[Activation of brain structures by fMRI data when viewing the video clips and recall of shown actions].

In 10 healthy volunteers, brain tomograms were recorded using an fMRI scanner with a 3T-field magnet. Emotionally neutral and emotionally involving videos were used for stimulation. Registration consisted of seven series: two series of viewing a fixation point and two kinds of video clips, one series of viewing of a succession of two types of video clips, two series of watching videos with subsequent recall, and two series of viewing the fixation point followed by recall of content online. Viewing content online caused the greatest degree of metabolism increase localized in the visual cortex. This activation was more pronounced during the presentation of an emotionally involving video clip. In addition to the occipital lobe, it actively involved the temporal, parietal and, to a lesser extent, the frontal cortex. Activation of the motor cortex was detected only in some subjects. The "interference" effect in which the increase in metabolism was minimal was observed during a consequent demonstration of video-clips. Immediate recall of video-clips after viewing caused the greatest activation of the posterior frontal and motor cortex. Delayed recall activated mostly the anterior frontal cortex. There was a decrease of metabolism in the visual cortex during the recall. The greatest reduction in the visual cortex was observed during immediate recall. Immediate and delayed recall activated the structures associated with the maintenance of consciousness, memory and a system of mirror neurons.

Mirror neurons are modulated by grip force and reward expectation in the sensorimotor cortices (S1, M1, PMd, PMv).

Mirror Neurons (MNs) respond similarly when primates make or observe grasping movements. Recent work indicates that reward expectation influences rostral M1 (rM1) during manual, observational, and Brain Machine Interface (BMI) reaching movements. Previous work showed MNs are modulated by subjective value. Here we expand on the above work utilizing two non-human primates (NHPs), one male Macaca Radiata (NHP S) and one female Macaca Mulatta (NHP P), that were trained to perform a cued reward level isometric grip-force task, where the NHPs had to apply visually cued grip-force to move and transport a virtual object. We found a population of (S1 area 1-2, rM1, PMd, PMv) units that significantly represented grip-force during manual and observational trials. We found the neural representation of visually cued force was similar during observational trials and manual trials for the same units; however, the representation was weaker during observational trials. Comparing changes in neural time lags between manual and observational tasks indicated that a subpopulation fit the standard MN definition of observational neural activity lagging the visual information. Neural activity in (S1 areas 1-2, rM1, PMd, PMv) significantly represented force and reward expectation. In summary, we present results indicating that sensorimotor cortices have MNs for visually cued force and value.

Towards a neurobiological understanding of alexithymia. / Hacia una comprensión neurobiológica de la alexitimia.

Although the specialized literature on the etiology of alexithymia is controversial, neurobiological research has shown relevant advances. The aim of this review is to analyze the available evidence regarding the neurophysiological bases of alexithymia. A comprehensive review of available articles from Medline/PubMed, EBSCO and SciELO was conducted. Previously, alexithymia was linked to a reduced interhemispheric brain connection. From a childhood traumatic perspective, the right prefrontal cortex and the default mode network would experience alterations, first hypermetabolic (dopaminergic and glutamatergic dysregulation) and then hypometabolic-dissociative (serotonergic and opioid dysregulation), resulting in a distorted interoceptive and emotional awareness. Mirror neurons are the essential neurobiological substrate of theory of mind and social cognition, intrinsically linked to alexithymia, involving parietal, temporal, premotor, and cingulate cortices, and inferior frontal gyrus. Other structures involved are the amygdala (facial expression and emotional reactivity), the insula (interoception, emotional integration and empathy) and the cerebellum (limbic cerebellum and somatosensory awareness). Molecular genetics has detected polymorphisms in genes of the serotonin transporter, in the enzyme genes of dopaminergic metabolism and brain-derived neurotrophic factor, while the role of oxytocin is controversial. To sum up, we found several studies demonstrating the overwhelming evidence of a neurobiological basis underlying alexithymia; nevertheless, research is still inconclusive and must include environmental, traumatic, social, and psychological factors that contribute to the origin of the alexithymia.

Si bien la literatura especializada sobre la etiología de la alexitimia es controvertida, la investigación neurobiológica sobre el fenómeno ha demostrado importantes avances. El objetivo de esta revisión es analizar la evidencia disponible en relación a las bases neurofisiológicas de la alexitimia. Se realizó una revisión exhaustiva de artículos disponibles en MEDLINE/PubMed, EBSCO y SciELO. Inicialmente, se vinculó a la alexitimia con una conexión cerebral interhemisférica reducida. Desde la perspectiva traumática infantil, la corteza prefrontal derecha y la red neuronal por defecto experimentarían alteraciones, primero hipermetabólicas (desregulación dopaminérgica y glutamatérgica) y luego hipometabólicas-disociativas (desregulación serotoninérgica y opioide), resultando en una consciencia interoceptiva y emocional distorsionada. Las neuronas espejo son el sustrato neurobiológico fundamental de la teoría de la mente y la cognición social, intrínsecamente vinculadas con la alexitimia, involucrando cortezas como la parietal, la temporal, la premotora, la cingulada y el giro frontal inferior. Otras estructuras involucradas son amígdala (expresión facial y reactividad emocional), ínsula (interocepción, integración emocional y empatía) y cerebelo (cerebelo límbico y consciencia somatosensorial). La genética molecular ha detectado polimorfismos en el gen del transportador de serotonina, en los genes de las enzimas del metabolismo dopaminérgico y del factor neurotrófico derivado del cerebro, mientras que el rol de la oxitocina es controvertido. En conclusión, numerosos estudios demuestran contundentemente la existencia de una neurobiología subyacente a la alexitimia. Sin embargo, la investigación es aún poco concluyente y debe considerar los factores ambientales, traumáticos, sociales y psicológicos que contribuyen al origen del fenómeno.

Neuroimaging in autism spectrum disorders: 1H-MRS and NIRS study.

Using proton magnetic resonance spectroscopy ((1)H-MRS), we measured chemical metabolites in the left amygdala and the bilateral orbito-frontal cortex (OFC) in children with autism spectrum disorders (ASD). The concentrations of N-acetylaspartate (NAA) in these regions of ASD were significantly decreased compared to those in the control group. In the autistic patients, the NAA concentrations in these regions correlated with their social quotient. These findings suggest the presence of neuronal dysfunction in the amygdala and OFC in ASD. Dysfunction in the amygdala and OFC may contribute to the pathogenesis of ASD. We performed a near-infrared spectroscopy (NIRS) study to evaluate the mirror neuron system in children with ASD. The concentrations of oxygenated hemoglobin (oxy-Hb) were measured with frontal probes using a 34-channel NIRS machine while the subjects imitated emotional facial expressions. The increments in the concentration of oxy-Hb in the pars opercularis of the inferior frontal gyrus in autistic subjects were significantly lower than those in the controls. However, the concentrations of oxy-Hb in this area were significantly elevated in autistic subjects after they were trained to imitate emotional facial expressions. The results suggest that mirror neurons could be activated by repeated imitation in children with ASD.

Papel de la corteza prefrontal en los problemas sensoriales de los niños con trastornos del espectro autista y su implicación en los aspectos sociales / The role of the prefrontal cortex in the sensory problems of children with autism spectrum disorder and its involvement in social aspects

Introducción. En las personas con trastornos del espectro autista (TEA), las percepciones sensoriales aberrantes podrían ser tan características y disruptivas como la presencia de anomalías en la comunicación e interacción social, así como de intereses restringidos y repetitivos. La mayoría presenta trastornos de la modulación sensorial (hiper o hiporresponsividad) en varios canales sensoriales. Además, muestra un déficit en la integración de la información procedente de varios sistemas sensoriales (por ejemplo, auditivo y visual). Todo ello agravaría los síntomas nucleares relacionados con la comunicación y aumentaría la aparición de problemas conductuales. Objetivo. Revisar la evidencia experimental que aborda el papel de la corteza prefrontal en las experiencias sensoriales inusuales en los TEA y su implicación en los aspectos sociales. Hay evidencia de hipoactivación y disfunción en redes neurales, que incluyen la corteza prefrontal y participan en la cognición social, como la red por defecto y el sistema de neuronas espejo en niños con TEA. Conclusiones. Los problemas sensoriomotores a edad temprana suponen una disrupción de la organización y regulación no sólo de la percepción y la acción, sino también del lenguaje, el pensamiento, la emoción e incluso la memoria (AU)

Introduction. In persons with autism spectrum disorders (ASD), aberrant sensory perceptions could be as characteristic and disruptive as the presence of anomalies in social communication and interaction or restricted and repetitive interests. Most of them present sensory modulation disorders (hyper- or hypo-responsiveness) in several sensory channels. Furthermore, there is a deficit in the integration of the information from a number of sensory systems (for example, auditory and visual). All this would worsen the core symptoms related with communication and increase the appearance of behavioural problems. Aims. This study aims to review the experimental evidence that addresses the role played by the prefrontal cortex in unusual sensory experiences in ASD and its involvement in social aspects. There is evidence of hypoactivation and dysfunction of the neural networks, which include the prefrontal cortex and participate in social cognition, such as the default mode and the mirror neuron system in children with ASD. Conclusions. Sensory-motor problems at an early age correspond to a disruption in the organisation and regulation not only of perception and action but also language, thought, emotion and even memory (AU)