Mechanisms of drug-induced driving impairment: a dimensional approach

Research output: Contribution to journalArticleAcademicpeer-review

18 Citations (Scopus)

Abstract

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.
Original languageEnglish
Pages (from-to)S49-S63
JournalHuman Psychopharmacology-Clinical and Experimental
Volume13
Issue number2
DOIs
Publication statusPublished - 1 Jan 1998

Cite this

@article{5d6443ceb6fc4dcb90213f827a9606da,
title = "Mechanisms of drug-induced driving impairment: a dimensional approach",
abstract = "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.",
author = "W.J. Riedel and A. Vermeeren and {van Boxtel}, Martin and E.F.P.M. Vuurman and F.R.J. Verhey and J. Jolles and J.G. Ramaekers",
year = "1998",
month = "1",
day = "1",
doi = "10.1002/(SICI)1099-1077(1998110)13:2+<S49::AID-HUP49>3.3.CO;2-T",
language = "English",
volume = "13",
pages = "S49--S63",
journal = "Human Psychopharmacology-Clinical and Experimental",
issn = "0885-6222",
publisher = "Wiley",
number = "2",

}

TY - JOUR

T1 - Mechanisms of drug-induced driving impairment: a dimensional approach

AU - Riedel, W.J.

AU - Vermeeren, A.

AU - van Boxtel, Martin

AU - Vuurman, E.F.P.M.

AU - Verhey, F.R.J.

AU - Jolles, J.

AU - Ramaekers, J.G.

PY - 1998/1/1

Y1 - 1998/1/1

N2 - 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.

AB - 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.

U2 - 10.1002/(SICI)1099-1077(1998110)13:2+<S49::AID-HUP49>3.3.CO;2-T

DO - 10.1002/(SICI)1099-1077(1998110)13:2+<S49::AID-HUP49>3.3.CO;2-T

M3 - Article

VL - 13

SP - S49-S63

JO - Human Psychopharmacology-Clinical and Experimental

JF - Human Psychopharmacology-Clinical and Experimental

SN - 0885-6222

IS - 2

ER -