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No tools are currently available to predict whether a patient suffering from major depressive disorder (MDD) will respond to a certain treatment. Machine learning analysis of magnetic resonance imaging (MRI) data has shown potential in predicting response for individual patients, which may enable personalized treatment decisions and increase treatment efficacy. Here, we evaluated the accuracy of MRI-guided response prediction in MDD. We conducted a systematic review and meta-analysis of all studies using MRI to predict single-subject response to antidepressant treatment in patients with MDD. Classification performance was calculated using a bivariate model and expressed as area under the curve, sensitivity, and specificity. In addition, we analyzed differences in classification performance between different interventions and MRI modalities. Meta-analysis of 22 samples including 957 patients showed an overall area under the bivariate summary receiver operating curve of 0.84 (95% CI 0.81–0.87), sensitivity of 77% (95% CI 71–82), and specificity of 79% (95% CI 73–84). Although classification performance was higher for electroconvulsive therapy outcome prediction (n = 285, 80% sensitivity, 83% specificity) than medication outcome prediction (n = 283, 75% sensitivity, 72% specificity), there was no significant difference in classification performance between treatments or MRI modalities. Prediction of treatment response using machine learning analysis of MRI data is promising but should not yet be implemented into clinical practice. Future studies with more generalizable samples and external validation are needed to establish the potential of MRI to realize individualized patient care in MDD.

Misophonia is characterized by intense rage and disgust provoked by hearing specific human sounds resulting in social isolation due to avoidance. We exposed patients with symptom provoking audiovisual stimuli to investigate brain activity of emotional responses. 21 patients with misophonia and 23 matched healthy controls were recruited at the psychiatry department of the Amsterdam UMC. Participants were presented with three different conditions, misophonia related cues (video clips with e.g. lip smacking and loud breathing), aversive cues (violent or disgusting clips from movies), and neutral cues (video clips of e.g. someone meditating) during fMRI. Electrocardiography was recorded to determine physiological changes and self-report measures were used to assess emotional changes. Misophonic cues elicited anger, disgust and sadness in patients compared to controls. Emotional changes were associated with increases in heart rate. The neuroimaging data revealed increased activation of the right insula, right anterior cingulate cortex and right superior temporal cortex during viewing of the misophonic video clips compared to neutral clips. Our results demonstrate that audiovisual stimuli trigger anger and physiological arousal in patients with misophonia, associated with activation of the auditory cortex and salience network.

In recent years, resting-state (RS) networks and RS function have received increased attention, highlighting their importance in both cognitive function and psychopathology. The neurochemical substrates underlying RS networks and their interactions, however, have not yet been well established. Even though prior research has provided first evidence for a negative association between brain GABA levels and RS connectivity, these findings have been limited to within network connectivity, and not network interactions. In this multi-modal imaging study, we investigated the role of the main inhibitory neurotransmitter У-aminobutyric acid (GABA) and the main excitatory neurotransmitter glutamate (Glx) on RS network function and network coupling of three core networks: the default-mode network (DMN), salience network (SN), and central executive network (CEN). Resting-state functional connectivity and GABA and Glx levels in the dorsal anterior cingulate cortex (dACC) were assessed in 64 healthy male participants using functional MRI and magnetic resonance spectroscopy (MRS). Analyses showed that dACC GABA levels were positively correlated with resting-state connectivity in the CEN, and negatively associated with functional coupling of the DMN and CEN. In contrast, GABA/Glx ratios were inversely correlated with the SN and DMN. These findings extend insights into the role of GABA and Glx in individual networks to interactions across networks, suggesting that GABA levels in the SN might play a role in RS functional connectivity within the central executive network, and network interactions with the default-mode network. Our results further suggest a potentially critical role of the relationship between GABA and Glx in RS network function.

Body Integrity Identity Disorder (BIID) is a condition in which individuals perceive a mismatch between their internal body scheme and physical body shape, resulting in an absolute desire to be either amputated or paralyzed. The condition is hypothesized to be of congenital nature, but evidence for a neuro-anatomical basis is sparse. We collected T1-weighted structural magnetic resonance imaging scans on a 3T scanner in eight individuals with BIID and 24 matched healthy controls, and analyzed the data using voxel-based morphometry. The results showed reduced grey matter volume in the left dorsal and ventral premotor cortices and larger grey matter volume in the cerebellum (lobule VIIa) in individuals with BIID compared to controls. The premotor cortex and cerebellum are thought to be crucial for the experience of body-ownership and the integration of multisensory information. Our results suggest that BIID is associated with structural brain anomalies and might result from a dysfunction in the integration of multisensory information, leading to the feeling of disunity between the mental and physical body shape.

Our body feels like it is ours. However, individuals with body integrity identity disorder (BIID) lack this feeling of ownership for distinct limbs and desire amputation of perfectly healthy body parts. This extremely rare condition provides us with an opportunity to study the neural basis underlying the feeling of limb ownership, since these individuals have a feeling of disownership for a limb in the absence of apparent brain damage. Here we directly compared brain activation between limbs that do and do not feel as part of the body using functional MRI during separate tactile stimulation and motor execution experiments. In comparison to matched controls, individuals with BIID showed heightened responsivity of a large somatosensory network including the parietal cortex and right insula during tactile stimulation, regardless of whether the stimulated leg felt owned or alienated. Importantly, activity in the ventral premotor cortex depended on the feeling of ownership and was reduced during stimulation of the alienated compared to the owned leg. In contrast, no significant differences between groups were observed during the performance of motor actions. These results suggest that altered somatosensory processing in the premotor cortex is associated with the feeling of disownership in BIID, which may be related to altered integration of somatosensory and proprioceptive information.

Trauma-focused psychotherapy is the first-line treatment for posttraumatic stress disorder (PTSD) but 30–50% of patients do not benefit sufficiently. We investigated whether structural and resting-state functional magnetic resonance imaging (MRI/rs-fMRI) data could distinguish between treatment responders and non-responders on the group and individual level. Forty-four male veterans with PTSD underwent baseline scanning followed by trauma-focused psychotherapy. Voxel-wise gray matter volumes were extracted from the structural MRI data and resting-state networks (RSNs) were calculated from rs-fMRI data using independent component analysis. Data were used to detect differences between responders and non-responders on the group level using permutation testing, and the single-subject level using Gaussian process classification with cross-validation. A RSN centered on the bilateral superior frontal gyrus differed between responders and non-responder groups (PFWE < 0.05) while a RSN centered on the pre-supplementary motor area distinguished between responders and non-responders on an individual-level with 81.4% accuracy (P < 0.001, 84.8% sensitivity, 78% specificity and AUC of 0.93). No significant single-subject classification or group differences were observed for gray matter volume. This proof-of-concept study demonstrates the feasibility of using rs-fMRI to develop neuroimaging biomarkers for treatment response, which could enable personalized treatment of patients with PTSD.

The classical cognitive-behavioral theory of obsessive-compulsive disorder (OCD) holds that compulsions are performed to reduce distress that is evoked by obsessions, whereas a recent neuroscience-inspired theory suggests that compulsivity results from a disbalance between goal-directed and habit-related neural networks. To bridge these theories, we investigated whether the balance between goal-directed and habit networks in patients with OCD was affected during psychological distress. Twenty-three OCD patients and twenty-three healthy controls participated in a controlled stress induction paradigm using the socially evaluated cold-pressor test in a crossover design. Stress responses were evaluated through cortisol levels, blood pressure, and anxiety ratings. Functional connectivity of the caudate nucleus and posterior putamen was assessed using seed region analysis of resting-state functional magnetic resonance imaging data, which are hubs of the goal-directed and habit network, respectively. Stress induction increased blood pressure and psychological stress measures across groups and resulted in blunted cortisol responses in patients. Furthermore, patients showed a blunted reduction in connectivity between the caudate nucleus and precuneus during psychological distress, which was positively correlated with compulsivity but not obsession severity. The posterior putamen showed no significant group differences in distress-induced connectivity. These results suggest that compulsivity in OCD is associated with altered connectivity between the goal-directed and default mode networks during psychological distress.

Acute psychological stress can trigger normal and abnormal motivated behaviors such as reward seeking, habitual behavior, and drug craving. Animal research suggests that such effects may result from actions of catecholamines and glucocorticoids that converge in brain regions that regulate motivated behaviors and incentive processing. At present, however, little is known about the acute effects of stress on these circuits in humans. During functional magnetic resonance imaging (fMRI), twenty-seven healthy young women performed a modified version of the monetary incentive delay (MID) task, which is known to robustly engage ventral striatal and medial prefrontal regions. To induce psychological stress, strongly aversive movie clips (versus neutral movie clips) were shown with the instruction to imagine being an eyewitness. Physiological (cortisol levels, heart rate frequency, and heart rate variability) and subjective measurements confirmed successful induction of moderate levels of acute psychological stress. Brain imaging data revealed that stress induction resulted in a significant decrease in reward-related responses in the medial prefrontal cortex (PFC) without affecting ventral striatal responses. Our results thus show that acute psychological stress induces regionally specific changes in functioning of incentive processing circuits. This regional specificity is in line with animal data showing inverted U-shaped relations between levels of stress-related neuromodulators and functioning of the PFC, a structure that is believed to be critical for coordinating behavior in accordance with higher order internal goals. Our findings thus suggest that stress-related increases in habitual and reward-seeking behaviors may be triggered primarily by an impairment of such PFC-dependent cognitive control mechanisms. ► Stress induces regionally specific changes in functioning of reward circuits. ► Acute stress reduces reward-related activity in the medial PFC specifically. ► Reduced medial PFC activity during stress may reflect impaired cognitive control. ► These findings help explain how stress increases habitual and reward-seeking behaviors.

Corticosteroids are potent modulators of human higher cognitive function. They are released in response to stress, and are thought to be involved in the modulation of cognitive function by inducing distinct rapid nongenomic, and slow genomic changes, affecting neural plasticity throughout the brain. However, their exact effects on the neural correlates of higher-order cognitive function as performed by the prefrontal cortex at the human brain system level remain to be elucidated. Here, we targeted these time-dependent effects of corticosteroids on prefrontal cortex processing in humans using a working memory (WM) paradigm during functional MRI scanning. Implementing a randomized, double-blind, placebo-controlled design, 72 young, healthy men received 10 mg hydrocortisone either 30 min (rapid corticosteroid effects) or 240 min (slow corticosteroid effects), or placebo before a numerical n-back task with differential load (0- to 3-back). Corticosteroids' slow effects appeared to improve working memory performance and increased neuronal activity during WM performance in the dorsolateral prefrontal cortex depending on WM load, whereas no effects of corticosteroids' rapid actions were observed. Thereby, the slow actions of corticosteroids seem to facilitate adequate higher-order cognitive functioning, which may support recovery in the aftermath of stress exposure.

Major depressive disorder (MDD) is associated with structural and functional brain abnormalities. MDD as well as brain anatomy and function are influenced by genetic factors, but the role of gene expression remains unclear. Here, this work investigates how cortical gene expression contributes to structural and functional brain abnormalities in MDD. This work compares the gray matter volume and resting‐state functional measures in a Chinese sample of 848 MDD patients and 749 healthy controls, and these case‐control differences are then associated with cortical variation of gene expression. While whole gene expression is positively associated with structural abnormalities, it is negatively associated with functional abnormalities. This work observes the relationships of expression levels with brain abnormalities for individual genes, and found that transcriptional correlates of brain structure and function show opposite relations with gene dysregulation in postmortem cortical tissue from MDD patients. This work further identifies genes that are positively or negatively related to structural abnormalities as well as functional abnormalities. The MDD‐related genes are enriched for brain tissue, cortical cells, and biological pathways. These findings suggest that distinct genetic mechanisms underlie structural and functional brain abnormalities in MDD, and highlight the importance of cortical gene expression for the development of cortical abnormalities. This paper investigates brain abnormalities in MDD, and observes opposite relationships of structural and functional abnormalities with gene expression in both Asian and European populations. Moreover, the transcriptional correlates of brain abnormalities show significant correlations with gene dysregulation in postmortem tissue samples from MDD patients. These findings suggest that distinct genetic mechanisms underlie brain abnormalities.