|Year : 2019 | Volume
| Issue : 3 | Page : 193-201
Chronic insomnia: A review
Suprakash Chaudhury1, Rakesh Kumar Singh2, Dolly Kumari3, Chetan Diwan4, Swaleha Mujawar1, Daniel Saldanha1
1 Department of Psychiatry, Dr. D. Y. Patil Medical College, Dr. D. Y. Patil Vidyapeeth, Pune, Maharashtra, India
2 Department of Psychiatry, Hind Institute of Medical Science, Lucknow, Uttar Pradesh, India
3 Department of Clinical Psychology, State Institute of Mental Health, Pt. B. D. Sharma University of Health Sciences, Rohtak, Haryana, India
4 Department of Social Work, Karve Institute of Social Service, Pune, Maharashtra, India
|Date of Submission||03-Mar-2019|
|Date of Acceptance||04-Apr-2019|
|Date of Web Publication||15-May-2019|
Department of Psychiatry, Dr. D. Y. Patil Medical College, Pimpri, Pune - 411 018, Maharashtra
Source of Support: None, Conflict of Interest: None
Chronic insomnia is a fairly common condition affecting one-fourth of the clinical population. It has been variously defined and is related to a large number of conditions. A thorough assessment of the patient presenting with chronic insomnia is of vital importance for the treatment. Treatment consists of modifying sleep habits to reduce autonomic and cognitive factors and education about healthier sleep practice. Drug treatment should be reserved for the short-term alleviation of insomnia. Appropriate treatment of chronic insomnia improves the quality of life. The prevention of insomnia consists of a balance of rest, recreational exercise in combination with stress management and a healthy diet.
Keywords: Benzodiazepines, chronic insomnia, cognitive behavior therapy, sleep habits
|How to cite this article:|
Chaudhury S, Singh RK, Kumari D, Diwan C, Mujawar S, Saldanha D. Chronic insomnia: A review. Med J DY Patil Vidyapeeth 2019;12:193-201
| Introduction|| |
Insomnia was the first psychosomatic disorder described by Johann Heinroth in 1818. Patients of insomnia characteristically present with difficulty in falling asleep, waking up often during the night and having trouble going back to the sleep, early morning awakening, and/or unrefreshing sleep., Most research studies adopt an arbitrary definition of insomnia as a delay of ≥30 min in sleep onset or sleep efficiency (the ratio of time asleep to time in bed) of <85%. Chronic insomnia is defined as difficulty with initiating or maintaining sleep at least 3 nights a week for at least 3 months.
| Epidemiology|| |
An estimated 6%–10% of the adult population suffers from chronic insomnia. However, insomnia is often underrecognized, underdiagnosed, and undertreated. The prevalence of chronic insomnia increases with age and is more common in women. Chronic insomnia interferes with personal functioning and causes distress, fatigue, poor cognitive functioning, and mood disturbance. The prevalence of chronic insomnia in a family medicine outpatient department in Bengaluru was 33%, and it was associated with increasing age and diabetes. In the elderly, 15%–45% had initial insomnia, 20%–65% middle insomnia, and 15%–54% late insomnia whereas 10% had poor sleep quality. In the elderly, chronic insomnia causes slower reaction times, greater difficulty in maintaining balance, and increased risk of falls resulting in increased risk of mortality. Chronic insomnia results in attention and memory deficits which could be misinterpreted as mild cognitive impairment or dementia.,
| Natural History|| |
One study found a remission rate of 13.1% after a 4-month follow-up in a population suffering from insomnia for 1 month or more.
| Pathophysiology|| |
Insomnia is a disorder of hyperarousal manifesting with problems in initiating and maintaining sleep at nighttime and daytime hypervigilance. Chronic activation of the neuroendocrine system's stress response causes this hyperarousal as shown by high levels of both cortisol and adrenocorticotropic hormone and dysregulation of corticotropin-releasing factor.
| Causes of Chronic Insomnia|| |
Although a genetic component is difficult to define except in fatal familial insomnia, a positive family history was present in 35% of people with insomnia.
Neurotransmitters and hormones
Low levels of melatonin (MT) were observed in chronic insomnia. The significance of role of MT is unclear due to the lack of consistent studies.
In people with chronic insomnia, cortisol levels were high only when their sleep was of poor quality. When they slept well, levels were lower. Possibly, the high levels of stress hormones are caused by poor sleep, rather than being the cause.
Growth hormone, secreted late in the night, is associated not only with growth but also with deep, slow-wave sleep. Normal aging is associated with a blunting of regular, cyclical surges of growth hormone, which may affect the sleep as one gets older.
Histamine and gamma-aminobutyric acid
These neurotransmitters regulate the sleep-wake switch.
Chronic insomnia and the immune system
Chronic insomnia is associated with higher levels of interleukin-6 and tumor necrosis factor during the day, but lower levels at night. These immune factors cause symptoms of fatigue. The implications of these immune changes in insomnia are not known.
Chronic insomnia often has a psychological or psychiatric basis, namely stress, anxiety, depression, bipolar disorder, schizophrenia, schizoaffective disorders, obsessive-compulsive disorders, dementias, attention deficit disorders, adjustment disorders, personality disorders, bereavement, and posttraumatic stress disorder; alcohol and other substance use/dependence/withdrawal.
Psychophysiologic insomnia occurs when an episode of transient insomnia disrupts the Person's circadian rhythm. The bed is associated not with rest and relaxation but with a struggle to sleep. As a result, a pattern of sleep failure emerges. Overtime, this event repeats, and bedtime becomes a source of anxiety. On the bed, the individual broods over his failure to sleep and the adverse effects of sleep loss, resulting in failure to sleep. Persistent worry about lack of sleep provides an automatic nightly trigger for anxiety and arousal. This is worsened by unsuccessful attempts to control thoughts, images, and emotions about insomnia. After such a cycle is established, insomnia becomes a self-fulfilling prophecy that can persist indefinitely.
| Theoretical Model Of Chronic Insomnia|| |
A conceptual framework to examine the causes of chronic insomnia begins with four general etiological factors (circadian, psychiatric, pharmacological, and medical/neurological) commonly noted in chronic insomnia. All these precipitating factors converge to form common psychological conditioning factors responsible for chronic insomnia [Figure 1].
|Figure 1: Causes of chronic insomnia (modified from Buysse and Reynold, 1990)|
Click here to view
Spielman's model of chronic insomnia classifies insomnia factors as predisposing, precipitating, or perpetuating. Predisposing factors include a tendency toward physiological hyperarousal or decreased homeostatic sleep drive.
Precipitating factors refers to events such as pain, job stress, a noisy sleep environment, or jet lag. Perpetuating factors refers to behavioral and cognitive aspects of insomnia which includes spending too much time in bed, excessive worry about the ability to sleep, a fear of being awake during the night, and increase caffeine intake during the night. These are phenomenon that emerges once an individual is experiencing increased wakefulness at night due to predisposing and precipitating factors. The relative importance of these factors in producing poor sleep, changes over the course of the insomnia. Before the start of the insomnia, each individual is hypothesized to have a certain level of predisposition to insomnia. The introduction of the precipitating factor interacts with the predisposing factor to trigger an episode of insomnia. As the duration of the insomnia increases, perpetuating factor plays an increasing role in maintaining the poor sleep. Although the precipitating factor recedes, sleep remains poor due to the perpetuating factors.
| Evaluation of a Patient With Insomnia|| |
A general characterization of the disorder, i.e., its duration, severity, variation, daytime consequences, and the following specific questions:
- Do you have difficulty primarily in
- Falling asleep
- Staying asleep
- Waking too early
- Combination of the above
- All of the above.
How long you are awake at each junction?When did the sleep problems start?How many nights per week/month does your insomnia occur? Any relation with season, menstruation, or any other cyclical factorsAny daytime consequences of your sleep problem? (fatigue, irritability, and difficulty in concentration)Is your occupation causing the sleep problems? (work schedule, shift duty, and jet lag).
It is of a specific value in estimating the severity of the problem, the night-to-night variability, and the presence of maladaptive sleeping habits such as naps or spending excessive time in the bed (≥8 h). Sleep diary also keeps track of compliance with behavioral intervention and response treatment.
Psychiatric rating scales for sleep
Insomnia severity index
It is a short, self-administered questionnaire, that assesses insomnia severity, satisfaction with sleep, impairment of daytime functioning, the perception of the sleep problem by others and the patient's level of concern.
Pittsburgh sleep quality index
This self-administered questionnaire assesses seven components of sleep quality comprising of quality, onset latency, duration, efficiency, disturbances, use of sleep medication, and daytime dysfunction. It helps in identifying the most affected parts of sleep. The scale had a sensitivity of 88.63%, a specificity of 74.99%, and a positive predictive value of 80.66%.
Presleep arousal scale
This simple self-administered scale consists of two subscales: somatic and cognitive. It helps to identify patients with sleep disturbance and the cognitive features associated with sleep.
Epworth sleepiness scale
This simple, short, self-administered scale rates the chance of dozing in certain situations, and thus provides information about the patient's daytime sleepiness which may be the cause or effect of insomnia at night.
Dysfunctional beliefs and attitudes about sleep questionnaire
This self-rating 28-item questionnaire is used to assess negative cognitions about sleep. A 16-item short form is available in Hindi.
Certain sleep disturbing pathologies such as chronic obstructive pulmonary diseases, asthma, or restless leg syndrome are assessed through physical examination.
These help to rule out subtle manifestations of thyroid diseases, iron deficiency anemia, and Vitamin B12 deficiency.
The gold standard for the assessment of sleep disorders uses EEG, EOG, EMG, ECG, and pulse oximetry to reveal a variety of disorders such as periodic limb movement disorder, sleep apnea, narcolepsy, or precipitous arousals with violent or injurious behavior. However, it is not recommended for routine use in the clinical assessment of insomnia.
Physical activity data, measured with a portable device worn on the wrist, are analyzed to determine sleep and wake time. This approach is useful to characterize circadian rhythm patterns or sleep disturbances in individuals with insomnia.
| The Treatment of Chronic Insomnia|| |
The treatment of chronic insomnia consists of the following:
- First, identify and manage comorbid medical or psychiatric disorders
- A trial of nonpharmacological interventions such as sleep hygiene, cognitive behavior therapy, and sleep restriction therapy
- A possible trial of hypnotics, although the long-term use of hypnotics for chronic insomnia is controversial
- Nonpharmacological interventions combined with pharmacotherapy probably are more effective than either approach alone.
It is based on the principle that since patient's condition themselves to be insomniacs, they can be deconditioned from associating the bedroom with a place of restlessness. Asking the patient to maintain a sleep diary for 2 weeks is very useful, since it provides objective evidence that can help us to improve the sleep hygiene. In addition, attempts are made to reduce behavior (such as lying in bed and worrying) that is not compatible with sleep, by advising the patient to leave the bed at these times.
Sleep hygiene education
Sleep as long as required to feel rested and then get out of bed. Health practices (e.g., diet, exercise, and substance use) and environmental factors (e.g., light, noise, temperature, and mattress) that may be either detrimental or beneficial to sleep are assessed. There are few habits which should be avoided before going to bed such as watching television and mobile phones. Similarly, heavy meals, excessive water intake, tea, coffee, alcohol, and exhausting exercises before bedtime also should be avoided. Our body has an internal clock to sleep and wake up at fix time which is called sleep-wake cycle, so it should be maintained for healthy sleep. The bed should be dedicated for sleep and sex only and not to other works. The patient is asked to follow the same rituals before going to bed which gives a psychological signal to the brain that now it is a time to fall asleep. Sleep hygiene counseling results in some improvement in sleep but less than cognitive-behavioral therapy (CBT) and pharmacotherapy.
Stimulus control therapy
According to this therapy, insomnia is a conditioned response to bedtime and environmental cues associated with sleep. When a patient is tossing and turning on the bed for a long time, the body learns to be awake on the bed or an association is made between awakening and bed, which leads to wakefulness. Stimulus control therapy tries to break this association between awakening and bed. Technique used: go to bed only when sleepy. The bed is to be used only for sleep and sex. Do not spend ≥20 min while tossing and turning on the bed. Leave the bed if you do not fall asleep within 20 min and do some relaxing activities and only return when you feel sleepy. Wake up at the regular time regardless of sleep duration at night. Avoid napping during the day. Activities which reward being awake such as watching television, using mobile phone, and eating are avoided. This therapy was found to be effective in randomized trials and its effects may be long lasting.
Relaxation therapies (RTs) are based on the observation that insomnia patients often display high levels of physiological and cognitive arousal. RT helps patients to attain physical and mental relaxation by reducing tension and negative thought process. All these techniques require regular practice over a period of several weeks, and professional guidance is necessary in the initial stage of training. Studies indicate that RTs are helpful for treating insomnia.,
Different types of relaxation techniques are as follows:
Deep breathing helps to reduce the patient's level of physiological and cognitive arousal.
Progressive muscle relaxation
In this technique, the patients progressively produces tightening and relaxing-specific groups of muscles of the whole body one by one to reduce stress and anxiety.
Visualizations and guided imagery
This type of relaxation is a systematic practice of generating detailed mental images and visualization of peaceful, pleasant, and beautiful scenes. Actually, it is a suggestion to the body and unconscious mind that the scenes are real and act accordingly. It results in relaxation and stress reduction which leads to good sleep. This can be done alone or with Jacobson's progressive muscular relaxation.
Meditation is helpful to improve sleep while doing it daytime or before bedtime. Mindfulness meditation has been widely reported to be useful in the treatment of insomnia.,
This is the type of relaxation in which the patient learns to consciously manipulate bodily responses such as breathing, heart rate, and brain activities using visual and auditory feedback from instrument to improve from stress, anxiety, and related insomnia.
This is a self-directed relaxation training which manipulating internal physiological process by focusing consciously on different body parts one by one. It emphasizing on making specific body parts warm and heavy through self-suggestion.
Cognitive therapy (CT) deals with patient's exaggerated and unrealistic beliefs about sleep. It discovers the patient's unhealthy belief and attitude about sleep and changes into a positive one. Patients often think that if they did not get sleep, the next day would be spoiled since he would feel heaviness in head the whole day and would not be able to do any work. Further, he may think that he would never sleep anymore and this was his destiny. This type of thought can be replaced by a more realistic appraisal on the lines of “yes it did happen with me, but for the last many days, I was able to do my work perfectly despite poor sleep. The occasional heaviness of head may have happened for some other reason. I am practicing the skills and hope it will help me, I should not worry about my sleep.”
CT is frequently combined with relaxation techniques.
CBT seeks to alter faulty beliefs and attitudes about sleep. The objective is to break the vicious cycle of sleep disturbance, mental distress, dysfunctional cognitions, and further sleep disturbances. CBT for insomnia (CBT-I) uses specific components together to change patient's thoughts and education on normal sleep behavior and sleep environment. It helps patients with chronic insomnia to discover, identify, and reframe the negative, unrealistic (e.g., “Every night I must get 8 h of sleep”) and dysfunctional thoughts and attitude of the patients about sleep and exaggerating its consequences (e.g., “With a poor night's sleep I cannot accomplish anything”). It is a goal-directed therapy which also teaches set of skills about how to recover from insomnia if it recurs later in life. It is effective therapy for patients with insomnia to improve sleep satisfaction. A meta-analysis of CBT-I in patients with chronic insomnia revealed significant reductions in self-reported time to sleep onset and time awake after falling asleep. Benefits of therapy were maintained for 6–12 months. Additional advantages of CBT-I include lack of medication side effects., The drawback is that while hypnotics act immediately, CBT-I takes weeks to show its effect.
Sleep restriction therapy consists of curtailing the amount of time spent in bed to more nearly match the subjective amount of time asleep. The patient is asked to maintain a sleep log which reports how many hours patient spends for sleep every day. It also records how many hours have been spent for sleeping and how many hours for tossing and turning on bed. The total time spent in bed and sleeping time are calculated which suggests sleep efficiency (ratio of total sleep/time in bed, ×100%) of the patient. This sleep efficiency is increased gradually while limiting bedtime. Sleep restriction creates a mild state of sleep deprivation and promotes a more rapid sleep onset, more efficient sleep, and less internight variability. To prevent excessive daytime sleepiness, time in bed should not be <5 h per night. Standalone sleep restriction therapy is efficacious for the treatment of chronic insomnia.
Exhausting and body tiring exercises during daytime help to improve sleep. However, it should not be done before bedtime. A systematic review found that exercise is effective in reducing insomnia, with effects similar to those observed after hypnotic medication. In addition, there is evidence of antidepressant and anxiolytic effects of exercise.
This therapy is based on the premise that onset of sleep is inhibited by performance anxiety. Therefore, instead of trying to sleep, if a patient genuinely attempts to stay awake, the performance anxiety will be alleviated and sleep may come easily. The patient is persuaded to engage in his/her most feared behavior, that is, staying awake. Paradoxical intention procedure is effective on several measures of sleep behavior as compared to either placebo or no treatment.
Drug therapy can be effective for short-term alleviation of insomnia but may not be sufficient for long-term management of chronic insomnia [Table 1]. Behavioral therapy, on the other hand, yields the most durable improvements in sleep patterns.
Benzodiazepines (BZDs) enhance the effect of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA). BZDs nonselectively bind to BZD receptor subtypes (1, 2, 3, and 5), which accounts for their sedative, anxiolytic, myorelaxant, and anticonvulsant properties. BZDs should be prescribed in the lowest effective dose to minimize side effects. The accumulation of active metabolites is problematic in elderly patients and those patients with impaired liver function. BZDs are contraindicated in patients with a history of substance abuse and during pregnancy. BZDs should be used cautiously in patients with chronic pulmonary insufficiency or untreated sleep apnea. The long-term use (beyond 4 weeks) is associated with dependence, discontinuation syndrome, psychomotor retardation, difficulty in new learning abilities, memory impairment, emotional anesthesia (blunting of emotions), and disinhibition manifesting as aggressive outburst and precipitation of suicide in depressed patients. Due to the potential for cognitive impairment, delirium, falls, fractures, and BZDs should be avoided in the elderly. Meta-analyses of randomized, placebo-controlled trials indicate that BZDs decrease sleep latency and the number of awakenings, while improving sleep duration and sleep quality.
Zolpidem, a non-BZD hypnotic, exhibits hypnotic effects with minimal myorelaxant, anticonvulsant, and anxiolytic properties, as it preferentially binds with the BNZ-1 receptor. It reduces sleep latency and nocturnal awakenings and increases total sleep time. Rebound effects are minimal. Adverse effects include drowsiness, nausea, headache, dizziness, nightmares, agitation, and in some patients anterograde amnesias.
Although similar to zolpidem, zaleplon has an ultrabrief duration of action. Zaleplon reduces sleep latency but does not reduce nighttime awakenings or increase total sleep time. Adverse effects include headache, dizziness, somnolence, and nausea.
The active stereoisomer of zopiclone predominantly binds with BNZ-2-3 receptors with lesser sensitivity for BNZ-1 receptor. The efficacy of eszopiclone in the treatment of insomnia as measured by sleep latency, total sleep time, and wake time after sleep onset was demonstrated by a 6-month, double-blind, placebo-controlled, parallel-group study of about 800 patients. The common side effects include an unpleasant taste, headache, somnolence, and dizziness., There was no evidence of tolerance or rebound insomnia after a 6-week trial of eszopiclone in patients with primary insomnia.
Ramelteon, a MT agonist reduces both polysomnographic and subjective sleep latencies in patients with chronic insomnia. Side effects include dizziness, nausea, and fatigue, but unlike zolpidem and eszopiclone, it does not affect patients' balance, thereby decreasing the risk of falls. It should be used with caution in pregnancy and is contraindicated in severe hepatic impairment.
Doxepin has a high affinity for H1 receptor is a sedating antidepressant. Review of nine randomized, placebo-controlled studies revealed that low-dose doxepin improved sleep maintenance and duration modestly with no effect on sleep initiation. No daytime somnolence was reported.
Trazodone due to its modulating effect on serotonin (5-HTA) receptors 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 is rare.
Mirtazapine has sedating properties due to antagonistic effects on histamine (H1) receptors.
Tricyclic antidepressants such as amitriptyline, imipramine, and nortriptyline are effective for inducing sleep and improving sleep continuity. They should be prescribed at the lowest effective dose to reduce chances of anticholinergic effects and cardiac conduction prolongation, especially in the elderly.
The most commonly prescribed antipsychotic for insomnia is quetiapine, followed by olanzapine and risperidone. These drugs have not been evaluated in the treatment of with primary insomnia and have serious side effects, such as metabolic syndrome and extrapyramidal effects. Routine use of these drug for the treatment of chronic insomnia is not recommended.
Antihistamines are effective for mild insomnia; however, next day sedation is a problem. Antihistamines commonly cause psychomotor impairment and anticholinergic effects. A randomized, double-blind, cross-over study demonstrated that tolerance to the sedative effect of diphenhydramine develops in 3 days. In addition, diphenhydramine and doxylamine are minimally effective in inducing sleep, but reduce sleep quality, and cause residual drowsiness and are not recommended for insomnia.
MT, a hormone produced by the pineal gland, helps regulate the circadian (sleep-wake) rhythms. Darkness stimulates while light inhibits MT production. The significant deterioration of sleep quality seen in many older people is correlated with a decline in MT secretion. MT may prevent jet lag in some travellers. It may help people who are dependent on sleeping medications withdraw from these agents and maintain good quality sleep. MT may be helpful for people who have difficulty in falling asleep at night but thereafter sleep normally. The most common side effects are sedation, drowsiness, and hypothermia. A randomized, double-blind, placebo-controlled study of prolonged-release MT for 3 weeks resulted in improvement in sleep latency, sleep quality, and morning alertness. Further, in a subset of patients who continued treatment for 6 months, the improvements were maintained. However, other studies gave contradictory results.
Valerian increases GABA concentrations in animal studies but its exact mechanism is not known. The hypnotic effect of valerian occurs after 2–4 weeks. Side effects include headache and daytime sedation. Other herbs used to promote sleep include kava, skullcap, passion flower, California poppy, and lemon balm. None of these are recommended at present. The optimum nutrient composition of diet and modest energy restriction was found to shorten sleep-onset latency in overweight and obese men with chronic insomnia.
| Prevention of Insomnia|| |
The promotion of a healthy lifestyle is the key.
- A lifestyle comprising a balance of rest, recreation, and physical exercise in combination with a healthy diet can greatly reduce the risk
- Learning physical and mental relaxation techniques are useful, and so is doing exercises before dinner. Exercising close to bedtime, however, may increase alertness
- Taking a hot bath about 2 h before bedtime alters the body's core temperature rhythm and eases the onset and maintenance of sleep. Avoid bathing shortly before the sleep as it increases alertness
- Relaxing activities such as reading, meditation, or a leisurely walk in the half-hour before bedtime. Is helpful
- A regular sleep schedule, with a regular bedtime and wake-up time and sticking to it, even on weekends, will set the body's internal clock in a way that will make nighttime sleep deeper and more consistent. However, this is easier said than done. Long naps, especially in the afternoon, should be avoided
- Dinner should be light and 2–3 h before bedtime. Avoid nicotine, caffeine, and other stimulants, especially in the evening
- Even though alcohol may help you fall asleep quicker, it actually worsens insomnia by causing shallow, nonrefreshing sleep, and therefore avoid alcohol.
| Conclusion|| |
The prevalence of chronic insomnia in outpatient and morbid populations is higher than in the general population. Factors associated with chronic insomnia include female sex, advanced years, poor general health, chronic medical diseases, present or past psychiatric disorders, painful conditions, increased health-care utilization, lower quality of life and disturbed social relationships, lower socioeconomic status, marital separation, unemployment, poorer working conditions, and impaired cognitive function. Longitudinal studies are needed to explore the risk factors and consequences of chronic insomnia. The treatment should start with nonpharmacological interventions. BZDs, non-BZDs and antidepressants are effective in the management of chronic insomnia, but all of them have side effects. BZDs have a greater risk of harm than non-BZDs.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Saddichha S. Diagnosis and treatment of chronic insomnia. Ann Indian Acad Neurol 2010;13:94-102.
] [Full text]
Carney PR, Berry RB, Geyer JD. Insomnia: Causes and treatment. In: Clinical Sleep Disorders. Philadelphia, PA: Lipincott William and Wilkins; 2005. p. 157-91.
Morin CM, Colecchi C, Stone J, Sood R, Brink D. Behavioral and pharmacological therapies for late-life insomnia: A randomized controlled trial. JAMA 1999;281:991-9.
American Psychiatric Association. Diagnostic and Statistical Manual of Mental disorders. 5th
ed. Arlington, Virginia: American Psychiatric Association; 2013.
Qaseem A, Kansagara D, Forciea MA, Cooke M, Denberg TD; Clinical Guidelines Committee of the American College of Physicians. Management of chronic insomnia disorder in adults: A clinical practice guideline from the American College of Physicians. Ann Intern Med 2016;165:125-33.
Bhaskar S, Hemavathy D, Prasad S. Prevalence of chronic insomnia in adult patients and its correlation with medical comorbidities. J Family Med Prim Care 2016;5:780-4.
] [Full text]
Praharaj SK, Gupta R, Gaur N. Clinical practice guideline on management of sleep disorders in the elderly. Indian J Psychiatry 2018;60:S383-96.
Lianqi L, Ancoli-Israel S. Insomnia in the older adult. Sleep Med Clin 2006;1:409-21.
Walsh JK, Benca RM, Bonnet M, Buysse DJ, Ricca J, Hauri PJ, et al
. Insomnia: Assessment and management in primary care. National Heart, Lung, and Blood Institute Working Group on Insomnia. Am Fam Physician 1999;59:3029-38.
Breslau N, Roth T, Rosenthal L, Andreski P. Sleep disturbance and psychiatric disorders: A longitudinal epidemiological study of young adults. Biol Psychiatry 1996;39:411-8.
Yang CM, Lin SC, Cheng CP. Transient insomnia versus chronic insomnia: A comparison study of sleep-related psychological/behavioral characteristics. J Clin Psychol 2013;69:1094-107.
Pinto LR Jr., Alves RC, Caixeta E, Fontenelle JA, Bacellar A, Poyares D, et al.
New guidelines for diagnosis and treatment of insomnia. Arq Neuropsiquiatr 2010;68:666-75.
Roth T, Roehrs T, Pies R. Insomnia: Pathophysiology and implications for treatment. Sleep Med Rev 2007;11:71-9.
Pizzorno J, Murray M. Textbook of Natural Medicine. 2nd
ed., Vol. 1. London: Churchill Livingstone; 1999. p. 821-6.
Heim C, Newport DJ, Heit S, Graham YP, Wilcox M, Bonsall R, et al.
Pituitary-adrenal and autonomic responses to stress in women after sexual and physical abuse in childhood. JAMA 2000;284:592-7.
Gillin JC. Psychiatric disorder. In: Kryger MH, Roth T, Dement WC. Principle and Practice of Sleep Medicine. 3rd
ed. Philadelphia: W.B. Saunders; 2000.
Buysse DJ, Reynold CF. Insomnia. In: Thorpy MJ. Handbook of Sleep Disorder. New York: Marcel Decker; 1990. p. 375-433.
Spielman AJ, Caruso LS, Glovinsky PB. A behavioral perspective on insomnia treatment. Psychiatr Clin North Am 1987;10:541-53.
Bonnet MH, Arand DL. Hyperarousal and insomnia. Sleep Med Rev 1997;1:97-108.
Besset A, Villemin E, Tafti M, Billiard M. Homeostatic process and sleep spindles in patients with sleep-maintenance insomnia: Effect of partial (21 h) sleep deprivation. Electroencephalogr Clin Neurophysiol 1998;107:122-32.
Bastien CH, Vallières A, Morin CM. Validation of the insomnia severity index as an outcome measure for insomnia research. Sleep Med 2001;2:297-307.
Buysse DJ, Reynolds CF 3rd
, Monk TH, Berman SR, Kupfer DJ. The Pittsburgh sleep quality index: A new instrument for psychiatric practice and research. Psychiatry Res 1989;28:193-213.
Nicassio PM, Mendlowitz DR, Fussell JJ, Petras L. The phenomenology of the pre-sleep state: The development of the pre-sleep arousal scale. Behav Res Ther 1985;23:263-71.
Johns MW. A new method for measuring daytime sleepiness: The Epworth sleepiness scale. Sleep 1991;14:540-5.
Morin CM, Stone J, Trinkle D, Mercer J, Remsberg S. Dysfunctional beliefs and attitudes about sleep among older adults with and without insomnia complaints. Psychol Aging 1993;8:463-7.
Dhyani M, Rajput R, Gupta R. Hindi translation and validation of dysfunctional beliefs and attitudes about sleep (DBAS – 16). Ind Psychiatry J 2013;22:80-5.
] [Full text]
Schutte-Rodin S, Broch L, Buysse D, Dorsey C, Sateia M. Clinical guideline for the evaluation and management of chronic insomnia in adults. J Clin Sleep Med 2008;4:487-504.
Lacks P, Rotert M. Knowledge and practice of sleep hygiene techniques in insomniacs and good sleepers. Behav Res Ther 1986;24:365-8.
Stepanski EJ, Wyatt JK. Use of sleep hygiene in the treatment of insomnia. Sleep Med Rev 2003;7:215-25.
Chen HY, Chiang CK, Wang HH, Hung KY, Lee YJ, Peng YS, et al.
Cognitive-behavioral therapy for sleep disturbance in patients undergoing peritoneal dialysis: A pilot randomized controlled trial. Am J Kidney Dis 2008;52:314-23.
Pallesen S, Nordhus IH, Kvale G, Nielsen GH, Havik OE, Johnsen BH, et al.
Behavioral treatment of insomnia in older adults: An open clinical trial comparing two interventions. Behav Res Ther 2003;41:31-48.
Means MK, Lichstein KL, Epperson MT, Johnson CT. Relaxation therapy for insomnia: Nighttime and day time effects. Behav Res Ther 2000;38:665-78.
Tsai HJ, Kuo TB, Lee GS, Yang CC. Efficacy of paced breathing for insomnia: Enhances vagal activity and improves sleep quality. Psychophysiology 2015;52:388-96.
Britton WB, Haynes PL, Fridel KW, Bootzin RR. Mindfulness-based cognitive therapy improves polysomnographic and subjective sleep profiles in antidepressant users with sleep complaints. Psychother Psychosom 2012;81:296-304.
Ong JC, Manber R, Segal Z, Xia Y, Shapiro S, Wyatt JK, et al.
A randomized controlled trial of mindfulness meditation for chronic insomnia. Sleep 2014;37:1553-63.
Trauer JM, Qian MY, Doyle JS, Rajaratnam SM, Cunnington D. Cognitive behavioral therapy for chronic insomnia: A systematic review and meta-analysis. Ann Intern Med 2015;163:191-204.
Sateia MJ, Buysse DJ, Krystal AD, Neubauer DN, Heald JL. Clinical practice guideline for the pharmacologic treatment of chronic insomnia in adults: An American Academy of sleep medicine clinical practice guideline. J Clin Sleep Med 2017;13:307-49.
Asnis GM, Thomas M, Henderson MA. Pharmacotherapy treatment options for insomnia: A primer for clinicians. Int J Mol Sci 2015;17. pii: E50.
Miller CB, Espie CA, Epstein DR, Friedman L, Morin CM, Pigeon WR, et al.
The evidence base of sleep restriction therapy for treating insomnia disorder. Sleep Med Rev 2014;18:415-24.
Yang PY, Ho KH, Chen HC, Chien MY. Exercise training improves sleep quality in middle-aged and older adults with sleep problems: A systematic review. J Physiother 2012;58:157-63.
Passos GS, Poyares DL, Santana MG, Tufik S, Mello MT. Is exercise an alternative treatment for chronic insomnia? Clinics 2012;67:653-9.
Ascher LM, Turner R. Paradoxical intention and insomnia: An experimental investigation. Behav Res Ther 1979;17:408-11.
Lie JD, Tu KN, Shen DD, Wong BM. Pharmacological treatment of insomnia. P
Buscemi N, Vandermeer B, Friesen C, Bialy L, Tubman M, Ospina M, et al.
The efficacy and safety of drug treatments for chronic insomnia in adults: A meta-analysis of RCTs. J Gen Intern Med 2007;22:1335-50.
Israel AG, Kramer JA. Safety of zaleplon in the treatment of insomnia. Ann Pharmacother 2002;36:852-9.
Krystal AD, Huang H, Zummo J, Grinnell T, Marshall RD. A WASO sub-group analysis of a 6-month study of eszopiclone 3 mg. Sleep Med 2012;13:691-6.
Roth T, Walsh JK, Krystal A, Wessel T, Roehrs TA. An evaluation of the efficacy and safety of eszopiclone over 12 months in patients with chronic primary insomnia. Sleep Med 2005;6:487-95.
Zammit GK, McNabb LJ, Caron J, Amato DA, Roth T. Efficacy and safety of eszopiclone across 6-weeks of treatment for primary insomnia. Curr Med Res Opin 2004;20:1979-91.
Yeung WF, Chung KF, Yung KP, Ng TH. Doxepin for insomnia: A systematic review of randomized placebo-controlled trials. Sleep Med Rev 2015;19:75-83.
Stahl SM. Mechanism of action of trazodone: A multifunctional drug. CNS Spectr 2009;14:536-46.
National Institutes of Health. National institutes of health state of the science conference statement on manifestations and management of chronic insomnia in adults, June 13-15, 2005. Sleep 2005;28:1049-57.
Richardson GS, Roehrs TA, Rosenthal L, Koshorek G, Roth T. Tolerance to daytime sedative effects of H1 antihistamines. J Clin Psychopharmacol 2002;22:511-5.
Ramakrishnan K, Scheid DC. Treatment options for insomnia. Am Fam Physician 2007;76:517-26.
Wade AG, Crawford G, Ford I, McConnachie A, Nir T, Laudon M, et al.
Prolonged release melatonin in the treatment of primary insomnia: Evaluation of the age cut-off for short-and long-term response. Curr Med Res Opin 2011;27:87-98.
Schultz V, Hansel R, Tyler VE. Restless and sleep disturbances. In: Rational Phytotherapy: A Physician's Guide to Herbal Medicine. 3rd
ed. Berlin: Springer-Verlag; 1998. p. 73-88.
Tan X, Alén M, Wang K, Tenhunen J, Wiklund P, Partinen M, et al.
Effect of six-month diet intervention on sleep among overweight and obese men with chronic insomnia symptoms: A randomized controlled trial. Nutrients 2016;8. pii: E751.