ABPN Sleep Medicine common mistakes
ABPN Sleep Medicine · Understand the traps and how to avoid them.
Treating a low or absent multiple sleep latency test mean sleep latency as diagnostic of narcolepsy without first confirming adequate sleep duration and excluding insufficient sleep syndrome, circadian misalignment, and OSA on the preceding polysomnogram and sleep log.
Candidates memorize the MSLT cutoffs (mean sleep latency ≤8 minutes, ≥2 SOREMPs) as a standalone rule and forget that the test is only interpretable after at least 2 weeks of adequate sleep and after the PSG has ruled out other causes of sleepiness and REM fragmentation.
What to do instead
Before scoring an MSLT, state the pretest conditions out loud: sleep diary and actigraphy for ≥2 weeks showing sufficient sleep, PSG demonstrating adequate total sleep time and no untreated OSA, and no REM-suppressing medications. If any are missing, the correct answer is usually to treat the confound first or repeat testing, not to diagnose narcolepsy.
Choosing an antidepressant or REM-suppressing agent as the answer for a patient whose REM sleep behavior disorder is being worked up, or attributing dream enactment to a psychiatric cause without checking for antidepressant use and comorbid neurodegeneration.
Candidates conflate the management of comorbid depression with the management of RBD and forget that SSRIs/SNRIs can both unmask and worsen dream enactment, and that RBD is a prodromal marker of synucleinopathies that warrants counseling and safety planning.
What to do instead
For any dream-enactment question, first ask whether the patient is on an SSRI/SNRI (a frequent trigger) and whether there are parkinsonian or autonomic features. The highest-yield answer is usually melatonin or clonazepam plus bedroom safety, with counseling about the association with future neurodegeneration.
Applying adult apnea-hypopnea index thresholds and adult polysomnography scoring conventions directly to a child, or dismissing snoring in a child as benign because the AHI is below 5.
Candidates carry over adult diagnostic cutoffs (AHI ≥5) and adult management pathways, but pediatric OSA is defined by an obstructive AHI ≥1 (with obstructive hypoventilation or a pattern of obstruction), and adenotonsillectomy is first-line rather than PAP.
What to do instead
For pediatric sleep-disordered breathing, anchor on pediatric thresholds (OAHI ≥1), remember adenotonsillectomy as first-line when tonsils are enlarged, and reserve PAP for children who are not surgical candidates or have persistent disease. Also remember that pediatric scoring uses different hypopnea and arousal rules.
Diagnosing restless legs syndrome from a description of leg discomfort alone, without confirming the four essential criteria (urge to move, worse at rest, relieved by movement, worse in the evening/night), and without distinguishing RLS from periodic limb movements or from neuropathic pain.
Candidates pattern-match 'leg discomfort at night' to RLS and skip the urge-to-move and circadian criteria, and they conflate PLMS (a polysomnographic finding) with RLS (a clinical diagnosis).
What to do instead
Recite the five IRLSSG criteria including the exclusion of mimics, and remember that PLMS on PSG supports but does not diagnose RLS. For treatment, check ferritin (target >75–100 ng/mL) before starting a dopamine agonist, and avoid augmenting agents when the history suggests augmentation.
Treating a delayed sleep-wake phase disorder with a bedtime hypnotic or with instructions to 'go to bed earlier' rather than with timed morning bright light, evening light restriction, and chronotherapy with gradual phase advancement.
Candidates see insomnia complaints and reflexively reach for sedative-hypnotics, missing that the core problem is circadian phase misalignment and that the treatment target is advancing the circadian clock, not sedating the patient at an earlier clock time.
What to do instead
When the sleep diary shows a consistent late sleep onset and late wake time with normal sleep duration when unconstrained, diagnose delayed phase and prescribe morning bright light plus fixed wake time and evening dim light; mention melatonin timed in the evening as an adjunct, not a hypnotic at bedtime.
Missing central sleep apnea or obesity hypoventilation syndrome because the candidate anchors on obstructive events and ignores the awake PaCO2, the overnight CO2 tracing, or the presence of Cheyne-Stokes respiration.
Candidates equate 'sleep apnea' with OSA and forget that hypoventilation is defined by awake PaCO2 ≥45 mmHg or disproportionate overnight CO2 elevation, and that central apnea with Cheyne-Stokes pattern points to heart failure or opioid use rather than to upper airway obstruction.
What to do instead
On any sleep-disordered breathing question, check three things explicitly: awake arterial or end-tidal CO2, the presence of central versus obstructive events, and the ejection fraction/opioid history. If PaCO2 is elevated, the answer involves noninvasive ventilation (BiPAP) rather than CPAP alone.
Misclassifying a parasomnia by timing and stage alone-labeling all confusional arousals or sleep terrors as REM-related, or labeling sleepwalking as occurring out of REM-without using the EEG stage at the time of the event and the patient's recall.
Candidates memorize 'NREM parasomnias are non-remembered, REM parasomnias are remembered' as a shortcut and misapply it, and they do not use the polysomnographic stage of the event or the typical first-third-of-night versus later-night timing to distinguish disorders of arousal from RBD.
What to do instead
Anchor on two axes: stage of origin (N3 for disorders of arousal, REM for RBD) and timing (first third of night for NREM, later for REM). Use video-PSG when the diagnosis is uncertain, and remember that NREM parasomnias can be triggered by sleep deprivation, fever, or another sleep disorder such as OSA.
Selecting a benzodiazepine or Z-drug as first-line pharmacotherapy for chronic insomnia in an older adult or in a patient with OSA, rather than CBT-I and, if a drug is needed, a low-risk agent such as a dual orexin receptor antagonist or low-dose doxepin.
Candidates default to the most familiar hypnotics and do not integrate age-related fall risk, respiratory depression risk in OSA, or the guideline recommendation that CBT-I is first-line for chronic insomnia in all adults.
What to do instead
For chronic insomnia, the first-line answer is almost always CBT-I (stimulus control, sleep restriction, relaxation, cognitive restructuring). When a medication is indicated, choose based on comorbidity: avoid benzodiazepines in older adults and in OSA, and consider melatonin-receptor agonists, DORAs, or low-dose doxepin depending on the clinical picture.
Interpreting an actigraphy or sleep-diary pattern as insomnia when the record actually shows a long time in bed with normal sleep efficiency and a short sleep duration, i.e., insufficient sleep syndrome, or missing a circadian misalignment that the diary reveals.
Candidates focus on the complaint ('I can't sleep') and do not systematically compare time in bed, total sleep time, and sleep timing across the record, so they miss the behavioral or circadian explanation and over-diagnose primary insomnia.
What to do instead
Read every diary or actigraph by computing time in bed, total sleep time, sleep efficiency, and the variability of sleep timing. If total sleep time is short with a long time in bed and daytime sleepiness, consider insufficient sleep syndrome; if timing is delayed or irregular, consider a circadian rhythm disorder.
Ignoring medication effects and substance use when explaining new-onset sleepiness, insomnia, or abnormal movements-for example missing that an SSRI, stimulant, opioid, or alcohol is the cause of the presenting sleep complaint.
Candidates treat sleep complaints as primary sleep disorders and do not routinely take a medication and substance timeline, even though many psychotropics, opioids, and alcohol alter sleep architecture, REM, and breathing.
What to do instead
For every sleep complaint, obtain a full medication and substance timeline with dates of initiation and dose changes, and ask specifically about caffeine, alcohol, cannabis, opioids, and REM-suppressing antidepressants. If the complaint began with a new drug, the first step is to address the drug before diagnosing a primary sleep disorder.