This review examines the structural validity of negative symptoms focusing on 2 questions: (1) Do negative symptoms represent a domain separate from other symptoms in schizophrenia? and (2) Within negative symptoms, is there a structure that suggests multidimensionality? Results from exploratory and confirmatory factor analytic studies are examined to address these questions. Across studies and symptom instruments, negative symptoms appear to consistently emerge as a factor separate from other dimensions of the illness in schizophrenia. Whether 2-, 3-, or 5-factor models are identified, negative symptoms consistently load on a factor separate from positive symptoms, affective symptoms of depression or anxiety, and symptoms of disorganization. Focusing on negative symptoms themselves, factor analytic findings suggest that this construct is multidimensional with at least 2 factors (involving diminished expression and anhedonia-asociality). Although these factors were replicable, serious limitations were noted in this literature. Thus, 2- (or even 3- or 5-) factor models of negative symptoms should not be considered definitive, but rather all converge to support the general conclusion of the multidimensionality of negative symptoms. The later findings indicate the importance of employing assessments that provide adequate coverage of the broad domain of negative symptoms. Importantly, caution is noted in the interpretability of findings based on existing instruments, and implications for future assessment are discussed.

Our understanding of the emotion deficits in schizophrenia is limited. Findings from studies employing trait emotion instruments suggest that patients have attenuated levels of positive emotion (ie, anhedonia) and increased levels of negative emotion. Conversely, patients and controls have not statistically differed in their subjective reactions to positive or negative valenced stimuli in most laboratory studies to date. Further obfuscating this issue is the fact that many of these laboratory studies are underpowered and a handful of emotion induction studies have found evidence of anhedonia. We conducted a meta-analysis of 26 published studies employing laboratory emotion induction procedures in patients with schizophrenia and healthy controls. Patients did not differ from controls when strictly rating their subjective hedonic reactions to the stimuli. However, they reported experiencing relatively strong aversion to both positive and neutral stimuli (Hedges D = .72 and .64, respectively). These findings were not the result of demonstrable sample or methodological differences across studies. Patients' ability to experience hedonic emotion is preserved, although they also show relatively strong, simultaneously occurring aversive emotion when processing laboratory stimuli considered by others to be pleasant or neutral.

Schizotypy refers to a set of personality traits thought to reflect the subclinical expression of the signs and symptoms of schizophrenia. Here, we review the cognitive and brain functional profile associated with high questionnaire scores in schizotypy. We discuss empirical evidence from the domains of perception, attention, memory, imagery and representation, language, and motor control. Perceptual deficits occur early and across various modalities. While the neural mechanisms underlying visual impairments may be linked to magnocellular dysfunction, further effects may be seen downstream in higher cognitive functions. Cognitive deficits are observed in inhibitory control, selective and sustained attention, incidental learning, and memory. In concordance with the cognitive nature of many of the aberrations of schizotypy, higher levels of schizotypy are associated with enhanced vividness and better performance on tasks of mental rotation. Language deficits seem most pronounced in higher-level processes. Finally, higher levels of schizotypy are associated with reduced performance on oculomotor tasks, resembling the impairments seen in schizophrenia. Some of these deficits are accompanied by reduced brain activation, akin to the pattern of hypoactivations in schizophrenia spectrum individuals. We conclude that schizotypy is a construct with apparent phenomenological overlap with schizophrenia and stable interindividual differences that covary with performance on a wide range of perceptual, cognitive, and motor tasks known to be impaired in schizophrenia. The importance of these findings lies not only in providing a fine-grained neurocognitive characterization of a personality constellation known to be associated with real-life impairments, but also in generating hypotheses concerning the aetiology of schizophrenia.

In the DSM5, negative symptoms are 1 of the 5 core dimensions of psychopathology evaluated for schizophrenia. However, negative symptoms are not pathognomonic—they are also part of the diagnostic criteria for other schizophrenia-spectrum disorders, disorders that sometimes have comorbid psychosis, diagnoses not in the schizophrenia-spectrum, and the general “nonclinical” population. Although etiological models of negative symptoms have been developed for chronic schizophrenia, there has been little attention given to whether these models have transdiagnostic applicability. In the current review, we examine areas of commonality and divergence in the clinical presentation and etiology of negative symptoms across diagnostic categories. It was concluded that negative symptoms are relatively frequent across diagnostic categories, but individual disorders may differ in whether their negative symptoms are persistent/transient or primary/secondary. Evidence for separate dimensions of volitional and expressive symptoms exists, and there may be multiple mechanistic pathways to the same symptom phenomenon among DSM-5 disorders within and outside the schizophrenia-spectrum (ie, equifinality). Evidence for a novel transdiagnostic etiological model is presented based on the Research Domain Criteria (RDoC) constructs, which proposes the existence of 2 such pathways—a hedonic pathway and a cognitive pathway—that can both lead to expressive or volitional symptoms. To facilitate treatment breakthroughs, future transdiagnostic studies on negative symptoms are warranted that explore mechanisms underlying volitional and expressive pathology.

Social anhedonia has been employed in psychometric high-risk studies to identify putative schizotypes. To date, this research has focused almost exclusively on college samples. The current study sought to examine the validity of social anhedonia as an indicator of risk for schizophrenia-spectrum disorders within a community sample. Furthermore, we evaluated the role of other individual difference variables in accounting for variable clinical severity within the social anhedonia group including trait affectivity, social support, and family environment. Following the mailed questionnaire screening of 2434 eighteen-year olds, laboratory assessments were conducted with individuals identified as being high in social anhedonia (n=86) and a comparison sample (n=89). Compared with the control group, individuals in the social anhedonia group were found to have higher rates of mood disorders, elevated schizophrenia-spectrum personality disorder characteristics, greater negative symptom characteristics, and lower global functioning. Individuals within the social anhedonia group also reported greater trait negative affectivity, lower positive affectivity, less social support, and more family conflict. Low social support and problematic family environment were found to be related to elevations in spectrum personality disorder characteristics and poorer functioning within the social anhedonia group. These cross-sectional findings from a community sample provide further support for social anhedonia as a possible indicator of schizotypy.