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How Do These Approaches Work?
The mechanism of action of behavioral and relaxation approaches can be considered at two levels: (1) determining how the procedure works to reduce cognitive and physiological arousal and to promote the most appropriate behavioral response and (2) identifying effects at more basic levels of functional anatomy, neurotransmitter and other biochemical activity, and circadian rhythms. The exact biological actions are generally unknown.
Pain
There appear to be two pain transmission circuits. Some data suggest that a spinal cord-thalamic-frontal cortex-anterior cingulate pathway plays a role in the subjective psychological and physiological responses to pain, whereas a spinal cord- thalamic-somatosensory cortex pathway plays a role in pain sensation. A descending pathway involving the periaqueductal gray region modulates pain signals (pain modulation circuit). This system can augment or inhibit pain transmission at the level of the dorsal spinal cord. Endogenous opioids are particularly concentrated in this pathway. At the level of the spinal cord, serotonin and norepinephrine appear to play important roles.
Relaxation techniques as a group generally alter sympathetic activity as indicated by decreases in oxygen consumption, respiratory and heart rate, and blood pressure. Increased electroencephalographic slow wave activity has also been reported. Although the mechanism for the decrease in sympathetic activity is unclear, one may infer that decreased arousal (due to alterations in catecholamines or other neurochemical systems) plays a key role.
Hypnosis, in part because of its capacity for evoking intense relaxation, has been reported to reduce several types of pain (e.g., lower back and burn pain). Hypnosis does not appear to influence endorphin production, and its role in the production of catecholamines is not known.
Hypnosis has been hypothesized to block pain from entering consciousness by activating the frontal-limbic attention system to inhibit pain impulse transmission from thalamic to cortical structures. Similarly, other CBT may decrease transmission through this pathway. Moreover, the overlap in brain regions involved in pain modulation and anxiety suggests a possible role for CBT approaches affecting this area of function, although data are still evolving.
CBT also appears to exert a number of other effects that could alter pain intensity. Depression and anxiety increase subjective complaints of pain, and cognitive-behavioral approaches are well documented for decreasing these affective states. In addition, these types of techniques may alter expectation, which also plays a key role in subjective experiences of pain intensity. They also may augment analgesic responses through behavioral conditioning. Finally, these techniques help patients enhance their sense of self control over their illness enabling them to be less helpless and better able to deal with pain sensations.
Insomnia
A cognitive-behavioral model for insomnia (see Figure 1) elucidates the interaction of insomnia with emotional, cognitive, and physiologic arousal; dysfunctional conditions, such as worry over sleep; maladaptive habits (e.g., excessive time in bed and daytime napping); and the consequences of insomnia (e.g., fatigue and impairment in performance of activities).
In the treatment of insomnia, relaxation techniques have been used to reduce cognitive and physiological arousal and thus assist the induction of sleep as well as decrease awakenings during sleep.
Relaxation is also likely to influence decreased activity in the entire sympathetic system, permitting a more rapid and effective "deafferentation" at sleep onset at the level of the thalamus. Relaxation may also enhance parasympathetic activity, which in turn will further decrease autonomic tone. In addition, it has been suggested that alterations in cytokine activity (immune system) may play a role in insomnia or in response to treatment.
Cognitive approaches may decrease arousal and dysfunctional beliefs and thus improve sleep. Behavioral techniques including sleep restriction and stimulus control can be helpful in reducing physiologic arousal, reversing poor sleep habits, and shifting circadian rhythms. These effects appear to involve both cortical structures and deep nuclei (e.g., locus ceruleus and suprachiasmatic nucleus).
Knowing the mechanisms of action would reinforce and expand use of behavioral and relaxation techniques, but incorporation of these approaches into the treatment of chronic pain and insomnia can proceed on the basis of clinical efficacy, as has occurred with adoption of other practices and products before their mode of action was completely delineated.
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