From the earliest descriptions of schizophrenia, disturbance of affect and aberrant emotion processing have been considered core features. Expressions of apathy and fear were central elements of Kraepelin's1
description of dementia praecox. In Bleuler's conceptualization,2
delusions and hallucinations were considered to be secondary to “the four A's,” which included disturbed affect. Bleuler also emphasized that individuals with schizophrenia may experience powerful affects despite reduced overt expression and that oversensitivity to emotion is often reported at the beginning of the onset of disease.2
Researchers have debated whether emotion abnormalities in schizophrenia are merely a reaction to living with a debilitating illness or, instead, intrinsic components of the pathophysiology of the disorder. More recent theoretical views describe hypohedonia (or “anhedonia”), an inability to experience pleasure, as core to schizophrenia.3
Meehl suggested that anhedonia stems from genetic factors and is integral to schizotypy, the basic predisposition to schizophrenia. Modern theoretical conceptualizations of schizophrenia continue to include descriptions of emotion disturbances. The most recent edition of the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision
) contains numerous references to emotion disturbance in schizophrenia, including affective flattening, inappropriate affect, anhedonia, depression, anxiety, and anger.4
Indeed, individuals with schizophrenia have now been shown to demonstrate abnormalities in emotion perception, emotion experience, emotion regulation, and emotional expression (articles in this issue). Generally, individuals with schizophrenia exhibit impaired emotion perception, intact experience of emotion in the laboratory, reduced self-reported positive experiences, and reduced emotion expression.5
In addition, individuals with schizophrenia demonstrate abnormal cognitive biases in the context of emotional information. More specifically, individuals with positive or disorganized symptoms exhibit a bias associated with negatively valenced information in the cognitive domains of attention,6,7
and language output.12,13
These emotional processing deficits impact social behavior.14,15
Thus, substantial evidence points to emotion abnormalities as being intrinsic to the origin of the illness.
Over the past 2 decades, investigation into emotion processing in schizophrenia has been extended to include at-risk groups. However, the extent to which these emotion-processing abnormalities are found in individuals considered at high risk (HR) for schizophrenia has not been systematically reviewed, in contrast to the many reviews of cognition in HR individuals. Research aimed at measuring HR for schizophrenia includes a number of possible populations and experimental approaches.16,17
As will be evident in this review, in certain domains, the abnormalities in those at HR resemble the performance of individuals with schizophrenia; while in others, those at risk demonstrate only attenuated abnormalities or performance comparable to that of healthy controls. The inclusion of HR groups adds insight into the pathophysiology of schizophrenia. By examining performance among different HR groups, constellations of abnormalities might emerge as vulnerability markers or predictors of subsequent onset of schizophrenia. Moreover, studies of HR persons avoid confounds that bedevil schizophrenia research (ie, effects of medications, psychosis, chronicity, and other environmental adversities) and help identify traits that are presumably core parts of the liability to the disorder.
We follow an organizational framework suggested for the study of emotion processing in schizophrenia (eg, Kring5
and Berenbaum and Oltmanns18
) that includes sections on emotion perception, emotion experience, and emotion expression. While research suggests that impairment in the processing of one emotion component may be independent of other areas of emotion processing (ie, experience and expression),19
it is possible that certain instances of emotion abnormality impact the integrity of other forms of emotion processing. Thus, tasks may measure more than one area of emotion processing. Whenever apparent, this overlap will be highlighted.
We review evidence of emotion-processing abnormalities in 3 populations who are at risk for schizophrenia: (1) nonpsychotic individuals (who may or may not be symptomatic) selected on the basis of a family history (FH) of schizophrenia (Persons with an FH of schizophrenia are considered to be at genetic HR because they are presumed to carry some of the same susceptibility genes for the illness as their affected biological relative.); (2) individuals from the general population who demonstrate relatively high levels of schizotypy or signs that resemble attenuated symptoms of schizophrenia; and (3) treatment-seeking individuals in the putative prodrome to schizophrenia, who are displaying early clinical signs of possible psychosis. Finally, we present an agenda for future research and highlight possible targets of intervention.
Articles included in this review were acquired through Medline searches that included terms relevant to emotion and risk for psychosis, such as “high risk,” “sibling,” “schizotypy,” “prodrome,” “emotion,” “affect,” “valence,” “arousal,” “psychophysiology,” “fMRI,” and “MRI.” Bibliographies in the selected articles also were reviewed for relevant publications. The period of search ended with articles published in June, 2007. Articles were excluded if they did not include reference to emotion and/or include emotion probes as part of the methods.