Absence of postexercise and delayed facilitation of motor cortex excitability in restless legs syndrome: evidence of altered cortical plasticity?

STUDY OBJECTIVE: Restless legs syndrome (RLS) is a neurologic disorder with well-defined clinical and diagnostic criteria but the pathophysiology of which is unclear. Previous studies have suggested alterations in motor cortex function in RLS. We aimed to compare motor cortex plasticity in subjects with RLS versus healthy controls. DESIGN: Biphasic single-pulse transcranial magnetic stimulation (TMS) of the nondominant hemisphere was used to define motor evoked potential (MEP) amplitude, motor threshold, and silent period. Subjects also performed 3 blocks (30-s, 60-s, and 90-s duration) of a bimanual motor task (exercise condition). Amplitude of MEPs elicited immediately after each block, and then after a 15-minute rest period were compared with baseline. The time course of intracortical inhibition was also tested using paired-pulse TMS at 1- to 6-millisecond interstimulus intervals. SETTING: Clinical neurophysiology laboratory in a General Hospital. STUDY PARTICIPANTS: For the single-pulse TMS procedures, the RLS group included 11 patients affected by primary RLS and the control group included 11 age- and sex-matched normal subjects. For the paired-pulse TMS procedures, there were 9 patients and 6 controls. INTERVENTIONS: None. RESULTS: There were no group differences in motor threshold and MEP amplitudes, but the silent period was significantly shorter in subjects with RLS. Compared with baseline, control subjects had larger MEP amplitudes after 30 and 60 seconds of exercise and also after the rest period. In contrast, MEP amplitudes in patients with RLS were not significantly different from baseline after any of the exercise conditions or following the rest period. Patients with RLS also had decreased short-latency paired-pulse inhibition. CONCLUSIONS: Findings show abnormal motor cortex inhibition and cortical excitability differences in RLS. We suggest the possibility of alterations in movement-related cortical plasticity in RLS.