Abnormalities of fixation, saccade and pursuit in posterior cortical atrophy

Shakespeare, Timothy J.; Kaski, Diego; Yong, Keir X. X.; Paterson, Ross W.; Slattery, Catherine F.; Ryan, Natalie S.; Schott, Jonathan M.; Crutch, Sebastian J.

doi:10.1093/brain/awv103

Cited by 84 publications

(81 citation statements)

References 78 publications

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“…Firstly, off-line manually coded saccade demonstrated significantly increased anticipatory saccade rates in the Alzheimer's disease group alone and in the horizontal gap condition alone, that was twice that found in aMCI and controls (33% versus 15%, p < 0.006). This outcome is consistent with a lack of inhibition of saccades in mild Alzheimer's disease that is sensitized by the gap paradigm [39,40]. Secondly, conventional post-hoc statistical analysis of manually coded error rates at antisaccades revealed that the mild Alzheimer's disease group had a reliably larger self-corrected error-rate than aMCI and controls, but self-correction was not significantly impaired in the aMCI group compared to controls.…”

Section: Discussionsupporting

confidence: 75%

“…A lower average gain was previously reported in mild Alzheimer's disease studies [8,10]. Lower gain/accuracy may be due to the degenerative process affecting parieto-occipital lobes and subcortical structures [39]. The mismatch between the latency distribution's intrinsic lognormal behavior, and Gaussian statistical assumptions underpinning conventional analyses likely yielded low statistical power, explaining the lack of significance found in the mild Alzheimer's disease group.…”

Section: Discussionmentioning

confidence: 67%

“…The resampling was repeated 300 times for all the statistical tests. Formally, the resulting bootstrap distribution is a standard-error distribution for the statistic of interest, given the sampled population [39]. Z-tests, computed from the bootstrapped lognormal parameter distributions of each patient group, were used to conduct statistical contrasts [40].…”

Section: Parametric Bootstrap (Resampling) Analysesmentioning

confidence: 99%

See 2 more Smart Citations

Prodromal Alzheimer’s Disease Demonstrates Increased Errors at a Simple and Automated Anti-Saccade Task

Holden

Cosnard

Laurens

et al. 2018

JAD

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Saccade alterations are potential early signs of Alzheimer's disease. However, uncertainty persists in how early and reliably automated saccade recording systems detect impairments. This multicenter pathophysiological case-control transversal study explored saccade execution in carefully diagnosed amnestic mild cognitive impairment patients fulfilling research criteria for prodromal Alzheimer's disease (n = 29), as compared to both aged-matched mild Alzheimer's disease patients (n = 23) and controls (n = 27). Auto-coded saccades from horizontal (gap) vertical (step) stimulus elicited pro-saccades, and anti-saccade (gap) tasks were compared across the 3 groups. Mild cognitive impairment patients committed significantly more anti-saccade errors compared to controls (46.9 versus 24.3%, p < 0.001). Conventional analyses of the auto-coded stimulus elicited saccades parameters did not distinguish the amnestic mild cognitive impairment from controls or the mild Alzheimer's disease group. However, an offline analysis of manually coded saccade latencies, using resampling statistics did reveal subtle differences among the groups. Analysis of the manually coded data revealed that the mild Alzheimer's disease group had a reliably larger self-corrected error-rate than in amnestic mild cognitive impairment and controls (p = 0.003). Analysis of the manually coded saccade latencies, using more sensitive lognormal bootstrap analysis revealed a continuum, from amnestic mild cognitive impairment to mild Alzheimer's disease, of an increased severity of impaired inhibition of stimulus elicited saccades and correct voluntary saccade initiation. Anti-saccade error rates and psychometric measures of executive and several other cognitive functions were moderately and negatively correlated. Overall, inhibitory impairments in stimulus elicited saccades, characteristic of Alzheimer's disease, may be detected early in presumed prodromal patients using a simple, automated anti-saccade task.

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Section: Discussionsupporting

confidence: 75%

Section: Discussionmentioning

confidence: 67%

Section: Parametric Bootstrap (Resampling) Analysesmentioning

confidence: 99%

See 1 more Smart Citation

Prodromal Alzheimer’s Disease Demonstrates Increased Errors at a Simple and Automated Anti-Saccade Task

Holden

Cosnard

Laurens

et al. 2018

JAD

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“…16 Saccadic eye movement impairments are one of the most commonly documented forms of oculomotor dysfunction in AD patients, 17–19 and have been recently reported in patients with the posterior cortical atrophy variant of AD. 20 Additional studies have also demonstrated that patients with amnestic MCI exhibit abnormal saccades. 21,22 These findings raise the possibility that a test of saccadic eye movement may have strong utility in the detection of cognitive impairment, in general, and AD, in particular.…”

Section: Introductionmentioning

confidence: 99%

Screening Utility of the King-Devick Test in Mild Cognitive Impairment and Alzheimer Disease Dementia

Galetta

Chapman

Essis

et al. 2017

Alzheimer Disease &Amp; Associated Disorders

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The King-Devick Test (K-D) is a 1–2-minute, rapid number naming test, often used to assist with detection of concussion, but also has clinical utility in other neurological conditions (e.g., Parkinson’s disease). The K-D involves saccadic eye and other eye movements, and abnormalities thereof may be an early indicator of Alzheimer’s disease (AD)-associated cognitive impairment. No study has tested the utility of the K-D in AD and we sought to do so. The sample included 206 (135 controls, 39 MCI, and 32 AD dementia) consecutive subjects from the Boston University Alzheimer’s Disease Center registry undergoing their initial annual evaluation between March 2013 and July 2015; the timeframe the K-D was administered. Areas under the receiver operating characteristic (ROC) curves generated from logistic regression models revealed the K-D test distinguished controls from subjects with cognitive impairment (MCI and AD dementia) (AUC=0.72), MCI (AUC=0.71) and AD dementia (AUC=0.74). K-D time scores between 48 and 52 seconds were associated with high sensitivity (>90.0%) and negative predictive values (>85.0%) for each diagnostic group. The K-D correlated strongly with validated attention, processing speed, and visual scanning tests. The K-D test may be a rapid and simple effective screening tool to detect cognitive impairment associated with AD.

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“…All these data combined have yielded very important findings. AD is linked to thicker retinal inner plexiform layer (IPL) (Snyder et al, 2016), thinner retinal NFL (Danesh-Meyer et al, 2006; Iseri et al, 2006; Paquet et al, 2007; Kesler et al, 2011; Gao et al, 2015; Thomson et al, 2015), a reduced number in ganglion cell axons (Blanks et al, 1996b; Danesh-Meyer et al, 2006), narrowing of retinal veins with decreased blood flow (Berisha et al, 2007), higher number of astrocytes in the NFL (Blanks et al, 1996a, 1996b), Aβ accumulation in GCL, NFL, IPL, outer retina (Alexandrov et al, 2011; Koronyo-Hamaoui et al, 2011) and lens (Goldstein et al, 2003), reduced amplitude and increased implicit times in ganglion cell responses (Katz et al, 1989; Trick et al, 1989; Krasodomska et al, 2010; Moschos et al, 2012), increased levels of inflammatory marker complement factor H in the retina (Alexandrov et al, 2011), and abnormalities in eye fixation, saccadic and pursuit movements (Chang et al, 2014; Shakespeare et al, 2015). …”

Section: Discussionmentioning

confidence: 99%

Retinal changes in the Tg-SwDI mouse model of Alzheimer’s disease

et al. 2017

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Alzheimer’s disease (AD), a debilitating neurodegenerative illness, is characterized by neuronal cell loss, mental deficits, and abnormalities in several neurotransmitter and protein systems. AD is also associated with visual disturbances, but their causes remain unidentified. We hypothesize that the visual disturbances stem from retinal changes, particularly changes in the retinal cholinergic system, and that the etiology in the retina parallels the etiology in the rest of the brain. To test our hypothesis, quantitative polymerase chain reaction (qPCR) and immunohistochemistry (IHC) were employed to assess changes in acetylcholine receptor (AChR) gene expression, number of retinal cells, and astrocytic gliosis in the Tg-SwDI mouse model as compared to age-matched wild type (WT). We observed that Tg-SwDI mice showed an initial upregulation of AChR gene expression early on (young adults and middle age adults), but a downregulation later on (old adults). Furthermore, transgenic animals displayed significant cell loss in the photoreceptor layer and inner retina of the young adult animals, as well as specific cholinergic cell loss, and increased astrocytic gliosis in the middle age adult and old adult groups. Our results suggest that the changes observed in AD cerebrum are also present in the retina and may be, at least in part, responsible for the visual deficits associated with the disease.

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Abnormalities of fixation, saccade and pursuit in posterior cortical atrophy

Cited by 84 publications

References 78 publications

Prodromal Alzheimer’s Disease Demonstrates Increased Errors at a Simple and Automated Anti-Saccade Task

Prodromal Alzheimer’s Disease Demonstrates Increased Errors at a Simple and Automated Anti-Saccade Task

Screening Utility of the King-Devick Test in Mild Cognitive Impairment and Alzheimer Disease Dementia

Retinal changes in the Tg-SwDI mouse model of Alzheimer’s disease

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