Restless legs syndrome (RLS) is characterized by an unpleasant sensation from the lower limbs with the urge to move them, motor restlessness, worsening of the symptoms at rest and partial relief from activity, worsening at bedtime and during nighttime. Most of the patients show nocturnal myoclonus (NM) of the lower limbs during polysomnography. Recently, some neurophysiologic studies were shown to support the hypothesis of a central (CNS) origin, in particular for NM, showing reduction of cortical motor inhibition (supraspinal inhibition) and increase in excitability of spinal cord motoneurons. Abnormal afferent inputs, as in the case of peripheral neuropathy, or abnormal sensorimotor integration at the spinal interneuronal level (i.e., spinal cord lesions) may act as a trigger of stimulus-induced modulations of RLS symptoms. Moreover, new studies of functional MRI and SPECT or PET techniques shed light on possible basal ganglia and dopaminergic involvement in the pathophysiology of RLS and NM. Concerning the treatment, several studies have estabilished the concept of the efficacy of dopaminergic drugs such as pramipexole, pergolide, and ropirinole, with fewer side effects than L-dopa. To date, these drugs seem to have less augmentation or rebound symptoms during the day than L-dopa. Recently, the treat- ment with iron therapy, when low ferritin levels are found, or with other agents as gabapentin, valproic acid and tramadol, support the involvement of other inhibitory/excitatory pathways in the mechanisms of RLS and NM. However, the more consistent and robust effect is still the dopaminergic one, in particular searching for drugs with a long half-life (i.e., cabergoline) and which are well tolerated.
|Issue number||4 SUPPL.|
|Publication status||Published - 2000|
ASJC Scopus subject areas
- Clinical Neurology