The current study assessed potential differences in emotion recognition ability between actively paranoid and non-paranoid patients with schizophrenia. Patients who were paranoid at the time of testing, relative to those who were not, showed a specific impairment in the ability to accurately identify neutral facial expressions. An analysis of error patterns revealed that this impairment was due to a greater tendency for AP patients to incorrectly attribute anger to neutral faces. These findings are consistent with previous behavioral studies showing an emotion recognition advantage for non-paranoid patients (An et al. 2006
; Russell et al. 2007
; Williams et al. 2007
) and clarify this work by demonstrating that impairments in AP patients are limited to neutral expressions. The over attribution of anger to neutral expressions is also consistent with work suggesting that delusional patients misattribute salience to neutral stimuli (Holt et al. 2006
) and hypotheses that paranoid ideation is related to heightened perception of threat, particularly in ambiguous situations (Green and Phillips 2004
; Phillips et al. 2000
). This latter finding may have important implications for the day-to-day social functioning of individuals with paranoia. Viewed within the framework of Couture and colleagues (2006)
, early misperceptions of facial emotion can lead to a cascade of negative attributions and resulting negative social interactions. Thus, it is possible that the tendency for AP patients to over attribute anger could play an important role in social impairment.
The present findings may also be informative for understanding findings of differential amygdala abnormalities in paranoid and non-paranoid patients. As noted above, several studies have demonstrated that paranoid patients show hypoactivation of the amygdala as compared to non-paranoid patients. Given that the amygdala is implicated in threat perception and that paranoia can be conceptualized as continually perceiving environmental threat, this finding seems somewhat counterintuitive. It is important to note, however, that our interpretations of these neuroimaging findings are limited by the fact that the vast majority of analyses of blood oxygenation level dependent (BOLD) imaging rely on a contrast between activation occurring during a specific event and activation that occurs during non-events, or a baseline. This renders it difficult to determine if reduced activations in paranoid patients reflect true reductions in neural responses to stimuli or differences in baseline activity that influence the BOLD estimate. It is therefore possible that paranoid individuals may actually show hyperactivation of the amygdala that results in a high baseline and subsequent ceiling effect that limit the signal change detected by BOLD techniques.
Two recent studies, one using BOLD imaging (Hall et al. 2008
) and the other using PET imaging (Fernandez-Egea et al. 2010
), provide support for the hypothesis that individuals with schizophrenia show increased amygdala responses. While these studies did not specifically examine paranoid and non-paranoid subgroups, Hall and colleagues reported that patients did not differ from controls in amygdala responses to fearful faces but that they did show abnormally greater amygdala activation in response to neutral faces. Similarly, using PET imaging, which does not follow the same potential limitations as BOLD imaging, Fernandez-Egea et al. found that patients showed a non-specific hyperactivation of the amygdala as compared to control participants. Consistent with the proposal of Aleman and Kahn (2005)
that high tonic levels of amygdala activation may result in assigning significance to neutral stimuli, over activation of the amygdala in paranoia would offer a potential causal mechanism for the results of the present study. Additionally, when considering the limitations of most current BOLD imaging analyses, generalized amygdala hyperactivation in paranoia would help explain previous imaging findings of reduced amygdala activation in this group. Further work is needed to substantiate these hypotheses; however, such work could be meaningful as several pharmacological agents show promise for attenuating amygdala responses during emotion processing (Pinkham et al., 2007
While this study offers new information about emotion recognition impairments in actively paranoid and non-paranoid individuals with schizophrenia, some limitations should be considered. First, potential group differences in cognitive ability were not assessed. Given that the impairments seen in the AP group were specific to neutral faces and did not generalize to all emotions, it is unlikely that cognitive impairments account for the present results; however, this possibility cannot be fully ruled out. Second, the present investigation assessed recognition for only the basic emotional expressions of happiness, sadness, anger, fear and neutral. It is possible that additional group differences would have emerged if more complex emotional displays were included. Finally, the AP group was significantly more symptomatic than the NAP group suggesting a greater level of psychopathology. While we did statistically control for this difference in our analyses and groups did not differ in response time or overall task accuracy, it is possible that an additional third factor related to symptom severity may have contributed to the results. Notwithstanding these limitations, the present study highlights the utility of considering symptom-based subgroups in efforts to understand social cognitive impairments in schizophrenia and lends support to work showing behavioral and neural differences between paranoid and non-paranoid patients.