ABPN Sleep Medicine cheat sheet

NREM stages: N1 (theta, vertex waves, slow eye movements), N2 (sleep spindles, K-complexes), N3 (delta ≥20% of epoch, slow-wave sleep).

REM: low-voltage mixed-frequency EEG, sawtooth waves, rapid eye movements, lowest EMG tone; phasic vs tonic REM distinguished by eye movements and muscle twitches.

Sleep onset normally follows a descending progression N1→N2→N3 then ascends to REM; first REM period typically 70–120 minutes after sleep onset.

Normal adult sleep architecture: N1 ~5%, N2 ~45–55%, N3 ~13–23%, REM ~20–25%; REM cycles recur approximately every 90 minutes.

Two-process model: homeostatic Process S (sleep pressure, adenosine-mediated) interacts with circadian Process C (suprachiasmatic nucleus pacemaker).

The SCN entrains via light input through the retinohypothalamic tract; melanopsin-containing retinal ganglion cells mediate non-image-forming photic entrainment.

Melatonin secretion from the pineal gland is suppressed by light and rises in dim light before habitual sleep; it acts as a chronobiotic, not a strong hypnotic.

Sleep-wake flip-flop: VLPO (GABAergic) and median preoptic neurons promote sleep; orexin/hypocretin neurons in the lateral hypothalamus stabilize wakefulness and prevent state instability.

Ontogeny: newborns have polyphasic sleep with ~50% REM; circadian rhythmicity emerges around 2–3 months; N3 peaks in early childhood and declines across adolescence.

PSG scoring: AASM rules use 30-second epochs; sleep onset is the first epoch of any sleep stage; wake after sleep onset (WASO) plus sleep latency plus total sleep time equals time in bed.

Apnea: ≥90% reduction in airflow for ≥10 seconds; hypopnea: ≥30% reduction with ≥3% desaturation or an arousal (AASM recommended rule).

AHI = apneas plus hypopneas per hour of sleep; ODI = desaturations ≥3% per hour; RERA = increasing respiratory effort leading to arousal without meeting apnea/hypopnea criteria.

PLM index = periodic limb movements per hour; a PLM is ≥0.5 s duration, 5–90 s apart, in series of ≥4; PLMS index ≥15 in adults is considered elevated.

MSLT: 4–5 naps at 2-hour intervals after overnight PSG; mean sleep latency ≤8 min is abnormal; ≥2 SOREMPs supports narcolepsy (1 SOREMP on preceding PSG also counts).

MWT: 4 trials of 40 minutes at 2-hour intervals; mean sleep latency ≤8 min indicates excessive sleepiness; used for safety/occupational assessments.

Actigraphy: wrist accelerometry estimating rest-activity patterns over ≥1–2 weeks; useful for circadian rhythm disorders, insomnia patterns, and total sleep time estimation.

Questionnaires: Epworth Sleepiness Scale (0–24; >10 excessive), STOP-BANG for OSA risk, Insomnia Severity Index, Pittsburgh Sleep Quality Index.

Home sleep apnea testing is appropriate for high pretest probability of moderate-severe OSA without significant cardiopulmonary or neurologic comorbidity; it is not used for central apnea or hypoventilation diagnosis.

DSM-5/ICSD-3 criteria: difficulty initiating or maintaining sleep ≥3 nights/week for ≥3 months with daytime impairment despite adequate opportunity for sleep.

CBT-I is first-line: sleep restriction, stimulus control, cognitive restructuring, sleep hygiene, and relaxation; effect sizes exceed hypnotics and benefits persist after treatment.

Sleep restriction therapy limits time in bed to average total sleep time (not <5–5.5 h), then extends by ~15–30 min weekly as sleep efficiency exceeds 85–90%.

Stimulus control: bed only for sleep and intimacy, leave bed if awake >20 minutes, fixed wake time regardless of sleep duration.

Benzodiazepine receptor agonists (zolpidem, eszopiclone, zaleplon) shorten sleep latency; risks include tolerance, complex sleep behaviors, and falls in older adults.

DORAs (suvorexant, lemborexant, daridorexant) antagonize orexin receptors; useful for sleep maintenance; avoid in narcolepsy.

Low-dose doxepin (3–6 mg) is FDA-approved for sleep maintenance; sedating antidepressants at higher doses risk anticholinergic and cardiac effects.

Melatonin receptor agonist ramelteon is indicated for sleep-onset insomnia; melatonin is best used for circadian phase shifting rather than primary insomnia.

Beers criteria: avoid benzodiazepines and Z-drugs in older adults due to falls, fractures, and cognitive impairment; CBT-I remains preferred.

OSA diagnosis: AHI ≥5 with symptoms, or AHI ≥15 regardless of symptoms; severity: mild 5–15, moderate 15–30, severe >30.

OSA pathophysiology: pharyngeal collapsibility, reduced compensatory muscle tone, loop gain instability, and low arousal threshold; obesity is the strongest risk factor.

Central sleep apnea: absent airflow and effort; Cheyne-Stokes respiration in heart failure has crescendo-decrescendo pattern with central events and prolonged circulation time.

Treatment-emergent central apnea: central events emerge when obstructive events are eliminated by PAP; often resolves with continued therapy.

Obesity hypoventilation syndrome: BMI ≥30, daytime PaCO2 ≥45 mmHg, and sleep-disordered breathing without other hypoventilation cause; PAP with volume assurance or NIV may be needed.

PAP titration: CPAP is first-line; BPAP used for intolerance or pressure needs >15 cm H2O; ASV is contraindicated in heart failure with LVEF ≤45% and predominant central apnea.

Alternatives to PAP: mandibular advancement device for mild-moderate OSA, hypoglossal nerve stimulation for CPAP-intolerant selected patients, positional therapy, and weight loss.

Congenital central hypoventilation syndrome: PHOX2B mutation, alveolar hypoventilation in sleep, impaired chemosensitivity; may require diaphragm pacing.

Pediatric OSA: adenotonsillar hypertrophy is the most common cause; adenotonsillectomy is first-line; AHI ≥10 or oxygen nadir <90% often triggers surgery.

Narcolepsy type 1: excessive daytime sleepiness plus cataplexy and/or CSF orexin-A ≤110 pg/mL; type 2 lacks cataplexy and orexin deficiency.

MSLT criteria for narcolepsy: mean sleep latency ≤8 min with ≥2 SOREMPs (one may be the preceding PSG REM latency ≤15 min).

Cataplexy is sudden bilateral loss of muscle tone triggered by emotion, preserved consciousness; treat with sodium oxybate, pitolisant, or antidepressants.

Narcolepsy treatments: modafinil/armodafinil, methylphenidate, pitolisant, solriamfetol for sleepiness; sodium oxybate for cataplexy and sleepiness.

Idiopathic hypersomnia: sleepiness with long unrefreshing naps, prolonged sleep (>10 h/24 h), no cataplexy, and ≤1 SOREMP on MSLT; orexin normal.

Kleine-Levin syndrome: recurrent episodes of hypersomnia with cognitive/perceptual disturbances and hyperphagia or hypersexuality, typically in adolescent males, with normal function between episodes.

Distinguish insufficient sleep syndrome by history and actigraphy showing short habitual sleep with resolution of sleepiness after sleep extension.

CSF orexin testing is indicated when narcolepsy is suspected with ambiguous MSLT or to confirm type 1; low orexin is highly specific.

Secondary causes of hypersomnia to exclude: sleep apnea, depression, hypothyroidism, medication effects, and substance use.

Delayed sleep-wake phase disorder: sleep onset and offset delayed ≥2 h beyond conventional times; common in adolescents; treat with morning bright light and evening low-dose melatonin.

Advanced sleep-wake phase disorder: early sleep onset and awakening, often familial (PER2, CSNK1D mutations), more common in older adults; treat with evening bright light.

Shift work disorder: insomnia and/or excessive sleepiness temporally linked to work schedule; management includes scheduled naps, strategic caffeine, and planned light exposure.

Jet lag disorder: transient misalignment after transmeridian travel; eastward travel advances require phase advance, westward travel delays; melatonin at destination bedtime aids adaptation.

Non-24-hour sleep-wake rhythm disorder: free-running rhythm, especially in totally blind individuals lacking photic entrainment; melatonin or tasimelteon can entrain.

Irregular sleep-wake rhythm: fragmented sleep without a clear circadian pattern, common in dementia and institutionalized patients; structured activity and light exposure help.

Actigraphy plus sleep logs over ≥2 weeks is the standard tool for diagnosing circadian phase disorders.

Chronotherapy for delayed phase: progressive phase delay of sleep times until desired schedule is reached; must be paired with light hygiene to prevent relapse.

Light is the strongest zeitgeber; exposure timing relative to the circadian phase determines whether it advances or delays the clock.

NREM parasomnias (confusional arousals, sleepwalking, sleep terrors) arise from N3 slow-wave sleep, often in the first third of the night with amnesia and partial recall.

REM sleep behavior disorder: dream enactment with loss of REM atonia; PSG shows REM without atonia; strongly associated with synucleinopathies (Parkinson disease, Lewy body dementia, MSA).

RBD management: melatonin or clonazepam first-line; bed safety measures; SSRI/SNRI and other serotonergic drugs can unmask or worsen RBD.

Sleep terrors: abrupt arousal with autonomic surge, inconsolable crying, no recall; typically in children, resolves with age.

Nightmare disorder: REM-related, full awakening with recall of frightening dream content; imagery rehearsal therapy and prazosin are evidence-based treatments.

Sleep enuresis is a NREM parasomnia in children; alarm therapy and desmopressin are first-line when treatment is indicated.

Sleep-related eating disorder can be associated with zolpidem and other sedative-hypnotics; consider medication effect in new-onset cases.

Parasomnia vs seizure: nocturnal frontal lobe epilepsy has stereotyped, brief events with dystonic posturing; PSG with extended EEG helps differentiate.

NREM parasomnias can be triggered by sleep deprivation, febrile illness, and obstructive sleep apnea; treating OSA may reduce events.

Restless legs syndrome: urge to move legs, worse at rest and in the evening, relieved by movement; diagnosis is clinical (ICSD-3/IRLSSG criteria).

RLS is associated with iron deficiency; check ferritin; consider iron supplementation when ferritin <75–100 ng/mL (with transferrin saturation assessment).

First-line RLS pharmacotherapy: alpha-2-delta ligands (gabapentin enacarbil, pregabalin) and dopamine agonists; augmentation is a major risk of dopamine agonists.

Augmentation: earlier onset, increased intensity, and spread of RLS symptoms with dopaminergic therapy; manage by reducing or switching agents.

Periodic limb movements of sleep: rhythmic extension of the big toe and dorsiflexion of the ankle, 5–90 s apart, in series; PLMS index ≥15 is elevated in adults.

PLMS are common in RLS, but PLMS alone without symptoms does not require treatment.

Bruxism: sleep-related tooth grinding; PSG shows masseter EMG bursts; associated with SSRIs and OSA; manage with oral appliance or biofeedback.

RLS differential includes peripheral neuropathy, akathisia, nocturnal leg cramps, and medication-induced restlessness; hypoglycemia and venous insufficiency can mimic symptoms.

Dopamine agonists in RLS: risk of impulse control disorders and augmentation; use lowest effective dose and monitor.

Depression: reduced REM latency, increased REM density, and decreased slow-wave sleep; insomnia is a risk factor for incident depression.

OSA is associated with hypertension, atrial fibrillation, stroke, and treatment-resistant hypertension; PAP may improve blood pressure modestly.

COPD: nocturnal hypoxemia from hypoventilation and V/Q mismatch; avoid supplemental oxygen alone that can worsen hypercapnia without ventilatory support.

Neurodegenerative disease: RBD precedes Parkinson disease; Alzheimer disease shows sleep fragmentation and sundowning; OSA may accelerate cognitive decline.

Epilepsy: sleep deprivation lowers seizure threshold; nocturnal seizures and interictal discharges can fragment sleep; some AEDs (barbiturates, benzodiazepines) cause sedation.

Medication effects: corticosteroids and stimulants cause insomnia; opioids and benzodiazepines can worsen central apnea; beta-blockers may cause nightmares.

Stroke: OSA is common and associated with worse outcomes; post-stroke sleep architecture shows reduced REM and increased wake.

Chronic pain and fibromyalgia show alpha-delta sleep and sleep fragmentation; treating the underlying pain and insomnia improves quality of life.

Thyroid disease: hypothyroidism causes hypersomnia; hyperthyroidism causes insomnia; both can be associated with sleep-disordered breathing.

Pediatric sleep architecture: REM proportion is high in infancy and declines with age; N3 is prominent in school-age children.

Pediatric OSA: adenotonsillar hypertrophy is the most common cause; AHI ≥10 or nadir SpO2 <90% often prompts adenotonsillectomy.

Infant sleep: circadian rhythm emerges around 2–3 months; safe sleep practices (supine, firm surface, no soft bedding) reduce SIDS risk.

Adolescent delayed sleep phase is common; school start times later than 8:30 a.m. are associated with improved sleep duration and academic outcomes.

Pregnancy: OSA and RLS increase; supine sleep in late pregnancy is associated with stillbirth risk; PAP may be used for OSA.

Older adults: reduced slow-wave sleep and increased awakenings; melatonin secretion decreases; advanced phase is common; screen for OSA and RLS.

Pediatric MSLT: normal mean sleep latency is longer than in adults; a mean sleep latency ≤8 min with ≥2 SOREMPs supports narcolepsy.

Neonatal sleep: active (REM-like) sleep predominates; sleep-wake cycling is not yet circadian; feeding and light cues help entrain.

Behavioral insomnia of childhood: sleep-onset association and limit-setting subtypes; extinction and graduated extinction are first-line.