RESUMO
Reduced thalamocortical facilitation of the motor cortex in PD leads to characteristic motor deficits such as bradykinesia. Recent research has highlighted improved motor function following tDCS, but a lack of neurophysiological evidence limits the progress of tDCS as an adjunctive therapy. Here, we tested the hypothesis that tDCS may modulate M1 hemodynamic activity in PD and healthy using functional near-infrared spectroscopy (fNIRS). In this randomized crossover experiment, fourteen PD and twelve healthy control participants attended three laboratory sessions and performed a regulated (3 Hz) right index finger tapping task before and after receiving tDCS. On each visit, participants received either anodal, cathodal, or sham tDCS applied over M1. Hemodynamic activity of M1 was quantified using fNIRS. Significant task related activity was observed in M1 and the inferior parietal lobe in PD and healthy (p < 0.05). PD additionally recruited the dorsal premotor cortex. During tDCS, while at rest, anodal and cathodal tDCS significantly increased the oxygenated hemoglobin concentration of M1 compared to sham (t62 = 4.09 and t62 = 4.25, respectively). Task related hemodynamic activity was unchanged following any tDCS intervention (p > 0.05). Task related hemodynamic activity of M1 is not modulated by tDCS in PD or healthy. During tDCS, both anodal and cathodal stimulation cause a significant increase of M1 oxygenation, the clinical significance of which remains to be clarified.