The CerebellumNeurosciencePeer-reviewed journal article
Investigation of neuromodulatory effect of anodal cerebellar transcranial direct current stimulation on the primary motor cortex using functional near-infrared spectroscopy
Zeshan ShoaibiD, Won Kee ChangiD, Jongseung LeeiD, Stephanie Hyeyoung LeeiD, Zephaniah Phillips ViD, Seung Hyun LeeiD, Nam‐Jong PaikiD, Han‐Jeong Hwang, Won‐Seok KimiD
Abstract
BackgroundCerebellar brain inhibition (CBI), a neural connection between the cerebellum and primary motor cortex (M1), has been researched as a target pathway for neuromodulation to improve clinical outcomes in various neurological diseases. However, conflicting results of anodal cerebellar transcranial direct current stimulation (acb-tDCS) on M1 excitability indicate that additional investigation is required to examine its precise effect. Objective/HypothesisThis study aimed to gather evidence of the neuromodulatory effect of acb-tDCS on the M1 using functional near-infrared spectroscopy (fNIRS). MethodsSixteen healthy participants were included in this cross-over study. Participants received real and sham acb-tDCS in a random order, with a minimum one-week washout period between them. The anode and cathode were placed on the right cerebellum and the right buccinator muscle, respectively. Stimulation lasted 20 min at an intensity of 2 mA, and fNIRS data were recorded for 42 min (including a 4 min baseline before stimulation and an 18 min post-stimulation duration) using eight channels attached bilaterally on the M1. Resultsacb-tDCS induced a significant decrease in oxyhemoglobin (HbO) concentration (inhibitory effect) in the left (contralateral) M1, whereas it induced a significant increase in HbO concentration (excitatory effect) in the right (ipsilateral) M1 compared to sham tDCS during (p < 0.05) and after stimulation (p < 0.01) in a group level analysis. At the individual level, variations in the response to acb-tDCS were observed. ConclusionOur findings demonstrate the neuromodulatory effects of acb-tDCS on the bilateral M1 in terms of neuronal hemodynamics.
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