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Transcranial magnetic stimulation (TMS) has become a promising strategy for bipolar disorder (BD). This study reviews neuroimaging findings, indicating functional, structural, and metabolic brain changes associated with TMS in BD. Web of Science, Embase, Medline, and Google Scholar were searched without any restrictions for studies investigating neuroimaging biomarkers, through structural magnetic resonance imaging (MRI), diffusion tensor imaging (DTI), functional MRI (fMRI), magnetic resonance spectroscopy (MRS), positron emission tomography (PET), and single photon emission computed tomography (SPECT), in association with response to TMS in patients with BD. Eleven studies were included (fMRI = 4, MRI = 1, PET = 3, SPECT = 2, and MRS = 1). Important fMRI predictors of response to repetitive TMS (rTMS) included higher connectivity of emotion regulation and executive control regions. Prominent MRI predictors included lower ventromedial prefrontal cortex connectivity and lower superior frontal and caudal middle frontal volumes. SPECT studies found hypoconnectivity of the uncus/parahippocampal cortex and right thalamus in non-responders. The post-rTMS changes using fMRI mostly showed increased connectivity among the areas neighboring the coil. Increased blood perfusion was reported post-rTMS in PET and SPECT studies. Treatment response comparison between unipolar depression and BD revealed almost equal responses. Neuroimaging evidence suggests various correlates of response to rTMS in BD, which needs to be further replicated in future studies.

Antisocial behavior involves actions that disregard the basic rights of others and may represent a threat to the social system. The neural processes associated with being subject to antisocial behavior, including social victimization, are still unknown. In this study, we used a social interaction task during functional magnetic resonance imaging to investigate the neural bases of social victimization. Brain activation and functional connectivity (FC) were estimated and correlated with the Big 5 Questionnaire, Temperament Evaluation in Memphis, Pisa and San Diego (TEMPS-M), and a Questionnaire of Daily Frustration scores. During social victimization, the right occipital and temporal cortex showed increased activation. The temporal cortex also had reduced FC with homotopic areas. Compared to the prosocial interaction, social victimization showed hyperactivation of the dorsomedial and lateral prefrontal cortex, putamen, and thalamus and increased FC of the medial-frontal–striatal–thalamic areas with the ventrolateral prefrontal cortex, insula, dorsal cingulate, and postcentral gyrus. Lastly, neuroticism, irritable temperament, and frustration scores were correlated with the magnitude of neural responses to social victimization. Our findings suggest that social victimization engages a set of regions associated with salience, emotional processing, and regulation, and these responses can be modulated by temperamental and personality traits.

Suicide ideation and behaviors are major health issues in the field of mental health. Several psychological and psychosocial factors have been taken into account as possible predictors of suicidality. Only recently affective temperaments have been considered as possible factors linked to suicide. This study aims to investigate the relationship between affective temperaments and suicidality, including the lifetime onset of suicide ideation, lifetime presence of suicide attempts and the total number of lifetime suicide attempts. This is a naturalistic multicentric observational study, involving outpatient units of seven University sites in Italy. Patients were administered with the short version of TEMPS-M and the Columbia Suicide Severity Rating Scale. A total of 653 participants were recruited, with a diagnosis of bipolar (55.7%), unipolar (35.8%) and cyclothymic disorder (8.4%). Regression models showed that the presence of lifetime suicide behaviors was increased in patients presenting trait related impulsivity (p < 0.0001), poor free-interval functioning (p < 0.05), higher number of affective episodes (p < 0.01), higher number of hospitalizations (p < 0.0001), cyclothymic and irritable affective temperaments (p < 0.05 and p < 0.05, respectively). Conversely, the presence of hyperthymic affective disposition reduced the likelihood of having suicidal behaviors (p < 0.01). Lifetime suicidal ideation was associated with trait-related impulsivity (p < 0.001), poor free-interval functioning (p < 0.05), higher number of affective episodes (p < 0.001) and of hospitalizations (p < 0.001). Depressive temperaments increased the likelihood of presenting suicidal ideation (p < 0.05), along with irritable temperaments (p < 0.01), contrary to hyperthymic affective (p < 0.05). Results of the present study confirm that affective disposition has a significant impact on the onset of suicidal ideation and behaviors, and that affective dispositions should be assessed in clinical settings to identify people at risk of suicide. Moreover, a wider clinical evaluation, including different clinical psychopathological dimensions, should be taken into consideration to develop effective preventive interventions.

Trait-related impulsiveness is highly prevalent in patients with mood disorders, being associated with negative outcomes. The predictive role of affective temperaments on trait-related impulsivity is still understudied. The aim of the present study is to investigate the relationship between impulsivity and affective temperaments in a sample of euthymic patients with mood disorders. This is a real-world multicentric observational study, carried out at the outpatient units of seven university sites in Italy. All patients filled in the short version of Munster Temperament Evaluation of the Memphis, Pisa, Paris and San Diego and the Barratt Impulsiveness Scale. The study sample included 653 participants, mainly female (58.2%), with a mean age of 46.9 (±14.1). Regression analyses showed that higher levels of trait-related impulsivity were associated to suicide attempts (p < 0.000), the presence of psychotic symptoms during acute phases (p < 0.05), a seasonal pattern (p < 0.05), a lower age at onset of the disorder (p < 0.05), cyclothymic (p < 0.01) and irritable temperaments (p < 0.01). The results of our study highlight the importance to screen patients with mood disorders for impulsivity and affective temperaments in order to identify patients who are more likely to present a worse outcome and to develop personalized and integrated early pharmacological and psychosocial treatment plans. Novelties of the present paper include the recruitment of patients in a stable phase, which reduced possible bias in patients’ self-reports, and the multicentric nature of the study, resulting in the recruitment of a large sample of patients with mood disorders, geographically distributed across Italy, thus improving the generalizability of study results.

The complex structure of the brain supports high-order cognition, which is crucial for mastering chess. Surface-based measures, including the fractional dimension (FD) and gyrification index (GI), may be more sensitive in detecting cortical changes relative to volumetric indexes. For this reason, structural magnetic resonance imaging data from 29 chess experts and 29 novice participants were analyzed using the CAT12 toolbox. FD and GI for each brain region were compared between the groups. A multivariate model was used to identify surface-based brain measures that can predict chess expertise. In chess experts, FD is increased in the left frontal operculum (p < 0.01), and this change correlates with the starting age of chess practice (ρ = −0.54, p < 0.01). FD is decreased in the right superior parietal lobule (p < 0.01). Chess expertise is predicted by the FD in a network of fronto-parieto-temporal regions and is associated with GI changes in the middle cingulate gyrus (p < 0.01) and the superior temporal sulcus (p < 0.01). Our findings add to the evidence that chess expertise is based on the complex properties of the brain surface of a network of transmodal association areas important for flexible high-level cognitive functions. Interestingly, these changes are associated with long-lasting practice, suggesting that neuroplastic effects develop over time.

Polyglutamine (polyQ) expansions in the androgen receptor (AR) gene cause spinal and bulbar muscular atrophy (SBMA), a neuromuscular disease characterized by lower motor neuron (MN) loss and skeletal muscle atrophy, with an unknown mechanism. We generated new mouse models of SBMA for constitutive and inducible expression of mutant AR and performed biochemical, histological and functional analyses of phenotype. We show that polyQ-expanded AR causes motor dysfunction, premature death, IIb-to-IIa/IIx fiber-type change, glycolytic-to-oxidative fiber-type switching, upregulation of atrogenes and autophagy genes and mitochondrial dysfunction in skeletal muscle, together with signs of muscle denervation at late stage of disease. PolyQ expansions in the AR resulted in nuclear enrichment. Within the nucleus, mutant AR formed 2% sodium dodecyl sulfate (SDS)-resistant aggregates and inclusion bodies in myofibers, but not spinal cord and brainstem, in a process exacerbated by age and sex. Finally, we found that two-week induction of expression of polyQ-expanded AR in adult mice was sufficient to cause premature death, body weight loss and muscle atrophy, but not aggregation, metabolic alterations, motor coordination and fiber-type switch, indicating that expression of the disease protein in the adulthood is sufficient to recapitulate several, but not all SBMA manifestations in mice. These results imply that chronic expression of polyQ-expanded AR, i.e. during development and prepuberty, is key to induce the full SBMA muscle pathology observed in patients. Our data support a model whereby chronic expression of polyQ-expanded AR triggers muscle atrophy through toxic (neomorphic) gain of function mechanisms distinct from normal (hypermorphic) gain of function mechanisms.