Road traffic accidents are largely determined by human errors in information processing and attention. Attentional functions constitute a vulnerable link in the human information processing chain. Three distinct attentional brain mechanisms are described that are considered to be involved in the supply of nervous energy for information processing. Arousal, phasic physiological responses to novel stimuli; Activation, tonic physiological readiness to respond; and Effort, the voluntarily exerted coordination between arousal and activation. These energy supply systems are mainly driven by noradrenergic, dopaminergic and cholinergic neurotransmission, respectively. Furthermore, they are affected by a behavioural inhibition system controlled by serotonin. The histamine neurotransmitter system is also associated with behavioural activation, whereas the neurotransmitter GABA has an inhibitory influence on the noradrenergic, dopaminergic and cholinergic systems. It is argued that the effects of drugs on driving can be predicted in terms of their effects on these neurochemical systems. Drugs that decrease noradrenaline-, acetylcholine-, dopamine- and histamine-neurotransmitter turn-over impair different facets of attention. GABAergic drugs are sedative, while serotonergic drugs seem to influence attention in a more subtle manner. Any pharmacological intervention on one or more of these systems via medicinal or other psychoactive drugs, can alter, and often impair, driving performance. The assessment of behavioural, psychophysiological and pharmacological markers of the attentional systems during driving performance may provide clues for the answer to the question how, rather than if, drugs have an influence on driving performance.
|Journal||Human Psychopharmacology-Clinical and Experimental|
|Publication status||Published - 1 Jan 1998|
Riedel, W. J., Vermeeren, A., van Boxtel, M., Vuurman, E. F. P. M., Verhey, F. R. J., Jolles, J., & Ramaekers, J. G. (1998). Mechanisms of drug-induced driving impairment: a dimensional approach. Human Psychopharmacology-Clinical and Experimental, 13(2), S49-S63. https://doi.org/10.1002/(SICI)1099-1077(1998110)13:2+<S49::AID-HUP49>3.3.CO;2-T