2016
DOI: 10.1007/s00213-016-4436-1
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Medications influencing central cholinergic neurotransmission affect saccadic and smooth pursuit eye movements in healthy young adults

Abstract: The prominent effects of the stronger central anticholinergic promethazine, on saccadic and smooth pursuit eye movements, potentially conveys the significance of central cholinergic pathways in the control of these centrally regulated oculomotor processes.

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Cited by 10 publications
(8 citation statements)
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“…Similarly, we found no relationship between pro‐saccades and cholinergic medication burden (determined with the Anticholinergic Drug Scale), which was unsurprising, as cholinergic therapies would likely increase rather than decrease reflexive saccade velocities through dampening saccadic inhibition . Similarly, cholinergic therapies may also increase saccadic latency and reduce amplitude (or gain) . Medication effect is one of the major challenges in interpretation of the results of saccadic impairments in PD, as it is difficult to determine whether deficits occur because of underlying PD pathology or the medications used to treat it.…”
Section: Discussionsupporting
confidence: 52%
See 1 more Smart Citation
“…Similarly, we found no relationship between pro‐saccades and cholinergic medication burden (determined with the Anticholinergic Drug Scale), which was unsurprising, as cholinergic therapies would likely increase rather than decrease reflexive saccade velocities through dampening saccadic inhibition . Similarly, cholinergic therapies may also increase saccadic latency and reduce amplitude (or gain) . Medication effect is one of the major challenges in interpretation of the results of saccadic impairments in PD, as it is difficult to determine whether deficits occur because of underlying PD pathology or the medications used to treat it.…”
Section: Discussionsupporting
confidence: 52%
“…37 Similarly, cholinergic therapies may also increase saccadic latency and reduce amplitude (or gain). 38 Medication effect is one of the major challenges in interpretation of the results of saccadic impairments in PD, as it is difficult to determine whether deficits occur because of underlying PD pathology or the medications used to treat it. However, studies regarding the impact of medications on saccades are inconsistent and often conflicting, which may be a result of the small sample sizes examined.…”
Section: Discussionmentioning
confidence: 99%
“…It also underscores the need to exclude confounding effects of comorbid conditions or psychoactive drugs that can secondarily alter eye movements. [58][59][60] Ocular motor studies in schizophrenia typically consider or control for medication effects, 59,61,62 but less so the mTBI literature.…”
Section: Ocular Motor Dysfunction In Traumatic Brain Injurymentioning
confidence: 99%
“…While disruption of normal neurological (Anderson and MacAskill 2013) or psychiatric (Lipton et al 1983) function can induce a range of characteristic eye-movement deficits; subtler modulations of neuronal function may also be detected in oculomotion. In this paper, we focus upon the neurochemical aspects of oculomotor control, and the sorts of oculomotor syndromes that may be induced by therapeutic agents (Naicker et al 2017; Reilly et al 2008). In doing so, we draw from recent theoretical work addressing the computational anatomy of oculomotion (Parr and Friston 2018a; Parr and Friston 2018c) and emerging themes in computational accounts of neuromodulation (Friston et al 2014; Marshall et al 2016; Parr et al 2018; Parr and Friston 2017b; Sales et al 2018; Schwartenbeck et al 2015).…”
Section: Introductionmentioning
confidence: 99%
“…organophosphate pesticides (Minton and Murray 1988)). As with the benzodiazepines, cholinergic effects have been associated with the velocity of a saccadic eye movement (Naicker et al 2017). This is interesting from the perspective of the scheme in Fig.…”
Section: Introductionmentioning
confidence: 99%