NEUROphysiology of CRACK Use Disorder in ITaly

Chronic crack cocaine use represents one of the most severe forms of substance use disorder, characterized by rapid onset, high compulsivity, and elevated relapse rates. Chronic consumption is known to induce profound neurobiological alterations in fronto-striatal circuits and disrupt dopaminergic regulation, particularly within reward systems and mechanisms of inhibitory control. This interplay between neurophysiology, clinical psychopathology, and systemic biological responses highlights the necessity for multidimensional treatment models. While traditional psychosocial and pharmacological interventions show limited efficacy for this specific population, qEEG-guided neurofeedback has emerged as a promising non-invasive neuromodulation technique. By providing real-time feedback of neural activity, neurofeedback allows participants to learn brain autoregulation strategies, promoting neuroplasticity and enhancing cognitive and emotional control. This study focuses on a specific neurofeedback training program implementing the Scott-Kaiser modification of the Peniston Alpha-Theta protocol. This approach suggests that targeted training of distinct cortical rhythms can directly modulate clinical symptoms such as impulsivity and craving. While preliminary evidence supports the use of EEG biofeedback in addiction, there is a critical need for rigorous, randomized controlled designs to systematically evaluate the clinical efficacy of this protocol on both neurophysiological patterns and objective behavioral outcomes in crack cocaine users.

Participants will be recruited from individuals hospitalized for crack cocaine use at the Short-Stay Accommodation Center (Centro di Pronta Accoglienza) of the ASP Palermo. It is planned to enroll a total sample of 104 participants (aged 18-55 years, stratified for sex and age). For initial assessment, interested subjects will be evaluated by using the Structured Clinical Interview for DSM-5 Disorders (SCID-5, incorporating the CV and PD modules), to operationalize psychiatric diagnoses and substance use profiles. Following the initial assessment and confirmation of eligibility, subjects will be randomized via an automated electronic system with allocation concealment to either the Experimental group or the Control group (1:1 ratio).

All experimental and training sessions will occur in a controlled setting within the laboratory.

* Neurophysiological parameters include qEEG spectral power analyses in the theta, alpha, SMR and beta bands, the beta/alpha and theta/beta ratios. * Behavioral and cognitive parameters include inhibitory control evaluated by a computerized Go/No-Go task, included in BFE-A battery. * Psychological assessment included: encompass current craving intensity (SCQ-NOW) and general psychopathology (GAD-7, PHQ-9).

Upon arrival (T0 - Baseline, executed within 72 hours of admission across two dedicated days), initial psychometric and behavioral parameters will be collected. Resting-state qEEG parameters will be recorded using the DigiTrack 32-channel system to establish neurophysiological baselines. Subsequently, participants will enter their assigned parallel arms for the duration of the institutional stay.

The Experimental group will receive standard institutional care (TAU) combined with 30 sessions of the modified Scott-Kaiser neurofeedback protocol, delivered via the DigiTrack system with interactive audiovisual feedback. This intervention is structured into two sequential phases at a rate of 1 daily sessions (45 minutes): Phase I consists of 5-10 sessions of Beta/SMR training to enhance cortical regulation and attentional control, followed by Phase II, consisting of 20 sessions of Alpha-Theta training focused on emotional regulation and craving reduction. The Control group will receive standard institutional TAU alone. The same assessment will be implemented at the end of the intervention protocol (T1) and at a 4 weeks follow-up (T2).

This research aims to provide robust evidence on the efficacy of a multi-phase Scott-Kaiser neurofeedback protocol as a complementary tool for crack cocaine use disorder. Understanding these specific neurobiological and psychological shifts can inform the integration of non-invasive neuromodulation techniques within public health addiction services (SerD). By utilizing a randomized controlled design, the study aims to differentiate the specific neuroplastic and cognitive benefits of targeted EEG biofeedback from the general outcomes of standard clinical care. The findings may contribute to a broader scientific understanding of how targeted brain training influences autonomic cortical regulation and behavioral control, ultimately facilitating the adherence at the TAU, reducing craving and increasing inhibitory control, finally increasing the possibility to an occupational reintegration for recovering individuals.

• Treatment Adherence and Retention [Time frame: Up to 4 weeks post-discharge (T2).]
• Clinical Relapse Rate [Time frame: 4 weeks post-discharge (T2).]
• Crack Cocaine Craving Intensity [Time frame: Baseline (T0, within 72 hours of admission), Post-Treatment (T1, approximately 40-45 days post-admission), and Follow-up (T2, 4 weeks post-discharge).]
• Depression Symptoms Severity [Time frame: Baseline (T0, within 72 hours of admission), Post-Treatment (T1, approximately 40-45 days post-admission), and Follow-up (T2, 4 weeks post-discharge).]
• Anxiety Symptoms Severity [Time frame: Baseline (T0, within 72 hours of admission), Post-Treatment (T1, approximately 40-45 days post-admission), and Follow-up (T2, 4 weeks post-discharge).]