(Arns et al. 2008; Chabot et al. 1999), and alcoholism (Cristini et al. 2003; Saletu-Zyhlarz et al. 2004). For example, Ford and colleagues (1986) measured EEG coherence in individuals with paranoid schizophrenia, dysthymia, and affective disorder who received tricyclics, neuroleptics, or no medication and found that coherence values were highest in paranoid schizophrenics, decreased with neuroleptic medication, and increased with tricyclic antidepressants. Similarly, Hegerl and colleagues (1992) found that responders to prophylactic lithium medication in affective psychosis showed a steeper slope of the amplitude/stimulus-intensity function (ASF slope) in N1 and P2 components than in nonresponders. The pronounced amplitude increases in the Loudness Dependence of the Auditory Evoked Potential (LDAEP), such as tangential dipole activity and N1-P2 components with increasing stimulus intensity (loudness), have been proposed as an indicator of a low serotonergic neurotransmission. This feature of augmented LDAEP has been observed during the alcohol-intoxicated state (Hegerl et al. 1996a) and after the intake of acamprosate during treatment (Hegerl et al. 1996b). Further, Pillay and colleagues (1996) showed that female patients with abnormal EEGs before starting the clozapine treatment had a significantly greater improvement in global assessment of functioning scores compared with female patients with normal EEGs. These results suggest that
