Background
Neurocognitive impairment is a well-studied feature of schizophrenia [
1‐
4], and its association with functional impairment has been well validated [
4‐
8]. For instance, people with schizophrenia scored lower on executive functioning, which is one aspect of neurocognitive functioning when compared to the healthy controls. Also, this impairment was related to negative symptoms in these people [
4]. However, prior studies often collapsed and treated neurocognition as one single domain [
9]. Since neurocognition is a broad construct encompassing visual and verbal learning, executive functioning, processing speed, and memory, further studies on the relationship between this construct and functional impairment or symptomatology are needed. The association of neurocognition with negative symptoms has been widely studied [
4,
10,
11], while positive and general symptoms have received much less attention in prior studies. The meta-analysis in 73 studies revealed that negative symptoms were associated with worse neurocognition and functional outcomes in schizophrenia [
11]. Specifically, negative symptoms were related to deficits in problem solving, reasoning, executive functioning [
4,
12,
13], and IQ [
14]. However, the findings regarding the association between neurocognition and positive symptoms were scarce and inconsistent [
11,
15,
16]. According to Ventura and colleagues [
11], positive symptoms were not significantly related to neurocognition and functional outcomes [
17], while Rabinowitz and colleagues found the opposite [
18]. Taken together, these findings suggest that neurocognition is more closely associated with negative than with positive symptoms. Moreover, general symptoms were often neglected in prior studies. Therefore, further studies are warranted for the investigation of the relation of neurocognition to symptomatology, including negative, positive, and general symptoms in schizophrenia. Prior longitudinal studies found that neurocognitive deficits predicted the onset of psychosis [
19,
20] as well as negative symptoms at the 1-year follow up in first-episode psychosis [
14]. Specifically, the review [
19] has revealed that neurocognitive deficits exist prior to the onset of psychosis. These findings were consistent with the argument by Comblatt and Keilp [
21] that neurocognitive deficits lead to social and emotional impairment, and this is reflected in the negative symptoms in schizophrenia. Hence, we hypothesized that neurocognitive deficits predicted the severity of symptoms instead of the other way around in the present study [
11].
Because neurocognition alone could account for only 20–60% of the variance in functional outcomes [
7], social cognition, which is a common correlate of both constructs [
6], has been speculated to be a potential candidate to explain the neurocognition-functional outcomes relation [
9,
22]. Social cognition, which is also impaired in people with schizophrenia [
23,
24], covers a range of constructs: theory of mind (ToM) or self-representation, emotion perception or empathy, and social perception [
25]. Specifically, regarding ToM, people with schizophrenia performed worse than healthy controls in the Faux Past Test after controlling for age and gender [
26] as well as in the “Reading the Mind in the Eyes” Test [
27]. In terms of empathy as measured by Interpersonal Reactivity Index (IRI), these people scored worse in two subscales (perspective taking and personal distress), but there was no significant difference in the other two subscales (fantasy and empathetic concern) [
28]. These suggest that some aspects of empathy might be retained even in neurocognitively impaired individuals.
A review of 15 prior studies showed that various social-cognitive domains, including ToM, emotion perception, empathy, and social perception, were significant mediators in such a relation [
9]. Also, [
29‐
31] found that social cognition assessed by objective measures such as the Facial Emotion Identification Test [
32] and the Half-profile of Nonverbal Sensitivity [
33] played a significant role in the functional outcomes in schizophrenia as well as in the clinical high-risk-for-psychosis group [
34]. These findings suggest that neurocognitive impairment may have an adverse impact on social-cognitive functioning, which in turn predisposes people with schizophrenia to poor functional outcomes. More importantly, it leads to the speculation that social cognition may also mediate the relation between neurocognition and symptomatology in schizophrenia [
35]. However, this hypothesis was scarcely examined.
Moreover, prior studies regarding social cognition suffered from a common limitation: they often focused on only one domain of the multi-dimensional social cognition construct at a time [
9]. It was found that only 3 out of 15 studies investigated more than one domain of social cognition [
9]. Among these studies, relatively few were done to explore empathy, which is also considered as one domain of social cognition [
36], and the findings have been inconsistent. For instance, empathy assessed by IRI, which is a self-report scale, was found to be negatively associated with negative symptoms in schizophrenia in some studies [
37,
38]. However, its association with symptomatology encompassing negative, positive, and disorganized symptoms was not significant in other studies using the same assessment, IRI [
39,
40]. These inconsistent results might be due to two factors: (1) Different types of psychotic disorders were examined in these studies. Specifically, people with schizophrenia [
37,
38] and people with first-episode psychosis [
39] were examined respectively. (2) Self- ratings of social cognition might be more biased when compared to the objective measures [
29,
31] in schizophrenia. Further studies are warranted to address these inconsistencies and speculations.
The present study extended previous studies by examining a broader concept of social cognition and symptomatology and separating neurocognition into various factors. Prior studies have focused on certain neurocognitive aspects such as executive functions, working memory, and attention and its relation with symptomatology in schizophrenia, while other aspects such as visual and spatial learning and memory were overlooked [
11]. Therefore, the present study investigated perception, which has been less investigated in prior literature. Besides that, executive functioning, which is the core neurocognitive impairment in schizophrenia and shares substantial variances with working-memory capacity (
r = .97), was also examined [
41]. All in all, the primary goals of the present study were to examine the neurocognitive (executive functioning and perception) and social cognitive (theory of mind and empathy) abilities and to examine whether social cognition played a mediating role in the relation of neurocognition to negative, positive, and general psychopathological symptoms in schizophrenia. It was hypothesized that both of these abilities were impaired in schizophrenia but not in healthy controls. Moreover, it was hypothesized that theory of mind as well as empathy would mediate the association between neurocognitive abilities (executive functioning or perception) and symptomatology (negative, positive, and general symptoms) in schizophrenia.
Discussion
To the best of our knowledge, this is the first study attempting to explore the role of social cognition in the relation between neurocognition and a broader spectrum of symptomatology in people with schizophrenia. Overall findings were consistent with prior studies’ findings that neurocognition and social cognition are impaired in schizophrenia [
1,
24]. More importantly, it was found that theory of mind (ToM) was a significant mediator explaining the relation of neurocognition to negative and positive symptoms [
9]. However, empathy was not a significant mediator of such a relation, which is contrary to our hypothesis and to prior findings [
22,
37,
38]. Overall findings suggest that social cognitive ability is one of the underlying factors of the neurocognition-symptomatology relation in schizophrenia, which has clinical implications for more cost-effective interventions for schizophrenia.
As expected, healthy controls had significantly better performance on perception, executive functioning [
1], and all ToM measures [
24], except for reasoning and inference of others’ mental states. These suggest that neurocognition, specifically the ability to perceive and understand the surrounding environment, along with visuo-spatial processing, planning, and problem-solving skills are impaired in people with schizophrenia. Furthermore, these findings suggest that these people also have social cognitive deficits in which they lack the ability to detect a faux pas and identify the person who has committed the faux pas in a social interaction.
However, empathy as measured by IRI was not impaired in these people, which is contrary to our hypothesis. One possible reason for the insignificant differences across groups might be that IRI [
50] is not sensitive enough to detect such social cognitive deficits in schizophrenia in the Chinese context. Another reason might be that IRI is a self-report empathy scale, and schizophrenic subjects might be biased about their self-ratings on their social cognitive abilities. Thus, it might be more sensitive to detect the difference using objective empathy measures. Third, the inconsistent results might also be due to the fact that possible aspects such as age and education level of the participants were not accounted for in the group comparison analyses in prior findings [
28] while the medication conditions were not accounted for in the present study. These speculations should be investigated in future studies.
In attempting to explain the relation between neurocognitive abilities and negative or positive symptoms in schizophrenia, ToM was found to be a full mediator. Specifically, the findings of the present study suggest that impairments in perception or executive functioning worsen the interpretation and understanding of others’ mental states or intentions. This in turn leads to more negative symptoms in schizophrenia [
6,
15]. In other words, the deficits in the organization, identification, and interpretation of sensory information in order to represent and understand the environment as well as problem-solving skills affect the ability to detect social cues and faux pas while interacting with others in schizophrenia. This in turn affects their social functioning including their ability to experience pleasure in their social interactions. In addition, it is suggested that impaired executive functioning leads to more positive symptoms through increased ToM deficits in schizophrenia. This suggests that the lack of ability to control and regulate cognitive processes such as working memory, reasoning, task flexibility, and execution in people with schizophrenia worsens their capacity to detect social cues and faux pas while interacting with others. This further leads to more abnormal outcomes such as hallucinations, delusions, and bizarre behaviors in these people.
Contrary to our expectation [
35], ToM could not explain the relation between perception and positive symptoms because perception was not related to positive symptoms (r = -0.06) in the present study [
11]. This inconsistent finding might be because the strength of the relation between positive symptoms and different neurocognitive domains varies or because different neurocognitive measures were used in prior studies [
11,
15,
16]. On the other hand, theory of mind (ToM) did not mediate the relation between neurocognition and general psychopathological symptoms, which was not expected. This finding suggests that the ability to understand and identify others’ mental states and intentions does not explain the relation of neurocognition to general symptoms in schizophrenia. One of the reasons for this finding is that the general psychopathological symptoms encompass a variety of symptoms, and it is possible that some of these symptoms are more closely related to certain domains of neurocognition and social cognition but that others are not. For instance, poor insight might be more associated with ToM than with empathy. Future studies should further examine the relation of specific general symptoms with neurocognition and social cognition. Furthermore, another social cognitive domain, empathy, was not related to any psychiatric symptoms, which is also inconsistent with prior findings. This might be because this domain was evaluated by different measures in different psychotic disorders previously [
22,
37‐
39].
Limitations
The current study suffers from five major limitations. First, the mediation analyses performed with neurocognition, social cognition, and symptomatology were based on cross-sectional data. Therefore, we could not conclude the causality of the mediated relationship found in the present study. However, the current study is an essential step toward confirming the association between neurocognition, social cognition, and symptomatology in schizophrenia before a longitudinal study in perception is undertaken. Second, due to the time constraints for assessing each participant, empathy and executive functioning were each only assessed by one scale, the Interpersonal Reactivity Index [
50] and the Tower of London [
43], respectively. This might not fully capture the whole dimension of empathy and executive functioning. Third, the present study only included theory of mind and empathy as the concept of social cognition, while only perception and executive functioning were included to represent neurocognition (also because of the time constraint factor). Future studies should include more measurement tools so to fully represent these concepts. For instance, social knowledge and attribution styles, which are social-cognitive domains and often neglected in prior studies, warrant further investigation [
9]. Also, working-memory and attention processes should also be assessed in the future. Fourth, the self-report measure was used to assess empathy in the present study while the other social cognition domain, theory of mind, was tested by objective measures. Since there might be bias in self-ratings of empathy by schizophrenia [
55]
, further studies should address this limitation in the future. Last but not least, the classic chlorpromazine (CPZ) equivalents that can be used to chart relative antipsychotic potencies of antipsychotic drugs were not recorded in the present study. Since it might be a factor in symptomology in schizophrenia, future studies should also include CPZ equivalents as a covariate.
Competing interests
All authors report no conflicts of interest relevant to the subject of this article.
Authors’ contributions
TMCL conceptualized the research idea. All authors designed the study. TMCL collected the clinical data. BYHL analyzed the data and wrote the first draft of the manuscript. TMC and AR supervised the research project and critically revised the manuscript. All authors contributed to and have approved the final manuscript.