Restless legs syndrome — structured clinical viva

This is chronic RLS with dopaminergic augmentation and probable impulse-control disorder on long-term ropinirole, plus stale low ferritin never readdressed. Escalating the agonist is the wrong vector — taper/switch, replete iron, and manage behavioural risk.[1][2][3]

1. Hierarchy. Chronic RLS; dopaminergic augmentation (earlier onset, anatomical spread, dose escalation); impulse-control behaviour (gambling); iron deficiency history; residual GAD; hypnotic/sedative review as needed.[1][2]

2. Why not higher ropinirole. Augmentation is iatrogenic disease progression on dopamine agonists. Further escalation worsens the phenotype. Guidelines emphasise prevention via α2δ-first strategies and structured management of established augmentation.[1][2][4]

3. Iron. Repeat morning fasting iron studies now. Historical ferritin 40 ng/mL is in the repletion zone used in RLS iron guidelines (commonly ≤75). Oral or IV iron per status, absorption, and severity — AASM emphasises iron evaluation in clinically significant RLS.[3][6]

4. Switch plan. Collaborative taper of ropinirole; introduce α2δ ligand (pregabalin/gabapentin pathway) as primary ongoing therapy; warn temporary symptom rebound; consider specialist input for refractory transition; avoid chronic levodopa rescue as routine long-term plan.[2][4][5]

5. Impulse control. Document gambling, finances, sexual/spending changes with collateral; stop/switch dopaminergic agent; financial and risk safeguards; follow-up for residual ICD after cessation.[2][4]

6. Safety-net. Mood/SI with sleep loss, falls if sedating α2δ titration aggressive in older adults, occupational impairment, and sleep medicine referral if refractory.[4][6]