Cocaine use disorder (CUD) is a global health problem with severe consequences, leading to behavioral, cognitive, and neurobiological disturbances. While consensus on treatments is still ongoing, repetitive transcranial magnetic stimulation (rTMS) has emerged as a promising approach for medication-resistant disorders, including substance use disorders. In this context, here we present the SUDMEX-TMS, a Mexican dataset from an rTMS clinical trial involving CUD patients. This longitudinal dataset comprises 54 CUD patients (including 8 females) with data collected at five time points: baseline (T0), two weeks (T1), three months (T2), six months (T3) follow-up, and twelve months (T4) follow-up. The clinical rTMS treatment followed a double-blinded randomized clinical trial design (n = 24 sham/30 active) for 2 weeks, followed by an open-label phase. The dataset includes demographic, clinical, and cognitive measures, as well as magnetic resonance imaging (MRI) data collected at all time points, encompassing structural (T1-weighted), functional (resting-state fMRI), and multishell diffusion-weighted (DWI-HARDI) sequences. This dataset offers the opportunity to investigate the impact of rTMS on CUD participants, considering clinical, cognitive, and multimodal MRI metrics in a longitudinal framework.

In amnestic mild cognitive impairment (aMCI), neuroinflammation evolves during disease progression, affecting microglial function and potentially accelerating the pathological process. Currently, no effective treatment exists, leading to explorations of various symptomatic approaches, though few target the underlying physiological mechanisms. Modulating inflammatory processes may be critical in slowing disease progression. Cognitive stimulation (CS) and transcranial direct current stimulation (tDCS) applied to the left dorsolateral prefrontal cortex (l-DLPFC) show promise, but the results are heterogeneous. Thus, a randomized, double-blind, placebo-controlled clinical trial is currently underway. The first-stage results were examined after three weeks of intervention in two groups: active tDCS combined with CS and sham tDCS combined with CS. Twenty-two participants underwent two assessments: T0 (baseline) and T1 (after 15 sessions of tDCS, active or sham, and 9 sessions of CS). The results demonstrated that CS improved cognition, increased brain-derived neurotrophic factor (BDNF) levels, and reduced peripheral proinflammatory cytokine levels (interleukin IL-6 and chemokine CX3CL1) in serum. This decrease in IL-6 may promote microglial proliferation and survival as a modulatory effect response, while the increase in BDNF might suggest a regulatory mechanism in microglia–neuron interaction responses. However, tDCS did not enhance the cognitive or modulatory effects of CS, suggesting that longer interventions might be required to achieve substantial benefits.

Cocaine use disorder (CUD) is a worldwide public health condition that is suggested to induce pathological changes in macrostructure and microstructure. Repetitive transcranial magnetic stimulation (rTMS) has gained attention as a potential treatment for CUD symptoms. Here, we sought to elucidate whether rTMS induces changes in white matter (WM) microstructure in frontostriatal circuits after 2 weeks of therapy in patients with CUD and to test whether baseline WM microstructure of the same circuits affects clinical improvement. This study consisted of a 2‐week, parallel‐group, double‐blind, randomized controlled clinical trial (acute phase) (sham [n = 23] and active [n = 27]), in which patients received two daily sessions of rTMS on the left dorsolateral prefrontal cortex (lDLPFC) as an add‐on treatment. T1‐weighted and high angular resolution diffusion‐weighted imaging (DWI‐HARDI) at baseline and 2 weeks after served to evaluate WM microstructure. After active rTMS, results showed a significant increase in neurite density compared with sham rTMS in WM tracts connecting lDLPFC with left and right ventromedial prefrontal cortex (vmPFC). Similarly, rTMS showed a reduction in orientation dispersion in WM tracts connecting lDLPFC with the left caudate nucleus, left thalamus, and left vmPFC. Results also showed a greater reduction in craving Visual Analogue Scale (VAS) after rTMS when baseline intra‐cellular volume fraction (ICVF) was low in WM tracts connecting left caudate nucleus with substantia nigra and left pallidum, as well as left thalamus with substantia nigra and left pallidum. Our results evidence rTMS‐induced WM microstructural changes in fronto‐striato‐thalamic circuits and support its efficacy as a therapeutic tool in treating CUD. Further, individual clinical improvement may rely on the patient's individual structural connectivity integrity.

Background Cocaine use disorder (CUD) is a worldwide public health condition which is suggested to induce pathological changes in macro- and microstructure. Treatments with psychosocial and pharmacological approaches achieve only low to moderate effects on dealing with cocaine clinical symptomatology. Novel approaches such as repetitive transcranial magnetic stimulation (rTMS) have gained attention to induce a reduction in CUD symptoms, yet its mechanisms remain partially understood. Here, we sought to elucidate whether rTMS induces changes on white matter (WM) microstructure in frontostriatal circuits after two weeks of therapy in patients with CUD, and to test whether baseline WM microstructure of the same circuits has an effect on clinical improvement. Methods This study consisted of a 2-week, parallel group, double-blind, randomized controlled clinical trial (acute phase) (sham [n = 23] and active [n = 27]), in which patients received two daily sessions of rTMS on the left dorsolateral prefrontal cortex (lDLPFC) as an add-on treatment. We acquired T1-weighted and HARDI-DWI 2-shell sequences at baseline and at two weeks. To elucidate the effects from active rTMS on frontostriatal WM tracts, we extracted NODDI metrics and performed a linear mixed model. We further evaluated the relationship between clinical outcomes in craving and impulsivity and the baseline white matter microstructure. Results After 2 weeks, active rTMS showed a significant increase in neurite density (ICVF or the density of axons and dendrites) compared to sham rTMS in WM tracts connecting left DLPFC with left (β = 0.038, d = -0.278) and right vmPFC (β = 0.034, d = -0.112). Similarly, rTMS showed reduction in orientation dispersion (OD or axon organization) in WM tracts connecting left DLPFC with left caudate nucleus (β = 0.009, d = -0.087), left thalamus (β = 0.006, d = -0.489) and left vmPFC (β = 0.027, d = 0.024). Results also show a greater reduction in craving VAS after 2 weeks rTMS when baseline ICVF was low in WM tracts connecting left caudate nucleus with substantia nigra (β = 22.61, d = 0.729), left pallidum (β = 21.13, d = 0.738), and those connecting left thalamus with substantia nigra (β = 16.30, d = 0.649) and left pallidum (β = 21.92, d = 0.723). Conclusions Our results suggest that rTMS induced white matter microstructural changes between fronto-striato-thalamic regions after 2 weeks. rTMS-induced microstructural changes may depend on the baseline integrity of the connections between the striatum, thalamus, and the substantia nigra. Connections that predicted clinical improvement in CUD. The current results support the efficacy of rTMS as a therapeutic tool in the treatment of CUD. However, the individual clinical improvement may rely on each patient’s state of structural connections integrity.