THRIVE score predicts clinical and radiological outcome after endovascular therapy or thrombolysis in patients with anterior circulation stroke in everyday clinical practice.

BACKGROUND AND PURPOSE: Based on the data of several trials the Totaled Health Risks in Vascular Events (THRIVE) score has been shown to predict outcome after either intravenous thrombolysis (IVT) or endovascular therapy (ET) in acute stroke patients. It is unknown whether the THRIVE score can also predict outcome in everyday clinical practice. Using our prospectively obtained stroke database the utility of the THRIVE score to predict clinical and radiological outcome in everyday clinical practice was analysed. METHODS: The relationships between THRIVE and good outcome (modified Rankin Scale ≤ 2 at discharge), poor outcome (modified Rankin Scale 5-6), in-hospital death, symptomatic intracranial haemorrhage (SICH) as well as infarct size were examined in patients with distal intracranial carotid artery, M1 and M2 occlusions after either IVT or ET. RESULTS: From January 2008 to October 2016 a total of 546 patients were treated with IVT and 492 patients received ET with stent retrievers (with or without IVT). In both treatment groups the THRIVE score predicted clinical outcome (Mantel-Haenszel chi-squared tests for trend P < 0.001 for good outcome, P < 0.001 for poor outcome and P < 0.001 for in-hospital death). In the ET group the THRIVE score remained an independent predictor of outcome after controlling for recanalization. The THRIVE score was associated with the infarct size after IVT or ET, whereas it did not predict SICH rates in either treatment group. CONCLUSIONS: In everyday clinical practice the THRIVE score strongly predicts clinical outcome and the extent of ischaemia after ET or IVT in patients with anterior circulation large vessel occlusions.

The neural basis of risk ratings: evidence from a functional magnetic resonance imaging (fMRI) study.

Research investigating risk perception suggests that not only the quantitative parameters used in technical risk assessment (i.e., frequency and severity of harm) but also 'qualitative' aspects such as the dread a hazard provokes or its controllability influence risk judgments. It remains to be elucidated, however, which neural mechanism underlie risk ratings in healthy subjects. Using fMRI to detect changes in neural activity we compared the neural activations elicited by risk ratings with those elicited by a letter detection task performed on the same stimuli. The latter task served to control for basic stimulus processing, response selection and button-pressing during task performance. Risk ratings differentially activated the medial prefrontal cortex, the inferior frontal gyrus, the cerebellum (P<0.05, FWE corrected, whole brain approach), and in an additional ROI analysis the amygdala (P<0.05, FWE corrected). Of these structures, particularly the amygdala and the prefrontal cortex have been previously associated with decisions about affective interference. Furthermore our data suggest both, similarities and differences between the neural correlates of risk ratings and risk taking as involved, for e.g., in gambling tasks.

fMRI data predict individual differences of behavioral effects of nicotine: a partial least square analysis.

Reorienting of visuospatial attention can be investigated by comparing reaction times to validly and invalidly cued targets ("validity effect"). The cholinergic agonist nicotine reduces the validity effect and neural activity in the posterior parietal cortex. Behavioral effects of nicotine in nonsmokers are weak and it has been suggested that differences in baseline behavior before nicotine exposure may influence the effect of nicotine. This study investigates whether individual differences in reorienting-related neural activity under placebo may be used to predict individual nicotine effects. Individual nicotine effects are defined as the behavioral effects under nicotine that cannot be predicted by the behavioral data under placebo. Fifteen nonsmoking subjects were given either placebo or nicotine gum (2 mg) prior to performing a cued target detection task inside a magnetic resonance imaging scanner. The results of a partial least square analysis suggest that neural data under placebo can be used to predict individual behavioral effects of nicotine. Neural activity in the left posterior cingulate cortex, the right superior parietal cortex, the right dorsal medial prefrontal cortex, and the left ventral medial prefrontal cortex significantly contributes to that prediction. We conclude that nicotine effects on reorienting attention depend on individual differences in reorienting-related neural activity under placebo and suggest that functional magnetic resonance imaging data can contribute to the prediction of individual drug effects.

The modulatory effects of nicotine on parietal cortex activity in a cued target detection task depend on cue reliability.

This functional magnetic resonance imaging study investigates the effects of nicotine in a cued target detection task when changing cue reliability. Fifteen non-smoking volunteers were studied under placebo and nicotine (Nicorette polacrilex gum 1 and 2 mg). Validly and invalidly cued trials were arranged in blocks with high, middle and low cue reliability. Two effects of nicotine were investigated: its influence on i) parietal cortex activity underlying the processing of invalid vs. valid trials (i.e. validity effect) and ii) neural activity in the context of low, middle and high informative value of the cue (i.e. cue reliability effect). Nicotine did not affect behavioral performance. However, nicotine reduced the difference in the blood oxygenation level dependent (BOLD) signal between invalid and valid trials in the right intraparietal sulcus. The reduction of parietal activity in invalid trials was smaller in the low cue reliability condition. The same posterior parietal region exhibited a nicotinic modulation of BOLD activity in valid trials which was dependent on cue reliability: Nicotine specifically enhanced the neural activity during valid trials in the context of low cue reliability, i.e. when subjects are already in a state of low certainty. We speculate that the right intraparietal sulcus might be part of two networks working in parallel: one responsible for reorienting attention and the other for the cholinergic modulation of cue reliability. By reducing the use of the cue, nicotine modulates parietal activity related to reorienting attention in conditions with higher cue certainty. On the other hand, nicotine increases parietal activity in states of low certainty. This enhanced activation might influence brain regions, such as the posterior cingulate, directly involved in the processing of cue reliability.