Insomnia & Mental Health – Clinical Psychology Page 1 of 8
1. MEASURING SLEEP — METHODS, USES & LIMITATIONS
Actigraphy Polysomnography (PSG) Questionnaires & Clinical Assessment
Wrist-worn device inferring sleep and wake from Electrodes on head and body recording brain and Self-report measures, sleep diaries, clinical
movement. Common in research for multi-night muscle activity. Detailed information on sleep interviews. Most common in routine clinical
data in natural environments. Output = actogram stages and architecture. Output = practice.
(blue = sleep, black = activity, yellow = light polysomnogram. Identifies NREM, REM, Why important: Insomnia is defined partly by
exposure). awakenings, physiological abnormalities. subjective complaint — dissatisfaction with
✗ Limitation: Can misclassify quiet Clinical implication: PSG is NOT usually sleep quantity or quality and associated daytime
wakefulness as sleep — particularly relevant in required to diagnose insomnia. Used in research impairment. Objective measurement is not always
insomnia where the person may lie still while or where another disorder is suspected (sleep the same as subjective sleep experience.
awake, worrying or monitoring sleep. apnoea, narcolepsy, parasomnia). People with insomnia may report poor sleep even
✗ Exam point: Do not write that PSG is "the when objective sleep duration is less severely
best" measure for insomnia — insomnia is disturbed.
assessed clinically using self-report and sleep
diary.
Key exam point: Objective measurement ≠ subjective sleep experience. This is why questionnaires and clinical interviews remain important in routine
practice alongside or instead of PSG.
THE HYPNOGRAM, SLEEP DEPTH & SLEEP ARCHITECTURE
Hypnogram — shows how sleep stages are distributed across the night: Why sleep architecture matters clinically:
Deep NREM sleep concentrated in the earlier part of the night In insomnia, the issue is often not only "how many hours" someone sleeps,
REM sleep becomes more prominent later in the night but also:
Typical night contains around 4–5 sleep cycles (varies with age, stress, Sleep continuity — repeated awakenings
substances, sleep deprivation) Sleep efficiency — time asleep ÷ time in bed
Perceived restoration — subjective quality of sleep
Auditory arousal threshold: The minimum amount of noise needed to Delayed sleep onset or repeated awakenings can disrupt the normal
wake someone from a particular sleep stage. Deeper sleep stages require a organisation of sleep stages.
louder stimulus to produce awakening. Relevant because noise pollution can
disturb sleep even without full remembered awakening.
, Insomnia & Mental Health – Clinical Psychology Page 2 of 8
2. WHAT CONTROLS SLEEP? THE THREE MAIN PROCESSES
A — HOMEOSTATIC B — CIRCADIAN C — PSYCHOLOGICAL
Process S = Sleep Pressure Biological Clock (~24-hour timing) Arousal, Learning & Automaticity
Sleep pressure builds from the moment a person Regulates when the body is biologically prepared Even when sleep pressure is high and circadian
wakes. The longer awake → stronger drive for for wakefulness and sleep. timing is appropriate, the brain can still "override"
sleep. Light is the key environmental cue. Intrinsically sleep if anxious, alert, frustrated, or trying hard to
Adenosine accumulates during wakefulness, photosensitive retinal ganglion cells detect light fall asleep.
contributing to sleep pressure; reduced during and help synchronise the sleep-wake rhythm. Sleep onset most likely when:
sleep. Light signals → suprachiasmatic nucleus Person is sleepy
Caffeine temporarily reduces perceived (master clock, in the hypothalamus) → melatonin It is the right biological time
sleepiness by blocking adenosine receptors — secretion. They are calm
but does not remove the underlying need for Melatonin rises in darkness; suppressed by light. Sleep environment is associated with rest
sleep. Bright light at night can delay sleepiness; morning
Core idea: Insomnia is often a problem of
Recommended: ~7–9 hours for adults (individual light strengthens circadian timing.
hyperarousal and learned wakefulness in a
need varies). Correction: SCN = hypothalamus. Pineal context where sleep should normally happen.
Exam wording: Process S explains why gland = melatonin secretion.
staying awake longer makes sleep more likely,
but it does not guarantee sleep if
psychological arousal is high.
5. THE 3P MODEL OF CHRONIC INSOMNIA (SPIELMAN)
PREDISPOSING PRECIPITATING PERPETUATING
Vulnerability factors that make sleep problems Stressors that trigger the initial acute sleep Maladaptive coping responses that maintain
more likely. e.g. anxiety proneness, hyperarousal disruption. e.g. bereavement, illness, relationship insomnia even after the original stressor
tendency, genetics, poor emotion regulation, breakdown, job loss, exam pressure. improves: spending longer in bed, napping,
perfectionism. monitoring, worrying, trying hard to sleep, clock-
watching.
Why the 3P model matters for essays: It explains why many people have short-term sleep disruption, but only some develop chronic insomnia. It prevents
an overly biological answer — insomnia can begin with a life stressor but become maintained by learned behaviours and cognitive arousal. The perpetuating
factors are the primary targets of CBT-I.
1. MEASURING SLEEP — METHODS, USES & LIMITATIONS
Actigraphy Polysomnography (PSG) Questionnaires & Clinical Assessment
Wrist-worn device inferring sleep and wake from Electrodes on head and body recording brain and Self-report measures, sleep diaries, clinical
movement. Common in research for multi-night muscle activity. Detailed information on sleep interviews. Most common in routine clinical
data in natural environments. Output = actogram stages and architecture. Output = practice.
(blue = sleep, black = activity, yellow = light polysomnogram. Identifies NREM, REM, Why important: Insomnia is defined partly by
exposure). awakenings, physiological abnormalities. subjective complaint — dissatisfaction with
✗ Limitation: Can misclassify quiet Clinical implication: PSG is NOT usually sleep quantity or quality and associated daytime
wakefulness as sleep — particularly relevant in required to diagnose insomnia. Used in research impairment. Objective measurement is not always
insomnia where the person may lie still while or where another disorder is suspected (sleep the same as subjective sleep experience.
awake, worrying or monitoring sleep. apnoea, narcolepsy, parasomnia). People with insomnia may report poor sleep even
✗ Exam point: Do not write that PSG is "the when objective sleep duration is less severely
best" measure for insomnia — insomnia is disturbed.
assessed clinically using self-report and sleep
diary.
Key exam point: Objective measurement ≠ subjective sleep experience. This is why questionnaires and clinical interviews remain important in routine
practice alongside or instead of PSG.
THE HYPNOGRAM, SLEEP DEPTH & SLEEP ARCHITECTURE
Hypnogram — shows how sleep stages are distributed across the night: Why sleep architecture matters clinically:
Deep NREM sleep concentrated in the earlier part of the night In insomnia, the issue is often not only "how many hours" someone sleeps,
REM sleep becomes more prominent later in the night but also:
Typical night contains around 4–5 sleep cycles (varies with age, stress, Sleep continuity — repeated awakenings
substances, sleep deprivation) Sleep efficiency — time asleep ÷ time in bed
Perceived restoration — subjective quality of sleep
Auditory arousal threshold: The minimum amount of noise needed to Delayed sleep onset or repeated awakenings can disrupt the normal
wake someone from a particular sleep stage. Deeper sleep stages require a organisation of sleep stages.
louder stimulus to produce awakening. Relevant because noise pollution can
disturb sleep even without full remembered awakening.
, Insomnia & Mental Health – Clinical Psychology Page 2 of 8
2. WHAT CONTROLS SLEEP? THE THREE MAIN PROCESSES
A — HOMEOSTATIC B — CIRCADIAN C — PSYCHOLOGICAL
Process S = Sleep Pressure Biological Clock (~24-hour timing) Arousal, Learning & Automaticity
Sleep pressure builds from the moment a person Regulates when the body is biologically prepared Even when sleep pressure is high and circadian
wakes. The longer awake → stronger drive for for wakefulness and sleep. timing is appropriate, the brain can still "override"
sleep. Light is the key environmental cue. Intrinsically sleep if anxious, alert, frustrated, or trying hard to
Adenosine accumulates during wakefulness, photosensitive retinal ganglion cells detect light fall asleep.
contributing to sleep pressure; reduced during and help synchronise the sleep-wake rhythm. Sleep onset most likely when:
sleep. Light signals → suprachiasmatic nucleus Person is sleepy
Caffeine temporarily reduces perceived (master clock, in the hypothalamus) → melatonin It is the right biological time
sleepiness by blocking adenosine receptors — secretion. They are calm
but does not remove the underlying need for Melatonin rises in darkness; suppressed by light. Sleep environment is associated with rest
sleep. Bright light at night can delay sleepiness; morning
Core idea: Insomnia is often a problem of
Recommended: ~7–9 hours for adults (individual light strengthens circadian timing.
hyperarousal and learned wakefulness in a
need varies). Correction: SCN = hypothalamus. Pineal context where sleep should normally happen.
Exam wording: Process S explains why gland = melatonin secretion.
staying awake longer makes sleep more likely,
but it does not guarantee sleep if
psychological arousal is high.
5. THE 3P MODEL OF CHRONIC INSOMNIA (SPIELMAN)
PREDISPOSING PRECIPITATING PERPETUATING
Vulnerability factors that make sleep problems Stressors that trigger the initial acute sleep Maladaptive coping responses that maintain
more likely. e.g. anxiety proneness, hyperarousal disruption. e.g. bereavement, illness, relationship insomnia even after the original stressor
tendency, genetics, poor emotion regulation, breakdown, job loss, exam pressure. improves: spending longer in bed, napping,
perfectionism. monitoring, worrying, trying hard to sleep, clock-
watching.
Why the 3P model matters for essays: It explains why many people have short-term sleep disruption, but only some develop chronic insomnia. It prevents
an overly biological answer — insomnia can begin with a life stressor but become maintained by learned behaviours and cognitive arousal. The perpetuating
factors are the primary targets of CBT-I.
