L O Bauer1, V M Hesselbrock. 1. Department of Psychiatry, University of Connecticut School of Medicine, Farmington, Connecticut 06030, USA.
Abstract
BACKGROUND: Longitudinal studies have demonstrated that childhood conduct disorder is a significant risk factor for a wide range of adult psychiatric disorders. The present study attempted to identify neurophysiologic differences that might underlie this risk factor. METHODS: The study examined 158 subjects, aged 14 to 20 years. Each subject was assigned to one of four groups defined by the factorial combination of the subject's gender and the relative number (-/+) of conduct problems exhibited before age 15. Event-related electroencephalographic potentials were recorded from each subject while he or she performed a memory scanning task. Each trial consisted of the brief presentation of either two or four consonant letters, a 2-sec memorization period, and a single "probe" letter. The subject was instructed to mentally compare the probe with the memory set and execute a discriminative (match vs. mismatch) key-press response. RESULTS: Analyses of P300 event-related potentials elicited by the probe stimuli revealed a significant interaction between probe stimulus membership and conduct problems: the P300 difference between trials with matching versus mismatching probes was significantly greater in the control (CP-) group than in the CP+ group. Current source density analyses, utilizing a realistic head-shape boundary element model, revealed that CP- subjects exhibited a robust activation of the left prefrontal cortex on matching versus mismatching trials. Among CP+ subjects, the degree of prefrontal cortex activation was not significant. CONCLUSIONS: The P300 results are consistent with those reported from previous studies of adolescents with conduct problems. Our study is unique in implementing current source density-boundary element method techniques for modeling P300 sources in "at-risk" adolescents. These techniques lend greater anatomical precision to the conclusion that conduct problems are associated with a specific dysfunction of the frontal brain.
BACKGROUND: Longitudinal studies have demonstrated that childhood conduct disorder is a significant risk factor for a wide range of adult psychiatric disorders. The present study attempted to identify neurophysiologic differences that might underlie this risk factor. METHODS: The study examined 158 subjects, aged 14 to 20 years. Each subject was assigned to one of four groups defined by the factorial combination of the subject's gender and the relative number (-/+) of conduct problems exhibited before age 15. Event-related electroencephalographic potentials were recorded from each subject while he or she performed a memory scanning task. Each trial consisted of the brief presentation of either two or four consonant letters, a 2-sec memorization period, and a single "probe" letter. The subject was instructed to mentally compare the probe with the memory set and execute a discriminative (match vs. mismatch) key-press response. RESULTS: Analyses of P300 event-related potentials elicited by the probe stimuli revealed a significant interaction between probe stimulus membership and conduct problems: the P300 difference between trials with matching versus mismatching probes was significantly greater in the control (CP-) group than in the CP+ group. Current source density analyses, utilizing a realistic head-shape boundary element model, revealed that CP- subjects exhibited a robust activation of the left prefrontal cortex on matching versus mismatching trials. Among CP+ subjects, the degree of prefrontal cortex activation was not significant. CONCLUSIONS: The P300 results are consistent with those reported from previous studies of adolescents with conduct problems. Our study is unique in implementing current source density-boundary element method techniques for modeling P300 sources in "at-risk" adolescents. These techniques lend greater anatomical precision to the conclusion that conduct problems are associated with a specific dysfunction of the frontal brain.
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