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Brain Advance Access originally published online on March 17, 2005
Brain 2005 128(6):1267-1276; doi:10.1093/brain/awh484
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© The Author (2005). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please e-mail: journals.permissions@oupjournals.org

Saccadic eye movement changes in Parkinson's disease dementia and dementia with Lewy bodies

Urs P. Mosimann1,2, René M. Müri2, David J. Burn1, Jacques Felblinger3, John T. O'Brien1 and Ian G. McKeith1

1 Institute for Ageing and Health, Newcastle General Hospital, Newcastle upon Tyne, UK, 2 Perception and Eye Movement Laboratory, Departments of Neurology and Clinical Research, Inselspital, Bern, Switzerland and 3 Department of Radiology, University Hospital of Nancy, Vandoeuvre, France

Correspondence to: Dr Urs P. Mosimann, Institute for Ageing and Health, Wolfson Research Centre, Newcastle General Hospital, Westgate Road, Newcastle upon Tyne NE4 6BE, UK E-mail: u.p.mosimann{at}ncl.ac.uk

Neurodegeneration in Parkinson's disease dementia (PDD) and dementia with Lewy bodies (DLB) affect cortical and subcortical networks involved in saccade generation. We therefore expected impairments in saccade performance in both disorders. In order to improve the pathophysiological understanding and to investigate the usefulness of saccades for differential diagnosis, saccades were tested in age- and education-matched patients with PDD (n = 20) and DLB (n = 20), Alzheimer's disease (n = 22) and Parkinson's disease (n = 24), and controls (n = 24). Reflexive (gap, overlap) and complex saccades (prediction, decision and antisaccade) were tested with electro-oculography. PDD and DLB patients had similar impairment in all tasks (P > 0.05, not significant). Compared with controls, they were impaired in both reflexive saccade execution (gap and overlap latencies, P < 0.0001; gains, P < 0.004) and complex saccade performance (target prediction, P < 0.0001; error decisions, P < 0.003; error antisaccades: P < 0.0001). Patients with Alzheimer's disease were only impaired in complex saccade performance (Alzheimer's disease versus controls, target prediction P < 0.001, error decisions P < 0.0001, error antisaccades P < 0.0001), but not reflexive saccade execution (for all, P > 0.05). Patients with Parkinson's disease had, compared with controls, similar complex saccade performance (for all, P > 0.05) and only minimal impairment in reflexive tasks, i.e. hypometric gain in the gap task (P = 0.04). Impaired saccade execution in reflexive tasks allowed discrimination between DLB versus Alzheimer's disease (sensitivity ≥60%, specificity ≥77%) and between PDD versus Parkinson's disease (sensitivity ≥60%, specificity ≥88%) when ±1.5 standard deviations was used for group discrimination. We conclude that impairments in reflexive saccades may be helpful for differential diagnosis and are minimal when either cortical (Alzheimer's disease) or nigrostriatal neurodegeneration (Parkinson's disease) exists solely; however, they become prominent with combined cortical and subcortical neurodegeneration in PDD and DLB. The similarities in saccade performance in PDD and DLB underline the overlap between these conditions and underscore differences from Alzheimer's disease and Parkinson's disease.


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