title: Changes in cognitive control in pre-manifest Huntington's disease examined using pre-saccadic EEG potentials - a longitudinal study.
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.
authors: Institute for Cognitive Neuroscience, Biopsychology, Ruhr-University, Bochum, Germany.
authors: Vanessa
authors: V
authors: Ness
authors: Institute for Cognitive Neuroscience, Biopsychology, Ruhr-University, Bochum, Germany.
authors: Anne-Kathrin
authors: AK
authors: Bestgen
authors: Department of Neurology, Huntington Centre NRW, St. Josef Hospital, Ruhr-University, Bochum, Germany.
authors: Carsten
authors: C
authors: Saft
authors: Institute for Cognitive Neuroscience, Biopsychology, Ruhr-University, Bochum, Germany Cognitive Neurophysiology, Department of Child and Adolescent Psychiatry, TU Dresden, Germany.
authors: Christian
authors: C
authors: Beste
mesh_terms: D000328:Adult; D001921:Brain / Q000503:physiopathology*; D016022:Case-Control Studies; D003072:Cognition Disorders / Q000209:etiology / Q000503:physiopathology*; D018450:Disease Progression; D004569:Electroencephalography; D005071:Evoked Potentials / Q000502:physiology*; D053483:Eye Movement Measurements; D005133:Eye Movements / Q000502:physiology; D005260:Female; D006801:Humans; D006816:Huntington Disease / Q000150:complications / Q000503:physiopathology*; D008137:Longitudinal Studies; D008297:Male; D062706:Prodromal Symptoms; D011930:Reaction Time; D012438:Saccades / Q000502:physiology*
keywords: EEG; Huntington's disease; antisaccade; cognitive control; inhibition; oculomotor control; saccade