Effects of anodal tDCS on electroencephalography correlates of cognitive control in mild-to-moderate traumatic brain injury

Abstract

BACKGROUND: Transcranial direct current stimulation (tDCS) may provide a potential therapy for cognitive deficits caused by traumatic brain injury (TBI), yet its efficacy and mechanisms of action are still uncertain. OBJECTIVE: We hypothesized that anodal tDCS over the left dorsolateral prefrontal cortex (DLPFC) would boost the influence of a cognitive training regimen in a mild-to-moderate TBI (mmTBI) sample. Cognitive enhancement was measured by examining event-related potentials (ERPs) during cognitive control tasks from pre- to post-treatment. METHODS: Thirty-four participants with mmTBI underwent ten sessions of cognitive training with active (n = 17) or sham (n = 17) anodal tDCS to the left DLPFC. ERPs were assessed during performance of an auditory oddball (3AOB), N-back, and dot pattern expectancy (DPX) task before and after treatment. RESULTS: P3b amplitudes significantly decreased from baseline to post-treatment testing, regardless of tDCS condition, in the N-back task. The active tDCS group demonstrated a significantly increased P3a amplitude in the DPX task. No statistically significant stimulation effects were seen during the 3AOB and N-back tasks. CONCLUSION: Active anodal tDCS paired with cognitive training led to increases in P3a amplitudes in the DPX, inferring increased cognitive control. P3b decreased in the N-back task demonstrating the effects of cognitive training. These dissociated P3 findings suggest separate mechanisms invoked by different neuroplasticity-inducing paradigms (stimulation versus training) in brain networks that support executive functioning.

Contrasting MEG effects of anodal and cathodal high-definition TDCS on sensorimotor activity during voluntary finger movements

“…Although it is not our intention here to fully review the vast literature on neural responses to TDCS, we note that even limiting ourselves to studies examining time-domain electromagnetic activity (ERPs and ERFs), examples can be found in line with our findings, contrary to our findings, and with null results from TDCS. Supporting the neural gain hypothesis, a fairly large number of studies have now demonstrated increases in the P300 potential after anodal stimulation, corresponding to behavioral improvements in cognitive control, target detection, and related measures (reviewed by Mendes et al, 2022 ; Liu et al, 2023 ; Mertens et al, 2023 ; Zhou et al, 2023 ). Some studies have also reported decreased N2 potentials after cathodal stimulation in a go/nogo paradigm (Friedrich and Beste, 2018 ), and increased auditory N2 (Hanenberg et al, 2019 ) and mismatch negativity (MMN) responses (Impey and Knott, 2015 ) after anodal stimulation.…”

Transcranial direct current stimulation promotes angiogenesis and improves neurological function via the OXA-TF-AKT/ERK signaling pathway in traumatic brain injury

“…tDCS has been established as an effective therapeutic approach for TBI, with research indicating its absence of side effects [ 34 , 35 ]. In terms of its therapeutic mechanism, specifically, anodal current exerts an excitatory effect on neuronal activity, while cathodal tDCS exhibits inhibitory properties [ 36 ]. A study has highlighted the ability of anodal tDCS to enhance reaction times in working memory tasks for patients with mild to moderate brain injuries, providing crucial therapeutic insights for their recovery [ 37 ].…”

“…Furthermore, anodal tDCS has demonstrated the potential to promote cerebrovascular reactivity in cerebral parenchymal arterioles, regulating average cerebral blood flow and tissue oxygenation in traumatized mice, thus potentially contributing to the improvement of neurological function [ 15 , 38 ]. Despite being considered an effective therapeutic modality for TBI, the molecular mechanisms governing the effects of tDCS are still not fully understood [ 36 ]. Hence, in this research, we proceeded to examine the impact of tDCS on vascular regeneration and angiogenesis in a rat model of TBI.…”