Restless Legs Syndrome
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Direct answer
Four essentials define restless legs syndrome: an urge to move the legs, worse at rest, worse in the evening or night, and relieved by movement — often with a creepy-crawling quality. It is frequently iron-related (ferritin below about 75–100 micrograms per litre is the treatment threshold) and commonly accompanies uraemia, pregnancy, neuropathy and Parkinson disease; current first-line pharmacotherapy favours the alpha-2-delta ligands gabapentin and pregabalin, with dopamine agonists reserved for selected patients because of augmentation.
What you must remember
- The four IRLSSG core criteria: urge to move; initiation or worsening at rest; partial or total relief by movement; and evening/night-time predominance — all four are required.
- Associated and secondary causes to hunt: iron deficiency, chronic kidney disease and dialysis, third-trimester pregnancy, peripheral neuropathy, Parkinson disease, and drugs (antihistamines, most antidepressants especially SSRIs and mirtazapine, dopamine antagonists, caffeine).
- Iron logic: check serum ferritin; treat with oral iron (with vitamin C co-administration on alternate days for absorption) when ferritin is below about 75 micrograms per litre or transferrin saturation is under 20 per cent; intravenous iron is an option for refractory deficiency or intolerance.
- First-line drugs by current guidance: gabapentin, pregabalin or gabapentin enacarbil (effective for sensory symptoms and sleep, and preferred when symptoms are frequent or neuropathic pain coexists); dose at night, hours before symptom onset.
- Dopamine agonists (pramipexole, ropinirole, rotigotine patch) work rapidly and at low doses but carry augmentation — earlier onset, greater intensity, spread to arms — with long-term use, plus impulse control disorders; levodopa has the highest augmentation risk and is short-term only.
- Opioids (low-dose, e.g., tramadol or stronger agents in refractory disease under specialist care) rescue severe cases and augmentation states.
- Sleep impact is the main morbidity — chronic sleep deprivation, depression and impaired daytime function — and polysomnography shows periodic limb movements of sleep in the majority.
- Non-pharmacological measures: sleep hygiene, evening stretching, avoidance of caffeine, alcohol and nicotine, and correction of any secondary cause.
One evening clinic, worked through
A 52-year-old woman on haemodialysis describes, almost apologetically, "insects inside my calves" every night at 11 pm; she must pace the terrace for an hour to settle, has stopped travelling by bus and cinema, and now sleeps four hours a night. The diagnosis is the history — all four criteria met, and the associated cause list narrows immediately: she is uraemic (RLS is highly prevalent in dialysis patients) and her ferritin comes back 38 micrograms per litre. Sequence the treatment. First, the iron: ferritin below the 75 threshold means replacement comes before any dopamine — oral iron on alternate-day dosing for absorption, or IV iron in dialysis, where oral iron routinely fails; reassess ferritin after some months. Second, the evening drug: an alpha-2-delta ligand — gabapentin or pregabalin given two hours before the usual symptom onset — suits her nightly symptoms, her neuropathic descriptor and her sleep debt, and avoids the augmentation pathway entirely. Third, the audit at 4–6 weeks: symptom timing diary, sleep hours, and the specific question about earlier onset — because earlier-onset symptoms on treatment signal augmentation, the dopamine-agonist complication that her prescription choice has just sidestepped. Had she instead presented on long-standing pramipexole with symptoms now beginning at 4 pm and spreading to her arms, the management would read the other way: taper the agonist, switch to an alpha-2-delta ligand or an opioid in refractory cases, and recheck the ferritin.
Where students slip
Two facts separate the prepared answer. First, the ferritin threshold: candidates quote anaemia-range numbers (below 15 or 30) when the RLS-specific target is 75 micrograms per litre or above — iron deficiency without anaemia is the classic driver. Second, the augmentation concept: "dopamine agonists are first line" was true for years but current guidance leads with gabapentinoids precisely because dopamine therapy worsens the disease timetable over time — an exam point that distinguishes new reading from old question banks. The four criteria themselves are the third slip: restless legs without rest-worsening, movement-relief or evening predominance is something else (neuropathy, cramps, akathisia, positional discomfort).
Frequently asked questions
What four features define restless legs syndrome?
An urge to move the legs that begins or worsens at rest, is partially or completely relieved by movement, and occurs or worsens in the evening or night.
What ferritin level triggers iron replacement in RLS?
Below about 75 micrograms per litre (with transferrin saturation under 20 per cent as a companion threshold); oral iron on alternate days or intravenous iron for intolerance or dialysis settings.
Why are gabapentinoids preferred to dopamine agonists now?
They treat sensory symptoms and sleep effectively without causing augmentation — the earlier-onset, intensifying, spreading phenomenon that complicates long-term pramipexole, ropinirole and especially levodopa.
What is augmentation in restless legs syndrome?
A treatment-emergent worsening: symptoms start earlier in the day, intensify, or spread beyond the legs, typically on dopaminergic therapy — managed by dose reduction and switching drug class.
Which patient groups have the highest RLS prevalence?
Patients with iron deficiency, chronic kidney disease on dialysis, third-trimester pregnancy, peripheral neuropathy and Parkinson disease — with antidepressants and antihistamines as aggravating drugs.