Understanding response inhibition lies at the core of behavioral control, which may be impaired across the spectrum of disinhibitory disorders (Zucker et al., 2011). Alcoholics not only manifest reduced P3 amplitudes to Go stimuli, but reduced P3 to NoGo stimuli as well (Pfefferbaum et al., 1991; Cohen et al., 1997b; Fallgatter et al., 1998; Rodriguez Holguin et al., 1999; Hada et al., 2000). Furthermore, chronic alcoholics manifest less differentiation between their responses to task-relevant target stimuli and task-irrelevant non-target stimuli, suggesting less effective inhibitory processes. Similarly, Cristini et al. (2003) reported reduced N2 in alcoholics in a Go/NoGo task. A recent study reported significantly reduced N2 amplitudes in alcohol-dependent subjects for Go and NoGo trials, particularly for NoGo trials in frontal regions where alcoholics did not show a more frontal distribution (Pandey et al., 2012) (Fig. 23.2); controls had significantly larger frontal amplitudes for NoGo, in line with a frontal generator for N2 (van Veen and Carter, 2002; Nieuwenhuis et al., 2004). The anteriorly distributed NoGo P3 potentials were also markedly reduced in amplitude in alcoholic subjects as well as
