Insomnia in Clinical Practice

 

Insomnia in Clinical Practice: A Contemporary Approach to Diagnosis and Management

Dr Neeraj Manikath , claude.ai

Abstract

Insomnia disorder affects 10-15% of adults and represents one of the most common complaints in internal medicine practice. Despite its prevalence, insomnia remains underdiagnosed and inadequately treated, often dismissed as a benign nuisance rather than recognized as a serious condition with significant morbidity. This review synthesizes current evidence on the pathophysiology, diagnostic approach, and management of chronic insomnia, with emphasis on practical clinical pearls for internists and consultants.

Introduction

Insomnia disorder is characterized by difficulty initiating or maintaining sleep, or early morning awakening with inability to return to sleep, occurring despite adequate opportunity for sleep and resulting in daytime impairment. While transient sleep difficulties are ubiquitous, chronic insomnia—defined as symptoms occurring at least three nights per week for three months or longer—warrants systematic evaluation and treatment.

The economic burden is substantial: insomnia accounts for over $100 billion annually in the United States through direct healthcare costs, reduced productivity, and increased accident rates. More critically for internists, chronic insomnia is bidirectionally associated with cardiovascular disease, metabolic syndrome, depression, and all-cause mortality, making it far more than a quality-of-life issue.

Pathophysiology: Beyond the Sleep-Wake Switch

Contemporary models conceptualize insomnia through the "3P model": predisposing factors (genetic vulnerability, hyperarousal tendency), precipitating factors (stressors, medical events), and perpetuating factors (maladaptive behaviors, conditioned arousal). Neurobiologically, insomnia involves hyperarousal across multiple systems—elevated cortisol and catecholamines, increased metabolic rate, heightened high-frequency EEG activity during sleep, and reduced GABA-ergic tone.

Pearl #1: The Hyperarousal Phenotype Patients with chronic insomnia often exhibit a 24-hour hyperarousal state. Clinically, look for elevated resting heart rate, difficulty relaxing even during the day, and heightened startle responses. This insight shifts treatment focus from simply inducing sleep to addressing underlying arousal mechanisms—explaining why sedating medications alone often fail.

Diagnostic Approach: The Art of Sleep History

The diagnosis of insomnia disorder is primarily clinical, based on detailed history. However, the nuanced approach distinguishes competent from excellent clinicians.

The Structured Sleep Interview

Begin with open-ended exploration: "Tell me about a typical night's sleep." This often reveals more than directed questioning. Subsequently, systematically assess:

1. Sleep architecture: Sleep onset latency, number of awakenings, wake after sleep onset, total sleep time, and final awakening time
2. Temporal patterns: Difficulty falling asleep suggests anxiety or circadian disorders; middle-of-night awakenings suggest depression, pain, or sleep apnea; early morning awakening classically associates with depression
3. Sleep opportunity: Actual time in bed versus time asleep (sleep efficiency)
4. Daytime consequences: Fatigue, mood disturbance, cognitive impairment, or functional impairment

Pearl #2: The "Trying Too Hard" Phenomenon Ask specifically: "What do you do when you can't sleep?" Patients who "try harder" to sleep—remaining in bed, forcing sleep—paradoxically worsen insomnia through conditioned arousal. This single question identifies candidates for stimulus control therapy.

Oyster #1: The Insomnia Mimic—Circadian Phase Disorders A young adult who "can't fall asleep until 3 AM" but sleeps well once asleep likely has delayed sleep-wake phase disorder, not insomnia. Treatment differs fundamentally: chronotherapy and morning light therapy versus cognitive-behavioral approaches. The diagnostic clue: weekends and vacations reveal their natural, delayed but consolidated sleep pattern.

Essential Screening

Every insomnia evaluation must screen for:

1. Obstructive sleep apnea (OSA): STOP-BANG questionnaire (sensitivity 90% for moderate-severe OSA). Loud snoring, witnessed apneas, obesity, and treatment-resistant hypertension are red flags.

2. Restless legs syndrome (RLS): "Do you have uncomfortable sensations in your legs that are worse in the evening, improved with movement, and interfere with sleep?" Affects 10% of adults and is vastly underrecognized.

3. Psychiatric comorbidity: Depression and anxiety disorders coexist in 40-50% of chronic insomnia cases. The relationship is bidirectional—treating insomnia improves mood, and vice versa.

4. Medications and substances: Stimulants, corticosteroids, beta-agonists, SSRIs (initial weeks), diuretics (if taken evening), alcohol (causes fragmented sleep despite sedation), and caffeine (half-life 5-7 hours).

Hack #1: The Sleep Diary Shortcut Rather than reconstructing sleep patterns from memory (notoriously inaccurate), have patients complete a two-week sleep diary before the follow-up visit. This provides objective data and increases patient engagement. Free validated diaries are available through Consensus Sleep Diary (CSD) tools.

Role of Objective Testing

Polysomnography is not routinely indicated for uncomplicated insomnia. Reserve it for:

• Suspected OSA, periodic limb movement disorder, or REM sleep behavior disorder
• Treatment-refractory insomnia despite appropriate therapy
• Unusual clinical features or excessive daytime sleepiness

Actigraphy—wrist-worn devices measuring movement—helps in selected cases to objectively quantify sleep-wake patterns, particularly useful in circadian disorders or when sleep diary reliability is questioned.

Management: The Paradigm Shift

The critical conceptual advance in insomnia management is recognizing cognitive-behavioral therapy for insomnia (CBT-I) as first-line treatment, superior to pharmacotherapy for long-term outcomes.

Cognitive-Behavioral Therapy for Insomnia (CBT-I)

CBT-I is a multicomponent intervention typically delivered over 4-8 sessions. Meta-analyses demonstrate 70-80% of patients achieve clinically significant improvement, with benefits sustained years after treatment cessation—unlike pharmacotherapy, which provides benefit only during active use.

Core Components:

1. Sleep restriction therapy: Paradoxically restricting time in bed to match actual sleep time increases sleep efficiency and consolidates sleep. For example, a patient sleeping 5 hours but spending 8 hours in bed restricts bed time to 5.5 hours initially, then gradually extends as sleep efficiency improves above 85%.

2. Stimulus control: Re-establishes bed as a conditioned stimulus for sleep rather than wakefulness. Key rules: use bed only for sleep and intimacy; if unable to sleep within 20 minutes, leave the bedroom; return only when sleepy; maintain consistent wake time regardless of sleep duration.

3. Cognitive therapy: Addresses dysfunctional beliefs about sleep ("I need 8 hours or I'll be useless," "I can't function without sleep") that perpetuate anxiety and arousal.

4. Sleep hygiene education: While insufficient alone, hygiene education complements other strategies—regular sleep schedule, bedroom environment optimization (cool, dark, quiet), avoiding clock-watching.

Pearl #3: The "Sleep Restriction Paradox" Sleep restriction often produces dramatic improvement within 1-2 weeks. The mechanism: mild sleep deprivation increases homeostatic sleep drive, overcoming conditioned arousal. However, explicitly discuss daytime sleepiness risk during initial restriction, particularly regarding driving safety.

Oyster #2: When CBT-I "Fails"—Look for Comorbidity If CBT-I produces minimal benefit, systematically reconsider: Is there unrecognized OSA? Is depression inadequately treated? Are circadian factors operating? Is the patient actually implementing recommendations (non-adherence is common)?

Pharmacological Management

Medications should be considered adjunctive or when CBT-I is unavailable/declined, though pragmatically, many patients receive medications as first-line therapy in primary care settings.

FDA-Approved Options:

1. Benzodiazepine receptor agonists (BzRAs): Include benzodiazepines (temazepam, triazolam) and Z-drugs (zolpidem, eszopiclone, zaleplon). Effective for sleep onset and maintenance but concerns include tolerance, dependence, cognitive impairment, fall risk (especially elderly), and complex sleep behaviors.

2. Melatonin receptor agonists: Ramelteon (MT1/MT2 agonist) shows modest efficacy, primarily for sleep onset, without abuse potential. Particularly useful in elderly patients where fall risk is paramount.

3. Orexin receptor antagonists: Suvorexant and lemborexant represent newer mechanisms, blocking wake-promoting orexin signaling. Effective for both sleep onset and maintenance with favorable safety profiles, though cost limits accessibility.

4. Dual orexin receptor antagonists (DORAs): Daridorexant, the newest addition, demonstrates efficacy without next-day residual effects in clinical trials.

Off-Label Options:

1. Sedating antidepressants: Trazodone (25-100 mg), doxepin (3-6 mg), and mirtazapine. Trazodone is widely used despite limited evidence for chronic insomnia. Low-dose doxepin (3-6 mg) has FDA approval and specifically targets histamine receptors with minimal anticholinergic effects.

2. Atypical antipsychotics: Quetiapine is commonly prescribed off-label but carries significant metabolic and extrapyramidal risks—use only when comorbid psychiatric indications exist.

3. Anticonvulsants: Gabapentin (100-300 mg) may help, particularly with comorbid pain or restless legs syndrome, though evidence is limited.

Hack #2: The "Intermittent Dosing" Strategy For patients requiring long-term medication, recommend intermittent (3-4 nights per week) rather than nightly dosing. This reduces tolerance development, minimizes side effects, and maintains efficacy. Patients often discover they sleep adequately on medication-free nights once anxiety about sleep diminishes.

Pearl #4: The Melatonin Misconception Over-the-counter melatonin (typically 3-10 mg) is vastly overused for insomnia. Physiological doses (0.3-0.5 mg) taken 3-4 hours before desired sleep time are most effective for circadian phase shifting. Higher doses may paradoxically cause grogginess without improving sleep architecture. Useful primarily for jet lag and delayed sleep phase disorder, not chronic insomnia.

Special Populations

Elderly Patients: Age-related sleep architecture changes (reduced slow-wave sleep, increased awakenings) are normal and shouldn't be overmedicated. Prioritize sleep hygiene, CBT-I, and if medications necessary, avoid benzodiazepines (Beers Criteria); consider low-dose doxepin or ramelteon.

Chronic Pain: Insomnia and pain bidirectionally worsen each other. Optimize pain management while addressing sleep specifically—gabapentinoids may serve dual purposes.

Comorbid Psychiatric Disorders: Treat both conditions simultaneously. Insomnia-specific treatment improves psychiatric outcomes and vice versa. SSRIs/SNRIs may initially worsen sleep; temporary adjunctive hypnotic during antidepressant initiation can improve tolerability.

Emerging Therapies and Future Directions

Digital CBT-I platforms (Sleepio, Somryst) deliver guideline-concordant treatment with comparable efficacy to therapist-delivered CBT-I, addressing the shortage of trained providers. These FDA-cleared platforms represent a significant advance in accessibility.

Novel pharmacologic targets under investigation include histamine H3 receptor inverse agonists and selective GABA-A receptor modulators with improved safety profiles over traditional BzRAs.

Practical Management Algorithm

1. Establish diagnosis: Detailed sleep history, screen for mimics (OSA, RLS, circadian disorders), assess comorbidities
2. First-line treatment: CBT-I (therapist-delivered or digital platform)
3. Adjunctive pharmacotherapy if needed: Choose based on phenotype (sleep onset vs. maintenance), comorbidities, and safety profile
4. Reassess at 4-6 weeks: If inadequate response, reconsider diagnosis, assess adherence, optimize comorbidity management
5. Long-term management: Taper medications once sleep consolidated; maintain behavioral strategies

Hack #3: The "Insomnia Passport" Create a brief summary document for patients outlining their personalized sleep strategies—optimal sleep window, stimulus control rules, medication plan. This "passport" reinforces adherence and provides continuity across healthcare settings.

Conclusion

Insomnia disorder warrants the same systematic, evidence-based approach as any chronic medical condition. The paradigm shift toward CBT-I as first-line treatment reflects growing recognition that insomnia is maintained by behavioral and cognitive factors amenable to non-pharmacologic intervention. Internists equipped with structured diagnostic skills and awareness of contemporary treatment options can significantly impact patients' sleep health, with downstream benefits for overall medical outcomes. The integration of digital therapeutics promises to democratize access to evidence-based treatment, though the clinician's role in diagnosis, phenotyping, and personalized management remains irreplaceable.

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Key References

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