Addressing the three core issues in research on cognitive control deficits in Internet Gaming Disorder (IGD)-unclear neural mechanisms, limited intervention targets, and poor patient compliance-this project innovatively constructs a pathological model of IGD characterized by "decline in social rewards → dysfunction of the dorsal Anterior Cingulate Cortex-Dorsolateral Prefrontal Cortex (dACC-DLPFC) cognitive control circuit → abnormalities in the frontal midline theta rhythm (Fmθ)." The investigators have developed a dual-target intervention system that integrates neurofeedback with social reward substitution, transforming social rewards into therapeutic reinforcers to enhance the effectiveness of the intervention.
Existing research has confirmed that cognitive control dysfunction is the core pathological mechanism underlying the onset and progression of Internet Gaming Disorder (IGD); however, there remain critical scientific questions in this field that urgently need to be addressed: First, the underlying neural mechanisms driving cognitive control abnormalities in IGD patients have not yet been clarified. Most existing studies remain at the level of phenomenological description and have not elucidated the mechanisms of dysfunction in brain circuits related to cognitive control or the upstream regulatory factors; Second, the cognitive control deficits in IGD patients have not yet been fundamentally remediated. Current intervention strategies focus solely on "inhibitory interventions" and fail to establish a healthy social reward system capable of replacing the immediate rewards of gaming. This leaves a gap in behavioral regulation following the correction of cognitive control deficits, resulting in a significant sense of psychological emptiness after withdrawal and persistently high rates of clinical relapse; Third, IGD patients exhibit low participation in restorative interventions targeting cognitive control deficits, and the effects of such interventions are short-lived. IGD is generally characterized by low sensitivity to social rewards and insufficient treatment motivation. The decline in social rewards and cognitive control deficits are causally interlinked; traditional psychotherapy models that rely on verbal communication and self-disclosure struggle to adapt to these characteristics, resulting in limited therapeutic efficacy. In light of these scientific issues, this project will conduct targeted research: First, the investigators will innovatively construct an IGD pathological model: "social reward decline → dysfunction of the dorsal Anterior Cingulate Cortex-Dorsolateral Prefrontal Cortex (dACC-DLPFC) cognitive control circuit → abnormalities in the frontal midline theta rhythm (Fmθ)." The investigators will systematically elucidate the mechanisms, upstream drivers, and specific biomarkers underlying the dysfunction of the cognitive control circuit; Second, based on the above theory and approaching IGD intervention from the perspective of organically combining "breaking with the old" and "establishing the new," the investigators will establish a dual-target system to repair the cognitive control circuit. Develop an Fmθ neurofeedback intervention device that "activates neural circuits and inhibits gaming behavior + promotes social rewards and substitutes for gaming behavior"; Third, transform social rewards into therapeutic reinforcers to effectively stimulate intrinsic motivation for cognitive control restoration, thereby significantly improving compliance and engagement in IGD cognitive control interventions.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
TREATMENT
Masking
NONE
Enrollment
120
Using the MATLAB environment, the PsychToolbox add-on, and the integrated EEGLAB toolbox for real-time EEG signal processing, a neural feedback system was constructed to enable precise, targeted regulation of the dACC-DLPFC circuit. Target 1 (activating neural circuits to inhibit gaming behavior \[breaking old habits\]) and Target 2 (promoting social rewards to replace gaming behavior \[establishing new habits\])-this dual-target design forms a complete learning loop of "inhibiting impulses → obtaining healthy rewards," simulating the behavioral patterns of a healthy brain. A three-group between-subjects design was employed to isolate the unique effects of the "social reward" component; each session consisted of 30 minutes of neurofeedback training, four times a week, for four consecutive weeks. Dual-regulation group: Received comprehensive "neural circuit activation + promotion of social reward" dual neurofeedback training.
1. Conduct a single-blind, randomized controlled trial. The 40 participants assigned to the single-modulation group will receive only "inhibitory" neurofeedback training targeting the dACC-DLPFC circuit (activating the neural circuit only, without promoting social reward). 2. Assessments will include standardized scales, behavioral tests, and neuroimaging, each administered once before and after the intervention. 3. During neurofeedback training, participants will undergo training four times per week, for a total of 16 sessions. 4. The entire intervention will last approximately one month. To track the immediacy and sustainability of the intervention's effects, the above measures will be collected at all four time points: baseline (T0), immediately post-intervention (T1), and at 6-month (T2) and 12-month (T3) follow-ups.
1\. Conduct a single-blind, randomized controlled trial. The 40 participants assigned to the sham feedback group will follow the same task protocol but receive sham feedback unrelated to their own brain activity. 2. Assessments, including standardized scales, behavioral tests, and neuroimaging, will be conducted once before and once after the intervention.3. During neurofeedback training, participants will undergo training four times per week, for a total of 16 sessions. 4. The entire intervention will last approximately one month. To track the immediacy and sustainability of the intervention's effects, the above measures will be collected at all four time points: baseline (T0), immediately post-intervention (T1), and at 6-month (T2) and 12-month (T3) follow-ups.
Bengbu Medical University
Bengbu, China
RECRUITINGSeverity of Gaming Disorder
The severity of gaming disorder was assessed using the Gaming Disorder Screening Scale (GDSS), which consists of 18 Likert-scale items. Each item has four response options (1 = never; 2 = sometimes; 3 = often; 4 = always), with a total score range of 18 to 72. Based on receiver operating characteristic (ROC) analysis using ICD-11 as the gold standard, a total score of ≥47 indicates a high risk of gaming disorder
Time frame: through neurofeedback training completion, an average of 1 month
Results of Neurofeedback Training
Results of Neurofeedback Training:Average increase in frontal midline theta (Fmθ) power during training. The higher the power, the better theresults
Time frame: through neurofeedback training completion, an average of 1 month
Results of Neurofeedback Training
Results of Neurofeedback Training:The time it takes for participants to reach a predetermined target energy level. The shorter the time, the better the training results.
Time frame: through neurofeedback training completion, an average of 1 month
Changes of Behavioral Indicators
Stop-Signal Reaction Time (SSRT) derived from the Social Reward-modified Stop-Signal Task. Shorter SSRT indicates better cognitive control performance under social-reward versus no-reward conditions.
Time frame: through neurofeedback training completion, an average of 1 month
Changes of Behavioral Indicators
Stop-Signal Delay (SSD) derived from the Social Reward-modified Stop-Signal Task. Higher SSD indicates better cognitive control performance under social-reward versus no-reward conditions.
Time frame: through neurofeedback training completion, an average of 1 month
Changes of Behavioral Indicators
Hit rate derived from the Social Incentive Delay Task. Reduced hit rate under social-reward cue conditions indicates impaired social reward processing.
Time frame: through neurofeedback training completion, an average of 1 month
Changes of Behavioral Indicators
Reaction time for correct hits derived from the Social Incentive Delay Task. Prolonged reaction time under social-reward cue conditions indicates impaired social reward processing.
Time frame: through neurofeedback training completion, an average of 1 month
Social Reward
The social reward function was measured using the "Social Pleasure" subscale of the Multidimensional Pleasure Deficit Scale. This subscale consists of four items. Participants were first asked to list two current or past social activities that had brought them pleasure, and then to respond to each item, assessing factors such as their willingness to participate in these activities and the level of pleasure experienced during participation. Scoring is based on a 10-point Likert scale, ranging from "Not at all" to "Very much." Higher scores indicate stronger social reward.
Time frame: through neurofeedback training completion, an average of 1 month
Executive Function
Executive function was evaluated using the Behavior Rating Inventory of Executive Function-Adult Version (BRIEF-A), comprising 75 items scored on a 3-point Likert scale ranging from "never" to "often." Higher scores on the Global Executive Composite (GEC) reflect greater executive function impairment.
Time frame: through neurofeedback training completion, an average of 1 month
Changes of Electrophysiological Indicators
Event-related potential (ERP) components N200 elicited during the Stop-Signal Task were analyzed with respect to amplitude . N200 amplitude indexed conflict monitoring.
Time frame: through neurofeedback training completion, an average of 1 month
Changes of Electrophysiological Indicators
Event-related potential (ERP) components P300 elicited during the Stop-Signal Task were analyzed with respect to latency. P300 latency reflected inhibitory control capacity.
Time frame: through neurofeedback training completion, an average of 1 month
Neuroimaging Indicators
Functional magnetic resonance imaging (fMRI) was used to assess the strength of functional connectivity between the dorsal anterior cingulate cortex (dACC) and the dorsolateral prefrontal cortex (DLPFC)
Time frame: through neurofeedback training completion, an average of 1 month
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