Restless-legs syndrome (RLS) is a sensorimotor disorder, characterized by an 
irresistible urge to move the legs usually accompanied or caused by 
uncomfortable and unpleasant sensations. It begins or worsens during periods of 
rest or inactivity, is partially or totally relieved by movements and is 
exacerbated or occurs at night and in the evening. RLS sufferers represent 2 to 
3% of the general population in Western countries. Supportive criteria include a 
family history, the presence of periodic-leg movements (PLM) when awake or 
asleep and a positive response to dopaminergic treatment. The RLS phenotypes 
include an early onset form, usually idiopathic with a familial history and a 
late onset form, usually secondary to peripheral neuropathy. Recently, an 
atypical RLS phenotype without PLM and l-DOPA resistant has been characterized. 
RLS can occur in childhood and should be distinguished from attention 
deficit/hyperactivity disorder, growing pains and sleep complaints in childhood. 
RLS should be included in the diagnosis of all patients consulting for sleep 
complaints or discomfort in the lower limbs. It should be differentiated from 
akathisia, that is, an urge to move the whole body without uncomfortable 
sensations. Polysomnographic studies and the suggested immobilization test can 
detect PLM. Furthermore, an l-DOPA challenge has recently been validated to 
support the diagnosis of RLS. RLS may cause severe-sleep disturbances, poor 
quality of life, depressive and anxious symptoms and may be a risk factor for 
cardiovascular disease. In most cases, RLS is idiopathic. It may also be 
secondary to iron deficiency, end-stage renal disease, pregnancy, peripheral 
neuropathy and drugs, such as antipsychotics and antidepressants. The 
small-fiber neuropathy can mimic RLS or even trigger it. RLS is associated with 
many neurological and sleep disorders including Parkinson's disease, but does 
not predispose to these diseases. The pathophysiology of RLS includes an altered 
brain-iron metabolism, a dopaminergic dysfunction, a probable role of pain 
control systems and a genetic susceptibility with nine loci and three 
polymorphisms in genes serving developmental functions. RLS treatment begins 
with the elimination of triggering factors and iron supplementation when 
deficient. Mild or intermittent RLS is usually treated with low doses of l-DOPA 
or codeine; the first-line treatment for moderate to severe RLS is dopaminergic 
agonists (pramipexole, ropinirole, rotigotine). In severe, refractory or 
neuropathy-associated RLS, antiepileptic (gabapentin, pregabalin) or opioid 
(oxycodone, tramadol) drugs can be used.