently weak sleep generating system. Psychological factors include worry or the tendency to be excessively ruminative. Social factors, although rarely a focus at the theoretical level, include such things as the bed partner keeping an incompatible sleep schedule or social/vocational pressures to sleep according to nonpreferred sleep schedule.
Precipitating factors are acute occurrences that interact with the patient’s predisposition for insomnia to produce transient sleep initiation and/or maintenance problems. As with the Predisposing factors, the factors which precipitate acute insomnia also span the biopsychosocial spectrum. Bio- logical factors include medical illness and injury, where these may either directly or indirectly give rise to insomnia. Psychological factors include acute stress reactions and/or the onset of psychiatric illness. Social factors include changes in the patient’s social environment that require an acute shift in, or disrupt, one’s preferred sleep phase (e.g., the need to provide infant care during the night).
Perpetuating factors refer to the variety of maladaptive strategies that individuals adopt in the face of transient insomnia in the attempt to get more sleep. Research and treatment have focused on two in particular:
excessive time in bed and the increase in non-sleep related behaviors occur- ring in the bedroom. Spielman’s three factor model tends to focus on the former: excessive time in bed. This refers to the tendency of patients with insomnia to go to bed earlier, get out of bed later, and/or nap. Such changes are enacted in order to increase the opportunity to get more sleep.
These behaviors, however, lead to mismatch between sleep opportunity and Figure 2.1. Nature of insomnia over time (Three-factor model from Spielman 1987).
sleep ability. The greater the mismatch the more likely it is that the indi- vidual will spend prolonged periods of time awake during the given sleep period.
While not formally embraced within the Spielman model, the second of the maladaptive strategies is also considered perpetuating factor (the increase in non-sleep related behaviors occurring in the bedroom). This is thought to produce stimulus dyscontrol (a reduced likelihood that bed/bedroom-related stimuli will elicit a singular response given that such stimuli are paired with a wide array of behaviors). This concept is central to Bootzin’s Stimulus Control perspective on insomnia (18).
The power of the behavioral model is that the therapeutic implications are clear. If chronic insomnia occurs primarily in relation to perpetuating factors, then the focus of behavioral treatment should be to eliminate the maladaptive behaviors that perpetuate the illness. That is, the focus of behavior therapy should be to control how much time is spent in bed (match sleep opportunity to sleep ability) and to prevent non-sleep behaviors from occurring in the bedroom. These are of course, the central components of Sleep Restriction (19) and Stimulus Control Therapy (18).
Finally, it is interesting to note that while the behavioral perspective allows for the concept of conditioned arousal, neither the Spielman Model nor Bootzin’s Stimulus Control Perspective embrace the concept. Both, it seems to us, focus on the instrumental side of the behavioral equation; on the behaviors that maintain insomnia. In the case of sleep restriction, it is the behavior of increasing time in bed that leads to the mismatch between sleep opportunity and sleep ability. In the case of stimulus control, it is the nonsleep related behaviors that are engaged in within the sleep environ- ment that weaken the association between sleep related cues and sleep.
Neither perspective, in their original formulations, directly suggests that being awake in bed sets the stage for a classical conditioning phenomena.
The repeated pairing of sleep related cues with wakefulness and/or arousal allows for the possibility that, in chronic insomnia, sleep related cues elicit arousal responses, and do so in the absence of (or in addition to) the other factors that maintain insomnia as a chronic illness.
It may well be the case that conditioned arousal is a final common factor or pathway for chronic insomnia. Put differently, the mismatch between sleep opportunity and sleep ability and poor stimulus control may perpet- uate insomnia but only do so on a contingent basis. If the maladaptive behaviors occur, there is insomnia. If the maladaptive behaviors are modi- fied or blocked, there is no insomnia. If, however, the contingency is protracted, there is the opportunity for a classical conditioning effect: con- ditioned arousal. This factor may perpetuate insomnia non-contingently and contribute to the disorder’s apparently self perpetuating nature. If one takes into account the possibility that Chronic Insomnia may also involve a classical conditioning effect, this allows us a way to understand two of the most reliable findings from the treatment outcome literature. First, CBT-I The Conceptual Framework for CBT-I 9
reliably produces about a 50% reduction in symptoms during the acute treatment phase* (e.g., 3;4). If only the traditional behavioral factors are responsible for chronic insomnia, one has to wonder why there is not a complete response to treatment. Second, following CBT-I patients continue to exhibit improvement over follow up periods as long as 12 months (e.g., 3;5). If only the traditional behavioral factors are responsible for chronic insomnia, one has to wonder why improvements occur beyond the acute treatment phase. If one allows for the possibility of conditioned arousal, then it may be that these effects occur as the conditioned arousal compo- nent abates with time (i.e., the repeated pairing of sleep related cues with sleep extinguishes the conditioned arousal). Thus, one can reasonably posit that classical conditioning or conditioned arousal is a factor in chronic insomnia and is appropriately subsumed under the Behavioral Perspective.
To allow for a representation of this possibility, a version of the four factor Figure 2.2. Nature of insomnia over time (four-factor model). As evident in Figure 2.1, the traditional Spielman Model does not extend to what occurs with treatment.
The model is usually represented as ending with the “chronic phase.” The “Acute Tx” and “+ Response” intervals are included here so that the reader may appreci- ate that (1) CBT-I eliminates the perpetuating factors and in so doing produces about 50% change and (2) the continued improvement over time may be the result of the counter-conditioning of hyperarousal (From Spielman 1987).
* The average 50% change from pre to post treatment applies to the combination of the symptoms that correspond to the patients presenting complaints “Can’t fall asleep” (sleep latency 43% change) and “can’t stay asleep” (wake after sleep onset 55%).
schematic is provided in Figure 2.2 which provides for this additional component.
Please note that while such a model as is presented in Figure 2.2 is plau- sible and well matched to the Behavioral perspective, there are a host of alternative explanations. It may be that with partial improvement (1) patients become more adherent with good maintenance strategies, (2) patients worry less as the problem becomes less frequent/severe, and (3) the stage is set for neurohormonal or functional brain changes that allow for continued recovery, and so on.
The Conceptual Framework for CBT-I 11
