Insomnia entails a spectrum of complaints reflecting dissatisfaction with the quality, duration, or continuity of sleep. These complaints may involve problems with falling asleep initially at bedtime (initial insomnia), waking up in the middle of the night and having difficulty going back to sleep (middle insomnia), waking up too early in the morning with an inability to sleep until planned rise time (late insomnia), or a perception of non restorative sleep. Insomnia may be transient, episodic, or persistent over time (Morin & Espie, 2003). Approximately one third of the adult population reports insomnia symptoms, whereas about 10% suffer from an insomnia disorder (Ohayon, 2002).
Along with subjective complaints of poor sleep, individuals with insomnia are often distressed about their sleep and also report significant fatigue and impairments of their daytime functioning. Common sleep-loss related daytime problems include difficulties with attention, concentration, memory, and completion of tasks, and negative mood. Chronic insomnia is also associated with reduced quality of life, decreased productivity, increased absenteeism from work, and increased risk for depression.
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Insomnia may be a primary sleep disorder or it may manifest itself as a co-occurring condition with another psychiatric, medical, or another sleep disorder (National Institutes of Health; NIH , 2005). The International Classification of Sleep Disorders recognizes at least three different subtypes of primary insomnia: psychophysiological, paradoxical, and idiopathic insomnia (American Academy of Sleep Medicine, 2005; AASM).
Up to 35%-40% of all insomnia cases are associated with an underlying psychopathology, with affective and anxiety disorders being the commonest comorbid disorders (Ford & Kamerow, 1989; Breslau et al., 1996). Insomnia may also result from one of several medical conditions such as hyperthyroidism, congestive heart failure, chronic obstructive pulmonary disease, dementia, and pain-related conditions. Several medications and over-the-counter preparations can also interfere with sleep. Insomnia may be a manifestation of an underlying sleep disorder such as restless legs syndrome, periodic limb movements during sleep, or sleep apnea (AASM, 2005). Finally, insomnia can result from circadian factors associated with jet lag, with alterations of the sleep/wake schedules required by shift work, or with a misalignment between endogenous circadian sleep phase and a person's chosen sleep-wake schedule.
Biological factors contributing to insomnia include homeostatic and circadian regulation of the sleep-wake system (Pigeon & Perlis, 2006). Hyperarousal is also considered a central feature of insomnia (Bonnet & Arand, 1996). Physiological markers of hyperarousal include increased heart rate, body temperature, metabolic rate, and cortisol levels. These markers may be state-related and conditioned to sleep-related stimuli or they may reflect a more enduring trait feature present throughout the 24-hour period. There is also evidence of increased cortical arousal in insomnia, as evidenced by higher quantity of fast EEG brain waves (alpha, beta) relative to the lower EEG frequency bands (delta, theta) among individuals with insomnia relative to good sleepers. This increased cortical arousal is consistent with the hypervigilance and racing mind that often characterized insomnia. It is likely that both biological and psychological factors contribute to increase arousal and to interfere with normal initiation and maintenance of sleep.
Psychological and behavioral factors also play an important role in the development and maintenance of insomnia as evidenced by higher levels of pre-sleep cognitive arousal (e.g., intrusive thoughts, worries) and general psychological reactivity among individuals with insomnia relative to good sleepers. Insomniacs also tend to present an anxiety-prone personality style that may predispose them to worry more about sleep. Life events contribute to trigger insomnia, but it is often the reduced ability to cope with daily stressors, combined with increased cognitive arousal at bedtime, that leads to sleep disturbances (Morin & Espie, 2003). Learning and conditioning are also involved in the maintenance or exacerbation of sleep disturbances. Potential risk factors for insomnia include female gender, advancing age, a worry-prone cognitive style, hyperarousal, and a past history of insomnia. For most individuals, insomnia is transient in nature, lasting a few days, and resolving itself once the initial precipitating event has subsided. For others, insomnia may persist long after the initial triggering event has disappeared; other factors would then perpetuate sleep disturbances. The course of insomnia may also be intermittent, with repeated brief episodes of sleep difficulties following a close association with the occurrence of stressful events.
Three types of factors are involved at different points during the course of insomnia.
The figure below (adapted from Spielman & Glovinsky, 1991) illustrates how transient insomnia can evolve into persistent insomnia. Everyone presents, to various degrees, some vulnerability to develop insomnia, which is more or less important depending on individual differences (predisposing factors). Different types of precipitating factor may trigger insomnia, even among those with little vulnerability. Once the initial precipitating event fades away, most people return to normal sleep. For others, perhaps those at greater risk for insomnia, sleep difficulties persist even after the initial precipitating event has been removed or managed. For these people, insomnia develops a life of its own and several psychological and behavioral factors contribute to perpetuate the sleep difficulties over time. Effective management of chronic insomnia must directly target these perpetuating factors.
The first step in treating symptomatic insomnia is to identify and remove contributing factors to the sleep problems. General sleep hygiene recommendations are also useful as preventative strategies. Insomnia-specific therapies include psychological and behavioral interventions, medications, and a variety of complementary and alternative therapies (e.g., dietary and herbal supplements).
The main objective of psychological and behavioral approaches is to alter those factors that perpetuate or exacerbate sleep disturbances.
Although these interventions can be used successfully as single therapies, they can also be effectively combined to improve sleep. Cognitive-behavioral therapy (CBT) that typically combine both cognitive and behavioral therapeutic approaches along with sleep hygiene education is becoming the standard non pharmacological approach for treating chronic insomnia. The efficacy of CBT is well established for treating chronic insomnia and one of its greatest benefits is that it produces long-term sleep improvements (Morin et al., 2006; NIH, 2005).
Medication (prescribed and over-the-counter) is the most common treatment used for insomnia. Only two classes of medications, benzodiazepine-receptor agonists (BRA) and melatonin-receptor agonists, are approved by the Food and Drug Administration of the United States of America for the treatment of insomnia. BRA include the traditional benzodiazepines (e.g., flurazepam, temazepam), and the more recent non-benzodiazepine receptor agonists (e.g., zolpidem, eszopiclone, zaleplon). The most recent hypnotic introduced on the market, ramelteon, is a melatonin-receptor agonist. These agents have all been found effective for the short-term treatment of insomnia. Despite a relative lack of data and no government-approved indication for insomnia, sedating antidepressants, such as the tricyclics, trazodone and mirtazapine, are commonly prescribed agents for treating chronic insomnia. There is relatively little efficacy data regarding the use of these agents specifically for insomnia (NIH, 2005). Overall, pharmacotherapy is a useful therapeutic option to alleviate transient insomnia. The role of long-term use of hypnotics, however, is controversial and there is limited evidence at this time to support this clinical practice. Behavioral approaches, alone or combined with brief pharmacotherapy, should be preferred to continuous long-term use of hypnotics to treat chronic insomnia.
An increasing number of natural (herbal/dietary) products are marketed as sleep aids. Such products include melatonin, valerian roots (valeriana officinalis), passionflower, chamomille, and L-Tryptophan. Despite their popularity and widespread use, there is currently not enough evidence to recommend the use of any herbal and dietary supplements for the management of clinical insomnia. In addition, there are always risks associated with products that are not monitored by government-regulated health agencies. In summary, insomnia is a prevalent public health problem that may be associated with negative psychosocial, economic and health outcomes. Several treatment options are available but the only two interventions that are currently supported by scientific evidence are cognitive behavioral therapy and the benzodiazepine-receptor agonists (NIH, 2005).
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