Our sample of patients with schizophrenia, dichotomized by the presence of clinically significant flat affect, showed that blunted affect is more common in men and is associated with distinct clinical features and deficits. The hypothesis that flat affect has an adverse effect on course of illness was strongly supported. Patients with FA had poorer premorbid adjustment, worse current quality of life, and worse outcome 1 year after affect was assessed. The poorer clinical picture begins with early adolescence and seems to span all facets of social adjustment. Notably, patients with FA also had more severe negative symptoms on other domains including avolition, alogia, anhedonia, and attention, while the positive symptoms in this group were slightly more severe. Although the focus of this prospective study was on flat affect, other domains that define negative symptoms, and their interrelation merit further examination (see the other articles in this issue).
Demographic characteristics of the 2 groups do not seem to explain why patients with FA have poorer clinical course and outcome. The groups did not differ in parental education and hence came from a similar sociodemographic background. Patients with FA attained a lower educational level, but that could be related to their younger age and earlier age at onset. The groups did not differ in duration of illness. Indeed, flat affect was evident in patients early in the course of illness. Notably, the results were sustained after controlling for these factors. Similarly, the results did not differ for inpatients and outpatients or by medication status, consistent with previous findings from our group that treatment with typical or atypical medications does not influence functional outcome.57
It is also noteworthy that the groups did not differ in dose or duration of treatment, except that patients with FA who were on atypicals only had a higher current dose than their counterparts without flat affect. While antipsychotics, in particular typicals, have been associated with akinesia, including the face, studies that have examined patients on and off antipsychotics reported no clear effect on expressivity and emotional experience.58,59
A major focus of the present study was to examine whether flat affect is associated with impaired emotion identification. As expected, patients with schizophrenia, compared with controls, were impaired on facial emotion processing tasks, one that required identification of happy and sad emotions and another that required differentiating among intensities within these emotions. Patients also showed the expectedly greater difficulties on the latter. Indeed, they displayed a “speed-accuracy decomposition,”37,38
whereby they responded inaccurately but fast, signifying “surrender.” These results suggest that future studies examining emotion processing deficits in schizophrenia should either use an emotion identification task or make intensity discrimination easier.
The main hypothesis of greater impairment in emotion processing for patients with FA was supported. Patients with FA performed more poorly on both tasks and showed a stronger decomposition of speed and accuracy for the intensity discrimination. Indeed, patients with FA responded even faster than controls. While performance on emotion processing tasks correlated moderately with neurocognitive performance across domains, the two groups did not differ in the neurocognitive profile except for verbal memory. Thus, the more impaired performance in emotion processing in patients with FA cannot be attributed to a greater generalized cognitive deficit. These results differ from an earlier study by our group using traditional paper-and-pencil neuropsychological measures.18
In that study we did not find differential deficit for emotion compared with an age identification task, but performance on the emotion task correlated with symptom severity and with measures of attention, verbal and spatial memory, and language. The present study has a much larger sample and shows moderate yet robust correlations between emotion processing and all neurocognitive measures. Furthermore, it shows unique associations for accuracy and speed that are not feasible with the traditional battery.
The link between cognition and emotion has been a topic of increased scrutiny.39,40,60
It appears that the memory system, particularly that related to “episodic,” “explicit,” or “source” memory,61,62
is closely associated with primary systems regulating emotion.40
Our results showed specific deficit in verbal memory associated with flat affect. It is unclear why only verbal memory distinguished the groups, and a replication is warranted. Possibly, given the association of verbal memory with left hemispheric function, this finding suggests greater left temporolimbic dysfunction in patients with flat affect. Functional imaging could help identify brain systems involved in emotion processing and their interaction with those regions recruited for processing of non-emotional stimuli.63
This study has several limitations. The emotion processing stimuli included only happy and sad faces. Processing of other “universal emotions” such as anger and fear may show a different or a more specific relation to clinical features. We have developed tasks that examine other emotions64
and have applied them to patients with schizophrenia.33
Another limitation of the study is its reliance on clinical ratings of flat affect. While these ratings are obtained under structured conditions and are highly reliable, a better understanding of deficits in the expression of emotions could be obtained from quantitative automated measures of facial affect change.65
Finally, the data on premorbid functioning is retrospective.22
Therefore, caution should be used in the interpretation of results. For example, our data suggest that FA patients are indistinguishable from NFA patients in their adjustment during childhood. Prospective studies of children at risk will help establish early signs of flat affect.66
Notwithstanding these limitations, the results of the present investigation give strong support to the hypothesis that patients with schizophrenia are impaired in emotion processing and that, among patients, those with flat affect are especially impaired. Furthermore, the association between flat affect and poor functioning underscores the need to examine this facet of the disorder. Other negative symptom domains, such as anhedonia, could likewise relate to emotion processing and outcome.67,68
However, our focus on flat affect is supported by the regression analysis and could yield mechanistic models, especially considering the overlap between neural systems involved in emotion processing and those involved in memory. The possibility that flat affect in schizophrenia may be associated with a unique neural substrate is therefore furthered by the impairment in verbal memory in patients with flat affect, while other neurocognitive measures were similar to patients without flat affect.