Affiliations: Institute for Cognitive Neuroscience, Biopsychology, Ruhr-University, Bochum, Germany | Department of Neurology, Huntington Centre NRW, St. Josef Hospital, Ruhr-University, Bochum, Germany | Cognitive Neurophysiology, Department of Child and Adolescent Psychiatry, TU Dresden, Germany
Note: [] Correspondence to: Christian Beste, Cognitive Neurophysiology, Department of Child and Adolescent Psychiatry, TU Dresden, Schubertstrasse 42, D-01309 Dresden, Germany. Tel.: +49 351 458 7072; Fax: +49 351 458 7318; E-mail: christian.beste@uniklinikum-dresden.de
Abstract: Background: It is well-known that Huntington's disease (HD) affects saccadic processing. However, saccadic dysfunctions in HD may be seen as a result of dysfunctional processes occurring at the oculomotor level prior to the execution of saccades, i.e., at a pre-saccadic level. Virtually nothing is known about possible changes in pre-saccadic processes in HD. Objective: This study examines pre-saccadic processing in pre-manifest HD gene mutation carriers (pre-HDs) by using clinically available EEG measures. Methods: Error rates, pre-saccadic EEG potentials and saccade onset EEG potentials were measured in 14 pre-HDs and case-matched controls performing prosaccades and antisaccades in a longitudinal study over a 15-month period. Results: The results show that pre-saccadic potentials were changed in pre-HDs, relative to controls and also revealed changes across the 15-month longitudinal period. In particular, pre-saccadic ERP in pre-HDs were characterized by lower amplitudes and longer latencies, which revealed longitudinal changes. These changes were observed for anti-saccades, but not for pro-saccades. Overt saccadic trajectories (potentials) were not different to those in controls, showing that pre-saccadic processes are sensitive to subtle changes in fronto-striatal networks in pre-HDs. Conclusions: Deficits in pre-saccadic processes prior the execution of an erroneous anti-saccade can be seen as an effect of dysfunctional cognitive control in HD. This may underlie saccadic abnormalities and hence a major phenotype of HD. Pre-saccadic EEG potentials preceding erroneous anti-saccades are sensitive to pre-manifest disease progression in HD.
