Categoría: Papers con abstracts

Disentangling interoception: insights from focal strokes affecting the perception of external and internal milieus. Autores Couto B, Adolfi F, Sedeño L, Salles A, Canales-Johnson A, Alvarez-Abut P, Garcia-Cordero I, Pietto M, Bekinschtein T, Sigman M, Manes F, Ibanez A. Año 2015 Journal  Couto B, Adolfi F, Sedeño L, Salles A, Canales-Johnson A, Alvarez-Abut P, Garcia-Cordero I, … Leer más

Impairments in negative emotion recognition and empathy for pain in Huntington’s disease families. Autores Báez S, Herrera E, Gershanik O, García A, Bocanegra Y, Kargieman L, Manes F, Ibanez A. Año 2015 Journal  Báez S, Herrera E, Gershanik O, García A, Bocanegra Y, Kargieman L, Manes F, Ibanez A. Volumen Abstract   Otra información    

The roles of interoceptive sensitivity and metacognitive interoception in panic. Autores Yoris A, Esteves S, Couto B, Melloni M, Kichic R, Cetkovich M, Favaloro R, Moser J, Manes F, Ibanez A, Sedeño L. Año 2015 Journal  Yoris A, Esteves S, Couto B, Melloni M, Kichic R, Cetkovich M, Favaloro R, Moser J, Manes F, Ibanez A, Sedeño … Leer más

Social cognition impairments are pervasive in the frontotemporal dementias (FTD). These deficits would be triggered by (a) basic emotion and face recognition processes as well as by (b) higher level social cognition (e.g., theory of mind, ToM). Both emotional processing and social cognition impairments have been previously reported in the behavioral variant of FTD (bvFTD) and also in other versions of FTDs, including primary progressive aphasia. However, no neuroanatomic comparison between different FTD variants has been performed. We report selective behavioral impairments of face recognition, emotion recognition, and ToM in patients with bvFTD and progressive non-fluent aphasia (PNFA) when compared to controls. Voxel-based morphometry (VBM) shows a classical impairment of mainly orbitofrontal (OFC), anterior cingulate (ACC), insula and lateral temporal cortices in patients. Comparative analysis of regional gray matter related to social cognition deficits (VBM) reveals a differential pattern of fronto-insulo-temporal atrophy in bvFTD and an insulo-temporal involvement in PNFA group. Results suggest that in spite of similar social cognition impairments reported in bvFTD and PNFA, the former represents an inherent ToM affectation whereas in the PNFA these deficits could be related to more basic processes of face and emotion recognition. These results are interpreted in the frame of the fronto-insulo-temporal social context network model (SCNM).

Objectives: To assess brain functional connectivity and variability in adults with attention deficit/hyperactivity disorder (ADHD) or euthymic bipolar disorder (BD) relative to a control (CT) group.

Methods: Electroencephalography (EEG) was measured in 35 participants (BD = 11; ADHD = 9; CT = 15) during an eyes-closed 10-min rest period, and connectivity and graph theory metrics were computed. A coefficient of variation (CV) computed also the connectivity’s temporal variability of EEG. Multivariate associations between functional connectivity and clinical and neuropsychological profiles were evaluated.

Results: An enhancement of functional connectivity was observed in the ADHD (fronto-occipital connections) and BD (diffuse connections) groups. However, compared with CTs, intrinsic variability (CV) was enhanced in the ADHD group and reduced in the BD group. Graph theory metrics confirmed the existence of several abnormal network features in both affected groups. Significant associations of connectivity with symptoms were also observed. In the ADHD group, temporal variability of functional connections was associated with executive function and memory deficits. Depression, hyperactivity and impulsivity levels in the ADHD group were associated with abnormal intrinsic connectivity. In the BD group, levels of anxiety and depression were related to abnormal frontotemporal connectivity.

Conclusions: In the ADHD group, we found that intrinsic variability was associated with deficits in cognitive performance and that connectivity abnormalities were related to ADHD symptomatology. The BD group exhibited less intrinsic variability and more diffuse long-range brain connections, and those abnormalities were related to interindividual differences in depression and anxiety. These preliminary results are relevant for neurocognitive models of abnormal brain connectivity in both disorders.

Recent advances in neuroscience have provided new insights into the understanding of heart-brain interaction and communication. Cardiac information to the brain relies on two pathways, terminating in the insular (IC) and anterior cingulate (ACC) cortices, along with the somatosensory cortex (S1-S2). Interoception relying on these neuroanatomical pathways has been shown to modulate social cognition. We report the case study of C.S., a patient with an «external heart » (an extracorporeal left-univentricular cardiac assist device, LVAD). The patient was assessed with neural/behavioral measures of cardiac interoception complemented by neuropsychological and social cognition measures. The patient’s performance on the interoception task (heartbeat detection) seemed to be guided by signals from the artificial LVAD, which provides a somatosensory beat, rather than by his endogenous heart. Cortical activity (heart-evoked potential, HEP) decreased in comparison to normal volunteers, particularly during interoceptive states. The patient accurately performed several cognitive tasks, expect for empathy, theory of mind and decision-making. This evidence suggests an imbalance in the patient’s cardiac interoceptive pathways that enhances sensation driven by the artificial pump over that from the cardiac vagal-ICC-ACC pathway. A patient with two hearts, one endogenous and one artificial, presents a unique opportunity to explore models of interoception and heart-brain interaction

This Research Topic features several papers tapping the situated nature of emotion and social cognition processes. The volume covers a broad scope of methodologies [behavioral assessment, functional magnetic resonance imaging (fMRI), structural neuroimaging, event-related potentials (ERPs), brain connectivity, and peripheral measures], populations (non-human animals, neurotypical participants, developmental studies, and neuropsychiatric and pathological conditions), and article types (original research, review papers, and opinion articles). Through this wide-ranging proposal, we introduce a fresh approach to the study of contextual effects in emotion and social cognition domains. We report four levels of evidence. First, we present studies examining how cognitive and neural functions are influenced by basic affective processes (interoception, motivation and reward, emotional impulsiveness, and appraisal of violent stimuli). A second set of behavioral and neuroscientific studies addresses how performance is modulated by different emotional variables (categorical and dimensional approaches to emotion, language-as-context for emotion, emotional suppression of the attentional blink, and reappraisal effects on the up-regulation of emotions). The studies in our third selection deal with different influences in social cognition (SC) domains (human and non-human comparative studies, long-term effects of social and physical stress, developmental theory of mind, neural bases of passionate love for others, social decision making in normal and psychopathic participants, and frontal lobe contributions to psychosocial adaptation models). Finally, the fourth set of papers investigates the blending of social and emotion-related processes (valence and social salience in amygdala networks, emotional contributions to identification of genuine and faked social expressions, emotional predispositions and social decision making bias, valence of fairness and social decisions, structural neuroimaging of emotional and social impairments in neurodegenerative diseases, and subjective reactivity to emotional stimuli and their association with moral cognition). A brief summary of all these studies is offered in the following sections.

Traditionally, Huntington´s disease (HD) has been known as a movement disorder, characterized by motor, psychiatric, and cognitive impairments. Recent studies have shown that motor and action–language processes are neurally associated. The cognitive mechanisms underlying this interaction have been investigated through the action compatibility effect (ACE) paradigm, which induces a contextual coupling of ongoing motor actions and verbal processing. The present study is the first to use the ACE paradigm to evaluate action–word processing in HD patients (HDP) and their families. Specifically, we tested three groups: HDP, healthy first-degree relatives (HDR), and non-relative healthy controls. The results showed that ACE was abolished in HDP as well as HDR, but not in controls. Furthermore, we found that the processing deficits were primarily linguistic, given that they did not correlate executive function measurements. Our overall results underscore the role of cortico-basal ganglia circuits in action–word processing and indicate that the ACE task is a sensitive and robust early biomarker of HD and familial vulnerability.

Although motor-language coupling is now being extensively studied, its underlying mechanisms are not fully understood. In this sense, a crucial opposition has emerged between the non-representational and the representational views of embodiment. The former posits that action language is grounded on the non-brain motor system directly engaged by musculoskeletal activity – i.e., peripheral involvement of ongoing actions. Conversely, the latter proposes that such grounding is afforded by the brain´s motor system – i.e., activation of neural areas representing motor action. We addressed this controversy through the action-sentence compatibility effect (ACE) paradigm, which induces a contextual coupling of motor actions and verbal processing. ACEs were measured in three patient groups – early Parkinson´s disease (EPD), neuromyelitis optica (NMO), and acute transverse myelitis (ATM) patients – as well as their respective healthy controls. NMO and ATM constitute models of injury to non-brain motor areas and the peripheral motor system, whereas EPD provides a model of brain motor system impairment. In our study, EPD patients exhibited impaired ACE and verbal processing relative to healthy participants, NMO, and ATM patients. These results indicate that the processing of action-related words is mainly subserved by a cortico-subcortical motor network system, thus supporting a brain-based embodied view on action language. More generally, our findings are consistent with contemporary perspectives for which action/verb processing depends on distributed brain networks supporting context-sensitive motor-language coupling.

An enduring question is unity vs. separability of executive deficits resulting from impaired frontal lobe function. In previous studies, we have asked how executive deficits link to a conventional measure of fluid intelligence, obtained either by standard tests of novel problem-solving, or by averaging performance in a battery of novel tasks. For some classical executive tasks, such as the Wisconsin Card Sorting Test (WCST), Verbal Fluency, and Trail Making Test B (TMTB), frontal deficits are entirely explained by fluid intelligence. However, on a second set of executive tasks, including tests of multitasking and decision making, deficits exceed those predicted by fluid intelligence loss. In this paper we discuss how these results shed light on the diverse clinical phenomenology observed in frontal dysfunction, and present new data on a group of 15 schizophrenic patients and 14 controls. Subjects were assessed with a range of executive tests and with a general cognitive battery used to derive a measure of fluid intelligence. Group performance was compared and fluid intelligence was introduced as a covariate. In line with our previous results, significant patient-control differences in classical executive tests were removed when fluid intelligence was introduced as a covariate. However, for tests of multitasking and decision making, deficits remained. We relate our findings to those of previous factor analytic studies describing a single principal component, which accounts for much of the variance of schizophrenic patients’ cognitive performance. We propose that this general factor reflects low fluid intelligence capacity, which accounts for much but not all cognitive impairment in this patient group. Partialling out the general effects of fluid intelligence, we propose, may clarify the role of additional, more specific cognitive impairments in conditions such as schizophrenia.