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En 2013, on estime que 40 à 50% des accidents corporels seraient dus à des défauts d'attention de la part du conducteur. Des études récentes ont mis en évidence la possibilité de détecter des états attentionnels dégradés afin de pouvoir mieux assister le conducteur ; ce thème de recherche représente donc un nouveau gisement de sécurité routière. Cette étude se concentre sur la détection de l'effort cognitif fournit par les conducteurs et cherche, par l'étude de la variation du rythme cardiaque, à identifier un indicateur d'effort sensible sur de courtes fenêtres temporelles.Chacun des 18 participants a passé 8 conditions expérimentales sur simulateur de conduite : la moitié où seule une tâche de comptage était demandée et l'autre moitié en réalisant une tâche supplémentaire de conduite sur simulateur. Il a été demandé aux participants soit d'effectuer la tâche cognitive soit de se relaxer et de ne pas prêter attention aux stimuli présentés (Effort Vs. Relaxation). Afin de réaliser la tâche de comptage, deux types de stimuli auditifs ont été présentés aux participants. Les participants ont effectué les conditions expérimentales dans des ordres partiellement contrebalancés. Le rythme cardiaque et la respiration ont été collectés.Les résultats de différents auteurs ont été répliqués y compris en conduite automobile. Dans les secondes qui suivent un effort cognitif, une légère décélération du rythme cardiaque puis une forte accélération ont été mises en évidence. A l'inverse, en condition de relaxation, une simple décélération cardiaque a été observée. Au terme de notre étude, il s'avère qu'il est possible de distinguer des patterns cardiaques d'effort et de relaxation sur de courtes fenêtre temporelle en observant la variation du rythme cardiaque moyenné sur un nombre conséquent d'épisodes. Toutefois, dans l'objectif de développer des systèmes capables de détecter en temps réel un effort cognitif important, ces dispositifs devront être capables de visualiser l'effort sur un unique évènement. Une piste intéressante consisterait à explorer la faisabilité de la suppression de l'influence de la respiration sur la variation du rythme cardiaque. Si cela s'avère efficace, des assistances pourraient ainsi permettre d'alerter le conducteur ou de pallier ses erreurs lorsque celui-ci ne peut plus assurer la tâche de conduite en raison d'un effort cognitif important.

The post-stimulus primary bradycardia-sometimes labelled as the first evoked cardiac response, ECR1-is regarded as a response which is independent of the stimulus novelty factor. Despite this however, in our previous research we have observed a noticeable variation of this response, which made us suspect that there could be some additional factor influencing it. To test this, we designed a habituation procedure to measure susceptibility of the ECR1 to stimulus repetition. In our experimental design, we also included a measure of the level of activation (arousal) as a possible additional factor influencing the time-course of the cardiac response. The level of arousal over the study was measured by the Activation-Deactivation Adjective Check List (AD ACL). Our results show that mere stimulus repetition does not influence the time-course of ECR1. However, another pattern of results appeared when one of the dimensions of AD ACL, namely Tense Arousal, was taken into account. We observed different ECR time-courses during the initial stimulus presentations for subjects with high and low levels of Tense Arousal. These results are interpreted within the framework of Preliminary Process Theory in terms of the different attentional patterns in subjects with high and low levels of Tense Arousal. © 2004 Elsevier B.V. All rights reserved.

The influence of two anxiolytics on basal heart rate and on the evoked cardiac response elicited by auditory stimuli, was studied in humans. Diazepam (Valium) (7.5 mg) and buspirone (Buspar) (7.5 mg), which differ in their psycho-pharmacological profiles, were used. Prestimulus vigilance and cognitive load were manipulated by instructions allowing the subjects to ignore the stimuli, or requiring them to count the tones. Drug effects were obtained in subjective alertness, basal heart rate level, and the evoked cardiac response. Diazepam reduced subjective alertness, while buspirone did not. Diazepam apparently increased heart rate levels relative to placebo, in contrast to buspirone, which produced an apparent decrease in heart rate. These drug-induced prestimulus heart rate level effects were associated with differential decelerations immediately following stimulus onset and appear to reflect differences in prestimulus vigilance. Opposite effects of the drugs were also observed in the second, acceleratory, component of the of the evoked cardiac response, and these were found to be independent of the prestimulus drug effects. Compared with placebo, buspirone appeared to enhance the acceleratory component in the count condition, while diazepam led to an apparent reduction of this component. Enhancement of this acceleration after buspirone may reflect an increase in cognitive effort directed to the performance of task-relevant behaviour, while the reduction of this component after diazepam can be regarded as a cognitive-motivational neutralisation of signal value. The differential effects of the two anxiolytics support the separation of the evoked cardiac response into different components and may also have implications for the clinical use of the drugs.

We investigated the mechanism of two evoked cardiac response components associated with different aspects of information processing. Innocuous stimuli presented in an irrelevant condition elicit a simple cardiac deceleration termed ECR1. The same stimuli presented in a relevant condition (such as results from requesting subjects to silently count the stimuli) elicit a complex biphasic response with a large secondary acceleration in heart rate. This difference is attributed to the additional effect of cognitive task performance, resulting in an addition response component, ECR2. This may be realised by subtraction of the two responses. We investigated the mechanisms involved by comparing cardiac response profiles from a neurologically-impaired group with those from a control group. amyotrophic lateral sclerosis (ALS) has been associated with a loss of synaptic connections in the frontal lobe. Twelve ALS clinically non-demented patients were age-matched with twelve neurological patients without pathological changes in the brain. Cardiac response profiles for ECR1 and ECR2 were examined as a function of group. ECR1 did not differ between the groups, but ECR2 was significantly impaired in the ALS patients. The results are discussed in terms of different brain regions associated with these two cardiac response components. ECR1 may be associated with automatic pre attentive stimulus registration involving, in the case of auditory stimuli, the auditory analyser and associated pathways, while ECR2 appears to be a correlate of controlled executive processing, involving the frontal cortex.