ABSTRACT
Transcranial static magnetic field stimulation (tSMS) is a recent low-cost non-invasive brain stimulation technique that decreases cortical excitability in healthy subjects. The objective of the present study was to test the ability of tSMS to modulate cortical excitability in patients with Parkinson's disease. We performed a randomized double-blind sham-controlled cross-over study to assess cortical excitability before and immediately after tSMS (or sham) applied for 10 min to the more affected motor cortex of patients with Parkinson's disease. Cortical excitability was quantified by the amplitude of motor evoked potentials (MEPs) elicited by single-pulse transcranial magnetic stimulation (TMS). tSMS significantly decreased MEP amplitudes in patients OFF medication (after overnight withdrawal of dopaminergic drugs), but not ON medication (after an acute dose of levodopa). The between-patients variability of tSMS-induced changes was significantly greater ON medication. The variability ON medication could be partly explained by disease progression, i.e. the more advanced the patient, the more likely it was to observe a switch from inhibitory tSMS plasticity OFF medication to paradoxical facilitatory plasticity ON medication. These results suggest that tSMS induces dopamine-dependent changes of cortical excitability in patients with Parkinson's disease.
Subject(s)
Cerebral Cortex/metabolism , Cerebral Cortex/physiopathology , Cortical Excitability , Dopamine/metabolism , Parkinson Disease/metabolism , Parkinson Disease/physiopathology , Transcranial Magnetic Stimulation , Adult , Aged , Cerebral Cortex/drug effects , Dopamine Agents/pharmacology , Dopamine Agents/therapeutic use , Evoked Potentials, Motor , Female , Humans , Male , Middle Aged , Motor Cortex/metabolism , Motor Cortex/physiopathology , Parkinson Disease/drug therapyABSTRACT
BACKGROUND: Transcranial static magnetic field stimulation (tSMS) in humans reduces cortical excitability. OBJECTIVE: The objective of this study was to determine if prolonged tSMS (2 h) could be delivered safely in humans. Safety limits for this technique have not been described. METHODS: tSMS was applied for 2 h with a cylindric magnet on the occiput of 17 healthy subjects. We assessed tSMS-related safety aspects at tissue level by measuring levels of neuron-specific enolase (NSE, a marker of neuronal damage) and S100 (a marker of glial reactivity and damage). We also included an evaluation of cognitive side effects by using a battery of visuomotor and cognitive tests. RESULTS: tSMS did not induce any significant increase in NSE or S100. No cognitive alteration was detected. CONCLUSIONS: Our data indicate that the application of tSMS is safe in healthy human subjects, at least within these parameters.
