Characteristic fear behaviour like putting the hands in front of the face and running for cover provides strong fear signals to observers who may not themselves be aware of any danger. Using event-related functional magnetic resonance imaging (fMRI) in humans, we investigated how such dynamic fear signals from the whole body are perceived. A factorial design allowed us to investigate brain activity induced by viewing bodies, bodily expressions of fear and the role of dynamic information in viewing them. Our critical findings are threefold. We find that viewing neutral and fearful body expressions enhances amygdala activity; moreover actions expressing fear activate the temporal pole and lateral orbital cortex more than neutral actions; and finally differences in activations between static and dynamic bodily expressions were larger for actions expressing fear in the STS and premotor cortex compared to neutral actions.

Most mental functions are associated with dynamic interactions within functional brain networks. Thus, training individuals to alter functional brain networks might provide novel and powerful means to improve cognitive performance and emotions. Using a novel connectivity-neurofeedback approach based on functional magnetic resonance imaging (fMRI), we show for the first time that participants can learn to change functional brain networks. Specifically, we taught participants control over a key component of the emotion regulation network, in that they learned to increase top-down connectivity from the dorsomedial prefrontal cortex, which is involved in cognitive control, onto the amygdala, which is involved in emotion processing. After training, participants successfully self-regulated the top-down connectivity between these brain areas even without neurofeedback, and this was associated with concomitant increases in subjective valence ratings of emotional stimuli of the participants. Connectivity-based neurofeedback goes beyond previous neurofeedback approaches, which were limited to training localized activity within a brain region. It allows to noninvasively and nonpharmacologically change interconnected functional brain networks directly, thereby resulting in specific behavioral changes. Our results demonstrate that connectivity-based neurofeedback training of emotion regulation networks enhances emotion regulation capabilities. This approach can potentially lead to powerful therapeutic emotion regulation protocols for neuropsychiatric disorders.

Being exposed to fear or anger signals makes us feel threatened and prompts us to prepare an adaptive response. Yet, while fear and anger behaviors are both threat signals, what counts as an adaptive response is often quite different. In contrast with fear, anger is often displayed with the aim of altering the behavior of the agent to which it is addressed. To identify brain responses that are common or specific to the perception of these two types of threat signals, we used functional magnetic resonance imaging and asked subjects to recognize dynamic actions expressing fear, anger and neutral behaviors. As compared with neutral actions, the perception of fear and anger behaviors elicited comparable activity increases in the left amygdala and temporal cortices as well as in the ventrolateral and the dorsomedial prefrontal cortex. Whereas the perception of fear elicited specific activity in the right temporoparietal junction, the perception of anger triggered condition-specific activity in a wider set of regions comprising the anterior temporal lobe, the premotor cortex and the ventromedial prefrontal cortex, consistent with the hypothesis that coping with threat from exposure to anger requires additional contextual information and behavioral adjustments.

Neuroscientific research on the perception of emotional signals has mainly focused on how the brain processes threat signals from photographs of facial expressions. Much less is known about body postures or about the processing of dynamic images. We undertook a systematic comparison of the neurofunctional network dedicated to processing facial and bodily expressions. Two functional magnetic resonance imaging (fMRI) experiments investigated whether areas involved in processing social signals are activated differently by threatening signals (fear and anger) from facial or bodily expressions. The amygdala (AMG) was more active for facial than for bodily expressions. Body stimuli triggered higher activation than face stimuli in a number of areas. These were the cuneus, fusiform gyrus (FG), extrastriate body area (EBA), temporoparietal junction (TPJ), superior parietal lobule (SPL), primary somatosensory cortex (SI), as well as the thalamus. Emotion-specific effects were found in TPJ and FG for bodies and faces alike. EBA and superior temporal sulcus (STS) were more activated by threatening bodies.

The ability to detect emotional meaning in others' behavior constitutes a central component of social competence. Expressions of anger in particular present salient signals that play a major role in the regulation of social interactions. Investigations of human anger signals have to date used still pictures of facial expressions but so far the neurobiological basis of bodily communication of anger remains largely unknown. Using functional magnetic resonance imaging, the present study investigated the neural bases involved in perceiving anger signals emanating from the whole body. Our study also investigates what the presence of dynamic information adds to the perception of body expressions of anger. Participants were scanned while viewing stimuli (stills or videos) of angry and neutral whole-body expressions. Whole-body expressions of anger elicit activity in regions including the amygdala and the lateral orbitofrontal cortex, which play a role in the affective evaluation of the stimuli. Importantly, the perception of dynamic body expressions of anger additionally engages the hypothalamus, the ventromedial prefrontal cortex, the temporal pole and the premotor cortex, brain regions that are coupled with autonomic reactions and motor responses related to defensive behaviors.

Although advances have been made regarding how the brain perceives emotional prosody, the neural bases involved in the generation of affective prosody remain unclear and debated. Two models have been forged on the basis of clinical observations: a first model proposes that the right hemisphere sustains production and comprehension of emotional prosody, while a second model proposes that emotional prosody relies heavily on basal ganglia. Here, we tested their predictions in two functional magnetic resonance imaging experiments that used a cue-target paradigm, which allows distinguishing affective from sensorimotor aspects of emotional prosody generation. Both experiments show that when participants prepare for emotional prosody, bilateral ventral striatum is specifically activated and connected to temporal poles and anterior insula, regions in which lesions frequently cause dysprosody. The bilateral dorsal striatum is more sensitive to cognitive and motor aspects of emotional prosody preparation and production and is more strongly connected to the sensorimotor speech network compared with the ventral striatum. Right lateralization during increased prosodic processing is confined to the posterior superior temporal sulcus, a region previously associated with perception of emotional prosody. Our data thus provide physiological evidence supporting both models and suggest that bilateralbasalgangliaareinvolvedinmodulatingmotorbehaviorasafunctionofaffectivestate.Rightlateralizationofcorticalregionsmobilized for prosody control could point to efficient processing of slowly changing acoustic speech parameters in the ventral stream and thus identify sensorimotor processing as an important factor contributing to right lateralization of prosody.

Negative emotional signals are known to influence task performance, but so far, investigations have focused on how emotion interacts with perceptual processes by mobilizing attentional resources. The attention-independent effects of negative emotional signals are less well understood. Here, we show that threat signals trigger defensive responses independently of what observers pay attention to. Participants were scanned using functional magnetic resonance imaging while watching short video clips of threatening actions and performed either color or emotion judgments. Seeing threatening actions interfered with performance in both tasks. Amygdala activation reflected both stimulus and task conditions. In contrast, threat stimuli prompted a constant activity in a network underlying reflexive defensive behavior (periaqueductal gray, hypothalamus, and premotor cortex). Threat stimuli also disrupted ongoing behavior and provoked motor conflict in prefrontal regions during both tasks. The present results are consistent with the view that emotions trigger adaptive action tendencies independently of task settings.

Patients with striate cortex damage and clinical blindness retain the ability to process certain visual properties of stimuli that they are not aware of seeing. Here we investigated the neural correlates of residual visual perception for dynamic whole-body emotional actions. Angry and neutral emotional whole-body actions were presented in the intact and blind visual hemifield of a cortically blind patient with unilateral destruction of striate cortex. Comparisons of angry vs. neutral actions performed separately in the blind and intact visual hemifield showed in both cases increased activation in primary somatosensory, motor, and premotor cortices. Activations selective for intact hemifield presentation of angry compared with neutral actions were located subcortically in the right lateral geniculate nucleus and cortically in the superior temporal sulcus, prefrontal cortex, precuneus, and intraparietal sulcus. Activations specific for blind hemifield presentation of angry compared with neutral actions were found in the bilateral superior colliculus, pulvinar nucleus of the thalamus, amygdala, and right fusiform gyrus. Direct comparison of emotional modulation in the blind vs. intact visual hemifield revealed selective activity in the right superior colliculus and bilateral pulvinar for angry expressions, thereby showing a selective involvement of these subcortical structures in nonconscious visual emotion perception.blindsight | body expressions | consciousness T he visual system encompasses a number of parallel visual pathways (1) of which the primary geniculostriate system processes a wide range of stimulus attributes. Other extrageniculostriate visual routes likely have a much more narrowly specified function, as indicated by their sensitivity to a limited range of spatial frequencies (2), spectral components (3), or motion parameters (4). However, we do not yet have a clear understanding of how these different extrageniculostriate pathways and the visual attributes they process match. Some visual attributes can also be processed by both the geniculostriate pathway and a more specialized extrageniculostriate one.One important example is movement perception. As originally discovered by Kohler and Held (5), movement perception elicits significant qualitative and quantitative differences at the neural as well as at behavioral level compared with static stimuli in the intact brain. These differences likely reflect the high evolutionary value of movement perception and may be especially important for understanding residual visual abilities in the case of striate cortex (V1) damage. In fact, after V1 damage, cortically blind patients retain a limited visual ability for movement discrimination (4, 6-9), akin to what has been previously observed in animals with V1 destruction (10,11). This spared ability to process simple movement is probably based on the extrageniculostriate connections that motion-sensitive human middle temporal/V5 complex (hMT/V5) has with subcortical structures like the lateral geniculate nucleus ...