Abstract Identifying factors whose fluctuations are associated with choice inconsistency is a major issue for rational decision theory. Here, we investigated the neuro-computational mechanisms through which mood fluctuations may bias human choice behavior. Intracerebral EEG data were collected in a large group of participants (n = 30), while they were performing interleaved quiz and choice tasks. Neural baseline activity preceding choice onset was confronted first to mood level, estimated by a computational model integrating the feedbacks received in the quiz task, and then to the weighting of option attributes, in a computational model predicting risk attitude in the choice task. Results showed that 1) elevated broadband gamma activity (BGA) in the ventromedial prefrontal cortex (vmPFC) and dorsal anterior insula (daIns) was respectively signaling periods of high and low mood, 2) increased vmPFC and daIns BGA respectively promoted and tempered risk taking by overweighting gain versus loss prospects. Thus, incidental feedbacks induce brain states that correspond to different moods and bias the comparison of safe and risky options. More generally, these findings might explain why people experiencing positive (or negative) outcome in some part of their life tend to expect success (or failure) in any other.
Assigning accurate conductivity values in human head models is an essential factor for performing precise electroencephalographic (EEG) source localization and targeting of transcranial electrical stimulation (TES). Unfortunately, the literature reports diverging conductivity values of the different tissues in the human head. The current study analyzes first the performance of in-vivo conductivity estimation for different configurations concerning the localization of the electrical source and measurement. Then, it presents conductivity estimates for three epileptic patients using scalp EEG and intracerebral stereotactic EEG (sEEG) acquired in simultaneous with intracerebral electrical stimulation. The estimates of the conductivities were based on finite-element models of the human head with five tissue compartments of homogeneous and isotropic conductivities. The results of this study show that in-vivo conductivity estimation can lead to different estimated conductivities for the same patient when considering different stimulation positions, different measurement positions or different measurement modalities (sEEG or EEG). This work provides important guidelines to in-vivo conductivity estimation and explains the variability among the conductivity values which have been reported in previous studies.
Using results from cortical stimulations, as well as the symptoms of spontaneous epileptic seizures recorded by stereoelectroencephalography we re-studied the phenomenon of the dreamy state, as described by Jackson (Jackson JH. Selected writings of John Hughlins Jackson. Vol 1. On epilepsy and epileptiform convulsions. Taylor J, editor. London: Hodder and Stoughton; 1931). A total of 15 sensations of déjà vécu, 35 visual hallucinations consisting of the image of a scene and 5 'feelings of strangeness' occurred. These were recorded during 40 stimulations in 16 subjects, and 15 seizures in 5 subjects. Forty-five per cent of dreamy states were evoked by stimulation of the amygdala, 37.5% by the hippocampus and 17.5% by the para-hippocampal gyrus. During both spontaneous and provoked dreamy state, the electrical discharge was localized within mesial temporal lobe structures, without involvement of the temporal neocortex. Early spread of the discharge to the temporal neocortex appeared to prevent the occurrence of the dreamy state. Semiological analysis showed a clinical continuity between déjà vécu and visual hallucinations, the latter often consisting of a personal memory that was 'relived' by the subject; such memories could be recent, distant or from childhood. With one exception, the particular memory evoked differed from one seizure to another, but were always drawn from the same period of the subject's life. Given the role of the amygdala and hippocampus in autobiographic memory, their pathological activation during seizures may trigger memory recall. This study of the dreamy state is in keeping with other evidence demonstrating the constant and central role of the amygdala and hippocampus (right as much as left) in the recall of recent and distant memories. It demonstrates the existence of large neural networks that produce recall of memories via activation of the hippocampus, amygdala and rhinal cortex.
