“…The PINV in schizophrenic patients has been attributed to "delayed CNV resolution"~Mantanus, Timsith-Berthier, Gerono, & Von Frenckell, 1981;Timsit, Koninckx, Dargent, Fontaine, & Dongier, 1970;Timsit-Berthier, Delaunoy, & Rousseau, 1973!, increased preparation for further stimulus and response evaluation~Birbaum-er, Elbert, Rockstroh, & Lutzenberger, 1986;Rockstroh et al, 1989!, andinability to resolve stimulus ambiguity~Delaunoy, Gerono, &Rousseau, 1978!, or has been termed a prolongated duration CNṼ Timsit-Berthier, Delaunoy, & Gerono, 1978!. Two studies have suggested that high as opposed to low working memory load during the matching of the S2 with the S1 augments the PINV amplitudes only in schizophrenic but not in healthy control individuals; furthermore, the execution of a motor response appears as a critical prerequisite for the rising of the PINV in both populations~Klein, 1997; Klein, Andresen, & Jahn, 1997;Klein, Cohen, Berg, & Rockstroh, 1996b;Werther, 1996!. Current and past etiological conceptions of schizophrenia have assumed the existence of a vulnerability dimension that ranges from healthy to pathological, with schizophrenic disorders representing extreme expressions of the dimensional vulnerability~e.g., Bleuler, 191101988;Kretschmer, 1921, cited in Kendler, 1985Meehl, 1962Meehl, , 1990Raine, Lencz, & Mednick, 1995!. Hence, ab-normalities that are observed in schizophrenic patients and are not a consequence of neuroleptic treatment or long-term hospitalization may be found also in individuals who are assumed to share dispositional factors with schizophrenic patients but who are not psychiatrically ill~Lenzenweger, 1994!.…”