Sleep hygiene / pathophysiology of insomnia and its management

SLEEP HYGIENE / PATHOPHYSIOLOGY OF INSOMNIA AND ITS MANAGEMENT — 15 MARKS ★ RECURRING NORMAL SLEEP AND CHANGES WITH AGE

Sleep is a reversible state of reduced responsiveness to the environment, comprising non-rapid eye movement (NREM) sleep — stages N1, N2 and N3 (slow-wave sleep) — and rapid eye movement (REM) sleep. NREM and REM alternate in cycles of about 90–110 minutes, with 4–6 cycles a night; slow-wave sleep dominates the first third of the night and REM periods lengthen toward morning.

Changes in old age: increased sleep-onset latency; reduced total sleep time and sleep efficiency; marked reduction in the absolute and relative amount of the deeper stages (N3) with a smaller reduction in REM; increase in light N1/N2 sleep; increased number and duration of awakenings (increased wake after sleep onset); circadian phase advance (earlier bedtime, earlier morning awakening); and increased daytime napping.

These changes are physiological, not pathological. The older person's ability to sleep declines while the need for sleep is largely unchanged. Therefore, insomnia in later life is usually explained by comorbidity, drugs, primary sleep disorders or circadian disruption, and must never be dismissed as "just ageing".

Insomnia disorder (ICSD-3 / DSM-5): dissatisfaction with sleep quantity or quality, with difficulty initiating sleep, difficulty maintaining sleep, or early-morning awakening with inability to return to sleep, occurring despite adequate opportunity and circumstances for sleep, and accompanied by daytime impairment (fatigue, mood disturbance, impaired attention or memory, social or occupational dysfunction). Chronic insomnia disorder = symptoms at least 3 nights a week for at least 3 months.

Characterise the pattern precisely, because it points to the cause: delayed sleep onset (anxiety, RLS, delayed phase, caffeine), frequent awakenings (pain, nocturia, sleep apnoea, PLMD, reflux), early-morning awakening (depression, phase advance, alcohol).

Hyperarousal is the core mechanism — chronic insomnia is a disorder of 24-hour hyperarousal, not merely of night-time sleep loss. Evidence: raised whole-body metabolic rate, elevated cortisol and ACTH, sympathetic overactivity with reduced heart-rate variability, increased high-frequency beta and gamma EEG activity at sleep onset and during NREM, and increased regional brain glucose metabolism during NREM sleep.

Neurochemistry of the sleep–wake switch: wakefulness is driven by the ascending arousal system — orexin/hypocretin (lateral hypothalamus), histamine (tuberomammillary nucleus), noradrenaline (locus coeruleus), serotonin (raphe), acetylcholine and dopamine. Sleep is driven by the ventrolateral preoptic nucleus (VLPO) through GABA and galanin, with adenosine as the principal endogenous somnogen. The mutually inhibitory VLPO–arousal "flip-flop switch" is stabilised by orexin; loss of stabilisation produces state instability and fragmented sleep.

Two-process model: Process S — homeostatic sleep pressure accumulating with wakefulness (adenosine-mediated); Process C — the circadian drive generated by the suprachiasmatic nucleus, entrained by light through the retinohypothalamic tract and expressed via pineal melatonin. Ageing reduces the amplitude of both processes.

Age-related circadian dysfunction: SCN neuronal loss and reduced SCN output, decreased and phase-advanced melatonin secretion, reduced daytime light exposure (cataract, reduced pupil size, indoor living, institutionalisation), and reduced physical and social activity (weak zeitgebers) → phase advance and reduced rhythm amplitude, expressed clinically as early-evening sleepiness, early-morning awakening, daytime napping and, in dementia, sundowning and irregular sleep–wake rhythm.

Spielman's 3-P behavioural model explains the transition from acute to chronic insomnia: Predisposing — age, female sex, family history, trait hyperarousal, anxious or ruminative personality. Precipitating — acute illness, hospitalisation, pain, bereavement, retirement, relocation, a new drug. Perpetuating — maladaptive behaviours (excessive time in bed, prolonged daytime napping, clock-watching, early bedtime) and dysfunctional beliefs ("I must sleep 8 unbroken hours or I will be ill"). Perpetuating factors are what CBT-I targets, and they are what keep insomnia going long after the trigger has resolved.

Conditioned (psychophysiological) insomnia — through repeated pairing, the bed and bedtime routine become learned cues for wakefulness and anxiety rather than for sleep. This is the rationale for stimulus-control therapy.

Physical symptoms underlying insomnia (elicit from the patient and the bed partner): pain from musculoskeletal disorders; orthopnoea, paroxysmal nocturnal dyspnoea or cough; nocturia; gastro-oesophageal reflux — all worsened by recumbency. Also breathlessness, anxiety and restlessness.

Symptoms of primary sleep disorders — periodic limb movements/restless legs (uncomfortable leg sensations with an urge to move; RLS prevalence rises to about 20% in those aged 80 and over); sleep apnoea (loud or irregular snoring, waking sweating, anxious and tachycardic, excessive movement, morning drowsiness); and REM sleep behaviour disorder (dream enactment, a prodrome of synucleinopathy).

Behavioural factors — daytime naps longer than 30 minutes, earlier bedtime, and increased time spent in bed not sleeping.

Drugs — hypnotic withdrawal, caffeine, alcohol (causes sleep fragmentation and rebound awakening in the second half of the night), certain antidepressants (SSRIs, SNRIs, bupropion), diuretics (nocturia) and corticosteroids; also theophylline, beta-blockers, levodopa, donepezil, decongestants and thyroxine excess.

Psychiatric — insomnia is a cardinal symptom of depression and anxiety and may be the presenting complaint. But it is also a good example of a symptom that must be evaluated for a treatable underlying cause: do not attribute insomnia to age or to depression before a comprehensive medical work-up is complete. Older adults may also hold unrealistic sleep expectations.

Assessment tools — a sleep diary for 1–2 weeks (the single most useful instrument), collateral history from the bed partner or carer, actigraphy where available, and validated scales: Insomnia Severity Index, Pittsburgh Sleep Quality Index, Epworth Sleepiness Scale.

Polysomnography is NOT routinely indicated for insomnia. Reserve it for suspected sleep apnoea, periodic limb movement disorder, REM sleep behaviour disorder or other parasomnia with injury, suspected nocturnal seizures, or insomnia refractory to adequate treatment.

Components of sleep hygiene: a fixed wake-up time seven days a week; get out of bed when unable to sleep; no clock-watching; the bedroom dark, quiet and cool and used only for sleep and sex; avoid caffeine after midday; avoid alcohol and nicotine in the evening; avoid heavy meals and large fluid volumes before bed; limit naps to under 30 minutes and before 3 pm; regular daytime exercise but not within 2–3 hours of bedtime; bright light exposure in the morning; a consistent wind-down routine; and no screens in bed.

In hospitals and care homes — reduce night-time noise and light, cluster nursing care and avoid routine nocturnal observations and medication rounds, keep the room cooler at night, increase daytime activity and daylight exposure, and treat nocturia. Sleep hygiene is listed among the environmental modifications of the Acute Care for Elders (ACE) unit.

Sleep hygiene alone is inadequate as monotherapy for chronic insomnia. It is one component of CBT-I, not a treatment in its own right — a frequent and heavily penalised error in examinations.

Treat the underlying cause first — analgesia and joint care; optimise heart failure and COPD; treat nocturia, prostatism and overactive bladder; treat reflux; treat depression and anxiety; correct iron deficiency in RLS (target ferritin above 75 ng/mL); CPAP for sleep apnoea; move diuretics and corticosteroids to the morning; and review every drug on the list.

Cognitive behavioural therapy for insomnia (CBT-I) is first-line for chronic insomnia in all ages, including older adults and those with comorbidity, delivered face-to-face, in groups, or digitally. Five components:

Stimulus control — bed only for sleep; go to bed only when sleepy; leave the bed after about 20 minutes of wakefulness; fixed rising time; no daytime naps.

Sleep restriction — restrict time in bed to actual sleep time (minimum 5–5.5 hours), then titrate upward as efficiency exceeds 85–90%. Use with caution in fall-prone patients, epilepsy, bipolar disorder and untreated OSA because of transient daytime sleepiness.

Relaxation training — progressive muscular relaxation, diaphragmatic breathing, mindfulness.

Cognitive restructuring — correcting catastrophic beliefs about sleep loss and unrealistic expectations.

Sleep hygiene education. CBT-I benefits are sustained after treatment ends, unlike hypnotics.

Circadian rhythm disorders and sundowning — there is currently no evidence for drug treatment. Non-pharmacological measures, principally good sleep hygiene practice and especially bright light therapy, are first-line, supported by structured daytime activity, exercise and social engagement.

Principles of drug therapy — hypnotics are an adjunct, for the shortest possible period (generally up to 4 weeks); start low and go slow; monitor target symptoms and side effects closely and adjust; never use long-acting benzodiazepines in geriatric patients; and anticipate rebound insomnia on stopping benzodiazepines and melatonin used regularly.

Agents — benzodiazepines: lorazepam 0.5–2.5 mg and temazepam 7.5–30 mg (intermediate acting, half-life 8–20 hours). Benzodiazepine receptor agonists: zolpidem 5–10 mg (short acting), zaleplon 5–20 mg (ultra-short), eszopiclone 1–3 mg (intermediate). Melatonin receptor agonist: ramelteon 8 mg. The effectiveness of short-term hypnotic use in older people has been questioned, and the long-term effects of chronic hypnotic use in this population are unknown.

AGS Beers Criteria — benzodiazepines, "Z-drugs" and first-generation antihistamines (diphenhydramine, hydroxyzine, promethazine) are potentially inappropriate in adults aged 65 and over because of cognitive impairment, delirium, falls, fractures and motor-vehicle crashes. Antipsychotics must not be used for insomnia; all second-generation antipsychotics carry increased mortality in dementia.

Insomnia in dementia — benzodiazepines are the most frequently used drugs but cause significant adverse effects. Low-dose trazodone is indicated in sleeping disorders, especially with night-time agitation, and long-term use may benefit both sleep parameters and cognitive decline in Alzheimer's disease. Mirtazapine 15 mg showed no improvement in nocturnal sleep duration or efficiency and increased daytime sleepiness. Suvorexant, an orexin receptor antagonist, improves total sleep time and cognitive performance in probable Alzheimer's dementia with insomnia. Trials of lemborexant in Alzheimer's disease and nelotanserin for REM sleep behaviour disorder in dementia with Lewy bodies are under way.

Deprescribing hypnotics — gradual dose tapering (about 25% every 1–2 weeks) combined with CBT-I is the most effective approach; direct-to-patient educational deprescribing (EMPOWER-type interventions) works and should be offered to every long-term hypnotic user.

Age changes in sleep: increased sleep latency and awakenings, reduced total sleep time, sleep efficiency and slow-wave sleep, circadian phase advance, more naps. Ability to sleep declines; need does not.

Definition: difficulty initiating or maintaining sleep, or early awakening, despite adequate opportunity, with daytime impairment; chronic if 3 nights a week for 3 months.

Pathophysiology: 24-hour hyperarousal (raised cortisol, sympathetic tone, beta EEG); orexin-stabilised VLPO– arousal flip-flop instability; declining Process S and Process C with SCN degeneration and reduced melatonin and light exposure; Spielman's predisposing–precipitating–perpetuating model; conditioned insomnia.

Causes: pain, orthopnoea/PND, nocturia, reflux; RLS/PLMD, sleep apnoea, RBD; naps over 30 minutes and excess time in bed; caffeine, alcohol, diuretics, steroids, SSRIs, hypnotic withdrawal; depression and anxiety.

Evaluation: sleep diary 1–2 weeks, bed-partner history, Insomnia Severity Index, Epworth; polysomnography only for suspected apnoea, PLMD, parasomnia or refractory insomnia.

Sleep hygiene (BEDROOM): fixed rising time, daytime exercise not late, dark/quiet/cool room, naps under 30 minutes, bed only for sleep and sex, out of bed if awake beyond 20 minutes, no evening caffeine, alcohol or heavy meals; morning bright light.

Management: treat the underlying cause; CBT-I first-line (stimulus control, sleep restriction, relaxation, cognitive restructuring, sleep hygiene); bright light therapy for circadian disorder and sundowning; drugs short-term only, avoiding long-acting benzodiazepines, Z-drugs and antihistamines per Beers; low-dose trazodone in dementia; taper and deprescribe long-term hypnotics alongside CBT-I. 3-point current update: (i) European Sleep Research Society guideline 2023 — CBT-I (including digital) first-line; BZD/BzRA and sedating antidepressants only up to 4 weeks; antihistamines, antipsychotics and phytotherapy not recommended; PR melatonin 2 mg up to 3 months if aged over 55. (ii) Dual orexin receptor antagonists (daridorexant, lemborexant, suvorexant) are the major advance; daridorexant has the shortest half-life (~8 h) with equal efficacy and safety in those aged 65 and over, and needs no special deprescribing protocol. (iii) ICSD-3-TR treats chronic insomnia as a disorder in its own right even when comorbid, and suvorexant's reduction in CSF tau and amyloid links sleep treatment to dementia-risk modification.