|March 26, 2016|
Insomnia is most frequently defined by an individual's report of sleeping difficulties. While the term is sometimes used in sleep literature to describe a disorder demonstrated by polysomnographic evidence of disturbed sleep, insomnia is often defined as a positive response to either of two questions: "Do you experience difficulty sleeping?" or "Do you have difficulty falling or staying asleep?"
Thus, insomnia is most often thought of as both a sign and a symptom that can accompany several sleep, medical and psychiatric disorders, characterized by persistent difficulty falling asleep and/or staying asleep or sleep of poor quality. Insomnia is typically followed by functional impairment while awake. One definition of insomnia is "difficulties initiating and/or maintaining sleep, or nonrestorative sleep, associated with impairments of daytime functioning or marked distress for more than 1 month."
Insomnia can be grouped into primary and secondary, or comorbid, insomnia. Primary insomnia is a sleep disorder not attributable to a medical, psychiatric, or environmental cause. A diagnosis will usually differentiate between:
Types of insomnia
Insomnia can be classified as transient, acute, or chronic.
Patterns of insomnia
Sleep-onset insomnia is difficulty falling asleep at the beginning of the night, often a symptom of anxiety disorders or the delayed sleep phase disorder .
Nocturnal awakenings are characterized by difficulty returning to sleep after awakening in the middle of the night or waking too early in the morning: middle-of-the-night insomnia and terminal insomnia. The former may be a symptom of pain disorders or medical illness; the latter is often a characteristic of clinical depression .
Poor sleep quality
Poor sleep quality can occur as a result of, for example, restless legs, sleep apnea or major depression. Poor sleep quality is caused by the individual not reaching stage 3 or delta sleep which has restorative properties. There are, however, people who are unable to achieve stage 3 sleep due to brain damage who lead perfectly normal lives.
Nocturnal polyuria, excessive nighttime urination, can be very disturbing to sleep.
Some cases of insomnia are not really insomnia in the traditional sense. People experiencing sleep state misperception often sleep for normal durations, yet severely overestimate the time taken to fall asleep. They may believe they slept for only 4 hours while, paradoxically, sleeping a full 8 hours.
Symptoms of insomnia can be caused by or can be co-morbid with:
Sleep studies using polysomnography have suggested that people who have sleep disruption have elevated nighttime levels of circulating cortisol and adrenocorticotropic hormone They also have an elevated metabolic rate, which does not occur in people who do not have insomnia but whose sleep is intentionally disrupted during a sleep study. Studies of brain metabolism using positron emission tomography (PET) scans indicate that people with insomnia have higher metabolic rates by night and by day. The question remains whether these changes are the causes or consequences of long-term insomnia.
A common misperception is that the amount of sleep required decreases as a person ages. The ability to sleep for long periods, rather than the need for sleep, appears to be lost as people get older. Some elderly insomniacs toss and turn in bed and occasionally fall off the bed at night, diminishing the amount of sleep they receive.
Specialists in sleep medicine are qualified to diagnose the many different sleep disorders. Patients with various disorders including delayed sleep phase syndrome are often mis-diagnosed with primary insomnia. When a person has trouble getting to sleep, but has a normal sleep pattern once asleep, a circadian rhythm disorder is a likely cause.
In many cases, insomnia is co-morbid with another disease, side effects from medications, or a psychological problem. Approximately half of all diagnosed insomnia is related to psychiatric disorders. In depression in many cases "insomnia should be regarded as a co-morbid condition, rather than as a secondary one;" insomnia typically predates psychiatric symptoms. "In fact, it is possible that insomnia represents a significant risk for the development of a subsequent psychiatric disorder."
Knowledge of causation is not necessary for a diagnosis.
It is important to identify or rule out medical and psychological causes before deciding on the treatment for insomnia. Attention to sleep hygiene is an important first line treatment strategy and should be tried before any pharmacological approach is considered. Pharmacological treatments have been used mainly to reduce symptoms in acute insomnia; their role in the management of chronic insomnia remains unclear.
Non-pharmacological strategies are superior to hypnotic medication for insomnia because tolerance develops to the hypnotic effects. In addition, dependence can develop with rebound withdrawal effects developing upon discontinuation. Hypnotic medication is therefore only recommended for short term use, especially in acute or chronic insomnia. Non pharmacological strategies however, have long lasting improvements to insomnia and are recommended as a first line and long term strategy of managing insomnia. The strategies include attention to sleep hygiene, stimulus control, behavioral interventions, sleep-restriction therapy, paradoxical intention, patient education and relaxation therapy.
EEG biofeedback has demonstrated effectiveness in the treatment of insomnia with improvements in duration as well as quality of sleep.
Stimulus control therapy is a treatment for patients who have conditioned themselves to associate the bed, or sleep in general, with a negative response. As stimulus control therapy involves taking steps to control the sleep environment, it is sometimes referred interchangeably with the concept of sleep hygiene. Examples of such environmental modifications include using the bed for sleep or sex only, not for activities such as reading or watching television; waking up at the same time every morning, including on weekends; going to bed only when sleepy and when there is a high likelihood that sleep will occur; leaving the bed and beginning an activity in another location if sleep does not result in a reasonably brief period of time after getting into bed (commonly ~20 min); reducing the subjective effort and energy expended trying to fall asleep; avoiding exposure to bright light during nighttime hours, and eliminating daytime naps.
A component of stimulus control therapy is sleep restriction, a technique that aims to match the time spent in bed with actual time spent asleep. This technique involves maintaining a strict sleep-wake schedule, only sleeping at certain times of the day and for specific amounts of time to induce mild sleep deprivation. Complete treatment usually lasts up to 3 weeks and involves making oneself sleep for only a minimum amount of time that they are actually capable of on average, and then, if capable (i.e. when sleep efficiency improves), slowly increasing this amount (~15 min) by going to bed earlier as the body attempts to reset its internal sleep clock. Bright light therapy, which is often used to help early morning wakers reset their natural sleep cycle, can also be used with sleep restriction therapy to reinforce a new wake schedule. Although applying this technique with consistency is difficult, it can have a positive effect on insomnia in motivated patients.
Paradoxical intention is a cognitive reframing technique where the insomniac, instead of attempting to fall asleep at night, makes every effort to stay awake (i.e. essentially stops trying to fall asleep). One theory that may explain the effectiveness of this method is that by not voluntarily making oneself go to sleep, it relieves the performance anxiety that arises from the need or requirement to fall asleep, which is meant to be a passive act. This technique has been shown to reduce sleep effort and performance anxiety and also lower subjective assessment of sleep-onset latency and overestimation of the sleep deficit (a quality found in many insomniacs).
Cognitive Behavioral Therapy for Insomnia
A recent study found that Cognitive Behavioral Therapy for Insomnia (CBT-I) is more effective than hypnotic medications in controlling insomnia. In this therapy, patients are taught improved sleep habits and relieved of counter-productive assumptions about sleep. Common misconceptions and expectations that can be modified include: (1) unrealistic sleep expectations (e.g., I need to have 8 hours of sleep each night), (2) misconceptions about insomnia causes (e.g., I have a chemical imbalance causing my insomnia), (3) amplifying the consequences of insomnia (e.g., I cannot do anything after a bad night's sleep), and (4) performance anxiety after trying for so long to have a good night's sleep by controlling the sleep process. Numerous studies have reported positive outcomes of combining cognitive behavioral therapy for insomnia treatment with treatments such as stimulus control and the relaxation therapies. Hypnotic medications are equally effective in the short term treatment of insomnia but their effects wear off over time due to tolerance . The effects of CBT-I have sustained and lasting effects on treating insomnia long after therapy has been discontinued. The addition of hypnotic medications with CBT-I adds no benefit in insomnia. The long lasting benefits of a course of CBT-I shows superiority over pharmacological hypnotic drugs. Even in the short term when compared to short term hypnotic medication such as zolpidem ( Ambien), CBT-I still shows significant superiority. Thus CBT-I is recommended as a first line treatment for insomnia.
Many insomniacs rely on sleeping tablets and other sedatives to get rest, with research showing that medications are prescribed to over 95% of insomniac cases. Certain classes of sedatives such as benzodiazepines and newer nonbenzodiazepine drugs can also cause physical dependence which manifests in withdrawal symptoms if the drug is not carefully tapered down. The benzodiazepine and nonbenzodiazepine hypnotic medications also have a number of side effects such as day time fatigue, motor vehicle crashes, cognitive impairments and falls and fractures. Elderly people are more sensitive to these side effects. The non-benzodiazepines zolpidem and zaleplon have not adequately demonstrated effectiveness in sleep maintenance. Some benzodiazepines have demonstrated effectiveness in sleep maintenance in the short term but in the longer term is associated with tolerance and dependence . Drugs are in development which may prove more effective and safer than existing drugs for insomnia.
In comparing the options, a systematic review found that benzodiazepines and nonbenzodiazepines have similar efficacy which was not significantly more than for antidepressants. Benzodiazepines did not have a significant tendency for more adverse drug reactions. Chronic users of hypnotic medications for insomnia do not have better sleep than chronic insomniacs who do not take medications. In fact, chronic users of hypnotic medications actually have more regular nighttime awakenings than insomniacs who do not take hypnotic medications. A further review of the literature regarding benzodiazepine hypnotic as well as the nonbenzodiazepines concluded that these drugs caused an unjustifiable risk to the individual and to public health and lack evidence of long term effectiveness. The risks include dependence , accidents and other adverse effects. Gradual discontinuation of hypnotics in long term users leads to improved health without worsening of sleep. Preferably hypnotics should be prescribed for only a few days at the lowest effective dose and avoided altogether wherever possible in the elderly.
The most commonly used class of hypnotics prescribed for insomnia are the benzodiazepines. Benzodiazepines bind unselectively to the GABAA receptor . These include drugs such as temazepam, flunitrazepam, triazolam, flurazepam, midazolam, nitrazepam and quazepam. These drugs can lead to tolerance , physical dependence and the benzodiazepine withdrawal syndrome upon discontinuation, especially after consistent usage over long periods of time. Benzodiazepines while inducing unconsciousness, actually worsen sleep as they promote light sleep whilst decreasing time spent in deep sleep such as REM sleep. A further problem is with regular use of short acting sleep aids for insomnia, day time rebound anxiety can emerge. Benzodiazepines can help to initiate sleep and increase sleep time but they also decrease deep sleep and increase light sleep. Although there is little evidence for benefit of benzodiazepines in insomnia and evidence of major harm prescriptions have continued to increase.
Nonbenzodiazepine sedative-hypnotic drugs, such as zolpidem, zaleplon, zopiclone and eszopiclone, are a newer classification of hypnotic medications. They work on the benzodiazepine site on the GABAA receptor complex similarly to the benzodiazepine class of drugs. Some but not all of the nonbenzodiazepines are selective for the ??1 subunit on GABAA receptors which is responsible for inducing sleep and may therefore have a cleaner side effect profile than the older benzodiazepines. Zopiclone and eszopiclone like benzodiazepine drugs bind unselectively to ??1, ??2, ??3 and ??5 GABAA benzodiazepine receptors. Zolpidem is more selective and zaleplon is highly selective for the ??1 subunit, thus giving them an advantage over benzodiazepines in terms of sleep architecture and a reduction in side effects. However, there are controversies over whether these non-benzodiazepine drugs are superior to benzodiazepines. These drugs appear to cause both psychological dependence and physical dependence though less than traditional benzodiazepines and can also cause the same memory and cognitive disturbances along with morning sedation.
Alcohol is often used as a form of self-treatment of insomnia to induce sleep. However, alcohol use to induce sleep can be a cause of insomnia. Long-term use of alcohol is associated with a decrease in NREM stage 3 and 4 sleep as well as suppression of REM sleep and REM sleep fragmentation. Frequent moving between sleep stages occurs, with awakenings due to headaches, polyuria, dehydration and diaphoresis. Glutamine rebound also plays a role as when someone is drinking, alcohol inhibits glutamine, one of the body's natural stimulants. When the person stops drinking, the body tries to make up for lost time by producing more glutamine than it needs.
The increase in glutamine levels stimulates the brain while the drinker is trying to sleep, keeping them from reaching the deepest levels of sleep. Stopping chronic alcohol use can also lead to severe insomnia with vivid dreams. During withdrawal REM sleep is typically exaggerated as part of a rebound effect.
Opioid medications such as hydrocodone, oxycodone, and morphine are used for insomnia which is associated with pain due to their analgesic properties and hypnotic effects. Opioids can fragment sleep and decrease REM and stage 2 sleep. By producing analgesia and sedation, opioids may be appropriate in carefully selected patients with pain-associated insomnia.
Some antidepressants such as amitriptyline, doxepin, mirtazapine, and trazodone can often have a very strong sedative effect, and are prescribed off label to treat insomnia. The major drawback of these drugs is that they have properties which can lead to many side effects, for example; amitriptyline and doxepin both have antihistaminergic, anticholinergic and antiadrenergic properties which contribute to their side effect profile, while mirtazapines side effects are primarily antihistaminergic, and trazadones side effects are primarily antiadrenergic. Some also alter sleep architecture. As with benzodiazepines, the use of antidepressants in the treatment of insomnia can lead to withdrawal effects; withdrawal may induce rebound insomnia.
Mirtazapine is known to decrease sleep latency, promoting sleep efficiency and increasing the total amount of sleeping time in patients suffering from both depression and insomnia.
Melatonin and melatonin agonists
The hormone melatonin, sold as a " dietary supplement" in some countries, is effective in several types of insomnia. Melatonin has demonstrated effectiveness equivalent to the prescription sleeping tablet zopiclone in inducing sleep and regulating the sleep/waking cycle. One particular benefit of melatonin is that it can treat insomnia without altering the sleep pattern which is altered by many prescription sleeping tablets. Another benefit is it does not impair performance related skills.
Melatonin agonists, including ramelteon (Rozerem) and tasimelteon, seem to lack the potential for misuse and dependence. This class of drugs has a relatively mild side effect profile and low likelihood of causing morning sedation. While these drugs show good effect for the treatment of insomnia due to jet lag and the chronic circadian rhythm disorders, the results for other forms of insomnia are less promising.
The antihistamine diphenhydramine is widely used in nonprescription sleep aids such as Benadryl. The antihistamine doxylamine is used in nonprescription sleep aids such as Unisom (USA) and Unisom 2 (Canada). In some countries, including Australia, it is marketed under the names Restavit and Dozile. It is the most effective over-the-counter sedative currently available in the United States, and is more sedating than some prescription hypnotics.
While the two drugs mentioned above are available over the counter in most countries, the effectiveness of these agents may decrease over time and the incidence of next-day sedation is higher than for most of the newer prescription drugs. Anticholinergic side effects may also be a draw back of these particular drugs. Dependence does not seem to be an issue with this class of drugs.
Cyproheptadine is a useful alternative to benzodiazepine hypnotics in the treatment of insomnia. Cyproheptadine may be superior to benzodiazepines in the treatment of insomnia because cyproheptadine enhances sleep quality and quantity whereas benzodiazepines tend to decrease sleep quality.
Low doses of certain atypical antipsychotics such as quetiapine, olanzapine and risperidone are also prescribed for their sedative effect but the danger of neurological, metabolic and cognitive side effects make these drugs a poor choice to treat insomnia. Over time, quetiapine may lose its effectiveness as a sedative. The ability of quetiapine to produce sedation is determined by the dosage. Higher doses (300 mg - 900 mg) are usually taken for its use as an antipsychotic, while lower doses (25 mg - 200 mg) have a marked sedative effect, e.g. if a patient takes 300 mg, he/she will more likely benefit from the drug's antipsychotic effects, but if the dose is brought down to 100 mg, it will leave the patient feeling more sedated than at 300 mg, because it primarily works as a sedative at lower doses.
Eplivanserin is an investigational drug with a mechanism similar to these antipsychotics, but probably with less side effects.
Insomnia may be a symptom of magnesium deficiency , or low magnesium levels, but this has not yet been proven. A healthy diet containing magnesium can help to improve sleep in individuals without an adequate intake of magnesium.
L- Arginine L-aspartate, S-adenosyl-L-homocysteine and Delta sleep-inducing peptide (DSIP) may be also helpful in alleviating insomnia. There is some evidence showing that 3 grams of L- Glycine before bedtime improves sleep quality.
A survey of 1.1 million residents in the United States conducted by the American Cancer Society found that those who reported sleeping about 7 hours per night had the lowest rates of mortality, whereas those who slept for fewer than 6 hours or more than 8 hours had higher mortality rates. Getting 8.5 or more hours of sleep per night increased the mortality rate by 15%. Severe insomnia - sleeping less than 3.5 hours in women and 4.5 hours in men - also led to a 15% increase in mortality. However, most of the increase in mortality from severe insomnia was discounted after controlling for co-morbid disorders. After controlling for sleep duration and insomnia, use of sleeping pills was also found to be associated with an increased mortality rate.
The lowest mortality was seen in individuals who slept between six and a half and seven and a half hours per night. Even sleeping only 4.5 hours per night is associated with very little increase in mortality. Thus mild to moderate insomnia for most people is associated with increased longevity and severe insomnia is only associated with a very small effect on mortality.
As long as a patient refrains from using sleeping pills there is little to no increase in mortality associated with insomnia but there does appear to be an increase in longevity. This is reassuring for patients with insomnia in that despite the sometimes unpleasantness of insomnia, insomnia itself appears to be associated with increased longevity.
Insomnia is 40% more common in women than in men.
The National Sleep Foundation's 2002 Sleep in America poll showed that 58% of adults in the U.S. experienced symptoms of insomnia a few nights a week or more. Although insomnia was the most common sleep problem among about one half of older adults (48%), they were less likely to experience frequent symptoms of insomnia than their younger counterparts (45% vs. 62%), and their symptoms were more likely to be associated with medical conditions, according to the poll of adults between the ages of 55 and 84.
As explained by Thomas Roth, estimates of the prevalence of insomnia depend on the criteria used as well as the population studied. About 30% of adults report at least one of the symptoms of insomnia. When daytime impairment is added as a criterium, the prevalence is about 10%. Primary insomnia persisting for at least one month yields estimates of 6%.
GNU Free Documentation License. It uses material from the Wikipedia article "Insomnia Prevention".
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