Neural Correlates of Antisocial Behavior: The Victim's Perspective.

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.

Neural Responses of Benefiting From the Prosocial Exchange: The Effect of Helping Behavior.

Prosocial behavior is critical for the natural development of an individual as well as for promoting social relationships. Although this complex behavior results from gratuitous acts occurring between an agent and a recipient and a wealth of literature on prosocial behavior has investigated these actions, little is known about the effects on the recipient and the neurobiology underlying them. In this study, we used functional magnetic resonance imaging to identify neural correlates of receiving prosocial behavior in the context of real-world experiences, with different types of action provided by the agent, including practical help and effort appreciation. Practical help was associated with increased activation in a network of regions spanning across bilateral superior temporal sulcus, temporoparietal junction, temporal pole, and medial prefrontal cortex. Effort appreciation was associated with activation and increased task-modulated connectivity of the occipital cortex. Prosocial-dependent brain responses were associated with positive affect. Our results support the role of the theory of mind network and the visual cortices in mediating the positive effects of receiving gratuitous help. Moreover, they indicate that specific types of prosocial behavior are mediated by distinct brain networks, which further demonstrates the uniqueness of the psychological processes underlying prosocial actions.

Teaching neurons to respond to placebos.

KEY POINTS: We analysed the placebo response at the single-neuron level in the thalamus of Parkinson patients to see the differences between first-time administration of placebo and administration after pharmacological pre-conditioning. When the placebo was given for the first time, it induced neither clinical improvement, as assessed through muscle rigidity reduction at the wrist, nor neuronal changes in thalamic neurons. However, if placebo was given after two, three or four prior administrations of an anti-Parkinson drug, apomorphine, it produced both clinical and neuronal responses. Both the magnitude and the duration of these placebo responses depended on the number of prior exposures to apomorphine, according to the rule: the greater the number of previous apomorphine administrations, the larger the magnitude and the longer the duration of the clinical and neuronal placebo responses. These findings show that learning plays a crucial role in the placebo response and suggest that placebo non-responders can be turned into placebo responders, with important clinical implications. ABSTRACT: Placebos have been found to affect the patient's brain in several conditions, such as pain and motor disorders. For example, in Parkinson's disease, a placebo treatment induces a release of dopamine in the striatum and changes the activity of neurons in both thalamic and subthalamic nuclei. The present study shows that placebo administration for the first time induces neither clinical nor neuronal improvement in Parkinson patients who undergo implantation of electrodes for deep brain stimulation. However, this lack of placebo responsiveness can be turned into substantial placebo responses following previous exposure to repeated administrations of the anti-Parkinson agent apomorphine. As the number of apomorphine administrations increased from one to four, both the clinical response and the neuronal activity in the ventral anterior and anterior ventrolateral thalamus increased. In fact, after four apomorphine exposures, placebo administration induced clinical responses that were as large as those to apomorphine, along with long-lasting neuronal changes. These clinical placebo responses following four apomorphine administrations were again elicited after a re-exposure to a placebo 24 h after surgery, but not after 48 h. These data indicate that learning plays a crucial role in placebo responsiveness and suggest that placebo non-responders can be turned into responders, with important implications in the clinical setting.

High-altitude headache: the effects of real vs sham oxygen administration.

High-altitude, or hypobaric hypoxia, headache has recently emerged as an interesting model to study placebo and nocebo responses, and particularly their peripheral mechanisms. In this study, we analyze the response of this type of headache to either real or sham (placebo) oxygen (O(2)) administration at an altitude of 3500 m, where blood oxygen saturation (SO(2)) drops from the normal value of about 98% to about 85%. In a trial in which a double-blind administration of either 100% O(2) or sham O(2) was administered, we tested pre- and post-exercise headache, along with fatigue, heart rate (HR) responses, and prostaglandin E(2) (PGE(2)) salivary concentration. Although real O(2) breathing increased SO(2) along with a decrease in pre- and post-exercise headache, fatigue, HR, and PGE(2), placebo O(2) changed neither pre-/post-exercise headache nor SO(2)/HR/PGE(2), but it decreased fatigue. However, in another group of subjects, when sham O(2) was delivered after 2 previous exposures to O(2) (O(2) preconditioning), it decreased fatigue, post-exercise headache, HR, and PGE(2), yet without any increase in SO(2). Three main findings emerge from these data. First, placebo O(2) is effective in reducing post-exercise headache, along with HR and PGE(2) decrease, only after O(2) preconditioning. Second, pre-exercise (at rest) headache is not affected by placebo O(2), which emphasizes the limits of a placebo treatment at high altitude. Third, fatigue is affected by placebo O(2) even without prior O(2) conditioning, which suggests the higher placebo sensitivity of fatigue compared with headache pain at high altitude.