title: Abnormal error-related antisaccade activation in premanifest and early manifest Huntington disease.
abstract: OBJECTIVE
  Individuals with the trinucleotide CAG expansion (CAG+) that causes Huntington's disease (HD) have impaired performance on antisaccade (AS) tasks that require directing gaze in the mirror opposite direction of visual targets. This study aimed to identify the neural substrates underlying altered antisaccadic performance.
  
  
  METHODS
  Three groups of participants were recruited: (1) Imminent and early manifest HD (early HD, n = 8); (2) premanifest (presymptomatic) CAG+ (preHD, n = 10); and (3) CAG unexpanded (CAG-) controls (n = 12). All participants completed a uniform study visit that included a neurological evaluation, neuropsychological battery, molecular testing, and functional MRI during an AS task. The blood oxygenation level dependent (BOLD) response was obtained during saccade preparation and saccade execution for both correct and incorrect responses using regression analysis.
  
  
  RESULTS
  Significant group differences in BOLD response were observed when comparing incorrect AS to correct AS execution. Specifically, as the percentage of incorrect AS increased, BOLD responses in the CAG- group decreased progressively in a well-documented reward detection network that includes the presupplementary motor area and dorsal anterior cingulate cortex. In contrast, AS errors in the preHD and early HD groups lacked this relationship with BOLD signal in the error detection network, and BOLD responses to AS errors were smaller in the two CAG+ groups as compared with the CAG- group.
  
  
  CONCLUSIONS
  These results are the first to suggest that abnormalities in an error-related response network may underlie early changes in AS eye movements in premanifest and early manifest HD. (PsycINFO Database Record (c) 2011 APA, all rights reserved).
authors.affiliation: Department of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN 46202-5251, USA.
authors.forename: Jason
authors.initials: J
authors.lastname: Rupp
authors.forename: Mario
authors.initials: M
authors.lastname: Dzemidzic
authors.forename: Tanya
authors.initials: T
authors.lastname: Blekher
authors.forename: Veronique
authors.initials: V
authors.lastname: Bragulat
authors.forename: John
authors.initials: J
authors.lastname: West
authors.forename: Jacqueline
authors.initials: J
authors.lastname: Jackson
authors.forename: Siu
authors.initials: S
authors.lastname: Hui
authors.forename: Joanne
authors.initials: J
authors.lastname: Wojcieszek
authors.forename: Andrew J
authors.initials: AJ
authors.lastname: Saykin
authors.forename: David
authors.initials: D
authors.lastname: Kareken
authors.forename: Tatiana
authors.initials: T
authors.lastname: Foroud
mesh_terms: D000293:Adolescent; D000328:Adult; D000367:Age Factors; D000368:Aged; D001921:Brain / Q000503:physiopathology*; D005260:Female; D006179:Gyrus Cinguli / Q000503:physiopathology; D006801:Humans; D006816:Huntington Disease / Q000235:genetics* / Q000503:physiopathology*; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D009044:Motor Cortex / Q000503:physiopathology; D009483:Neuropsychological Tests; D012307:Risk Factors; D012438:Saccades / Q000502:physiology*; D019680:Trinucleotide Repeat Expansion; D055815:Young Adult