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The Effects of Fetal Alcohol Syndrome on Response Execution and Inhibition: An Event‐Related Potential Study
Author(s) -
Burden Matthew J.,
Andrew Colin,
SaintAmour Dave,
Meintjes Ernesta M.,
Molteno Christopher D.,
Hoyme H. Eugene,
Robinson Luther K.,
Khaole Nathaniel,
Nelson Charles A.,
Jacobson Joseph L.,
Jacobson Sandra W.
Publication year - 2009
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.2009.01038.x
Subject(s) - fetal alcohol syndrome , response inhibition , alcohol , event (particle physics) , fetal alcohol , fetus , medicine , psychology , chemistry , neuroscience , biology , pregnancy , physics , biochemistry , cognition , genetics , quantum mechanics
Background: Both executive function deficits and slower processing speed are characteristic of children with fetal alcohol exposure, but the temporal dynamics of neural activity underlying cognitive processing deficits in fetal alcohol spectrum disorder have rarely been studied. To this end, event‐related potentials (ERPs) were used to examine the nature of alcohol‐related effects on response inhibition by identifying differences in neural activation during task performance. Methods: We recorded ERPs during a Go/No‐go response inhibition task in 2 groups of children in Cape Town, South Africa ( M age = 11.7 years; range = 10 to 13)—one diagnosed with fetal alcohol syndrome (FAS) or partial FAS (FAS/PFAS; n = 7); the other, a control group whose mothers abstained or drank only minimally during pregnancy ( n = 6). Children were instructed to press a “Go” response button to all letter stimuli presented except for the letter “X,” the “No‐go” stimulus, which occurred relatively infrequently. Results: Task performance accuracy and reaction time did not differ between groups, but differences emerged for 3 ERP components—P2, N2, and P3. The FAS/PFAS group showed a slower latency to peak P2, suggesting less efficient processing of visual information at a relatively early stage (∼200 ms after stimulus onset). Moreover, controls showed a larger P2 amplitude to Go versus No‐go, indicating an early discrimination between conditions that was not seen in the FAS/PFAS group. Consistent with previous literature on tasks related to cognitive control, the control group showed a well‐defined, larger N2 to No‐go versus Go, which was not evident in the FAS/PFAS group. Both groups showed the expected larger P3 amplitude to No‐go versus Go, but this condition difference persisted in a late slow wave for the FAS/PFAS group, suggesting increased cognitive effort. Conclusions: The timing and amplitude differences in the ERP measures suggest that slower, less efficient processing characterizes the FAS/PFAS group during initial stimulus identification. Moreover, the exposed children showed less sharply defined components throughout the stimulus and response evaluation processes involved in successful response inhibition. Although both groups were able to inhibit their responses equally well, the level of neural activation in the children with FAS/PFAS was greater, suggesting more cognitive effort. The specific deficits in response inhibition processing at discrete stages of neural activation may have implications for understanding the nature of alcohol‐related deficits in other cognitive domains as well.