Sleep disorders in psychiatry — structured clinical viva

This is chronic insomnia disorder comorbid with late-life depression/anxiety, long-term benzodiazepine use with falls, and high pretest probability of OSA. The daughter’s request for a stronger hypnotic is the wrong vector — deprescribe, start CBT-I-adapted care, and evaluate OSA.[1][2][4]

1. Hierarchy. List: chronic insomnia disorder; sedative-hypnotic dependence/long-term use; possible OSA; residual depression/anxiety; fall risk and cognitive adverse-effect burden. Exclude RLS, periodic limb movements, nocturia/medical causes, alcohol.[6]

2. Why not stronger BZD. Meta-analysis in older adults shows modest sleep benefits offset by harms (cognitive events, falls). Guidelines prioritise CBT-I; AASM pharmacologic recommendations are weak and short-term-oriented, not indefinite escalation.[1][2][5]

3. CBT-I components. Stimulus control; sleep restriction (cautious in frail elderly — collaborative titration); cognitive therapy; relaxation; education. Digital or face-to-face; involve daughter as ally for schedule, not enforcer of more pills.[3]

4. OSA path. BMI, snoring, sleepiness → sleep study referral; weight, alcohol, CPAP if indicated; explain that untreated OSA can look like treatment-resistant mood/cognitive impairment.[4]

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

6. Safety net. Further falls, escalating SI, daytime sleepiness with driving, witnessed apnoeas — clear return precautions and crisis contacts.[6]