Delineating common and separable neural alterations in substance use disorders (SUD) is imperative to understand the neurobiological basis of the addictive process and to inform substance-specific treatment strategies. Given numerous functional MRI (fMRI) studies in different SUDs, a meta-analysis could provide an opportunity to determine robust shared and substance-specific alterations. The present study employed a coordinate-based meta-analysis covering fMRI studies in individuals with addictive cocaine, cannabis, alcohol, and nicotine use. The primary meta-analysis

Background: Post-traumatic stress disorder (PTSD) is characterized by deficits in the self-regulation of cognitions and emotions. Neural networks of emotion regulation may exhibit reduced control mediated by the anterior cingulate cortex (ACC), contributing to aberrant limbic responses in PTSD.Methods: Real-time fMRI neurofeedback (rt-fMRI NF) assessed self-regulation of the ACC in nine patients with PTSD after single trauma exposure and nine matched healthy controls. All participants were instructed to train ACC upregulation on three training days.Results: Both groups achieved regulation, which was associated with wide-spread brain activation encompassing the ACC. Compared to the controls, regulation amplitude and learning rate was lower in patients, correlating with symptom severity. In addition, a frontopolar activation cluster was associated with self-regulation efforts in patients.Conclusions: For the first time, we tested self-regulation of the ACC in patients with PTSD. The observed impairment supports models of ACC-mediated regulation deficits that may contribute to the psychopathology of PTSD. Controlled trials in a larger sample are needed to confirm our findings and to directly investigate whether training of central regulation mechanisms improves emotion regulation in PTSD.

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The autonomic nervous system (ANS) receives modulatory input from high-level supra-tentorial brain structures, which affects peripheral physiological measures such as heart rate variability (HRV), respiration, and electrodermal activity (see Beissner, Meissner, Bär, & Napadow, 2013 for a meta-analysis). For instance, in the neurovisceral integration model for HRV (Thayer & Lane, 2009), neocortical areas such as the prefrontal and cingulate cortex exert tonic inhibitory control over brainstem circuitry underlying the ANS regulation. A similar cortico-limbic model has been proposed for sensorimotor integration of respiration (Evans, 2010), with an interplay of volitional respiratory control (pre-motor and supplementary motor area (SMA)) and interoceptive integration areas (anterior cingulate cortex (ACC), insula, and amygdala). These models overlap in core autonomic network areas, including the cingulate cortex, insula, and amygdala

Mismatch responses reflect neural mechanisms of early cognitive processing in the auditory domain. Disturbances of these mechanisms on multiple levels of neural processing may contribute to clinical symptoms in major depression (MD). A functional magnetic resonance imaging (fMRI) study was conducted to identify neurobiological foundations of altered mismatch processing in MD. Twenty‐five patients with major depression and 25 matched healthy individuals completed an auditory mismatch paradigm optimized for fMRI. Brain activity during mismatch processing was compared between groups. Moreover, seed‐based connectivity analyses investigated depression‐specific brain networks. In patients, mismatch processing was associated with reduced activation in the right auditory cortex as well as in a fronto‐parietal attention network. Moreover, functional coupling between the right auditory cortex and frontal areas was reduced in patients. Seed‐to voxel analysis on the whole‐brain level revealed reduced connectivity between the auditory cortex and the thalamus as well as posterior cingulate. The present study indicates deficits in sensory processing on the level of the auditory cortex in depression. Hyposensitivity in a fronto‐parietal network presumably reflects altered attention mechanisms in depression. The observed impairments may contribute to psychopathology by reducing the ability of the affected individuals to orient attention toward important environmental cues.

Compulsivity and loss of behavioral control represent core symptoms in obsessive–compulsive disorder (OCD), substance use disorder (SUD), and internet gaming disorder (IGD). Despite elaborated animal models suggesting that compulsivity is mediated by cortico‐striatal circuits and a growing number of neuroimaging case–control studies, common neurofunctional alterations in these disorders have not been systematically examined. The present activation likelihood estimation (ALE) meta‐analysis capitalized on previous functional magnetic resonance imaging (fMRI) studies to determine shared neurofunctional alterations among the three disorders. Task‐based fMRI studies of individuals with SUD, OCD, or IGD were obtained. ALE was performed within each disorder. Next, contrast and conjunction meta‐analyses were performed to determine differential and common alterations. Task‐paradigm classes were group according to Research Domain Criteria (RDoC) domains to determine contributions of underlying behavioral domains. One hundred forty‐four articles were included representing data from n = 6897 individuals (SUD = 2418, controls = 2332; IGD = 361, controls = 360; OCD = 715, controls = 711) from case–control studies. Conjunction meta‐analyses revealed shared alterations in the anterior insular cortex between OCD and SUDs. SUD exhibited additionally pronounced dorsal‐striatal alterations compared with both, OCD and IGD. IGD shared frontal, particularly cingulate alterations with all SUDs, while IGD demonstrated pronounced temporal alterations compared with both, SUD and OCD. No robust overlap between IGD and OCD was observed. Across the disorders, neurofunctional alterations were mainly contributed by cognitive systems and positive valence RDoC domains. The present findings indicate that neurofunctional dysregulations in prefrontal regions engaged in regulatory‐control represent shared neurofunctional alterations across substance and behavioral addictions, while shared neurofunctional dysregulations in the anterior insula may mediate compulsivity in substance addiction and OCD.

Highlights We found neurofeedback-specific attenuation of amygdala responses. Trauma symptoms and the affective state improved in patients at one-month follow-up. Reduced amygdala responses were associated with improved well-being at follow-up. 75% of individuals with PTSD used the learned strategies in daily life. Left lateral prefrontal cortex responses were reduced during neurofeedback training.