Specific visuomotor deficits due to alcohol intoxication: Evidence from the pro- and antisaccade paradigms

Vorstius, Christian; Radach, Ralph; Lang, Alan R.; Riccardi, Christina J.

doi:10.1007/s00213-007-0954-1

Cited by 31 publications

(50 citation statements)

References 48 publications

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“…As compared to placebo, low-dose lorazepam (1-2 mg) significantly increases saccade latency and decreases peak velocity (Masson et al 2000). Similar effects can be seen after consumption of moderate amounts of ethanol (Vorstius et al 2008). In addition, specific and marked impairment of saccadic eye movements have been reported in early Alzheimer's (Yang et al 2012), mild frontotemporal dementia (Boxer et al 2006), and in post concussion syndrome (Heitger et al 2008).…”

Section: Introductionsupporting

confidence: 56%

Cognitive performance in high-altitude climbers: a comparative study of saccadic eye movements and neuropsychological tests

et al. 2013

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Impairment of cognitive performance during and after high-altitude climbing has been described in numerous studies and has mostly been attributed to cerebral hypoxia and resulting functional and structural cerebral alterations. To investigate the hypothesis that highaltitude climbing leads to cognitive impairment, we used of neuropsychological tests and measurements of eye movement (EM) performance during different stimulus conditions. The study was conducted in 32 mountaineers participating in an expedition to Muztagh Ata (7,546 m). Neuropsychological tests comprised figural fluency, line bisection, letter and number cancellation, and a modified pegboard task. Saccadic performance was evaluated under three stimulus conditions with varying degrees of cortical involvement: visually guided pro-and anti-saccades, and visuo-visual interaction. Typical saccade parameters (latency, mean sequence, post-saccadic stability, and error rate) were computed off-line. Measurements were taken at a baseline level of 440 m and at altitudes of 4, 497, 5,533, 6,265, and again at 440 m. All subjects reached 5,533 m, and 28 reached 6,265 m. The neuropsychological test results did not reveal any cognitive impairment. Complete eye movement recordings for all stimulus conditions were obtained in 24 subjects at baseline and at least two altitudes and in 10 subjects at baseline and all altitudes. Measurements of saccade performances showed no dependence on any altitude-related parameter and were well within normal limits. Our data indicates that acclimatized climbers do not seem to suffer from significant cognitive deficits during or after climbs to altitudes above 7,500 m. We demonstrated that investigation of EMs is feasible during high-altitude expeditions.

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Section: Introductionsupporting

confidence: 56%

Cognitive performance in high-altitude climbers: a comparative study of saccadic eye movements and neuropsychological tests

et al. 2013

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“…Interest in this paradigm surged after the discovery that frontal lobe lesions specifically and severely affect human performance of antisaccades, while prosaccades (i.e., saccades directed to the visual stimulus) are facilitated [3]. Vorstius et al [168] showed that the saccade latency data strongly suggest that alcohol intoxication impairs temporal aspects of saccade generation, irrespective of the level of processing triggering the saccade. Furthermore, the specific impairment of saccade amplitude in the anti-saccade task under alcohol suggests that higher level processes involved in the spatial remapping of target location in the absence of a visually specified saccade goal are specifically affected by alcohol intoxication.…”

Section: Antisaccade Paradigmmentioning

confidence: 99%

Chronic alcoholism: Insights from neurophysiology

Campanella¹,

Petit²,

Maurage³

et al. 2009

Neurophysiologie Clinique/Clinical Neurophysiology

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SummaryIntroduction. -Increasing knowledge of the anatomical structures and cellular processes underlying psychiatric disorders may help bridge the gap between clinical signs and basic physiological processes. Accordingly, considerable insight has been gained in recent years into a common psychiatric condition, i.e., chronic alcoholism. Material and methods. -We reviewed various physiological parameters that are altered in chronic alcoholic patients compared to healthy individuals -continuous electroencephalogram, oculomotor measures, cognitive event-related potentials and event-related oscillations -to identify links between these physiological parameters, altered cognitive processes and specific clinical symptoms. Results. -Alcoholic patients display: (1) high beta and theta power in the resting electroencephalogram, suggesting hyperarousal of their central nervous system; (2) abnormalities in smooth pursuit eye movements, in saccadic inhibition during antisaccade tasks, and in prepulse inhibition, suggesting disturbed attention modulation and abnormal patterns of prefrontal activation that may stem from the same prefrontal ''inhibitory'' cortical dysfunction; (3) decreased amplitude for cognitive event-related potentials situated along the continuum of informationprocessing, suggesting that alcoholism is associated with neurophysiological deficits at the level of the sensory cortex and not only disturbances involving associative cortices and limbic structures; and (4) decreased theta, gamma and delta oscillations, suggesting cognitive disinhibition at a functional level. Discussion. -The heterogeneity of alcoholic disorders in terms of symptomatology, course and outcome is the result of various pathophysiological processes that physiological parameters * Corresponding author. E-mail address: salvatore.campanella@chu-brugmann.be (S. Campanella).

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“…This is broadly consistent with some previous reports of acute effects of alcohol on saccadic inhibitory control tasks. For example, more studies report a lack of alcohol effect or even a positive alcohol effect on anti-saccade task performance (Blekher et al, 2002;Khan et al, 2003;Vassallo et al, 2002;Vorstius et al, 2008) than report an impairment (Crevits et al, 2000;Marinkovic et al, 2013). Nonetheless, studies considering the effect of alcohol on the delayed ocular response task find significant effects of alcohol on premature saccades (e.g., Abroms et al, 2006;Weafer and Fillmore, 2012).…”

Section: Alcohol Does Not Affect Saccadic Ssrtmentioning

confidence: 99%

“…Participants make either a reflexive saccade to a target location (pro-saccade) or a saccade to the opposite location (anti-saccade) inhibiting their reflexive response. While two studies found alcohol to increase anti-saccade error rates in either head-injured participants (Crevits et al, 2000; blood alcohol levels between 1.89 and 3.84 g/l) or healthy participants (Marinkovic et al, 2013; alcohol dose 0.6 g/kg for males and 0.55 g/kg for females), two studies found no effect (healthy participants, Blekher et al, 2002; breath alcohol concentration 80 mg/dl; Vorstius et al, 2008; breath alcohol concentration 65 mg/dl). Counter-intuitively, two studies even found decreases in error rates (healthy participants, Khan et al, 2003; blood alcohol concentration 0.08%; Vassallo et al, 2002; blood alcohol concentration 0.044%), which may be due to alcohol attenuating the reflexive response rather than the inhibitory control process (Fillmore and Weafer, 2013).…”

Section: Introductionmentioning

confidence: 98%

Impairment of manual but not saccadic response inhibition following acute alcohol intoxication

Campbell

Chambers

Allen

et al. 2017

Drug and Alcohol Dependence

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A B S T R A C TBackground: Alcohol impairs response inhibition; however, it remains contested whether such impairments affect a general inhibition system, or whether affected inhibition systems are embedded in, and specific to, each response modality. Further, alcohol-induced impairments have not been disambiguated between proactive and reactive inhibition mechanisms, and nor have the contributions of action-updating impairments to behavioural 'inhibition' deficits been investigated. Methods: Forty Participants (25 female) completed both a manual and a saccadic stop-signal reaction time (SSRT) task before and after a 0.8 g/kg dose of alcohol and, on a separate day, before and after a placebo. Blocks in which participants were required to ignore the signal to stop or make an additional 'dual' response were included to obtain measures of proactive inhibition as well as updating of attention and action. Results: Alcohol increased manual but not saccadic SSRT. Proactive inhibition was weakly reduced by alcohol, but increases in the reaction times used to baseline this contrast prevent clear conclusions regarding response caution. Finally, alcohol also increased secondary dual response times of the dual task uniformly as a function of the delay between tasks, indicating an effect of alcohol on action-updating or execution. Conclusions: The modality-specific effects of alcohol favour the theory that response inhibition systems are embedded within response modalities, rather than there existing a general inhibition system. Concerning alcohol, saccadic control appears relatively more immune to disruption than manual control, even though alcohol affects saccadic latency and velocity. Within the manual domain, alcohol affects multiple types of action updating, not just inhibition.

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Specific visuomotor deficits due to alcohol intoxication: Evidence from the pro- and antisaccade paradigms

Cited by 31 publications

References 48 publications

Cognitive performance in high-altitude climbers: a comparative study of saccadic eye movements and neuropsychological tests

Cognitive performance in high-altitude climbers: a comparative study of saccadic eye movements and neuropsychological tests

Chronic alcoholism: Insights from neurophysiology

Impairment of manual but not saccadic response inhibition following acute alcohol intoxication

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