Objective
Recent studies have shown that alcoholism is characterized by a deficit in the processing of emotional facial expressions (EFE), and that this deficit could be “emotion specific”. The present study explored the hypothesis that there is a specific deficit for the EFE of anger compared to another negative emotion (disgust). Moreover, on the basis of event-related potentials (ERPs), this study aimed at determining the locus of this deficit in the information-processing stream.
Methods
Fifteen patients suffering from alcoholism and fifteen matched healthy controls took part in the study, which used a “modified emotional” oddball paradigm. ERPs were recorded in response to repetitions of a particular facial expression (i.e. anger) and in response to two deviant (rare) stimuli obtained by a morphing procedure, one depicting the same emotion as the frequent stimulus, the other depicting a different emotion (i.e. disgust). The participants' task was to press a key as soon as they spotted the deviant stimulus.
Results
Behavioural data showed an absence of categorical perception effect for anger (but not for disgust) stimuli among alcoholic patients. Moreover, electrophysiological data revealed that alcoholism is associated with an impaired processing of anger at the attentional level (N2b/P3a complex), extending to the decisional level (P3b).
Conclusion
This study demonstrated disturbed processing of anger in alcoholism, at behavioural and electrophysiological levels. These preliminary results strengthen the proposition of a specific deficit for anger, and localize its possible origin to the attentional level (N2b/P3a complex) of the information processing stream. The clinical implications of these results are discussed.
The decoding of emotional facial expressions (EFE) has been extensively investigated in normal individuals over the last decades, leading to a huge amount of data (Camras et al., 1993 and Ekman, 1984). The appropriate processing of EFE is clearly a major skill for the development and maintenance of adapted interpersonal relations (Ekman, 1989 and Feldman et al., 1991). In this perspective, studies have explored EFE decoding deficits in different psychopathologies (Power and Dalgleish, 1997), such as schizophrenia (Archer et al., 1992), social phobia (Winton et al., 1995) and depression (Hale, 1998).
More specifically, recent electrophysiological studies demonstrated the usefulness of an “emotional oddball paradigm” (based on the detection of an infrequent deviant stimulus among a succession of frequent standard stimuli) in the exploration of EFE deficits: One possible use of this paradigm is to define, for each clinical population showing an EFE deficit, where the disturbance originates in the information processing stream (Campanella and Philippot, 2006). Psychopathy (Campanella et al., 2005), anxiety (Rossignol et al., 2005), drug addiction (Mejias et al., 2005) and schizophrenia (Campanella et al., 2006) have been investigated using this technique, with results suggesting that the initial level of impairment leading to disturbed EFE processing is specific for each population (i.e. perceptual level for schizophrenia, attention level for depression, decisional level for anxiety and psychopathy). Nevertheless, all the stimuli used in these experiments were faces depicting a neutral expression for the frequent stimulus and an EFE for the rare stimuli, as illustrated in Fig. 1 (part A). The key limitation of this method is that it leads to major physical differences between the frequent (neutral) and rare (emotional) stimuli, as the physical distance between a face displaying a neutral or an emotional state is not controlled for. This bias weakens the conclusions that can be drawn from this paradigm, because one cannot exclude the possibility that the differences observed between frequent and rare stimuli could at least partly be explained by uncontrolled physical variations (and not by the explored emotional dimension).
