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Dose‐dependent sensorimotor impairment in human ocular tracking after acute low‐dose alcohol administration
KEY POINTS: Oculomotor behaviours are commonly used to evaluate sensorimotor disruption due to ethanol (EtOH). The current study demonstrates the dose‐dependent impairment in oculomotor and ocular behaviours across a range of ultra‐low BACs (<0.035%). Processing of target speed and direction, as...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7898833/ https://www.ncbi.nlm.nih.gov/pubmed/33332605 http://dx.doi.org/10.1113/JP280395 |
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author | Tyson, Terence L. Feick, Nathan H. Cravalho, Patrick F. Flynn‐Evans, Erin E. Stone, Leland S. |
author_facet | Tyson, Terence L. Feick, Nathan H. Cravalho, Patrick F. Flynn‐Evans, Erin E. Stone, Leland S. |
author_sort | Tyson, Terence L. |
collection | PubMed |
description | KEY POINTS: Oculomotor behaviours are commonly used to evaluate sensorimotor disruption due to ethanol (EtOH). The current study demonstrates the dose‐dependent impairment in oculomotor and ocular behaviours across a range of ultra‐low BACs (<0.035%). Processing of target speed and direction, as well as pursuit eye movements, are significantly impaired at 0.015% BAC, suggesting impaired neural activity within brain regions associated with the visual processing of motion. Catch‐up saccades during steady visual tracking of the moving target compensate for the reduced vigour of smooth eye movements that occurs with the ingestion of low‐dose alcohol. Saccade dynamics start to become ‘sluggish’ at as low as 0.035% BAC. Pupillary light responses appear unaffected at BAC levels up to 0.065%. ABSTRACT: Changes in oculomotor behaviours are often used as metrics of sensorimotor disruption due to ethanol (EtOH); however, previous studies have focused on deficits at blood‐alcohol concentrations (BACs) above about 0.04%. We investigated the dose dependence of the impairment in oculomotor and ocular behaviours caused by EtOH administration across a range of ultra‐low BACs (≤0.035%). We took repeated measures of oculomotor and ocular performance from sixteen participants, both pre‐ and post‐EtOH administration. To assess the neurological impacts across a wide range of brain areas and pathways, our protocol measured 21 largely independent performance metrics extracted from a range of behavioural responses ranging from ocular tracking of radial step‐ramp stimuli, to eccentric gaze holding, to pupillary responses evoked by light flashes. Our results show significant impairment of pursuit and visual motion processing at 0.015% BAC, reflecting degraded neural processing within extrastriate cortical pathways. However, catch‐up saccades largely compensate for the tracking displacement shortfall caused by low pursuit gain, although there still is significant residual retinal slip and thus degraded dynamic acuity. Furthermore, although saccades are more frequent, their dynamics are more sluggish (i.e. show lower peak velocities) starting at BAC levels as low as 0.035%. Small effects in eccentric gaze holding and no effect in pupillary response dynamics were observed at levels below 0.07%, showing the higher sensitivity of the pursuit response to very low levels of blood alcohol, under the conditions of our study. |
format | Online Article Text |
id | pubmed-7898833 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-78988332021-03-03 Dose‐dependent sensorimotor impairment in human ocular tracking after acute low‐dose alcohol administration Tyson, Terence L. Feick, Nathan H. Cravalho, Patrick F. Flynn‐Evans, Erin E. Stone, Leland S. J Physiol Neuroscience KEY POINTS: Oculomotor behaviours are commonly used to evaluate sensorimotor disruption due to ethanol (EtOH). The current study demonstrates the dose‐dependent impairment in oculomotor and ocular behaviours across a range of ultra‐low BACs (<0.035%). Processing of target speed and direction, as well as pursuit eye movements, are significantly impaired at 0.015% BAC, suggesting impaired neural activity within brain regions associated with the visual processing of motion. Catch‐up saccades during steady visual tracking of the moving target compensate for the reduced vigour of smooth eye movements that occurs with the ingestion of low‐dose alcohol. Saccade dynamics start to become ‘sluggish’ at as low as 0.035% BAC. Pupillary light responses appear unaffected at BAC levels up to 0.065%. ABSTRACT: Changes in oculomotor behaviours are often used as metrics of sensorimotor disruption due to ethanol (EtOH); however, previous studies have focused on deficits at blood‐alcohol concentrations (BACs) above about 0.04%. We investigated the dose dependence of the impairment in oculomotor and ocular behaviours caused by EtOH administration across a range of ultra‐low BACs (≤0.035%). We took repeated measures of oculomotor and ocular performance from sixteen participants, both pre‐ and post‐EtOH administration. To assess the neurological impacts across a wide range of brain areas and pathways, our protocol measured 21 largely independent performance metrics extracted from a range of behavioural responses ranging from ocular tracking of radial step‐ramp stimuli, to eccentric gaze holding, to pupillary responses evoked by light flashes. Our results show significant impairment of pursuit and visual motion processing at 0.015% BAC, reflecting degraded neural processing within extrastriate cortical pathways. However, catch‐up saccades largely compensate for the tracking displacement shortfall caused by low pursuit gain, although there still is significant residual retinal slip and thus degraded dynamic acuity. Furthermore, although saccades are more frequent, their dynamics are more sluggish (i.e. show lower peak velocities) starting at BAC levels as low as 0.035%. Small effects in eccentric gaze holding and no effect in pupillary response dynamics were observed at levels below 0.07%, showing the higher sensitivity of the pursuit response to very low levels of blood alcohol, under the conditions of our study. John Wiley and Sons Inc. 2020-12-17 2021-02-15 /pmc/articles/PMC7898833/ /pubmed/33332605 http://dx.doi.org/10.1113/JP280395 Text en © 2020 San Jose State University. The Journal of Physiology published by John Wiley & Sons Ltd on behalf of The Physiological Society This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes. |
spellingShingle | Neuroscience Tyson, Terence L. Feick, Nathan H. Cravalho, Patrick F. Flynn‐Evans, Erin E. Stone, Leland S. Dose‐dependent sensorimotor impairment in human ocular tracking after acute low‐dose alcohol administration |
title | Dose‐dependent sensorimotor impairment in human ocular tracking after acute low‐dose alcohol administration |
title_full | Dose‐dependent sensorimotor impairment in human ocular tracking after acute low‐dose alcohol administration |
title_fullStr | Dose‐dependent sensorimotor impairment in human ocular tracking after acute low‐dose alcohol administration |
title_full_unstemmed | Dose‐dependent sensorimotor impairment in human ocular tracking after acute low‐dose alcohol administration |
title_short | Dose‐dependent sensorimotor impairment in human ocular tracking after acute low‐dose alcohol administration |
title_sort | dose‐dependent sensorimotor impairment in human ocular tracking after acute low‐dose alcohol administration |
topic | Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7898833/ https://www.ncbi.nlm.nih.gov/pubmed/33332605 http://dx.doi.org/10.1113/JP280395 |
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