Insomnia

Author: Erasmo A Passaro, MD, FAAN, Director, Comprehensive Epilepsy Program/Clinical Neurophysiology Lab,

Bayfront Medical Center Florida Center for Neurology
Contributor Information and Disclosures
Updated: Sep 28, 2010

Introduction

Background
Insomnia is defined as repeated difficulty with the initiation, duration, maintenance, or quality of sleep that
occurs despite adequate time and opportunity for sleep that results in some form of daytime impairment.
Approximately one third of adults report some difficulty falling asleep and/or staying asleep during the
past 12 months, with 17% reporting this problem as a significant one. Insomnia can be acute or chronic.
Acute adjustment insomnia occurs in the context of an identifiable stressor (eg, personal loss, change in
interpersonal relationships, bereavement, occupational stress, job loss) that acts as a precipitating factor.
It typically lasts 3 months or less, and resolves as the stressor is no longer present or as the individual
adapts to the stressor. The 1-year prevalence of adjustment insomnia in adults is approximately 10-15%.

Despite inadequate sleep, many patients with insomnia do not complain of excessive daytime sleepiness,
such as involuntary episodes of drowsiness in boring, monotonous, nonstimulating situations. However,
they do complain of feeling tired and fatigued with poor concentration. This may be related to a
physiological state of hyperarousal (seePathophysiology). In fact, despite not getting adequate sleep,
patients with insomnia oftentimes have difficulty falling asleep even during daytime naps.

Chronic insomnia also has numerous health consequences. For example, patients with chronic insomnia
report reduced quality of life comparable to other conditions such as diabetes, arthritis, and heart disease.
Quality of life improves with treatment but still does not reach the level seen in the general population. In
addition, chronic insomnia is associated with impaired occupational and social performance and an
elevated absenteeism rate that is 10-fold greater than controls. Furthermore, insomnia is associated with
higher healthcare use, including a 2-fold increase in hospitalizations and office visits.

Insomnia can also be a risk factor for depression and a symptom of a number of medical, psychiatric, and
sleep disorders. In fact, insomnia appears to be predictive of a number of disorders, including depression,
anxiety, alcohol dependence, drug dependence, and suicide. The annual cost of insomnia is not
inconsequential with the estimated annual costs for insomnia at $12 billion dollars for healthcare and $2
billion dollars for sleep promoting agents.

In 2005, the National Institutes of Health held a State of the Science Conference on the Manifestations of
Chronic Insomnia in Adults. This conference focused on the definition, classification, etiology, prevalence,
risk factors, consequences, comorbidities, public health consequences and the available treatments and
evidence for their efficacy. A summary of this conference can be obtained at the NIH Consensus
Development Program home page. Prior to this conference, most cases of chronic insomnia were widely
believed to be secondary to another medical or psychiatric condition and effective treatment of the
primary condition was believed to effectively address secondary insomnia. However, at this 2005
conference, based on the review of the literature and the panel experts, the following was concluded:

Most causes of insomnia are co-morbid with other conditions. Historically, this has been termed
secondary insomnia. However, the limited understanding of the mechanistic pathways precludes drawing
firm conclusions about the nature of these associations or directions of causality. Furthermore, there is
concern that the term secondary insomnia may promote under treatment. Therefore, we propose the term
comorbid insomnia.

This is an important point since insomnia is often only a secondary symptom that will resolve once the
primary cause, whether it be medical or psychiatric, is treated. Consequently, this results in the
underrecognition and undertreatment of insomnia. Furthermore, oftentimes if sleep difficulties are not the
presenting complaint, there is too little time to address them at an office visit. There is also very little
training in medical school on sleep disorders and their impact on patient overall health and quality of life.
In fact, most providers rate their knowledge of sleep medicine as only fair. Finally, many providers are not
aware of the safety issues, efficacy of cognitive behavioral and pharmacologic therapies, or when to refer
a patient to a sleep medicine specialist.

Insomnia often persists despite treatment of the underlying medical or psychiatric condition and the
persistence of insomnia can increase the risk of relapse of the primary condition in certain cases. In this
regard, the clinician needs to understand that insomnia is a condition in its own right that requires prompt
recognition and treatment to prevent morbidity and improve quality of life for their patients.

For related information, see Medscape's Sleep Disorders Resource Center.

Pathophysiology
In the late 1980s, Spielman created a model of insomnia in terms of predisposing, precipitating, and
perpetuating factors.
 
Predisposing factors

Genetic and neurobiologic factors likely determine a person’s risk of developing insomnia in the context of
a precipitating factor (psychosocial, medical, or psychiatric). Many of these have not been identified.
Sleep and wakefulness is an active, tightly regulated process that may differ between individuals who
have different susceptibilities to exogenous influences. 

Recent studies indicate differential genetic susceptibility to exogenous influences such as caffeine, light,
and stress. For example, one study found that differences in the adenosine 2A receptor gene (ADORA2)
determine differential sensitivity to caffeine’s effect on sleep. The ADORA2A 1083T>C genotype
determined how closely the caffeine-induced changes in brain electrical activity (increased beta activity)
during sleep resembled the alterations observed in patients with insomnia. 

In addition, circadian clock genes (Clock, Per2) have been identified that regulate the circadian rhythm.
For example, a mutation or functional polymorphism in the clock gene (Per2) can lead to circadian rhythm
disorders such as advance sleep phase syndrome (sleep and morning awakening occur earlier than
normal), and delayed sleep phase syndrome (sleep and morning awakening are delayed). Furthermore, a
study examining the association between Clock gene polymorphisms and insomnia revealed a higher
recurrence of initial, middle, and terminal insomnia in patients homozygous for the Clock genotype. 

A missense mutation has been found in the gene encoding the GABAA beta 3 subunit in a patient with
chronic insomnia. Polymorphisms in the serotonin receptor transporter gene may modulate the ability of
an individual to handle stress or may confer susceptibility to depression. In depression, serotonin is an
important neurotransmitter for arousal mechanisms. Furthermore, antagonism of the 5-HT2 receptor
promotes slow wave sleep. Therefore, preliminary basic science evidence indicates a possible genetic
predisposition to hyperarousal and insomnia.

Clinical research has also shown that patients with chronic insomnia show evidence of increased brain
arousal. For example, studies have indicated that patients with chronic primary insomnia demonstrate
increased fast frequency activity during NREM sleep, an EEG sign of hyperarousal, and evidence of
reduced deactivation in key sleep/wake regions during NREM sleep when compared with controls.
Furthermore, patients with insomnia have higher day and night body temperatures, urinary cortisol and
adrenaline secretion, and ACTH than patients with normal sleep. A study of normal sleepers
demonstrated that these changes were not due to sleep deprivation. Only a fraction of patients with
medical and psychiatric conditions develop insomnia, which suggests that some patients have an inherent
susceptibility (whether psychosocial, medical, or psychiatric) to develop insomnia in the context of a
stressful event.

Precipitating factors
 
In retrospective studies, a large proportion of patients with insomnia (78%) can identify a precipitating
trigger for their insomnia. Morin and colleagues showed that these patients demonstrate an increased
response to stress as compared with controls. A number of factors can trigger insomnia in vulnerable
individuals. These factors include depression, anxiety, sleep-wake schedule changes, medications, other
sleep disorders, and medical conditions. In addition, positive or negative family, work-related, and health
events are common insomnia precipitants.

Perpetuating factors
 
Insomnia, regardless of how it is triggered, is generally accepted to be perpetuated by cognitive and
behavioral mechanisms. Cognitive mechanisms include misconceptions about normal sleep requirements
and excessive worry about the ramifications of the daytime effects of inadequate sleep. As a result, these
patients often become obsessive about their sleep or try too hard to fall asleep. These dysfunctional
beliefs often produce sleep disruptive behaviors such as trying to catch up on lost sleep with daytime
naps or sleeping in late, which in turn reduces their natural homeostatic drive to sleep at their habitual
bedtime. Learned sleep-preventing associations are characterized by overconcern about inability to fall
asleep.

Consequently, these patients develop conditioned arousal to stimuli that would normally be associated
with sleep (ie, heightened anxiety and ruminations about going to sleep in their bedroom). A cycle then
develops in which the more the patients strive to sleep, the more agitated they become, and the less they
are able to fall asleep. They also have ruminative thoughts or clock watching as they are trying to fall
asleep in their bedroom. Thus, conditioned environmental cues causing insomnia develop from the
continued association of sleeplessness with situations and behaviors that are typically related to sleep.
Theoretical model of the factors causing chronic insomnia. Chronic insomnia is believed to
primarily occur in patients with predisposing or constitutional factors. These factors may
cause the occasional night of poor sleep but not chronic insomnia. A precipitating factor,
such as a major life event, causes the patient to have acute insomnia. If poor sleep habits
or other perpetuating factors occur in the following weeks to months, chronic insomnia
develops despite the removal of the precipitating factor. Adapted from Spielman AJ, Caruso
LS, Glovinsky PB: A behavioral perspective on insomnia treatment. Psychiatr Clin North Am.
1987 Dec;10(4):541-53.

Overview of mechanisms of normal sleep and wakefulness 

A basic understanding of mechanisms of sleep and wakefulness is essential to understanding potential

mechanisms of insomnia and how insomnia medications affect these pathways to promote sleep.

Both animal and human studies support a model of 2 processes that regulate sleep and wakefulness:
homeostatic and circadian. The homeostatic process is the drive to sleep that is influenced by the
duration of wakefulness. The circadian process transmits stimulatory signals to arousal networks to
promote wakefulness in opposition to the homeostatic drive to sleep.

Sleep-wake cycle.

The suprachiasmatic nucleus (SCN) is entrained to the external environment by the cycle of light and
darkness. The retinal ganglion cells transmit light signals via the retinohypothalamic tract to stimulate the
SCN. A multisynaptic pathway from the SCN projects to the pineal gland, which produces melatonin.
Melatonin synthesis is inhibited by light and stimulated by darkness. The nocturnal rise in melatonin
increases between 8 and 10 am and peaks between 2 and 4 am, then declines gradually over the
morning. Melatonin acts via specific melatonin receptors MT1 which attenuates the alerting signal and
MT2 which phase shifts the SCN clock. The novel sleep-promoting drug ramelteon acts specifically at the
MT1 and MT2 receptors to promote sleep.

Brain areas critical for wakefulness include the tuberomammillary nucleus (TMN) in the posterior
hypothalamus that contains histamine neurons, which project stimulatory inputs to brainstem arousal
centers such as the locus coeruleus (LC) (norepinephrine), the dorsal raphe nuclei (DRN) (serotonin), the
ventral tegmental area (VTA) (dopamine), and the basal forebrain (acetylcholine), which project diffusely
to cortical areas to promote arousal.

The TMN also inhibits sleep-promoting areas, such as the anterior hypothalamus. Similarly, the brainstem
arousal regions inhibit sleep-promoting regions in the anterior hypothalamus. Adenosine, a
neurotransmitter, accumulates in the brain during prolonged wakefulness and inhibits wake-promoting
regions in the posterior hypothalamus and the basal forebrain. Acetylcholine in the basal forebrain also
projects diffusely to cortical areas and the TMN to promote wakefulness.

The ascending arousal system. Adapted from Saper et al. Hypothalamic Regulation of Sleep
and Circadian Rhythms. Nature 2005;437:1257-1263.

The anterior hypothalamus, which includes the ventrolateral preoptic nucleus (VLPO) contains GABA and
the peptide galanin, which are inhibitory and promote sleep. They project to the TMN and the brainstem
arousal regions to inhibit wakefulness. GABA is the predominant inhibitory neurotransmitter in the central
nervous system.
Ventrolateral pre-optic nucleus inhibitory projections to main components of the arousal
system to promote sleep.

Saper and colleagues proposed the flip-flop switch model of sleep-wake regulation.1 This flip-flop circuit
consists of 2 sets of mutually inhibitory components. The sleep side is the VLPO and the arousal side
includes TMN histaminergic neurons and brainstem arousal regions (the DRN serotonergic neurons, VTA
dopaminergic neurons, and LC noradrenergic neurons). Each side of the switch inhibits the other. For
example, when activation of one side is slightly stronger, the weaker side has increased inhibition, thus
further tipping the balance toward the stronger side. This flip-flop switch allows for rapid state transitions.

Schematic flip-flop switch model. Adapted from Saper C et al. Hypothalamic regulation of
sleep and circadian rhythms. Nature 2005;437:1257-1263.

Hypocretin neurons in the posterolateral hypothalamus are active during wakefulness and project to all of
the wakefulness arousal systems described above. Hypocretin neurons interact with both the sleep-active
and the sleep-promoting systems and act as stabilizers between wakefulness-maintaining and sleep-
promoting systems to prevent sudden and inappropriate transitions between the 2 systems.2 For example,
patients with narcolepsy with cataplexy have a greater than 90% loss of hypocretin neurons, and they
have sleep-wake state instability with bouts of NREM/REM sleep intruding into wakefulness.

Benzodiazepine receptor agonists (BZRAs) and nonbenzodiazepine receptor agonists (NBZRAs), for
example, work through GABAA receptors to promote sleep by inhibiting brainstem monoaminergic arousal
pathways, through facilitation of VLPO inhibitory GABAergic projections to arousal centers such as the
anterior hypothalamus TMN, the posterolateral hypothalamic hypocretin neurons, and the brainstem
arousal regions (see Medication for further information about BZRAs and NBZRAs).

In summary, sleep and wakefulness is a tightly regulated process with reciprocal connections that
produce consolidated periods of wakefulness and sleep that are entrained by environmental light to occur
at specific times of the 24-hour cycle.

Frequency
United States

In a 1991 survey, 30-35% of American adults reported difficulty sleeping in the past year and 10%
reported the insomnia to be chronic and/or severe. Despite the high prevalence, only 5% of persons with
chronic insomnia visited their physician specifically to discuss their insomnia. Only 26% discussed their
insomnia during a visit made for another problem.

International

A study from Quebec indicated an overall prevalence of insomnia of approximately 20% of French
Canadians. A study of young adults in Switzerland indicated a 9% prevalence of chronic insomnia. A
World Health Organization (WHO) study conducted in 15 centers found a prevalence of approximately
27% for the complaint "difficulty sleeping."

Mortality/Morbidity
Consequences of chronic insomnia  

 Patients with insomnia report decreased quality of life compared with normal controls in all
dimension of the SF-36.
 Patients with insomnia report excessive fatigue as measure by the Fatigue Severity Scale and the
Profiles of Mood Status (POMS).
 Patients with insomnia are more than twice as likely as the general population to have a fatigue-
related motor vehicle accident.
 Increased occupational dysfunction and decreased work performance are likely due to chronic
hyperarousal state or perceptions of sleep deprivation rather than actual sleep loss from
insomnia. For example, unlike patients with chronic sleep deprivation from other causes, patients
with insomnia report less excessive daytime sleepiness and less psychomotor and cognitive
impairment.
 Knutson et al found that the quantity and quality of sleep correlate with future blood pressure. In
an ancillary to the Coronary Artery Risk Development in Young Adults (CARDIA) cohort study,
measurement of sleep for 3 consecutive days in 578 subjects showed that shorter sleep duration
and lower sleep maintenance predicted both significantly higher blood pressure levels and
adverse changes in blood pressure over the next 5 years (P<0.05).3

Associations of insomnia with depression and anxiety

One of the early descriptions of an association between insomnia and depression and anxiety was by
Ford and Kamerow.4  What is still unknown is the nature of the association. For example, does insomnia
presage the development of an incipient mood disorder and/or do mood disorders independently
predispose to insomnia.
After adjusting for medical disorders, ethnicity, and sex, patients with insomnia were 9.8 times more likely
to have clinically significant depression and 17.3 times more likely to have clinically significant anxiety
than persons who did not have insomnia.

Ohayon and Roth found that symptoms of insomnia were reported to occur before the first episode of an
anxiety disorder 18% of the time, simultaneously 39% of the time, and after the onset of an anxiety
disorder 44% of the time.5 

In contrast, insomnia symptoms were reported to occur before a first episode of a mood disorder 41% of
the time, simultaneously 29% of the time, and after the onset of a mood disorder 29% of the time.

Race
At this time, no data are available to suggest an association for or against race as a risk factor for
insomnia.

Sex
The prevalence of chronic insomnia is 1.2-2.0 times greater in women than men. One study by Strine and
colleagues indicated that women who have menstrual-related problems are more likely to have insomnia
as compared with women without such problems.6 In fact, after adjustments were made for age, race and
ethnicity, education, marital status, and employment status, women who had menstrual-related problems
were 2.4 times as likely to report insomnia than women without such problems. At this time, whether
social factors or neurobiologic factors contribute to the increased prevalence in women is not known.

Age
Chronic insomnia increases in frequency with age and is more common in the elderly. This is presumed
due to greater psychosocial stressors, losses, and medical illnesses. Recent epidemiologic data indicate
that the prevalence of chronic insomnia increases form 25% in the adult population to 50% in the elderly
population.

Clinical

History
The history is the most important part of evaluating insomnia. It must include a complete sleep history,
medical history, psychiatric history, social history, and careful medication review.

Sleep history

Determining the timing of insomnia, the patient's sleep habits (commonly referred to as sleep hygiene),
and symptoms of sleep disorders associated with insomnia is important.

 Timing of insomnia: Patients should be asked about any difficulty falling asleep, frequent or early
morning awakening, problems in sleep onset, and whether they feel sleepy when getting into bed.
 Sleep schedule: Patients must be asked what time they go to bed and rise from bed in the
morning. Determine whether the sleep schedule is consistent and if the schedule has changed
recently.
  Sleep environment: Patients should be asked about temperature, bed comfort, noise, and light
levels. Ask whether the patient sleeps better in his or her own bed or in a chair or a foreign
environment (like a hotel).
 Sleep habits: Patients with insomnia often have poor sleep hygiene. They should be asked about
activities prior to bedtime (ie, relaxation or work), whether they read or watch TV in bed, and
whether the TV or light is kept on during the night. Also, ask patients what they do if unable to fall
asleep and whether they fall asleep after waking up in the middle of the night. Ask patients about
daytime naps and whether they exercise and the time of exercise.
 Patients should be asked about symptoms of other sleep disorders such as obstructive sleep
apnea (eg, snoring, witnessed apneas, gasping) and restless legs syndrome/periodic limb
movement disorder (ie, restless feeling in legs on lying down, which improves with movement;
rhythmic kicking during the night; sheets in disarray in the morning).
 Daytime effects: Patients should experience daytime effects if they truly are not sleeping at night.
In fact, if a patient is having no daytime effects, he or she is probably getting adequate sleep and
the complaint of insomnia is truly subjective. Common complaints are fatigue, tiredness, lack of
energy, irritability, reduced work performance, and difficulty concentrating. These complaints
should be distinguished from the complaint of excessive sleepiness, which is uncommon in
insomnia. For example, if a patient complains of excessive daytime sleepiness (ie Epworth
Sleepiness Scale Score >10), another sleep disorder should also be considered. (See Media file
12 for the Epworth Sleepiness Scale.)

Medical history

A thorough medical history and review of systems should be performed, with particular emphasis on
those disorders mentioned in Causes.

Psychiatric history

A review of signs and symptoms of anxiety or depression should be sought. A 2-question case-finding
instrument can help screen for depression.

Diagnostic algorithm for major depression.

Diagnostic criteria for generalized anxiety disorder.

Social history

For transient or short-term insomnia, inquire about new situational stresses such as a new job, new
school, relationship change, or bereavement. For chronic insomnia, attempt to relate the onset of
insomnia to past stresses or medical illnesses. Inquire about tobacco, caffeinated products, alcohol, and
illegal drug use.

Medication history

Medications that commonly cause insomnia include beta-blockers, clonidine, theophylline (acutely),
certain antidepressants (protriptyline or fluoxetine), decongestants, and stimulants. Also inquire about
over-the-counter and herbal remedies that the patient may be taking.

Physical
The physical examination can provide clues to comorbid insomnia.

 A large neck size of 18 inches or greater in males, elevated BMI of 30 kg/m2, enlarged tonsils,
Mallampati airway score of 3 or 4 (see Media file 2), low lying soft palate particularly in patients
with hypertension or cardiac disease, and obstructive sleep apnea/hypopnea syndrome should be
considered. Other features include enlarged tongue, retrognathia, micrognathia, or a steep
mandibular angle.
 If patients have evidence of peripheral neuropathy (ie, stocking distribution loss of temperature
sensation) with or without trophic changes, they should be asked about painful symptoms (ie,
burning sensation) in their feet, and history of diabetes, alcohol abuse, and neurologic
consultation should be requested.
 If patients complain of symptoms of restless legs syndrome or symptoms suggestive of a
neurologic disorder, such as nocturnal seizures, Parkinson disease, or a neuromuscular disorder,
a neurologic consultation should be requested.
 In patients with chronic pain syndromes or rheumatologic syndromes, referral to a pain
management specialist and/or rheumatologist should be considered.
 If chest examination shows reduced breath sounds; clubbing or wheezing in the setting of clinical
signs; and symptoms suggestive of chronic obstructive pulmonary disease, asthma, or obesity
hypoventilation syndrome, pulmonary consultation should be requested.

Causes
Many clinicians often assume that insomnia is secondary to a psychiatric disorder, However, a large
epidemiologic survey showed that half of insomnia diagnoses were not related to a primary psychiatric
disorder. As mentioned earlier, an insomnia diagnosis does increase the future risk for depression or
anxiety (see Morbidity).

Frequency of insomnia causes.

Classification of Insomnia
The International Classification of Sleep Disorders classifies insomnia into 11 categories, listed below. 

Adjustment insomnia (acute insomnia)

This occurs in the context of an identifiable stressor (eg, personal loss, change in interpersonal
relationship, bereavement, occupational stress, job loss) that acts as a precipitating factor. It typically last
3 months or less and resolves as the stressor is no longer present or as the individual adapts to the
stressor . 
 
Chronic insomnia

The following are diagnoses of chronic insomnia and meet the criteria for chronic insomnia:

1. Repeated difficulty with the initiation, duration, maintenance, or quality of sleep that occurs
despite adequate time and opportunity for sleep that results in some form of daytime impairment.
2. Number 1 must be present for at least 1 month.

Psychophysiologic insomnia (primary insomnia) 

 The patient has evidence of conditioned sleep difficulty and or/heightened arousal in bed as
indicated by one or more of the following:
o Excessive focus on and heightened anxiety about sleep
o Difficulty falling asleep at the desired bedtime or during planned naps, but no difficulty
falling asleep during other monotonous activities when not intending to sleep
o Ability to sleep better away from home than at home
o Mental arousal in bed characterized either by intrusive thoughts or a perceived inability to
volitionally cease sleep-preventing mental activity
 o Heightened somatic tension in bed reflected by a perceived inability to relax the body
sufficiently to allow the onset of sleep
 The sleep disturbance is not better explained by another sleep disorder, medical or neurologic
disorder, medication use, or substance abuse disorder.

Paradoxical insomnia 

 One or more of the following criteria apply:

o The patient reports a chronic pattern of little or no sleep most nights, with rare nights
during which relatively normal amounts of sleep are obtained.
o Sleep log data from one or more weeks of monitoring show an average sleep time often
with no sleep at all indicated for several nights each week; typically daytime naps are
absent following such nights.
o The patients typically show a mismatch between objective findings from
polysomnography or actigraphy and subjective sleep estimates from self-reported sleep
diary.
 At least one of the following is observed:
o The patient reports constant or near constant awareness of environmental stimuli
throughout most nights.
o The patient reports a pattern of conscious thoughts or rumination throughout most nights
while maintaining a recumbent posture.
 The daytime impairment reported is consistent with that reported by other insomnia subtypes but
is much less severe than expected given the extreme level of sleep deprivation reported.
 The sleep disturbance is not better explained by another sleep disorder, medical or neurologic
disorder, medication use, or substance abuse disorder.

Insomnia due to medical condition

 The patient has a coexisting medical condition known to disrupt sleep.

 The insomnia is clearly associated with the medical condition. The insomnia began near the time
of onset or with significant progression of the medical condition and waxes and wanes with the
severity of this condition.
 The sleep disturbance is not better explained by another sleep disorder, medical or neurologic
disorder, medication use, or substance abuse disorder.

Insomnia due to mental disorder

 A mental disorder has been diagnosed according to the criteria of DSM-IV-TR.

 The insomnia is temporally associated with the mental disorder; however, in some cases,
insomnia may appear a few days or weeks before the emergence of the underlying mental
disorder.
 The insomnia is more prominent than that typically associated with the mental disorders, as
indicated by causing marked distress or constituting an independent focus of treatment.
 The sleep disturbance is not better explained by another sleep disorder, medical or neurologic
disorder, medication use, or substance abuse disorder.

Insomnia due to drug or substance abuse

  One of the following applies:
o The patient has current ongoing dependence on or abuse of a drug or substance known
to have sleep disruptive properties either during periods of use or intoxication or during
periods of withdrawal.
o The patient has current ongoing use of or exposure to a medication, food, or toxin known
to have sleep-disruptive properties in susceptible individuals.
 The insomnia is temporally associated with the substance exposure, use, or abuse, or acute
withdrawal.
 The sleep disturbance is not better explained by another sleep disorder, medical or neurologic
disorder, medication use, or substance abuse disorder.

Insomnia not due to substance or known physiological condition, unspecified

This diagnosis is used for forms of insomnia that cannot be classified elsewhere in ICSD-2, but are
suspected to be due to an underlying mental disorder, psychological factors, or sleep disruptive
processes. This diagnosis can be used on a temporary basis until further information is obtained to
determine the specific mental condition or psychological or behavioral factors responsible for the sleep
difficulty.

Inadequate sleep hygiene

 Inadequate sleep hygiene practices are evident by the presence of at least 1 of the following:
o Improper sleep scheduling consisting of frequent daytime napping, selecting highly
variable bed or rising times or spending excessive amounts of time in bed.
o Routine use of products containing alcohol, nicotine, or caffeine, especially in the period
preceding bedtime.
o Engagement in mentally stimulating, physically activating, or emotionally upsetting
activities too close to bedtime.
o Frequent use of the bed for activities other than sleep (eg, television watching, reading,
studying, snacking, thinking, planning).
o Failure to maintain a comfortable sleeping environment.
 The sleep disturbance is not better explained by another sleep disorder, medical or neurologic
disorder, medication use, or substance abuse disorder.

Idiopathic insomnia 

A longstanding complaint of insomnia with insidious onset in infancy or childhood. No precipitant or cause
is identifiable. There is a persistent course with no sustained periods of remission. This condition is
present in 0.7% of adolescents and 1% of very young adults.

Behavioral insomnia of childhood

 A child's symptoms meet the criteria for insomnia based on parents or other adult caregivers
observations.
 The child shows a pattern consistent with either sleep-onset association or limit-setting type of
insomnia:
o Sleep onset association type
 Falling asleep is an extended process that requires special conditions.
  Sleep onset associations are highly problematic or demanding.
 In the absence of associated conditions, sleep onset is significantly delayed or
sleep is otherwise disrupted.
 Nightime awakenings require caregiver intervention for the child to return to
sleep.
o Limit-setting type
 The individual has difficulty initiating or maintaining sleep.
 The individual stalls or refuses to go to bed at an appropriate time or refuses to
return to bed following a nighttime awakening.
 The caregiver demonstrates insufficient or inappropriate limit setting to establish
appropriate sleeping behavior in the child.

Primary sleep disorders causing insomnia

 Restless legs syndrome (RLS) is a sleep disorder characterized by the following:

o An urge to move the legs, usually accompanied by uncomfortable and unpleasant
physical sensations in the legs.
o The urge to move or the unpleasant sensations begin or worsen during periods of rest or
inactivity such as lying or sitting.
o The urge to move or the unpleasant sensations are partially or totally relieved by moving,
such as walking or stretching, at least as long as the activity continues.
o The urge to move or the unpleasant sensations are worse or only occur in the evening or
the night.
 Obstructive sleep apnea/hypopnea syndrome:A minority of patients complain of insomnia rather
than hypersomnolence. They frequently complain of multiple awakenings or sleep-maintenance
difficulties. They may also have nocturia causing frequent nocturnal awakenings.
 Circadian rhythm disorders
o Advanced sleep phase syndrome: The patient feels sleepy earlier than their desired
bedtime (ie, 8 pm) and they wake up earlier than they would like to (ie, 4-5 am). This
condition is more common in the elderly. These patients typically complain of sleep
maintenance insomnia.
o Delayed sleep phase syndrome: The patient does not feel sleepy until much later than
the desired bedtime, and he or she wakes up later than desired or socially acceptable.
On sleep diaries or actigraphy, these patients show a consistent sleep time with earlier
wake times that correspond to school or work days, and delayed wake times on
weekends, time off, and vacations. This condition often begins in adolescence and may
be associated with a family history in up to 40% of patients. These patients report
difficulty falling asleep at usually socially desired bedtimes, and complain of excessive
daytime sleepiness during the school or work week.
o Shift work sleep disorder: A complaint of insomnia or excessive sleepiness is typically
temporally related to a recurring work schedule that overlaps the usual sleep time. This
can occur with early morning shifts (4-6 am), where the patient is anxious about waking
up in time for their early shift particularly when they have a rotating shift schedule.
Evening shifts that end at 11 pm can result in insomnia in that the patient may need some
time to wind down from work before retiring to bed. Night shift can be associated with
both sleep onset and maintenance insomnia due to exposure to sunlight on their drive
 home from work, daylight exposure in their bedroom, and social and environmental cues
(picking up children at school, paying bills, household chores, etc).
o Irregular sleep-wake rhythm: This is typically seen in patients with poor sleep hygiene,
patients who live or work alone with minimal exposure to light, activity, and social cues.
These patients randomly nap throughout the day making it difficult, if not impossible, to
fall asleep at a habitual bedtime with a consolidated sleep period.