Saccadic intrusions in Alzheimer-type dementia

Jones, Ashby; Friedland, Robert P.; Koss, B; Stark, Lawrence; Thompkins-Ober, B A

doi:10.1007/bf00313742

Cited by 56 publications

(27 citation statements)

References 27 publications

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“…Both groups exhibited a decreased period of fixation, which was associated in PCA with increased frequency of large intrusive saccades and in typical Alzheimer's disease with an increased frequency of square wave jerks. These findings of impaired fixation stability are consistent with previous reports of saccadic intrusions during fixation in Alzheimer's disease (Jones et al, 1983;Schewe et al, 1999), though it should be noted that square wave jerks are not specific to Alzheimer's disease, with increased frequency associated with advancing age (Herishanu and Sharpe, 1981) and other neurological conditions such as progressive supranuclear palsy, cerebellar disease and Parkinson's disease (Troost and Daroff, 1977;White et al, 1983;Rascol et al, 1991;Rabiah et al, 1997). The increased frequency of square wave jerks in patients with typical Alzheimer's disease likely reflects changes in basic oculomotor mechanisms rather than higher order cognitive processes, as these eye movements are not under cognitive control.…”

Section: Fixation Stabilitysupporting

confidence: 93%

Abnormalities of Fixation, Saccade and Pursuit in Posterior Cortical Atrophy

Shakespeare¹,

Kaski²,

Yong³

et al. 2015

J Neurol Neurosurg Psychiatry

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See Antoniades and Kennard (doi:10.1093/brain/awv124) for a scientific commentary on this article.The clinico-neuroradiological syndrome posterior cortical atrophy is the cardinal 'visual dementia' and most common atypical Alzheimer's disease phenotype, offering insights into mechanisms underlying clinical heterogeneity, pathological propagation and basic visual phenomena (e.g. visual crowding). Given the extensive attention paid to patients' (higher order) perceptual function, it is surprising that there have been no systematic analyses of basic oculomotor function in this population. Here 20 patients with posterior cortical atrophy, 17 patients with typical Alzheimer's disease and 22 healthy controls completed tests of fixation, saccade (including fixation/target gap and overlap conditions) and smooth pursuit eye movements using an infrared pupil-tracking system. Participants underwent detailed neuropsychological and neurological examinations, with a proportion also undertaking brain imaging and analysis of molecular pathology. In contrast to informal clinical evaluations of oculomotor dysfunction frequency (previous studies: 38%, current clinical examination: 33%), detailed eyetracking investigations revealed eye movement abnormalities in 80% of patients with posterior cortical atrophy (compared to 17% typical Alzheimer's disease, 5% controls). The greatest differences between posterior cortical atrophy and typical Alzheimer's disease were seen in saccadic performance. Patients with posterior cortical atrophy made significantly shorter saccades especially for distant targets. They also exhibited a significant exacerbation of the normal gap/overlap effect, consistent with 'sticky fixation'. Time to reach saccadic targets was significantly associated with parietal and occipital cortical thickness measures. On fixation stability tasks, patients with typical Alzheimer's disease showed more square wave jerks whose frequency was associated with lower cerebellar grey matter volume, while patients with posterior cortical atrophy showed large saccadic intrusions whose frequency correlated significantly with generalized reductions in cortical thickness. Patients with both posterior cortical atrophy and typical Alzheimer's disease showed lower gain in smooth pursuit compared to controls. The current study establishes that eye movement abnormalities are near-ubiquitous in posterior cortical atrophy, and highlights multiple aspects of saccadic performance which distinguish posterior cortical atrophy from typical Alzheimer's disease. We suggest the posterior cortical atrophy oculomotor profile (e.g. exacerbation of the saccadic gap/overlap effect, preserved saccadic velocity) reflects weak input from degraded occipito-parietal spatial representations of stimulus location into a superior collicular spatial map for eye movement regulation. This may indicate greater impairment of identification of oculomotor targets rather than generation of oculomotor movements. The results highlight the critical role of spatial attention an...

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Section: Fixation Stabilitysupporting

confidence: 93%

Abnormalities of Fixation, Saccade and Pursuit in Posterior Cortical Atrophy

Shakespeare¹,

Kaski²,

Yong³

et al. 2015

J Neurol Neurosurg Psychiatry

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“…A problem with classifying SI is that it can be difficult to distinguish the saccades taking the eye away from and towards the target in the presence of large numbers of SI [18]. Many studies of fixation have concentrated on characterising the features of SI in a range of test conditions, to the exclusion of other features such as fixation periods (FP) that may occur between SI [4,7,8,13,23,[32][33][34]. Concentrating solely on SI characteristics to the exclusion of other features recorded during fixation, introduces the possibility of missing other features that may provide clinically useful insights into neurological function [18].…”

Section: Introductionmentioning

confidence: 99%

An exploration of ocular fixation in Parkinson’s disease, multiple system atrophy and progressive supranuclear palsy

et al. 2009

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Since the basal ganglia are thought to have a role in controlling ocular fixation it is expected that patients with parkinsonian conditions would show impaired performance in fixation tasks. Our study examines ocular fixation in patients with a range of parkinsonian conditions (Idiopathic Parkinson's Disease, Multiple System Atrophy and Progressive Supranuclear Palsy). Eye movements were recorded from 44 patients and 50 age matched control subjects during ocular fixation both with and without a visible target. The data for each patient were then characterised in terms of fixation periods and saccadic intrusions (SI). Patient groups exhibited larger and more frequent SI as well as greater displacement from the fixation target. Patients with Progressive Supranuclear Palsy exhibit larger SI than control subjects when fixation targets are visible, this difference is reversed in the absence of a fixation target. Patients with Multiple System Atrophy show increased frequency of SI both with and without a visible target. Our findings show that ocular fixation is impaired in patients with parkinsonian conditions and may prove useful as part of an oculomotor profile to aid with the differentiation of parkinsonian conditions.

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“…Although abnormalities of both saccadic [1, 2, 3, 4, 5, 6, 7, 8, 9]and smooth pursuit [10, 11, 12]eye movements exist in Alzheimer’s disease (AD), neither prolonged saccadic latencies nor reduced pursuit gains per se are significant contributors to the eventually overwhelming disability experienced by the AD patient. Their importance lies instead in the information which ocular motor deficits can convey about dysfunction of the visuomotor pathways in the brain.…”

Section: Introductionmentioning

confidence: 99%

Effects of Stimulus Predictability and Interstimulus Gap on Saccades in Alzheimer’s Disease

Abel

Unverzagt²,

Yee

2002

Dement Geriatr Cogn Disord

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Objectives: Studies of saccadic eye movement impairment in Alzheimer’s disease (AD) have largely focused on simple reflexive eye movements and the antisaccade task. The effects of manipulating stimulus timing have been little studied. Methods: Fourteen patients with mild to severe AD and 11 age-matched controls were studied on the antisaccade task, while latencies on simultaneous, gap and predictable tasks were recorded from 11 patients and 11 controls. Dementia severity was assessed with the Mini-Mental State Examination. Results: As a group, patients’ latencies were significantly higher and more variable on the simultaneous and gap tasks. Predictable task performance was similar in mean but significantly more variable. Grossly anticipatory responses by patients were common on the predictable, simultaneous and gap tasks. Exclusion of these from subject means revealed that AD patients, when making target-driven saccades, demonstrated a gap effect of similar magnitude to normal subjects. Patients made significantly fewer correct antisaccades and significantly more reflexive errors not followed by a corrective antisaccade than did controls. Conclusions: The frequent presence of grossly anticipatory saccades may reflect dysfunction of fixation mechanisms possibly involving projections from frontal lobe to superior colliculus. The less frequently seen, marked prolongation of latency may reflect changes in posterior parietal mechanisms mediating reflexive saccade generation. The presence of the gap effect demonstrates a continued ability to benefit from externally controlled stimulus disengagement. Patients’ ability to make appropriately timed saccades to targets of known locations was particularly impaired, but the target sequence itself was at least grossly correctly learned. Larger studies may be able to identify clinically distinct populations of AD patients.

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Saccadic intrusions in Alzheimer-type dementia

Cited by 56 publications

References 27 publications

Abnormalities of Fixation, Saccade and Pursuit in Posterior Cortical Atrophy

Abnormalities of Fixation, Saccade and Pursuit in Posterior Cortical Atrophy

An exploration of ocular fixation in Parkinson’s disease, multiple system atrophy and progressive supranuclear palsy

Effects of Stimulus Predictability and Interstimulus Gap on Saccades in Alzheimer’s Disease

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