Diagnostic
Precision
Not Wellness
Fluff.
A rigorous repository of AASM scoring protocols, ICSD-3 diagnostic criteria, and localized clinical calculators for sleep medicine professionals and researchers.
Core Modalities
Diagnostic HardwarePolysomnography
The gold standard Level I sleep study. Full 10-20 EEG montage, EOG, submental EMG, ECG, respiratory effort, airflow, and oximetry.
View Montages →Home Sleep Apnea Test
Level III/IV studies. Type 3 devices measuring minimum 4 channels. Limitations in detecting arousal-based hypopneas (RERAs).
Clinical Limits →Multiple Sleep Latency
Objective measure of daytime sleepiness. 5-nap protocol following overnight PSG. Crucial for Narcolepsy and IH diagnosis.
View Protocol →Beyond the AHI:
OSA Phenotyping
The Apnea-Hypopnea Index (AHI) is an incomplete metric. Modern sleep medicine targets specific pathophysiological traits responsible for Obstructive Sleep Apnea using the PALM scale.
- P: Pharyngeal Critical Closing Pressure (Pcrit)
- A: Arousal Threshold (High vs Low)
- L: Loop Gain (Ventilatory Instability)
- M: Muscle Responsiveness (Genioglossus)
Clinical Calculators
Standardized scoring tools running entirely client-side. Zero data retention.
Pharmacokinetics Table
Half-life data derived from FDA prescribing information. Note the reduced next-morning grogginess potential in compounds with shorter terminal half-lives.
The Orexin System & DORAs
Unlike traditional Z-drugs (GABA-A receptor agonists) which broadly depress the central nervous system, Dual Orexin Receptor Antagonists (DORAs) specifically target the wake-promoting neuropeptide orexin (hypocretin).
This mechanism acts to "turn off wakefulness" rather than "force sleep," preserving sleep architecture closer to physiologic norms and minimizing rebound insomnia.
Review DORA Efficacy DataAASM Standard PSG Montage
Electrode placement specifications based on the International 10-20 System for standard adult Polysomnography.
EEG Derivations
- F4-M1 Recommended Frontal
- C4-M1 Recommended Central
- O2-M1 Recommended Occipital
- Backup electrodes (F3, C3, O1, M2) placed to allow switching if artifacts occur.
EOG Derivations
- E1-M2 Left lower canthus (1cm below/lateral)
- E2-M2 Right upper canthus (1cm above/lateral)
- Out-of-phase deflections indicate conjugate eye movements (crucial for REM and wake scoring).
EMG Derivations
- Submental 3 electrodes (1 midline, 2 lateral)
- Tibialis Ant. Left and right legs for PLMs
- Submental EMG tonus drop is a required criterion for scoring Stage R (REM) sleep.
Circadian Rhythm: DLMO
Dim Light Melatonin Onset (DLMO) is the most reliable clinical marker of the endogenous circadian pacemaker.
Read Clinical Utility →Salivary Testing Protocol
Samples collected hourly or half-hourly in dim light (<30 lux) beginning 4-5 hours before anticipated bedtime. The onset is typically defined when concentrations cross the 3 pg/mL threshold.
Phase Angle of Entrainment
In healthy adults, DLMO occurs approximately 2-3 hours before spontaneous sleep onset. Abnormal phase angles indicate circadian rhythm sleep-wake disorders (CRSWD) like DSPD or ASPD.
The Limitations of Consumer Wearables
Why wrist-worn PPG cannot accurately score sleep architecture.
The PPG vs EEG Gap
Consumer trackers (Oura, Whoop, Apple Watch) rely primarily on Photoplethysmography (PPG) to measure heart rate variability (HRV) and accelerometers for movement. They use machine learning algorithms to *infer* sleep stages based on autonomic nervous system fluctuations.
However, true sleep staging (N1, N2, N3, REM) is defined neurologically via EEG (brainwaves). Autonomic surrogate markers frequently fail to distinguish between light sleep (N1/N2) and Wake in individuals with insomnia or fragmentation.
Clinical Reliability Index
- Total Sleep Time (TST) Moderate
- Sleep Latency (SOL) Poor (Overestimates sleep)
- REM Sleep Accuracy Poor (~60% agreement vs PSG)
- Deep Sleep (N3) Accuracy Poor (Highly variable)
- Oximetry (SpO2) Drops Moderate (Good for gross screening)
PAP Titration & Algorithms
Understanding device response to flow limitation, snoring, and apneas.
CPAP
Delivers a constant fixed pressure (e.g., 10 cmH2O). Requires formal in-lab titration to determine optimal pressure that eliminates events in all sleep stages and positions.
APAP
Fluctuates pressure between a set min/max based on proprietary algorithms detecting flow limitation. Often struggles with central sleep apnea or severe hypoventilation.
BiPAP (BPAP)
Provides two pressures: IPAP (inspiration) and EPAP (expiration). Used for high pressure requirements, pressure intolerance, or specific hypoventilation syndromes.
RLS & Iron Metabolism
Restless Legs Syndrome (RLS) is a clinical diagnosis (URGE criteria), not a polysomnographic one, though often accompanied by PLMD.
The Ferritin Protocol
Central nervous system iron deficiency is a primary pathophysiologic driver of RLS. Current guidelines recommend checking fasting serum ferritin. If ferritin is < 75 mcg/L (or transferrin saturation < 20%), oral iron supplementation with Vitamin C is the first-line therapy before initiating dopamine agonists or alpha-2-delta ligands.
RBD & Synucleinopathies
REM Sleep Behavior Disorder involves the loss of normal REM atonia (RSWA), allowing patients to enact their dreams. It is a highly specific prodromal marker for alpha-synucleinopathies (Parkinson's disease, Lewy Body Dementia, Multiple System Atrophy).
Polysomnographic Criteria
Diagnosis requires PSG demonstration of RSWA (sustained muscle activity in chin EMG or excessive transient muscle activity in chin/limb EMG during REM sleep) combined with clinical history of dream enactment.
Clinical Implications
Over 80% of patients with idiopathic RBD will eventually convert to a neurodegenerative disease, often 10-15 years after RBD onset, making it a critical window for future neuroprotective trials.
CBT-I is not
Sleep Hygiene
Sleep hygiene (dark room, cool temp, no screens) is insufficient as a standalone treatment for chronic insomnia. The first-line treatment is Cognitive Behavioral Therapy for Insomnia (CBT-I).
View Core CBT-I ComponentsThe Two Pillars of CBT-I
Sleep Restriction Therapy (SRT)
Consolidates fragmented sleep by matching Time in Bed (TIB) to subjective Total Sleep Time (TST). Increases homeostatic sleep drive. E.g., if a patient sleeps 5.5 hours but spends 9 hours in bed, TIB is restricted to ~5.5-6 hours initially.
Stimulus Control
Breaks the conditioned response of the bed = wakefulness/anxiety. Rule: Only use the bed for sleep and sex. If unable to sleep within ~20 minutes, get out of bed and do a quiet activity under dim light until sleepy.
Pediatric Scoring Differences
AASM scoring rules for children differ significantly from adults, reflecting different physiological thresholds.
Apnea Criteria
In adults, an apnea must last ≥ 10 seconds. In children (< 18 yrs), an apnea is scored if it lasts for ≥ 2 missed breaths (or the duration of 2 breaths relative to baseline breathing rate), regardless of absolute duration.
AHI Severity
Adult mild OSA begins at an AHI of 5. Pediatric mild OSA begins at an OAHI (Obstructive Apnea-Hypopnea Index) of just 1 event per hour, reflecting the higher vulnerability of the developing brain to hypoxia and fragmentation.
Pathophysiology:
Untreated OSA
The recurrent intermittent hypoxia and hypercapnia characteristic of OSA trigger intense sympathetic nervous system surges at the end of apneic events.
This sympathetic hyperactivation, combined with intrathoracic pressure swings and systemic inflammation, drives severe cardiovascular sequelae over time.
- → Drug-Resistant Hypertension
- → Atrial Fibrillation (High recurrence rate post-ablation)
- → Stroke (Ischemic)
- → Heart Failure with Preserved Ejection Fraction (HFpEF)
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