Rapid detection of fear in body expressions, an ERP study.

Recent findings indicate that the perceptual processing of fearful expressions in the face can already be initiated around 100-120 ms after stimulus presentation, demonstrating that emotional information of a face can be encoded before the identity of the face is fully recognized. At present it is not clear whether fear signals from body expressions may be encoded equally as rapid. To answer this question we investigated the early temporal dynamics of perceiving fearful body expression by measuring EEG. Participants viewed images of whole body actions presented either in a neutral or a fearful version. We observed an early emotion effect on the P1 peak latency around 112 ms post stimulus onset hitherto only found for facial expressions. Also consistent with the majority of facial expression studies, the N170 component elicited by perceiving bodies proved not to be sensitive for the expressed fear. In line with previous work, its vertex positive counterpart, the VPP, did show a condition-specific influence for fearful body expression. Our results indicate that the information provided by fearful body expression is already encoded in the early stages of visual processing, and suggest that similar early processing mechanisms are involved in the perception of fear in faces and bodies.

[The cortico-thalamic theory for generalised spike-wave discharges]. / Kortikotalamicheskaia teoriia proiskhozhdeniia generalizovannykh pik-volnovykh razriadov.

The origin of generalized absence epilepsy is still not known. In the last century, four theories have dominated the debate about the origin of the bilateral synchronous generalized spike-wave discharges associated with absence seizures: the "centrencephalic" theory [Penfield and Jasper], the "cortical" [Bancaud, Niedermeyer, Luders], the "cortico-reticular" theory [Gloor, Kostop[oulos, Avoli] and the "thalamic clock" theory [Buzsaki]. There is now some evidence that absence epilepsy, as studied in the WAG/Rij model, is a corticothalamic type of epilepsy. A new hypothesis is proposed which suggests that a cortical focus in the somatosensory cortex is driving the widespread corticothalamic networks during spontaneous absence seizures. This modern theory was given the name "hot spot' theory" [Meeren et al., 2002]. According to the present view three brain structures are critically involved and their integrity seems a minimal and sufficient condition for the occurrence of spike-wave discharges. Firstly, the reticular thalamic nucleus is involved and most likely its rostral pole. Secondly, the thalamocortical relay cells in the ventrobasal complex play a role and, thirdly and most importantly, the cerebral cortex with its epileptic zone. The zone in which the epileptic focus seems to be localised is located on the somato-sensory cortex, and more precisely in the area on which the peri-oral region including the upper lip, projects.