We have come a long way in understanding this key restorative activity. The history of this field is full of interesting developments and it continues to be a source of fervent research to this day. Learn more about the early days of sleep research, the main milestones and modern developments in the field.
For most of early history, many cultures focused on the interpretation of dreams. Yet, they were largely uninterested in the role of sleep as a factor in human health. Only in the 18th century did scientists actually begin to research sleep patterns. He noticed that the plants continued to grow even in constant darkness and understood that circadian rhythms are independent of the environment. In , a British doctor named John Davy studied the connection between body temperatures and sleep patterns.
This marked the first time in history when rest was studied as a health issue. In the following years, sleep research blossomed as a rich field for scientists.
Constantin von Economo, a Romanian neurologist, went on to identify the hypothalamus as the area of the brain responsible for regulating sleep cycles. In , a German psychiatrist named Hans Berger became the first to record electroencephalogram EEG wave patterns produced by the brain and study the difference between sleep and wakefulness.
In the s, Dr. Based on the severity, it classifies insomnia into three types as follows. Mild insomnia:This term describes an almost nightly complaint of an insufficient amount of sleep or not feeling rested after the habitual sleep episode. It is accompanied by little or no evidence of impairment of social or occupational functioning.
Mild insomnia is often associated with feelings of restlessness, irritability, mild anxiety, daytime fatigue, and tiredness. Moderate insomnia: This term describes a nightly complaint of an insufficient amount of sleep or not feeling rested after the habitual sleep episode. It is accompanied by mild or moderate impairment of social or occupational functioning.
Moderate insomnia is always associated with feelings of restlessness, irritability, anxiety, daytime fatigue, and tiredness. Severe insomnia: This term describes a nightly complaint of an insufficient amount of sleep or not feeling rested after the habitual sleep episode. It is accompanied by severe impairment of social or occupational functioning.
Severe insomnia is associated with feelings of restlessness, irritability, anxiety, daytime fatigue, and tiredness. The treatment of chronic insomnia consists of initially diagnosing and treating the underlying medical or psychological problems. The identification of behaviors that may worsen insomnia follows and stopping or reducing them would help eliminate insomnia. Next, a possible trial of pharmacology can be tried, although the long-term use of drugs for chronic insomnia is controversial.
This is in spite of the fact that the US FDA has approved three medications for the treatment of insomnia with no limitation on the duration of their use. A trial of behavioral techniques to improve sleep, such as relaxation therapy, sleep restriction therapy, and reconditioning, is however useful. Behavioral intervention combined with pharmacologic agents may be more effective than either approach alone.
Non-pharmacologic interventions for insomnia consist primarily of short-term cognitive-behavioral therapies. These methods act primarily by reducing heightened autonomic and cognitive arousal, modifying self-perpetuating maladaptive sleep habits, altering dysfunctional beliefs and attitudes about sleep, and educating patients about healthier sleep practices.
Evidence suggests that stimulus control therapy is effective and well suited for the clinical management of insomnia in the elderly[ 30 ] with effect sizes ranging from 0.
Sleep restriction therapy consists of restricting the amount of time spent in bed to nearly match the subjective amount of time spent sleeping. Periodic adjustments are made usually on a weekly basis until an optimal sleep duration is achieved. Sleep restriction therefore creates a mild state of sleep deprivation and is said to "promote a more rapid sleep onset, more efficient sleep, and less inter-night variability.
Evidence suggests that sleep restriction therapy is moderately effective with effect sizes ranging from 0. Relaxation-based interventions are based on the observation that insomnia patients often display high levels of arousal physiological and cognitive , both at night and during daytime.
Progressive muscle relaxation and biofeedback techniques seek to reduce somatic arousal, whereas attention focusing procedures such as imagery training and thought stopping are intended to lower presleep cognitive arousal e. Additional relaxation therapies e. Cognitive therapy seeks to alter faulty beliefs and attitudes about sleep. Examples of treatment targets for cognitive therapy include having unrealistic sleep expectations e.
The advocates of cognitive therapy believe that "it consists of identifying patient-specific dysfunctional sleep cognitions, challenging their validity, and replacing them with more adaptive substitutes through the use of restructuring techniques such as reattribution training, decatastrophizing, hypothesis testing, reappraisal, and attention shifting. Paradoxical intention is a method that consists of persuading a patient to engage in his or her most feared behavior, i.
Thus, if a patient stops trying to sleep and contrarily attempts to stay awake, performance anxiety will be reduced and sleep may come more easily. This procedure may be conceptualized as a form of cognitive restructuring technique to alleviate performance anxiety. Effect sizes reported have been moderate in sleep latency 0. Sleep hygiene education targets health practices e. Additional recommendations, which tend to overlap with stimulus control and sleep restriction, may also include curtailing daytime napping and time spent in bed.
While poor sleepers are generally better informed about sleep hygiene, they also engage in more unhealthy practices than good sleepers. Thus, the objectives of sleep hygiene are to promote better health practices. In a meta-analysis of sleep hygiene, effect size observed was modest in all parameters.
Having the patient keep a sleep diary for 2 weeks may be helpful. Depending on the findings in the sleep diary, a discussion of sleep hygiene may be beneficial to the patient. Adopting the practices of good sleep hygiene is often helpful regardless of whether the patient has primary insomnia or a sleep disturbance related to a medical condition.
Patients can condition themselves to be insomniacs, and treatment focuses on de-conditioning the patient from associating the bedroom with a place of restlessness. There are three recently published meta-analyses which serve to establish the efficacy of psychological and behavioral methods. Significant effect sizes in sleep latency 0.
Drug treatment is indicated for patients as short-term alleviation of insomnia but is insufficient for long-term management of chronic insomnia.
In combination with behavioral therapy, it however, yields the most durable improvements in sleep patterns. Although clinical trials of pharmacotherapeutic agents recently approved by the FDA have demonstrated their efficacy and safety, common general practice dictates that five basic principles be followed which characterize rational pharmacotherapy for insomnia, especially chronic insomnia, in both adult and geriatric patients:[ 43 ] using the lowest effective dose, using intermittent dosing two to four times weekly , prescribing medication for short-term use i.
These drugs carry the highest level of evidence supporting efficacy and safety. Benzodiazepines are frequently prescribed to treat insomnia. These hypnotics reduce latency to sleep onset and total awakenings by increasing total sleep duration.
Benzodiazepines enhance the effect of the inhibitory neurotransmitter gamma-amino butyric acid GABA by increasing the affinity of GABA for its receptor. Benzodiazepines non-selectively bind to an allosteric site and affect the GABA-A receptor complex to allow a greater number of chloride ions to enter the cell when GABA interacts with the receptor and therefore enhance the inhibitory action of GABA.
This accounts for their sedative, anxiolytic, myorelaxant, and anticonvulsant properties. Five benzodiazepines estazolam, flurazepam, quazepam, temazepam, and triazolam have an FDA-approved indication for the management of insomnia.
Dose, distinguishing pharmacokinetic properties absorption rate, distribution, and elimination half-life , and risk-benefit ratio should be considered when selecting the most appropriate medication. The lowest effective dose should be used to minimize side effects, and long-acting benzodiazepines with active metabolites should be avoided in the elderly. Major side effects of short-acting benzodiazepines include rebound insomnia and anterograde amnesia.
Intermediate-and longer-acting benzodiazepines are less effective for inducing sleep, but are indicated for sleep maintenance and decreasing nocturnal awakenings. Accumulation of active metabolites is problematic in elderly patients and in those patients with impaired liver function as it can cause confusion and cognitive dysfunction.
Benzodiazepines are contraindicated in patients with acute alcohol intoxication with depressed vital signs, a history of substance abuse, and during pregnancy. Benzodiazepines should be used cautiously in patients with chronic pulmonary insufficiency or untreated sleep apnea.
They are frequently used in mood disorders but a worsening of the dysphoric symptoms and precipitation of suicide has been noted in depression, while hypomania or frank mania and paradoxical hyper-excited states can also occur.
Non-benzodiazepine hypnotics include zopiclone, zolpidem, and zaleplon. Zopiclone is a non-benzodiazepine hypnotic of the cyclopryrrolone class. It is effective for reducing sleep latency and nocturnal awakenings and increasing total sleep time.
Zopiclone delays the onset of rapid eye movement REM sleep but does not reduce consistently the total duration of REM periods. Rebound effects have been reported but are minimal. The incidence of adverse effects is low at recommended doses 3. Zolpidem is a non-benzodiazepine hypnotic of the imidazopyridine class. It exhibits hypnotic effects with minimal myorelaxant, anticonvulsant, and anxiolytic properties, as it preferentially binds with the GABA-A receptor complexes with an alpha-1 subtype.
Zolpidem is effective for reducing sleep latency and nocturnal awakenings and increasing total sleep time. Rebound effects are minimal. Common side effects include drowsiness, dizziness, and headache. Zaleplon, like zolpidem, belongs to the imidazopyridine class of non-benzodiazepine hypnotics.
The pharmacology of these two drugs is similar; however, zaleplon has an ultra-brief duration of effect. No next-day sedation or rebound insomnia is documented with zaleplon at recommended doses 5—10 mg. Eszopiclone, which is the active stereoisomer of zopiclone, acts as an agonist at benzodiazepine BNZ receptors.
Well absorbed orally, about 3 mg of eszopiclone is equivalent to 10 mg of diazepam. It has also recently been approved for the treatment of insomnia and is the only non-scheduled prescription drug available in the United States for the treatment of insomnia.
It has been shown to be effective in the elderly. These drugs have moderate level of evidence supporting their efficacy and tolerability. Tricyclic antidepressants TCAs such as amitriptyline, doxepin, and nortriptyline are effective for inducing sleep and improving sleep continuity.
The overdose potential of TCAs is greater than with other hypnotic agents, and daytime sedation can be significant. Trazodone is a potent sedating antidepressant. Trazodone improves sleep continuity and is an attractive option in persons prone to substance abuse, as addiction or tolerance is not a problem. Adrenergic blockade can result in oversedation and orthostatic hypotension, especially in elderly patients.
The risk of priapism, a condition of painful, prolonged erection in men, is rare. Other antidepressants used include Mirtazapine due to its sedative properties. Evidence for their efficacy when used alone is relatively weak and hence no specific agent within this group is recommended as preferable to the others in this group. Antihistamines are found in many over-the-counter OTC sleep aids.
These agents are effective for mild insomnia; however, next-day sedation may be a problem. Antihistamines commonly cause psychomotor impairment and anticholinergic effects. Greater severity of insomnia at baseline was associated with higher rates of persistence over time, as one might expect. The data from these studies suggest that once insomnia persists for some unknown time period, remission is unlikely.
One of the major limitations of the longitudinal studies thus far is that they provide only a snapshot of the course of insomnia that is low in resolution, with most assessments occurring with a frequency of once per year. A finer grained analysis is needed in order to resolve phenomena that are conceptualized as occurring within shorter time frames. As important, the current studies only provide descriptive, numerical analyses regarding prevalence, incidence, and persistence.
They do not provide information regarding the process of how insomnia develops over time. In order to accomplish this, longitudinal studies would need to be deployed that have a high sampling resolutions e. What We Know Models of Insomnia Up until the mids there were very few theories regarding the etiology and pathophysiology of insomnia and only two gained widespread acceptance and served as platforms for treatment: the Stimulus Control Model 34 , 35 and the 3 Factor Model. Stimulus Control Perspective Stimulus control, which is based on principles of instrumental conditioning, was originally applied to the problem of insomnia by Bootzin and Nicassio.
When a stimulus is always paired with a single behavior there is a high probability that the stimulus will yield only one response. In a more complex conditioning history, a stimulus is paired with a variety of behaviors and this leads to a low probability that the stimulus will yield only one response.
From the patient point of view, engagement in these behaviors is justified because 1 leaving the bedroom would make it more likely that the bout of wakefulness would be prolonged and 2 staying in bed is restful and thus is somewhat recuperative. From the conditioning point of view, the increase in the number of non-sleep behaviors in the bed and bedroom leads to stimulus dyscontrol: the reduced probability that sleep-related stimuli will occur in association with sleepiness and sleep.
Stimulus dyscontrol can therefore be conceptualized as a problem that grows out of a normal process: instrumental conditioning. The latter, while not an explicit focus of the stimulus control perspective, is also thought to be problem that grows out of a normal process: classical conditioning. Interestingly, patients often allude to this state of affairs when they report being sleepy while watching TV in the living room only to become inexplicably alert and awake upon crossing the threshold into the bedroom.
Most would agree that the stimulus control perspective is compelling. Further, the important role of stimulus dyscontrol as a perpetuating factor for insomnia is supported by the finding that Stimulus Control Therapy which involves reestablishing a one-to-one correspondence between sleep-related stimuli and sleep by eliminating non-sleep activities in the bed and bedroom is highly efficacious.
To date, no prospective study has been undertaken to shown that the transition from acute insomnia to chronic insomnia is associated with an increased occurrence of or time spent in non-sleep related behaviors in the bed and bedroom.
Chronic insomnia occurs as a result of maladaptive coping behaviors perpetuating factors. Predisposing factors include: trait hyperarousal; personality characteristics such as the tendency to worry or ruminate; and social factors, such as incompatible sleep schedules between bed partners and social pressures to sleep according to a non-preferred sleep schedule e.
Precipitating factors are acute occurrences that trigger sleep continuity disturbance. Perpetuating factors refer to the behaviors adopted by the individual, which are intended to compensate for sleep loss.
In the original conceptualization of the behavioral model, Spielman focused on the role of sleep extension. The consequence of sleep extension, however, is the dysregulation of sleep homeostasis. There is no doubt that the Spielman model is powerful and persuasive.
Further, the important role of sleep extension is supported by the findings 1 of low sleep efficiency in patients with insomnia and 2 that Sleep Restriction Therapy, which involves limiting time spent in bed both at night and during the day, is highly efficacious.
To date no prospective study has shown that patients with acute insomnia who develop chronic insomnia do indeed compensate for sleep loss with sleep extension and that this differentiates them from both good sleepers and subjects who recover from acute insomnia.
The Neurocognitive Model The Neurocognitive model 37 , 41 is based on, and is an extension of, the Spielman model. Cognitive Models The cognitive perspective has been, in principle, around since time immemorial and is essentially the proposition that worry has a central etiologic role in the precipitation and perpetuation of insomnia.
Consistent with this view, are the results from a variety of studies that show that patients with chronic insomnia exhibit higher scores on instruments measuring factors related to worry 50 , 51 and that patients with insomnia engage in more sleep-related worry during the pre-sleep period. With respect to the perpetuation of insomnia, the role of worry was not formally explicated until Morin 55 suggested that dysfunctional beliefs about sleep specifically this type of worry may serve to perpetuate insomnia.
This point of view is buttressed by several studies which show that patients with insomnia endorse sleep related dysfunctional beliefs to a greater extent than good sleepers, and that treatment of insomnia is associated with a reduction in these beliefs.
More recently, the cognitive perspective has been greatly elaborated to include an information processing perspective. That is, insomnia not only occurs in association with worry but with a fundamental alteration in the way that individuals perceive, remember, and respond to events related to the experience of insomnia. This paradigmatic shift was nearly simultaneously initiated by the group at Oxford University led by Dr.
Colin Espie. According to the Harvey 2 model , acute insomnia occurs in association with life stress, sub-chronic insomnia occurs with worry about sleeplessness, and chronic insomnia is maintained by selective attention, distorted perceptions of daytime deficits, and counterproductive safety behaviors. Selective attention refers to the development of an attentional set where the individual regularly monitors the internal e. Detection of sleep-related threats increases both cognitive and physiologic arousal and reinforces monitoring behavior and is therefore self-perpetuating.
In addition to the sleep-related alterations in attentional processes, Harvey also points to increased attention to the daytime consequences of insomnia e. Individuals with insomnia are concerned about the consequences of sleeplessness and are thought to selectively attend to daytime problems and attribute these problems exclusively to poor sleep.
Unlike the monitoring that occurs at night which directly interferes with sleep initiation and maintenance , the detection of daytime consequences prompts the engagement of safety behaviors. This term, which is borrowed from the anxiety disorders literature, refers to the engagement of compensatory behaviors which are thought to mitigate the social or personal costs of sleeplessness.
For example, if one is particularly irritable owing to sleep loss, one might avoid social interactions and thereby the occurrence of adverse events. From the patient point of view, this may seem a reasonable strategy and a successful one.
The consequence of the strategy is that safety behaviors become self reinforcing and thus ensures that the insomnia always has daytime effects and this contributes to illness chronicity, if not severity.
It should be noted that the behavioral phenomenon of sleep extension could easily be considered one kind of safety behavioral i. To our knowledge, Harvey and colleagues do not specify that this is the case. That is, whether these factors distinguish between patients with acute and chronic insomnia, and at what point do these factors come into play across the illness trajectory relative to other factors e. The failure to inhibit wakefulness is, in turn, thought to result in two cognitive phenomena.
First, when individuals are unable to sleep, attention is drawn to what is otherwise an automatic process. Increased attention prevents the perceptual and behavioral disengagement necessary for sleep onset to occur. Second, attentional focus produces an intention to sleep, where sleep becomes a purposeful goal; one which cannot be attained simply by virtue of the occurrence of attention and intention. This effort, like enhanced attention and intention, serves only to extend wakefulness.
Both the Harvey and Espie models provide formidable conceptualizations of the role of cognitive processes in the development of chronic insomnia. The models are similar owing to a common focus on attentional processes.
It is also much more elaborative when it comes to diurnal effects of insomnia and how selective attention and safety behaviors in that context serve to make insomnia self-perpetuating. A distinction of the Espie model is that it is more articulate with respect to how the attentional bias comes to be and how it leads to sleep effort, with the latter proposed as a primary precipitating and perpetuating factor.
Finally, the Espie model provides for a paradigmatic shift in how the pathophysiology of insomnia is conceptualized. The central etiologic agent is not hyperarousal, it is the failure to inhibit wakefulness. To date, the sequence as whole has not been evaluated in a longitudinal study from good sleep to chronic insomnia.
Cross sectional studies have provided support for the models to the extent that patients with chronic insomnia exhibit more of these signs than good sleepers, subjects with acute insomnia, or subjects with forms of insomnia that are presumably more biologically based e. Longitudinal studies with limited sampling and large temporal windows i. More specifically, the following issues need to be addressed. The data from this study have been informative and are likely to continue to yield important findings in the future.
This said, the Laval study needs to be followed up with an investigation that has enhanced temporal resolution ideally daily assessments over months to years and uses instruments that allow one to assess the constructs of interest ideally dedicated and validated measures.
Such a study will 1 allow for an assessment of the relative importance of the putative causal factors and 2 position the field to develop not only better therapies but also preventive strategies. Notes Conflicts of Interest. It has been reported that one in every 20 people in Turkey suffers from sleep apnea, which occurs when a person's breathing is interrupted during sleep.
People with untreated sleep apnea stop breathing repeatedly during their sleep, sometimes hundreds of times. This means the brain - and the rest of the body - may not get enough oxygen.
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