Objective: An electrocortical “disinhibition” to transcranial magnetic stimulation (TMS) was observed in restless legs syndrome (RLS), resulting in a hyperexcitability state [1]. In addition, the sensory complaints suggest a central sensitization in the RLS pathophysiology [2]. We aimed to probe the role of inhibitory repetitive TMS (rTMS) over the primary motor (M1) and somatosensory cortices (S1) in patients with idiopathic RLS. Materials: Resting motor threshold (rMT), motor evoked potentials (MEPs) and cortical silent period (CSP) were recorded using a figure-of-eight coil from the first dorsal interosseus muscle of the dominant hand of 6 RLS patients age-matched with 6 controls. Methods: Participants were randomly assigned to a stimulation sequence including, in differing order, motor, sensory and sham stimulations. By using a stimulus intensity of 110% of the rMT, a session of low-frequency rTMS over the M1 and S1 cortices and sham stimulation was performed in three different days, at the same time (evening). In each session, 20 rTMS trains were delivered, with 50 stimuli at 1 Hz for each train and an intertrain interval of 30 s (1,000 stimuli in total). Clinical assessment and TMS measures of cortical excitability were repeated after every stimulation procedure. Results: Data analysis confirmed the neurophysiological pattern described in patients with RLS: normal rMT and MEPs latency, shorter CSP duration, smaller MEPs amplitude. Patients reported an improvement of initiating sleep after the S1 rTMS, whereas the overall quality of sleep did not change significantly. Compared to baseline, a slightly prolonged CSP after M1 and S1 stimulation and a trend toward a higher rMT and smaller MEPs amplitude after M1 stimulation were observed in patients; conversely, rMT significantly decreased after S1 stimulation, especially in controls. Sham rTMS did not produce any variation. Discussion: The effect of the rTMS on the S1-M1 connectivity and central somatosensory processing may alleviate the sensory complaints of RLS patients. Compared to controls, RLS subjects exhibited only partially inhibitory rTMS-induced cortical plasticity over the S1, and did not respond to the M1 stimulation. The Shortening of CSP and the absence of rTMS-induced phenomena of long-term depression might be considered as a “proof of evidence” for impaired GABA-mediated mechanisms of cortical excitability and plasticity in RLS. Conclusion: The distinctive TMS profile in RLS is useful for the diagnosis and monitoring [3] and it might be viewed as a target of specific non-invasive brain stimulation techniques modulating sensorymotor cortical networks.

Repetitive TMS on primary sensorimotor areas of patients with RLS: a “proof of evidence” study

Lanza G;Bella R;
2015

Abstract

Objective: An electrocortical “disinhibition” to transcranial magnetic stimulation (TMS) was observed in restless legs syndrome (RLS), resulting in a hyperexcitability state [1]. In addition, the sensory complaints suggest a central sensitization in the RLS pathophysiology [2]. We aimed to probe the role of inhibitory repetitive TMS (rTMS) over the primary motor (M1) and somatosensory cortices (S1) in patients with idiopathic RLS. Materials: Resting motor threshold (rMT), motor evoked potentials (MEPs) and cortical silent period (CSP) were recorded using a figure-of-eight coil from the first dorsal interosseus muscle of the dominant hand of 6 RLS patients age-matched with 6 controls. Methods: Participants were randomly assigned to a stimulation sequence including, in differing order, motor, sensory and sham stimulations. By using a stimulus intensity of 110% of the rMT, a session of low-frequency rTMS over the M1 and S1 cortices and sham stimulation was performed in three different days, at the same time (evening). In each session, 20 rTMS trains were delivered, with 50 stimuli at 1 Hz for each train and an intertrain interval of 30 s (1,000 stimuli in total). Clinical assessment and TMS measures of cortical excitability were repeated after every stimulation procedure. Results: Data analysis confirmed the neurophysiological pattern described in patients with RLS: normal rMT and MEPs latency, shorter CSP duration, smaller MEPs amplitude. Patients reported an improvement of initiating sleep after the S1 rTMS, whereas the overall quality of sleep did not change significantly. Compared to baseline, a slightly prolonged CSP after M1 and S1 stimulation and a trend toward a higher rMT and smaller MEPs amplitude after M1 stimulation were observed in patients; conversely, rMT significantly decreased after S1 stimulation, especially in controls. Sham rTMS did not produce any variation. Discussion: The effect of the rTMS on the S1-M1 connectivity and central somatosensory processing may alleviate the sensory complaints of RLS patients. Compared to controls, RLS subjects exhibited only partially inhibitory rTMS-induced cortical plasticity over the S1, and did not respond to the M1 stimulation. The Shortening of CSP and the absence of rTMS-induced phenomena of long-term depression might be considered as a “proof of evidence” for impaired GABA-mediated mechanisms of cortical excitability and plasticity in RLS. Conclusion: The distinctive TMS profile in RLS is useful for the diagnosis and monitoring [3] and it might be viewed as a target of specific non-invasive brain stimulation techniques modulating sensorymotor cortical networks.
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/20.500.11769/372434
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