Insomnia Disorder

Clinical picture

• Difficulty initiating sleep, maintaining sleep, or early morning awakening despite adequate opportunity and favorable circumstances.
• Daytime consequences dominate the complaint: fatigue, irritability, impaired concentration, and anticipatory worry about the next night.
• Patients show sleep-effort behaviors such as excessive time in bed, clock-watching, and daytime napping that perpetuate the problem.
• Conditioned arousal presents classically as overwhelming sleepiness on the couch that vanishes the moment the patient enters the bedroom.
• Subjective and objective sleep estimates diverge, and patients typically underestimate total sleep time by roughly 30 to 60 minutes.
• A sleep diary kept for 1 to 2 weeks reveals variable schedules and low sleep efficiency that the clinical interview alone will miss.

Criteria snapshot

• Sleep dissatisfaction involving initiation, maintenance, or early awakening, present at least 3 nights per week for at least 3 months.
• Clinically significant daytime distress or impairment is required, so poor sleep without daytime consequence does not meet the threshold.
• The difficulty must occur despite adequate opportunity for sleep, which excludes insufficient sleep caused by schedule constraints.
• DSM-5-TR dropped the primary versus secondary split, so insomnia is diagnosed alongside depression or pain rather than subordinated to it.
• Other sleep-wake disorders, substance effects, and coexisting medical conditions must not better account for the presenting complaint.

Neurobiology

• Hyperarousal is the core model, with elevated cortisol and ACTH, raised metabolic rate, and increased high-frequency EEG at sleep onset.
• Sleep-promoting VLPO GABAergic neurons compete with arousal systems using orexin, histamine, norepinephrine, and acetylcholine.
• Dual orexin receptor antagonists target orexin signaling, reducing wake drive rather than broadly sedating the entire brain.
• Homeostatic sleep pressure builds through adenosine accumulation, and caffeine antagonizes adenosine receptors for roughly 5 to 7 hours.
• Chronic insomnia roughly doubles the risk of incident depression and is linked to hypertension and cardiometabolic disease.
• Heritability is about 30% to 40%, with genome-wide studies implicating loci shared with anxiety and depressive phenotypes.

Psychology

• The 3P model of predisposing, precipitating, and perpetuating factors explains how acute situational insomnia becomes chronic.
• Perpetuating behaviors such as extending time in bed reduce sleep efficiency and strengthen the association of bed with wakefulness.
• Dysfunctional beliefs about sleep, including catastrophic predictions about tomorrow, sharply raise pre-sleep cognitive arousal.
• Classical conditioning turns the bed and the bedtime routine into learned cues for alert wakefulness rather than for sleep onset.
• Threat monitoring, clock-checking, and effortful trying to sleep are paradoxical behaviors that directly maintain wakefulness.

Differential & comorbidity

• Screen for obstructive sleep apnea using STOP-BANG, plus restless legs syndrome, both of which are frequently missed contributors.
• Delayed sleep-wake phase disorder presents as sleep-onset insomnia with normal sleep when the schedule is allowed to run free.
• Insomnia is bidirectional with depression, anxiety, and PTSD, and treating the insomnia improves the comorbid disorder as well.
• Evaluate substances: alcohol, caffeine, nicotine, stimulants, and SSRI-related sleep disruption are common and reversible contributors.
• Insomnia is an independent suicide risk factor, and nightmares with short sleep raise risk beyond depression severity alone.

Pharmacologic treatment

• Medication is second-line: CBT-I should be offered first, with pharmacotherapy used short-term or as a targeted adjunct.
• Dual orexin receptor antagonists lemborexant 5-10 mg and suvorexant 10-20 mg are preferred for sleep-maintenance insomnia.
• Zolpidem 5-10 mg and eszopiclone 1-3 mg work short-term; counsel on complex sleep behaviors and next-day psychomotor impairment.
• Doxepin 3-6 mg and ramelteon 8 mg are non-scheduled options with favorable safety profiles in older adults.
• Avoid antihistamines, antipsychotics, and long-term benzodiazepines; trazodone 25-100 mg is widely used but weakly supported.

Psychotherapy

• CBT-I over 4 to 8 sessions is first-line, matching hypnotics acutely and clearly outperforming them at 6 to 12 month follow-up.
• Sleep restriction therapy raises sleep efficiency by limiting time in bed to actual sleep time plus roughly 30 minutes.
• Stimulus control reserves the bed for sleep and sex, with the patient leaving bed when awake beyond about 15 to 20 minutes.
• Cognitive restructuring targets catastrophic sleep beliefs, while relaxation training addresses residual somatic arousal.
• Digital CBT-I programs achieve effects approaching in-person therapy and help offset the shortage of trained providers.

Adjunct options

• Use consensus sleep diaries and the Insomnia Severity Index to track outcomes, where a 7-point ISI drop is clinically meaningful.
• Actigraphy or a wearable can supplement diaries, while polysomnography is reserved for suspected apnea or periodic limb movements.
• Optimize circadian inputs: morning outdoor light, evening dimming, a fixed wake time, exercise timing, and a cool dark bedroom.
• Taper hypnotics gradually while delivering CBT-I, which prevents rebound insomnia and reduces the risk of reinstatement.
• Treat comorbid apnea, chronic pain, and nocturia concurrently, since insomnia rarely resolves while these remain unaddressed.

Clinical pearls

• Treat insomnia in its own right; it does not simply remit when depression lifts.
• Restricting time in bed feels wrong to patients and outperforms every other step.
• Sleepy on the couch but wide awake in bed means conditioned arousal.