Insomnia disorder — structured clinical viva

This is chronic insomnia disorder with residual anxiety/depression, long-term benzodiazepine use, clear perpetuating behaviours (extended TIB, clock-watching, alcohol), fall risk, and possible OSA. The request for a stronger hypnotic is the wrong vector — deprescribe, start CBT-I, and evaluate OSA.[1][2][6]

1. Hierarchy. Chronic insomnia disorder; sedative-hypnotic long-term use/dependence risk; possible OSA; residual GAD/depression; fall risk. Exclude RLS, nocturia/medical causes, circadian delay if schedule history supports it.[5][6]

2. Mechanisms. Spielman 3P: predisposing (trait anxiety), precipitating (past episode/stressor), perpetuating (extended TIB, clock-watching, alcohol, conditioned arousal). Hyperarousal model explains cognitive and physiological maintenance. CBT-I targets perpetuating limb.[6]

3. Why not stronger BZD. Modest benefit vs falls/cognitive harm signals; guidelines prioritise CBT-I; AASM pharmacologic recommendations are weak and short-term-oriented, not indefinite escalation.[1][2][4]

4. CBT-I components. Stimulus control; sleep restriction (collaborative, plan driving/falls); cognitive therapy; relaxation; education. Digital or face-to-face. Hygiene alone is not CBT-I.[3]

5. OSA path. BMI, snoring → sleep study referral; weight, alcohol reduction, CPAP if indicated; explain untreated OSA can look like residual mood/cognitive impairment.[5]

6. Deprescribing plan. Shared decision; slow taper (e.g. 10–25% reductions every 1–2+ weeks as tolerated — individualise); warn rebound insomnia; temporary non-BZD strategies within CBT-I; avoid automatic high-dose quetiapine; falls prevention; document agreement and safety-net.[1][5]