RESUMEN
OBJECTIVE: Guilt increases prior to objective binge-eating episodes (OBE) and decreases following OBE, suggesting that OBE may function to regulate negative affective states. Rapid eating, a common feature of OBE, may be an observable indication of difficulty regulating eating. Heart rate variability (HRV), a measure of parasympathetic activity, is an indicator of top-down inhibitory control and indicates emotion regulation attempts. We aimed to test the effect of guilt on consumption rate and change in HRV among individuals with (+) and without (-) OBE. METHOD: Participants (N = 86) underwent a mood induction (randomized to either a neutral mood or a guilt condition) and were then provided with 32 ounces (0.95 L) of Boost® meal replacement shake (960 kcal) and instructed to consume until they felt satisfied. Guilt was measured at baseline, prior to consumption, and following consumption. HRV was measured throughout. RESULTS: Participants in the guilt condition reported higher guilt prior to consumption than individuals in the neutral mood condition, primarily driven by individuals with low HRV. Guilt decreased following consumption among individuals with low HRV in the guilt condition. The OBE+ individuals did not consume more or at an overall faster rate than OBE- individuals. Guilt prior to consumption did not lead to faster initial rates among OBE+ individuals; although, OBE+ individuals who experienced an increase in HRV from prior to during consumption demonstrated faster initial rates and greater changes in rate over time. DISCUSSION: When experiencing negative emotions, individuals with OBE may experience increases in parasympathetic functioning while eating, reinforcing OBE as a facilitator of emotion regulation.
Asunto(s)
Trastorno por Atracón , Bulimia , Emociones , Conducta Alimentaria , Frecuencia Cardíaca , HumanosRESUMEN
Two aspects of the EEG literature lead us to revisit mu suppression in Autism Spectrum Disorder (ASD). First and despite the fact that the mu rhythm can be functionally segregated in two discrete sub-bands, 8-10 Hz and 10-12/13 Hz, mu-suppression in ASD has been analyzed as a homogeneous phenomenon covering the 8-13 Hz frequency. Second and although alpha-like activity is usually found across the entire scalp, ASD studies of action observation have focused on the central electrodes (C3/C4). The present study was aimed at testing on the whole brain the hypothesis of a functional dissociation of mu and alpha responses to the observation of human actions in ASD according to bandwidths. Electroencephalographic (EEG) mu and alpha responses to execution and observation of hand gestures were recorded on the whole scalp in high functioning subjects with ASD and typical subjects. When two bandwidths of the alpha-mu 8-13 Hz were distinguished, a different mu response to observation appeared for subjects with ASD in the upper sub-band over the sensorimotor cortex, whilst the lower sub-band responded similarly in the two groups. Source reconstructions demonstrated that this effect was related to a joint mu-suppression deficit over the occipito-parietal regions and an increase over the frontal regions. These findings suggest peculiarities in top-down response modulation in ASD and question the claim of a global dysfunction of the MNS in autism. This research also advocates for the use of finer grained analyses at both spatial and spectral levels for future directions in neurophysiological accounts of autism.
Asunto(s)
Ondas Encefálicas/fisiología , Corteza Cerebral/fisiopatología , Trastornos Generalizados del Desarrollo Infantil/fisiopatología , Adulto , Ritmo alfa , Electroencefalografía , Femenino , Humanos , Masculino , Adulto JovenRESUMEN
Compulsive drug use and a persistent vulnerability to relapse are key features of addiction. Imaging studies have suggested that these features may result from deficits in prefrontal cortical structure and function, and thereby impaired top-down inhibitory control over limbic-striatal mechanisms of drug-seeking behaviour. We tested the hypothesis that selective damage to distinct subregions of the prefrontal cortex, or to the amygdala, after a short history of cocaine taking would: (i) result in compulsive cocaine seeking at a time when it would not usually be displayed; or (ii) facilitate relapse to drug seeking after abstinence. Rats with selective, bilateral excitotoxic lesions of the basolateral amygdala or anterior cingulate, prelimbic, infralimbic, orbitofrontal or anterior insular cortices were trained to self-administer cocaine under a seeking-taking chained schedule. Intermittent mild footshock punishment of the cocaine-seeking response was then introduced. No prefrontal cortical lesion affected the ability of rats to withhold their seeking responses. However, rats with lesions to the basolateral amygdala increased their cocaine-seeking responses under punishment and were impaired in their acquisition of conditioned fear. Following a 7-day abstinence period, rats were re-exposed to the drug-seeking environment for assessment of relapse in the absence of punishment or cocaine. Rats with prelimbic cortex lesions showed decreased seeking responses during relapse, whereas those with anterior insular cortex lesions showed an increase. Combined, these results show that acute impairment of prefrontal cortical function does not result in compulsive cocaine seeking after a short history of self-administering cocaine, but further implicates subregions of the prefrontal cortex in relapse.