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Antisaccade Latency Is Sensitive to Longitudinal Change of Motor and Cognitive Symptoms in Parkinson's Disease

2020; Wiley; Volume: 36; Issue: 1 Linguagem: Inglês

10.1002/mds.28374

1531-8257

Josefine Waldthaler, Lena Stock, Johanna Sommerkorn, Charlotte Krüger‐Zechlin, Lars Timmermann,

Transcranial Magnetic Stimulation Studies

Considerable efforts have been made to evaluate different aspects of saccadic eye movements as potential biomarkers in Parkinson's disease (PD). The antisaccade task is a widely used eye-tracking paradigm that requires the suppression of a reflexive response to a visual target and the execution of a volitional saccade in the opposite direction instead1 (Fig. 1A). Despite a large body of evidence regarding alterations of antisaccades in PD,2 no studies have reported changes in antisaccade performance over time within the same subjects so far. Although comparisons of patients in different disease stages suggest prolongation of antisaccade latency with disease progression,3, 4 a conclusive statement about the usefulness of eye-tracking measures as potential biomarkers cannot be made without longitudinal data. In this pilot study, we investigated the changes in antisaccade latency and error rate in 25 patients with PD (age 61.4 ± 6.8, disease duration 6.0 ± 4.5 years) over a period of 12.3 ± 2.4 months in correlation with the evolution of motor and cognitive symptoms. Of the 25 patients, 10 received deep brain stimulation (DBS) in the subthalamic nucleus during the follow-up period (time between DBS activation and follow-up visit 4.5 ± 2.1 months). All patients were tested in the on medication and ON DBS states and adjustments of dopaminergic medication were allowed during the follow-up period. Patients without DBS who showed relevant improvement in motor symptoms after 1 year also received higher levodopa equivalent dose at follow-up (non-DBS group baseline: 578 ± 342 mg, mean change +12 ± 199 mg; DBS group baseline: 1033 ± 365 mg, mean change −335 ± 344 mg). Overall, mean antisaccade latency (baseline: 339 ± 72 milliseconds, mean change: +9 ± 51.1 milliseconds) and error rate (baseline: 0.52, mean change −0.02 ± 0.3) remained stable in the non-DBS group. In the DBS group, the antisaccade latency tended to increase (baseline: 295 ± 78 milliseconds, mean change: +48 ± 75 milliseconds [P = 0.09]), whereas the error rate improved at follow-up (baseline: 0.76, mean change: −0.21 ± 0.3 [P = 0.048]). The change in antisaccade latency correlated with change in MDS-UPDRS III in both groups (non-DBS group baseline: 25.7 ± 13.3, mean change +0.3 ± 7.4; DBS group baseline: 27.2 ± 16.5, mean change: −5.2 ± 17.8) and with the change in MoCA score in the non-DBS group (25.8 ± 3.1, mean change −1.3 ± 3.1) (Fig. 1B and 1C). Antisaccade latency at baseline was predictive of the MoCA score at follow-up in a univariate linear model (Fig. 1D). Building on earlier studies that have already proposed antisaccade measures as markers for PD severity,5, 6 we provide first data indicating that antisaccade latency may be sensitive to longitudinal intraindividual improvement and deterioration of motor and cognitive symptoms in PD. Our preliminary results pave the way for future longitudinal studies with larger cohorts and longer follow-up periods. The ethical committee approval was provided by the Ethical Committee of the Faculty of Medicine, Philipps University Marburg and written informed consents were obtained from all participants. We thank our patients for their dedicated cooperation in this study. Open access funding enabled and organized by Projekt DEAL. (1) Research Project: A. Conception, B. Organization, C. Execution; (2) Statistical Analysis: A. Design, B. Execution, C. Review and Critique; (3) Manuscript: A. Writing of the First Draft, B. Review and Critique. J.W.: 1A, 1A, 2A, 2B, 3A L.S.: 1C, 3B J.S.: 1C, 2C, 3B C.K.-Z.: 1C, 3B L.T.: 2C, 3B In the past year until March 2020, Lars Timmermann received payments as a consultant for Boston Scientific, and L.T. received honoraria as a speaker on symposia sponsored by UCB, Desitin, Boston Scientific, and Abbott. The institution of L.T., not L.T. personally, received funding by the German Research Foundation, the German Ministry of Education and Research, and the Deutsche Parkinson Vereinigung. Neither L.T. nor any member of his family holds stocks, stock options, patents, or financial interests in any of the aforementioned companies or their competitors. Professor Timmermann is member of the oversight Guidelines Commission of the German Neurological Society. He is participating in the Guideline of Treatment of Parkinson Syndromes. He will be the official delegate of the German Neurological Society in the EU medical devices commission and is appointed be become delegate of the German Neurological Society in the Arbeitsgemeinschaft der Wissenschaftlichen Medizinischen Fachgesellschaften (AWMF) (German National Institute for Medical Guidelines). Appendix S1. Supporting Information Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.