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Cognitive Aging
Published in Rachael E. Docking, Jennifer Stock, International Handbook of Positive Aging, 2017
Nelson A. Roque, Walter R. Boot
Our ability to limit the influence of task-irrelevant information taps directly into the construct of inhibition. This construct has been considered by some to be largely responsible for explaining age-related declines in cognitive function. One paradigm used to measure inhibition is the antisaccade task (Munoz & Everling, 2004), in which observers are asked to look in the opposite direction of the stimulus that is presented on the screen (to the left or right of a fixation cross). There is evidence that age-related declines in the frontostriatal systems may be contributing to a reduced capacity to voluntarily suppress an eye movement towards the target amongst older adults compared to younger adults (Sweeney et al., 2001). The evidence for age differences in inhibition is mixed, with an early meta-analysis on measuring inhibitory control mechanisms using the Stroop task (Stroop, 1935) finding no age differences in inhibition (Verhaeghen & De Meersman, 1998), compared to a large-scale study looking at the Stroop task that found age differences not attributed to general slowing (Troyer, Leach & Strauss, 2006).
Neurology with dementia with Lewy bodies
Published in John O'Brien, Ian McKeith, David Ames, Edmond Chiu, Dementia with Lewy Bodies and Parkinson's Disease Dementia, 2005
Certain aspects of saccadic eye movements (rapid eye movements that shift the fovea to a visual target) are abnormal in DLB (Mosimann et al, 2003). Thus, mean saccadic latency is significantly increased and mean gain of the first saccade is reduced in DLB patients compared with AD and normal controls, while both DLB and AD patients make more errors in an antisaccade task compared with normal controls. The pathophysiological basis for these changes is uncertain, but is likely to reflect both cortical and subcortical pathology.
Special Considerations in Gaze
Published in Vivek Lal, A Clinical Approach to Neuro-Ophthalmic Disorders, 2023
Mohamed Elkasaby, Aasef G. Shaikh
Wernicke's encephalopathy, characterized by the triad of encephalopathy, ophthalmoplegia and gait ataxia, is caused by thiamine deficiency [119]. There is a frequent association with chronic alcoholism, but it may be seen with other conditions like hyperemesis, acquired immunodeficiency syndrome, gastrointestinal surgery especially bariatric surgery and malnutrition in general [119]. Nystagmus, the most common finding, presents in form of gaze-evoked, upbeat or downbeat nystagmus; in some cases, upbeat nystagmus switches to downbeat with convergence [120, 121]. Early impairment in horizontal vestibulo-ocular reflexes are noted, but as disease progresses there is impairment in abduction, horizontal and vertical gaze palsies and inter-nuclear ophthalmoplegia that eventually becomes complete ophthalmoplegia [122–124]. Saccade slowing is rare finding in Wernicke's encephalopathy [125]. Without immediate parenteral administration thiamine, Wernicke's disease can progress to Korsakoff syndrome in which there is a striking disorder of selective anterograde and retrograde amnesia along with psychiatric symptoms. In rare cases, individuals may create imaginary events to fill in gaps in their memory (confabulation). Korsakoff syndrome may include significant abnormalities of eye movement, which include abnormal horizontal smooth pursuit eye movements, hypometria and increased saccadic durations [126, 127]. An increased number of directional errors on an antisaccade task may also be seen in these patients [128]. Wernicke's encephalopathy affects extracerebellar brainstem regions, including those responsible for burst generation, and is not predominantly cerebellar [121, 129]. Impairment of saccade burst generation is, therefore, the likely cause of the rare saccadic slowing in Wernicke's encephalopathy. In atypical cases, Wernicke's encephalopathy may also affect the substantia nigra, which could affect saccades through lack of tectal inhibition [130]. In such cases, parkinsonism is expected in addition to the slow saccades.
Central vestibular dysfunction: don’t forget vestibular rehabilitation
Published in Expert Review of Neurotherapeutics, 2022
Sulin Zhang, Dan Liu, E. Tian, Jun Wang, Zhaoqi Guo, Weijia Kong
The anti-saccade task, first developed by Peter Hallett [56], has been used extensively for investigating mechanisms of voluntary saccade control. Anti-saccade suddenly appears in the field of vision at the mirror position of the target. It was initially developed as a way to dissociate between the stimulus location and the goal of the saccade [57]. Memory-guided saccade is based on the position of the target that appeared in memory. When an action is memory-guided, its control must access a stored representation of the target, and this stored representation cannot be provided by the visuomotor mechanisms in the dorsal pathway [58]. Both are the endogenous higher cortex eye movement reflex and include cortical-subcortical eye movements. Such reflexes involve the center and structure alone the random eye movement pathways, with the will, the higher cortex and the cognitive processing process being implicated in them. The difference between the two saccades lies in that the visual target moves in different manners. In anti-saccade, the examiner raises the target with both hands, and randomly indicates one of the two visual targets. With patient’s head staying static, and the eyes quickly scan in the opposite direction of the indicated target. With memory-guided saccade, the examiner holds two vision targets with both hands. At a certain angle, the patient stares at the two vision targets on the left and the right. After allowing for adaptation for some time, the patient closes eyes and imagines the eye movement when eyes are open and move eyes to the left and right. The session is repeated 5 times.
Eye movement performance and clinical outcomes among female athletes post-concussion
Published in Brain Injury, 2020
Virginia Gallagher, Brian Vesci, Jeffrey Mjaanes, Hans Breiter, Yufen Chen, Amy Herrold, James Reilly
Primary eye movement measurements of interest (see Table 1) on the prosaccade task included (a) latency: the time (in milliseconds [ms]) between the appearance of the stimuli and the initiation of a saccade, which reflects the speed of reflexive shifts of visual attention and response execution; (b) gain: the spatial accuracy of the saccade to the target location, which is derived from the ratio of the saccade amplitude to the target amplitude (gain of 1 reflects perfect spatial accuracy, < 1 indicates participant undershot the target [hypometric], and > 1 indicates participant overshot the target [hypermetric]; (c) accuracy: the spatial accuracy of the primary saccade, derived from the difference between the location of the target position (in x-coordinate pixels) and the location of the end point of the primary saccade; (d) duration: the time (ms) taken to complete a saccade; and (e) peak velocity: the highest velocity reached during the saccade, which is linearly related to the saccade duration (41). On the anti-saccade task, the primary eye movement measurements of interest were primary saccade latency, which reflects the speed of executive shifts of visual attention, and anti-saccade error rate (error trials/total trials), a measure of executive inhibition and cognitive control; an error trial occurred when the participant incorrectly looked ≥ 20% of the distance toward the peripheral target.
Saccade eye movement in children with attention deficit hyperactivity disorder
Published in Nordic Journal of Psychiatry, 2020
Jui-Hsiang Huang, Yuan-Shuo Chan
In the present eye tracking research for the normal children population, we used different ocular motor paradigms in order to elicit these different types of saccades. Some paradigms were used to cause horizontal visually guided saccades (step, gap, overlap paradigms) and anti-saccades. These paradigms differ in the delay between the destroying fixation point and the illumination of a peripheral target. This delay can influence the latency of saccades and trigger reflexive or more voluntary saccades. In the anti-saccade task, there can be a more complex voluntary saccade than the overlap paradigm generated. This was done by asking the participant to inhibit eye movement towards a peripheral target and then to generate a voluntary saccade of the same amplitude in the opposite direction. Anti-saccade tasks are usually used in developmental and clinical research [25,26]. For amplitude gain, there was a statistically significant interaction between saccade size and age. Small saccades (<5°) were not as significantly affected [27].