ABOHNS Sleep Medicine cheat sheet

NREM stage N1 occupies ~5% of sleep; N2 ~45-55%; N3 (slow-wave) ~15-25%; REM ~20-25% in healthy adults.

Sleep cycles last ~90 minutes; slow-wave sleep predominates in the first third of the night and REM in the last third.

Wake-promoting arousal system: orexin/hypocretin neurons in the lateral hypothalamus plus cholinergic, noradrenergic, serotonergic, histaminergic, and dopaminergic projections.

Sleep-promoting pathways: ventrolateral preoptic nucleus (GABA/galanin) and the thalamocortical circuit generating sleep spindles and slow waves.

Two-process model: homeostatic Process S (adenosine accumulation) and circadian Process C (suprachiasmatic nucleus pacemaker) jointly gate sleep propensity.

Circadian rhythm is entrained by light via the retinohypothalamic tract; melatonin secretion from the pineal begins ~2 hours before habitual sleep onset (dim-light melatonin onset).

REM sleep is characterized by low-voltage mixed-frequency EEG, episodic rapid eye movements, muscle atonia (loss of chin EMG tone), and irregular respiration and heart rate.

K-complexes and sleep spindles define N2; spindles arise from thalamocortical 11-14 Hz oscillations.

Normal sleep efficiency is typically >=85%; sleep-onset latency <=30 minutes and wake after sleep onset <=30 minutes are common normative thresholds.

Polysomnography channels: EEG (frontal, central, occipital), EOG, chin EMG, ECG, airflow (thermistor and nasal pressure), respiratory effort (thoracic/abdominal belts), pulse oximetry, body position, and limb EMG.

Apnea = >=90% drop in airflow for >=10 seconds; hypopnea = >=30% airflow reduction with >=3% desaturation or an arousal (AASM scoring rules).

AHI = apneas plus hypopneas per hour of sleep; obstructive apnea is scored when respiratory effort persists, central when effort is absent.

Oximetry-only or single-channel home testing cannot reliably distinguish obstructive from central events or quantify arousals.

Home sleep apnea testing (HSAT) is appropriate for adults with high pretest probability of moderate-to-severe OSA without significant cardiopulmonary comorbidity; a negative result warrants in-lab PSG.

Multiple sleep latency test (MSLT): mean sleep latency <=8 minutes plus >=2 sleep-onset REM periods supports narcolepsy; performed after overnight PSG.

Maintenance of wakefulness test (MWT) measures ability to stay awake; used to assess treatment response and fitness for duty rather than to diagnose narcolepsy.

Actigraphy estimates sleep-wake patterns from wrist movement over days to weeks; useful for circadian rhythm disorders and insomnia patterns but not for apnea scoring.

Pulse oximetry alone is insufficient to diagnose OSA; oxygen desaturation index (ODI) is a screening metric, not equivalent to AHI.

OSA severity by AHI: mild 5-14.9, moderate 15-29.9, severe >=30 events/hour.

Key risk factors: obesity (especially increased neck circumference), male sex, age, retrognathia, large tonsils, nasal obstruction, alcohol/sedatives, and menopause.

STOP-BANG (snoring, tiredness, observed apnea, pressure, BMI, age, neck circumference, gender) scores >=3 indicate elevated OSA risk.

Untreated OSA is associated with hypertension, atrial fibrillation, stroke, insulin resistance, and increased motor vehicle crash risk.

First-line therapy for moderate-to-severe OSA is positive airway pressure (CPAP); adherence is often defined as >=4 hours/night on >=70% of nights.

Oral appliances (mandibular advancement devices) are reasonable for mild-to-moderate OSA or CPAP-intolerant patients with adequate dentition.

Positional therapy benefits patients whose events predominate in the supine position.

Weight loss, including bariatric surgery, can meaningfully reduce AHI; hypoglossal nerve stimulation is an option for selected CPAP-intolerant patients.

OSA should be considered in patients with resistant hypertension, unexplained daytime sleepiness, nocturia, or difficult-to-control atrial fibrillation.

Pediatric OSA is most often caused by adenotonsillar hypertrophy and craniofacial factors, not obesity alone, though obesity is an increasing contributor.

Pediatric AHI thresholds differ from adults: AHI 1-4.9 mild, 5-9.9 moderate, >=10 severe; an obstructive apnea index >=1 may be abnormal.

Adenotonsillectomy is first-line surgical therapy for pediatric OSA with adenotonsillar hypertrophy; residual disease occurs in a substantial minority.

Symptoms include snoring, witnessed apneas, mouth breathing, restless sleep, enuresis, and daytime behavioral or attention problems.

Untreated pediatric OSA is linked to growth failure, pulmonary hypertension, and neurobehavioral deficits.

PSG is the reference standard for pediatric diagnosis; home testing is less validated in children.

The Pediatric Sleep Questionnaire and OSA-18 are validated screening and quality-of-life instruments.

Craniofacial syndromes (e.g., Down syndrome, Pierre Robin sequence) carry elevated OSA risk and may require additional airway evaluation.

Weight management and treatment of allergic rhinitis are adjuncts in obese or atopic children.

Central apnea = absent airflow with absent respiratory effort for >=10 seconds; central AHI >=5 defines central sleep apnea.

Cheyne-Stokes respiration is a crescendo-decrescendo breathing pattern with central apneas, classically in heart failure with reduced ejection fraction.

Treatment-emergent central sleep apnea can appear when CPAP is started for OSA and often resolves; persistent cases need alternative therapy.

Obesity hypoventilation syndrome: BMI >=30, daytime PaCO2 >=45 mmHg, and sleep-disordered breathing without another cause.

Hypoventilation is scored when PaCO2 rises >55 mmHg for >=10 minutes or >10 mmHg above awake supine value with desaturation.

Adaptive servo-ventilation is used for central sleep apnea and Cheyne-Stokes respiration; it is contraindicated in symptomatic heart failure with LVEF <=45%.

Congenital central hypoventilation syndrome is linked to PHOX2B mutations and requires lifelong ventilatory support.

Neuromuscular and chest wall disorders cause nocturnal hypoventilation; noninvasive positive pressure ventilation is a mainstay.

Opioid-induced central apnea and ataxic breathing respond to reducing opioids and to positive pressure or oxygen therapy.

Insomnia disorder requires difficulty initiating or maintaining sleep with daytime consequences despite adequate opportunity, >=3 nights/week for >=3 months.

Cognitive behavioral therapy for insomnia (CBT-I) is first-line; components include sleep restriction, stimulus control, cognitive restructuring, and relaxation.

Sleep restriction therapy builds sleep pressure by limiting time in bed to average total sleep time, then extending gradually.

Stimulus control: use the bed only for sleep and intimacy, leave bed if awake >20 minutes, and maintain a fixed wake time.

Hypnotics have limited roles; benzodiazepines and Z-drugs carry tolerance and fall risk, and sedating antidepressants are used off-label.

Delayed sleep-wake phase disorder is treated with morning bright light and timed low-dose melatonin in the evening.

Advanced sleep-wake phase disorder is treated with evening bright light exposure.

Shift work disorder management includes strategic napping, planned caffeine use, and timed light exposure; melatonin may aid adaptation.

Non-24-hour sleep-wake rhythm disorder occurs most often in blind individuals and is treated with timed melatonin.

Narcolepsy type 1: cataplexy plus CSF hypocretin-1 <=110 pg/mL or MSLT criteria; it reflects orexin neuron loss.

Narcolepsy type 2 lacks cataplexy and hypocretin deficiency; MSLT shows mean sleep latency <=8 minutes with >=2 SOREMPs.

Cataplexy is sudden loss of muscle tone triggered by emotion, typically without loss of consciousness.

Other narcolepsy features: sleep paralysis, hypnagogic/hypnopompic hallucinations, and fragmented nocturnal sleep.

Kleine-Levin syndrome: recurrent episodes of hypersomnia with cognitive changes and hyperphagia.

Idiopathic hypersomnia: excessive daytime sleepiness with long unrefreshing naps and no SOREMPs on MSLT.

Wake-promoting agents include modafinil, armodafinil, pitolisant, and solriamfetol; sodium oxybate treats cataplexy and sleepiness in narcolepsy.

MSLT should follow adequate sleep (>=7 hours/night) and a drug-free interval to avoid false positives.

Distinguishing sleep insufficiency and circadian misalignment from central hypersomnia requires sleep logs or actigraphy before MSLT.

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

REM sleep behavior disorder features dream enactment with loss of REM atonia, usually later in the night, and can precede synucleinopathies.

REM sleep behavior disorder is treated with melatonin or clonazepam and requires safety measures to prevent injury.

Restless legs syndrome: urge to move the legs, worse at rest and in the evening, relieved by movement; associated with iron deficiency.

Periodic limb movements in sleep are scored when movements last 0.5-10 seconds and occur in sequences of >=4.

Sleep-related bruxism has a central origin and is not simply a malocclusion problem; it can cause dental wear and jaw pain.

Sleep enuresis, sleep-related eating disorder, and exploding head syndrome are other recognized parasomnias.

Ferritin testing and iron repletion are relevant in RLS; dopamine agonists and alpha-2-delta ligands are treatment options.

Video-polysomnography helps distinguish parasomnias from nocturnal seizures, especially when events are stereotyped or occur at sleep onset.

Major depression is associated with reduced REM latency, increased REM density, and reduced slow-wave sleep.

Insomnia is a risk factor for incident depression and relapse; treating insomnia can improve mood outcomes.

Bipolar disorder can present with decreased need for sleep during mania and hypersomnia during depression; sleep deprivation can trigger mania.

Post-traumatic stress disorder features nightmares and hyperarousal; imagery rehearsal therapy and prazosin are used for nightmares.

Chronic pain and fibromyalgia are associated with fragmented sleep and nonrestorative sleep complaints.

Heart failure, atrial fibrillation, and resistant hypertension are linked to OSA; treatment of OSA may improve cardiovascular outcomes.

Nocturnal asthma and COPD worsen at night due to circadian airway changes and supine position.

Gastroesophageal reflux worsens in the supine position and can mimic or exacerbate nocturnal airway symptoms.

Substance use (alcohol, opioids, stimulants) disrupts sleep architecture and can induce sleep-disordered breathing.

CPAP remains the most effective therapy for OSA; humidification and mask fitting improve adherence.

Mandibular advancement devices are best for mild-to-moderate OSA and CPAP-intolerant patients; they can cause temporomandibular symptoms.

Uvulopalatopharyngoplasty reduces AHI variably and is less predictable than CPAP; patient selection matters.

Maxillomandibular advancement is among the most effective surgical options for OSA in selected patients.

Hypoglossal nerve stimulation requires favorable anatomy and CPAP intolerance; it is not appropriate for all OSA phenotypes.

Tracheostomy is a definitive but last-resort option for severe OSA or upper airway obstruction.

Weight loss, including bariatric surgery, is a key adjunct in obese OSA patients.

Positional therapy and nasal surgery address specific anatomic contributors but rarely cure OSA alone.

Combination therapy (e.g., surgery plus PAP or oral appliance) is used when single-modality treatment is inadequate.

Upper airway collapsibility depends on pharyngeal anatomy, mandibular position, tongue base, and soft palate; the velopharynx is a common collapse site.

Mallampati score, tonsil size, neck circumference, and craniofacial features help assess OSA risk.

Drug-induced sleep endoscopy can identify levels of obstruction to guide surgical planning.

Preoperative OSA screening with STOP-BANG and communication with anesthesia can reduce perioperative complications.

Perioperative risks in OSA include difficult airway, opioid sensitivity, and postoperative respiratory depression.

Postoperative monitoring and multimodal analgesia sparing opioids improve safety in OSA patients.

Adenotonsillectomy is the most common pediatric OSA surgery; postoperative respiratory complications are higher in severe OSA and young children.

Practice management includes documenting AHI severity, adherence to PAP, and objective testing to support medical necessity.

Nasal obstruction from septal deviation or turbinate hypertrophy can impair PAP tolerance and should be evaluated.

Sleep center accreditation standards address facility, staffing, equipment, and quality assurance.

Documentation for PAP therapy typically requires a qualifying sleep test and evidence of adherence for continued coverage.

Adherence for insurance purposes is often >=4 hours/night on >=70% of nights over a 30-day period.

Home sleep apnea testing requires appropriate patient selection and follow-up pathways for negative or inconclusive results.

Sleep study scoring should follow AASM rules and be performed by qualified technologists.

Quality metrics include test turnaround time, PAP adherence rates, and patient follow-up completion.

Telehealth and remote PAP data monitoring can improve access and adherence tracking.

Infection control and equipment sanitation are required for reusable sleep testing devices.

Multidisciplinary collaboration among otolaryngology, pulmonology, neurology, and dentistry supports comprehensive sleep care.

The pharynx has three levels: retropalatal (velopharyngeal), retroglossal, and epiglottic; obstruction may occur at one or multiple levels.

Friedman tongue position and tonsil size predict surgical outcomes and OSA severity.

Adenotonsillar hypertrophy is the dominant cause of pediatric OSA; tonsil size grading informs surgical decisions.

Nasal valve collapse and septal deviation increase upstream resistance and can worsen snoring and PAP intolerance.

Drug-induced sleep endoscopy uses sedation to simulate sleep and map obstruction patterns.

Perioperative OSA risk is increased by opioids, sedatives, and supine positioning; anesthesia planning should account for airway difficulty.

Postoperative monitoring is especially important after airway surgery in patients with severe OSA.

Craniofacial abnormalities such as retrognathia and micrognathia increase OSA risk and affect surgical planning.

A team approach with anesthesia and sleep medicine improves perioperative safety in OSA patients.

A comprehensive sleep history includes sleep schedule, symptoms, medications, alcohol/caffeine use, and bed partner observations.

Sleep diaries and actigraphy help characterize circadian patterns and insomnia before advanced testing.

PSG is required for suspected narcolepsy, parasomnias, and some pediatric cases; HSAT is not equivalent for these indications.

MSLT interpretation requires adequate prior sleep and attention to medication effects.

Oximetry and home testing have limited negative predictive value; a negative HSAT in a high-risk patient should prompt PSG.

Objective adherence data from PAP devices support clinical and insurance decision-making.

Standardized questionnaires (Epworth Sleepiness Scale, STOP-BANG, Insomnia Severity Index) support screening and monitoring.

Accreditation, documentation, and quality assurance are core components of a sleep practice.

Referral pathways should match the suspected disorder to the appropriate specialist and testing modality.