67.1 Chronic Insomnia & Obstructive Sleep Apnea

Two Disorders That Share a Complaint

Roughly one adult in three reports insomnia symptoms and roughly one in seven middle-aged adults meets criteria for at least moderate obstructive sleep apnea, yet the two conditions demand opposite first moves: chronic insomnia disorder is treated behaviorally before it is treated pharmacologically, while obstructive sleep apnea (OSA) requires objective testing before it is treated at all. They coexist often enough (comorbid insomnia and sleep apnea, "COMISA") that the safest primary care habit is to screen for both whenever a patient complains of poor sleep or daytime sleepiness.

The distinction the examination rewards is "I cannot sleep" versus "I sleep but I am not rested." Difficulty initiating or maintaining sleep points toward insomnia; loud snoring, witnessed apneas, morning headache, and unrefreshing sleep with excessive daytime somnolence point toward sleep-disordered breathing.

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Chronic Insomnia Disorder: Definition and Diagnosis

Chronic insomnia disorder is a clinical diagnosis requiring all of the following:

1. Difficulty initiating sleep, maintaining sleep, or waking earlier than desired;
2. Occurring at least 3 nights per week;
3. Persisting for at least 3 months;
4. Producing daytime impairment (fatigue, mood disturbance, cognitive complaint, impaired occupational or social function);
5. Despite adequate opportunity and circumstance for sleep.

That fifth criterion separates insomnia from insufficient sleep syndrome, in which the patient simply does not allow enough time in bed. No sleep study is needed to diagnose insomnia; polysomnography is not indicated for uncomplicated insomnia and is reserved for suspected comorbid sleep apnea, periodic limb movement disorder, or treatment-refractory presentations.

Structured evaluation

• Sleep diary for 1 to 2 weeks — the single most useful instrument, capturing bedtime, sleep latency, awakenings, rise time, naps, caffeine, alcohol, and screen use.
• Insomnia Severity Index (ISI) — a validated 7-item measure used for baseline severity and treatment response.
• Secondary causes to exclude: depression and anxiety, chronic pain, nocturia, gastroesophageal reflux, restless legs syndrome, menopause-associated vasomotor symptoms, and medications (stimulants, bupropion, corticosteroids, beta-agonists, decongestants, evening diuretics, and — paradoxically — alcohol, which shortens latency but fragments the second half of the night).

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Treating Chronic Insomnia: Behavior First

Cognitive behavioral therapy for insomnia (CBT-I) is first-line therapy for all adults with chronic insomnia disorder and should be initiated before pharmacotherapy is considered. This is a strong recommendation from the American College of Physicians (2016) and is echoed by the American Academy of Sleep Medicine and the 2025 VA/DoD guideline. Effect sizes match or exceed hypnotics in the short term and, unlike hypnotics, are durable after treatment ends.

[!IMPORTANT] A frequent distractor is offering sleep hygiene education alone as definitive treatment. Sleep hygiene is one component of CBT-I and performs poorly as a stand-alone intervention. Digital and app-delivered CBT-I are acceptable delivery routes when in-person therapy is unavailable, and access limitations are not a reason to skip straight to a hypnotic.

When pharmacotherapy is added

Medication is adjunctive, short-term, and shared-decision territory. AASM gives only weak recommendations for the agents it endorses, and explicitly recommends against several commonly used ones.

• Suggested (weak) options: eszopiclone, zolpidem, zaleplon, temazepam, triazolam, low-dose doxepin (sleep maintenance), ramelteon (sleep onset), and dual orexin receptor antagonists (suvorexant, lemborexant, daridorexant).
• Recommended against: trazodone, diphenhydramine and other sedating antihistamines, melatonin, valerian, tiagabine, and L-tryptophan for chronic insomnia — evidence of benefit is insufficient relative to harms.
• Older adults: the AGS Beers Criteria designate benzodiazepines and the non-benzodiazepine "Z-drugs" (zolpidem, eszopiclone, zaleplon) as potentially inappropriate, because they increase falls, fractures, delirium, and motor vehicle crashes without meaningful improvement in sleep latency. Anticholinergic antihistamines are likewise Beers-listed. Prescribing zolpidem to a 78-year-old with insomnia is a reliably wrong answer.

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Obstructive Sleep Apnea: Pathophysiology and Definitions

OSA is repetitive collapse of the pharyngeal airway during sleep despite continued respiratory effort, producing intermittent hypoxemia, sympathetic surges, and arousals.

• Apnea: cessation of airflow for at least 10 seconds.
• Hypopnea: at least a 30% reduction in airflow lasting at least 10 seconds accompanied by a ≥3% oxygen desaturation or an arousal.
• Apnea–hypopnea index (AHI): events per hour of sleep.

Diagnosis requires an AHI of ≥ 5 with symptoms or relevant comorbidity (sleepiness, unrefreshing sleep, insomnia, gasping, witnessed apnea, hypertension, mood disorder, cognitive dysfunction, coronary disease, atrial fibrillation, heart failure, stroke, or type 2 diabetes) or an AHI of ≥ 15 regardless of symptoms.

Screening: what the USPSTF actually says

The USPSTF concluded in 2022 that the evidence is insufficient (I statement) to assess the balance of benefits and harms of screening asymptomatic adults for OSA — including adults with unrecognized symptoms. The Task Force explicitly noted that an I statement is neither a recommendation for nor against screening, and that clinicians should use judgment for individual patients. This does not apply to symptomatic patients, who should be evaluated on clinical grounds.

STOP-BANG remains the most widely used case-finding instrument in symptomatic or high-risk patients:

A score of 0–2 is low risk, 3–4 intermediate, and ≥ 5 high risk. The Epworth Sleepiness Scale quantifies subjective sleepiness (score > 10 is abnormal) but does not diagnose OSA.

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Testing: Home Study Versus In-Laboratory Polysomnography

Home sleep apnea testing (HSAT) is appropriate for uncomplicated adults with a high pretest probability of moderate-to-severe OSA. In-laboratory polysomnography (PSG) is preferred — and an HSAT should not be substituted — when any of the following are present:

• Significant cardiopulmonary disease (advanced heart failure, moderate-to-severe COPD, suspected hypoventilation or hypoxemic disease);
• Neuromuscular disease or advanced primary neurologic disease;
• Chronic opioid or sedative-hypnotic use;
• History of stroke;
• Significant chronic insomnia or other sleep disruption that undermines the recording;
• Suspected central sleep apnea, narcolepsy, or parasomnia;
• Low pretest probability, or a negative/technically inadequate HSAT in a patient with persistent clinical suspicion — this last scenario is the classic stem, and the correct answer is in-laboratory PSG, not repeat HSAT or empiric CPAP.

Because HSAT records time recorded rather than true sleep time, it reports a respiratory event index (REI) that systematically underestimates the AHI. A negative home study therefore never excludes OSA.

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Treatment of OSA

1. Positive airway pressure (PAP) is first-line for moderate-to-severe OSA and for symptomatic mild OSA. Auto-titrating CPAP is acceptable for uncomplicated OSA; in-laboratory titration is used for complex patients. Adherence is the outcome that matters — troubleshoot mask fit, nasal congestion, aerophagia, and claustrophobia rather than abandoning therapy.
2. Weight management is disease-modifying, not merely supportive; clinically meaningful weight loss lowers AHI, and bariatric surgery or incretin-based pharmacotherapy is reasonable in eligible patients with obesity.
3. Mandibular advancement devices are a reasonable alternative for mild-to-moderate OSA or for PAP-intolerant patients.
4. Positional therapy helps supine-predominant disease.
5. Hypoglossal nerve stimulation is an option for selected PAP-intolerant adults with moderate-to-severe OSA within device-specific AHI and BMI limits.
6. Avoid evening alcohol, benzodiazepines, and opioids, all of which worsen upper-airway collapsibility and blunt arousal.

Consequences the examination expects you to connect

• OSA is the most common identifiable cause of secondary and resistant hypertension — a patient on three antihypertensives with a non-dipping nocturnal profile should be evaluated for OSA before further drug escalation.
• Associations include atrial fibrillation recurrence after cardioversion or ablation, heart failure, pulmonary hypertension, stroke, insulin resistance, and perioperative respiratory complications.
• Occupational safety: untreated moderate-to-severe OSA with excessive sleepiness carries clear drowsy-driving risk. Commercial drivers and other safety-sensitive workers require documented evaluation and treatment adherence, and clinicians should counsel all sleepy patients about driving.

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Board Exam Traps

1. Chronic insomnia in a 70-year-old → CBT-I, not zolpidem (Beers-listed) and not trazodone (recommended against).
2. "Sleep hygiene handout" offered as the definitive treatment → insufficient as monotherapy.
3. Resistant hypertension plus loud snoring → test for OSA before adding a fourth antihypertensive.
4. Negative home sleep apnea test with high clinical suspicion → in-laboratory polysomnography, because HSAT underestimates AHI.
5. Asymptomatic adult, no complaints, request to "screen for sleep apnea" → USPSTF I statement; there is no graded screening recommendation.
6. Patient on chronic opioids or with advanced heart failure needing OSA testing → in-laboratory PSG, not HSAT.