Skip to main content
NIHPA Author Manuscripts logoLink to NIHPA Author Manuscripts
. Author manuscript; available in PMC: 2022 Dec 1.
Published in final edited form as: Psychiatry Res. 2021 Sep 23;306:114224. doi: 10.1016/j.psychres.2021.114224

Reciprocal Social Behavior and Related Social Outcomes in Individuals at Clinical High Risk for Psychosis

Denise S Zou a, Henry R Cowan a, Matilda Azis a, Vijay A Mittal b
PMCID: PMC8643304  NIHMSID: NIHMS1745479  PMID: 34610542

Abstract

Reciprocal social behavior (RSB) deficits have been noted in formal psychotic disorders and may play a role in the clinical high-risk for psychosis (CHR) syndrome. The present study examined RSB deficits and clinical and social functioning correlates in 45 individuals meeting criteria for a CHR syndrome and 47 healthy comparisons (HC). Further, this study examined associations with number of friends, problematic social Internet use, and perceived social support. Compared to the HC group, the CHR group exhibited greater deficits in total RSB and in all RSB subdomains. Total RSB deficits were associated with greater negative but not positive symptom severity in the CHR group, and greater social functional impairment. RSB deficits also may have related to fewer friendships, more problematic social Internet use, and less perceived belonging and tangible social support, although relationships with Internet use and perceived social support did not survive FDR-correction. These findings provide further evidence that RSB is impaired in the CHR syndrome and suggest specific social outcomes that may be affected. Further investigations with larger, diverse samples and repeated measures can confirm these findings.

Keywords: clinical high risk for psychosis, reciprocal social behavior, social functioning, friends, problematic social Internet use, negative symptoms

1. Introduction

Deficits in reciprocal social behavior (RSB) are seen in formal psychotic disorders (Solomon et al., 2011). RSB is the extent to which an individual “engages in emotionally appropriate turn-taking social interactions with others” (Constantino et al., 2000). RSB was initially described in autism spectrum disorder (ASD) populations, where it is found to be related but distinct from theory of mind (e.g., Lei & Ventola, 2018). Whereas theory of mind reflects cognitive abilities to mentalize about others’ inner experiences, RSB reflects behavioral abilities to notice and interpret social cues, exhibit appropriate social behaviors, express motivation to socialize, and engage beyond restricted interests and stereotyped behaviors (Constantino et al., 2000; Jalbrzikowski et al., 2013). Although RSB is characteristic of ASD, it has also been observed in individuals with schizophrenia (Morrison et al., 2017; Solomon et al., 2011) and may account for overlap between autistic symptoms and negative psychotic symptoms (Isvoranu et al., 2021; Trevisan et al., 2020).

Several lines of research suggest that RSB deficits are also present in the clinical high risk for psychosis (CHR) syndrome, which can precede the onset of psychosis (Fusar-Poli et al., 2013; Fusar-Poli et al., 2015). The CHR syndrome describes individuals who do not meet criteria for a DSM-5 psychotic disorder, but who experience attenuated psychotic symptoms, brief intermittent psychotic symptoms (BIPS), or genetic risk and recent declines in functioning (Addington et al., 2015; Cannon et al., 2008; Haroun et al., 2006). Deficits have been observed in CHR samples in social cognition, social communication, and overall social functioning (Carrión et al., 2016; Cotter et al., 2017; Glenthøj et al., 2016; Glenthøj et al., 2020; Osborne et al., 2019). Genetic risk for psychosis relates to poorer theory of mind, a related construct to RSB (Gibson et al., 2010; Lee et al., 2015), and broad social cognitive impairments also appear to predict conversion to psychosis in CHR samples (Bora et al., 2008; Healey et al., 2013). Social behavioral processes are particularly relevant given the developmental stage of the CHR syndrome: as youth become independent, their development of reciprocal social skills—or lack thereof—set the stage for a lifetime of social functioning (Häfner et al., 1999; Roisman et al., 2004).

These impairments in social cognition and functioning are likely to manifest through turn-taking social interactions with others. Direct examination of RSB, therefore, offers a critical opportunity to better understand social behavioral deficits and inform clinical perspectives for individuals that meet criteria for a CHR syndrome. Accordingly, one previous study has examined RSB in the CHR syndrome, finding that RSB deficits were associated with both negative attenuated psychotic symptoms and impaired social functioning (Jalbrzikowski et al., 2013). Despite the relevance of RSB and important ongoing research on related constructs, Jalbrzikowski and colleagues’ (2013) initial investigation has not yet been replicated. Therefore, the first goal of the current study was to replicate Jalbrzikowski and colleagues’ 2013 study.

Moreover, the current study extended previous research by examining links between RSB deficits and specific social outcomes which are known to impact everyday social functioning and quality of life in the CHR syndrome (Cotter et al., 2017; Glenthøj et al., 2016; Glenthøj et al., 2020). First, an individual’s ability to build friendships is likely affected by RSB, as friendships are known to depend on social awareness, social cognition, and social communication (Burleson, 1994; Ojanen et al., 2010; von Salisch et al., 2014). Second, problematic social Internet use is more common among individuals with social cognition difficulties, and RSB deficits may affect online as well as in-person interactions (Caplan, 2005). Third, perceived social support affects mental health outcomes, setting the stage for more difficulties with perceived social support for those who develop psychosis (Wang et al., 2018). These social outcomes—friendships, problematic social Internet use, and perceived social support—speak to specific real-world difficulties and may explain how RSB deficits impact overall social functioning in the CHR syndrome.

The present study’s primary aim was to assess RSB in a new sample of individuals meeting criteria for a CHR syndrome, compared to a healthy comparison (HC) group. Replicating and building on Jalbrzikowski and colleagues’ (2013) approach, the current study examined group differences in multiple RSB domains, as well as associations between RSB deficits, clinical symptoms, and overall functional impairment. We hypothesized that RSB deficits would be greater in the CHR group, compared to the HC group, and would relate positively to clinical symptomology and social functioning impairment. The second aim examined relationships between RSB deficits and specific social outcomes (i.e., friendships, problematic social internet use, and perceived social support) in the CHR group. We hypothesized that RSB deficits would relate to fewer friendships, more problematic social Internet use, and lower perceived social support.

2. Method

In this cross-sectional study, participants included 45 CHR and 47 HC participants whose parent or guardian reported on the participant’s RSB. Recruitment for the study took place at the Adolescent Development and Preventative Treatment Program in Boulder, Colorado between the years of 2011 and 2015. Participants were recruited using phone screens, email, flyers, bus advertisements, Internet postings, and in-person presentations. In addition, those in the CHR group were recruited through referrals from high schools, hospitals, counselors, psychiatrists, and community mental health centers.

Participants were included in the CHR group based on the presence of a psychosis-risk syndrome per the Structured Interview for Psychosis-Risk Syndromes (SIPS; McGlashan et al., 2010). The current study did not include those that met criteria for BIPS. Participants were excluded from the CHR group if they met criteria for a psychotic disorder based on the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV; American Psychiatric Association, 2000), which was the diagnostic standard at the time of the study. HC participants were included if they did not have significant psychopathology measured by the Structured Clinical Interview for the DSM-IV (SCID-I; First et al., 1997), did not have a first degree relative with a psychotic disorder, and did not meet criteria for a CHR syndrome. None of the participants in the study endorsed ASD or developmental disorders based on self- and parent-report of community diagnosis. Exclusion criteria for both groups were presence of intellectual disability, significant head injury, neurological disorder, suicidality, or lifetime substance dependence assessed by clinical interviewers using the SCID, the Alcohol Use Scale (AUS), and the Drug Use Scale (DUS) (DUS; McHugo et al., 1995).

2.1. Materials

2.1.1. Clinical Interviews.

The Structured Interview for Psychosis-Risk Syndromes (SIPS; McGlashan et al., 2010) was administered to all participants to assess psychosis-risk symptoms. This study examined the positive and negative SIPS subscales, which measure assessor-rated positive and negative symptoms. For each subscale, a composite score was calculated by summing individual symptoms. A corrected negative symptoms score was created by removing N1 (social anhedonia) from the negative symptoms composite because of construct overlap with the social relationship measures. All analyses used the corrected negative symptoms score.

The Structured Clinical Interview for the DSM-IV (SCID-I; First et al., 1997) was administered to rule out psychotic disorders in all participants and to rule out Axis I disorders in the HC group. The Global Functioning Scales (GFS; Cornblatt et al., 2007) consist of prompts regarding participants’ social functioning (e.g., friendship, family, and romantic relationships) and role functioning (e.g., work, school, and chores). Assessors rated social and role functioning on a 10-point scale. All clinical interviews were administered by advanced graduate students and post-doctoral researchers, trained to a high standard of reliability (κ > .80), with diagnostic decisions made in meetings supervised by a licensed clinical psychologist.

2.1.2. RSB Deficits.

The Social Responsiveness Scale (SRS; Constantino & Gruber, 2012) is a 65-item measure completed by the parent or guardian to describe their relative’s behavior since the last research visit. The SRS assesses problems in five domains of RSB (Social Awareness, Social Cognition, Social Communication, Social Motivation, and Autistic Mannerisms) with satisfactory reliability and validity (Bölte et al., 2008; Gau et al., 2013; Wigham et al., 2012). Participants’ parent or guardian completed the SRS by mail. Items were summed to create five domain scores as well as a total score (with higher scores indicating worse RSB deficits).

2.1.3. Social Outcome and Support Variables.

Number of friends was measured by one item from the Social Network Index (SNI; Cohen, et al., 1997), a measure of social network diversity, which asks, “How many friends do you see or talk to at least once every two weeks?”

The Internet Addiction Test (IAT; Young, 1998) measured problematic social Internet use. The IAT consists of 20 items on a 5-point Likert scale which measure the frequency with which the individual engages in Internet behaviors across several domains, including social, time management, and reality substitution (i.e., reliance on Internet use to relieve real-world issues) (Mittal, Dean, & Pelletier, 2013).

The Interpersonal Support Evaluation List-12 (ISEL; Cohen & Hoberman, 1983) measured perceived social support, consisting of three subscales with four items each: appraisal (e.g., advice and guidance), belonging (e.g., empathy, acceptance, and concern), and tangible social support (e.g., help and assistance, such as material aid).

The social outcome and support variables were only available for a subset of participants because these measures were added after some data collection had been completed. See Table 2 for number of participants completing each measure.

Table 2.

Descriptive statistics for study variables

HC CHR
Variable n M SD n M SD t p
SRS Subscales
—SRS-Awareness 47 3.51 2.02 45 5.76 3.62 3.69 < .001
—SRS-Cognition 47 3.23 3.82 45 6.71 5.69 3.46 < .001
—SRS-Communication 47 5.49 6.23 45 12.08 10.96 3.56 < .001
—SRS-Motivation 47 3.85 3.46 45 9.02 7.28 4.38 < .001
—SRS-Mannerisms 47 2.19 3.44 45 5.82 5.96 3.60 < .001
Clinical Phenomenology
—SIPS-Negative 47 0.30 0.83 45 7.33 5.97 8.00 < .001
—SIPS-Positive 47 0.62 1.42 45 10.51 5.60 11.74 < .001
Social Functioning
—GFS-Social 47 8.64 0.67 44 6.80 1.67 −7.00 < .001
—GFS-Role 47 8.53 0.72 44 6.98 1.76 −5.59 < .001
Social Outcome/Support
—SNI-Friends 22 3.95 1.73 22 2.77 2.31 −1.92 .031
—IAT-Social Problems 43 4.93 5.06 39 6.44 5.65 1.27 .104
—IAT-Time Management 45 7.76 5.16 41 10.05 5.20 2.05 .022
—IAT-Reality Substitution 46 2.17 2.31 42 4.10 2.76 3.55 < .001
—ISEL-Belonging 23 13.96 1.92 22 10.77 3.15 −4.11 < .001
—ISEL-Tangible 23 14.37 1.65 22 11.39 2.44 −4.82 < .001
—ISEL-Appraisal 23 15.04 1.36 22 11.86 2.85 −4.81 < .001

Abbreviations: SRS, Social Responsiveness Scale; SIPS, Structured Interview for Psychosis-risk Syndromes; GFS, Global Functioning Scales; SNI, Social Network Index; IAT, Internet Addiction Test; ISEL, Interpersonal Support Evaluation List.

2.2. Analysis

This study includes measures collected from a larger longitudinal study focusing on motor, cognitive, and socio-emotive processes in the psychosis prodrome (Bernard et al., 2017; Dean et al., 2018; Mittal et al., 2014), but the target variables and research questions are novel. All analyses were planned a priori. For the study’s primary aim, independent samples t-tests examined group differences in RSB deficit and subscale scores and clinical variables, and Pearson correlations examined relationships between RSB deficits and clinical variables. The study’s second aim examined relationships between RSB deficits and social outcome and support variables in the CHR group through t-tests of group differences in social outcomes, and correlations between RSB deficits and social outcomes. Number of friends, an ordinal variable, was examined using Spearman correlation. All variables were normally distributed with the exception of the IAT social subscale, with skewness of 1.43 (SE = .38). A supplemental analysis found similar results when IAT was transformed to correct for skew; therefore, the study reports untransformed IAT values. Outliers were not removed in our analyses. To account for multiple comparisons, we report p-values corrected for the False Discovery Rate (FDR) using the Benjamini-Hochberg method (Benjamini & Hochberg, 1995).

Sample sizes for social outcomes were smaller than for the primary analyses (see Table 2 below). Data were likely missing at random, given that study recruitment procedures did not change over time, and that marginal plots of missing data showed the distribution of SRS scores was similar for missing and non-missing data. Therefore, the use of partial data reduces statistical power for these tests but is unlikely to introduce systematic biases. Missing data were addressed by pairwise deletion rather than multiple imputation because of the relatively large proportion of missing data in these exploratory analyses.

3. Results

See Table 1 for demographics of the CHR and HC samples. Chi-squared tests and t-tests found a significant difference in age and no significant differences in gender, race, or parental education between the groups. Age positively correlated with positive symptoms and negative symptoms, and negatively correlated with social functioning. For variables that correlated with age, we report raw Pearson correlations as well as partial correlations adjusted for age. No other demographic variables correlated with study measures.

Table 1.

Participant characteristics

HC CHR χ2 or t p
Gender
—Male 25 (53%) 26 (58%)
—Female 22 (47%) 19 (42%) 0.20 .66
—Total 47 45
Race
—White 30 (64%) 32 (71%)
—South/Central American 12 (26%) 9 (20%)
—Asian 2 (4%) 1 (2%)
—Multiracial 1 (2%) 1 (2%)
—Black 1 (2%) 1 (2%)
—Native American 1 (2%) 1 (2%) 2.78 .84
Age
—Mean Years (SD) 17.70 (2.94) 18.92 (1.83) 2.38 .02
Parent Education
—Mean Years (SD) 16.04 (2.61) 15.72 (2.44) −0.61 .55

3.1. RSB in the CHR Group

3.1.1. Comparison of CHR and HC groups.

The independent samples t-test revealed a difference in overall RSB. To test if the effect was accounted for by age or gender, we calculated a simultaneous multiple regression model with age, gender, and group (dummy-coded as 1 = CHR and 2 = HC) entered as predictors. The effect for group was significant, β = −0.39, p <.001, indicating that group differences in SRS scores were not accounted for by age or gender. Follow-up t-tests revealed that individuals in the CHR group were markedly impaired in overall RSB (see Figure 1) and all individual facets of RSB (all p < .001, see Table 2). The RSB subscales were highly inter-correlated (r = 0.75 to 0.88). As a result, subsequent analyses were conducted with the RSB total rather than individual subscales. Follow up t-tests demonstrated that individuals in the CHR group were impaired in negative symptoms, positive symptoms, social functioning, and role functioning (see Table 2).

Figure 1.

Figure 1.

The clinical high risk for psychosis group showed more reciprocal social behavior deficits than the healthy comparison group, t(90) = 4.10, p <.001, d = .86. Social Responsiveness Scale (SRS) total scores shown here. Similar results were found for all 5 SRS subscales (Awareness, Cognition, Communication, Motivation, and Mannerisms).

3.1.2. Clinical phenomenology.

The individuals in the CHR group showed a positive relationship between RSB deficits and negative symptoms, r(43) = 0.45, p =.001, which was not accounted for by the effect of age, rpartial(42) = 0.47, p =.001, pFDR = .006. RSB deficits were not related to positive symptoms, r(43) = 0.07, p =.317, rpartial(42) = 0.11, p =.242, pFDR = .289.

3.1.3. Social functioning.

RSB deficits were negatively correlated with social functioning in the CHR group, r(42)= −0.45, p = .002, and this correlation was not accounted for by the effect of age, rpartial(41)= −0.50, p < .001, pFDR = .006 (see Figure 2a). There was some evidence of specificity. Although RSB deficits were also negatively correlated with role functioning, r(42) = −0.26, p = .044, pFDR = .075, this was a small-medium effect size that did not survive FDR correction.

Figure 2.

Figure 2.

(a) RSB deficits were associated with poorer social functioning in the CHR group. Pearson correlation shown here, r(42)= −0.45, p = .002, was not accounted for by the effect of age, rpartial(41)= −0.50, p < .001, pFDR = .006. (b) RSB deficits were associated with problematic social Internet use, r(37) = 0.27, p =.048, pFDR = .088. Note: RSB deficits = Social Responsiveness Scale; social functioning = Global Functioning Scale: Social; problematic social Internet use = Internet Addiction Test (IAT) social problems domain.

3.2. Social Outcome and Support Variables

3.2.1. Comparison of CHR and HC groups.

As shown in Table 2, t-tests indicated that individuals in the CHR group had fewer friends; less perceived appraisal, belonging, and tangible support; and more Internet-related reality substitution and time management problems than HC. Interestingly, we did not observe group differences in problematic social Internet use.

3.2.2. Friends.

As shown in Table 3, within the CHR group, RSB deficits were negatively correlated with number of friends, with a large effect size.

Table 3.

Correlations between reciprocal social behavior and social outcome and support variables

Variable Correlation with RSB p p FDR
SNI-Friends −0.51 .007** .026*
IAT-Social Problems 0.27 .048* .088
IAT-Time Management 0.10 .263 .289
IAT-Reality Substitution 0.12 .224 .289
ISEL-Belonging −0.39 .037* .081
ISEL-Tangible −0.41 .028* .077
ISEL-Appraisal 0.07 .387 .387

Note: Correlations were Pearson’s r, except for SNI-Friends, which was Spearman’s rho.

*

Significant at p < 0.05

**

Significant at p < 0.01

3.2.3. Problematic social Internet use.

As shown in Table 3, RSB deficits were positively correlated with problematic social Internet use, with a medium effect size (see Figure 2b). However, the effect was no longer significant after FDR correction. To test specificity, we also examined relationships between RSB and other types of problematic Internet use. RSB was not associated with Internet time management problems or reality substitution problems even before FDR correction.

3.2.4. Perceived social support.

As shown in Table 3, RSB deficits were negatively correlated with perceived belonging and perceived tangible social support, but not perceived appraisal support. Relationships between RSB deficits, perceived belonging, and perceived tangible social support were no longer significant after FDR correction.

4. Discussion

This study provides further evidence that RSB impairments are present in the CHR syndrome. Moreover, it also suggests that RSB impairments may be associated with real-world social outcomes including friendships, problematic social Internet use, and perceived social support. These social phenomena are critical as they may put individuals at risk for an unpleasant cycle of worsening outcomes (Sündermann et al., 2013).

Replicating previous research, we found substantial RSB deficits in individuals meeting criteria for a CHR syndrome (Jalbrzikowski et al., 2013). Extending previous research, we showed that RSB deficits in the CHR group were broad and not specific to any domain of social behavior. Moreover, where Jalbrzikowski et al. (2013) reported a trend-level association between RSB deficits and negative symptoms (r = .25, p = .06), we found a stronger link (r = .45, p = .001, pFDR = .006), suggesting that social behavioral impairments may play a larger role in the expression of negative symptoms than was previously known. By contrast, RSB deficits were not related to positive symptoms, reinforcing recent evidence that positive symptom duration and severity are not associated with poorer social outcomes for those at risk for psychosis (Carrión et al., 2016). Finally, the present findings replicated links between RSB deficits and lower social functioning in the CHR group (Jalbrzikowski et al., 2013).

In the CHR group, participants with more severe RSB deficits reported having fewer friends. RSB deficits may be a mediator explaining previous findings that social networks in the CHR syndrome are characterized by fewer friends and more family members (Gayer-Anderson & Morgan, 2013; Robustelli et al., 2017). RSB deficits may alter the social landscape for individuals meeting criteria for a CHR syndrome, impairing their ability to form and maintain friendships and leaving them reliant on family for social support.

RSB deficits also had a positive association with problematic social Internet use. Although this result did not survive correction for multiple comparisons, it provides preliminary evidence that RSB deficits may carry over into Internet use. This is particularly interesting given that problematic social Internet use did not differ between CHR and HC groups. These results suggest that problematic social Internet use is not unique to CHR samples, but when it does occur in CHR samples it may be linked to RSB deficits. As interactions among young people increasingly take place online, it will be important to explore the role(s) of social Internet use within the CHR syndrome, including the impact of RSB deficits on Internet social behavior.

Finally, RSB deficits had a negative relationship with perceived empathy, acceptance, and concern; and perceived material support from others. Although these results did not survive FDR correction, their medium-large effect sizes suggest that they may be meaningful effects warranting follow-up study. RSB deficits may impact individuals’ social networks in part through beliefs and cognitive biases about social relationships, making individuals less likely to pursue intimate friendships and romantic relationships.

These data add some nuance to distinctions between RSB and negative symptoms. Interestingly, in the present study, family-rated RSB deficits related to clinician-rated negative symptoms, suggesting that these effects are not due to common rater bias. There is some conceptual overlap between RSB deficits and the negative symptom domains of poverty of speech and expression (De Crescenzo et al., 2019; Kincaid et al., 2017; Trevisan et al., 2020). Yet, RSB deficits in ASD and negative symptoms in the CHR syndrome have distinct features (Nenadid et al., 2021), such as prevalence rates and the severity of repetitive behaviors and stereotyped interests (Jalbrzikowski et al., 2013; Kincaid et al., 2017). Although both negative symptoms (Gupta et al., 2021; Schlosser et al., 2015) and RSB deficits (Jalbrzikowski et al., 2013) predict social dysfunction in CHR populations, RSB deficits may capture social dysfunction in a unique way. By focusing on specific aspects of social behavior and developmental trends over time, future research could further explore conceptual overlap and points of departure between RSB and negative symptoms.

The current study had some limitations. The sample sizes for analyses in the second aim limit inferences from those analyses. Follow-up studies could address this limitation by recruiting larger and more diverse samples. Moreover, future research could include the full range of CHR syndromes, including BIPS, and conduct formal screenings for ASD. It is important to note that this study was not powered to detect differences in correlations between the CHR and HC groups. One strength of the current study is that RSB deficits were measured with family-reports, whereas social outcomes were measured with self-reports, and social functioning was rated by clinical interviewers. This multimethod design eliminates potential sources of common method bias (Podsakoff et al., 2003). However, other methods could be used to assess basic RSB mechanisms, for example through electromyography (EMG) or emotion recognition software (Gupta et al., 2019; Riehle & Lincoln, 2017). Lastly, number of friends is only one way to operationalize friendship outcomes. Some investigations have suggested that number of friends may be independent of quality of friends, and may not predict adjustment (Demir & Urberg, 2004; Eckert, 1989). Future studies with multiple measures of friendship outcomes would be valuable in teasing apart these nuances.

In sum, the present research replicated previous findings of RSB deficits in the CHR syndrome and showed that these deficits relate to negative symptoms and specific social outcomes, suggesting RSB as a rich topic for future study in this crucial developmental period.

Acknowledgements

This research was supported by the National Institute of Mental Health grants R21/33MH103231, R01MH094650, and R01MH112545 to Dr. Mittal. The data that support the findings of this study are available from the corresponding author upon reasonable request.

Footnotes

Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

Conflicts of Interest

The authors have no conflicts of interest to report.

References

  1. Addington J, Liu L, Buchy L, Cadenhead KS, Cannon TD, Cornblatt BA, Perkins DO, Seidman LJ, Tsuang MT, Walker EF, Woods SW, Bearden CE, Mathalon DH, & McGlashan TH (2015). North American Prodrome Longitudinal Study (NAPLS 2): The Prodromal Symptoms. The Journal of Nervous and Mental Disease, 203(5), 328–335. 10.1097/NMD.0000000000000290 [DOI] [PMC free article] [PubMed] [Google Scholar]
  2. American Psychiatric Association, & American Psychiatric Association (Eds.). (2000). Diagnostic and statistical manual of mental disorders: DSM-IV-TR (4th ed., text revision). American Psychiatric Association. [Google Scholar]
  3. Benjamini Y, & Hochberg Y (1995). Controlling the False Discovery Rate: A Practical and Powerful Approach to Multiple Testing. Journal of the Royal Statistical Society. Series B (Methodological), 57(1), 289–300. [Google Scholar]
  4. JSTOR.Bölte S, Poustka F, & Constantino JN (2008). Assessing autistic traits: Cross-cultural validation of the social responsiveness scale (SRS). Autism Research, 1(6), 354–363. 10.1002/aur.49 [DOI] [PubMed] [Google Scholar]
  5. Bernard JA, Orr JM, & Mittal VA (2017). Cerebello-thalamo-cortical networks predict positive symptom progression in individuals at ultra-high risk for psychosis. NeuroImage: Clinical, 14, 622–628. 10.1016/j.nicl.2017.03.001 [DOI] [PMC free article] [PubMed] [Google Scholar]
  6. Bora E, Gökçen S, Kayahan B, & Veznedaroglu B (2008). Deficits of Social-Cognitive and Social-Perceptual Aspects of Theory of Mind in Remitted Patients With Schizophrenia: Effect of Residual Symptoms. The Journal of Nervous and Mental Disease, 196(2), 95–99. 10.1097/NMD.0b013e318162a9e1 [DOI] [PubMed] [Google Scholar]
  7. Burleson BR (1994). Friendship and similarities in social-cognitive and communication abilities: Social skill bases of interpersonal attraction in childhood. Personal Relationships, 1(4), 371–389. 10.1111/j.1475-6811.1994.tb00071.x [DOI] [Google Scholar]
  8. Cannon TD, Cadenhead K, Cornblatt B, Woods SW, Addington J, Walker E, Seidman LJ, Perkins D, Tsuang M, McGlashan T, & Heinssen R (2008). Prediction of Psychosis in Youth at High Clinical Risk: A Multisite Longitudinal Study in North America. Archives of General Psychiatry, 65(1), 28–37. 10.1001/archgenpsychiatry.2007.3 [DOI] [PMC free article] [PubMed] [Google Scholar]
  9. Caplan SE (2005). A Social Skill Account of Problematic Internet Use. Journal of Communication, 55(4), 721–736. 10.1111/j.1460-2466.2005.tb03019.x [DOI] [Google Scholar]
  10. Carrión RE, Demmin D, Auther AM, McLaughlin D, Olsen R, Lencz T, Correll CU, & Cornblatt BA (2016). Duration of attenuated positive and negative symptoms in individuals at clinical high risk: Associations with risk of conversion to psychosis and functional outcome. Journal of Psychiatric Research, 81, 95–101. 10.1016/j.jpsychires.2016.06.021 [DOI] [PMC free article] [PubMed] [Google Scholar]
  11. Cohen S, & Hoberman HM (1983). Positive events and social supports as buffers of life change stress. Journal of Applied Social Psychology, 13(2), 99–125. 10.1111/j.1559-1816.1983.tb02325.x [DOI] [Google Scholar]
  12. Cohen S, Doyle WJ, Skoner DP, Rabin BS, & Gwaltney JM (1997). Social ties and susceptibility to the common cold. JAMA, 277(24), 1940–1944. 10.1001/jama.1997.03540480040036 [DOI] [PubMed] [Google Scholar]
  13. Constantino JN, Przybeck T, Friesen D, & Todd RD (2000). Reciprocal social behavior in children with and without pervasive developmental disorders. Journal of Developmental and Behavioral Pediatrics, 21(1), 2–11. 10.1097/00004703-200002000-00001 [DOI] [PubMed] [Google Scholar]
  14. Constantino JN, & Gruber CP (2012). Social responsiveness scale: SRS-2. Western Psychological Services Torrance, CA. [Google Scholar]
  15. Cornblatt BA, Auther AM, Niendam T, Smith CW, Zinberg J, Bearden CE, & Cannon TD (2007). Preliminary Findings for Two New Measures of Social and Role Functioning in the Prodromal Phase of Schizophrenia. Schizophrenia Bulletin, 33(3), 688–702. 10.1093/schbul/sbm029 [DOI] [PMC free article] [PubMed] [Google Scholar]
  16. Cotter J, Bartholomeusz C, Papas A, Allott K, Nelson B, Yung AR, & Thompson A (2017). Examining the association between social cognition and functioning in individuals at ultra-high risk for psychosis. The Australian and New Zealand Journal of Psychiatry, 51(1), 83–92. 10.1177/0004867415622691 [DOI] [PubMed] [Google Scholar]
  17. De Crescenzo F, Postorino V, Siracusano M, Riccioni A, Armando M, Curatolo P, & Mazzone L (2019). Autistic Symptoms in Schizophrenia Spectrum Disorders: A Systematic Review and Meta-Analysis. Frontiers in Psychiatry, 10. 10.3389/fpsyt.2019.00078 [DOI] [PMC free article] [PubMed] [Google Scholar]
  18. Dean DJ, Walther S, Bernard JA, & Mittal VA (2018). Motor Clusters Reveal Differences in Risk for Psychosis, Cognitive Functioning, and Thalamocortical Connectivity: Evidence for Vulnerability Subtypes. Clinical Psychological Science, 6(5), 721–734. 10.1177/2167702618773759 [DOI] [PMC free article] [PubMed] [Google Scholar]
  19. Demir M, & Urberg KA (2004). Friendship and adjustment among adolescents. Journal of Experimental Child Psychology, 88(1), 68–82. 10.1016/j.jecp.2004.02.006 [DOI] [PubMed] [Google Scholar]
  20. Eckert P (1989). Jocks and Burnouts: Social Categories and Identity in the High School. Teachers College Press. [Google Scholar]
  21. First MB (1997). SCID-I: Clinician version. American Psychiatric Press. [Google Scholar]
  22. Fusar-Poli P, Borgwardt S, Bechdolf A, Addington J, Riecher-Rössler A, Schultze-Lutter F, Keshavan M, Wood S, Ruhrmann S, Seidman LJ, Valmaggia L, Cannon T, Velthorst E, De Haan L, Cornblatt B, Bonoldi I, Birchwood M, McGlashan T, Carpenter W, … Yung A (2013). The psychosis high-risk state: A comprehensive state-of-the-art review. JAMA Psychiatry, 70(1), 107–120. 10.1001/jamapsychiatry.2013.269 [DOI] [PMC free article] [PubMed] [Google Scholar]
  23. Fusar-Poli P, Cappucciati M, Rutigliano G, Schultze-Lutter F, Bonoldi I, Borgwardt S, Riecher-Rössler A, Addington J, Perkins D, Woods SW, McGlashan TH, Lee J, Klosterkötter J, Yung AR, & McGuire P (2015). At risk or not at risk? A meta-analysis of the prognostic accuracy of psychometric interviews for psychosis prediction. World Psychiatry, 14(3), 322–332. 10.1002/wps.20250 [DOI] [PMC free article] [PubMed] [Google Scholar]
  24. Gau SS-F, Liu L-T, Wu Y-Y, Chiu Y-N, & Tsai W-C (2013). Psychometric properties of the Chinese version of the Social Responsiveness Scale. Research in Autism Spectrum Disorders, 7(2), 349–360. 10.1016/j.rasd.2012.10.004 [DOI] [Google Scholar]
  25. Gayer-Anderson C, & Morgan C (2013). Social networks, support and early psychosis: A systematic review. Epidemiology and Psychiatric Sciences, 22(2), 131–146. 10.1017/S2045796012000406 [DOI] [PMC free article] [PubMed] [Google Scholar]
  26. Gibson CM, Penn DL, Prinstein MJ, Perkins DO, & Belger A (2010). Social Skill and Social Cognition in Adolescents at Genetic Risk for Psychosis. Schizophrenia Research, 122(1–3), 179–184. 10.1016/j.schres.2010.04.018 [DOI] [PMC free article] [PubMed] [Google Scholar]
  27. Glenthøj LB, Fagerlund B, Hjorthøj C, Jepsen JRM, Bak N, Kristensen TD, Wenneberg C, Krakauer K, Roberts DL, & Nordentoft M (2016). Social cognition in patients at ultra-high risk for psychosis: What is the relation to social skills and functioning? Schizophrenia Research: Cognition, 5, 21–27. 10.1016/j.scog.2016.06.004 [DOI] [PMC free article] [PubMed] [Google Scholar]
  28. Glenthøj LB, Kristensen TD, Wenneberg C, Hjorthøj C, & Nordentoft M (2020). Investigating Cognitive and Clinical Predictors of Real-Life Functioning, Functional Capacity, and Quality of Life in Individuals at Ultra-High Risk for Psychosis. Schizophrenia Bulletin Open, 1(1). 10.1093/schizbullopen/sgaa027 [DOI] [Google Scholar]
  29. Gupta T, Haase CM, Strauss GP, Cohen AS, & Mittal VA (2019). Alterations in facial expressivity in youth at clinical high-risk for psychosis. Journal of Abnormal Psychology, 128(4), 341–351. 10.1037/abn0000413 [DOI] [PMC free article] [PubMed] [Google Scholar]
  30. Gupta T, Cowan HR, Strauss GP, Walker EF, & Mittal VA (2021). Deconstructing Negative Symptoms in Individuals at Clinical High-Risk for Psychosis: Evidence for Volitional and Diminished Emotionality Subgroups That Predict Clinical Presentation and Functional Outcome. Schizophrenia Bulletin, 47(1), 54–63. 10.1093/schbul/sbaa084 [DOI] [PMC free article] [PubMed] [Google Scholar]
  31. Häfner H, Löffler W, Maurer K, Hambrecht M, & an der Heiden W. (1999). Depression, negative symptoms, social stagnation and social decline in the early course of schizophrenia. Acta Psychiatrica Scandinavica, 100(2), 105–118. 10.1111/j.1600-0447.1999.tb10831.x [DOI] [PubMed] [Google Scholar]
  32. Haroun N, Dunn L, Haroun A, & Cadenhead KS (2006). Risk and Protection in Prodromal Schizophrenia: Ethical Implications for Clinical Practice and Future Research. Schizophrenia Bulletin, 32(1), 166–178. 10.1093/schbul/sbj007 [DOI] [PMC free article] [PubMed] [Google Scholar]
  33. Healey KM, Penn DL, Perkins D, Woods SW, & Addington J (2013). Theory of mind and social judgments in people at clinical high risk of psychosis. Schizophrenia Research, 150(2), 498–504. 10.1016/j.schres.2013.08.038 [DOI] [PMC free article] [PubMed] [Google Scholar]
  34. Isvoranu A, Ziermans T, Schirmbeck F, Borsboom D, Geurts H, Haan L, Amelsvoort T, Bartels-Velthuis A, Simons C, & Os J (2021). Autistic Symptoms and Social Functioning in Psychosis: A Network Approach. Schizophrenia Bulletin. 10.1093/schbul/sbab084 [DOI] [PMC free article] [PubMed] [Google Scholar]
  35. Jalbrzikowski M, Krasileva KE, Marvin S, Zinberg J, Andaya A, Bachman P, Cannon TD, & Bearden CE (2013). Reciprocal social behavior in youths with psychotic illness and those at clinical high risk. Development and Psychopathology, 25(4), 1187–1197. 10.1017/S095457941300045X [DOI] [PMC free article] [PubMed] [Google Scholar]
  36. Kincaid DL, Doris M, Shannon C, & Mulholland C (2017). What is the prevalence of autism spectrum disorder and ASD traits in psychosis? A systematic review. Psychiatry Research, 250, 99–105. 10.1016/j.psychres.2017.01.017 [DOI] [PubMed] [Google Scholar]
  37. Lee TY, Hong SB, Shin NY, & Kwon JS (2015). Social cognitive functioning in prodromal psychosis: A meta-analysis. Schizophrenia Research, 164(1–3), 28–34. 10.1016/j.schres.2015.02.008 [DOI] [PubMed] [Google Scholar]
  38. Lei J, & Ventola P (2018). Characterising the relationship between theory of mind and anxiety in children with Autism Spectrum Disorder and typically developing children. Research in Autism Spectrum Disorders, 49, 1–12. 10.1016/j.rasd.2018.01.005 [DOI] [Google Scholar]
  39. McGlashan T, Walsh B, & Woods S (2010). The Psychosis-Risk Syndrome: Handbook for Diagnosis and Follow-Up. Oxford University Press, USA. [Google Scholar]
  40. McHugo GJ, Drake RE, Burton HL, & Ackerson TH (1995). A scale for assessing the stage of substance abuse treatment in persons with severe mental illness. The Journal of Nervous and Mental Disease, 183(12), 762–767. 10.1097/00005053-199512000-00006 [DOI] [PubMed] [Google Scholar]
  41. Mittal VA, Dean DJ, & Pelletier A (2013). Internet addiction, Reality Substitution, and Longitudinal Changes in Psychotic-like Experiences in Young Adults. Early Intervention in Psychiatry, 7(3), 261–269. 10.1111/j.1751-7893.2012.00390.x [DOI] [PMC free article] [PubMed] [Google Scholar]
  42. Mittal VA, Dean DJ, Bernard JA, Orr JM, Pelletier-Baldelli A, Carol EE, Gupta T, Turner J, Leopold DR, Robustelli BL, & Millman ZB (2014). Neurological Soft Signs Predict Abnormal Cerebellar-Thalamic Tract Development and Negative Symptoms in Adolescents at High Risk for Psychosis: A Longitudinal Perspective. Schizophrenia Bulletin, 40(6), 1204–1215. 10.1093/schbul/sbt199 [DOI] [PMC free article] [PubMed] [Google Scholar]
  43. Morrison KE, Pinkham AE, Penn DL, Kelsven S, Ludwig K, & Sasson NJ (2017). Distinct profiles of social skill in adults with autism spectrum disorder and schizophrenia. Autism Research, 10(5), 878–887. 10.1002/aur.1734 [DOI] [PMC free article] [PubMed] [Google Scholar]
  44. Nenadid I, Meller T, Evermann U, Schmitt S, Pfarr J-K, Abu-Akel A, & Grezellschak S (2021). Subclinical schizotypal vs. Autistic traits show overlapping and diametrically opposed facets in a non-clinical population. Schizophrenia Research, 231, 32–41. 10.1016/j.schres.2021.02.018 [DOI] [PubMed] [Google Scholar]
  45. Ojanen T, Sijtsema JJ, Hawley PH, & Little TD (2010). Intrinsic and extrinsic motivation in early adolescents’ friendship development: Friendship selection, influence, and prospective friendship quality. Journal of Adolescence, 33(6), 837–851. 10.1016/j.adolescence.2010.08.004 [DOI] [PubMed] [Google Scholar]
  46. Osborne KJ, Vargas T, & Mittal VA (2019). Early childhood social communication deficits in youth at clinical high-risk for psychosis: Associations with functioning and risk. Development and Psychopathology, 1–14. 10.1017/S0954579419000385 [DOI] [PMC free article] [PubMed] [Google Scholar]
  47. Podsakoff PM, MacKenzie SB, Lee J-Y, & Podsakoff NP (2003). Common method biases in behavioral research: A critical review of the literature and recommended remedies. Journal of Applied Psychology, 88(5), 879–903. 10.1037/0021-9010.88.5.879 [DOI] [PubMed] [Google Scholar]
  48. Riehle M, & Lincoln TM (2017). Social consequences of subclinical negative symptoms: An EMG study of facial expressions within a social interaction. Journal of Behavior Therapy and Experimental Psychiatry, 55, 90–98. 10.1016/j.jbtep.2017.01.003 [DOI] [PubMed] [Google Scholar]
  49. Robustelli BL, Newberry RE, Whisman MA, & Mittal VA (2017). Social relationships in young adults at ultra high risk for psychosis. Psychiatry Research, 247, 345–351. 10.1016/j.psychres.2016.12.008 [DOI] [PMC free article] [PubMed] [Google Scholar]
  50. Roisman GI, Masten AS, Coatsworth JD, & Tellegen A (2004). Salient and Emerging Developmental Tasks in the Transition to Adulthood. Child Development, 75(1), 123–133. 10.1111/j.1467-8624.2004.00658.x [DOI] [PubMed] [Google Scholar]
  51. Wang J, Mann F, Lloyd-Evans B, Ma R, & Johnson S (2018). Associations between loneliness and perceived social support and outcomes of mental health problems: A systematic review. BMC Psychiatry, 18(1), 156. 10.1186/s12888-018-1736-5 [DOI] [PMC free article] [PubMed] [Google Scholar]
  52. Wigham S, McConachie H, Tandos J, & Le Couteur AS (2012). The reliability and validity of the Social Responsiveness Scale in a UK general child population. Research in Developmental Disabilities, 33(3), 944–950. 10.1016/j.ridd.2011.12.017 [DOI] [PubMed] [Google Scholar]
  53. von Salisch M, Zeman J, Luepschen N, & Kanevski R (2014). Prospective Relations Between Adolescents’ Social-emotional Competencies and Their Friendships. Social Development, 23(4), 684–701. 10.1111/sode.12064 [DOI] [Google Scholar]
  54. Schlosser DA, Campellone TR, Biagianti B, Delucchi KL, Gard DE, Fulford D, Stuart BK, Fisher M, Loewy RL, & Vinogradov S (2015). Modeling the role of negative symptoms in determining social functioning in individuals at clinical high risk of psychosis. Schizophrenia Research, 169(1–3), 204–208. 10.1016/j.schres.2015.10.036 [DOI] [PMC free article] [PubMed] [Google Scholar]
  55. Solomon M, Olsen E, Niendam T, Ragland JD, Yoon J, Minzenberg M, & Carter CS (2011). From lumping to splitting and back again: Atypical social and language development in individuals with clinical-high-risk for psychosis, first episode schizophrenia, and autism spectrum disorders. Schizophrenia Research, 131(1), 146–151. 10.1016/j.schres.2011.03.005 [DOI] [PMC free article] [PubMed] [Google Scholar]
  56. Sündermann O, Onwumere J, Bebbington P, & Kuipers E (2013). Social networks and support in early psychosis: Potential mechanisms. Epidemiology and Psychiatric Sciences, 22(2), 147–150. 10.1017/S2045796012000601 [DOI] [PMC free article] [PubMed] [Google Scholar]
  57. Trevisan DA, Foss-Feig JH, Naples AJ, Srihari V, Anticevic A, & McPartland JC (2020). Autism spectrum disorder and schizophrenia are better differentiated by positive symptoms than negative symptoms. Frontiers in Psychiatry, 11. 10.3389/fpsyt.2020.00548 [DOI] [PMC free article] [PubMed] [Google Scholar]
  58. Young KS (1998). Internet Addiction: The Emergence of a New Clinical Disorder. CyberPsychology & Behavior, 1(3), 237–244. 10.1089/cpb.1998.1.237 [DOI] [Google Scholar]

RESOURCES