Log your accrued CPD hours

APS members get exclusive access to the logging tool to monitor and record accrued CPD hours.

2018 APS Congress

The 2018 APS Congress will be held in Sydney from Thursday 27 to Sunday 30 September 2018


Not a member? Join now

Password reminder

Enter your User ID below and we will send you an email with your password. If you still have trouble logging in please contact us.

Back to

Your password has been emailed to the address we have on file.

Australian Psychology Society This browser is not supported. Please upgrade your browser.

InPsych 2014 | Vol 36

April | Issue 2

Cover feature : Disordered sleep

Managing insomnia: What we’ve learnt in the last 10 years

Sleep is a building block essential for our physical and mental wellbeing, potentially providing a period of restoration but also a time when we do not have to think, feel or act. However, when sleep is disrupted the result may be one of feeling tired, grumpy and cheated, where everything appears to require considerably more effort. If better sleep is not restored within a few days increased negative feelings can potentially impact on mood.

Insomnia is the most common sleep disorder and one of the most common health complaints in the general population. Insomnia is a distressing difficulty where sleep onset, sleep maintenance, early morning wakening or a combination of these symptoms occurs and sleep is insufficient for an individual’s needs, despite adequate time spent in bed to achieve sleep. The last decade has seen a significant increase in interest in insomnia and its impact on health, mental health and wellbeing. This interest has been matched by considerable advances in the understanding and treatment of insomnia, including its important bi-directional relationship with depression.

Diagnosis of insomnia disorder

According to the DSM-5, acute insomnia relates to symptoms being present for less than one month, while chronic insomnia is defined as sleep difficulties being present for at least one month and occurring three times or more per week (American Psychiatric Association, 2013). The International Classification of Sleep Disorders (ICSD, 2005), however, classifies insomnia as chronic after six months and is currently under revision.

Traditionally insomnia was perceived as a symptom of ‘other’ physical and psychosocial factors, but is now defined as a disorder due to its negative and pathological sequelae (Roth, 2007). Previously insomnia was divided into primary insomnia and secondary insomnia, but the new DSM-5 has a single diagnosis of insomnia disorder, which is the most useful construct. Diagnostic criteria which must be met include specific daytime consequences of complaints of fatigue, daytime sleepiness, cognitive impairment, mood disturbance, and impaired work function or impaired interpersonal functioning. A strength of this definition is the underlying premise that insomnia is a recognisable 24-hour disorder with significant daytime consequences. The DSM-5 has also recognised that other mental/medical disorders, the physiological effects of a substance (such as drug or alcohol abuse, or medication) or another sleep-wake disorder (such as a breathing disorder, circadian rhythm disorder or parasomnias) can be present, but do not explain the predominant complaint of insomnia.


When non-restrictive definitions of insomnia are used, insomnia is found in 33 per cent of the general population (Ohayon, 2002). Ohayon & Reynolds (2009) undertook a cross sectional study of six European countries via telephone interviews and found 37 percent of the population reported sleep difficulties, including short sleep (20%), light sleep (17%) and global sleep dissatisfaction (8%). A general population prospective study (Singareddy et al., 2012) found chronic insomnia in nine per cent of the population after a 7.5-year follow-up.

In Australia, the prevalence of insomnia is estimated between 13 and 33 per cent of the population (Lack, Miller, & Turner, 1988; Bartlett, Marshall, Williams , & Grunstein, 2007). The BEACH Report (Bettering the Evaluation and Care of Health programs between April 2006 and March 2008; Charles, Harrison, & Britt, 2009) highlights the frequency of sleep disorders encountered in general practitioner consultations. Across Australia, for every 100 GP encounters sleep disorders were managed at a rate of 1.6 contacts, with insomnia represented in eight out of 10 sleep disorders managed.

Who is most likely to have insomnia?

Individuals who:

  • Are over 45 years of age
  • Are overweight or obese
  • Have conditions such as pain, hypertension, cardiovascular disease, upper airway disease, restless legs syndrome and/or periodic limb movement
  • Have major depression, anxiety or bipolar disorder
  • Are shift workers
  • Consume large amounts of caffeinated products, alcohol or recreational drugs

Theoretical perspectives on insomnia

The aetiology of insomnia is complex and usually multi-factorial. The Spielman Model is useful and proposes three main factors (predisposing, precipitating and perpetuating – the ‘3 Ps’) which potentially trigger, establish and maintain insomnia (Spielman, Saskin, & Thorpy, 1987).

Predisposing factors include demographic factors (e.g., ageing, female gender, living alone), familial/hereditary conditions (a personal or family history of insomnia), psychological factors (e.g., anxiety, depression, personality traits), and physiological and lifestyle factors (e.g., increased arousability, caffeine and alcohol intake, and smoking). There is little or no longitudinal research at present to identify whether these factors are a trigger or an effect.

Precipitating factors include stressful life events (e.g., relationships, divorce, grief, financial worries, work-related stressors), as well as psychological and health-related factors (e.g., pain, cardiovascular disease, mental health problems). These precipitating factors are initially responsible for the acute insomnia.

Perpetuating factors include maladaptive sleep habits, spending excessive amounts of time in bed to make up for perceived sleep loss, and distress and concern about poor sleep, sleep ‘performance anxiety’ and other dysfunctional/unhelpful beliefs and cognitions about the ability to sleep, which with time become self-fulfilling prophecies.

Early intervention is the key to managing insomnia but rarely occurs, even when the identifiable insomnia trigger is addressed (as within 75 per cent of cases) yet the insomnia remains (Bastien, Morin, Quellet, Blais, & Bouchard, 2004). Individuals generally fail to recognise how the combination of poor sleep, sleep anxiety, and an inability to ‘down-regulate’ arousal levels at bedtime is feeding the insomnia on a nightly basis.

Cognitive model of insomnia

The ‘wired and tired’ or hyperarousal state is a common distressing feature of insomnia. Excessive negative cognitive activity leads to increased physiological hyperarousal and selective attention (Harvey, 2002). Chronic insomnia is maintained by worry, unhelpful beliefs about sleep, use of safety behaviours, monitoring of the sleep-related threats, and inaccurate perceptions of sleep and the consequences of sleep loss.

Worry precipitates and/or perpetuates insomnia. Worry about the daytime consequences of not obtaining enough sleep (associated with increased absenteeism and performance anxiety) triggers the flight or fight response (Bonnet & Arand, 1997), resulting in more emotional distress and worsening sleep. Unhelpful or dysfunctional beliefs about sleep include statements such as “I need 8 hours of sleep every night to feel refreshed” and “If I don’t sleep well at night I know I cannot possibly function well the following day”, which exemplify the unrealistic beliefs maintained by worry.

Safety behaviour is a paradox as the individual engages in behaviour that is more likely to make their sleep worse (e.g., napping, sleeping late, consuming large amounts of caffeine/alcohol, erratic use of medications). Monitoring of sleep-related threats further perpetuates the worry, and this attentional bias results in continual internal checking for a reason why the individual is not sleeping (e.g., too hot, too cold, stiff shoulder, breathing partner) or for an external cause for sleeplessness (e.g., dog barking, tap dripping).

All of these perceptions have a negative effect on daytime mood and performance. An inaccurate perception of sleep is common. Good sleepers tend to overestimate their sleep and individuals with insomnia underestimate their sleep. Interestingly, a difference of only 35 minutes of objectively measured sleep was found between good sleepers and those with insomnia (Chambers & Keller, 1993).

Depression and insomnia

Insomnia was in the past seen as a symptom of ‘something else’ or, if associated with depression, the general consensus was that the insomnia would just ‘go away’ when the depression was treated. This concept was first challenged with the finding that if individuals had previously experienced depression, sleep disturbance in the form of insomnia was found to be a prodromal symptom of a recurring bout of depression (Breslau, Roth, Rosenthal, & Andreski., 1996). More direct relationships between untreated insomnia and depression have since been established (Riemann & Voderholzer, 2003; Cole & Dendukuri, 2003)

Three influential prospective community samples have been instrumental in providing evidence for a bidirectional relationship between insomnia and depression. In a study of 3,000 Swedish residents (Jansson-Frojmark & Lindblom, 2008), high anxiety and depression at baseline predicted insomnia whilst untreated insomnia at baseline predicted depression and anxiety at the one-year follow-up. Another prospective study of 2,363 adults in the UK found depression at baseline predicted insomnia at the one-year follow-up (Morphy, Dunn, Lewis, Boardman, & Croft, 2007). Johnson and colleagues (Johnson, Roth, & Breslau, 2006) found clinical insomnia predicted the onset of depression, but there was no correlation with previous depression.

In the HUNT Study of 24,715 people (Siversten et al., 2012), prospective data was collected from 1995-1997 (HUNT 2) and from 2006-2008 (HUNT3) and used to investigate the directionality of the relationship between depression and insomnia. Strong longitudinal associations between insomnia and depression were found in these two studies that were 11 years apart. The associations between both insomnia and depression were bidirectional, and although lifestyle and anxiety also accounted for some of these associations, this was apparent for both disorders.

Both aspects of the relationship between insomnia and depression, whatever the direction, require equal attention and treatment. The most common residual symptom following successful treatment for a major depressive episode is sleep disturbance (Nierenberg et al., 2010), whilst non-depressed individuals with insomnia have a two-fold increased risk of developing depression when left untreated (Baglioni et al., 2011).

Management of insomnia in Australia

The BEACH Report (Charles et al., 2009) found that insomnia was managed in 95 per cent of cases by general practitioners prescribing medication. Eighty per cent of medications prescribed were benzodiazepine derivatives, 15 per cent were benzodiazepine-related drugs, and the remaining medications were antidepressants. Lower than average rates of advice/counselling were found, and referral rates per 100 insomnia problems were considerably lower than the BEACH average for referral for other presentations (0.8 vs. 8.3).

Management of insomnia with medication can be efficacious in the short term, but has the negative consequences of dependence and can be ineffective over time. The low rate of referral for psychological assistance for insomnia found in the general practice study is concerning, as psychological interventions involving cognitive behaviour therapy for insomnia have been shown to be highly effective. Collaboration with the referring medical practitioner is essential, particularly in relation to medical conditions which may be contributing to insomnia and for managing any medications that may have been prescribed. A general rule is to maintain individuals on their current medications and then to taper hypnotics as sleep confidence and sleep behaviours improve. Antidepressant medication is maintained as required.

Many individuals with insomnia experience physiological hyperarousal and cognitive hypervigilance, whilst daytime sleepiness appears the least reported daytime impairment (Espie, 2012). When insomnia is present with daytime sleepiness it is important to look for the possibility of other sleep disorders including obstructive sleep apnoea, restless legs syndrome, periodic limb movement, narcolepsy/cataplexy, parasomnias, an undiagnosed medical disorder, head injury or severe depression, and to discuss these matters with the referring practitioner.

In a clinical setting the most common presentation of the individual with insomnia is one of being ‘wired and tired’, reporting high levels of fatigue on questionnaires but rarely sleepiness on the Epworth Sleepiness Scale (ESS; Johns, 1991). This scale is widely used in sleep medicine to assess daytime sleepiness, with any score greater than 10 reflecting excessive sleepiness. Approximately 10 per cent of individuals diagnosed with insomnia have a delayed sleep phase disorder (DSPD) where sleep onset is delayed by at least 2-4 hours, resulting in difficulties with waking and a feeling of perpetual jet lag. DSPD is also very common in depression and requires additional treatment to realign sleep with the environment (see article on page 14 for further information on this disorder).

Psychological treatment of insomnia

Cognitive behavioural therapy for insomnia (CBT-I) targets maladaptive sleep behaviours and thoughts. CBT-I is the most effective objectively measured treatment for insomnia (Morin, Le Blanc, Daley, Gregoire, & Merette, 2006) and is more efficacious compared with hypnotic medication (Siversten et al., 2006). It has been shown to be effective in older age groups (Lichstein, Wilson, & Johnson, 2000), community groups (Espie et al., 2007) and in depressed individuals (Manber et al., 2008). Demonstrable large effect size changes are found in primary outcomes (sleep latency, increased total sleep time and sleep efficiency, fewer wakes) and maintained at long-term follow-up (Smith et al., 2002).

A key message in the psychological treatment of insomnia is that current sleep behaviours have not been working and for any improvement to occur the individual needs to do something different. Treatment usually commences with psychoeducation to provide a good understanding of sleep, sleep staging, circadian rhythm and healthy sleep practices. Behavioural interventions such as stimulus control, sleep/bed restriction and relaxation techniques are then introduced as the first change required for effective treatment. Recent research shows that brief behavioural treatment is effective for many individuals, while a stepped care model that incorporates cognitive therapy (including mindfulness and acceptance and commitment therapy) is recommended for more complex issues. These various psychological techniques for insomnia are briefly reviewed below, with some adaptations for treating individuals with depression presented in italics.

Sleep hygiene and circadian rhythm education

The aim of psychoeducation is to provide information on the environmental, physiological and behavioural factors and habits that promote sound sleep. The most important component of psycheducation in relation to insomnia is to provide information about the circadian rhythm and to encourage rising at the same time each day regardless of the previous night’s sleep. Individuals should ensure that they experience morning light after the minimum core body temperature time in order to suppress the sleep hormone (melatonin) and reset the body clock, and reduce exposure to bright light in the evening.

Regular exercise should be encouraged within this framework, and long naps within the daytime should be avoided. Individuals should also be made aware of the effect on sleep of alcohol and stimulants such as caffeine and nicotine. Visual access to a clock when in bed should be avoided, and the bedroom kept dark, quiet, clean and comfortable.

Stimulus control

Stimulus control is usually recommended for individuals with sleep onset insomnia and involves strategies that enable them to learn to discriminate between the daytime and night time sleep environment. The aim is to promote a positive association between the bedroom environment and sleepiness, whereas for many individuals the bedroom has become a cue for being awake and aroused. Treatment involves removing all stimuli from the bedroom that are potentially sleep-incompatible (e.g., books, television, iPads, mobile phones, electronic games), and not sleeping in living areas. The individual is instructed to get out of bed if not asleep within 15-20 minutes, when wakeful during the night and/or when experiencing increasing distress in relation to the insomnia, and to do a non-stimulating activity until feeling ready to try to sleep again.

For individuals with severe depression the bedroom frequently becomes a place of refuge which enables escape through sleep and not having to feel or think. Encouraging sleep boundaries (particularly a set time to get up each morning, regardless of the previous night’s sleep quality), reducing time in bed, and not retiring to bed when overwhelmed are key components of treatment.

Sleep/bed restriction therapy

Sleep restriction (or bed restriction) is a technique that increases sleep ‘drive’ and reduces time in bed lying awake by matching the time spent asleep with the individual’s average actual reported sleep time. A strict rising schedule and/or bedtime is set to match the individual’s reported average hours of sleep. The time in bed is slowly increased by 15-30 minutes when the time spent asleep is at least 85 per cent of the allowed time in bed. A significant side effect of this treatment is an increase in natural sleepiness (Kyle et al., 2014), and gives the individual a sense of assurance that bed is now a safe place to sleep.

Reducing time in bed for the individual with severe depression can be a challenge and requires considerable understanding and a carefully negotiated plan.

Worry time and letting go of the day

Preparation time out in the early part of the evening to enable the individual to address issues that are important for the next day or help to ‘let go’ of the day are important components in boundary setting in preparation for sleep. Choosing a soothing activity just before bed can also be useful.

Relaxation techniques

Progressive relaxation, imagery training, biofeedback, meditation, hypnosis and autogenic training, are all useful, with few randomised controlled trials to show that one approach is better than another. Practice and perseverance are important to enable the individual to feel comfortable undertaking these techniques. Be aware that a last minute relaxation attempt just before sleep will only put more pressure on the sleep process and inevitably increase night time arousal. Even a few minutes of relaxation two to four times a day is useful. Relaxation is less effective as a stand-alone treatment for insomnia but is a useful technique in combination with other treatment interventions.

In depression, relaxation techniques can initially exacerbate the ‘feelings of hopelessness’. Helping the individual sit with these feelings along with mindfulness techniques can be very useful. Offering many different strategies provides choice but care should be taken to ensure expectations about efficacy are managed.

Cognitive therapy

There are a number of cognitive techniques that aim to identify and target beliefs that may be interfering with adherence to all the components of CBT-I and in particular to stimulus control and sleep restriction techniques described above. These cognitions may include fears about the techniques and how they reduce the opportunity to sleep, but frequently it is about facing ‘the fear of the fear of not sleeping’! Other unhelpful cognitions associated with insomnia that can be targeted with cognitive techniques include excessive worry about the consequences of not obtaining enough sleep, an over-estimation of the hours of sleep required each night to maintain health, or an under-estimation of the actual sleep obtained. All of these beliefs need to be addressed slowly and other interpretations introduced. Strategies such as thought blocking can also assist in addressing faulty cognitions – repeating the word ‘the’ or ‘no thinking’ every three seconds can occupy the short-term memory store (used in processing information), potentially allowing sleep to happen.

These strategies are effective with depression but may require a slower approach to address the additional perseveration of negative thought patterns.

Paradoxical intention

Putting the effort into remaining wakeful rather than ‘trying’ to fall asleep (a de-catastrophising technique) can strengthen the sleep drive and reduce performance effort (Morin, Bootzin, et al., 2006). Sitting on the edge of the bed, with back straight, tummy pulled in, shoulders down, eyes open and staring ahead, can be a wonderful incentive to let sleep happen. However, this may need to be addressed a number of times – it is also very boring.

Mindfulness and acceptance and commitment therapy

Mindfulness is an easy adjunct with CBT-I which enables the individual to learn to deal better with the ‘here and now’ of being awake and/or in a hypervigilant state. An active brain is necessary for sleep, so it is not about emptying the mind or ‘switching off’, but rather learning to let go of thinking about past or future events at night. Mindfulness emphasises being non-judgmental in the present. Mindfulness treatment interventions for insomnia have been shown to result in reductions in pre-sleep arousal, sleep effort, and dysfunctional sleep-related cognitions (Ong, Shapiro, & Manber, 2008).

Acceptance and commitment therapy (ACT) may be helpful in teaching individuals with insomnia to be more accepting of wakefulness and to understand and manage their hyperarousal state better. ACT appears to be a useful therapy in insomnia and depression interventions, but as yet there are no randomised controlled trials investigating the treatment of insomnia in depression.


In the last 10 years there have been significant advances in the understanding of insomnia, and there is now a wealth of good research evidence on the effectiveness of CBT interventions for this distressing disorder. A particularly important development in knowledge is the bi-directional relationship between insomnia and depression which has been shown through clinical and epidemiological studies. These disorders can no longer be seen as separate entities, and it is even more imperative that currently underutilised psychological interventions for insomnia are made more readily available. Psychologists need good sleep knowledge to work with individuals with insomnia, and many of the well-known psychological principles and skills can be used to enhance the wellbeing and health of people struggling to get those precious hours of restorative sleep.

The author can be contacted at delwyn.bartlett@sydney.edu.au


  • American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Arlington, VA: American Psychiatric Publishing.
  • Baglioni, C., Battagliese, G., Feige, B., Spiegelhalder, K., Nissen, C., et al. (2011). Insomnia as a predictor fo depression: a meta-analytic evaluation of longitudinal studies. Journal of Affective Disorders, 135, 10-19.
  • Bartlett, D. J., Marshall, N. S., Williams , A., & Grunstein, R. R. (2007). Sleep health New South Wales: chronic sleep restriction and daytime sleepiness. Internal Medicine Journal, 1-8.
  • Bastien, C., Morin, C., Quellet, M.-C., Blais, F., & Bouchard, S. (2004). Cognitive-Behavioral Therapy for insomnia:comparison of individual therapy, group therapy and telephone consultations. Journal of Consulting and Clinical Psychology, 72, 653-659.
  • Bonnet, M., & Arand, D. (1997). Hyperarousal and insomnia. Sleep Medicine Reviews, 1, 97-108.
  • Breslau, N., Roth, T., Rosenthal, L., & Andreski., P. (1996). Sleep Disturbance and Psychiatric Disorders: A Longitudinal Epidemiological Study of Young Adults. Biological Psychiatry, 39, 411-418.
  • Chambers, M., & Keller, B. (1993). Alert Inosmniacs: Are they areally sleep deprived? Clinical Psychology Review, 13, 649-666.
  • Charles, J., Harrison, C., & Britt, H. (2009). Insomnia. Australian Family Physician, 38(5), 283.
  • Cole, M., & Dendukuri, N. (2003). Risk factors for depression among elderly subjects: a systematic review and meta-analysis. The American Journal of Psychiatry, 160, 1147-1156.
  • Espie, C. (2012). The Daytime Impact of DSM-5 Insomnia Disorder: Comparative Analysis of Insomnia Subtypes from the Great British Sleep Survey. Journal of Clinical Psychiatry, 73(12), e1478-31484.
  • Espie, C., MacMahon, K., Kelly, H.-L., Broomfield, N., Douglas, N., et al. (2007). Randomised clinical effectiveness trial of nurse-administered small-group cognitive behavior therapy for persistent insomnia in general practice. Sleep, 30(5), 574-584.
  • Harvey, A. (2002). A cognitive model of insomnia. Behaviour Research Therapy, 40, 869-893.
  • ICSD. (2005). The international classification of sleep disorders revised: diagnostic and coding manual. American Sleep Disorders Association.
  • Jansson-Frojmark, M., & Lindblom, K. (2008). A bidirectional relationship between anxiety and depression, and insomnia? A prospective study in the general population. Journal of Psychosomatic Research, 64, 443-449.
  • Johns, M. W. (1991). A new method for measuring daytime sleepiness: the Epworth sleepiness scale. Sleep, 14(6), 540-545.
  • Johnson, E. O., Roth, T., & Breslau, N. (2006). The association of insomnia with anxiety disorders and depression: exploration of the direction of risk. Journal of Psychiatric Research, 40(8), 700-708.
  • Kyle, S. D., Miller, C. B., Roger, Z., Siriwardena, M., Mac Mahon, K. M., & Espie, C. A. (in press). Sleep restriction therapy for insomnia is associated with reduced objective total sleep time, increased daytime somnolence, and objectively-impaired vigilance: implications for the clinical management of insomnia disorder. Sleep.
  • Lack, L., Miller, W., & Turner, D. (1988). A Survey of Sleeping Difficulties in an Australian Population. Community Health Studies, 12(2), 200-207.
  • Lichstein, K., Wilson, N., & Johnson, C. (2000). Psychological treatment of secondary insomnia. Psychological Aging, 15, 232-240.
  • Manber, R., Edinger, J., Gress, J., San Pedro-Salcedo, M., Kuo, T., & Kalista, T. (2008). Cognitive Behavioral Therapy for insomia enhances depression outcomes in patients with comorbid major depressive disorder and insomnia. Sleep, 31, 489-495.
  • Morin, C., Bootzin, R., Buysse, D., Edinger, J., Espie, C., & Lichstein, K. L. (2006). Psychological And Behavioral Treatment Of Insomnia: Update Of The Recent Evidence (1998-2004). Sleep, 29, 1398-1414.
  • Morin, C., Le Blanc, M., Daley, M., Gregoire, J., & Merette, C. (2006). Epidemiology of insomnia:prevalence, self-help treatments, consultations and determinants of self-seeking behaviours. Sleep Medicine, 7, 123-130.
  • Morphy, H., Dunn, K. M., Lewis, M., Boardman, H. F., & Croft, P. R. (2007). Epidemiology of insomnia: a longitudinal study in a UK population. Sleep, 30(3), 274.
  • Nierenberg, A., Husain, M. M., Trivedi, M., Fava, M., Warden, D., et al. (2010). Residual symptoms after remission of major depressive disorder with citalopram and risk of relapse: a STAR*D report. Psychological Medicine, 40, 41-50.
  • Ohayon, M. (2002). Epidemiology of insomnia: what we know and what we still need to learn. Sleep Medicine Reviews, 6(2), 97-111.
  • Ohayon, M., & Reynolds, C. (2009). Epidemiological and clinical relevance of insomnia diagnosis algorithms according to the DSM-IV and the International Classification of Sleep Disorders (ICSD). Sleep Medicine, 10, 952-960.
  • Ong, J., Shapiro, C., & Manber, R. (2008). Combining mindfulness meditation with cognitive behavior therapy for insomnia: a treatment development study. Behavior Therapy, 39, 171-182.
  • Riemann, D., & Voderholzer, U. (2003). Primary insomnia: a risk factor to develop depression? Journal of Affective Disorders, 76, 255-259.
  • Roth, T. (2007). Insomnia: definition, prevalence, etiology, and consequences. Journal of clinical sleep medicine: JCSM: official publication of the American Academy of Sleep Medicine, 3(5 Suppl), S7.
  • Singareddy, R., Vgontzas, A. N., Fernandez-Mendoza, J., Liao, D., Calhoun, S., Shaffer, M. L., & Bixler, E. O. (2012). Risk factors for incident chronic insomnia: a general population prospective study. Sleep Medicine, 13(4), 346-353.
  • Siversten, B., Omvik, S., Pallesen, S., Bjorvatn, B., Havik, O., et al. (2006). Cognitive behavioral therapy vs Zopicone for treatment of chronic primary insomnia in older adults. Journal of the American Medical Association, 295, 2851-2858.
  • Siversten, B., Salo, P., Mykletun, A., Hysing, M., Pallesen, S., et al. (2012). The Bidirectional Association between Depression and Insomnia: The HUNT Study. Psychosomatic Medicine, 74, 1-8.
  • Smith, M., Perlis, M., Park, A., Smith, M., Pennington, J., Giles, D., & Buysse, D. (2002). Comparative meta-analysis of pharmacotherapy and behavior therapy for peristent insomnia. American Journal of Psychiatry, 159, 5-11.
  • Spielman, A., Saskin, P., & Thorpy, M. (1987). Treatment of chronic insomnia by restriction of time in bed. Sleep, 10, 45-56.

Disclaimer: Published in InPsych on April 2014. The APS aims to ensure that information published in InPsych is current and accurate at the time of publication. Changes after publication may affect the accuracy of this information. Readers are responsible for ascertaining the currency and completeness of information they rely on, which is particularly important for government initiatives, legislation or best-practice principles which are open to amendment. The information provided in InPsych does not replace obtaining appropriate professional and/or legal advice.