Idiopathic insomnia …

Sleep Disorders

Updated 08.29.2023
Released 09.02.1993
Expires For CME 08.29.2026

Idiopathic insomnia

Authors: Muna Irfan MD, Stephen Talsness DO, Wajahat Khalil MD

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Editor: Antonio Culebras MD FAAN FAHA FAASM

Idiopathic insomnia

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Introduction

Overview

The following article discusses a rare form of insomnia: idiopathic or childhood-onset insomnia. It is a chronic and serious inability to initiate and maintain sleep, often observed as early as the first few weeks of life. The most recent advancement in the treatment of this condition is the demonstration that melatonin not only improves sleep, but also improves overall health status in these patients.

Key points

	• The onset of idiopathic insomnia is usually in childhood, but not every case of childhood-onset insomnia is idiopathic insomnia.
	• Its course is chronic and life-long, and there is no clearly identifiable cause.
	• Polysomnography offers little diagnostic value in idiopathic insomnia; actigraphy might be more helpful.
	• Benzodiazepine receptor agonists or melatonin, in addition to strict sleep hygiene practices, may be effective in treating idiopathic insomnia patients.

Historical note and terminology

In the 1979 Sleep Nosology developed by the Association of Sleep Disorders Centers, now the American Academy of Sleep Medicine, a new category titled "childhood onset insomnia" was presented. It was described as "a sleep-onset and sleep-maintenance insomnia, resulting in daytime symptoms of inadequate sleep, that is characterized by a distinctive history of (unexplained) development before puberty and persistence into adulthood." It was postulated that this new entity represented "a CNS shift or dysfunction of the sleep-arousal equilibrium" (06). Research in the 1980s documented the existence of such an insomnia by showing that childhood-onset insomnia was different from adult-onset insomnia on polysomnographic grounds and that it could be distinguished from other types of insomnia in a cluster analysis. The International Classification of Sleep Disorders defines idiopathic insomnia as a lifelong sleep difficulty with insidious onset occurring during infancy or early childhood that causes distress or functional impairment and is not better explained by another sleep disorder, medical or neurologic condition, psychiatric disorder, medication use, or substance use (01). However, not everyone agrees that this disorder is a separate and unique type of insomnia. For example, the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders regards the apparent neurologic predisposition toward insomnia described here as a component of a broader entity named "primary insomnia disorder" (PI) that includes idiopathic insomnia, psychophysiological insomnia, and sleep state misperception (paradoxical insomnia). The International Classification of Sleep Disorders, third edition (ICSD-3) describes idiopathic insomnia as a pathophysiological subtype of chronic insomnia disorder (02).

Clinical manifestations

Presentation and course

Idiopathic insomnia is a chronic and serious inability to initiate and maintain sleep that can often be observed as early as the first few weeks of life. Sleep latency is long. Sleep is riddled with many awakenings and may show sleep-stage abnormalities, such as REM sleep with few eye movements or ill-formed sleep spindles during stage II sleep. Paradoxically, idiopathic insomniacs may show fewer body movements per unit of sleep than normal sleepers do. As the presumed underlying neurologic abnormality may vary from mild to severe, the range of insomnia encountered in this condition may also vary from mild (essentially a light sleeper) to severe and incapacitating. Daytime features typically include decreased attention and vigilance, low levels of energy and concentration, and a deterioration of mood commonly described as grim and subdued, rather than obviously depressed or anxious. In mild or moderate idiopathic insomnia, psychological functioning is remarkably intact. In severe cases, daytime functioning may be severely disrupted, and affected patients may be unable to hold a job. During childhood and adolescence, idiopathic insomnia is often associated with soft neurologic signs (eg, as dyslexia or hyperactivity). Many cases show diffuse nonspecific abnormalities on the EEG (03).

The broad diagnostic criteria according to the third edition of the International Classification of Sleep Disorders are as follows:

Criteria A through F should be met:

(A) The patient experiences repeated problems with one or more of the following:
	• sleep initiation
	• maintenance
	• waking up earlier
(B) The patient experiences one or more of the following due to nighttime sleep difficulty:
	• fatigue/malaise
	• attention, concentration, or memory impairment
	• impaired social, family, occupational, or academic performance
	• mood disturbance/irritability
	• daytime sleepiness
	• behavioral problems
	• reduced motivation/energy/initiative
	• proneness for errors/accidents
	• dissatisfaction with sleep
(C) The sleep complaint cannot be explained by inadequate opportunity/circumstances for sleep
(D) The sleep disturbance and associated daytime symptoms occur at least 3x/week
(E) The course is chronic with symptoms longer than 3 months (typically onset in infancy or childhood, the lack of an identifiable etiology, and a persistent course without prolonged episodes of remission)
(F) The sleep difficulty is not explained by another sleep disorder
(02)

Prognosis and complications

The suspected underlying neurologic abnormality in idiopathic insomnia is presumably life-long. Complications often involve attempts to treat the condition either by self-medication (such as in alcohol) or by prescriptions (high doses of benzodiazepines or barbiturates). Other complications involve excessive use of stimulants to promote wakefulness (03).

Clinical vignette

A 36-year-old, right-handed man presented to the sleep center clinic for a first-time evaluation concerning his longstanding inability to fall asleep or stay asleep. He stated that as far back as he could remember, even as a child in grade school, he had trouble falling asleep. His mother had told him that as a newborn he slept much less than his siblings. He went to bed around 10 PM and tossed and turned for an hour or so before he fell asleep. The patient stated that his sleep was very light, and he tended to wake up once or twice in the middle of the night and stay awake for an undetermined amount of time. Whenever he was unable to fall asleep, he became restless, constantly watching the digital clock on his bedside table or, rarely, getting out of bed to watch television. He went to bed every night anticipating not falling asleep. The patient routinely received only 4 to 5 hours of sleep a night and did not feel refreshed in the morning. Rarely, after a few bad nights with little sleep, he could sleep for one night up to 7 hours, after which he would awaken refreshed. He denied feeling subjectively sleepy during the day and never fell asleep in inappropriate situations. The patient reported the inability to nap and stated that no matter where he attempted to sleep (at home or away), he had difficulty falling and staying asleep. He denied symptoms suggestive of restless legs syndrome, obstructive sleep apnea, or narcolepsy. In the past, treatments with over-the-counter sleeping aids and zaleplon were not effective. Although trazodone helped him sleep, it produced an intolerable hangover effect. He did not drink excessive caffeinated or alcoholic beverages, but he did chew tobacco throughout the day into the late evening. He had no other complaints.

Family history was significant for a similar type of insomnia in his grandmother and mother, but not in his father or siblings.

Physical examination was normal.

All night polysomnogram revealed increased sleep latency and poor sleep efficiency at 48% due to prolonged unexplained awakenings. An actigraph, worn for a week, confirmed his subjective reports of 4 to 5 hours of fragmented sleep at night.

With strict compliance with sleep hygiene regulations and 1 mg of estazolam at bedtime, he was able to improve his sleep efficiency to a considerable degree but not to resolve his insomnia entirely.

Biological basis

Etiology and pathogenesis

Idiopathic insomnia may be due to some dysfunction in the sleep-wake center in the brain. It may represent either hyperactivity in the wake center or hypoactivity in the sleep center (24). Due to early onset, lifelong, and stable course over time, it is presumed to be genetically determined or congenital due to anomaly in central nervous system sleep inducing or arousal system or both. No specific genetic loci or neuropathology have been identified.

Central sleep-wake mechanisms include the basic sleep onset systems (which involve nuclei in the preoptic area of the hypothalamus, the brainstem raphe nuclei, and the medial forebrain area) and the basic wake-promoting systems of the ascending reticular activating system (which include the perifornical lateral and tuberomammillary nuclei of the hypothalamus and the locus coeruleus and pedunculopontine/lateral dorsal tegmental nuclear complex of the brainstem) (03; 24; 13). Whether a person is awake or asleep depends on the neurophysiological balance between the reticular activating system and the sleep-inducing maintenance systems (16). Idiopathic insomnia presumably is due to a shift of this balance toward arousal. Patients coming to clinical attention may simply represent the wakeful end of the normal spectrum of sleep. Other patients may have a neurochemical, neuroanatomical, or neurophysiological dysfunction or lesions interfering with normal sleep (16). Either hyperactivity in the arousal system or hypoactivity in the sleep system may cause idiopathic insomnia (24). Empirically, idiopathic insomniacs are hyperaroused during wakefulness on questionnaires, auditory evoked potentials, and EEG. Physiologic hyperarousal in many systems (cardiac, core temperature, corticosteroids, etc.) is also frequently found in other types of insomnia, including idiopathic insomnia (08). High-density EEG of insomnia patients (based on DSM-V criteria) shows broad beta band activity during wakefulness that, combined with prior reports of this activity during sleep, suggests a state of persistent hyperarousal in patients with insomnia (11). Daytime symptom patterns characterized by mood disturbance and low sleepiness also support an internal etiologic component to idiopathic insomnia, in contrast to learned forms of insomnia (23). Although insomniac animals have been created with lesions (eg, in the medial forebrain), no direct human evidence for structural neuropathology exists for such a lesion in idiopathic insomnia. A study investigating the phase angle between self-selected bedtime and the dim light melatonin onset among patients with insomnia (60 patients with primary insomnia) without obvious circadian phase disorders demonstrated that a substantial proportion of patients (10% to 22%) initiate sleep at too early a circadian phase, leading to the complaints of long sleep latency and, hence, implicating circadian contribution (15).

Another resting state functional magnetic resonance imaging study aimed to assess whether the brain activity of primary insomnia patients varied according to age and gender and whether these factors could affect the distribution of hyper-arousal brain regions (31). The results suggested that the gender-related difference of brain activity mainly existed in superior temporal gyrus, cerebellum posterior lobe, and middle frontal gyrus; the age-related difference mainly existed in cerebellum anterior lobe, superior temporal gyrus, brainstem, para hippocampal gyrus, anterior cingulate, and cingulate gyrus. Furthermore, the gender factor did not influence the distribution of the altered regions, whereas the age factor could affect the distribution. The age-related and gender-related difference of brain activity in primary insomnia patients were found to be associated with emotional and cognitive function, which was suggested to be the possible cause of different insomnia incidence, sleep experience, and efficacy of intervention in primary insomnia patients with different gender and age.

Differential diagnosis

Not all insomnia in childhood is idiopathic or childhood-onset insomnia. In children, insomnia is most frequently caused by environmental, behavioral, and psychological factors (07). Unlike the fairly common behavioral insomnia of childhood, idiopathic insomnia has no identifiable precipitating or perpetuating factors.

Although the complaints of insomnia are seen in up to 41% of children (05), idiopathic insomnia in its pure form is rarely seen. This is due to the fact that a lifetime of serious, chronic insomnia typically results in complications such as poor sleep hygiene, alcohol or drug abuse, or maladaptive associations aggravating the insomnia. Idiopathic insomnia is diagnosed when insomnia predates the development of these complications and when the imbalance of the sleep-wake system plays a paramount role (03).

Childhood-onset restless legs syndrome is differentiated from idiopathic insomnia by the dysesthesias associated with restless legs syndrome. This irresistible urge to move the limbs tends to occur primarily in the evening or at night, typically getting better in the early morning hours. The associated insomnia, therefore, is mainly sleep onset insomnia (17).

Idiopathic insomnia is differentiated from short sleeping by the accompanying fatigue and daytime performance impairment. Short sleepers feel and function well during waking hours and do not routinely have difficulties falling asleep, nor suffer from repeated awakenings and poor-quality sleep.

Idiopathic insomnia can be difficult to distinguish from psychophysiological insomnia, which is also accompanied by an innate predisposition toward poor sleep. In idiopathic insomnia, the presumed sleep-wake imbalance is enough to cause the insomnia by itself; in psychophysiological insomnia, the inherent sleep-wake disturbance is weaker, needing the addition of the stress of maladaptive conditioning to trigger the insomnia, and it typically begins during adulthood (01).

Psychologically, most patients with idiopathic insomnia are remarkably healthy, given their chronic lack of sleep. Also, the insomnia is relentless and almost unvaried through both poor and good periods of emotional adaptation (03).

Management

Behavioral intervention. Impeccable sleep hygiene is essential, including regular, somewhat curtailed sleep hours, excellent relaxation skills, and active waking lifestyles (16). Cognitive behavioral therapy for insomnia, an approach often cited by patients as preferable to pharmacotherapy and more effective in relapse prevention, can be helpful in addressing dysfunctional beliefs about sleep and, alternatively or adjunctively, acceptance-based psychotherapeutic approaches may be more beneficial to patients with idiopathic insomnia (14).

Pharmacological intervention. Benzodiazepines and zolpidem are effective as hypnotics (24). Long-term use of drugs has raised the question of tolerance and dependence (24). Some studies, however, have shown that the risk for tolerance, dependence, and addiction is minimal in patients using long-term benzodiazepines for insomnia or for other sleep disorders (20; 22; 12). Melatonin has been shown to be helpful in treating chronic insomnia in school-aged children (26; 29) and in improving health status and advancing the sleep-wake rhythm in children with chronic insomnia (27; 28; 09). It is recommended to use melatonin in doses of 0.05 mg/kg 1 to 2 hours before dim light melatonin onset and before bedtime (29). A metaanalysis of 13 studies showed that short-term use of ramelteon (melatonin receptor 1 and 2 agonist) was associated with some improvement in sleep parameters such as subjective sleep latency and sleep quality, but overall clinical impact was modest (18).

Another review of four randomized trials demonstrated that suvorexant, which is a dual orexin receptor antagonist, was associated with significant improvements in subjective time to sleep onset, subjective total sleep time, and subjective quality of sleep (19).

Alternative medical strategies. A patient-assessor-blinded, randomized, sham-controlled acupuncture trial suggests that acupuncture can improve clinical symptoms (30). Also, the combination of multi-acupoints may enhance clinical efficacy further. The study showed improvement in the clinical outcomes of PSQI (Pittsburg sleep quality index) and TST (total sleep time) on polysomnogram.

Other strategies such as transcranial magnetic stimulation have also been explored by scientists to demonstrate some effect but have not been established as standard treatment option yet (04).

References

01: American Academy of Sleep Medicine. International classification of sleep disorders: Diagnostic and coding manual. 2nd edition. Westchester, IL: American Academy of Sleep Medicine, 2005.
02: American Academy of Sleep Medicine. International classification of sleep disorders: Diagnostic and coding manual. 3nd edition. Darien, IL: American Academy of Sleep Medicine, 2014.
03: American Sleep Disorders Association. International classification of sleep disorders: Diagnostic and coding manual. Rochester, MN: American Sleep Disorders Association, 1997.
04: Arana-Lechuga DY, Escandón OS, Corona MC, et al. Electroencephalographic abnormalities in patients with idiopathic insomnia. Neurosci Med 2011;2. Available at: www.scirp.org. Accessed 2019.
05: Archbold KH, Pituch KJ, Panahi P, Chervin RD. Symptoms of sleep disturbances among children at two general pediatric clinics. J Pediatr 2002;140(1):97-102. PMID 11815771
06: Association of Sleep Disorders Centers. Diagnostic classification of sleep and arousal disorders. Sleep 1979;2:1-137.
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08: Bonnet MH, Arand DL. 24-hour metabolic rate in insomniacs and matched normal sleepers. Sleep 1995;18:581-8. PMID 8552929
09: Braam W, Didden R, Smits M, Curfs L. Melatonin treatment in individuals with intellectual disability and chronic insomnia: a randomized placebo-controlled study. J Intellect Disabil Res 2008;52(Pt 3):256-64. PMID 18261024
10: Buysse DJ, Reynolds CF 3rd, Kupfer DJ, et al. Clinical diagnoses in 216 insomnia patients using the International Classification of Sleep Disorders (ICSD), DSM-IV and ICD-10 categories: a report from the APA/NIMH DSM-IV Field Trial. Sleep 1994;17:630-7. PMID 7846462
11: Colombo MA, Ramautar JR, Wei Y, et al. Wake high-density electroencephalographic spatiospectral signatures of insomnia. Sleep 2016;39(5):1015-27. PMID 26951395
12: Darcourt G, Pringuey D, Salliere D, Lavoisy J. The safety and tolerability of zolpidem--an update [Review]. J Psychopharmacol 1999;13(1):81-93. PMID 10221362
13: Dyken ME, Yamada T, Ali M. Treatment of Hypersomnias. In: Kushida CA, editor. Handbook of Sleep Disorders. 2nd edition. New York: Informa HealthCare, 2009:299-320.
14: Espie CA, Barrie LM, Forgan GS. Comparative investigation of the psychophysiologic and idiopathic insomnia disorder phenotypes: psychologic characteristics, patients' perspectives, and implications for clinical management. Sleep 2012;35(3):385-93. PMID 22379245
15: Flynn-Evans E, Shekleton J, Miller B, et al. Circadian phase and phase angle disorders in primary insomnia. Sleep 2017;40(12). PMID 29029340
16: Hauri PJ. Insomnia. Clin Chest Med 1998;19(1):157-68. PMID 9554225
17: Kotagal S, Silber MH. Childhood-onset restless legs syndrome. Ann Neurol 2004;56(6):803-7. PMID 15505786
18: Kuriyama A, Honda M, Hayashino Y. Ramelteon for the treatment of insomnia in adults: a systematic review and meta-analysis. Sleep Med 2014;15(4):385-92. PMID 24656909
19: Kuriyama A, Tabata H. Suvorexant for the treatment of primary insomnia: A systematic review and meta-analysis. Sleep Med Rev 2017;35:1-7. PMID 28365447
20: Mahowald MW. Diagnostic testing: sleep disorders. Neurol Clin 1996;14:183-200. PMID 8676843
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27: Smits MG, van Stel HF, van der Heijden K, Meijer AM, Coenen AM, Kerkhof GA. Melatonin improves health status and sleep in children with idiopathic chronic sleep-onset insomnia: a randomized placebo-controlled trial. J Am Acad Child Adolesc Psychiatry 2003;42(11):1286-93. PMID 14566165
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31: Wang YK, Shi XH, Wang YY, et al. Evaluation of the age-related and gender-related differences in patients with primary insomnia by fractional amplitude of low-frequency fluctuation: A resting-state functional magnetic resonance imaging study. Medicine (Baltimore) 2020b;99(3):e18786. PMID 32011475

Contributors

All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.

Authors

Muna Irfan MD

Dr. Irfan of Minnesota Regional Sleep Disorders Center has no relevant financial relationships to disclose.
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Stephen Talsness DO

Dr. Talsness of Minneapolis Veterans Affairs Medical Center and University of Minnesota has no relevant financial relationships to disclose.
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Wajahat Khalil MD

Dr. Khalil of the University of Minnesota Medical School has no relevant financial relationships to disclose.
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Editor

Antonio Culebras MD FAAN FAHA FAASM

Dr. Culebras of SUNY Upstate Medical University at Syracuse has no relevant financial relationships to disclose.
See Profile

Former Authors

Peter Hauri PhD (original author), Hrayr P Attarian MD, Kyoung Bin Im MD, and Mark Eric Dyken MD

Patient Profile

Age range of presentation: 1 month to 65+ years
Sex preponderance: male=female
Heredity: heredity may be a factor
Population groups selectively affected: none selectively affected
Occupation groups selectively affected: none selectively affected

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Idiopathic insomnia

Differential Diagnosis

behavioral insomnia of childhood
childhood-onset restless legs syndrome
psychophysiological insomnia
inadequate sleep hygiene
insomnia due to drug or substance
- short sleeper
- secondary insomnia

Also Relevant

Attention deficit hyperactivity disorder
Insomnia
Insufficient sleep syndrome
Paradoxical insomnia
Pharmacological treatment of insomnia
- Psychophysiological insomnia
- Sleep disorders
- Sleep disorders associated with anxiety disorders
- Sleep state misperception

Clinical Categories

Sleep Disorders

Patient Handouts

Web References

Clinical Trials

NIH: Sleep Disorders

Idiopathic insomnia …

Idiopathic insomnia

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Prognosis and complications

Clinical vignette

Biological basis

Etiology and pathogenesis

Epidemiology

Prevention

Differential diagnosis

Diagnostic workup

Management

References

Contributors

Authors

Editor

Former Authors

Patient Profile

ICD & OMIM codes

This is an article preview.
Start a Free Account
to access the full version.

Questions or Comment?

Also in This Category

Telehealth and cognitive behavioral therapy for insomnia (CBT-I)

NonREM parasomnias

Neurologic disorders associated with obesity

Hypersomnolence

Sleep disorders in women

Sleep, stroke, and vascular dementia

Parasomnia overlap disorder and status dissociatus

Stimulant-dependent sleep disorder

Idiopathic insomnia

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Prognosis and complications

Clinical vignette

Biological basis

Etiology and pathogenesis

Epidemiology

Prevention

Differential diagnosis

Diagnostic workup

Management

References

Contributors

Authors

Editor

Former Authors

Patient Profile

ICD & OMIM codes

This is an article preview. Start a Free Account to access the full version.

Questions or Comment?

Also in This Category

Telehealth and cognitive behavioral therapy for insomnia (CBT-I)

NonREM parasomnias

Neurologic disorders associated with obesity

Hypersomnolence

Sleep disorders in women

Sleep, stroke, and vascular dementia

Parasomnia overlap disorder and status dissociatus

Stimulant-dependent sleep disorder

This is an article preview.
Start a Free Account
to access the full version.