Sleep Disorders

Sleep disorders are a group of conditions that impair the ability to initiate, maintain, or regulate sleep or wakefulness, resulting in disrupted sleep patterns and daytime functional impairment.

2. Epidemiology

3. Sleep Physiology — Anatomy and Function

To understand sleep disorders, you must first understand normal sleep. This section covers the neuroanatomy, neurochemistry, and architecture of sleep from first principles.

3.1 The Two-Process Model of Sleep Regulation

Sleep is regulated by two interacting processes: ^[1]^[3]

Governed by the suprachiasmatic nucleus (SCN) of the anterior hypothalamus — the master circadian pacemaker ^[1]^[3]
The SCN has an intrinsic ~24.2-hour rhythm (slightly longer than 24 hours) → must be entrained daily
Primary zeitgeber (time-giver): light ^[3]
- Light enters the eye → melanopsin-containing intrinsically photosensitive retinal ganglion cells (ipRGCs) → retinohypothalamic tract → SCN
- Light exposure in the morning advances the clock; light in the evening delays it
The SCN signals the pineal gland to release melatonin via a multisynaptic pathway (SCN → paraventricular nucleus → superior cervical ganglion → pineal gland) ^[1]^[3]
- Melatonin: released in darkness ("hormone of darkness"), suppressed by light ^[3]
- Melatonin promotes sleep onset and signals nighttime to the body
- This is why bright light therapy works for circadian rhythm disorders, and why blue light from screens delays sleep onset
Core body temperature rhythm: drops in the evening (promoting sleep onset), reaches a nadir in the early morning hours (~04:00), and rises before awakening ^[3]
Cortisol rhythm: peaks in the early morning (cortisol awakening response), lowest at midnight ^[3]

The interaction of Process S and Process C determines when you feel sleepy and when you feel alert. Process S builds up during the day (increasing sleep pressure), while Process C provides an alerting signal during the day that opposes Process S. In the evening, as Process C's alerting signal wanes and Process S is high, you feel sleepy. ^[3]

Why do you get a 'second wind' at night?

In the early evening, Process C's alerting signal is near its peak (the "wake maintenance zone" or "forbidden zone for sleep," roughly 19:00–21:00). Even though Process S has accumulated significantly, the circadian alerting signal counterbalances it. Once this alerting signal declines after ~21:00–22:00, the accumulated Process S "wins" and sleepiness hits hard. This is also why shift workers find it very difficult to sleep during the day — Process C is sending a strong alerting signal.

3.2 Neuroanatomy of the Sleep–Wake Switch

The "flip-flop" switch model (Saper, 2005): ^[3]

These are located in the brainstem and hypothalamus:

Centre	Neurotransmitter	Location	Role
Locus coeruleus (LC)	Noradrenaline (NA)	Dorsal pons	Cortical arousal, attention
Raphe nuclei	Serotonin (5-HT)	Brainstem midline	Wakefulness, mood regulation
Tuberomammillary nucleus (TMN)	Histamine	Posterior hypothalamus	Cortical arousal — this is why antihistamines cause drowsiness
Basal forebrain (BF)	Acetylcholine (ACh)	Basal forebrain	Cortical activation, especially REM
Ventral tegmental area (VTA)	Dopamine	Midbrain	Motivation, reward-based arousal
Lateral hypothalamus	Orexin/Hypocretin	Lateral hypothalamus	Stabilizes wakefulness and prevents inappropriate transitions into sleep

3.3 Sleep Architecture — Stages and Cycles

Sleep is divided into two fundamentally different states: ^[1]^[3]

Feature	NREM Sleep	REM Sleep
EEG	Synchronised, high-amplitude, low-frequency waves	Desynchronised, low-amplitude, high-frequency waves (resembles wakefulness — hence "paradoxical sleep")
Muscle tone	Maintained (reduced but present)	Atonia (generalised skeletal muscle paralysis except diaphragm and extraocular muscles)
Eye movements	Slow rolling (Stage 1) → absent (Stage 2, 3)	Rapid conjugate eye movements
Dreaming	Thought-like mental activity, less vivid	Vivid, bizarre, narrative dreams
Autonomic activity	↓HR, ↓BP, ↓RR — stable	Variable — ↑HR, ↑BP, penile/clitoral engorgement
Thermoregulation	Maintained (can still sweat or shiver)	Poikilothermic (thermoregulation suspended)

Stage	% of Total Sleep	EEG Features	Key Features
N1	2–5%	Theta waves (4–7 Hz), vertex sharp waves	Lightest sleep, easily aroused, "drifting off," hypnic jerks, slow rolling eye movements
N2	45–55%	Sleep spindles (11–16 Hz bursts) + K-complexes	True sleep onset, memory consolidation begins, harder to arouse
N3 (Slow-Wave Sleep, SWS)	13–23%	Delta waves ( < 2 Hz), high-amplitude ( > 75 µV)	Deepest sleep, most restorative, hardest to arouse, GH secretion, immune function, NREM parasomnias occur here

Sleep spindles are generated by the thalamic reticular nucleus — they serve as a "gate" that blocks external sensory information from reaching the cortex (why you don't hear things during sleep)
K-complexes are large-amplitude, biphasic waves — they represent cortical responses to external stimuli and help maintain sleep by suppressing cortical arousal
Slow-wave sleep (N3) is maximal in the first third of the night → this is why NREM parasomnias (sleepwalking, sleep terrors) tend to occur in the first half of the night ^[2]

Age Group	Recommended Sleep (hrs)
Neonates	14–17
Infants	12–15
Toddlers	11–14
Preschool	10–13
School-age	9–11
Teens	8–10
Adults	7–9
Older adults	7–8

Method to determine individual sleep need: sleep/wake in a free-running manner (i.e., no alarm clock, sleep as long as needed) for ≥1 week. If tired or sleepy in the daytime = not getting enough. ^[2]

Sleep deprivation produces widespread physiological, neuropsychiatric, and systemic effects: ^[2]

Domain	Effect	Mechanism
Physiological	↑ evening cortisol, ↑ sympathetic nervous activity, ↑ TSH, ↓ insulin response (→ ↓ glucose tolerance)	HPA axis dysregulation; sympathetic overdrive from inadequate VLPO restoration
Neuropsychiatric	↑ amygdala activation → ↑ negative emotions; irritability; cognitive impairment; memory lapses; impaired moral judgement; hallucinations; symptoms similar to ADHD	Failure of prefrontal cortical regulation of the amygdala; impaired memory consolidation
Motor	Increased reaction time, decreased accuracy, tremors	Cerebellar and cortical dysfunction
Chronic effects	Associated with obesity, CVD, ↑ overall mortality ( < 5h/day during weekends associated with 52% ↑ mortality compared to 7h/day)	Metabolic dysregulation (leptin ↓, ghrelin ↑), chronic inflammation, sympathetic overdrive
Immune	Impaired immune function	↓ NK cell activity, altered cytokine profiles

Partial sleep deprivation and short duration ( < 7h vs 7–8h) is associated with mental and physical health risk, especially cardiovascular. Long duration ( > 9h) is also associated with health risks (U-shaped curve). ^[2]

4. Aetiology (with Focus on Hong Kong Context) and Pathophysiology

This is the single most important aetiological framework for understanding insomnia: ^[1]^[2]

The 3Ps are: Predisposing, Precipitating, and Perpetuating factors.

Factor	Definition	Examples	Timeframe
Predisposing	Trait-level vulnerabilities that lower the threshold for insomnia	Anxious temperament, female sex, older age, family history, hyperarousability (elevated cortisol, ↑ metabolic rate, ↑ beta EEG activity), comorbid psychiatric/medical conditions	Always present
Precipitating	Acute stressors/events that trigger insomnia	Life events (bereavement, job loss, exams), acute illness, pain, medication changes, jet lag, shift work	Acute phase
Perpetuating	Maladaptive behaviours and cognitions that maintain insomnia after the precipitant has resolved	Spending excessive time in bed, irregular sleep–wake schedule, daytime napping, clock-watching, catastrophising about sleep, using bed for non-sleep activities, stimulant use	Chronic phase

Key Insight: Why Chronic Insomnia Persists

As insomnia becomes chronic, perpetuating factors become the dominant driver, even as the original precipitating factor resolves. ^[2] This is why CBT-I (which specifically targets perpetuating factors — maladaptive behaviours and dysfunctional cognitions) is so effective for chronic insomnia, often more so than medications which only address symptoms.

The classic diagram shows:

Pre-morbid: only predisposing factors present (below threshold)
Acute insomnia: predisposing + precipitating exceed threshold
Early insomnia: predisposing + precipitating + emerging perpetuating factors
Chronic insomnia: precipitating factors have largely resolved, but perpetuating factors maintain insomnia above threshold

4.4 Aetiologies by Sleep Disorder Category

Orexin (hypocretin) deficiency: ^[2]

CSF orexin deficiency in narcolepsy type 1 (with cataplexy) but not type 2
Orexin: released by orexin neurons in the lateral hypothalamus
Function: released during wakefulness → increases activity of brain regions promoting wakefulness → stabilizes wakefulness and prevents inappropriate transition into REM or NREM sleep
Deficiency → allows REM sleep-related phenomena to intrude into wakefulness, e.g., cataplexy, hypnagogic hallucinations, sleep paralysis

Genetics and autoimmune hypothesis: ^[2]

HLA-DQB10602 found in 98% of type 1, 50% of type 2*
This led to the autoimmune hypothesis of selective orexin neuronal death by autoimmune process
Also explains why onset is common in spring (?streptococcal infection as trigger — molecular mimicry)

Secondary narcolepsy: ^[2]

Rare, can be due to posterior hypothalamic or midbrain lesions (?direct injury to orexin neurons)

Pathophysiological basis of narcolepsy symptoms:

Symptom	Pathophysiology
Excessive daytime sleepiness	Loss of orexin → destabilised flip-flop switch → inappropriate transition from wakefulness to sleep
Cataplexy	Intrusion of REM atonia into wakefulness, triggered by strong emotions (which normally activate the amygdala → lateral hypothalamus pathway, but without orexin stabilization, this triggers the REM atonia circuit)
Sleep paralysis	REM atonia persisting into the wake transition — unable to move upon waking/falling asleep
Hypnagogic/hypnopompic hallucinations	REM dreaming intruding at sleep–wake transitions (hypnagogic = at sleep onset; hypnopompic = upon awakening)
Fragmented nocturnal sleep	Instability of sleep states → frequent arousals

5. Classification

Three major classification systems are used for sleep disorders: ^[2]

ICSD-3 (2014)	ICD-10	DSM-5
~60 specific diagnoses under 7 categories:	Non-organic sleep disorders (F51):	10 disorder categories:
1. Insomnia	Dyssomnias (insomnia, hypersomnia, disorder of sleep–wake cycle)	Insomnia disorder
2. Sleep-related breathing disorders	Parasomnias (sleepwalking, sleep terrors, nightmares)	Hypersomnolence disorder
3. Central disorders of hypersomnolence	Sleep disorders of organic origin (G47):	Narcolepsy
4. Circadian rhythm sleep–wake disorders	Narcolepsy	Breathing-related sleep disorders
5. Parasomnias	Kleine-Levin syndrome	Circadian rhythm sleep–wake disorders
6. Sleep-related movement disorders	Sleep apnoea	NREM sleep arousal disorders
7. Other sleep disorders	Others (R33): primary nocturnal enuresis	Nightmare disorders
		REM sleep behaviour disorder
		Restless leg syndrome
		Substance/medication-induced sleep disorder

This table is high-yield and frequently tested: ^[2]

Feature	NREM Parasomnia	REM Parasomnia
Timing	First half of the night (SWS predominates)	Latter half of the night (REM predominates)
Duration	Seconds to several minutes	Brief, lasting seconds (for RBD)
Age	Usually begins in early childhood and resolves by adolescence	Primarily affects older adults (usually male)
Eyes	Open eyes (for disorders of arousal)	Closed eyes (for RBD)
Memory recall	Partial or no recall (deep sleep — hippocampus offline)	Reasonable dream recall congruent with behaviour performed
Behaviour	Complex, semi-purposeful, may walk around	Typically short, may appear purposeful, often violent

Type	Epidemiology	Features	Treatment
Delayed (80%)	3.3–4.6% adolescents and young adults	"Night owl" circadian preference; ↓ sleep time when combined with early school/work	Gradual advancing bedtime; 0.5 mg melatonin 1h before target bedtime; morning light (2h 5000 lux); evening light restriction
Advanced	0.25–7% adults, ↑ in older males	Excessive evening sleepiness; chronic early morning awakening	Bright light therapy in the evening
Non-24h	Average onset 20 years; majority blind	Inability to align endogenous clock to 24h → continuous delay → eventual day-night reversal	Behavioural changes; timed melatonin (1h before bed); melatonin agonist (tasimelteon)

6. Clinical Features — Symptoms and Signs (with Pathophysiological Basis)

Clinical features — remember the number "3": ≥30 min delay/awake/early awakening for 3×/week × 3 months ^[2]

Symptoms:

Symptom	Pathophysiological Basis
Difficulty initiating sleep (sleep onset latency ≥30 min)	Hyperarousal state → elevated sympathetic tone, cortisol, and high-frequency EEG activity prevents the VLPO from adequately suppressing wake centres. Conditioned arousal (bed = anxiety about not sleeping) further raises arousal. Most well-rested adults fall asleep in ≤10–20 min.
Difficulty maintaining sleep (≥30 min awake during the night)	Fragmentation due to cortical hyperarousal → insufficient "depth" of sleep → frequent micro-arousals → subjective awakening. May also be driven by comorbidities (pain, OSA, PLMD).
Early morning awakening (≥30 min before desired wake time, cannot return to sleep)	May reflect advanced circadian phase, HPA axis dysregulation (early cortisol surge), or mood disorder (depression classically causes terminal insomnia due to REM pressure and cortisol dysregulation).
Non-restorative sleep	Even if total sleep time is adequate, fragmentation prevents sufficient SWS → impaired glymphatic clearance, impaired GH secretion, impaired immune restoration.
Daytime fatigue, malaise, ↓ concentration, ↓ work performance	Sleep deprivation → ↓ prefrontal cortical function → cognitive impairment; ↑ amygdala reactivity → emotional dysregulation; ↓ vigilance and psychomotor performance.
Worry about sleep ("cycle of worry")	Worry that lack of sleep will compromise daytime function → ↑ stress → ↑ arousal → ↑ difficulty sleeping → self-fulfilling prophecy. This is the key perpetuating cognitive factor in the 3P model. ^[2]

Signs (often limited in insomnia):

May appear fatigued, irritable, with ↓ concentration on MSE
No specific physical signs (unlike OSA where you may see obesity, crowded oropharynx, etc.)

Four characteristic symptoms (the "narcolepsy tetrad"): ^[2]

Symptom	Pathophysiological Basis
1. Excessive daytime sleepiness (EDS)	Loss of orexin → destabilised flip-flop switch → unable to sustain wakefulness. Sleep attacks: severe sleepiness resulting in rapid dozing off with little warning. Sleepiness usually improves temporarily after a nap (unlike idiopathic hypersomnia where naps are unrefreshing).
2. Cataplexy	Intrusion of REM atonia into wakefulness. Triggered by strong emotions (laughter, surprise, anger). Ranges from jaw drop, head nod, knee buckling to complete collapse. Consciousness preserved. Pathognomonic for narcolepsy type 1. Mechanism: emotional circuits (amygdala, hypothalamus) normally held in check by orexin; without orexin, emotional arousal triggers the pontine REM-atonia circuit.
3. Sleep paralysis	REM atonia persisting into the transition from sleep to wakefulness or vice versa. Patient is awake but unable to move for seconds to minutes. Frightening but benign. Can also occur in isolation in healthy individuals (especially with sleep deprivation).
4. Hypnagogic/hypnopompic hallucinations	REM dreaming intruding at sleep–wake transitions. Hypnagogic = at sleep onset (hypn- = sleep, -agogic = leading to); hypnopompic = upon awakening (-pompic = sending away). Often vivid, visual, sometimes frightening. Due to direct transition into REM at sleep onset (sleep-onset REM periods, SOREMPs) rather than the normal N1 → N2 → N3 → REM progression.

Additional features:

Fragmented nocturnal sleep — instability of sleep states (wakefulness intruding into sleep, the converse of daytime symptoms)
Automatic behaviours (continuing activities in a semi-conscious state)
Weight gain (orexin also regulates metabolism and appetite)
Depression and anxiety (common comorbidities)

Signs:

May observe sleep attacks during clinical encounter
Formal testing: MSLT shows mean sleep latency < 5 min and ≥2 SOREMPs (≥1 if narcolepsy suspected) ^[2]

Symptoms and their basis: ^[2]

Symptom	Pathophysiological Basis
Loud and habitual snoring	Partial upper airway obstruction → turbulent airflow → soft palate/uvula vibration
Witnessed apnoeas / choking episodes	Complete upper airway collapse → cessation of airflow (apnoea) → arousal with gasping/choking to restore airway patency
Insomnia with daytime sleepiness (frequent arousals)	Repeated arousals to terminate apnoeas fragment sleep → poor sleep quality → EDS
Excessive sleep movements	Arousals and respiratory effort against closed airway cause body movements
Dry mouth	Mouth breathing due to nasal obstruction and/or during apnoeic recovery
Nocturia	Arousal from apnoeas → awareness of bladder; ↑ abdominal pressure against closed glottis → ↑ intrathoracic negative pressure → ↑ venous return → ↑ ANP secretion → diuresis
Morning headache	Nocturnal desaturation + CO₂ retention → cerebral vasodilation → headache ^[2]
Unrefreshing sleep, cognitive impairment, mood changes	Chronic intermittent hypoxia + sleep fragmentation → hippocampal and prefrontal cortical damage

Signs:

Obesity (especially central/neck obesity, collar size > 17 inches in males)
Crowded oropharynx (Mallampati grade III/IV)
Retrognathia
Hypertension (especially resistant/refractory HTN)
Signs of right heart failure (in severe, chronic cases — cor pulmonale)

Feature	Pathophysiological Basis
Urge to move legs, unpleasant leg sensations when sitting/lying down	Dopaminergic dysfunction in the A11 diencephalospinal pathway → failure of descending dopaminergic inhibition of sensory processing in the spinal cord → uncomfortable sensory experiences
Symptoms worse at rest, relieved by movement	Movement activates alternative sensory/motor circuits that override the abnormal sensory input
Symptoms worse in the evening/night	Dopamine levels have a circadian variation — lowest in the evening/night → symptoms peak
Partner reports restless sleep, limb jerks	May overlap with periodic limb movement disorder (PLMD) — repetitive stereotypical limb movements during sleep
Sleep-onset insomnia	Inability to keep legs still prevents relaxation needed for sleep onset

6.6 NREM Parasomnias

Feature	Pathophysiological Basis
Complex behaviours during sleep (walking, sitting, repetitive movements)	Incomplete arousal from SWS → motor cortex active but prefrontal cortex and hippocampus remain in deep sleep → complex motor activity without executive control or memory encoding
Begin with confusional arousal	Partial cortical activation
Typically NO recollection	Hippocampus offline → no memory consolidation
Can be violent if attempts to restrain	Amygdala activation without prefrontal modulation → fight response
Eyes open, glazed expression	Partial cortical activation — enough for visual processing but not full awareness

6.7 REM Parasomnias

Feature	Pathophysiological Basis
Dream enactment behaviour: short episodes ( < 60s), appear purposeful (throwing, punching, vocalising)	Loss of REM sleep atonia → failure to suppress motor activity during REM → patient physically acts out dreams
Change in dream content: frequent, vivid, action-packed, violent dreams	Unknown mechanism; possibly altered dream generation in a brain undergoing neurodegeneration
Can injure self or bed partner	Violent dream enactment without cortical awareness of surroundings
50% associated with neurological conditions	Synucleinopathies (PD, DLB, MSA) → degeneration of pontine REM-atonia centres (subcoeruleus/sublaterodorsal nucleus)
Eyes closed during episodes	In REM, eyes are closed (unlike NREM disorders of arousal where eyes are open)
Can recall dream content upon awakening	Cortex active during REM → memory consolidation intact

7. Evaluation of Sleep Disorders

Systematic approach to evaluating a patient with a sleep complaint: ^[2]

Investigation	Indication
Actigraphy	Adjunct to sleep diary when suspecting circadian sleep–wake disorder — wrist-worn accelerometer measures rest-activity cycles over days to weeks
Polysomnography (PSG)	Only when suspecting another sleep disorder, e.g., OSA, RBD, PLMD — NOT routinely indicated for insomnia alone
MSLT	Narcolepsy, idiopathic hypersomnia
Chronotype questionnaire	Determine circadian preference — Morningness-Eveningness Questionnaire
Dim light melatonin onset (DLMO) protocol	Periodic blood/salivary sampling every 30–60 min for melatonin level under dim light → should show ↑ level 90–120 min before habitual bedtime — gold standard for circadian phase assessment
Blood tests	Ferritin ( < 75 µg/L suggests iron deficiency → RLS), TFTs (hypothyroidism → hypersomnia), HbA1c
Video PSG	RBD diagnosis — demonstrates REM without atonia + dream enactment
CSF orexin levels	Narcolepsy type 1 — ≤110 pg/mL (or < 1/3 of normal)
HLA typing	HLA-DQB1*0602 — supportive but not diagnostic for narcolepsy

High Yield Summary

Sleep regulation: Two-process model — Process S (homeostatic, adenosine-driven) + Process C (circadian, SCN/melatonin-driven). Their interaction determines sleep timing.
Flip-flop switch: VLPO (GABA/galanin, sleep) ↔ ARAS (NA, 5-HT, histamine, ACh, DA, orexin, wake) — mutually inhibitory. Orexin stabilises the wake state. Loss of orexin → narcolepsy type 1.
Sleep architecture: NREM (N1 → N2 → N3) → REM in 90-min cycles. SWS predominates early (NREM parasomnias first half). REM predominates late (REM parasomnias second half).
3P model of insomnia: Predisposing (trait) + Precipitating (trigger) + Perpetuating (maladaptive behaviours/cognitions). Chronic insomnia is driven primarily by perpetuating factors.
Comorbid insomnia: "Secondary" insomnia concept abandoned → now "comorbid" because causality is bidirectional.
Narcolepsy type 1: Orexin deficiency → REM intrusion phenomena (cataplexy, sleep paralysis, hypnagogic hallucinations) + sleep instability. HLA-DQB1*0602 → autoimmune hypothesis.
RBD: Loss of REM atonia → dream enactment. Strongly associated with synucleinopathies (prodromal PD/DLB). M > F 9:1. Eyes closed (vs NREM open). Dream recall present.
Assessment: Sleep diary (2 weeks), ESS (≥10 = excessive sleepiness), MSLT (mean latency < 5 min = pathological; ≥2 SOREMPs = narcolepsy), PSG only if suspecting OSA/RBD/PLMD — NOT for routine insomnia.
CSWRD workup: Sleep diary + actigraphy + chronotype questionnaire + DLMO protocol.
Clinical pearl — insomnia type by presentation: Initial → anxiety/DSWPD/RLS; Middle → OSA/PLMD/pain; Terminal → depression/ASWPD.

Active Recall - Sleep Disorders (Definition to Clinical Features)

Differential Diagnosis of Sleep Disorders

Differential Diagnosis of Insomnia

This is the most common presentation, so the differential is extensive. The table below is adapted from DSM-5 and ICSD-3 differential listings ^[2].

Differential	Salient Differentiating Features	Why It Matters / First Principles Explanation
Normal sleep variations (short sleepers)	Some individuals require little sleep and do not feel difficulty falling/staying asleep or daytime sleepiness. May mimic insomnia if they try to stay in bed for a longer time. Inadequate opportunity of sleep due to e.g., shift work, other disturbances. ^[2]	The key distinction is absence of daytime impairment. A true short sleeper (genetic — e.g., DEC2 gene mutation) sleeps 4–6 hours and functions perfectly. They only present when they (or a partner) believe they "should" sleep more. Spending excessive time in bed trying to force more sleep actually fragments it (paradoxically worsening sleep quality).
Situational (adjustment) insomnia	Lasts days to weeks and is associated with life events or changes in sleep schedules. Classified under other specified insomnia disorder under DSM-5 if < 3 months but otherwise meets criteria. ^[2]	This is the acute insomnia that everyone experiences — exam stress, bereavement, jet lag. The distinction from chronic insomnia disorder is duration < 3 months and clear temporal relationship to a stressor. Most cases self-resolve. The concern is when perpetuating factors (3P model) develop and it transitions to chronic insomnia.
Delayed sleep-wake phase disorder (DSWPD)	Classified under delayed sleep phase type of circadian rhythm sleep-wake disorder. Usually report sleep-onset insomnia when trying to sleep at socially normal times, but do not complain of insomnia when following endogenous circadian rhythm. ^[2]	This is a crucial mimic of insomnia. The patient says "I can't fall asleep until 3 AM" — sounds like initial insomnia. But if you let them sleep 3 AM–11 AM, their sleep quality and quantity are completely normal. The problem is timing, not the sleep itself. The circadian clock is set late (SCN intrinsic period too long, or insufficient morning light exposure / excessive evening light). Distinguish by sleep diary + actigraphy showing a consistent late sleep phase.
Restless leg syndrome (RLS)	Often produces difficulties initiating and maintaining sleep. Should have urge to move legs, unpleasant leg sensation when sitting/lying down. Partner may report history of restless sleep or limb movements/muscle twitches during sleep. ^[2]	RLS causes sleep-onset insomnia because the patient cannot keep their legs still when trying to relax in bed → uncomfortable sensory symptoms → forced to move → can't fall asleep. The pathophysiology is dopaminergic — symptoms are worst in the evening when dopamine is lowest. Always check ferritin (iron deficiency exacerbates RLS as iron is a cofactor for tyrosine hydroxylase in dopamine synthesis).
Breathing-related sleep disorders (OSA)	Majority have history of loud snoring, breathing pauses during sleep. May report interrupted sleep (frequent arousal due to apnoea) and daytime sleepiness. ^[2]	OSA can present as insomnia (especially "maintenance insomnia" from repeated arousals). The patient may not be aware of the apnoeas — it's the bed partner who describes snoring and witnessed apnoeas. Morning headache (from CO₂ retention and desaturation), dry mouth, and nocturia are clues. OSA also worsens RBD and NREM parasomnias by causing arousals from deep sleep.
Narcolepsy	Predominantly presents with excessive daytime sleepiness, but may also have cataplexy (intense emotions precipitate drop attack), sleep paralysis, sleep-related hallucinations. ^[2]	Narcolepsy patients often have fragmented nocturnal sleep (from flip-flop switch instability) and may complain of "insomnia." However, the predominant complaint is EDS, and the characteristic tetrad (EDS, cataplexy, sleep paralysis, hypnagogic hallucinations) distinguishes it. Important: not all features need to be present (type 2 lacks cataplexy).
Parasomnias	Characterised by unusual behaviour/events during sleep. May lead to intermittent wakening and difficulty resuming sleep. ^[2]	Parasomnias cause sleep disruption but the primary complaint is usually the abnormal behaviour (or its consequences — injury, bed partner disturbance) rather than difficulty initiating sleep. The insomnia is secondary to the arousals.

This is where you must be especially careful, because insomnia is both a symptom and a comorbid condition in psychiatric disorders. The modern approach says: diagnose insomnia as comorbid with the psychiatric disorder rather than dismissing it as "secondary" ^[2].

Psychiatric Condition	Sleep Pattern	Why This Pattern Occurs
Major Depressive Disorder	Most classically early morning awakening ^[4]. Also middle insomnia, initial insomnia (less common). Some atypical features include hypersomnia.	Terminal insomnia in depression is thought to relate to HPA axis dysregulation — cortisol rises too early (advanced cortisol nadir), and REM pressure shifts earlier in the night. SWS is reduced. The depressed brain is in a state of hyperarousal (contrary to the subjective experience of low energy).
Generalised Anxiety Disorder (GAD)	Usually difficulty falling asleep with persistent worrying thoughts, intermittent unrefreshing sleep with unpleasant dreams/night terrors ^[5]. Early morning awakening is NOT a feature of GAD and strongly suggests depressive disorders ^[5].	Anxiety causes cognitive hyperarousal at bedtime — the "racing mind." The sympathetic nervous system is activated, opposing the VLPO's sleep-promoting activity. The key differentiator from depression: GAD causes initial and middle insomnia (can't switch off the worrying), NOT terminal insomnia.
PTSD	Initial insomnia (hyperarousal, fear of sleep/nightmares), middle insomnia (nightmares cause awakenings), nightmares (re-experiencing)	The traumatised brain maintains a persistent state of threat detection (amygdala hyperactivation, impaired prefrontal regulation). Sleep is perceived as a vulnerable state → resistance to falling asleep. Nightmares are a core re-experiencing symptom.
Bipolar Affective Disorder	Mania/hypomania: ↓ need for sleep (distinct from insomnia — patient feels refreshed after little sleep). Depressive phase: insomnia or hypersomnia.	In mania, the reduced sleep need is driven by dopaminergic and noradrenergic overactivity — the wake-promoting system is overactive. The patient doesn't want to sleep and doesn't feel tired — this is fundamentally different from insomnia where the patient wants to sleep but cannot.
Schizophrenia	Severely disrupted sleep architecture — delayed sleep phase, fragmented sleep, reversed sleep–wake cycle	Dopaminergic dysregulation, social withdrawal (reduced zeitgeber exposure), medication effects, and circadian rhythm disruption from disorganised behaviour.
Substance use disorders	Varies by substance (see below)	Direct pharmacological effects on sleep architecture.

Exam Trap: Decreased Need for Sleep vs Insomnia

Decreased need for sleep (mania) is fundamentally different from insomnia:

Mania: Patient sleeps 2–3 hours and wakes feeling energised, refreshed, and ready to go. They do not complain about poor sleep — they don't feel they need it.
Insomnia: Patient wants to sleep, tries to sleep, cannot sleep, and suffers daytime impairment as a result.

If a patient reports sleeping 3 hours and feels great with increased energy and grandiosity, think mania, not insomnia. This distinction is frequently tested.

Medical Condition	Mechanism of Sleep Disruption
Chronic pain (arthritis, neuropathy, malignancy)	Pain → cortical arousal → inability to maintain sleep. Pain perception is actually heightened at night due to loss of descending inhibitory modulation.
GERD	Supine position → ↑ reflux → oesophageal irritation → arousals. Also, oesophageal acid exposure can cause microarousals without conscious awareness.
Heart failure	Paroxysmal nocturnal dyspnoea (PND) → awakening with SOB. Orthopnoea. Cheyne-Stokes respiration (central sleep apnoea). Fluid redistribution when supine → upper airway oedema → OSA.
COPD / Asthma	Nocturnal bronchoconstriction (cortisol nadir at ~4 AM → peak airway inflammation) → dyspnoea → arousal. Medications (theophylline, β-agonists) are stimulatory.
Hyperthyroidism	↑ metabolic rate → ↑ sympathetic activation → hyperarousal → difficulty sleeping. Also causes anxiety, tremor, palpitations that contribute.
Menopause	Hot flushes → sudden autonomic arousal → awakening. Oestrogen decline also affects serotonergic and GABAergic regulation of sleep.
Nocturia (BPH, DM, HF)	Repeated awakening to urinate → fragmented sleep. Must distinguish from nocturia secondary to arousals from another cause (patient wakes from OSA → notices bladder → attributes awakening to nocturia).
Neurological (Parkinson's, dementia, epilepsy)	PD: RBD, PLMD, dyskinesias. Dementia: "sundowning" (reversed sleep–wake). Epilepsy: nocturnal seizures mimicking parasomnias.

Substance	Effect on Sleep
Caffeine	Adenosine receptor antagonist → blocks Process S → insomnia. Half-life ~5–6 hours. A cup at 4 PM still has 50% caffeine at 10 PM.
Alcohol	Initial sedation (enhances GABA) → BUT second-half rebound arousal as alcohol is metabolised → fragmented sleep, ↓ REM, ↑ SWS early then ↓ later. Chronic use → tolerance → withdrawal insomnia.
Nicotine	Stimulant at low doses (nicotinic ACh receptor agonist) → arousal. Withdrawal during sleep → nocturnal arousal in dependent smokers.
Stimulants (amphetamines, cocaine, methylphenidate)	↑ DA, NA release → potent wake-promoting → severe insomnia
SSRIs/SNRIs	↑ serotonin → can cause insomnia, vivid dreams, ↓ REM, periodic limb movements. SSRIs also cause/exacerbate RBD.
Corticosteroids	↑ cortisol → HPA axis activation → hyperarousal → insomnia
β-blockers	Suppress melatonin secretion (via β₁-receptor blockade of pineal gland) → insomnia, nightmares
Benzodiazepine withdrawal	Rebound insomnia — GABA receptor downregulation → hyperexcitability → severe insomnia, anxiety, potential seizures

Causes of excessive daytime sleepiness: ^[2]

Category	Conditions	Key Distinguishing Features
Insufficient sleep	Behavioural (most common cause globally)	History of voluntarily restricting sleep. Resolves when adequate sleep is obtained. Very common in Hong Kong's work-hard culture.
Poor sleep quality	OSA, periodic limb movement disorder (PLMD)	OSA: snoring, witnessed apnoeas, obesity. PLMD: bed partner reports limb jerks (patient often unaware). Both cause fragmented sleep → EDS.
Narcolepsy	Type 1 and Type 2	Cataplexy pathognomonic for type 1. MSLT: mean latency < 5 min + ≥2 SOREMPs. Naps are refreshing (unlike idiopathic hypersomnia).
Idiopathic hypersomnia	—	Naps are unrefreshing and prolonged. Severe sleep inertia ("sleep drunkenness"). MSLT: mean latency < 8 min but < 2 SOREMPs.
Secondary to medical conditions	Hypothyroidism, Prader-Willi syndrome	Check TFTs. Prader-Willi: obesity, hyperphagia, intellectual disability.
Secondary to psychiatric disorders	Depression	EDS can be a feature of atypical depression (hypersomnia, hyperphagia, leaden paralysis, rejection sensitivity). Also seen in bipolar depressive episodes.
Secondary to medications	Antihistamines, gabapentinoids, anticonvulsants, benzodiazepines	Temporal correlation with medication initiation. Antihistamines cause drowsiness by blocking H₁ receptors in the TMN (wake-promoting centre).

Sleepiness vs Fatigue: A Critical Distinction

Sleepiness is the propensity to fall asleep — it differs from fatigue/tiredness: ^[2]

Sleepiness is worst during inactivity and improves with stimulation. Ask: "Do you actually fall asleep or nearly fall asleep during the day?"
Fatigue is worst during exertion and not relieved by sleep. Ask: "Do you feel exhausted and lacking energy but couldn't actually fall asleep if you tried?"

Sleepiness → think sleep disorders (OSA, narcolepsy, insufficient sleep). Fatigue → think medical conditions (anaemia, hypothyroidism, HF) or psychiatric (depression).

Some conditions cause both (e.g., depression, OSA), but asking the patient to distinguish helps narrow the differential.

This is where the distinction between NREM and REM parasomnias, nocturnal epilepsy, and psychiatric conditions becomes critical.

Differential	Key Differentiating Features	First Principles
NREM parasomnias (sleepwalking, sleep terrors, confusional arousals)	First half of night, eyes open, no recall, onset in childhood, usually resolves by adolescence. Precipitated by sleep deprivation, fever, stress, OSA, PLMD.	Arise from incomplete arousal from SWS — motor cortex active but hippocampus/prefrontal cortex still in deep sleep.
REM sleep behaviour disorder (RBD)	Latter half of night, eyes closed, dream recall present, older adults (usually male, M:F = 9:1), can be precipitated by OSA ^[2]. Loss of REM sleep atonia → dream enactment. Short episodes ( < 60s).	Degeneration or dysfunction of pontine REM-atonia generators (sublaterodorsal nucleus) → failure to inhibit spinal motor neurons during REM.
Nightmare disorder	Latter half of night (REM), patient wakes fully and is rapidly alert, vivid recall of frightening dream content, no motor enactment (atonia preserved).	Normal REM atonia is intact — patient is paralysed and experiences the dream passively. The distress comes from the content, not the behaviour.
Nocturnal (sleep-related) epilepsy	Can occur at any time of night, stereotyped movements (identical from episode to episode), may have tongue biting / incontinence, post-ictal confusion, EEG abnormalities.	Epileptic discharges during sleep. Frontal lobe epilepsy is particularly difficult to distinguish from NREM parasomnias — both cause complex motor behaviours from sleep. Key: epileptic events are stereotyped (same movement every time), while parasomnias are variable.
Nocturnal panic attacks	Occur from NREM sleep (usually N2/N3), patient wakes with intense fear + autonomic symptoms (palpitations, sweating, SOB), fully alert within minutes, recalls the event but NOT dream content.	Panic attacks can arise from sleep — not triggered by dreams (unlike nightmares). The autonomic surge during NREM arouses the patient into a full panic. Distinguished from sleep terrors by full alertness and recall.
Sleep-related eating disorder	Episodes of involuntary eating during partial arousals from NREM sleep. Often bizarre food choices (raw meat, inedible items). Partial or no recall.	A variant of NREM disorder of arousal. Distinguished from nocturnal eating syndrome (NES) where patient is fully conscious during eating.
Nocturnal dissociative episodes	Complex behaviours arising from wakefulness during the night (PSG shows wake EEG during episodes). Often in context of childhood trauma.	Not a true parasomnia — patient is electrophysiologically awake. Distinguished by video-PSG showing wake pattern during the episode.

How to Distinguish Nocturnal Frontal Lobe Epilepsy from NREM Parasomnias

Both cause complex motor behaviours from sleep, but:

Feature	NREM Parasomnia	Nocturnal Frontal Lobe Epilepsy
Stereotypy	Variable from episode to episode	Highly stereotyped (identical each time)
Duration	Usually longer (minutes)	Usually shorter (seconds to 1–2 minutes)
Frequency	Infrequent (weekly to monthly)	Can occur multiple times per night
Age of onset	Childhood (usually resolves)	Any age (persists)
Family history	Common for parasomnias	Less common; may have FHx of epilepsy
EEG	Normal	May show epileptiform discharges (but often normal inter-ictally in frontal epilepsy)

If in doubt → video-PSG is the gold standard investigation.

Differential	How to Distinguish
DSWPD vs Insomnia	DSWPD: normal sleep quality/quantity when allowed to follow own schedule. Insomnia: sleep is disturbed regardless of timing. Confirm with sleep diary + actigraphy showing consistent delayed sleep phase.
ASWPD vs Depression	Both cause early morning awakening. ASWPD: patient also has excessive evening sleepiness and wants to go to bed early. Depression: no desire to go to bed early, wakes with low mood, ruminative thoughts. Check for other depressive features (anhedonia, worthlessness, suicidal ideation).
Shift work disorder vs Insomnia	Clear temporal relationship to shift schedule. Worker sleeps well on days off. Resolved or improved when shifted to day work.
Non-24-hour sleep–wake disorder vs Irregular sleep	Non-24h: progressive daily delay of sleep–wake times, eventually cycling through the 24-hour day. Most common in blind individuals (no light entrainment). Sighted individuals: extremely rare, consider psychiatric comorbidity.

When facing a patient with a sleep complaint, use this structured thinking:

Step 1: What is the predominant complaint?

Insomnia? Hypersomnolence? Abnormal behaviour? Timing?

Step 2: Rule out insufficient sleep and poor sleep hygiene

The most common cause of EDS globally is simply not sleeping enough
Ask about sleep opportunity, caffeine, screen time, irregular schedule

Step 3: Screen for psychiatric comorbidity

Depression (terminal insomnia, anhedonia, low mood)
Anxiety (initial insomnia, racing thoughts)
PTSD (nightmares, hyperarousal)
Mania (decreased need for sleep — patient feels fine)

Step 4: Screen for medical comorbidity

Pain, GERD, respiratory disease, thyroid disease, menopause
Review medication list (SSRIs, steroids, β-blockers, stimulants)
Substance use (caffeine, alcohol, nicotine, recreational drugs)

Step 5: Consider specific sleep disorders

OSA (snoring, witnessed apnoeas, obesity, morning headache)
RLS (urge to move legs, worse at rest and evening)
Narcolepsy (EDS + cataplexy/sleep paralysis/hallucinations)
CSWRD (timing complaint, normal sleep when on own schedule)
Parasomnias (abnormal behaviours — characterise timing, recall, stereotypy)

Step 6: Use appropriate investigations

Sleep diary (2 weeks) for all
Actigraphy for CSWRD
PSG for suspected OSA, RBD, PLMD, epilepsy — NOT for routine insomnia
MSLT for suspected narcolepsy/idiopathic hypersomnia
DLMO for circadian phase confirmation

The insomnia is not better explained by and does not occur exclusively during the course of another sleep-wake disorder (e.g., narcolepsy, a breathing-related sleep disorder, a circadian rhythm sleep-wake disorder, a parasomnia). The insomnia is not attributable to the physiological effects of a substance. Coexisting mental disorders and medical conditions do not adequately explain the predominant complaint of insomnia. — DSM-5 Criteria S, T, U ^[2]

This is important: the DSM-5 insomnia criteria explicitly require you to rule out (or at least consider) all of the above differentials. But remember — you can diagnose insomnia disorder comorbidly with these conditions if the insomnia is a prominent independent complaint that warrants treatment in its own right.

High Yield Summary — Differential Diagnosis of Sleep Disorders

Insomnia DDx: Normal short sleepers (no impairment), situational insomnia ( < 3 months), DSWPD (normal sleep on own schedule), RLS (urge to move legs), OSA (snoring, apnoeas), narcolepsy (EDS dominant), depression (terminal insomnia), anxiety (initial insomnia), substance/medication effects.
EDS DDx: Insufficient sleep (most common), OSA, narcolepsy (refreshing naps, cataplexy), idiopathic hypersomnia (unrefreshing naps, sleep drunkenness), depression (fatigue > sleepiness), medications (antihistamines, BZDs).
Parasomnia DDx: NREM (first half, eyes open, no recall, children) vs REM (second half, eyes closed, dream recall, older males) vs nocturnal epilepsy (stereotyped, any time) vs nocturnal panic (NREM, fully alert, no dream content).
Key distinguishing concepts: Decreased need for sleep (mania) ≠ insomnia; sleepiness ≠ fatigue; DSWPD ≠ insomnia; ASWPD ≠ depression.
Comorbid approach: Insomnia can be diagnosed alongside psychiatric/medical conditions — causality is bidirectional.

Active Recall - Differential Diagnosis of Sleep Disorders

References

^[1] Lecture slides: GC 165. I can't fall asleep Sleep physiology and Sleep disorders.pdf ^[2] Senior notes: ryanho-psych.md (Chapter 9.2 Sleep Disorders) ^[4] Senior notes: ryanho-psych.md (Chapter 7.1 Approach to Low Mood — sleep disturbance in depression) ^[5] Lecture slides: GC 167. I feel very nervous Anxiety disorders.pdf (GAD sleep features)

Diagnostic Criteria, Algorithm, and Investigations for Sleep Disorders

1. Diagnostic Criteria by Condition

This is the most commonly tested set of criteria. Walk through each criterion to understand why it exists ^[2]:

Criterion	DSM-5 Text	Rationale / First Principles
A	A predominant complaint of dissatisfaction with sleep quantity or quality, associated with one or more of: (1) Difficulty initiating sleep; (2) Difficulty maintaining sleep, characterised by frequent awakenings or problems returning to sleep after awakenings (in children, may manifest as difficulty returning to sleep without caregiver intervention); (3) Early-morning awakening with inability to return to sleep	These three patterns map to initial, middle, and terminal insomnia respectively. At least one must be present. Each has different differential implications (initial → anxiety/RLS/DSWPD; terminal → depression/ASWPD).
B	The sleep disturbance causes clinically significant distress or impairment in social, occupational, educational, academic, behavioural, or other important areas of functioning	This separates pathological insomnia from normal short sleepers. Without daytime impairment, there is no disorder — the patient may simply have a lower sleep need.
C	The sleep difficulty occurs ≥3 nights per week	Frequency threshold — occasional poor nights are normal. ≥3/week establishes a pattern.
D	The sleep difficulty is present for ≥3 months	Duration threshold — separates chronic insomnia disorder from short-term/adjustment insomnia ( < 3 months). This criterion increased specificity when DSM-5 replaced DSM-IV's 1-month threshold, reducing prevalence from 22.1% to 10.8%.
E	The sleep difficulty occurs despite adequate opportunity for sleep	Critical exclusion — if someone works 80-hour weeks and sleeps 4 hours, that's insufficient sleep opportunity, not insomnia. The sleep environment and schedule must be permissive of sleep.
F	The insomnia is not better explained by and does not occur exclusively during the course of another sleep-wake disorder (e.g., narcolepsy, a breathing-related sleep disorder, a circadian rhythm sleep-wake disorder, a parasomnia)	Requires consideration of primary sleep disorder mimics — especially DSWPD (normal sleep on own schedule), OSA (fragmentation from apnoeas), and RLS (can't keep legs still).
G	The insomnia is not attributable to the physiological effects of a substance (e.g., a drug of abuse, a medication)	Rule out substance-induced sleep disorder — caffeine, alcohol, stimulants, SSRIs, steroids, etc.
H	Coexisting mental disorders and medical conditions do not adequately explain the predominant complaint of insomnia	Modern "comorbid" approach — you CAN diagnose insomnia disorder alongside depression/anxiety, but only if the insomnia is prominent enough to warrant independent clinical attention. If insomnia is a minor symptom fully explained by severe depression, it doesn't need a separate diagnosis.

Specify course: ^[2]

Episodic: ≥1 month, < 3 months
Persistent: ≥3 months
Recurrent: ≥2 episodes per year

Remember the number "3": ≥30 min delay/awake/early awakening, for ≥3×/week, for ≥3 months ^[2]

ICD-10 Non-Organic Insomnia (F51.0) — Key Differences

The ICD-10 criteria are broadly similar but require:

The complaint occurs at least 3 nights per week for at least 1 month (shorter than DSM-5's 3 months)
The sleep disturbance is the predominant complaint
Preoccupation with not sleeping and excessive concern about consequences
No organic cause (unlike DSM-5's comorbid approach, ICD-10 retains the organic/non-organic split)
Must cause marked distress or interference with functioning

For HKU exams, know DSM-5 criteria primarily, but be aware the ICD-10 threshold is 1 month (not 3).

Diagnosed by polysomnography (PSG):

Apnoea-Hypopnoea Index (AHI) ≥5 events/hour with symptoms (EDS, snoring, witnessed apnoeas, gasping), OR
AHI ≥15 events/hour regardless of symptoms

Severity classification:

Severity	AHI
Mild	5–14 events/hour
Moderate	15–29 events/hour
Severe	≥30 events/hour

Where:

Apnoea = complete cessation of airflow for ≥10 seconds
Hypopnoea = ≥30% reduction in airflow for ≥10 seconds with ≥3% oxygen desaturation or arousal

3. Investigation Modalities — Detailed Guide

3.1 Clinical Assessment Tools (Bedside / Outpatient)

Prefer sleep diary over a 2-week period ^[2]

This is the single most important "investigation" for any sleep complaint. It costs nothing and provides more diagnostic information than most laboratory tests.

What to record each day:

Parameter	Why It Matters
Bedtime	Identifies irregular schedules (perpetuating factor)
Duration until sleep onset (sleep onset latency)	≥30 min suggests insomnia or DSWPD
Number and duration of awakenings	Frequent brief awakenings → OSA/PLMD; prolonged awakenings → insomnia
Final awakening time	Early → depression/ASWPD; Late → DSWPD
Nap times and length	Excessive napping perpetuates insomnia; short refreshing naps suggest narcolepsy
Self-rated sleep quality	Subjective perception — poor quality despite adequate duration suggests fragmented sleep or paradoxical insomnia
Alcohol, caffeine, medication intake	Identifies substance-related contributions
Exercise timing	Late exercise is stimulatory

A standard sleep diary format from the reference ^[2] includes columns for: date, bedtime, lights-off, estimated sleep onset, number of awakenings, total wake time after sleep onset, final awakening, out-of-bed time, naps, subjective quality rating.

Tool	What It Measures	Scoring / Interpretation
Pittsburgh Sleep Quality Index (PSQI)	Global sleep quality over past month	7 component scores (0–3 each): subjective quality, latency, duration, efficiency, disturbances, medication use, daytime dysfunction. Total 0–21. Significant sleep disturbance = > 5 points ^[2]
Sleep Problems Questionnaire	Frequency of specific sleep problems	Significant sleep disturbance = ≥4 on any single item ^[2]
Epworth Sleepiness Scale (ESS)	Subjective daytime sleepiness	Score 0–24. Excessive sleepiness ≥10. Rates likelihood of dozing in 8 situations (0 = never to 3 = high chance) ^[2]
STOP-BANG Questionnaire	OSA risk screening	Snoring, Tired, Observed apnoeas, blood Pressure, BMI > 35, Age > 50, Neck > 40 cm, Gender male. Score 0–8. High risk ≥5.
Insomnia Severity Index (ISI)	Insomnia severity	7 items, 0–28. No insomnia 0–7; subthreshold 8–14; moderate 15–21; severe 22–28
International RLS Study Group Rating Scale	RLS severity	10 items, 0–40
PHQ-9 and GAD-7	Depression and anxiety screening	Essential because psychiatric comorbidity is so common. PHQ-9 ≥10 suggests moderate depression; GAD-7 ≥10 suggests moderate anxiety

Physical examination should screen for medical comorbidities: ^[2]

System	What to Look For	Why
Oropharynx	Mallampati grade, tonsillar hypertrophy, crowding, retrognathia, macroglossia	OSA risk assessment — anatomical narrowing of upper airway
Neck	Circumference ( > 40 cm / 17 inches in males = high risk OSA)	Fat deposition around pharyngeal airway
Cardiovascular	HTN (especially resistant), signs of HF	OSA → chronic intermittent hypoxia → sympathetic overdrive → HTN. HF → Cheyne-Stokes / orthopnoea
Respiratory	COPD, asthma signs	Nocturnal bronchoconstriction → arousals
GI	GERD symptoms	Supine reflux → arousals
Neurological	Tremor, rigidity, bradykinesia, cognitive assessment	RBD → screen for synucleinopathies (PD, DLB)
General	BMI, thyroid status, signs of iron deficiency	Obesity → OSA; hypothyroidism → hypersomnia; iron deficiency → RLS

3.2 Objective Sleep Investigations

Only indicated when you suspect another sleep disorder, e.g., OSA — NOT for routine insomnia evaluation ^[2]

What it measures — a "multi-channel" overnight recording:

Channel	What It Records	Why It's Needed
EEG (electroencephalogram, typically 6+ channels)	Brain electrical activity	Determines sleep stage (N1/N2/N3/REM/wake), identifies arousals, detects epileptiform activity
EOG (electrooculogram)	Eye movements	Distinguishes REM (rapid conjugate eye movements) from NREM (slow rolling or absent)
EMG (electromyogram — chin + tibialis anterior)	Muscle tone	Chin EMG: REM atonia vs RSWA (for RBD). Leg EMG: periodic limb movements (PLMD)
ECG	Heart rhythm	Detects arrhythmias associated with apnoeas (bradycardia during apnoea → tachycardia on arousal)
Nasal airflow (thermistor + pressure transducer)	Breathing	Detects apnoeas (complete cessation) and hypopnoeas (partial reduction)
Chest/abdominal effort (respiratory inductance plethysmography)	Respiratory effort	Distinguishes obstructive (effort present, airflow absent) from central (effort absent, airflow absent) apnoeas
Pulse oximetry	SpO₂	Detects desaturations associated with apnoeas — quantifies hypoxaemic burden
Body position sensor	Supine vs lateral	Positional OSA (worse supine due to gravity pulling tongue posteriorly)
Snore microphone	Snoring	Documents snoring and its relationship to respiratory events
Video (for video-PSG)	Visible behaviour	Essential for parasomnia evaluation — correlates visible behaviour with electrophysiological data

Key findings and interpretation by condition:

Condition	Key PSG Findings	Interpretation
OSA	AHI ≥5 with obstructive apnoeas/hypopnoeas; oxygen desaturations (often cyclical "sawtooth" pattern); respiratory effort present during airflow cessation; arousal at termination of events	Upper airway collapse → effort continues against closed airway → desaturation → arousal to reopen → cycle repeats. The AHI quantifies severity.
Central Sleep Apnoea	AHI ≥5 with central apnoeas; absent respiratory effort during airflow cessation; may see Cheyne-Stokes pattern in HF	Brain fails to generate respiratory drive. In HF: cyclical crescendo-decrescendo breathing due to high loop gain from pulmonary congestion.
RBD	REM sleep without atonia (RSWA) on chin/limb EMG during REM + video showing dream enactment behaviour ^[2]	Pontine REM-atonia generators dysfunctional → persistent muscle tone during REM → motor output not suppressed → enactment.
PLMD	Periodic limb movement index ≥15/hour; stereotyped, repetitive leg movements (dorsiflexion of ankle + flexion of knee/hip) in NREM, occurring in runs	Dopaminergic dysfunction → repetitive involuntary limb movements. Each movement may cause a microarousal → fragmented sleep → EDS.
Narcolepsy	Early REM entry (≤15 min from sleep onset), spontaneous awakenings, increased light NREM sleep, fragmented sleep architecture ^[2]	Destabilised flip-flop switch → rapid transitions between wake and REM; inadequate consolidation of sleep states.
NREM parasomnia	Arousal from N3 (SWS) — EEG shows sudden shift from high-amplitude delta to mixed alpha/theta; behaviour on video (walking, screaming)	Partial cortical arousal from deep sleep — motor cortex active, hippocampus and prefrontal cortex remain in sleep.
Nocturnal epilepsy	Epileptiform discharges (spikes, sharp waves) on EEG during or between events; stereotyped movements on video	Epileptic focus generating abnormal electrical activity. May need extended EEG montage for frontal lobe foci.

When to Order PSG — A Common Exam Question

DO order PSG for:

Suspected OSA (snoring + EDS + witnessed apnoeas + risk factors)
Suspected RBD (dream enactment in older adult)
Suspected PLMD (bed partner reports repetitive limb jerks)
Pre-MSLT assessment for narcolepsy (must rule out OSA first and document preceding night's sleep)
Suspected nocturnal epilepsy (when history is ambiguous)
Treatment-resistant insomnia where another sleep disorder is suspected

Do NOT order PSG for:

Routine insomnia evaluation — insomnia is a clinical diagnosis
Circadian rhythm disorders — use actigraphy + DLMO instead
RLS — diagnosed clinically using IRLSSG criteria
Uncomplicated NREM parasomnias in children — diagnosed clinically

Objective measure of sleepiness ^[2]

Purpose: Quantifies physiological sleepiness and detects pathological REM intrusion (SOREMPs)
Process: patient asked to try to sleep for 20 min, repeated every 2 hours (Q2H), starting 2–4 hours after awakening, performed 4–5 times throughout the day ^[2]
Prerequisites (critical — invalid without these):
- Preceding night's PSG to confirm ≥6 hours of sleep (and rule out OSA causing EDS)
- Sleep diary for ≥1 week before showing adequate habitual sleep (≥7 hours)
- Discontinuation of REM-suppressing medications (SSRIs, SNRIs, TCAs) ≥2 weeks before (these suppress REM and reduce SOREMPs, causing false negatives)
- No caffeine, alcohol, or recreational drugs on test day

Interpretation: ^[2]

Finding	Interpretation
Mean sleep latency < 5 min	Pathological sleepiness — the patient is so sleepy they fall asleep within 5 minutes, indicating severe sleepiness that could impair functioning and driving safety
Mean sleep latency 5–8 min	Borderline / indeterminate
Mean sleep latency > 8 min	Normal — argues against pathological sleepiness
≥2 SOREMPs out of 4–5 naps	Narcolepsy (type 1 or 2) — pathological REM intrusion. A SOREMP on the preceding nocturnal PSG can count as one of the two.
< 2 SOREMPs with short latency	Idiopathic hypersomnia, insufficient sleep, or other cause of EDS

≥2 trials with positive REM sleep indicates narcolepsy ^[2]

Test	Indication	Rationale
Ferritin	RLS evaluation	Iron repletion if ferritin < 75 µg/L ^[2] — iron is a cofactor for tyrosine hydroxylase (rate-limiting enzyme in dopamine synthesis). Low iron → low dopamine → RLS symptoms. Note: target is 75 µg/L, NOT the standard lab "normal" cutoff of ~15–20 µg/L
TFTs	EDS evaluation	Hypothyroidism → ↓ metabolic rate → hypersomnia, fatigue
HbA1c / Fasting glucose	OSA evaluation	OSA ↔ metabolic syndrome (bidirectional relationship); screen for T2DM
ABG	Severe OSA / Obesity hypoventilation	Chronic CO₂ retention (↑ PaCO₂, ↑ HCO₃⁻) indicates alveolar hypoventilation
CSF hypocretin-1 (orexin-A)	Narcolepsy type 1 diagnosis	Low in narcolepsy type 1 (≤110 pg/mL or < 1/3 of normal) ^[2]. Highly specific and sensitive. Useful when MSLT is equivocal or cannot be performed.
*HLA-DQB10602**	Narcolepsy risk assessment	Positive in 98% of narcolepsy type 1, 50% of type 2, but also 12–40% of healthy individuals ^[2] — therefore it is supportive but not diagnostic. High sensitivity, low specificity. A negative result makes narcolepsy type 1 very unlikely.

Suspected Condition	First-Line Investigation	Confirmatory / Additional
Insomnia disorder	Sleep history + 2-week sleep diary + screening tools (PSQI, ISI) ^[2]	PSG only if another sleep disorder suspected; psychiatric screening (PHQ-9, GAD-7)
OSA	STOP-BANG screening → PSG (or home sleep apnoea test if high pre-test probability and no comorbidities)	SpO₂ trend, ABG if severe, TFTs, HbA1c
Narcolepsy	Clinical assessment (tetrad) + ESS → PSG followed by MSLT	CSF orexin-A (if type 1 suspected), HLA-DQB1*0602 (supportive)
Idiopathic hypersomnia	Clinical assessment + ESS → PSG followed by MSLT	MSLT: mean latency < 8 min but < 2 SOREMPs
RLS	Clinical diagnosis (IRLSSG criteria) + ferritin level	PSG only if PLMD needs documentation; nerve conduction studies if neuropathy suspected
RBD	Clinical history (dream enactment, bed partner Hx) → video PSG ^[2]	Neurological assessment for synucleinopathies; DaTscan if PD suspected
NREM parasomnias	Clinical history (usually sufficient in children)	Video PSG if diagnosis uncertain, events are frequent/injurious, or nocturnal epilepsy needs exclusion
CSWRD	Sleep diary ≥2 weeks + actigraphy ^[2]	Chronotype questionnaire + DLMO protocol ^[2]

High Yield Summary — Diagnosis and Investigation of Sleep Disorders

Insomnia Disorder DSM-5: Sleep complaint (initial/middle/terminal) + distress/impairment + ≥3 nights/week + ≥3 months + adequate sleep opportunity + not explained by other sleep disorder/substance/medical condition. Remember "3-3-3": 30 min, 3x/week, 3 months.
Insomnia is a CLINICAL diagnosis — PSG is NOT indicated for routine insomnia. Only order PSG when suspecting OSA, RBD, PLMD, or treatment-resistant cases.
PSG channels: EEG (sleep stages), EOG (eye movements), EMG (atonia/RSWA/PLMS), ECG, airflow, respiratory effort, SpO2, position, video. Know which channel answers which clinical question.
MSLT: Objective sleepiness test. Mean latency < 5 min = pathological sleepiness. ≥2 SOREMPs = narcolepsy. Must have preceding PSG + adequate prior sleep + withdrawal of REM-suppressants.
DLMO: Gold standard for circadian phase. Sample melatonin under dim light ( < 30 lux) every 30–60 min. Normal rise 90–120 min before habitual bedtime. Delayed rise = DSWPD.
Actigraphy: Wrist-worn accelerometer for rest-activity cycles over weeks. Best for CSWRD and as adjunct to sleep diary. Cannot stage sleep.
Key blood tests: Ferritin < 75 µg/L → iron repletion for RLS. CSF orexin-A ≤110 pg/mL → narcolepsy type 1. HLA-DQB1*0602: supportive not diagnostic (98% type 1, but 12–40% healthy).
OSA diagnosis: AHI ≥5 + symptoms or AHI ≥15 regardless. Mild 5–14, Moderate 15–29, Severe ≥30.
RBD diagnosis: History + video PSG showing RSWA + dream enactment. Always screen for synucleinopathies.
RLS diagnosis: Purely clinical (IRLSSG 5 criteria). Check ferritin. PSG only for PLMD documentation.

Active Recall - Diagnostic Criteria, Algorithm and Investigations

References

^[1] Lecture slides: GC 165. I can't fall asleep Sleep physiology and Sleep disorders.pdf ^[2] Senior notes: ryanho-psych.md (Chapter 9.2 Sleep Disorders)

Management of Sleep Disorders

1. Management of Insomnia

Sleep hygiene is the universal foundation — every patient with any sleep disorder should receive sleep hygiene counselling. ^[2] Think of it as the "lifestyle modification" equivalent in hypertension — necessary but often insufficient alone for moderate-severe disease.

Principles of sleep education (sleep hygiene): ^[2]

Category	Recommendations	Rationale / First Principles
Sleep environment	Familiar and comfortable, Dark, Quiet	Darkness promotes melatonin secretion (pineal gland responds to absence of light via the retinohypothalamic tract → SCN → pineal). Noise causes cortical arousals. An unfamiliar environment activates the amygdala ("first night effect").
Encourage	Bedtime routines	Conditioned relaxation response — consistent pre-sleep ritual signals to the brain that sleep is approaching
	Consistent time for going to bed and waking up	Entrains the circadian clock (SCN); irregular schedules cause internal desynchrony (similar to perpetual jet lag)
	Going to bed only when tired	Prevents lying awake in bed → prevents conditioned arousal (bed = frustration)
	Thinking about problems before going to bed	"Worry time" earlier in the evening offloads cognitive arousal before the sleep period
	Regular exercise	Exercise ↑ adenosine accumulation (↑ Process S), ↓ anxiety, ↑ SWS — but timing matters
Avoid	Late-evening exercise	Exercise is sympathetically activating; core body temperature needs to drop for sleep onset — exercise delays this drop
	Caffeine-containing drinks late in the day	Caffeine blocks adenosine A₁/A₂A receptors → blocks Process S → delays sleep onset. Half-life ~5–6h, so afternoon caffeine is still active at bedtime
	Using mobile devices or watching TV in bed	Blue light from screens suppresses melatonin via ipRGCs → delays circadian phase. Also, bed becomes associated with stimulating activity (conditioned arousal)
	Excessive alcohol and smoking	Alcohol: initial sedation → second-half rebound arousal + ↓ REM. Nicotine: stimulant effect
	Excessive daytime sleep	Dissipates Process S → reduces homeostatic sleep drive at night
	Large late meals	GERD risk; thermogenic effect of digestion raises core temperature, opposing the temperature drop needed for sleep onset
	Too much time in bed lying awake	Perpetuates conditioned arousal — the bed becomes a cue for wakefulness, not sleep

Sleep Hygiene Alone Is Usually Insufficient for Chronic Insomnia

Sleep hygiene is necessary but rarely sufficient as monotherapy for chronic insomnia disorder. It is best thought of as the "baseline" that enables other treatments (CBT-I, medications) to work. Studies show sleep hygiene education alone has modest effect sizes (~0.2). Always combine with CBT-I or pharmacotherapy for chronic insomnia. Do NOT dismiss a patient with chronic insomnia by telling them to "just practice good sleep hygiene."

CBT for insomnia (CBT-I): 1st line but not readily available ^[2]

CBT-I is the gold standard treatment for chronic insomnia. It is recommended as first-line by AASM, European Sleep Research Society, and NICE guidelines. It has equivalent short-term efficacy to medications but superior long-term outcomes because it addresses perpetuating factors (3P model) rather than just symptoms.

Techniques: ^[2]

Technique	What It Is	How It Works (First Principles)
Sleep education	Teaching the patient about normal sleep, sleep architecture, the 3P model, and realistic sleep expectations	Corrects misconceptions (e.g., "I need 8 hours or I'll be destroyed") that fuel anxiety about sleep. Reduces the cognitive component of hyperarousal.
Stimulus control	Instructions to re-associate the bed/bedroom with sleep only. Rules: go to bed only when sleepy; if unable to sleep within ~20 min, leave the bed and return only when sleepy; use bed only for sleep and sex; fixed wake time regardless of sleep quality; no napping.	Targets conditioned arousal — the classical conditioning where bed = wakefulness/frustration. By breaking this association and rebuilding bed = sleep, you restore the automatic sleep response. This is arguably the single most powerful CBT-I component.
Sleep restriction	Reduce time in bed to match actual sleep time (e.g., if patient sleeps 5 hours but spends 8 hours in bed → restrict to 5 hours in bed). Gradually increase by 15–30 min as sleep efficiency improves. Target: sleep efficiency ≥85%.	Builds up Process S (homeostatic sleep drive) by mild sleep deprivation → consolidates sleep → improves sleep efficiency. Counter-intuitive but extremely effective. Sleep efficiency = (total sleep time / time in bed) × 100%. Normal ≥85%.
Relaxation training	Progressive muscle relaxation, diaphragmatic breathing, guided imagery, autogenic training	Directly opposes physiological hyperarousal — ↓ sympathetic tone, ↓ cortisol, ↓ muscle tension → lowers the arousal threshold to allow VLPO activation
Cognitive therapy	Identifying and challenging dysfunctional beliefs about sleep (e.g., "If I don't sleep 8 hours, I'll collapse at work tomorrow"; "I've never been a good sleeper and never will be")	Addresses the cognitive perpetuating factors — catastrophising, unrealistic expectations, and attentional bias toward sleep-related threat. Reduces the "worry cycle" described in the 3P model.

Delivery formats: ^[2]

Form: self-help, individual, group, face-to-face, telephone-administered
Delivery: by nurse or therapist
Number of sessions: 1–8 (typically 4–6 weekly sessions)
Digital CBT-I (dCBT-I) is increasingly available and has good evidence (e.g., Sleepio, SHUTi). HKU's CBT-I project by Dr KF Chung is a local resource ^[2]

Why Is CBT-I First Line Over Medications?

Equivalent short-term efficacy to pharmacotherapy for chronic insomnia
Superior long-term efficacy — effects persist after treatment ends (because you've changed the perpetuating factors), unlike medications where insomnia returns upon discontinuation
No dependence risk — unlike benzodiazepines and Z-drugs
No side effects — no hangover sedation, no falls risk, no cognitive impairment
Addresses root cause — targets the perpetuating factors of the 3P model, not just the symptom

The main barrier is availability — there are not enough trained CBT-I therapists. This is why digital CBT-I programmes are increasingly important.

1.3 Pharmacotherapy for Insomnia

Pharmacological therapy: only Z drugs and Ramelteon recommended in guidelines, also 1st line ^[2]

Medications are appropriate when:

CBT-I is unavailable or the patient declines
Acute/short-term insomnia where rapid symptom relief is needed
As adjunct to CBT-I in severe cases
Always aim for short-term use (2–4 weeks), with planned tapering

Drug Class	Specific Agents	Mechanism	Indications	Key Features	Cautions/Contraindications
Z drugs (BZD receptor agonists)	Zolpidem (Stilnox), Zopiclone (Imovane) ^[2]^[6]	Non-benzodiazepine drugs acting as specific agonists at BZD receptors (ω₁ receptors) ^[6]. The ω₁ (alpha-1 subunit of GABA-A) receptor is selectively targeted → sedation without significant anxiolytic, muscle relaxant, or anticonvulsant effects (which require ω₂/ω₃).	Sleep onset insomnia primarily. Stilnox CR can be used for sleep maintenance insomnia ^[6].	Produces ↓ changes in sleep architecture and has ↓ duration of action compared to BZDs ^[6]. Stilnox has shorter half-life (↓ propensity for hangover), less bitter, but may be less effective for sleep maintenance and may be more expensive. Imovane may cause bitter aftertaste. ^[6]	Residual effects (slow, drowsiness, ↓ daytime performance, ↑ risk of falls), rarely behavioural disturbances (confusion, amnesia, ↓ mood) ^[6]. Complex sleep behaviours (sleep-driving, sleep-eating) — rare but serious. Elderly: start low dose. Avoid in pregnancy. Short-term use only (2–4 weeks).
Melatonin receptor agonist	Ramelteon ^[2]^[6]	Selective MT₁ and MT₂ receptor agonist ^[6]. MT₁ receptors in SCN → promote sleepiness; MT₂ receptors → shift circadian phase. Unlike melatonin supplements, Ramelteon has higher receptor affinity and longer half-life.	Sleep onset insomnia, especially in elderly (no abuse potential, no next-day impairment).	No abuse potential, no dependence risk, not a controlled substance. Minimal next-day sedation. Safe in elderly.	Avoid with fluvoxamine (strong CYP1A2 inhibitor → ↑ Ramelteon levels). Less effective for sleep maintenance.
Low-dose doxepin	Doxepin (Silenor) 3–6 mg ^[2]	Tricyclic antidepressant — at low doses, acts primarily as H₁ antihistamine (blocks histamine at the TMN → blocks wake-promoting signal). At antidepressant doses (75–150 mg), additional NA and 5-HT reuptake inhibition.	Sleep maintenance insomnia, especially in elderly.	At 3–6 mg, essentially a pure antihistamine with minimal anticholinergic or adrenergic effects. Only FDA-approved TCA for insomnia.	Avoid in glaucoma (anticholinergic at higher doses), urinary retention. Very low doses are remarkably well-tolerated.

Why the ω₁ selectivity of Z drugs matters: Traditional benzodiazepines bind non-selectively to all GABA-A receptor subtypes (ω₁, ω₂, ω₃). ω₁ → sedation; ω₂ → anxiolysis + muscle relaxation; ω₃ → anticonvulsant. By targeting only ω₁, Z drugs provide hypnotic effect with fewer muscle-relaxant and amnestic effects, less disruption to sleep architecture, and (theoretically) less dependence potential. In practice, however, dependence can still develop with prolonged use.

Other drugs (not recommended): ^[2]

Drug Class	Specific Agents	Mechanism	When Used	Why Not First-Line
Off-label sedating antidepressants	Mirtazapine (Remeron), Trazodone, Paroxetine ^[2]	Mirtazapine: H₁ antagonist + 5-HT₂A/2C antagonist → sedation + ↑ appetite. Trazodone: 5-HT₂A antagonist + weak SARI → sedation at low dose. Paroxetine: SSRI with some sedating properties.	When comorbid depression exists, or when primary agents fail. Trazodone is very widely used off-label (50–100 mg) despite limited evidence.	Insufficient RCT evidence for insomnia specifically. SE profile: Mirtazapine → weight gain; Trazodone → priapism (rare but serious), orthostatic hypotension; Paroxetine → weight gain, sexual dysfunction, withdrawal symptoms.
Off-label sedating antipsychotics	Quetiapine (Seroquel) ^[2]	At low doses (25–50 mg): primarily H₁ and α₁ antagonism → sedation. At higher doses: D₂ and 5-HT₂A antagonism.	Sometimes used when comorbid psychotic illness or severe agitation. Widely (mis)used off-label for insomnia.	NOT recommended for insomnia — metabolic syndrome risk (weight gain, dyslipidaemia, hyperglycaemia), QTc prolongation, extrapyramidal symptoms with chronic use. Disproportionate risk for a "sleep aid."
Short-acting benzodiazepines	Lorazepam (Ativan) ^[2]	Non-selective GABA-A receptor agonist → sedation + anxiolysis + muscle relaxation + anticonvulsant	Acute severe insomnia with significant anxiety, very short-term use ( < 2–4 weeks)	↑ risk of dependence ^[2]. Disrupt sleep architecture (↓ SWS, ↓ REM). Rebound insomnia on discontinuation. Falls risk in elderly. Cognitive impairment. Tolerance develops.
OTC drugs	Promethazine (Phenergan), melatonin ^[2]	Promethazine: 1st-generation antihistamine (H₁ blocker). Melatonin: MT₁/MT₂ agonist (OTC formulation).	Self-medication by patients.	Promethazine: anticholinergic SE (dry mouth, blurred vision, urinary retention, constipation), next-day sedation, not evidence-based. OTC melatonin: variable bioavailability, unregulated dosing, modest effect mainly on sleep latency (15–20 min reduction).

Benzodiazepines for Insomnia — What You Must Know for Exams

Benzodiazepines should NOT be used as primary treatment for insomnia ^[6]:

Prefer short-acting drugs for sleep induction to minimise hangover (e.g., temazepam, lormetazepam) ^[6]
May inhibit REM sleep and disrupt sleep architecture, resulting in a rebound increase when discontinued ^[6]
Should avoid using hypnotics regularly or for long periods of time ^[6]
Maximum recommended duration: 2–4 weeks
Risk of tolerance (need escalating doses) and dependence (physical withdrawal symptoms)
Withdrawal symptoms: rebound insomnia (worse than baseline), anxiety, tremor, seizures (in severe cases)
Elderly: ↑ falls risk, ↑ cognitive impairment, ↑ hip fractures

If you must use a BZD for insomnia, choose short-acting, prescribe the lowest effective dose, limit to < 4 weeks, and have an exit plan.

Other non-pharmacological: mindfulness, TCM, hypnosis ^[2]

Approach	Evidence	Mechanism
Mindfulness-Based Therapy for Insomnia (MBTI)	Moderate evidence — can be combined with CBT-I elements	Reduces cognitive and physiological arousal through present-moment awareness; breaks the "worry cycle"
Acupuncture / TCM	Limited but growing evidence; popular in Hong Kong	Proposed mechanism: modulation of autonomic nervous system, endorphin release. Evidence quality is generally low.
Hypnosis	Limited evidence as standalone; may augment relaxation training	Suggestion-based approach to reduce arousal and modify sleep-related cognitions
Exercise	Good evidence as adjunct	↑ adenosine, ↑ SWS, ↓ anxiety, ↑ core body temperature (subsequent cooling promotes sleep) — must be timed correctly (not late evening)

2. Management of Excessive Daytime Sleepiness and Narcolepsy

Treatment for sleepiness in general: ^[2]

Measure	Rationale
Sleep hygiene: regular and adequate sleep, caffeine not later than 4 PM ^[2]	Ensuring adequate sleep opportunity addresses the most common cause of EDS (insufficient sleep). Caffeine after 4 PM disrupts subsequent night's sleep → perpetuates cycle.
Short naps: 15 min ^[2]	Short naps dissipate Process S without entering deep sleep (which causes sleep inertia upon waking). In narcolepsy, short naps are characteristically refreshing. Longer naps enter SWS → grogginess.
Bright light: especially for shift work, jet lag, seasonal affective disorder ^[2]	Light suppresses melatonin and activates the SCN alerting signal → promotes wakefulness at desired times. Strategic light exposure can phase-shift the circadian clock.
Adjust shift work: forward shift, regular night shift, 12h 2-shift ^[2]	Forward rotation (morning → afternoon → night) follows the natural tendency of the circadian clock to delay. Rapid backward rotations cause severe desynchrony. Consistent schedules allow partial adaptation.

Management of narcolepsy: ^[2]

Symptom Targeted	Drug	Mechanism	Key Points
Daytime sleepiness	Modafinil: 1st line ^[2]	?Amphetamine-like inhibition of dopamine reuptake ^[2] → ↑ DA in wake-promoting circuits (VTA, LC). Also may affect norepinephrine and histamine pathways. Exact mechanism not fully elucidated.	100–400 mg/day. Well-tolerated. SE: headache, nausea, anxiety. Lower abuse potential than traditional stimulants.
	Other options: armodafinil, methylphenidate, amphetamines ^[2]	Armodafinil: R-enantiomer of modafinil (longer-acting). Methylphenidate/amphetamines: ↑ DA and NA release.	Methylphenidate and amphetamines are second-line due to higher abuse potential, cardiovascular SE (↑ HR, ↑ BP), and Schedule II controlled substance status.
Cataplexy	SSRI/SNRI/(TCA) ^[2]: e.g., venlafaxine, atomoxetine, fluoxetine, (clomipramine)	MoA: brainstem circuits that generate REM sleep are strongly inhibited by noradrenaline and serotonin ^[2]. These drugs ↑ NA and/or 5-HT → suppress the pontine REM-atonia generator → prevent cataplexy (which is intrusion of REM atonia into wakefulness).	Venlafaxine is often preferred (potent NA + 5-HT reuptake inhibition). Clomipramine (TCA) is highly effective but has more SE (anticholinergic). Abrupt discontinuation can cause "status cataplecticus" — prolonged cataplexy episode.
Both EDS and cataplexy	Sodium oxybate (sodium γ-hydroxybutyrate / GHB) ^[2]	GABA metabolite → ?acts through GABA-B receptors, exact mechanism unknown ^[2]. Consolidates nocturnal sleep (↑ SWS) → ↓ daytime sleepiness. Also suppresses cataplexy through unclear mechanisms.	Given in two divided doses at night (at bedtime and 2.5–4 hours later — short half-life). Powerful but tightly regulated (Schedule III). SE: nausea, dizziness, enuresis, sleep-disordered breathing. Risk of abuse.
	Pitolisant (newer agent)	Histamine H₃ receptor inverse agonist/antagonist → blocks presynaptic H₃ autoreceptors → ↑ histamine release from TMN → promotes wakefulness. Also modulates other neurotransmitters.	EU/US approved. Oral, once daily. Lower abuse potential. Also effective for cataplexy.
	Solriamfetol (newer agent)	Dual dopamine and norepinephrine reuptake inhibitor (DNRI)	Approved for EDS in narcolepsy and OSA. Fast onset.

Driving advice for narcolepsy: ^[2]

Majority safe to drive but may need time limit (prolonged wakefulness → ↑ attacks) ^[2]
Patients should avoid long, monotonous drives
Strategic napping before driving
Some jurisdictions require medical clearance

Other drugs to avoid: ^[2]

Avoid BZD, opiates, antipsychotics, alcohol — all suppress wakefulness and worsen EDS

Treatment	Indication	Mechanism	Key Considerations
Lifestyle modifications	All patients	Weight loss: ↓ fat around pharyngeal airway → ↑ airway calibre. Positional therapy: avoid supine sleeping (tongue falls back). Avoid alcohol/sedatives: these relax pharyngeal muscles → ↑ collapsibility.	Weight loss of 10% can ↓ AHI by ~50% in moderate OSA. Positional therapy works for positional OSA (AHI ≥2× in supine vs lateral).
Continuous Positive Airway Pressure (CPAP)	First line for moderate-severe OSA (AHI ≥15)	Pneumatic splint — delivers continuous positive pressure via mask → prevents upper airway collapse by maintaining intraluminal pressure above the critical closing pressure	Gold standard. Highly effective. Main barrier: adherence (~50% patients struggle). Adequate use = ≥4 hours/night for ≥70% of nights. SE: mask discomfort, nasal dryness, aerophagia, claustrophobia. Heated humidification and proper mask fitting improve tolerance.
Mandibular Advancement Device (MAD)	Mild-moderate OSA or CPAP-intolerant patients	Custom-fitted oral appliance that protrudes the mandible forward → pulls the tongue and soft palate anteriorly → ↑ posterior airway space	Less effective than CPAP but better adherence. Custom devices (fitted by dentist) superior to OTC boil-and-bite devices.
Surgery	Selected patients with identifiable anatomical obstruction or CPAP/MAD failure	Uvulopalatopharyngoplasty (UPPP): removes excess tissue. Maxillomandibular advancement: moves jaw forward. Hypoglossal nerve stimulation: stimulates genioglossus → opens airway.	Highly variable success rates. UPPP: ~50% response, often diminishes over time. Hypoglossal nerve stimulation (Inspire device) is promising for selected patients who fail CPAP.
Adjuncts	As indicated	Nasal surgery for obstruction. Tonsillectomy/adenoidectomy (first-line in paediatric OSA). Myofunctional therapy (tongue exercises).	Paediatric OSA: adenotonsillectomy is curative in most cases.

4. Management of Parasomnias

Key principle: determine severity and frequency → highly variable but important treatment implications ^[2]

Infrequent → no treatment required ^[2]
Once every few months → need treatment + search for precipitating factors ^[2]

Treatment	Details	Mechanism
Treat precipitating factors	Sleep deprivation, alcohol, medications (especially BZD, BZRA), fever, OSA, PLMD ^[2]	These factors increase SWS depth or cause incomplete arousals → more parasomnia events. Treating OSA alone can resolve NREM parasomnias.
Environment modification	Use padding in bedroom, lock doors, remove sharp objects ^[2]. Alarms on doors/windows. Sleep on ground floor.	Prevent injury during episodes. The patient is unaware during the event and cannot protect themselves.
Reassurance and education	Explain to parents (for children) that this is developmental and usually self-limiting	Most childhood NREM parasomnias resolve by adolescence as SWS proportion naturally decreases
Scheduled awakening	Wake the child ~15–30 min before the typical time of the parasomnia event, nightly for several weeks	Disrupts the SWS cycle before the partial arousal occurs. Effective in children with predictable timing.
Pharmacotherapy: low-dose clonazepam	Best studied, rarely necessary ^[2]. Typical dose: 0.25–0.5 mg at bedtime.	Clonazepam suppresses SWS (reduces depth of N3) → fewer partial arousals. Also ↓ arousal threshold. Reserve for frequent, dangerous, or injurious episodes.

SRED (Sleep-Related Eating Disorder): ^[2]

Management: SSRI, topiramate, clonazepam ^[2]
Topiramate: appetite suppressant + GABAergic properties → reduces eating episodes

4.2 REM Parasomnias

Management of RBD: ^[2]

Treatment	Details	Mechanism
Safe sleeping environment	First priority ^[2]. Remove bedside tables, sharp objects. Place mattress on floor. Separate beds if necessary. Pad the floor and furniture edges.	RBD episodes can cause serious injury — falling out of bed, punching partner, breaking furniture. Safety comes first.
Melatonin	Augments REM sleep ^[2]. Dose: 3–12 mg at bedtime.	Melatonin may partially restore REM atonia through unclear mechanisms — possibly by modulating GABAergic and glycinergic transmission in the brainstem. Has fewer SE than clonazepam. Increasingly used as first-line pharmacotherapy.
Clonazepam	0.25–2 mg at bedtime ^[2]	Suppresses phasic muscle activity during REM. Does NOT restore normal REM atonia (EMG still shows RSWA on PSG). May work by raising the arousal threshold. Effective but risk of sedation, falls (elderly), worsening OSA (muscle relaxation).
Address underlying cause	Withdraw offending serotonergic antidepressants if possible. Treat comorbid OSA (which can precipitate RBD). Screen for neurodegenerative disease (PD, DLB).	Serotonergic antidepressants (SSRIs, SNRIs, mirtazapine) can cause/exacerbate RBD by altering serotonergic modulation of pontine REM-atonia centres.

Management of nightmares: ^[2]

Treatment	Details	Mechanism
Good sleep hygiene	Address sleep deprivation, which increases REM rebound → more intense dreams ^[2]	Sleep deprivation → REM rebound → ↑ dream intensity and emotional content
Treat comorbid disorder	Especially depression, PTSD ^[2]	Nightmares are often a manifestation of underlying psychopathology
Psychotherapy	Image Rehearsal Therapy (IRT): patient rehearses a modified, non-threatening version of the nightmare during daytime → "rewrites" the dream script ^[2]	Cognitive restructuring of the nightmare content. Highly effective (NNT ~3 for PTSD-related nightmares).
Prazosin	α₁-adrenergic antagonist ^[2]. Dose: 1–15 mg at bedtime (start low, titrate up).	Blocks noradrenergic hyperactivation during sleep — in PTSD, the locus coeruleus is overactive, causing increased noradrenergic tone during REM → nightmares. Prazosin blocks post-synaptic α₁ receptors → reduces this hyperarousal. SE: orthostatic hypotension (first dose effect), dizziness.

Stepwise approach: ^[2]

Step	Treatment	Details
1	Iron repletion if ferritin < 75 µg/L ^[2]	Oral iron (ferrous sulfate 325 mg with vitamin C on empty stomach) or IV iron if oral intolerant. Target ferritin > 75 µg/L (NOT the standard lab "normal" of 15–20). Iron is the cofactor for tyrosine hydroxylase → rate-limiting enzyme for dopamine synthesis → ↓ iron = ↓ dopamine.
2	α₂δ ligand (gabapentin, pregabalin) ^[2] OR non-ergot dopamine agonists (pramipexole, ropinirole) ^[2]	α₂δ ligands: Bind α₂δ subunit of presynaptic voltage-dependent Ca²⁺ channels → block release of excitatory neurotransmitters → ↓ sensory symptoms. SE: somnolence, dizziness, ↑ appetite, mood changes, confusion, ataxia ^[6]. DA agonists: directly stimulate D₂/D₃ receptors in A11 diencephalospinal pathway. SE: nausea, augmentation (worsening of symptoms with chronic use — paradoxical earlier onset and spread to arms), impulse control disorders (gambling, hypersexuality). Current guidelines (IRLSSG 2024) favour α₂δ ligands as first-line over DA agonists due to augmentation risk.
	Levodopa ^[2]	Dopamine precursor (converted to DA by DOPA decarboxylase). Effective for intermittent RLS but high augmentation risk with daily use (up to 70% over years). Best reserved for as-needed/intermittent use.
3 (Refractory)	± Opioid, clonazepam ^[2]	Low-dose opioids (oxycodone, tramadol, codeine): activate mu-opioid receptors → modulate dopaminergic and sensory pathways. Very effective but addiction risk. Clonazepam: ↓ arousals from PLMS but doesn't treat RLS sensation.

Augmentation — The Nemesis of Dopamine Agonist Therapy in RLS

Augmentation is the most important long-term complication of dopamine agonist treatment for RLS. It manifests as:

Earlier onset of symptoms (e.g., afternoon instead of evening)
Faster onset when at rest
Spread to previously unaffected body parts (arms, trunk)
Shorter duration of drug effect

This occurs because chronic dopamine receptor stimulation → receptor desensitisation → compensatory upregulation of symptoms. It is more common with levodopa (70%) and less common with longer-acting DA agonists (pramipexole ~8% at 10 years). This is the main reason current guidelines prefer α₂δ ligands over DA agonists as initial therapy.

Disorder	Treatment	Mechanism
Delayed Sleep-Wake Phase Disorder (80%)	Gradual advancing bedtime with strict sleep/wake schedule; 0.5 mg melatonin 1h before target bedtime; morning light (2h 5000 lux); evening light restriction ^[2]	Chronotherapy (gradually advancing bedtime): shifts the clock earlier. Melatonin: exogenous melatonin given 1h before desired bedtime acts as a "darkness signal" → advances the circadian phase via MT₁/MT₂ receptors in SCN. Must be low dose (0.5 mg) and correctly timed — higher doses can cause daytime sedation without better phase-shifting. Morning bright light: suppresses residual melatonin and provides a phase-advancing zeitgeber to the SCN. Evening light restriction: prevents the blue light phase-delay signal.
Advanced Sleep-Wake Phase Disorder	Bright light therapy in the evening ^[2]	Evening bright light delays the circadian clock (sends "it's still daytime" signal to the SCN → delays melatonin onset → delays sleep phase).
Non-24-hour Sleep-Wake Disorder	Behavioural changes; timed melatonin (1h before bed); melatonin agonist (tasimelteon) ^[2]	Tasimelteon ("tasi" from the MT₁/MT₂ receptor targets): dual MT₁/MT₂ agonist specifically approved for non-24-hour disorder in totally blind adults. Provides the entrainment signal that missing light input cannot.
Shift work disorder	Strategic light/dark exposure; scheduled napping; melatonin before desired sleep time; optimise shift schedules ^[2]	Forward rotation (morning → afternoon → night): aligns with natural circadian delay tendency. Bright light at start of night shift → promotes alertness. Dark sunglasses on drive home in morning → prevents phase-advancing light exposure. Melatonin before daytime sleep → promotes sleep during biological day.
Jet lag	Strategic light exposure at destination, melatonin, short-acting hypnotic (one-off)	Eastward travel (phase advance required): morning light at destination, melatonin in evening. Westward travel (phase delay required): evening light at destination, avoid morning light.

Drug	Class	Mechanism	Primary Use
Zolpidem, Zopiclone	Z drugs	ω₁-selective GABA-A agonist	Insomnia (sleep onset)
Ramelteon	Melatonin agonist	MT₁/MT₂ agonist	Insomnia (sleep onset, elderly)
Low-dose doxepin	TCA (at low dose = antihistamine)	H₁ antagonist	Insomnia (sleep maintenance)
Modafinil	Wakefulness promoter	DA reuptake inhibition	Narcolepsy EDS, shift work
Sodium oxybate	GHB	GABA-B agonist	Narcolepsy (EDS + cataplexy)
Venlafaxine, Fluoxetine	SNRI / SSRI	↑ NA and/or 5-HT → suppress REM	Cataplexy, sleep paralysis
Pitolisant	H₃ inverse agonist	↑ histamine release from TMN	Narcolepsy EDS + cataplexy
Melatonin	Neurohormone	MT₁/MT₂ agonist	RBD, CSWRD, insomnia
Clonazepam	BZD	Non-selective GABA-A agonist	RBD, NREM parasomnias, PLMD
Prazosin	α₁ antagonist	Blocks noradrenergic hyperactivation	Nightmares (PTSD)
Gabapentin, Pregabalin	α₂δ ligand	Blocks presynaptic Ca²⁺ channels	RLS (first-line)
Pramipexole, Ropinirole	DA agonist	D₂/D₃ agonist	RLS (second-line, augmentation risk)
Tasimelteon	Melatonin agonist	MT₁/MT₂ agonist	Non-24h CSWRD

High Yield Summary — Management of Sleep Disorders

Insomnia first-line: CBT-I (sleep education, stimulus control, sleep restriction, relaxation, cognitive therapy). 1–8 sessions. Superior long-term outcomes to drugs. Address perpetuating factors of 3P model.
Insomnia pharmacotherapy: Only Z drugs (zolpidem, zopiclone) and Ramelteon recommended. Low-dose doxepin for maintenance insomnia. Short-term use only (2–4 weeks). BZDs are NOT first-line and carry dependence risk.
Z drugs: ω₁-selective GABA-A agonists → less sleep architecture disruption and shorter action than BZDs. Stilnox (shorter half-life, less hangover). Imovane (bitter taste).
Narcolepsy: Modafinil first-line for EDS. SSRI/SNRI for cataplexy (suppress REM via ↑ NA/5-HT in brainstem). Sodium oxybate for both (GABA-B agonist, consolidates sleep). Pitolisant (H₃ inverse agonist) is newer option.
OSA: CPAP first-line for moderate-severe. Weight loss in all. MAD if CPAP-intolerant. Surgery for selected cases.
RBD: Safe environment first. Melatonin (augments REM, first-line drug). Clonazepam (suppresses phasic muscle activity). Screen for synucleinopathies.
RLS: Iron repletion if ferritin < 75. α₂δ ligand (gabapentin/pregabalin) preferred over DA agonists (augmentation risk). Opioids/clonazepam if refractory.
DSWPD: Low-dose melatonin 1h before target bedtime + morning bright light + evening light restriction + gradual schedule advance.
Nightmares: Sleep hygiene + treat comorbid PTSD/depression + Image Rehearsal Therapy + prazosin (α₁ antagonist blocks noradrenergic hyperactivation).
Sleep paralysis: SSRI/SNRI/TCA to suppress REM + reassurance + address precipitants.

Active Recall - Management of Sleep Disorders

References

^[1] Lecture slides: GC 165. I can't fall asleep Sleep physiology and Sleep disorders.pdf ^[2] Senior notes: ryanho-psych.md (Chapter 9.2 Sleep Disorders) ^[6] Senior notes: ryanho-psych.md (Chapter 3.1.4 Non-benzodiazepine Anxiolytics and Hypnotics; Chapter 3.1.4.1 Benzodiazepines)

Complications of Sleep Disorders

1. Systemic Complications of Chronic Sleep Disruption

These complications are shared across insomnia, OSA, narcolepsy, shift work disorder, and any condition causing chronic sleep loss. They represent the downstream effects of sustained physiological stress from inadequate or fragmented sleep.

Complication	Pathophysiological Mechanism
Hypertension	Chronic sleep deprivation → ↑ sympathetic nervous (SN) activity ^[2] → sustained elevation of catecholamines → peripheral vasoconstriction → ↑ SVR → HTN. In OSA specifically: repetitive apnoeas cause cyclical hypoxia–reoxygenation → chemoreceptor sensitisation → persistent sympathetic overdrive that continues even during the daytime. OSA is the leading secondary cause of resistant HTN.
Coronary artery disease and MI	Chronic effect: associated with ↑ overall mortality ^[2]. Chronic sympathetic overdrive → endothelial dysfunction → ↑ inflammatory markers (CRP, IL-6, TNF-α) → accelerated atherosclerosis. Intermittent hypoxia (OSA) → oxidative stress → lipid peroxidation → foam cell formation in arterial walls. Sleep deprivation → ↑ evening cortisol → metabolic syndrome → further CVD risk.
Heart failure	OSA → chronic intermittent hypoxia + large negative intrathoracic pressure swings (Müller manoeuvre against closed glottis) → ↑ LV transmural pressure → ↑ afterload → LV hypertrophy → eventual failure. Also, sympathetic overdrive → direct myocardial toxicity over years.
Arrhythmias (especially AF)	OSA: each apnoeic episode causes vagal surge (hypoxia-mediated) → bradycardia → followed by sympathetic surge on arousal → tachycardia. This "autonomic seesaw" predisposes to atrial fibrillation, ventricular ectopy, and heart block. AF prevalence in severe OSA is ~5× that of the general population.
Stroke	Combination of HTN, atherosclerosis, AF (cardioembolic), and endothelial dysfunction. Partial sleep deprivation and short duration ( < 7h vs 7–8h) is associated with mental and physical health risk, especially cardiovascular ^[2]. Paradoxically, long duration ( > 9h) is also associated with health risks ^[2] — a U-shaped mortality curve.
↑ Heart rate variability	Increased heart rate variability ^[2] reflects autonomic dysregulation — loss of the normal circadian pattern of parasympathetic dominance during sleep.

The U-Shaped Curve of Sleep Duration and Mortality

Partial sleep deprivation and short duration ( < 7h vs 7–8h) is associated with mental and physical health risk, especially CVS. Long duration ( > 9h) is also associated with health risks. ^[2]

Why the U-shape? Short sleep → the mechanisms described above (sympathetic overdrive, inflammation, metabolic dysfunction). Long sleep → may be a marker of underlying illness (depression, chronic inflammation, obesity, undiagnosed sleep disorders like OSA that fragment sleep leading to compensatory oversleeping), rather than long sleep being directly harmful. Sleep < 5h/day during weekends is associated with 52% ↑ mortality compared to 7h/day. ^[2]

Complication	Pathophysiological Mechanism
Obesity	Chronic effect: associated with obesity ^[2]. Sleep deprivation → ↓ leptin (satiety hormone, produced by adipocytes during sleep) + ↑ ghrelin (hunger hormone, produced by stomach when awake) → net effect: ↑ appetite, particularly for calorie-dense carbohydrates. Also: fatigue → ↓ physical activity → ↓ energy expenditure. Sympathetic overdrive → cortisol excess → visceral fat deposition.
↓ Glucose tolerance / Type 2 Diabetes	Physiological: ↓ insulin response (→ ↓ glucose tolerance) ^[2]. Sleep deprivation → ↓ insulin sensitivity at the cellular level (mechanism: sympathetic activation → ↑ cortisol and catecholamines → counter-regulatory hormones oppose insulin action; also, direct ↓ pancreatic β-cell function). Even one week of sleep restriction (5–6 hours/night) in healthy adults shifts glucose tolerance to a pre-diabetic range. Risk of diabetes Type 2 ^[2]. OSA: intermittent hypoxia independently impairs insulin signalling.
Dyslipidaemia	Sleep deprivation → ↑ cortisol → ↑ hepatic VLDL production → ↑ triglycerides, ↓ HDL. Insulin resistance further exacerbates dyslipidaemia.
Metabolic syndrome	The convergence of obesity + HTN + dyslipidaemia + insulin resistance. OSA is now considered an independent component of metabolic syndrome — some authors call the combination "Syndrome Z" (metabolic syndrome + OSA).

Complication	Pathophysiological Mechanism
Cognitive impairment	Brain: cognitive impairment, memory lapses or loss ^[2]. Sleep (especially SWS and REM) is essential for memory consolidation — hippocampal replay during SWS transfers episodic memories from hippocampus to neocortex. REM consolidates procedural and emotional memories. Chronic disruption → ↓ working memory, ↓ attention, ↓ executive function.
Irritability and emotional dysregulation	Neuropsychiatric: ↑ amygdala activation → ↑ negative emotions ^[2]. Sleep deprivation weakens prefrontal cortical inhibition of the amygdala → unchecked emotional reactivity. The medial prefrontal cortex normally provides top-down regulation of limbic responses; this regulatory pathway is impaired by even one night of poor sleep.
Impaired moral judgement	Impaired moral judgement ^[2]. The prefrontal cortex (especially ventromedial PFC) mediates moral reasoning. Sleep loss → prefrontal hypofunction → ↓ empathy, ↓ social judgement, ↓ ethical decision-making.
Depression and anxiety	Sleep disorders may be a cause of psychological symptoms → contribute to onset of psychiatric disorders ^[2]. Insomnia is a robust risk factor for incident depression (RR ~2–3×). The bidirectional relationship: insomnia → HPA dysregulation + amygdala hyperactivation + serotonergic pathway disruption → depression; depression → circadian disruption + hyperarousal → insomnia. Treating insomnia reduces depression risk and improves treatment outcomes in existing depression.
Hallucinations	Hallucinations ^[2]. Severe sleep deprivation ( > 72h) can cause visual and auditory hallucinations — effectively, REM-like intrusion phenomena into wakefulness (the brain begins generating dream content while still awake). This is a recognised phenomenon in sleep-deprived military personnel and medical residents.
Symptoms similar to ADHD	Symptoms similar to ADHD ^[2]. Sleep-deprived children and adults show inattention, hyperactivity, impulsivity — mimicking ADHD. In children, sleep deprivation paradoxically causes hyperactivity rather than sleepiness (unlike adults). This has important clinical implications: always screen for sleep disorders before diagnosing ADHD in children.

Complication

Mechanism

Impaired immune system

Impaired immune system ^[2]. During SWS, the immune system is most active — pro-inflammatory cytokines (IL-1, TNF-α) are released, natural killer (NK) cell activity peaks, and adaptive immune responses are consolidated. Sleep deprivation → ↓ NK cell activity, ↓ antibody response to vaccination (e.g., influenza and hepatitis B vaccine responses are significantly blunted by sleep restriction), ↑ susceptibility to infection (sleeping < 6h → 4.2× risk of catching the common cold vs > 7h).

Chronic inflammation

Chronic sleep loss → sustained low-grade inflammation (↑ CRP, IL-6, TNF-α) → contributes to atherosclerosis, insulin resistance, and possibly carcinogenesis.

Complication	Mechanism
Growth suppression	Growth suppression ^[2]. Growth hormone (GH) is predominantly secreted during SWS (especially the first SWS episode of the night). Chronic sleep deprivation in children → ↓ GH → growth retardation.
↓ Core body temperature	Decreased temperature ^[2]. Sleep deprivation disrupts normal thermoregulation — the circadian temperature nadir becomes less pronounced, and overall core body temperature may be lower during the day.
Tremors, aches	Tremors, aches ^[2]. Prolonged wakefulness → neuromuscular fatigue → fine tremor, myalgia. Also related to ↑ sympathetic tone and ↑ cortisol effects on muscle.
Severe yawning	Severe yawning ^[2]. The exact mechanism of yawning is debated, but it is a universal marker of sleepiness — possibly serves to ↑ cerebral blood flow or ↑ arousal through stretching of pharyngeal muscles.

2. Complications Specific to Individual Sleep Disorders

Complication	Explanation
Perpetuation and chronicity	Chronic insomnia is notoriously persistent — lasts ≥1 year in 74%, ≥3 years in 46%, resolves in 54% but recurs in > 50% of those recovered within 4 years ^[2]. The perpetuating factors (3P model) become self-sustaining — maladaptive sleep behaviours and catastrophic cognitions about sleep become deeply ingrained habits. Exacerbation: often connected to medical, psychiatric, psychosocial stressors ^[2].
Development of psychiatric disorders	Chronic insomnia is an independent risk factor for: major depression (RR ~2.5), anxiety disorders (RR ~2), substance use disorders (self-medication with alcohol, OTC sedatives, benzodiazepines), and suicidal ideation. Insomnia may be a cause of psychological symptoms → contribute to onset of psychiatric disorders ^[2].
Substance dependence	Patients with chronic insomnia may self-medicate with alcohol (initial sedation, but ultimately worsens sleep), over-the-counter antihistamines, or escalate benzodiazepine use → dependence. The "cycle of worry" ^[2] drives patients to seek any solution, increasing vulnerability to substance misuse.
Functional impairment	Compromised daytime function: fatigue, malaise, ↓ concentration, ↓ work performance ^[2]. Chronic insomnia is associated with ↑ absenteeism, ↓ productivity (presenteeism), and ↑ healthcare utilisation — the economic burden is substantial.
↑ Cardiovascular mortality	Chronic insomnia with short objective sleep duration ( < 6h on PSG) is associated with ↑ all-cause mortality and ↑ CVS mortality — this "hyperarousal insomnia" phenotype carries the highest risk.

Complication	Mechanism
Resistant hypertension	OSA is the most common secondary cause. Cyclical hypoxia → chemoreceptor sensitisation → persistent sympathetic overdrive. ↑ aldosterone secretion also contributes (OSA is associated with ↑ aldosterone levels). Treating OSA with CPAP ↓ BP by ~2–3 mmHg in compliant patients.
Cor pulmonale	Chronic intermittent hypoxia → pulmonary vasoconstriction (hypoxic pulmonary vasoconstriction, same mechanism as in COPD) → pulmonary hypertension → right ventricular hypertrophy → right heart failure.
Polycythaemia	Chronic hypoxaemia → ↑ EPO secretion from kidney → ↑ red cell mass → ↑ blood viscosity → further ↑ risk of thrombosis and stroke.
Road traffic accidents (RTA)	Impact: RTA, work-related accidents, ↓ neuropsychological and motor function, ↓ QoL ^[2]. EDS from OSA → ↑ risk of drowsy driving. Untreated OSA patients have a 2–7× increased risk of RTA compared to the general population. This is one of the most important reasons to treat.
Neurocognitive decline	Chronic intermittent hypoxia → hippocampal and prefrontal cortical neuronal damage → progressive memory loss, executive dysfunction. OSA is now recognised as a modifiable risk factor for dementia.
Perioperative risk	Undiagnosed OSA ↑ risk during general anaesthesia — difficult intubation (obese, crowded airway), sensitivity to sedatives/opioids (further ↓ pharyngeal tone), post-operative respiratory complications. Always screen for OSA preoperatively.
Nocturia	Nocturia due to arousal and ↑ abdominal pressure ^[2]. During obstructive apnoeas, large negative intrathoracic pressure → ↑ venous return → atrial distension → ↑ ANP release → ↑ diuresis. Also, arousals → awareness of bladder fullness. Nocturia resolves with CPAP in many patients.

Complication	Mechanism
Accidents and injuries	Sleep attacks during driving, operating machinery, or cooking → RTA, burns, falls. Majority safe to drive but may need time limit ^[2].
Psychosocial impact	Narcolepsy is profoundly disabling — falling asleep at work/school, cataplexy causing embarrassment, sleep paralysis causing fear. Depression affects ~25–50% of narcolepsy patients. Social isolation, unemployment, and relationship difficulties are common.
Obesity	Orexin regulates metabolism in addition to wakefulness. Orexin deficiency → ↓ basal metabolic rate + ↓ physical activity from sleepiness → weight gain. BMI is on average higher in narcolepsy type 1 patients than age-matched controls.
Status cataplecticus	Prolonged or near-continuous cataplexy episodes, usually precipitated by abrupt withdrawal of anticataplectic medications (SSRIs, SNRIs, TCAs, sodium oxybate). REM-suppressing drugs should never be discontinued abruptly in narcolepsy — always taper.

Complication	Affected Condition	Mechanism
Physical injury (self or bed partner)	Sleepwalking, RBD, sleep terrors	NREM parasomnias: walking into furniture, falling down stairs, exiting through windows. RBD: dream enactment behaviour, usually short ( < 60s), appear purposeful (e.g., throwing a ball, vocalisation) ^[2] → punching, kicking, falling out of bed → ecchymoses, fractures, subdural haematomas (in elderly).
Neurodegenerative conversion	RBD	50% of RBD is associated with neurological conditions ^[2]. Idiopathic RBD has ~80–90% conversion to synucleinopathies (PD, DLB, MSA) over 10–15 years. The degeneration of pontine REM-atonia centres (sublaterodorsal nucleus) in RBD reflects early alpha-synuclein pathology that will eventually spread to the substantia nigra (PD) or cortex (DLB). This is the most important long-term complication of RBD.
Sleep-related injuries in children	NREM parasomnias (sleepwalking)	Children may walk out of the house, fall down stairs, or injure themselves on household objects. Environment modification is the priority.
Psychosocial distress	Nightmares, sleep paralysis	Nightmares: fear response, ↑ awareness, ↑ SN tone upon awakening with vivid recall of content ^[2]. Recurrent nightmares (especially PTSD-related) cause fear of going to sleep → avoidance behaviour → worsening insomnia → vicious cycle. Sleep paralysis with hypnagogic hallucinations can be profoundly terrifying and may be misinterpreted as supernatural experiences.
Obesity from SRED	Sleep-related eating disorder	May be associated with obesity and ingestion of inedible substances (e.g., cat food, frozen food) ^[2]. Unconscious high-calorie consumption during sleep → significant weight gain over time.

Complication	Mechanism
Chronic insomnia	RLS → inability to relax in bed → severe sleep-onset insomnia → chronic sleep deprivation with all its systemic sequelae.
Depression and anxiety	Chronic sleep disruption + distressing sensory symptoms → high rates of comorbid depression and anxiety. Other features: insomnia, depression, anxiety ^[2].
Augmentation (iatrogenic)	The most important complication of dopamine agonist treatment for RLS (covered in Management section). Paradoxical worsening with chronic DA agonist use → earlier onset, more severe, spread to arms.
Iron deficiency consequences	If secondary to iron deficiency: the underlying anaemia may have its own complications (fatigue, tachycardia, koilonychia, pica).

Complication	Mechanism
Academic and occupational failure	DSWPD in adolescents → ↓ sleep time when combined with early school or work start times ^[2] → chronic partial sleep deprivation → ↓ academic performance, ↓ concentration, absenteeism, school dropout. This is a major public health issue in Hong Kong's education system.
Metabolic syndrome	Shift work disorder → chronic circadian misalignment → eating during the biological night (when insulin sensitivity is lowest) → ↑ T2DM risk, ↑ obesity. Shift workers have ~20–40% increased risk of CVD events.
Mental health	Circadian disruption → serotonergic and dopaminergic rhythm disruption → ↑ depression, ↑ anxiety. Seasonal affective disorder is related to photoperiod (light exposure duration) changes affecting circadian function.
Cancer risk	The International Agency for Research on Cancer (IARC) classified shift work involving circadian disruption as a "probable carcinogen" (Group 2A). Mechanism: melatonin suppression → loss of melatonin's oncostatic properties (free radical scavenging, immune surveillance enhancement, anti-proliferative effects). Night shift workers have ↑ breast cancer risk.

Treatment	Complication	Mechanism
Benzodiazepines / Z drugs	Dependence, tolerance, rebound insomnia, falls (elderly), cognitive impairment, complex sleep behaviours (sleep-driving, sleep-eating with zolpidem), respiratory depression (especially in OSA — BZDs relax pharyngeal muscles → worsen apnoeas)	GABA-A receptor down-regulation with chronic use → tolerance → dose escalation → dependence. Sudden withdrawal → receptor hypoexcitability reversed → rebound hyperexcitability → insomnia worse than baseline, anxiety, potentially seizures.
Dopamine agonists (for RLS)	Augmentation (most important), impulse control disorders (pathological gambling, hypersexuality, compulsive shopping, binge eating)	Augmentation: D₂/D₃ receptor desensitisation. Impulse control: mesolimbic DA pathway overstimulation → reward circuit dysregulation.
CPAP	Non-adherence (the main "complication"), mask discomfort, nasal dryness/congestion, aerophagia (air swallowing → bloating), claustrophobia, skin breakdown at mask interface	Positive pressure → dries nasal mucosa; constant mask pressure → skin irritation; air entering oesophagus; psychological claustrophobia. Solutions: heated humidification, proper mask fitting, desensitisation therapy, alternative interfaces.
Sodium oxybate	CNS depression (especially if combined with alcohol or other sedatives), enuresis, nausea, abuse potential, respiratory depression	GABA-B agonism → potent CNS depression. Strictly regulated due to history of GHB abuse.
SSRIs/SNRIs (for cataplexy)	May precipitate or worsen RBD; status cataplecticus if abruptly withdrawn	Serotonergic modulation of pontine REM-atonia centres → paradoxically can reduce REM atonia in some patients. Abrupt withdrawal → rebound REM + rebound cataplexy.
Modafinil	Headache, nausea, anxiety, insomnia (if taken too late in the day), rare serious skin reactions (Stevens-Johnson syndrome — very rare)	Dopaminergic stimulation can cause anxiety/insomnia if dosing is not timed correctly (take in the morning). Rare hypersensitivity reactions.

Exam Pearl: The Vicious Cycles of Sleep Disorders

Sleep disorders create multiple self-reinforcing vicious cycles that explain their chronicity:

Insomnia vicious cycle: Poor sleep → daytime impairment → worry about sleep → hyperarousal → worse sleep → more worry (the "cycle of worry" ^[2])

OSA vicious cycle: OSA → sleep fragmentation → EDS → ↓ physical activity → weight gain → worsens OSA

Insomnia-Depression cycle: Insomnia → HPA dysregulation + serotonergic disruption → depression → worsens insomnia

RLS-Iron cycle: Low iron → low dopamine → RLS → poor sleep → ↓ dietary intake/↓ absorption → worsens iron deficiency

Medication dependence cycle: Insomnia → BZD use → tolerance → dose escalation → dependence → rebound insomnia on discontinuation → re-initiation

Breaking these vicious cycles is the therapeutic goal. CBT-I breaks the insomnia worry cycle. CPAP + weight loss breaks the OSA cycle. Iron repletion breaks the RLS-iron cycle. Gradual tapering with CBT-I support breaks the medication cycle.

Issue	Explanation
Academic underperformance in adolescents	DSWPD + early school start times (typically 08:00–08:30 in Hong Kong) → chronic partial sleep deprivation in a significant proportion of secondary school students → ↓ concentration, ↓ grades, ↓ wellbeing. Compounded by heavy homework load and screen use at night.
Occupational injuries in shift workers	Hong Kong's 24/7 service economy (healthcare, transport, hospitality, finance) has a large shift-working population → circadian disruption → ↑ accidents, ↑ metabolic disease.
Undiagnosed OSA	East Asian craniofacial anatomy predisposes to OSA at lower BMIs. Many Hong Kong patients with "lean OSA" go undiagnosed because the classic obese phenotype is not present. Late diagnosis → longer exposure to chronic intermittent hypoxia → ↑ CVD burden.
Benzodiazepine/Z drug overuse	Due to limited CBT-I availability in Hong Kong, hypnotics are over-prescribed → dependence, falls in elderly (significant cause of hip fractures in ageing Hong Kong population), cognitive impairment.

High Yield Summary — Complications of Sleep Disorders

Cardiovascular: HTN (especially resistant — OSA is top secondary cause), CAD, HF, AF, stroke. Mechanism: sympathetic overdrive, intermittent hypoxia, endothelial dysfunction, chronic inflammation.
Metabolic: Obesity (↓ leptin, ↑ ghrelin), T2DM (↓ insulin sensitivity), dyslipidaemia, metabolic syndrome ("Syndrome Z" when combined with OSA).
Neuropsychiatric: Cognitive impairment, ↑ amygdala activation (emotional dysregulation), depression (RR ~2.5×), anxiety, hallucinations (severe deprivation), ADHD-mimicking symptoms in children.
Immune: ↓ NK cell activity, ↓ vaccine response, ↑ susceptibility to infection.
OSA-specific: Cor pulmonale, polycythaemia, RTA (2–7×), perioperative risk, nocturia.
RBD-specific: Physical injury (self/partner) and 80–90% conversion to synucleinopathies (PD, DLB, MSA) over 10–15 years.
RLS-specific: Chronic insomnia, depression/anxiety, augmentation from DA agonists.
Iatrogenic: BZD/Z drug dependence and rebound insomnia, DA agonist augmentation and impulse control disorders, CPAP non-adherence, status cataplecticus from abrupt SSRI withdrawal.
Mortality: U-shaped curve — both short ( < 7h) and long ( > 9h) sleep associated with ↑ all-cause mortality. Short sleep + insomnia phenotype carries highest CVS mortality risk.
Vicious cycles: Sleep disorders are self-perpetuating through multiple reinforcing loops (worry cycle in insomnia, weight gain cycle in OSA, medication dependence cycle). Breaking these cycles is the therapeutic goal.

Active Recall - Complications of Sleep Disorders

References

^[1] Lecture slides: GC 165. I can't fall asleep Sleep physiology and Sleep disorders.pdf ^[2] Senior notes: ryanho-psych.md (Chapter 9.2 Sleep Disorders)

High Yield Summary

Sleep regulation: Two-process model — Process S (homeostatic, adenosine-driven) + Process C (circadian, SCN/melatonin-driven). Their interaction determines sleep timing.
Flip-flop switch: VLPO (GABA/galanin, sleep) ↔ ARAS (NA, 5-HT, histamine, ACh, DA, orexin, wake) — mutually inhibitory. Orexin stabilises the wake state. Loss of orexin → narcolepsy type 1.
Sleep architecture: NREM (N1 → N2 → N3) → REM in 90-min cycles. SWS predominates early (NREM parasomnias first half). REM predominates late (REM parasomnias second half).
3P model of insomnia: Predisposing (trait) + Precipitating (trigger) + Perpetuating (maladaptive behaviours/cognitions). Chronic insomnia is driven primarily by perpetuating factors.
Comorbid insomnia: "Secondary" insomnia concept abandoned → now "comorbid" because causality is bidirectional.
Narcolepsy type 1: Orexin deficiency → REM intrusion phenomena (cataplexy, sleep paralysis, hypnagogic hallucinations) + sleep instability. HLA-DQB1*0602 → autoimmune hypothesis.
RBD: Loss of REM atonia → dream enactment. Strongly associated with synucleinopathies (prodromal PD/DLB). M > F 9:1. Eyes closed (vs NREM open). Dream recall present.
Assessment: Sleep diary (2 weeks), ESS (≥10 = excessive sleepiness), MSLT (mean latency < 5 min = pathological; ≥2 SOREMPs = narcolepsy), PSG only if suspecting OSA/RBD/PLMD — NOT for routine insomnia.
CSWRD workup: Sleep diary + actigraphy + chronotype questionnaire + DLMO protocol.
Clinical pearl — insomnia type by presentation: Initial → anxiety/DSWPD/RLS; Middle → OSA/PLMD/pain; Terminal → depression/ASWPD.

High Yield Summary — Differential Diagnosis of Sleep Disorders

Insomnia DDx: Normal short sleepers (no impairment), situational insomnia ( < 3 months), DSWPD (normal sleep on own schedule), RLS (urge to move legs), OSA (snoring, apnoeas), narcolepsy (EDS dominant), depression (terminal insomnia), anxiety (initial insomnia), substance/medication effects.
EDS DDx: Insufficient sleep (most common), OSA, narcolepsy (refreshing naps, cataplexy), idiopathic hypersomnia (unrefreshing naps, sleep drunkenness), depression (fatigue > sleepiness), medications (antihistamines, BZDs).
Parasomnia DDx: NREM (first half, eyes open, no recall, children) vs REM (second half, eyes closed, dream recall, older males) vs nocturnal epilepsy (stereotyped, any time) vs nocturnal panic (NREM, fully alert, no dream content).
Key distinguishing concepts: Decreased need for sleep (mania) ≠ insomnia; sleepiness ≠ fatigue; DSWPD ≠ insomnia; ASWPD ≠ depression.
Comorbid approach: Insomnia can be diagnosed alongside psychiatric/medical conditions — causality is bidirectional.

High Yield Summary — Diagnosis and Investigation of Sleep Disorders

Insomnia Disorder DSM-5: Sleep complaint (initial/middle/terminal) + distress/impairment + ≥3 nights/week + ≥3 months + adequate sleep opportunity + not explained by other sleep disorder/substance/medical condition. Remember "3-3-3": 30 min, 3x/week, 3 months.
Insomnia is a CLINICAL diagnosis — PSG is NOT indicated for routine insomnia. Only order PSG when suspecting OSA, RBD, PLMD, or treatment-resistant cases.
PSG channels: EEG (sleep stages), EOG (eye movements), EMG (atonia/RSWA/PLMS), ECG, airflow, respiratory effort, SpO2, position, video. Know which channel answers which clinical question.
MSLT: Objective sleepiness test. Mean latency < 5 min = pathological sleepiness. ≥2 SOREMPs = narcolepsy. Must have preceding PSG + adequate prior sleep + withdrawal of REM-suppressants.
DLMO: Gold standard for circadian phase. Sample melatonin under dim light ( < 30 lux) every 30–60 min. Normal rise 90–120 min before habitual bedtime. Delayed rise = DSWPD.
Actigraphy: Wrist-worn accelerometer for rest-activity cycles over weeks. Best for CSWRD and as adjunct to sleep diary. Cannot stage sleep.
Key blood tests: Ferritin < 75 µg/L → iron repletion for RLS. CSF orexin-A ≤110 pg/mL → narcolepsy type 1. HLA-DQB1*0602: supportive not diagnostic (98% type 1, but 12–40% healthy).
OSA diagnosis: AHI ≥5 + symptoms or AHI ≥15 regardless. Mild 5–14, Moderate 15–29, Severe ≥30.
RBD diagnosis: History + video PSG showing RSWA + dream enactment. Always screen for synucleinopathies.
RLS diagnosis: Purely clinical (IRLSSG 5 criteria). Check ferritin. PSG only for PLMD documentation.

High Yield Summary — Management of Sleep Disorders

Insomnia first-line: CBT-I (sleep education, stimulus control, sleep restriction, relaxation, cognitive therapy). 1–8 sessions. Superior long-term outcomes to drugs. Address perpetuating factors of 3P model.
Insomnia pharmacotherapy: Only Z drugs (zolpidem, zopiclone) and Ramelteon recommended. Low-dose doxepin for maintenance insomnia. Short-term use only (2–4 weeks). BZDs are NOT first-line and carry dependence risk.
Z drugs: ω₁-selective GABA-A agonists → less sleep architecture disruption and shorter action than BZDs. Stilnox (shorter half-life, less hangover). Imovane (bitter taste).
Narcolepsy: Modafinil first-line for EDS. SSRI/SNRI for cataplexy (suppress REM via ↑ NA/5-HT in brainstem). Sodium oxybate for both (GABA-B agonist, consolidates sleep). Pitolisant (H₃ inverse agonist) is newer option.
OSA: CPAP first-line for moderate-severe. Weight loss in all. MAD if CPAP-intolerant. Surgery for selected cases.
RBD: Safe environment first. Melatonin (augments REM, first-line drug). Clonazepam (suppresses phasic muscle activity). Screen for synucleinopathies.
RLS: Iron repletion if ferritin < 75. α₂δ ligand (gabapentin/pregabalin) preferred over DA agonists (augmentation risk). Opioids/clonazepam if refractory.
DSWPD: Low-dose melatonin 1h before target bedtime + morning bright light + evening light restriction + gradual schedule advance.
Nightmares: Sleep hygiene + treat comorbid PTSD/depression + Image Rehearsal Therapy + prazosin (α₁ antagonist blocks noradrenergic hyperactivation).
Sleep paralysis: SSRI/SNRI/TCA to suppress REM + reassurance + address precipitants.

High Yield Summary — Complications of Sleep Disorders

Cardiovascular: HTN (especially resistant — OSA is top secondary cause), CAD, HF, AF, stroke. Mechanism: sympathetic overdrive, intermittent hypoxia, endothelial dysfunction, chronic inflammation.
Metabolic: Obesity (↓ leptin, ↑ ghrelin), T2DM (↓ insulin sensitivity), dyslipidaemia, metabolic syndrome ("Syndrome Z" when combined with OSA).
Neuropsychiatric: Cognitive impairment, ↑ amygdala activation (emotional dysregulation), depression (RR ~2.5×), anxiety, hallucinations (severe deprivation), ADHD-mimicking symptoms in children.
Immune: ↓ NK cell activity, ↓ vaccine response, ↑ susceptibility to infection.
OSA-specific: Cor pulmonale, polycythaemia, RTA (2–7×), perioperative risk, nocturia.
RBD-specific: Physical injury (self/partner) and 80–90% conversion to synucleinopathies (PD, DLB, MSA) over 10–15 years.
RLS-specific: Chronic insomnia, depression/anxiety, augmentation from DA agonists.
Iatrogenic: BZD/Z drug dependence and rebound insomnia, DA agonist augmentation and impulse control disorders, CPAP non-adherence, status cataplecticus from abrupt SSRI withdrawal.
Mortality: U-shaped curve — both short ( < 7h) and long ( > 9h) sleep associated with ↑ all-cause mortality. Short sleep + insomnia phenotype carries highest CVS mortality risk.
Vicious cycles: Sleep disorders are self-perpetuating through multiple reinforcing loops (worry cycle in insomnia, weight gain cycle in OSA, medication dependence cycle). Breaking these cycles is the therapeutic goal.

Sleep Disorders

1. Definition

2. Epidemiology

2.1 Insomnia

2.2 Narcolepsy

2.3 Obstructive Sleep Apnoea (OSA)

2.4 Restless Leg Syndrome (RLS)

2.5 REM Sleep Behaviour Disorder (RBD)

2.6 Parasomnias (NREM)

2.7 Circadian Rhythm Sleep–Wake Disorders

3. Sleep Physiology — Anatomy and Function

3.1 The Two-Process Model of Sleep Regulation

Process S — Homeostatic Sleep Drive ("Sleep Pressure")

Process C — Circadian Rhythm ("Body Clock")

3.2 Neuroanatomy of the Sleep–Wake Switch

Wake-Promoting Centres (Ascending Reticular Activating System, ARAS)

Sleep-Promoting Centre

The Flip-Flop Switch

3.3 Sleep Architecture — Stages and Cycles

NREM Stages (N1, N2, N3)

REM Sleep

Sleep Cycle

3.4 Sleep Requirements Across the Lifespan

3.5 Consequences of Sleep Deprivation

4. Aetiology (with Focus on Hong Kong Context) and Pathophysiology

4.1 The 3P Model of Insomnia (Spielman Model)

4.2 Paradigm Shift: Primary vs Secondary vs Comorbid Insomnia

4.3 Common Comorbid Conditions (Hong Kong Relevant)

4.4 Aetiologies by Sleep Disorder Category

4.4.1 Insomnia — Aetiology

4.4.2 Narcolepsy — Aetiology and Pathophysiology

4.4.3 Obstructive Sleep Apnoea (OSA) — Aetiology and Pathophysiology

4.4.4 Restless Leg Syndrome (RLS) / Willis-Ekbom Disease — Aetiology

4.4.5 Circadian Rhythm Sleep–Wake Disorders — Aetiology

4.4.6 Parasomnias — Aetiology

5. Classification

5.1 Overview of Classification Systems

5.2 Insomnia Classification (ICSD-3)

5.3 Parasomnia Classification

5.4 Comparison: REM vs NREM Parasomnias

5.5 Circadian Rhythm Sleep–Wake Disorders

6. Clinical Features — Symptoms and Signs (with Pathophysiological Basis)

6.1 Insomnia

6.2 Narcolepsy

6.3 Idiopathic Hypersomnia

6.4 Obstructive Sleep Apnoea (OSA)

6.5 Restless Leg Syndrome (RLS) / Willis-Ekbom Disease

6.6 NREM Parasomnias

Sleepwalking (Somnambulism) [2]

Sleep Terrors [2]

Confusional Arousals

6.7 REM Parasomnias

Nightmare Disorder

REM Sleep Behaviour Disorder (RBD) [2]

6.8 Circadian Rhythm Sleep–Wake Disorders

6.9 Assessment of Sleepiness

7. Evaluation of Sleep Disorders

7.1 Sleep History and Diary

7.2 Screening Tools

7.3 Physical Examination

7.4 Special Investigations

Active Recall - Sleep Disorders (Definition to Clinical Features)

References

The Conceptual Approach

Differential Diagnosis of Insomnia

Psychiatric Differentials of Insomnia

Medical Differentials of Insomnia

Substance/Medication Differentials

Differential Diagnosis of Excessive Daytime Sleepiness (EDS)

Differential Diagnosis of Parasomnias and Abnormal Nocturnal Behaviours

Differential Diagnosis of Circadian Rhythm Complaints

A Systematic Approach to Sleep Disorder Differentials

Active Recall - Differential Diagnosis of Sleep Disorders

Guiding Principle

1. Diagnostic Criteria by Condition

1.1 Insomnia Disorder — DSM-5 Criteria

1.2 Narcolepsy — Diagnostic Criteria (ICSD-3 / DSM-5)

1.3 Obstructive Sleep Apnoea — Diagnostic Criteria

1.4 Restless Leg Syndrome — IRLSSG Diagnostic Criteria

1.5 REM Sleep Behaviour Disorder — ICSD-3 Criteria