Insomnia

Insomnia is most often defined by an individual’s report of sleeping difficulties. While the term is sometimes used in sleep literature to describe a disorderdemonstrated 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:

  • insomnia as secondary to another condition,
  • primary insomnia co-morbid with one or more conditions, or
  • free-standing primary insomnia.

Types of insomnia

Insomnia can be classified as transient, acute, or chronic.

  1. Transient insomnia lasts for less than a week. It can be caused by another disorder, by changes in the sleep environment, by the timing of sleep, severe depression, or by stress. Its consequences – sleepiness and impaired psychomotor performance – are similar to those of sleep deprivation.
  2. Acute insomnia is the inability to consistently sleep well for a period of less than a month.
  3. Chronic insomnia lasts for longer than a month. It can be caused by another disorder, or it can be a primary disorder. Its effects can vary according to its causes. They might include muscular fatigue, hallucinations, and/or mental fatigue; but people with chronic insomnia often show increased alertness. Some people that live with this disorder see things as if they are happening in slow motion, wherein moving objects seem to blend together. Can cause double vision.
Potential complications of insomnia

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.

Major depression leads to alterations in the function of the hypothalamic-pituitary-adrenal axis, causing excessive release of cortisol which can lead to poor sleep quality.

Nocturnal polyuria, excessive nighttime urination, can be very disturbing to sleep.

Subjective insomnia

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 they, in fact, slept a full 8 hours.

Causes and co-morbidities

Symptoms of insomnia can be caused by or can be co-morbid with:

  • Use of psychoactive drugs or stimulants, including certain medications, herbs, caffeine, nicotine, cocaine, amphetamines, methylphenidate, MDMA and modafinil
  • Use of fluoroquinolone antibiotic drugs, see fluoroquinolone toxicity, associated with more severe and chronic types of insomnia[11]
  • Restless Legs Syndrome, which can cause sleep onset insomnia due to the discomforting sensations felt and the need to move the legs or other body parts to relieve these sensations.
  • Periodic limb movement disorder (PLMD), which occurs during sleep and can cause arousals that the sleeper is unaware of.
  • Pain[12] An injury or condition that causes pain can preclude an individual from finding a comfortable position in which to fall asleep, and can in addition cause awakening.
  • Hormone shifts such as those that precede menstruation and those during menopause
  • Life events such as fear, stress, anxiety, emotional or mental tension, work problems, financial stress, birth of a child and bereavement.
  • Mental disorders such as bipolar disorder, clinical depression, generalized anxiety disorder, post traumatic stress disorder, schizophrenia, obsessive compulsive disorder, Dementia or Excessive Alcohol intake.[13]
  • Disturbances of the circadian rhythm, such as shift work and jet lag, can cause an inability to sleep at some times of the day and excessive sleepiness at other times of the day. Chronic circadian rhythm disorders are characterized by similar symptoms.
  • Certain neurological disorders, brain lesions, or a history of traumatic brain injury
  • Medical conditions such as hyperthyroidism and rheumatoid arthritis[14]
  • Abuse of over-the counter or prescription sleep aids can produce rebound insomnia
  • Poor sleep hygiene, e.g., noise
  • Parasomnias, which include such disruptive sleep events as nightmares, sleepwalking, night terrors, violent behavior while sleeping, and REM behavior disorder, in which the physical body moves in response to events within dreams
  • A rare genetic condition can cause a prion-based, permanent and eventually fatal form of insomnia called fatal familial insomnia.[15]
  • Physical exercise. Exercise-induced insomnia is common in athletes, causing prolonged sleep onset latency.

Treatment

Non-pharmacological

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 effectsdeveloping 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, sleeping only 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.

Medications

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 asbenzodiazepines and newer nonbenzodiazepine drugs can also cause physical dependence, which manifests in withdrawal symptoms if the drug is not carefully tapered down. The benzodiazepine andnonbenzodiazepine 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 are associated with tolerance and dependence. Drugs that may prove more effective and safer than existing drugs for insomnia are in development.

In comparing the options, a systematic review found that benzodiazepines and nonbenzodiazepines have similar efficacy that is 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 not taking medications. In fact, chronic users of hypnotic medications have more regular nighttime awakenings than insomniacs not taking hypnotic medications. A further review of the literature regarding benzodiazepine hypnotic as well as the nonbenzodiazepines concluded that these drugs cause 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. It is preferred that hypnotics be prescribed for only a few days at the lowest effective dose and avoided altogether wherever possible in the elderly.

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