Insomnia Mechanisms: The Hyperarousal Model
Insomnia involves chronic hyperarousal: elevated 24-hour cortisol, higher metabolic rate, and increased high-frequency EEG activity at night; CBT-I achieves remission in 70–80% of patients and outperforms sleep medication.
| Measure | Value | Unit | Notes |
|---|---|---|---|
| Metabolic rate elevation in insomnia | +7 | % higher 24h metabolic rate | Bonnet & Arand 1995; insomniacs vs matched controls with normal sleep |
| CBT-I remission rate | 70–80 | % | Multiple meta-analyses; first-line treatment per ACP guidelines |
| Insomnia prevalence | 10–15 | % of adults | Chronic insomnia (3+ nights/week for 3+ months); 30–35% have occasional symptoms |
| High-frequency EEG in insomnia | Elevated | gamma/beta power | Insomniacs show higher beta-frequency EEG during sleep — 'first night effect' permanently |
| Cortisol 24-hour levels | Elevated | vs good sleepers | HPA axis hyperactivity; particularly elevated evening cortisol |
The Hyperarousal Model
Insomnia disorder is defined clinically as difficulty initiating or maintaining sleep, or early morning awakening, occurring ≥3 nights/week for ≥3 months, causing significant daytime impairment. Its prevalence is 10–15% of adults for chronic insomnia; 30–35% experience occasional insomnia symptoms.
The hyperarousal model, proposed by Bonnet and Arand (1995) and elaborated by Riemann et al. (2010), proposes that insomnia is not simply “not sleeping” but a state of chronic physiological and psychological hyperarousal that prevents the deactivation necessary for sleep onset.
Evidence for hyperarousal in insomnia:
| Marker | Finding in Insomniacs |
|---|---|
| 24h metabolic rate | +7% above matched controls |
| Resting heart rate | Higher throughout 24h |
| Core body temperature | Less pronounced nocturnal decline |
| Cortisol (24h) | Elevated; evening cortisol particularly higher |
| EEG during sleep | More high-frequency (beta) activity |
| Waking EEG (alpha) | Higher frontal alpha in daytime |
| Brain imaging (fMRI) | Greater activity in arousal-promoting regions at sleep onset |
The 3P Model
The 3P (Spielman) model explains how acute sleep difficulty becomes chronic insomnia:
- Predisposing factors: biological (arousal system sensitivity, HPA axis reactivity) and psychological (anxiety trait, perfectionism) factors that lower the threshold for insomnia
- Precipitating factors: acute stressors that trigger sleep disruption (job change, illness, divorce, grief)
- Perpetuating factors: behaviors and cognitions that maintain insomnia beyond the precipitating event: spending excessive time in bed, irregular sleep schedules, daytime napping, cognitive arousal (worry about sleep, clock-watching), and conditioned wakefulness (the bedroom becomes associated with arousal rather than sleep)
CBT-I targets perpetuating factors through sleep restriction therapy, stimulus control, sleep hygiene, and cognitive restructuring.
CBT-I: First-Line Treatment
Cognitive Behavioral Therapy for Insomnia (CBT-I) is a structured 6–8 week program comprising:
- Sleep restriction: reduces time in bed to actual sleep time, building sleep pressure
- Stimulus control: re-associates the bed with sleepiness only (no screens, reading, worrying in bed)
- Sleep hygiene: consistent wake time, light exposure, caffeine timing, temperature optimization
- Cognitive restructuring: addresses catastrophic beliefs about sleep (“I must get 8h or I can’t function”)
- Relaxation techniques: reduces pre-sleep physiological arousal
Meta-analyses consistently show CBT-I produces remission in 70–80% of patients, with effects maintained at 1-year follow-up. The American College of Physicians (2016) and virtually all sleep medicine societies recommend CBT-I over pharmacotherapy as first-line treatment.
Related Pages
Sources
- Bonnet MH & Arand DL — 24-Hour metabolic rate in insomniacs and matched normal sleepers. Sleep (1995)
- Riemann D et al. — The hyperarousal model of insomnia: a review of the concept. Sleep Med Rev (2010)
- Morin CM et al. — Cognitive-behavioral therapy for late-life insomnia. J Consult Clin Psychol (1993)
- Qaseem A et al. — Management of chronic insomnia disorder in adults: ACP Clinical Guideline. Ann Intern Med (2016)
Frequently Asked Questions
What causes insomnia?
The most accepted model is the 3P model (predisposing, precipitating, perpetuating factors): predisposing factors include genetic hyperarousal traits and anxiety-prone personalities; precipitating factors trigger onset (stress, illness, life change); perpetuating factors maintain it long-term (excessive time in bed, napping, worrying about sleep, conditioned arousal to the bedroom). CBT-I addresses perpetuating factors.
Is insomnia primarily a nighttime or daytime problem?
The hyperarousal model characterizes insomnia as a 24-hour disorder, not just a nighttime problem. Insomniacs show elevated cortisol, higher resting metabolic rate, faster heart rate, and more beta-frequency brain activity throughout the day — not only at night. This physiological hyperarousal state makes the brain resistant to sleep even when the individual desperately wants to sleep.
Should sleeping pills be used for insomnia?
Clinical guidelines (American College of Physicians, 2016) recommend cognitive behavioral therapy for insomnia (CBT-I) as first-line treatment, not sleep medications. CBT-I produces durable remission (70–80%) without dependency or rebound insomnia. Pharmacotherapy is recommended only when CBT-I is unavailable or insufficient, and for limited duration. Z-drugs (zolpidem, eszopiclone) and benzodiazepines carry risks of dependency and next-day impairment.