test of everyday attention

  • 文章类型: Journal Article
    持续注意力的自然波动会导致日常任务中的注意力失败,甚至是危险的事件。这些波动取决于个人因素,以及任务特征。到目前为止,我们对持续关注的理解部分是由于实验室设置和任务的常见用法,以及行为和大脑活动之间复杂的相互作用。因此,当前研究的重点是测试在一系列生态任务中应用单通道无线EEG监测持续注意力模式的可行性。在日常注意力测试(TEA)和跟踪测试(TMT)的听觉和视觉任务中,连续记录了42名健康志愿者的EEG注意力标记(BEI-大脑参与指数)。随着任务复杂性的增加,我们发现听觉任务中的性能和BEI的下降模式,而在视觉任务上性能的增加和BEI的减少。此外,BEI在复杂任务中的模式被用来通过探索性模型检测异常值和最佳注意范围。当前的研究支持在生态任务中对持续注意进行电生理和神经认知联合研究的可行性,从而对持续注意模式作为任务模态和任务复杂性的函数产生了独特的见解。
    Natural fluctuations in sustained attention can lead to attentional failures in everyday tasks and even dangerous incidences. These fluctuations depend on personal factors, as well as task characteristics. So far, our understanding of sustained attention is partly due to the common usage of laboratory setups and tasks, and the complex interplay between behavior and brain activity. The focus of the current study was thus to test the feasibility of applying a single-channel wireless EEG to monitor patterns of sustained attention during a set of ecological tasks. An EEG marker of attention (BEI-Brain Engagement Index) was continuously recorded from 42 healthy volunteers during auditory and visual tasks from the Test of Everyday Attention (TEA) and Trail Making Test (TMT). We found a descending pattern of both performance and BEI in the auditory tasks as task complexity increases, while the increase in performance and decrease in BEI on the visual task. In addition, patterns of BEI in the complex tasks were used to detect outliers and the optimal range of attention through exploratory models. The current study supports the feasibility of combined electrophysiological and neurocognitive investigation of sustained attention in ecological tasks yielding unique insights on patterns of sustained attention as a function of task modality and task complexity.
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  • 文章类型: Journal Article
    Recent animal studies have shown that the synapses between inner hair cells and the dendrites of the spiral ganglion cells they innervate are the elements in the cochlea most vulnerable to excessive noise exposure. Particularly in rodents, several studies have concluded that exposure to high level octave-band noise for 2 h leads to an irreversible loss of around 50% of synaptic ribbons, leaving audiometric hearing thresholds unaltered. Cochlear synaptopathy following noise exposure is hypothesized to degrade the neural encoding of sounds at the subcortical level, which would help explain certain listening-in-noise difficulties reported by some subjects with otherwise \'normal\' hearing. In response to this peripheral damage, increased gain of central stages of the auditory system has been observed across several species of mammals, particularly in association with tinnitus. The auditory brainstem response (ABR) wave I amplitude and waves I-V amplitude ratio have been suggested as non-invasive indicators of cochlear synaptopathy and central gain activation respectively, but the evidence for these hearing disorders in humans is inconclusive. In this study, we evaluated the influence of lifetime noise exposure (LNE) on the human ABR and on speech-in-noise intelligibility performance in a large cohort of adults aged 29 to 55. Despite large inter-subject variability, results showed a moderate, but statistically significant, negative correlation between the ABR wave I amplitude and LNE, consistent with cochlear synaptopathy. The results also showed (a) that central gain mechanisms observed in animal studies might also occur in humans, in which higher stages of the auditory pathway appear to compensate for reduced input from the cochlea; (b) that tinnitus was associated with activation of central gain mechanisms; (c) that relevant cognitive and subcortical factors influence speech-in-noise intelligibility, in particular, longer ABR waves I-V interpeak latencies were associated with poorer performance in understanding speech in noise when central gain mechanisms were active; and (d) absence of a significant relationship between LNE and tinnitus, central gain activation or speech-in-noise performance. Although this study supports the possible existence of cochlear synaptopathy in humans, the great degree of variability, the lack of uniformity in central gain activation and the significant involvement of attention in speech-in-noise performance suggests that noise-induced cochlear synaptopathy is, at most, one of several factors that play a role in humans\' speech-in-noise performance.
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