Predictors for Returning to Paid Work after Transient Ischemic Attack and Minor Ischemic Stroke.

This study aims to determine which factors within the first week after a first-ever transient ischemic attack (TIA) or minor ischemic stroke (MIS) are associated with stroke survivors' ability to return to either partial or full time paid external work (RTpW). In this single-center prospective cohort study, we recruited 88 patients with first-ever TIA or MIS (NIHSS ≤ 5). Bivariate analyses were conducted between patients that did (RTpW) or did not return to paid work (noRTpW) within 7 days after stroke onset and at 3-months follow-up. Then, we conducted multivariate logistic and negative binomial regression analyses assessing (i) which factors are associated with RTpW at 3 months (ii) the likelihood that patients would RTpW at 3 months and (iii) the number of months necessary to RTpW. Overall, 43.2% of the patients did not RTpW at 3 months. At 3-months follow-up, higher anxiety/depression and fatigue-related disabilities were associated with noRTpW. Multivariate analysis showed that higher NIHSS scores at onset and hyperlipidemia (LDL cholesterol > 2.6 mmol/L or statins at stroke onset) were associated with noRTpW at 3 months. Stroke severity and/or newly diagnosed hypercholesterolemia at stroke onset in TIA or MIS patients were associated with not returning to paid work at 3 months.

Neural correlates of expectations-induced effects of caffeine intake on executive functions.

Placebo effects are defined as the beneficial subjective or behavioral outcomes of an intervention that are not attributable to its inherent properties; Placebo effects thus follow from individuals' expectations about the effects of the intervention. The present study aimed at examining how expectations influence neurocognitive processes. We addressed this question by contrasting three double-blinded within-subjects experimental conditions in which participants were given decaffeinated coffee, while being told they had received caffeinated (condition i) or decaffeinated coffee (ii), and given caffeinated coffee while being told they had received decaffeinated coffee (iii). After each of these three interventions, performance and electroencephalogram was recorded at rest as well as during sustained attention Rapid Visual Information Processing task (RVIP) and a Go/NoGo motor inhibitory control task. We first aimed to confirm previous findings for caffeine-induced enhancement on these executive components and on their associated electrophysiological indexes (The Attention-P3 component, response conflict NoGo-N2 and inhibition NoGo-P3 components (ii vs iii contrast); and then to test the hypotheses that expectations also induce these effects (i vs ii), although with a weaker amplitude (i vs iii). We did not confirm any of our hypotheses for caffeine-induced behavioral improvements and thus did not test the effect of caffeine-related expectations. At the electrophysiological level, however, we confirmed that caffeine increased the Attention-P3 and NoGo-P3 components amplitude but did not confirm an effect on the response-conflict N2 component. We did not confirm that expectations influence any of the investigated electrophysiological indices, but we confirmed that the Attention-P3 Global Field Power values were larger for the caffeine compared to the expectations conditions. We conclude that previously identified behavioral effect size of caffeine and of the related expectations for sustained attention and inhibitory control may have been overestimated, and that caffeine primarily influences the cognitive processes and brain areas supporting attention allocation. Finally, we confirm that caffeine-related expectations induce smaller effects than the substance itself.

Experience with opioids does not modify the brain network involved in expectations of placebo analgesia.

Placebo analgesia (PA) is defined as a psychobiological phenomenon triggered by the information surrounding an analgesic drug instead of its inherent pharmacological properties. PA is hypothesized to be formed through either verbal suggestions or conditioning. The present study aims at disentangling the neural correlates of expectations effects with or without conditioning through prior experience using the model of PA. We addressed this question by recruiting two groups of individuals holding comparable verbally-induced expectations regarding morphine analgesia but either (i) with or (ii) without prior experience with opioids. We then contrasted the two groups' neurocognitive response to acute heat-pain induction following the injection of sham morphine using electroencephalography (EEG). Topographic ERP analyses of the N2 and P2 pain evoked potential components allowed to test the hypothesis that PA involves distinct neural networks when induced by expectations with or without prior experience. First, we confirmed that the two groups showed corresponding expectations of morphine analgesia (Hedges' gs < .4 positive control criteria, gs = .37 observed difference), and that our intervention induced a medium-sized PA (Hedges' gav ≥ .5 positive control, gav = .6 observed PA). We then tested our hypothesis on the recruitment of different PA-associated brain networks in individuals with versus without prior experience with opioids and found no evidence for a topographic N2 and P2 ERP components difference between the two groups. Our results thus suggest that in the presence of verbally-induced expectations, modifications in the PA-associated brain activity by conditioning are either absent or very small.

Acute alcohol intoxication and expectations reshape the spatiotemporal functional architecture of executive control.

While the deleterious effects of acute ethyl alcohol intoxication on executive control are well-established, the underlying spatiotemporal brain mechanisms remain largely unresolved. In addition, since the effects of alcohol are noticeable to participants, isolating the effects of the substance from those related to expectations represents a major challenge. We addressed these issues using a double-blind, randomized, parallel, placebo-controlled experimental design comparing the behavioral and electrical neuroimaging acute effects of 0.6 vs 0.02 â€‹g/kg alcohol intake recorded in 65 healthy adults during an inhibitory control Go/NoGo task. Topographic ERP analyses of covariance with self-reported dose expectations allowed to dissociate their neurophysiological effects from those of the substance. While alcohol intoxication increased response time variability and post-error slowing, bayesian analyses indicated that it did not modify commission error rates. Functionally, alcohol induced topographic ERP modulations over the periods of the stimulus-locked N2 and P3 components, arising from pre-supplementary motor and anterior cingulate areas. In contrast, alcohol decreased the strength of the response-locked anterior cingulate error-related component but not its topography. This pattern indicates that alcohol had a locally specific influence within the executive control network, but disrupted performance monitoring processes via global strength-based mechanisms. We further revealed that alcohol-related expectations induced temporally specific functional modulations of the early N2 stimulus-locked medio-lateral prefrontal activity, a processing phase preceding those influenced by the actual alcohol intake. Our collective findings thus not only reveal the mechanisms underlying alcohol-induced impairments in impulse control and error processing, but also dissociate substance- from expectations- related functional effects.