Abstract
Previous studies provide partly contradictory results about the characteristics of saccades in PD and the possible effects of levodopa, which may be attributed to different study design regarding disease stages, medication state or cognitive functioning. We studied horizontal and vertical visually guided saccades (VGS) and antisaccades (AS) in 40 patients with PD with and without postural instability in On and Off medication state as well as in 20 healthy controls (HC). Motor and cognitive performance were assessed using UPDRS, Montreal Cognitive Assessment (MoCA) and Frontal Assessment Battery (FAB). The PD group showed decreased VGS amplitudes and increased vertical VGS and AS latencies. Only relatively few studies had assessed vertical saccades in PD so far. However, our results indicate that vertical saccadic amplitude may be a supportive marker in diagnosing PD since upwards gain demonstrated an AUC of 0.85 for the discrimination of PD and HC. Only more advanced patients in Hoehn & Yahr stage 3 executed higher numbers of AS errors than HC. Since the AS error rate correlated with FAB and MoCA scores, AS performance seems to reflect cognitive ability in PD. Furthermore, the correlation of AS latency with the UPDRS axial subscore promotes the recently highlighted connection between postural control and executive function in PD. Levodopa did not alter saccade amplitudes and had opposing effects on the initiation of VGS and AS: Levodopa intake prolonged VGS latency, but decreased AS latency. Possible mechanisms by which levodopa may be capable of partially reversing the impaired balance between voluntary and reflexive cortical saccade initiation of PD are discussed.
Highlights
Visual disturbances are common in Parkinson’s disease (PD)[1] which is partly attributed to impaired oculomotor control.Saccades are the most studied eye movements since different patterns of saccade impairment reflect pathology in corresponding brain regions which, in turn, allows to distinguish between neurological conditions with similar symptoms but different pathophysiological substrate.[2]
Post-hoc multiple comparisons showed that the gain of upwards, downwards, and horizontal saccades was reduced in H&Y2 and in H&Y3 compared to healthy controls (HC) (Table 1 for detailed results)
The upwards and downwards gain were correlated with the total UPDRS III score, the correlations did not remain significant after correction for multiple testing (Table 2)
Summary
Visual disturbances are common in Parkinson’s disease (PD)[1] which is partly attributed to impaired oculomotor control.Saccades are the most studied eye movements since different patterns of saccade impairment reflect pathology in corresponding brain regions which, in turn, allows to distinguish between neurological conditions with similar symptoms but different pathophysiological substrate.[2]. The only clinical finding regarding eye movements in earlier stages of the disease may be a mild-upwards gaze palsy, surprisingly few studies assessed both horizontal and vertical saccades in the same session.[4] previous studies trials provided contradictory data regarding several aspects of saccades in PD which may be attributed to different methodology and composition of study cohorts, such as various disease stages, ON vs OFF medication state or exclusion of cognitively impaired patients.[5] In PD patients, visually guided saccades (VGS) and voluntary saccades are hypometric[6] which results in the need for multiple correction saccades to reach a visual target.[7] This fragmentation of gaze shift is remarkable and has been proposed as a biomarker.[8] Both, saccade amplitude and latency tend to worsen during the course of the disease[9] whereby VGS latency is prolonged in PD patients with mild cognitive impairment or dementia.[10] PD patients make more directional antisaccade (AS) errors than healthy controls (HC).[11] The performance in the AS task is related to functional and imaging markers of executive function in healthy elderly as well as patients with mild cognitive impairment.[12,13] Recently, the same association was demonstrated in early, drug-naive PD patients.[14] Ito et al
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