Pre-pulse inhibition and antisaccade performance indicate impaired attention modulation of cognitive inhibition in 22q11.2 deletion syndrome (22q11DS).

[22q11.2 deletion syndrome]

22 q 11 .2 deletion syndrome (22 q 11 DS ) is associated with a number of physical anomalies and neuropsychological deficits including impairments in executive and sensorimotor function . It is estimated that 25 % of children with 22 q 11 DS will develop schizophrenia and other psychotic disorders later in life . Evidence of genetic transmission of information processing deficits in schizophrenia suggests performance in 22 q 11 DS individuals will enhance understanding of the neurobiological and genetic substrates associated with information processing . In this report , we examine information processing in 22 q 11 DS using measures of startle eyeblink modification and antisaccade inhibition to explore similarities with schizophrenia and associations with neurocognitive performance .Startle modification (passive and active tasks ; 120 - and 480 -ms pre-pulse intervals ) and antisaccade inhibition were measured in 25 individuals with genetically confirmed 22 q 11 DS and 30 healthy control subjects .Individuals with 22 q 11 DS exhibited increased antisaccade error as well as some evidence (trend-level effect ) of impaired sensorimotor gating during the active condition , suggesting a dysfunction in controlled attentional processing , rather than a pre-attentive dysfunction using this paradigm .The findings from the present study show similarities with previous studies in clinical populations associated with 22 q 11 DS such as schizophrenia that may indicate shared dysfunction of inhibition pathways in these groups .