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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.
Saccadic Eye Movements in Patients with Mild Cognitive Impairment: A Longitudinal Study
Published in Journal of Motor Behavior, 2023
Müge Akkoyun, Koray Koçoğlu, Hatice Eraslan Boz, Pembe Keskinoğlu, Gülden Akdal
Six parameters were measured in saccade paradigms: (1) The saccadic reaction time (SRT) was measured as the time between the target onset and the onset of the correct saccade. (2) A saccade was defined as correct when it was made toward the target stimulus for the pro-saccade paradigm, in the opposite direction for the anti-saccade paradigm (3) Corrected errors were calculated for anti-saccades and defined as the responses which were redirected to the correct response location after the initiated incorrect saccade response. (4) Uncorrected errors are defined as the percentage of incorrect saccades made toward the stimulus during the anti-saccade task. (5) Express saccade was defined as a rapidly saccade responses with SRTs between 80 ms and 130 ms. (6) A saccade was defined as anticipatory if its SRT was shorter than 80 ms before target onset.
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
Our finding that CON demonstrated increased inhibitory errors relative to HC (21.88% vs. 13.22% of anti-saccade trials, averaged across conditions, respectively) is consistent with prior studies comprised predominantly of male participants presenting to the emergency department (23,32,37,59). Increased errors on the anti-saccade task among CON – but similar performance to controls on the stimulus-driven, reflexive prosaccade task (e.g. latency, gain, accuracy, duration and peak velocity) – suggests an acute, isolated, deficit in oculomotor executive control. That is, patients in the acute recovery phase following concussion exhibited increased difficulty inhibiting the automatic response to look toward the target. This finding is consistent with previous investigations of acute post-concussion functioning that reveal frontal networks dysfunction, which anatomically implicates the frontal and parietal cortices, as well as their subcortical connections and functionally implicates abilities such as executive functioning, problem solving, divided attention, sustained attention, and working memory (60–63). Anti-saccade errors may also be due to difficulty maintaining attention (more specifically, maintaining instructions in active working memory), suggesting deficits in the fronto-parietal working memory network (64); although the fact that CON and HC had comparable rates of self-correction of errors and latency of corrective saccades argues against this and suggest errors are likely attributable to reduced top-down executive control of attention.
Associations between Attention-Deficit/Hyperactivity Disorder and Ocular Abnormalities in Children: A Population-based Study
Published in Ophthalmic Epidemiology, 2020
Jau-Der Ho, Jau-Jiuan Sheu, Yi-Wei Kao, Ben-Chang Shia, Herng-Ching Lin
Attention-deficit/hyperactivity disorder (ADHD) is one of the most common neurodevelopmental disorders of childhood, characterized by symptoms of impulsivity, hyperactivity, and inattention.1–3 ADHD is estimated to affect 3–5% of elementary school children, and for some, these symptoms can persist into adulthood.4,5 Several studies showed that ADHD is associated with different dysfunctions and abnormal problems, such as allergic processes, obesity, enuresis, febrile seizures, headaches, congenital heart diseases, ocular abnormalities, and dental caries.6,7 Moreover, ADHD was reported to be associated with disturbances in the prefrontal circuitry and seems to be associated with dysfunctions of eye motility on the antisaccade task and memory-guided saccade task.4,8,9