Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/12182
Title: Saccade reprogramming in Friedreich ataxia reveals impairments in the cognitive control of saccadic eye movement.
Austin Authors: Hocking, Darren R;Corben, Louise A;Fielding, Joanne;Cremer, Phillip D;Millist, Lynette;White, Owen B;Delatycki, Martin B 
Affiliation: Clinical Genetics, Department of Medicine, Austin Health, The University of Melbourne, Heidelberg, Victoria, Australia
School of Psychological Science, La Trobe University, Bundoora, Victoria 3086, Australia
Bruce Lefroy Centre for Genetic Health Research, Murdoch Childrens Research Institute, Parkville, Victoria, Australia
Department of Neurology, Royal Melbourne Hospital, Parkville, Victoria, Australia
Royal North Shore Hospital, St. Leonards, New South Wales, Australia
School of Psychology and Psychiatry, Monash University, Clayton, Victoria, Australia
Issue Date: 19-Apr-2014
Publication information: Brain and Cognition 2014; 87(): 161-7
Abstract: Although cerebellar dysfunction has known effects on motor function in Friedreich ataxia (FRDA), it remains unclear the extent to which the reprogramming of eye movements (saccades) and inhibition of well-learned automatic responses are similarly compromised in affected individuals. Here we examined saccade reprogramming to assess the ability of people with FRDA to respond toward unexpected changes in either the amplitude or direction of an "oddball" target. Thirteen individuals with genetically confirmed FRDA and 12 age-matched controls participated in the study. The saccade reprogramming paradigm was used to examine the effect of an unpredictable "oddball" target on saccade latencies and accuracy when compared to a well-learned sequence of reciprocating movements. Horizontal eye movements were recorded using a scleral search coil eye tracking technique. The results showed a proportionally greater increase in latencies for reprogrammed saccades toward an oddball-direction target in the FRDA group when compared to controls. The FRDA group were also less accurate in primary saccade gain (i.e. ratio of saccade amplitude to target amplitude) when reprogramming saccades toward an unexpected change in direction. No significant group differences were found on any of the oddball-amplitude targets. Significant correlations were revealed between latency and disease severity as measured by the Friedreich Ataxia Rating Scale. These findings provide further support to the view that cognitive changes in FRDA may arise from disruption of cerebellar connections to cortical structures.
Gov't Doc #: 24752035
URI: https://ahro.austin.org.au/austinjspui/handle/1/12182
DOI: 10.1016/j.bandc.2014.03.018
Journal: Brain and cognition
URL: https://pubmed.ncbi.nlm.nih.gov/24752035
Type: Journal Article
Subjects: Attention
Cerebellum
Cognition
Inherited ataxias
Adult
Cognition.physiology
Friedreich Ataxia.physiopathology
Humans
Middle Aged
Saccades
Appears in Collections:Journal articles

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