Impairment of Saccadic Eye Movements by Scopolamine Treatment

Oliva, Giulia Anna; Bucci, Maria Pia; Fioravanti, R.

doi:10.2466/pms.1993.76.1.159

Cited by 15 publications

(3 citation statements)

References 8 publications

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“…For example, the anticholinesterase inhibitor pyridostigmine decreased visual smooth pursuit in nonhuman primates while not impacting manual tasks (Vercher, Dusticier, Ebihara, Nieoullon, & Gauthier, 1990). The acetylcholine receptor antagonist scopolamine has been demonstrated to impair stability of visual fixation, decrease saccade accuracy and increase latency, and robustly decrease peak saccade velocity in healthy individuals even at low doses (Oliva, Bucci, & Fioravanti, 1993). And, atropine, another anticholinergic drug, impairs smooth pursuit performance at doses where changes in neuropsychological measures of attention were not detected (Penetar, Haegerstrom-Portnoy, & Jones, 1988).…”

Section: Pharmacologic Effects On Eye Movements In Healthy Individmentioning

confidence: 99%

Pharmacological treatment effects on eye movement control

Reilly

Lencer

Bishop

et al. 2008

Brain and Cognition

207

142

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The increasing use of eye movement paradigms to assess the functional integrity of brain systems involved in sensorimotor and cognitive processing in clinical disorders requires greater attention to effects of pharmacological treatments on these systems. This is needed to better differentiate disease and medication effects in clinical samples, to learn about neurochemical systems relevant for identified disturbances, and to facilitate identification of oculomotor biomarkers of pharmacological effects. In this review, studies of pharmacologic treatment effects on eye movements in healthy individuals are summarized and the sensitivity of eye movements to a variety of pharmacological manipulations is established. Primary findings from these studies of healthy individuals involving mainly acute effects indicate that: (i) the most consistent finding across several classes of drugs, including benzodiazepines, first- and second-generation antipsychotics, anticholinergic agents, and anticonvulsant/mood stabilizing medications is a decrease in saccade and smooth pursuit velocity (or increase in saccades during pursuit); (ii) these oculomotor effects largely reflect the general sedating effects of these medications on central nervous system functioning and are often dose-dependent; (iii) in many cases changes in oculomotor functioning are more sensitive indicators of pharmacological effects than other measures; and (iv) other agents, including the antidepressant class of serotonergic reuptake inhibitors, direct serotonergic agonists, and stimulants including amphetamine and nicotine, do not appear to adversely impact oculomotor functions in healthy individuals and may well enhance aspects of saccade and pursuit performance. Pharmacological treatment effects on eye movements across several clinical disorders including schizophrenia, affective disorders, attention deficit hyperactivity disorder, Parkinson's disease, and Huntington's disease are also reviewed. While greater recognition and investigation into pharmacological treatment effects in these disorders is needed, both beneficial and adverse drug effects are identified. This raises the important caveat for oculomotor studies of neuropsychiatric disorders that performance differences from healthy individuals cannot be attributed to illness effects alone. In final sections of this review, studies are presented that illustrate the utility of eye movements for use as potential biomarkers in pharmacodynamic and pharmacogenetic studies. While more systematic studies are needed, we conclude that eye movement measurements hold significant promise as tools to investigate treatment effects on cognitive and sensorimotor processes in clinical populations and that their use may be helpful in speeding the drug development pathway for drugs targeting specific neural systems and in individualizing pharmacological treatments.

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Section: Pharmacologic Effects On Eye Movements In Healthy Individmentioning

confidence: 99%

Pharmacological treatment effects on eye movement control

Reilly

Lencer

Bishop

et al. 2008

Brain and Cognition

207

142

View full text Add to dashboard Cite

show abstract

“…Hyoscine (a.k.a. scopolamine), an antimuscarinic (anticholinergic) drug (Corallo et al 2009) used to treat motion sickness, slows the velocity of saccades (Oliva et al 1993), consistent with Fig. 3.…”

Section: Introductionmentioning

confidence: 58%

The computational pharmacology of oculomotion

Parr

Friston

2019

Psychopharmacology

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Many physiological and pathological changes in brain function manifest in eye-movement control. As such, assessment of oculomotion is an invaluable part of a clinical examination and affords a non-invasive window on several key aspects of neuronal computation. While oculomotion is often used to detect deficits of the sort associated with vascular or neoplastic events; subtler (e.g. pharmacological) effects on neuronal processing also induce oculomotor changes. We have previously framed oculomotor control as part of active vision, namely, a process of inference comprising two distinct but related challenges. The first is inferring where to look, and the second is inferring how to implement the selected action. In this paper, we draw from recent theoretical work on the neuromodulatory control of active inference. This allows us to simulate the sort of changes we would expect in oculomotor behaviour, following pharmacological enhancement or suppression of key neuromodulators—in terms of deciding where to look and the ensuing trajectory of the eye movement itself. We focus upon the influence of cholinergic and GABAergic agents on the speed of saccades, and consider dopaminergic and noradrenergic effects on more complex, memory-guided, behaviour. In principle, a computational approach to understanding the relationship between pharmacology and oculomotor behaviour affords the opportunity to estimate the influence of a given pharmaceutical upon neuronal function, and to use this to optimise therapeutic interventions on an individual basis.

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“…The patient's transdermal scopolamine exposure may also have contributed to her symptoms since cholinergic pathways play a role in oculomotor function [5,12]. Central anticholinergic medications such as scopolamine can impair eye movements in healthy individuals due to decreased cholinergic transmission, in addition to the better-known effects of mydriasis and increased intraocular pressure [5,6,[13][14][15][16]. Anticholinergic activity may not completely explain her extraocular symptoms, however, so we concluded her presentation was likely a combination of her anesthetic and anticholinergic drug exposure to which her mild chronic white matter microvascular ischemia may have rendered her susceptible.…”

Section: Discussionmentioning

confidence: 99%

Transient Bilateral Ophthalmoplegia: A Case of a Forgotten Anesthetic Medication Effect

Hyland

Kavi

Smith

et al. 2021

Cureus

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A 58-year-old woman was found to have bilateral ptosis and downward gaze deviation immediately after elective shoulder surgery with general anesthesia and supraclavicular nerve block. A code stroke was activated due to concern for the neurologic process, but neuroimaging did not reveal acute changes or vascular abnormality. Her symptoms gradually resolved in the following hours with supportive care and were ultimately deemed to be related to anesthetic and transdermal scopolamine exposures layered upon her underlying comorbidities. Transient bilateral ophthalmoplegia after general anesthetics has been previously described; drug effect should be considered in the differential of this alarming presentation, which can mimic acute stroke and/or Horner syndrome.

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Impairment of Saccadic Eye Movements by Scopolamine Treatment

Cited by 15 publications

References 8 publications

Pharmacological treatment effects on eye movement control

Pharmacological treatment effects on eye movement control

The computational pharmacology of oculomotion

Transient Bilateral Ophthalmoplegia: A Case of a Forgotten Anesthetic Medication Effect

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