Event-related potential studies show reduced P300 amplitudes in alcohol use disorders (AUDs). Alcohol exposure, genetic vulnerability to alcoholism, and comorbid psychopathology may contribute to this reduction. Most previous research has studied treated adult AUD samples, which have more severe alcoholism, a greater family history of AUDs, and more comorbidity than untreated samples. Untreated AUD samples tend to have little or no P300 amplitude reduction. We compared P300 between treatment-naïve alcohol-dependent (TNAD) adolescents with no diagnosable substance abuse or psychiatric comorbidity and nonsubstance-abusing control (NSAC) adolescents.
Individuals between the ages of 13 and 18 years were recruited into either TNAD (n = 45) or NSAC (n = 64) groups. Alcohol use variables, family history density of alcohol problems, and psychiatric symptom counts were assessed in a clinician-administered evaluation. EEGs were recorded during performance of a 3-condition visual target detection task.
P300 amplitudes were of comparable size in TNAD adolescents and NSAC adolescents. Boys demonstrated larger P3a and P3b amplitudes than girls. Within TNAD, P3b amplitude was reduced in those who drank more frequently, and P3a latency was more prolonged in subjects with higher internalizing symptom counts.
The P300 deficit was not present in TNAD adolescents without comorbidities. In comparison to results of reduced P300 in treated adolescent AUD samples, this finding likely reflects moderate alcohol exposure, lower genetic vulnerability to alcoholism, and lack of comorbidity in our sample. Further work is needed to determine the relative contributions of these factors to changes in the P300.
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