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The complexity of contemporary cities requires new tools for the Urban Resilience: old approaches based on the "defensive control" and corrective contingency responses, are replaced by "synergy policies" addressed through preventive, adaptable and reversible actions. In this framework, the term Resili(g)ence proposes to combine "Intelligent" values (information, knowledge, anticipation, projection and adaptation) and "Resilient" valences (resistance and recycling, reaction and recovery, renovation and adaptation) in a new responsive and reactive condition, sensory, sensorized and sensitive, at time. In the context of a new Resili(g)ent approach this new sensibility must take in consideration six resilient main topics (water, earth, fire, air, land-use, eco-systems and communities) referring them to a more complex and crossed network of six possible strategic fields of investigation and prospection (Mapping/Managing – Planning/ Landing – Designing/Socializing), which, interconnected, configure also the framework of multiple innovative experiences and integrated approaches today, infra-, intra-, intro-, eco-, info-… and trans- structural and systemic at time. The 3 IN combination "information (trended) + interaction (threaded) + integration (tended)" announces new dynamics of urban planning aimed at advanced interdisciplinary research, oriented to a strategic integration of operating systems and to a holistic view of its multiple dimensions (patrimonial, sensorial, environmental, cultural and social) in new scenarios not only associated with pure informational management (Smart Cities), but also to its network systematic and to its strategic-planning projection (Intelligent Cities). All this, in the same terms of exploration that are defining a new and emerging Advanced Urbanism linked with the KA-AU Project (Knowledge Alliance for Advanced Urbanism), associated to the European Erasmus Project (2015-2018). The contribution proposes a reflection on this new Resili(g)ent approach and on how it influences and modifies urban dynamics and morphology, going beyond the conventional – and conventioned – term of "Resilience" as a rational adaptation to environmental stress to conceive it in a more complex way, with a new eco-, socio- and info- urban-territorial (and cultural) dimension, passing from an space-territory understood (to all scales) as a relational landscape-scenario to a new interactive (land & far) scape-scenario.

Despite the ubiquitous interdependence between one’s own decisions and others’ welfare, and the controversial evidence on the behavioral effect of choosing for others, the neural bases of making decisions for another versus oneself remain unexplored. We investigated whether loss aversion (LA; the tendency to avoid losses over approaching equivalent gains) is modulated by (i) choosing for oneself, other individuals, or both; (ii) knowing or not knowing the other recipients; or (iii) an interaction between these factors. We used fMRI to assess the brain activations associated with choosing whether to accept or reject mixed gambles, either for oneself, for another player, or both, in 2 groups of 28 participants who had or had not briefly interacted with the other players before scanning. Participants displayed higher LA for choices involving their payoff compared with those affecting only the payoff of other, known, players. This “social” modulation of decision-making was found to engage the dorsomedial prefrontal cortex and its inhibitory connectivity to the middle cingulate cortex. This pattern might underpin decision-making for known others via self-other distinction processes associated with dorsomedial prefrontal areas, with this in turn promoting the inhibition of socially oriented responses through the downregulation of the midcingulate node of the empathy network.

Increased decision latency in alcohol use disorder (AUD) has been generally explained in terms of psychomotor slowing. Recent results suggest that AUD patients’ slowed decision-making might rather reflect alterations in the neural circuitry underlying the engagement of controlled processing by salient stimuli. We addressed this hypothesis by testing a relationship between decision latency at the Cambridge Gambling Task (CGT) and intrinsic brain activity in 22 individuals with AUD and 19 matched controls. CGT deliberation time was related to two complementary facets of resting-state fMRI activity, i.e. coherence and intensity, representing early biomarkers of functional changes in the intrinsic brain architecture. For both metrics, we assessed a multiple regression (to test a relationship with deliberation time in the whole sample), and an interaction analysis (to test a significantly different relationship with decision latency across groups). AUD patients’ slowed deliberation time (p

The development of alcohol habits is considered a form of maladaptive reinforced learning, with sustained alcohol use resulting in the strengthening of associative links between consumption and either rewarding, or the lack of aversive, experiences. Despite recent efforts in characterizing decision-making skills in alcohol-use-disorder (AUD), it is still unknown whether impaired behavioural learning in AUD patients reflects a defective processing and anticipation of choice-related, cognitively mediated, emotions such as regret or relief for what might have been under a different choice. We administered a Wheel-of-Fortune (WoF) task to 26 AUD patients and 19 healthy controls, to investigate possible alterations in adjusting choices to the magnitude of experienced regret/relief, and in other facets of decision-making performance such as choice latency. AUD patients displayed both longer deliberation time than healthy controls, and impaired adaptations to previous outcome-related negative emotions. Although further evidence is needed to unveil the cognitive mechanisms underlying AUD patients’ abnormal choice, the present results highlight important implications for the clinical practice, e.g. in terms of cognitive treatments aiming to shape faulty perceptions about negative emotions associated with excessive alcohol exposure.

Decreased punishment sensitivity in alcohol use disorder (AUD) might reflect a reduction in the typical human tendency to overweigh negative choice outcomes compared with equivalent positive ones, that is, 'loss aversion.' While this hypothesis is supported by previous reports of reduced loss aversion in AUD, it is still unknown whether such decreased sensitivity to prospective losses represents a specific facet of altered decision-making or a secondary effect of executive/working-memory impairments. We addressed this issue by assessing whether lower loss aversion in 22 AUD patients compared with 19 healthy controls is explained by their differential executive or working-memory performance and by investigating its neural basis in terms of grey matter density and cortical thickness via voxel- and surface-based morphometry, respectively. A significant decrease of loss aversion in patients, unrelated to their impaired executive/working-memory performance, reflected the reduction of posterior fronto-medial grey matter density and right frontopolar cortical thickness. Rather than their executive deficits, patients' reduced loss aversion reflects the structural damage of the posterior fronto-medial cortex previously associated with solving conflicts at the response level, where earlier functional magnetic resonance imaging (fMRI) studies have shown a 'neural loss aversion' pattern of steeper deactivation for losses than activation for gains, and of the frontopolar cortex in charge of managing competing goals. These findings highlight possible directions for addressing AUD patients' high relapse rate, for example, cognitive-behavioural rehabilitative interventions enhancing the awareness of the adverse outcomes of addiction or neurostimulation protocols targeting the regions processing their salience.

The persistence of addictive behaviours despite their adverse consequences highlights decreased punishment sensitivity as a facet of decision-making impairments in Alcohol Use Disorder (AUD). This attitude departs from the typical loss aversion (LA) pattern, i.e. the stronger sensitivity to negative than positive outcomes, previously associated with striatal and limbic-somatosensory responsiveness in healthy individuals. Consistent evidence highlights decreased LA as a marker of disease severity in AUD, but its neural bases remain largely unexplored. AUD-specific modulations of frontolateral activity by LA were previously related to the higher executive demands of anticipating losses than gains, but the relationship between LA and executive/working-memory performance in AUD is debated. Building on previous evidence of overlapping neural bases of LA during decision-making and at rest, we investigated a possible neural signature of altered LA in AUDs, and its connections with executive skills, in terms of complementary facets of resting-state functioning. In patients, smaller LA than controls, unrelated to executive performance, reflected reduced connectivity within striatal and medial temporal networks, and altered connectivity from these regions to the insular-opercular cortex. AUD-specific loss-related modulations of intrinsic connectivity thus involved structures previously associated both with drug-seeking and with coding the trade-off between appetitive and aversive motivational drives. These findings fit the hypothesis that altered striatal coding of choice-related incentive value, and interoceptive responsiveness to prospective outcomes, enhance neural sensitivity to drug-related stimuli in addictions. LA and its neural bases might prove useful markers of AUD severity and effectiveness of rehabilitation strategies targeting the salience of negative choice outcomes.

Growing evidence highlights the potential of innovative rehabilitative interventions such as cognitive remediation and neuromodulation, aimed at reducing relapses in Alcohol Use Disorder (AUD). Enhancing their effectiveness requires a thorough description of the neural correlates of cognitive alterations in AUD. Past related attempts, however, were limited by the focus on selected neuro-cognitive variables. We aimed to fill this gap by combining, in 22 AUD patients and 18 controls, an extensive neuro-cognitive evaluation and metrics of intrinsic connectivity as highlighted by resting-state brain activity. We addressed an inherent property of intrinsic activity such as intra-network coherence, the temporal correlation of the slow synchronous fluctuations within resting-state networks, representing an early biomarker of alterations in the functional brain architecture underlying cognitive functioning. AUD patients displayed executive impairments involving working-memory, attention and visuomotor speed, reflecting abnormal coherence of activity and grey matter atrophy within default mode, in addition to the attentional and the executive networks. The stronger relationship between fronto-lateral coherent activity and executive performance in patients than controls highlighted possible compensatory mechanisms counterbalancing the decreased functionality of networks driving the switch from automatic to controlled behavior. These results provide novel insights into AUD patients’ cognitive impairments, their neural bases, and possible targets of rehabilitative interventions.

While the discussion on the foundations of social understanding mainly revolves around the notions of empathy, affective mentalizing, and cognitive mentalizing, their degree of overlap versus specificity is still unclear. We took a meta‐analytic approach to unveil the neural bases of cognitive mentalizing, affective mentalizing, and empathy, both in healthy individuals and pathological conditions characterized by social deficits such as schizophrenia and autism. We observed partially overlapping networks for cognitive and affective mentalizing in the medial prefrontal, posterior cingulate, and lateral temporal cortex, while empathy mainly engaged fronto‐insular, somatosensory, and anterior cingulate cortex. Adjacent process‐specific regions in the posterior lateral temporal, ventrolateral, and dorsomedial prefrontal cortex might underpin a transition from abstract representations of cognitive mental states detached from sensory facets to emotionally‐charged representations of affective mental states. Altered mentalizing‐related activity involved distinct sectors of the posterior lateral temporal cortex in schizophrenia and autism, while only the latter group displayed abnormal empathy related activity in the amygdala. These data might inform the design of rehabilitative treatments for social cognitive deficits., The relationship between affective Theory of Mind (ToM), cognitive ToM, and empathy is still unclear. We addressed this issue via coordinate‐based meta‐analyses of previous fMRI data. Empathy and mentalizing engaged frontoinsular and classical ToM nodes, respectively. Adjacent regions might underpin graded transitions between ToM and mentalizing. Autistic and schizophrenic patients displayed specific patterns of altered activity.

Previous inconsistencies on the effects of implicitly processing positively - vs. negatively - connotated emotional words might reflect the influence of uncontrolled psycholinguistic dimensions, and/or social facets inherent in putative “emotional” stimuli. Based on the relevance of social features in semantic cognition, we developed a socio-emotional Stroop task to assess the influence of social vs. individual (non-social) emotional content, besides negative vs. positive valence, on implicit word processing. The effect of these variables was evaluated in terms of performance and RTs, alongside associated brain activity/connectivity. We matched conditions for several psycholinguistic variables, and assessed a modulation of brain activity/connectivity by trial-wise RT, to characterize the maximum of condition- and subject-specific variability. RTs were tracked by insular and anterior cingulate activations likely reflecting implicit attention to stimuli, interfering with task-performance based on condition-specific processing of their subjective salience. Slower performance for negative than neutral/positive words was tracked by left-hemispheric structures processing negative stimuli and emotions, such as fronto-insular cortex, while the lack of specific activations for positively-connotated words supported their marginal facilitatory effect. The speeding/slowing effects of processing positive/negative individual emotional stimuli were enhanced by social words, reflecting in specific activations of the right anterior temporal and orbitofrontal cortex, respectively. RTs to social positive and negative words modulated connectivity from these regions to fronto-striatal and sensorimotor structures, respectively, likely promoting approach vs. avoidance dispositions shaping their facilitatory vs. inhibitory effect. These results might help assessing the neural correlates of impaired social cognition and emotional regulation, and the effects of rehabilitative interventions.

We have previously shown that activity and connectivity within and between the action observation and mentalizing brain systems reflect the degree of positive dimensions expressed by social interactions such as cooperativity and affectivity, respectively. Here we aim to extend this evidence by investigating the neural bases of processing negative dimensions of observed interactions, such as competition and affective conflict, possibly representing a benchmark for different pathological conditions. In this fMRI study 34 healthy participants were shown pictures depicting interactions characterized by two crossed dimensions, i.e. positively- vs. negatively- connotated social intentions mainly expressed in terms of motor acts vs. mental states, i.e. cooperative, competitive, affective and conflicting interactions. We confirmed the involvement of the action observation and mentalizing networks in processing intentions mainly expressed through motor acts (cooperative/competitive) vs. mental states (affective/conflicting), respectively. Results highlighted the selective role of the left pSTS/TPJ in decoding social interactions, even when compared with parallel actions by non-interacting individuals. Its right-hemispheric homologue displayed stronger responses to negative than positive social intentions, regardless of their motor/mental status, and decreased connectivity with the medial prefrontal cortex (mPFC) when processing negative interactions. The resulting mPFC downregulation by negative social scenes might reflect an adaptive response to socio-affective threats, via decreased mentalizing when facing negative social stimuli. This evidence on the brain mechanisms underlying the decoding of real complex interactions represents a baseline for assessing both the neural correlates of impaired social cognition, and the effects of rehabilitative treatments, in neuro-psychiatric diseases or borderline conditions such as loneliness.

Alcohol Use Disorder (AUD) is a chronic relapsing condition characterized by excessive alcohol consumption despite its multifaceted adverse consequences, associated with impaired performance in several cognitive domains including decision-making. While choice deficits represent a core component of addictive behavior, possibly consecutive to brain changes preceding the onset of the addiction cycle, the evidence on grey-matter and white-matter damage underlying abnormal choices in AUD is still limited. To fill this gap, we assessed the neurostructural bases of decision-making performance in 22 early-abstinent alcoholic patients and 18 controls, by coupling the Cambridge Gambling Task(CGT) with quantitative magnetic resonance imaging metrics of grey-matter density and white-matter integrity. Regardless of group, voxel based morphometry highlighted an inverse relationship between deliberation time and grey-matter density, with alcoholics displaying slower choices related to grey-matter atrophy in key nodes of the motor control network. In particular, grey-matter density in the supplementary motor area, reduced in alcoholic patients, explained a significant amount of variability in their increased deliberation time. Tract-based spatial statistics revealed a significant relationship betweenCGT deliberation time and all white-matter indices, involving the most relevant commissural, projection and associative tracts. The lack of choice impairments other than increased deliberation time highlights reduced processing speed, mediated both by grey-matter and white-matter alterations, as a possible marker of a generalized executive impairment extending to the output stages of decision-making. These results pave the way to further studies aiming to tailor novel rehabilitation strategies and assess their functional outcomes.

Highlights • Alcohol User Disorder (AUD) entails widespread white-matter (WM) alterations. • WM alterations underlie the typical profile of executive impairment in AUD. • Executive profile in AUD is related to WM tracts connecting large-scale networks. • Altered large-scale structural connections may promote maladaptive behavior in AUD., Alcohol Use Disorders (AUD) is associated with negative consequences on global functioning, likely reflecting chronic changes in brain morphology and connectivity. Previous attempts to characterize cognitive impairment in AUD addressed patients’ performance in single domains, without considering their cognitive profile as a whole. While altered cognitive performance likely reflects abnormal white-matter microstructural properties, to date no study has directly addressed the relationship between a proxy of patients’ cognitive profile and microstructural damage. To fill this gap we aimed to characterize the microstructural damage pattern, and its relationship with cognitive profile, in treatment-seeking AUD patients. Twenty-two AUD patients and 18 healthy controls underwent a multimodal MRI protocol including diffusion tensor imaging (DTI), alongside a comprehensive neurocognitive assessment. We used a principal component analysis (PCA) to identify superordinate components maximally explaining variability in cognitive performance, and whole-brain voxelwise analyses to unveil the neural correlates of AUD patients’ cognitive impairment in terms of different white-matter microstructural features, i.e. fractional anisotropy (FA), mean diffusivity (MD), axial diffusivity (AD) and radial diffusivity (RD). PCA revealed a basic executive component, significantly impaired in AUD patients, associated with tasks tapping visuo-motor processing speed, attention and working-memory. Within a widespread pattern of white-matter damage in patients, we found diverse types of relationship linking WM microstructure and executive performance: (i) in the whole sample, we observed a linear relationship involving MD/RD metrics within both ‘superficial’ white-matter systems mediating connectivity within large-scale brain networks, and deeper systems modulating their reciprocal connections; (ii) in AUD patients vs. controls, a performance-by-group interaction highlighted a MD/AD pattern involving two frontal white-matter systems, including the genu of corpus callosum and cingulum bundle, mediating structural connectivity among central executive, salience and default mode networks. Alterations of prefrontal white-matter pathways are suggestive of abnormal structural connectivity in AUD, whereby a defective interplay among large-scale networks underpins patients’ executive dysfunction. These findings highlight different directions for future basic and translational research aiming to tailor novel rehabilitation strategies and assess their functional outcomes.

The neural bases of cognitive impairment(s) in alcohol use disorders (AUDs) might reflect either a global brain damage underlying different neuro-cognitive alterations, or the involvement of specific regions mostly affected by alcohol neuro-toxic effects. While voxel-based-morphometry (VBM) studies have shown a distributed atrophic pattern in fronto-limbic and cerebellar structures, the lack of comprehensive neuro-cognitive assessments prevents previous studies from drawing robust inferences on the specificity of the association between neuro-structural and cognitive impairments in AUDs. To fill this gap, we addressed the neuro-structural bases of cognitive impairment in AUDs, by coupling VBM with an in-depth neuropsychological assessment. VBM results highlighted a diffuse pattern of grey matter reduction in patients, involving the key-nodes of the meso-cortico-limbic (striatum, hippocampus, medial prefrontal cortex), salience (insular and dorsal anterior cingulate cortex) and executive (inferior frontal cortex) networks. Grey matter density in the insular and anterior cingulate sectors of the salience network, significantly decreased in patients, explained almost half of variability in their defective attentional and working-memory performance. The multiple cognitive and neurological impairments observed in AUDs might thus reflect a specific executive deficit associated with the selective damage of a salience-based neural mechanism enhancing access to cognitive resources required for controlled cognition and behaviour.

Background: Alzheimer’s Disease (AD) is a multifactorial disorder driven by genetic and modifiable lifestyle risk factors. Lifestyle primary prevention initiatives may reduce the prevalence and incidence of dementia in older adults. Objectives: The E.Mu.N.I study is a randomized controlled trial investigating the effect of multilevel non-pharmacologic interventions on cognitive performances (primary outcome) and structural and vascular brain MRI markers (secondary outcome), as well as markers of brain functional connectivity change (exploratory outcome), in older adults with subjective memory decline (SMD). Here, we present the study design and the baseline features of the sample. Methods: Cognitively intact older adults with SMD, enrolled between February 2016 and June 2017, were randomly assigned to one of the 3 interventions for 1 year: Active Control Intervention (ACI), i.e., educational lessons; Partial Intervention (PI), i.e., homotaurine administration (100 mg/die) and lessons on the Mediterranean diet; Multilevel Intervention (MI), i.e., PI plus computerized cognitive training and physical exercise training. Results: One-hundred and twenty-eight eligible participants were enrolled (66% female; age: 68 ± 5 years). Eighty-two percent of the sample was composed of volunteers with SMD from the community. Participants were randomly allocated to the interventions as follows: ACI (N = 40), PI (N = 44), MI (N = 44). No significant differences among groups emerged on socio-demographic, clinical–neuropsychological variables and MRI markers at baseline. Conclusions: The outcomes obtained from the E.Mu.N.I. study will clarify the efficacy of multilevel non-pharmacologic interventions on cognitive and neuroimaging markers in SMD individuals. This is a crucial step forward for the development of cost-effective non-pharmacologic primary prevention initiatives for AD.

Alcohol Use Disorder (AUD) entails chronic effects on brain structure. Neurodegeneration due to alcohol toxicity is a neural signature of executive impairment typically observed in AUD, previously related to both gray-matter volume/density and white-matter abnormalities. Recent studies highlighted the role of meso-cortico-limbic structures supporting the salience and executive networks, in which the extent of neurostructural damage is significantly related to patients' executive performance. Here we aim to integrate multimodal information on gray-matter and white-matter features with a multivariate data-driven approach (joint Independent Component Analysis, jICA), and to assess the relationship between the extent of damage in the resulting neurostructural superordinate components and executive profile in AUD. Twenty-two AUD patients and 18 matched healthy controls (HC) underwent a Magnetic Resonance Imaging (MRI) protocol, alongside clinical and neuropsychological examinations. We ran jICA on five neurostructural features, including gray-matter density and different diffusion tensor imaging metrics. We extracted 12 Independent Components (ICs) and compared the resulting mixing coefficients in patients vs. HC. Finally, we correlated significant ICs with executive and clinical variables. One out of 12 ICs (IC11) discriminated patients from healthy controls and correlated positively both with executive performance in all subjects, and with lifetime duration of alcohol abuse in patients. In line with previous related evidence, this component involved widespread gray-matter and white-matter patterns including key nodes and fiber tracts of salience, default-mode and central executive networks. These findings highlighted the role of multivariate data integration as a valuable approach revealing superordinate hallmarks of neural changes related to cognition in neurological and psychiatric populations.

The neural bases of cognitive impairment(s) in alcohol use disorders (AUDs) have been explained either with the specific involvement of frontal regions mostly affected by alcohol neurotoxic effects, or with a global brain damage underlying different neuro-cognitive alterations. Novel insights into this issue might come from the analysis of resting-state brain activity, representing a baseline level of intrinsic connectivity within and between the networks underlying cognitive performance. We thus addressed the neural bases of cognitive impairment(s) in 22 AUD patients, compared with 18 healthy controls, by coupling resting-state fMRI with an in-depth neuropsychological assessment of the main cognitive domains. We assessed a relationship between AUD patients' cognitive impairment and two complementary facets of intrinsic brain functioning, i.e., intensity of activation and functional network connectivity, related to the strength of connectivity within and between resting-state networks, respectively. Alcoholic patients' decreased cognitive performance involved specifically an executive domain associated with attentional and working-memory tasks. This impairment reflected an abnormal relationship, in patients versus controls, between cognitive performance and the intensity of intrinsic activity in the dorsolateral prefrontal and striatal nodes of the executive control network. Functional connectivity between the same structures was positively correlated with executive performance in the whole sample, but significantly reduced in patients. The present data suggest that AUD patients' executive impairment reflects dysfunctional connectivity between the cortical and subcortical nodes of the networks underlying cognitive control on goal-directed behavior. This evidence provides a baseline for future studies addressing the abnormal neural architecture underlying cognitive impairment in AUDs and the outcome of rehabilitative treatment.

Decoding the meaning of others’ actions, a crucial step for social cognition, involves different neural mechanisms. While the “mirror” and “mentalizing” systems have been associated with, respectively, the processing of biological actions versus more abstract information, their respective contribution to intention understanding is debated. Processing social interactions seems to recruit both neural systems, with a different weight depending on cues emphasizing either shared action goals or shared mental states. We have previously shown that observing cooperative and affective social interactions elicits stronger activity in key nodes of, respectively, the mirror (left posterior superior temporal sulcus (pSTS), superior parietal cortex (SPL), and ventral/dorsal premotor cortex (vPMC/dPMC)) and mentalizing (ventromedial prefrontal cortex (vmPFC)) systems. To unveil their causal organization, we investigated the effective connectivity underlying the observation of human social interactions expressing increasing cooperativity (involving left pSTS, SPL, and vPMC) versus affectivity (vmPFC) via dynamic causal modeling in 36 healthy human subjects. We found strong evidence for a model including the pSTS and vPMC as input nodes for the observed interactions. The extrinsic connectivity of this model undergoes oppositely valenced modulations, with cooperativity promoting positive modulations of connectivity between pSTS and both SPL (forward) and vPMC (mainly backward), and affectivity promoting reciprocal positive modulations of connectivity between pSTS and vmPFC (mainly backward). Alongside fMRI data, such divergent effective connectivity suggests that different dimensions underlying the processing of social interactions recruit distinct, although strongly interconnected, neural pathways associated with, respectively, the bottom–up visuomotor processing of motor intentions, and the top–down attribution of affective/mental states.

Background and aim Despite an extensive literature on cognitive impairments in focal and generalized epilepsy, only a few number of studies specifically explored social cognition disorders in epilepsy syndromes. The aim of our study was to investigate social cognition abilities in patients with temporal lobe epilepsy (TLE) and in patients with idiopathic generalized epilepsy (IGE). Materials and methods Thirty-nine patients (21 patients with TLE and 18 patients with IGE) and 21 matched healthy controls (HCs) were recruited. All subjects underwent a basic neuropsychological battery plus two experimental tasks evaluating emotion recognition from facial expression (Ekman-60-Faces test, Ek-60F) and mental state attribution (Story-based Empathy Task, SET). In particular, the latter is a newly developed task that assesses the ability to infer others' intentions (i.e., intention attribution — IA) and emotions (i.e., emotion attribution — EA) compared with a control condition of physical causality (i.e., causal inferences — CI). Results Compared with HCs, patients with TLE showed significantly lower performances on both social cognition tasks. In particular, all SET subconditions as well as the recognition of negative emotions were significantly impaired in patients with TLE vs. HCs. On the contrary, patients with IGE showed impairments on anger recognition only without any deficit at the SET task. Discussion Emotion recognition deficits occur in patients with epilepsy, possibly because of a global disruption of a pathway involving frontal, temporal, and limbic regions. Impairments of mental state attribution specifically characterize the neuropsychological profile of patients with TLE in the context of the in-depth temporal dysfunction typical of such patients. Conclusion Impairments of socioemotional processing have to be considered as part of the neuropsychological assessment in both TLE and IGE in view of a correct management and for future therapeutic interventions.

Neuroeconomics is providing insights into the neural bases of decision-making in normal and pathological conditions. In the neuropsychiatric domain, this discipline investigates how abnormal functioning of neural systems associated with reward processing and cognitive control promotes different disorders, and whether such evidence may inform treatments. This endeavor is crucial when studying different types of addiction, which share a core promoting mechanism in the imbalance between impulsive subcortical neural signals associated with immediate pleasurable outcomes and inhibitory signals mediated by a prefrontal reflective system. The resulting impairment in behavioral control represents a hallmark of alcohol use disorders (AUDs), a chronic relapsing disorder characterized by excessive alcohol consumption despite devastating consequences. This review aims to summarize available magnetic resonance imaging (MRI) evidence on reward-related decision-making alterations in AUDs, and to envision possible future research directions. We review functional MRI (fMRI) studies using tasks involving monetary rewards, as well as MRI studies relating decision-making parameters to neurostructural gray- or white-matter metrics. The available data suggest that excessive alcohol exposure affects neural signaling within brain networks underlying adaptive behavioral learning via the implementation of prediction errors. Namely, weaker ventromedial prefrontal cortex activity and altered connectivity between ventral striatum and dorsolateral prefrontal cortex likely underpin a shift from goal-directed to habitual actions which, in turn, might underpin compulsive alcohol consumption and relapsing episodes despite adverse consequences. Overall, these data highlight abnormal fronto-striatal connectivity as a candidate neurobiological marker of impaired choice in AUDs. Further studies are needed, however, to unveil its implications in the multiple facets of decision-making.

Background Limbic encephalitis (LE) is characterized by an acute or subacute onset with memory impairments, confusional state, behavioral disorders, variably associated with seizures and dystonic movements. It is due to inflammatory processes that selectively affect the medial temporal lobe structures. Voltage-gate potassium channel (VGKC) autoantibodies are frequently observed. In this study, we assessed at the individual level FDG-PET brain metabolic dysfunctions and neuropsychological profiles in three autoimmune LE cases seropositive for neuronal VGKC-complex autoantibodies. Materials and methods LGI1 and CASPR2 potassium channel complex autoantibody subtyping was performed. Cognitive abilities were evaluated with an in-depth neuropsychological battery focused on episodic memory and affective recognition/processing skills. FDG-PET data were analyzed at single-subject level according to a standardized and validated voxel-based Statistical Parametric Mapping (SPM) method. Results Patients showed severe episodic memory and fear recognition deficits at the neuropsychological assessment. No disorder of mentalizing processing was present. Variable patterns of increases and decreases of brain glucose metabolism emerged in the limbic structures, highlighting the pathology-driven selective vulnerability of this system. Additional involvement of cortical and subcortical regions, particularly in the sensorimotor system and basal ganglia, was found. Conclusions Episodic memory and fear recognition deficits characterize the cognitive profile of LE. Commonalities and differences may occur in the brain metabolic patterns. Single-subject voxel-based analysis of FDG-PET imaging could be useful in the early detection of the metabolic correlates of cognitive and non-cognitive deficits characterizing LE condition.

Impairments in the ability to recognize and attribute emotional states to others have been described in amyotrophic lateral sclerosis patients and linked to the dysfunction of key nodes of the emotional empathy network. Microstructural correlates of such disorders are still unexplored. We investigated the white-matter substrates of emotional attribution deficits in a sample of amyotrophic lateral sclerosis patients without cognitive decline. Thirteen individuals with either probable or definite amyotrophic lateral sclerosis and 14 healthy controls were enrolled in a Diffusion Tensor Imaging study and administered the Story-based Empathy Task, assessing the ability to attribute mental states to others (i.e., Intention and Emotion attribution conditions). As already reported, a significant global reduction of empathic skills, mainly driven by a failure in Emotion Attribution condition, was found in amyotrophic lateral sclerosis patients compared to healthy subjects. The severity of this deficit was significantly correlated with fractional anisotropy along the forceps minor, genu of corpus callosum, right uncinate and inferior fronto-occipital fasciculi. The involvement of frontal commissural fiber tracts and right ventral associative fronto-limbic pathways is the microstructural hallmark of the impairment of high-order processing of socio-emotional stimuli in amyotrophic lateral sclerosis. These results support the notion of the neurofunctional and neuroanatomical continuum between amyotrophic lateral sclerosis and frontotemporal dementia.

Background bvFTD patients display an impairment in the attribution of cognitive and affective states to others, reflecting GM atrophy in brain regions associated with social cognition, such as amygdala, superior temporal cortex and posterior insula. Distinctive patterns of abnormal brain functioning at rest have been reported in bvFTD, but their relationship with defective attribution of affective states has not been investigated. Objective To investigate the relationship among resting-state brain activity, gray matter (GM) atrophy and the attribution of mental states in the behavioral variant of fronto-temporal degeneration (bvFTD). Methods We compared 12 bvFTD patients with 30 age- and education-matched healthy controls on a) performance in a task requiring the attribution of affective vs. cognitive mental states; b) metrics of resting-state activity in known functional networks; and c) the relationship between task-performances and resting-state metrics. In addition, we assessed a connection between abnormal resting-state metrics and GM atrophy. Results Compared with controls, bvFTD patients showed a reduction of intra-network coherent activity in several components, as well as decreased strength of activation in networks related to attentional processing. Anomalous resting-state activity involved networks which also displayed a significant reduction of GM density. In patients, compared with controls, higher affective mentalizing performance correlated with stronger functional connectivity between medial prefrontal sectors of the default-mode and attentional/performance monitoring networks, as well as with increased coherent activity in components of the executive, sensorimotor and fronto-limbic networks. Conclusions Some of the observed effects may reflect specific compensatory mechanisms for the atrophic changes involving regions in charge of affective mentalizing. The analysis of specific resting-state networks thus highlights an intermediate level of analysis between abnormal brain structure and impaired behavioral performance in bvFTD, reflecting both dysfunction and compensation mechanisms., Highlights • bvFTD patients are impaired in the attribution of mental states to others (theory of mind, ToM). • bvFTD patients' ToM deficit involves mainly the attribution of affective states. • Affective ToM deficits in bvFTD reflect gray matter atrophy in frontolimbic areas. • Affective ToM deficits in bvFTD reflect altered frontomedial resting-state activity. • Brain activity at rest reflects both dysfunction and compensation mechanisms in bvFTD.