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C. J. Herold et al.: Co gnitive GeroPsych Performance (2017), in©Schizophren 2017 30 (1), Hogrefe 35–44 ia Full-Length Research Report This document is copyrighted by the American Psychological Association or one of its allied publishers. This article is intended solely for the personal use of the individual user and is not to be disseminated broadly. Cognitive Performance in Patients with Chronic Schizophrenia Across the Lifespan Christina Josefa Herold1, Lena Anna Schmid1, Marc Montgomery Lässer1, Ulrich Seidl2, and Johannes Schröder1,3 1 Section of Geriatric Psychiatry, Department of General Psychiatry, University of Heidelberg, Heidelberg, Germany 2 Center for Mental Health, Klinikum Stuttgart, Stuttgart, Germany 3 Institute of Gerontology, University of Heidelberg, Heidelberg, Germany Abstract: Chronic schizophrenia involves neuropsychological deficits that primarily strike executive functions and episodic memory. Our study investigated these deficits throughout the lifespan in patients with chronic schizophrenia and in healthy controls. Important neuropsychological functions were tested in 94 patients and 66 healthy controls, who were assigned to three age groups. Compared with the healthy controls, patients performed significantly poorer on all tests applied. Significant age effects occurred on all tests except the digit span forward, with older subjects scoring well below the younger ones. With respect to cognitive flexibility, age effects were more pronounced in the patients. These findings underline the importance of cognitive deficits in chronic schizophrenia and indicate that diminished cognitive flexibility shows age-associated differences. Keywords: schizophrenia, cognition, aging, executive functions, memory Cognitive impairment is a hallmark of schizophrenia. The pattern of deficits and their relationship to psychosocial functioning have been illustrated in a large number of neuropsychological studies over the past few decades (Dickinson & Gold, 2008; Green, 1996; Schröder, Tittel, Stockert, & Karr, 1996). It is generally assumed that cognitive function is often already below average in premorbid periods (Reichenberg et al., 2006; Woodberry, Giuliano, & Seidman, 2008) and decreases with manifestation of the disease (Bilder et al., 2000; Mesholam-Gately, Giuliano, Goff, Faraone, & Seidman, 2009). The respective deficits continue in patients with chronic schizophrenia, including those in whom symptoms have partially remitted (Barbarotto, Castignoli, Pasetti, & Laiacona, 2001; Heinrichs & Zakzanis, 1998). Cognitive and functional losses occur with normal aging in the entire population. The frontal-lobe hypothesis (West, 1996) posits that the frontal lobe is particularly susceptible to age-related deterioration in healthy adults. This assumption is supported by neuroimaging data that demonstrate both structural and functional changes in the frontal lobe with aging (Hazlett et al., 1998; Raz et al., 1997; Salat et al., 2004). In addition, neuropsychological studies describe a worsening of frontal executive functions with aging in healthy adults (Salthouse, Atkinson, & Berish, 2003; Sorel & Pennequin, 2008). The question of the extent to which this decline of frontal functions with age also applies to patients with chronic schizophrenia remains unresolved. While some studies indicate that © 2017 Hogrefe certain cognitive domains such as information processing and executive functioning might bear a greater risk of worsening with age (Bowie, Reichenberg, McClure, Leung, & Harvey, 2008; Fucetola et al., 2000; Irani et al., 2012; Loewenstein, Czaja, Bowie, & Harvey, 2012), others did not find any differential aging effects (Heaton et al., 2001; Hijman, Hulshoff Pol, Sitskoorn, & Kahn, 2003; Mockler, Riordan, & Sharma, 1997). These divergent findings may reflect methodological differences between the studies, which are detailed in the Discussion section below. Recently, Kirkpatrick et al. (2008) established the hypothesis that schizophrenia is a syndrome of accelerated aging – as already conceptualized by the term “dementia praecox” (Kraepelin, 1913) – since cognitive deficits in chronic schizophrenia primarily strike those domains that are typically affected in the physiological aging process. This hypothesis also conforms to the frontal cortex changes frequently described in patients with schizophrenia in neuroimaging studies (Bachmann et al., 2004; Buchsbaum et al., 1982; DeLisi, Szulc, Bertisch, Majcher, & Brown, 2006; Schröder, Buchsbaum et al., 1996). Despite the renewed interest in cognition in old age schizophrenia, considerable controversy still lingers over this topic. The current study examines the association between age and cognitive performance in chronic schizophrenia. We concentrate specifically on patients and psychiatrically healthy controls ranging in age from young adulthood to old age. GeroPsych (2017), 30 (1), 35–44 DOI 10.1024/1662-9647/a000164 36 We hypothesized that patients with chronic schizophrenia of all ages show substantial cognitive deficits. In addition, we expected these deficits to worsen with age. This effect should primarily involve executive functions, while episodic memory deficits should remain more stable. Methods This document is copyrighted by the American Psychological Association or one of its allied publishers. This article is intended solely for the personal use of the individual user and is not to be disseminated broadly. Subjects and Procedures Cognitive performance was assessed in healthy subjects and patients with chronic schizophrenia in the age range 18 to 82 years. The patients and healthy controls were each subdivided into three age groups (“young” ≤ 34 years, “middle” 35–49 years, and “older” ≥ 50 years). 94 patients with chronic or subchronic schizophrenia according to DSM-IV (American Psychiatric Association, 2000) were recruited from three psychiatric long-term units (n = 40) and a mental state hospital (n = 54). All patients were in a stable condition and had received antipsychotic therapy; dosage was evaluated in mg chlorpromazine (CPZ) equivalents (Woods, 2003). The diagnosis was established by experienced psychiatrists. Inclusion criteria for patients were (1) a diagnosis of schizophrenia according to DSM-IV (American Psychiatric Association, 2000), (2) German as the primary language, and (3) a minimum of 8 years school education. Patients with late onset schizophrenia with a manifestation of the disease after age 45 were not included as this condition may have involved a different etiology (Howard, Rabins, Seeman, & Jeste, 2000; Schmid, Lässer, & Schröder, 2011). Further exclusion criteria included a history of any neurological condition affecting the central nervous system, head injury, or substance abuse. Healthy controls (n = 66) were recruited among the hospital staff and through advertisements in a newspaper. The Mini International Neuropsychiatric Interview (interrater and retestreliability Cohen’s κ > 0.75, Sheehan et al., 1998) and the Beck Depression Inventory II (Cronbach’s α = 0.89, retest-reliability r = 0.78, Hautzinger, Keller, & Kühner, 2006) were performed to screen controls for current psychopathology. They were carefully matched to patients with respect to age and sex (main effect “diagnosis,” p > .30). Informed consent was obtained from all participants after the study had been fully explained. The study was approved by the local ethics committee. C. J. Herold et al.: Cognitive Performance in Schizophrenia Krausz, 1997; Overall & Gorham, 1962), the Scale for the Assessment of Positive Symptoms (SAPS) and the Scale for the Assessment of Negative Symptoms (SANS) (34 and 25 items respectively, maximum global score = 20 and 25 respectively, interrater-reliability r = 0.63 and r = 0.52 for SAPS and SANS respectively, Cronbach’s α SAPS = 0.77–0.91 and SANS = 0.83–0.92; Andreasen & Olsen, 1982; Norman, Malla, Cortese, & Diaz, 1996). Important neuropsychological domains typically involved in chronic schizophrenia were assessed by using a comprehensive test battery. Therefore, verbal learning and memory, short-term and working memory, processing speed, and cognitive flexibility were taken into account; the Mini-Mental State Examination (MMSE, maximum score = 30, retest-reliability r = 0.80, Cronbach’s α = 0.91) was used as a screening instrument for cognitive ability (Folstein, Folstein, & McHugh, 1975; Marioni, Chatfield, Brayne, & Matthews, 2011). All subjects completed the logical memory subtests of the Wechsler Memory Scale (Härting et al., 2000) to assess verbal learning and memory (logical memory I and logical memory II, maximum score each = 50, retest-reliability r = 0.79, interrater-reliability r = 0.99), and the digit span forward and backward subtests, assessing short-term and working memory (each maximum score = 12, retest-reliability r = 0.83). As an index of processing speed and cognitive flexibility, we used the scores of the Trail Making Test (TMT A – max. 180 s, TMT B – max. 240 s, retest-reliability r = 0.74 and r = 0.43 for TMT A and B, respectively (Conway Greig, Nicholls, Wexler, & Bell, 2004; Reitan, 1992)). Statistical Analyses The effects of diagnosis and age were examined using multivariate analyses of variance (MANOVA) with diagnosis (patients, controls) and age group (young, middle, older) as the betweengroup factors, and the different demographical/clinical characteristics and the cognitive parameters as the dependent variables, while controlling for years of education in the latter. These analyses were followed by Bonferroni posthoc tests. An α level of 0.05 (two-tailed) was used for all statistical tests. Analyses were conducted by means of the Predictive Analysis Soft Ware (PASW/SPSS 18.0). Results Sample Characteristics Measures Symptoms were assessed using the Brief Psychiatric Rating Scale (BPRS, 18 items, maximum score = 108, interrater-reliability r = 0.8; Ligon & Thyer, 2000; Mass, Burmeister, & GeroPsych (2017), 30 (1), 35–44 In a first step, demographic and clinical characteristics of the three age groups were tested for significant group differences (Table 1). Patient and control groups showed only minor, nonsignificant differences with regard to age and sex (main effect © 2017 Hogrefe This document is copyrighted by the American Psychological Association or one of its allied publishers. This article is intended solely for the personal use of the individual user and is not to be disseminated broadly. C. J. Herold et al.: Cognitive Performance in Schizophrenia © 2017 Hogrefe 37 GeroPsych (2017), 30 (1), 35–44 This document is copyrighted by the American Psychological Association or one of its allied publishers. This article is intended solely for the personal use of the individual user and is not to be disseminated broadly. 38 C. J. Herold et al.: Cognitive Performance in Schizophrenia Figure 1. Neuropsychological profiles of patients (black lines) and healthy controls (gray lines). Raw test scores of all cognitive parameters were transformed to z-scores, based on the norm values of the specific test. “diagnosis,” p > .30), while the healthy subjects had received a significantly longer school education than the patients (mean of years of education M = 12.47 (SD = 2.78) vs. M = 13.58 (SD = 2.30), F(1, 154) = 6.755, p = .010, η2 = 0.042). Further analysis of the patient group revealed that the three age groups did not differ in dosage of antipsychotic medication (CPZ equivalents), negative and positive symptoms, with a trend-level significant effect for SAPS global score, indicating more distinctive positive symptoms in the young patient group, F(2, 91) = 2.870, p = .062. With respect to BPRS sum score a significant effect for “age,” F(2, 91) = 5.238, p = .007, shows additionally evidence for a more severe psychopathology in younger patient groups. Posthoc tests revealed significant differences between the older patients and both patient groups of middle (p = .015) and young (p = .032) age. As expected, significant differences were noticeable with regard to illness duration, F(2, 91) = 64.016, p < .001, the patient groups differed each with p < .001, and age at onset of the illness, F(2, 91) = 5.631, p = .005. Posthoc tests showed a significant difference between young and old patients (p = .004), whereas other comparisons failed to reach significance (p > .09). There was a significant age cohort effect for dwelling status, χ² = 9.542, p = .008, with middle and older patients being more GeroPsych (2017), 30 (1), 35–44 often hospitalized in comparison to young patients at the time point of study. Age Effects on Cognitive Performance In a second step it was shown that, compared with the healthy controls, patients performed lower on all tests applied (Figure 1). Test performance tended to be lower in the oldest than the young and middle-aged groups. With respect to TMT B, this effect was more pronounced in the patient groups in whom a sharper decline of performance with age became evident (Figure 2). These findings were confirmed by a MANOVA (Table 2) which yielded a significant main effect for “diagnosis,” F(7, 147) = 19.227, p < .001, η2 = 0.478. Further comparisons revealed significant differences between patients and healthy controls for all neuropsychological tests applied, thus indicating a pronounced performance deficit of the patients (0.04 > p = .000). The main effect for “age” reached significance level too, F(14, 296) = 4.280, p < .001, η2 = 0.168, with older subjects being more impaired (0.03 > p = .000), except for digit span forward (p = .145). © 2017 Hogrefe 39 This document is copyrighted by the American Psychological Association or one of its allied publishers. This article is intended solely for the personal use of the individual user and is not to be disseminated broadly. C. J. Herold et al.: Cognitive Performance in Schizophrenia Figure 2. TMT A (above) and TMT B (below) performance as a function of age for patients (black lines) and healthy subjects (gray lines). Posthoc tests revealed that MMSE performance was significantly lower for old than for young subjects (p = .007), while the difference between groups of old and middle-aged subjects failed to reach significance (p = .062). In case of logical memory I, the old subjects had significant impairments in contrast to the young subjects (p = .044); in the case of logical memory II, the old subjects showed marked deficits in comparison to both younger groups (p < .02). Working memory performance, as indicated by digit span backward, was significantly reduced in the old subject group in contrast to the young group (p = .003). © 2017 Hogrefe GeroPsych (2017), 30 (1), 35–44 40 This document is copyrighted by the American Psychological Association or one of its allied publishers. This article is intended solely for the personal use of the individual user and is not to be disseminated broadly. Information processing speed, assessed via TMT A, was also significantly impaired in the older subjects compared to both younger groups (p < .001). With respect to cognitive flexibility, as assessed using TMT B, significant differences between each age group and the other groups were evident (.05 > p = .000). The interaction “diagnosis × age” showed a significant effect for TMT B, F(2, 153) = 4.869, p = .009, with trend-level significance for TMT A, F(2, 153) = 2.716, p = .069. A trend-level significant “diagnosis × age” interaction with respect to MMSE also appeared, additionally indicating a cognitive deterioration in older patients, F(2, 153) = 2.774, p = .066. Discussion The present study revealed three major findings regarding cognitive impairment of patients with chronic schizophrenia: (1) a confirmation of broad deficits in a variety of important neuropsychological domains which (2) apply to all life periods from young adulthood to early age; and (3) evidence that cognitive flexibility is particularly affected in the older patients. The poorer test performance of patients with chronic schizophrenia in comparison to healthy subjects covers a wide range of cognitive domains. This was particularly evident with regard to verbal learning and memory, where z-scores nearly reached the mark of z = –1.5 for all age groups. Information processing speed and cognitive flexibility were impaired to a comparable extent with a considerable stronger dip in the older patients. In contrast, short-term memory remained rather spared with performance still ranging in low average levels. These results corroborate findings from previous studies on cognitive deficits in young and middle-aged patients with chronic schizophrenia (Heinrichs & Zakzanis, 1998; Irani et al., 2012) and extend them for an older group. One of the studies investigating cognition in schizophrenia over a wide age range was conducted by Fucetola et al. (2000), who examined 87 patients and 94 healthy controls assigned to three groups with an average age of M = 30.0 (SD = 3.6), M = 41.1 (SD = 4.2) and M = 58.3 (SD = 5.6) years in the patient groups and M = 28.5 (SD = 4.4), M = 41.3 (SD = 3.8) and M = 62.5 (SD = 7.2) years in the control groups, respectively. Cognitive deficits in the patient group involved verbal memory, perceptual motor skills, and abstraction, with z-scores below –1 throughout the three age groups. As in the present study, performance in memory and learning, information processing, and cognitive flexibility was well within the range of that typically obtained in older patients with a diagnosis of mild cognitive impairment (Sattler, 2012). At this point it should be emphasized that even the marked deficits typically observed in older patients with chronic schizophrenia are not directly comparable to the impairments characteristic of neurodegenerative illnesses such as Alzheimer’s GeroPsych (2017), 30 (1), 35–44 C. J. Herold et al.: Cognitive Performance in Schizophrenia disease (AD), since declarative memory remains relatively spared and does not further deteriorate with progression of the disease. As in the present study, a consistent pattern of neuropsychological deficits was already described by McBride et al. (2002) and Ting et al. (2009). The MMSE scores of our patient group were – though reduced and at trend-level deteriorating with increasing age – not comparable to that of patients with AD (Barth, Schönknecht, Pantel, & Schröder, 2005; Dos Santos et al., 2011). These findings parallel results from a review of neuropathological studies, which concluded that AD pathology does not occur more frequently among patients with schizophrenia than in the general population (Niizato, Genda, Nakamura, Iritani, & Ikeda, 2001). While a wealth of studies investigated cognitive performance in schizophrenia in general, only few authors focused on the potential interaction effects between age and illness with regard to cognitive functioning. The present study demonstrated that older patients showed a significantly poorer performance in cognitive flexibility compared to their younger counterparts. Along with this, a trend toward significant interaction of diagnosis with age was found for information processing. In contrast, none of the other cognitive domains examined showed such a differential effect of aging in the patient group compared to the healthy controls. In the study cited above, Fucetola et al. (2000) found similar age-related performance differences between patients and controls across various domains, while a significant interaction was restricted to abstract thinking as assessed on the Wisconsin Card Sorting Test. In a recent study, Irani et al. (2012) tested two groups of 624 patients with schizophrenia and healthy controls on a computerized version of the Continuous Performance Test and on a Letter-N-Back Test and came to similar conclusions. Compared with the healthy controls, the patients showed significantly lower values regardless of age in most indices of cognitive performance. However, the older group under investigation showed a reduced speed but not accuracy in the N-back task compared to the younger patients. This indicates that the executive component of working memory performance was predominantly affected. Loewenstein et al. (2012) analyzed age-associated cognitive differences in a sample of 226 patients with chronic schizophrenia and 834 healthy controls, which were compiled from different databases. All participants were older than 40 years; the clinical course of the disorder was not further specified. The study yielded greater age effects for patients than for controls on measures of information processing i.e., the TMT A, the Stroop and the Digit Symbol Test, which also assess at least to a certain extent cognitive flexibility. The results of our study indicate that patients with chronic schizophrenia show a slope of cognitive decline with advancing age similar to controls in all cognitive domains except for cognitive flexibility as a typical executive function. Although this effect was rather small, it clearly refers to progressive cerebral changes in normal aging, which particularly strike the frontal lobes (DeCarli et al., 2005; Raz et al., 1997; Salat et al., 2004). © 2017 Hogrefe This document is copyrighted by the American Psychological Association or one of its allied publishers. This article is intended solely for the personal use of the individual user and is not to be disseminated broadly. C. J. Herold et al.: Cognitive Performance in Schizophrenia Longitudinally, the extent of progressive brain tissue decrease in patients with schizophrenia is found to be twice that of healthy subjects and particularly affects frontal areas (Hulshoff Pol & Kahn, 2008; Olabi et al., 2011). Similar significant reductions in superior frontal gyrus and orbitofrontal regions were observed in a small male sample of young patients with schizophrenia and older healthy subjects in comparison to a young healthy control group (Convit et al., 2001). Moreover, gray matter decreases in frontal cortex were greater in chronic than in first-episode schizophrenia (Chan, Di, McAlonan, & Gong, 2011; Ellison-Wright, Glahn, Laird, Thelen, & Bullmore, 2008). Except for cognitive flexibility, our pattern of findings with rather stable deficits across different groups is consistent with the results of previous studies. Mockler et al. (1997) confirmed widespread cognitive deficits, but did not report any significant age effects on cognitive functioning in 62 patients with chronic schizophrenia between 18 and 69 years of age. However, the majority of patients were below 50 years, and just 6 patients formed the oldest group (60 to 69 years). Moreover, executive functions were not specifically addressed. Similarly, Hijman et al. (2003) who compared performance on four subtests of the Wechsler Adult Intelligence Test between 112 patients with chronic schizophrenia and 70 healthy controls (age range: 16 to 56 years) did not describe a significant interaction effect of age with group, while patients performed worse on all subtests. The oldest group (46 to 56 years) comprised 17 patients; the majority of patients were below 46 years of age. Performance on the subtest picture arrangement, which shares aspects of executive functioning, decreased with age, a process which appeared to be slightly more pronounced in the patient group. Bowie and colleagues (2008) also reported deficits in a number of important neuropsychological domains including psychomotor speed and cognitive flexibility. Performance levels compare to the “middle-aged” and “older” patient subgroups investigated in the present study. However, Bowie et al. (2008) recruited a group of old patients (50–85 years), but did not include younger patients with chronic schizophrenia. In light of the reduced life expectancy of patients with chronic schizophrenia (Laursen, 2011), the subgroup of old patients (70–85 years) may represent a number of survivors who either had a more favorable course of the disorder or were less vulnerable to its consequences during the aging process. The study showed evidence for age-associated cognitive decline on the more complex components of an information-processing test, which Bowie et al. (2008) alternatively referred to “the course of illness and the processing demands of the cognitive measure of interest.” However, their results mirror our findings because they did not only show a significant age-associated decline in the TMT A, but also a similar although nonsignificant trend toward for the TMT B in the patients. In the present study, executive functions were only addressed by using the TMT, while other tests such as the Wisconsin Card Sorting Test were not applied. Because of reduced © 2017 Hogrefe 41 cognitive capacity of especially the older patients, we restricted our cognitive assessment to a few tests. While groups were carefully matched for age and sex, in the patients years of education were significantly reduced, which may be expected in a group of patients with a chronic course of the disease, of whom 20–60% were hospitalized. For this reason years of education were controlled for in the MANOVA. Negative symptoms differed nonsignificantly between the patient groups, while positive symptoms (trend-level only) and BPRS total score were lower in older than younger patients. These differences correspond to the amelioration of acute schizophrenic symptoms with increasing age (Schmid et al., 2011), already described by Bleuler (1949). That the older patients are nonetheless severely affected is indicated by their dwelling status, illustrating that older patients are more often institutionalized. Given that age and duration of illness coincide because of onset of the disease in early adulthood and the exclusion of patients with late onset schizophrenia, the three age groups differed significantly with respect to illness duration. The marginal, albeit significant group difference of age at illness onset, determined on basis of the patients’ history and case notes, may well be explained by the fact that the youngest group per definitionem does not comprise patients with a later onset, which is also reflected by the respective standard deviations. Data concerning the predominant treatment of the patients in the past were unfortunately not available. At the time of assessment the majority of the patients were receiving atypical antipsychotics only or typical and atypical antipsychotic medication in combination. Potential medication effects cannot be entirely excluded as patients were examined cross-sectionally, although the three patient groups showed only marginally, nonsignificant differences with respect to CPZ equivalents. Similarly, significant medication effects were not identified in the large meta-analysis by Irani and colleagues (2011). In contrast, other studies indicate a beneficial impact of atypical (Guilera, Pino, Gómez-Benito, & Rojo, 2009; Thornton, Van Snellenberg, Sepehry, & Honer, 2006; Woodward, Purdon, Meltzer, & Zald, 2005) and typical (Davidson et al., 2009; Mishara & Goldberg, 2004; Schröder, Tittel et al., 1996) antipsychotic medication on cognition in schizophrenia. Especially the latter findings are important given that particularly the older patients of our sample might have received mainly classical antipsychotics in the past. Additional factors other than age are likely to affect cognitive flexibility: The large meta-analysis cited above (Irani et al., 2011) revealed a significant role for both demographic (age, sex, education, race) and clinical factors (living status, age of onset, duration of illness, clinical symptoms). From a clinical standpoint, co-morbid somatic conditions and other life-style factors should also be added in longitudinal studies, as physical illnesses like the metabolic syndrome, which increases in incidence with rising age and is associated with cognitive deterioration (Schröder & Pantel, 2011), are more common in patients GeroPsych (2017), 30 (1), 35–44 42 This document is copyrighted by the American Psychological Association or one of its allied publishers. This article is intended solely for the personal use of the individual user and is not to be disseminated broadly. with schizophrenia (Oud & Meyboom-de Jong, 2009; Sebastian & Beer, 2007). The results of the present cross-sectional study underline the importance of cognitive deficits in chronic schizophrenia and indicate that diminished cognitive flexibility undergoes age-associated differences, which can be assigned to frontal lobe changes. This pattern of cognitive deficits facilitates the differentiation from neurodegenerative diseases such as mild cognitive impairment and AD and underlines the need for appropriate training programs for elderly patients with chronic schizophrenia. Declaration of Conflicts of Interest The authors declare that no conflicts of interest exist. Acknowledgments The study was supported by the Dietmar Hopp Foundation, Germany. References American Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders – DSM-IV-TR. Washington, DC: American Psychiatric Association. Andreasen, N. C., & Olsen, S. (1982). Negative vs. positive schizophrenia: Definition and validation. Archives of General Psychiatry, 39, 789–794. 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Chlorpromazine equivalent doses for the newer atypical antipsychotics. Journal of Clinical Psychiatry, 64, 663–667. Woodward, N. D., Purdon, S. E., Meltzer, H. Y., & Zald, D. H. (2005). A meta-analysis of neuropsychological change to clozapine, olanzapine, quetiapine, and risperidone in schizophrenia. International Journal of Neuropsychopharmacology, 8, 457–472. doi 10.1017/S146114570500516X Manuscript received: 17.07.2015 Manuscript accepted after revision: 17.12.2015 Dipl.-Psych. Dr. Christina Herold Section of Geriatric Psychiatry University of Heidelberg Voßstr. 4 69115 Heidelberg Germany christina-j.herold@med.uni-heidelberg.de © 2017 Hogrefe Directions: In the library, using Academic Search Premiere and PsycArticles (and relevant advanced search options), find five research articles (NOT meta-analyses, literature reviews, commentaries, or book reviews) on a topic of interest to you and complete the table below. Article #1 APA Reference of Article Subjects/Participants used in study Method used Summary of main findings (2-3 sentences) Article #2 APA Reference of Article Subjects/Participants used in study Method used Summary of main findings (2-3 sentences) Article #3 APA Reference of Article Subjects/Participants used in study Method used Summary of main findings (2-3 sentences) Article #4 APA Reference of Article Subjects/Participants used in study Method used Summary of main findings (2-3 sentences) Article #5 APA Reference of Article Subjects/Participants used in study Method used Summary of main findings (2-3 sentences) Neuropsychology 2017, Vol. 31, No. 2, 209 –219 © 2016 American Psychological Association 0894-4105/17/$12.00 http://dx.doi.org/10.1037/neu0000309 The Effect of Positive Symptoms on Social Cognition in First-Episode Schizophrenia Is Modified by the Presence of Negative Symptoms Vibeke Bliksted Poul Videbech and Birgitte Fagerlund Aarhus University Hospital Risskov, Denmark, and Aarhus University Mental Health Centre Glostrup, Denmark Chris Frith This document is copyrighted by the American Psychological Association or one of its allied publishers. This article is intended solely for the personal use of the individual user and is not to be disseminated broadly. Aarhus University and University College London Objective: There is considerable evidence that patients with schizophrenia have neurocognitive and social– cognitive deficits. It is unclear how such deficits in first-episode schizophrenia relate to current clinical symptoms. Method: Fifty-nine patients with first-episode schizophrenia (FES) were tested using the Danish version of NART (premorbid IQ), subtests from WAIS-III (current IQ), and global cognition using Brief Assessment of Cognition in Schizophrena (BACS), a neurocognitive test battery. Social perception was tested using film clips of everyday interactions (TASIT). Theory of mind (ToM) was tested using silent animations (Animated Triangles Task). The FES subjects had been experiencing psychotic symptoms for several years (mean duration 9.5 years 95% confidence interval (CI [7.6;11.3]). The FES patients were divided into clinical subgroups based on their level of positive and negative symptoms (using SANS and SAPS). Healthy controls were matched to the patients. Results: High levels of negative symptoms were associated with low estimated functional IQ and poor neurocognition and social cognition. All SANS subscales, but Avolition-Apathy, had significant negative impact on social cognition. The effects of positive symptoms were complex. High levels of delusions were associated with higher premorbid IQ. In the presence of high levels of negative symptoms, high levels of positive symptoms were associated with the most comprehensive deficits in social perception, while, in the absence of negative symptoms, high levels of positive symptoms were not associated with such deficits. Conclusion: The results suggest that social– cognitive training will need to take account of the above mentioned effects of symptoms. Keywords: social cognition, neurocognition, negative symptoms, positive symptoms, theory of mind deficit in the patients’ theory of mind abilities (Frith, 1992). Frith et al. proposed four subgroups of schizophrenia with different theory of mind abilities (Corcoran, Cahill, & Frith, 1997; Frith & Corcoran, 1996; Pickup & Frith, 2001). Most severely affected were patients with behavioral signs of negative symptoms and/or incoherence. Patients with paranoid symptoms such as delusion of persecution, delusions of reference, and third-person hallucinations were thought to be only moderately affected. Patients with passivity experiences such as delusions of control, thought insertion, and thought broadcasting and finally patients in remission were thought to have normal theory of mind abilities. Sprong et al. (Sprong, Schothorst, Vos, Hox, & van Engeland, 2007) looked at subgroups according to Frith et al.’s suggestion in 29 studies of theory of mind in schizophrenia. They found deficits of theory of mind in all the subgroups, including remitted patients (patients with no behavioral signs and no positive symptoms on the day of testing), indicating that these deficits are trait related and even more comprehensive than in the model from 1992. Patients with symptoms of disorganization had more severe theory of mind deficits than the other patient subgroups. Besides Theory of Mind (ToM), the social– cognitive domains most affected in schizophrenia are social perception, social knowledge, attributional bias, and emotional processing (Green et al., 2008; Penn et al., 2008). A meta-analysis of the above-mentioned social– cognitive domains concluded that ToM and social percep- In recent years, there has been an increasing interest in the importance of social– cognitive deficits in schizophrenia and how aspects of social cognition might be able to explain the heterogeneity of symptoms in people with this disorder (Bliksted, Fagerlund, Weed, Frith, & Videbech, 2014; Fletcher & Frith, 2009; M. F. Green & Leitman, 2008; Green et al., 2008; Penn, Sanna, & Roberts, 2008). In 1992, Chris Frith proposed a model suggesting that specific psychotic symptoms in schizophrenia could be explained by a This article was published Online First November 3, 2016. Vibeke Bliksted, Psychosis Research Unit, Aarhus University Hospital Risskov, Denmark, and Interactive Minds Centre, Aarhus University; Poul Videbech, Mental Health Services, Capital Region of Denmark, Mental Health Centre Glostrup, Denmark; Birgitte Fagerlund, Mental Health Centre, Mental Health Services, Capital Region of Denmark, Glostrup, and Lundbeck Foundation Centre for Clinical Intervention and Neuropsychiatric Schizophrenia Research (CINS), Mental Health Centre Glostrup; Chris Frith, Interactive Minds Centre, Aarhus University, and Leopold Müller Functional Imaging Laboratory, Wellcome Trust Centre for Neuroimaging, University College London. Correspondence concerning this article should be addressed to Vibeke Bliksted, Psychosis Research Unit, Aarhus University Hospital Risskov, Denmark, Skovagervej 2, 8240 Risskov, Denmark. E-mail: vibeke.bliksted@ ps.rm.dk 209 BLIKSTED, VIDEBECH, FAGERLUND, AND FRITH This document is copyrighted by the American Psychological Association or one of its allied publishers. This article is intended solely for the personal use of the individual user and is not to be disseminated broadly. 210 tion were the social– cognitive domains most affected in schizophrenia (Savla, Vella, Armstrong, Penn, & Twamley, 2012). Recent studies have suggested that social– cognitive deficits in schizophrenia are trait related and independent of the phase and duration of the illness (Bliksted, Ubukata, & Koelkebeck, 2016; Green et al., 2012; Horan et al., 2012). Similar impairments of social cognition have been found in first-episode and chronic schizophrenia and their first degree relatives, and no changes in the social– cognitive deficits were seen at 12 months follow-up in first-episode schizophrenia (Bora & Pantelis, 2013; Bora, Yucel, & Pantelis, 2009; Green et al., 2012; Horan et al., 2012). This adds to the complexity of understanding the interaction between specific social– cognitive domains and the clinical symptoms of schizophrenia such as psychotic and negative symptoms. It also raises the question of social– cognitive subgroups in schizophrenia. Bell et al. found that patients with schizophrenia could be divided into three subgroups: (a) Patients with high levels of negative symptoms, (b) patients with low levels of negative symptoms but high social– cognitive scores, and (c) patients with low levels of negative symptoms and low social– cognitive scores (Bell, Corbera, Johannesen, Fiszdon, & Wexler, 2013). These subgroups were based on a principal component analysis of the subscales of negative symptoms and the social– cognitive tests that was followed by a cluster analysis that specified the above subgroups. Other researchers argue that there is no simple delineation of deficit profiles, but instead a complex matrix of correlations between clinical symptoms, neurocognitive domains, social– cognitive domains, and functional outcome (Bliksted et al., 2014; Mancuso, Horan, Kern, & Green, 2011). It has furthermore been argued that patients with schizophrenia show deficits in all aspects of neurocognitive and social– cognitive domains compared with healthy controls, but to varying degrees (Green, Horan, & Sugar, 2013). However, a recent review suggests that some reflexive aspects of social cognition, such as emotion experience, might be intact in patients with schizophrenia (Green, Horan, & Lee, 2015). In this study, we examined 59 patients with first-episode schizophrenia to account for the correlations between aspects of negative and positive symptoms as well as neurocognition and social cognition. For this purpose we divided the patients into four groups with high versus low levels of negative symptoms, and high versus low levels of positive symptoms. A healthy control group was included. It was hypothesized that patients in general would perform worse than the healthy control subjects on all neurocognitive and social– cognitive tasks. We expected the social– cognitive deficits to be most pronounced in patients with many negative symptoms (Bell et al., 2013; Frith, 1992), and in very paranoid patients (Frith, 1992). Method Subjects The patients were recruited from OPUS which is an intensive 2-year assertive community treatment program for first-episode schizophrenia (Bertelsen et al., 2008). The patients had recently been diagnosed with first-episode schizophrenia (FES) by experienced psychiatrists according to ICD-10 criteria. The patients were included during two time periods: from January 1, 2009 until February 1, 2010, and from August 1, 2011 until August 1, 2012 as consecutive parts of the same study. Some of the data from time period one have been used in statistical analyses that differ from the analyses in this article (Bliksted et al., 2014). Healthy control subjects were recruited via advertisements in four local newspapers and were tested during the same time period as their patient match. FES Subjects The first-episode schizophrenia (FES) patients were from 18 to 34 years old. Thirty-six patients were included during 2009 and 2010. None of the patients had received any antipsychotic medication for more than 3 months before inclusion. Twenty-three patients were included during 2011 and 2012. These patients were either antipsychotic-naïve or had received no more than 6 weeks’ lifetime psychopharmacological treatment at inclusion. Twenty-nine from the entire group of patients received atypical antipsychotics; 13 atypical antipsychotics and antidepressants; 4 atypical antipsychotics and other medication; 1 typical antipsychotic and other medication; 1 atypical antipsychotic, antidepressant, and benzodiazepine; 1 antidepressant; 1 patient had stopped taking his atypical antipsychotic two weeks ago; and 9 patients were antipsychotic-naïve. Other medication was for example, insulin and gastric ulcer medication. Exclusion criteria were a history of neurological disorder, severe head trauma, or drug- and alcohol dependency according to ICD10. Patients were excluded if they did not understand spoken Danish sufficiently to understand the testing procedures or if they had an estimated premorbid IQ below 70 based on their history. Healthy Control Subjects The healthy controls and patients were individually matched to the patients based on age, gender, handedness, educational level (based on the last commenced education), community of residence, and parental socioeconomic status (based on the highest parental education and expected parental income regarding wages according to Statistics Denmark). Parental educational level (rather than the patients’s educational level) was chosen as the matching variable because the onset of a mental illness interferes with education. Thus, we presumed that the parental educational level would reflect the potential level of function of the FES patients more presisely. The parental socioeconomic groups were divided into high (N ⫽ 19; 32.20%), middle (N ⫽ 30; 50.85%), and low (N ⫽ 10; 16.95%). In two cases the patients and healthy control subjects did not match perfectly one-to-one. This meant that there was one more female in the healthy subject population than in the FES patient group. The 59 healthy control subjects had no history of mental illness and neither had their first-degree relatives. They did not have a history of neurological illness, severe head injury or drug- or alcohol dependence according to ICD-10 criteria. This was controlled for by blood and urine tests. Ethics The participants received written and oral information about the project, and written informed consent was obtained before inclu- SOCIAL COGNITIVE SUBGROUPS IN SCHIZOPHRENIA sion. The study was approved by The Central Denmark Region Committees on Biomedical Research Ethics (Ref: M-2009 – 0035) and the Danish Data Protection Agency. The project complied with the Helsinki-II-declaration. This document is copyrighted by the American Psychological Association or one of its allied publishers. This article is intended solely for the personal use of the individual user and is not to be disseminated broadly. Measures Social– cognitive measures. Social perception. We used five sincere and five simple sarcastic film clips from the Danish translation of TASIT (The Awareness of Social Inference Test—Part A2 Social Inference minimal; Bliksted et al., 2014). The test is composed of small video clips with professional actors performing everyday interactions (McDonald et al., 2006; McDonald, Flanagan, Rollins, & Kinch, 2003). The clips last for 16 –53 s. After seeing each clip one has to figure out if the people were being sincere or sarcastic based on paralinguistic cues such as tone of voice, facial expressions, and verbal content. Each clip was followed by four questions concerning the communicative intentions of the persons (what they were doing, saying, thinking, and feeling; max score of each clip was 4 points). The TASIT film clips can also be analyzed as a signal detection task, that is, how good the subjects are at distinguishing sarcastic from sincere behavior. For this purpose we developed a sensitivity score. We also constructed a bias score that measured whether subjects were neutral (⫽0) or biased toward interpreting the clips sincerely (⬎0) or sarcastic (⬍0). The TASIT film clips were translated and back-translated for the purpose of this project in agreement with Pearson Assessment in London. Theory of mind. The Animated Triangles (Abell, Happé, & Frith, 2000; Castelli, Happe, Frith, & Frith, 2000) were used to measure ToM. We used four random clips where the two triangles had no intended interaction (e.g., bouncing about) and four ToM clips where the triangles interacted intentionally (e.g., the large triangle trying to persuade the small triangle to come outside). The duration of the animations is 38 – 41 s. The subjects were asked to interpret what was going on in each animation and their answers were recorded, transcribed, and scored according to the level of intentionality (degree of mental state attribution, range 0 –5 per animation, where a score of 4 or 5 meant use of words describing different degrees of mental interaction), and appropriateness (accuracy of the description, range 0 –3 per animation, where 3 meant a perfect description of the interaction intended by the animator; Castelli et al., 2000). Also target items were recorded referring to whether the right type of description was used to tell the degree of intentionality being used in the animations (e.g., score 4 or 5 in intentionality of the ToM clips and score 0 or 1 in the random clips), no matter if the subject’s answer was appropriate or not (max score of 4 per type of animation; Russell, Reynaud, Herba, Morris, & Corcoran, 2006). VB and a research student (MLT) evaluated each answer from the 59 FES patients and 59 controls separately, and their mean scores were calculated. Interrater agreement was substantial to almost perfect (Random animations: ␬ ⫽ 0.75; ToM animations: ␬ ⫽ 0.84; ToM Appropriateness: ␬ ⫽ 0.63; Random Appropriateness: ␬ ⫽ 0.72). Neuropsychological measures. Neurocognition. We used the Danish translation of the Brief Assessment of Cognition in Schizophrenia (BACS-DK), to measure verbal memory, working memory, motor speed, verbal flu- 211 ency, executive functions, attention, and speed of processing (Keefe et al., 2004, 2008; Keefe, Poe, Walker, & Harvey, 2006). Intelligence. Current functional intelligence was estimated by the four following subtests from WAIS-III (Wechsler Adult Intelligence Scale, Third version; Wechsler, 1997), chosen because of their high correlation with the total WAIS-III IQ score: Matrix Reasoning, Block Design, Vocabulary, Similarities (Wechsler, 1997). Premorbid intelligence was estimated using DART (Danish Adult Reading Test), which is the Danish version of the NART (The Nelson Adult Reading Test; Nelson & O’Connell, 1978). Psychopathology, Clinical Measures, and Drugs Screening During inclusion at the OPUS clinic, all FES patients were interviewed with the PSE-interview (Present State Examination, ICD-10) by experienced psychiatrists regarding schizophrenia and drug dependence (WHO, 1994). All healthy control subjects were interviewed by VB using the entire PSE interview. All subjects were SANS and SAPS rated by VB (Andreasen, 1984a, 1984b). SANS (Scale for the Assessment of Negative Symptoms) consists of 25 items divided into 4 subscales: Affective flattening or blunting, Alogia, Avolition-Apathy, Anhedonia-Asociality. SAPS (Scale for the Assessment of Positive Symptoms) consists of 34 items which measure 4 psychotic domains: Hallucinations, Delusions, Bizarre behavior, Positive formal thought disorder. The severity of each symptom is rated from 0 –5 and an overall global score of each subscale is found (range 0 –5). Urine samples were collected on the day of psychological testing measuring use of amphetamine, benzodiazepines, cannabis, codeine, morphine, and cocaine. The subjects tested during 2009 and 2010 were also tested for potential alcohol dependence by blood samples (P-Carbohydrat-Deficient-Transferrin). Data Analysis Statistical analyses were carried out with Stata IC 11.2 software. The data were examined for distribution and outliers. Continuous variables were examined by Wilcoxon’s rank sum test (Mann–Whitney) and effect size in terms of Harrell’s C. Harrell’s C is a rank parameter measuring the ordinal predictive power of a model. Categorical variable were examined by Fisher’s exact test and reported with the counts and proportions of the group total. Means and 95 or 99% confidential intervals plus effect sizes were calculated in accordance with the data distribution of each variable. Composite scores of the BACS-DK were calculated as the weighted mean of z-scores, separately computed for each subtest relative to the mean and standard deviation of the healthy control subjects (M ⫽ 0, SD ⫽ 1) as described by Keefe et al. (Keefe et al., 2004). The same procedure was followed regarding the calculation of the social– cognitive composite score. Correlations between social cognition, neurocognition, IQ, and symptoms in the FES patients were calculated by Spearman’s rank correlation (because not all variables were normally distributed). Social– cognitive patient subgroups were found by dividing the 59 patients into subgroups on the basis of SANS and SAPS. Data were split at the mean (SANS: ⱕ10 vs. ⬎10; SAPS: ⱕ12 vs. ⬎12) BLIKSTED, VIDEBECH, FAGERLUND, AND FRITH 212 resulting in four groups. Results were adjusted for multiple testing using Bonferroni corrections. Comparison between symptom subgroups within patients and controls was done using Kruskal-Wallis rank test. These p values were from 3 df ␹2 tests corrected. Subgroup analyses were performed by comparing patients with their matched controls on a group basis. This procedure lead us to the exclusion of two control subjects who could not be directly matched to a patient (Table 1). Correlations Between SANS/SAPS Subscales and Neurocognition, Social Cognition, and IQ Results Demographics, Psychopathology, and IQ This document is copyrighted by the American Psychological Association or one of its allied publishers. This article is intended solely for the personal use of the individual user and is not to be disseminated broadly. no correlation between positive symptoms (SAPS total score) and the social– cognitive composite score (␳ ⫽ 0.14, p ⫽ .29). The application of TASIT as a detection task showed that the patients were poor at making the distinction between sincerity and sarcasm (TASIT sensitivity), t(96.37) ⫽ 4.33, p ⬍ .0001; d ⫽ 0.80 95% CI (0.42;1.17), but also had a bias toward treating the sarcastic behavior as sincere (TASIT bias), t(116) ⫽ ⫺2.77, p ⫽ .0066; d ⫽ ⫺0.51 95% CI (⫺0.87; ⫺0.14; Figure 2). Demographics and psychopathology are summarized in Table 2. Patients and controls did not differ in age and sex. The age range in the FES subjects was 18 –34 years with a mean age of 22.9 years. Twenty-three of the patients were women (39%). As expected, the educational level of the patients was lower, probably because the illness had interfered with their educational plans. The patients reported having had psychotic symptoms on average 9.5 years before inclusion. As expected, the FES patients had lower premorbid IQ and lower estimated current functional IQ than the controls. Neurocognition The FES patients performed significantly worse in all 6 BACS subtests compared with the healthy controls (p ⬍ .0003). The BACS composite score was 1.80 SDs below the healthy controls (p ⫽ 1.6e-9; Harrell’s C (0.83) 99% CI (0.73;0.92)). There was a significant negative correlation between negative symptoms (SANS total score) and neurocognition (␳ ⫽ ⫺0.36, p ⫽ .005), but no correlation between positive symptoms (SAPS total score) and neurocognition (␳ ⫽ 0.16, p ⫽ .22; Figure 1). Social Cognition A social– cognitive composite score was derived based on the statistically significant subscores of the social– cognitive tests. This composite score was 1.91 SDs below the mean of the healthy controls (p ⫽ 2.2e-11; Harrell’s C 0.86 99% CI (0.77;0.95), which is remarkably similar to the BACS composite score. There was a significant negative correlation between negative symptoms (SANS total score) and the social– cognitive composite score (␳ ⫽ ⫺0.39; p ⫽ .002), but Table 1 FES Subgroups Based on SANS and SAPS Symptom Scores Measure SANS Measure Low High Total SAPS Low High Total 17 13 30 12 17 29 29 30 59 Note. FES ⫽ first-episode schizophrenia; SANS ⫽ Scale for Assessment of Negative Symptoms; SAPS ⫽ Scale for Assessment of Positive Symptoms. We started our subgroup analyses by looking at correlations (using Spearmann’s Rank Correlations) between the subscales of SAPS and SANS and neurocognition, social cognition, and IQ (see Table 3). In the SAPS subscales, the only significant correlation was a positive correlation between the global score of delusion and premorbid IQ (DART) (␳ ⫽ 0.32, p ⫽ .01), with the presence of delusions being associated with higher IQ. The Four SANS Subscores All Showed Numerous Significant Correlations Global rating of Affective flattening (e.g., unchanging facial expression, poor eye contact, and lack of vocal inflections) correlated negatively with the Animated Triangles total Appropriateness scores (␳ ⫽ ⫺0.30, p ⫽ .02) and the Appropriateness score of the random animations (␳ ⫽ ⫺0.33, p ⫽ .01), the Social– cognitive composite score (␳ ⫽ ⫺0.29, p ⫽ .03), and estimated functional IQ (WAIS-III; ␳ ⫽ ⫺0.33, p ⫽ .01). However, no correlations were found between Affective flattening and social perception (TASIT: Sincere ␳ ⫽ ⫺0.03, p ⫽ .83; Simple sarcasm ␳ ⫽ ⫺0.16, p ⫽ .22). Global rating of Alogia (e.g., poverty of content of speech, blocking, and increased latency of response) correlated negatively with several aspects of social perception (TASIT: Sincere ␳ ⫽ ⫺0.27, p ⫽ .04; Simple sarcasm ␳ ⫽ ⫺0.29, p ⫽ .03; Sensitivity ␳ ⫽ ⫺0.32, p ⫽ .01) and the Animated Triangles total Appropriateness score (␳ ⫽ ⫺0.32, p ⫽ .01) and the overall level of social cognition (Social– cognitive composite score ␳ ⫽ ⫺0.28, p ⫽ .03) and estimated functional IQ (WAIS-III; ␳ ⫽ ⫺0.44, p ⬍ .001). Global rating of Avolition-Apathy (e.g., impersistence at work or school, poor personal hygiene, and physical anergia) correlated negatively with the neurocognitive BACS composite score (␳ ⫽ ⫺0.30, p ⫽ .02). Finally, the global rating of Anhedonia-Asociality (e.g., problems regarding ability to feel intimacy and closeness and have relationships with friends and peers) correlated negatively with social perception (TASIT: Simple sarcasm ␳ ⫽ ⫺0.32, p ⫽ .01; Sensitivity ␳ ⫽ ⫺0.31, p ⫽ .02). There was also a negative correlation with neurocognition (BACS composite score ␳ ⫽ ⫺0.38, p ⫽ ⬍0.01), estimated functional IQ (WAIS-III; ␳ ⫽ ⫺0.36, p ⬍ .01) and the Social– cognitive composite score (␳ ⫽ ⫺0.39, p ⬍ .01). We adjusted the data for multiple comparisons (nine tests) using the Bonferroni methods after which only four correlations remained significant: Alogia and estimated functional IQ; Anhedonia-Asociality (AA) and estimated functional IQ; AA and BACS composite score and AA and the social– cognitive composite score. SOCIAL COGNITIVE SUBGROUPS IN SCHIZOPHRENIA 213 Table 2 Comparison of Patients With First-Episode Schizophrenia (FES) and Controls on demographics, Psychopathology, and IQ Age Females Years of education Current occupation Unemployed Work Student Sick leave Pension Vocational training Days of FES-diagnosis Years of untreated illness SANS SAPS DART (estimated premorbid IQ) WAIS-III (estimated functional IQ) First-episode schizophrenia (N ⫽ 59) Healthy controls (N ⫽ 59) 22.9 [22.0;23.8] 23 (39.0%) 12.1 [11.4;12.7] 23.1 [22.2;23.9] 24 (40.7%) 14.1 [13.4;14.7] 31 (52.5%) 1 (1.7%) 12 (20.3%) 5 (8.5%) 1 (1.7%) 9 (15.3%) 129.1 [98.3; 159.9] 9.5 [7.6; 11.3]c 10.1 [8.8;11.3] 12.1 [10.9; 13.3] 29.2 [27.3; 31.2]d 87.7 [82.7; 92.7] 4 (6.8%) 22 (37.3%) 33 (55.9%) 0 0 0 0 0 0 0 32.9 [31.5; 34.3] 103.0 [99.3; 106.7] Harrell’s C p value .51 (.41–.62) .81a 1.00b 2.1e-5a 1.7e-15b .73 (.63–.82) .66 (.56–.76) .74 (.65–.83) 2.4e-3a 8.9e-6a Note. Continuous variables were examined by Wilcoxon Rank-Sum Test (Mann-Whitney) and reported with mean (95% CI, confidence interval) and effect size by terms of Harrell’s C (95% CI). Categorical variables were examined by Fisher’s Exact Test and reported with the counts and proportions of group total, N (Percentage). FES ⫽ first-episode schizophrenia; SANS ⫽ Scale for Assessment of Negative Symptoms; SAPS ⫽ Scale for Assessment of Positive Symptoms; DART ⫽ Danish Adult Reading Test; WAIS-III ⫽ Wechsler Adult Intelligence Scale-III (Matrix Reasoning, Block Design, Vocabulary, and Similarities). a Mann-Whitney test. b Fisher’s exact test. c N ⫽ 58. d N ⫽ 57. Based on the above findings, we concluded that various aspects of social cognition, neurocognition, and functional IQ had significant associations with different aspects of negative symptoms in our FES sample. FES Subgroups We compared the patients from the four symptom subgroups with their matched controls on a subgroup basis. Two patients were not matched one to one to a control subject which made us leave out two nonmatched controls from the analysis (see Table 4). Patients with a combination of high levels of positive symptoms and high levels of negative symptoms had the most severe deficits in -4 -2 0 2 As mentioned in the data analysis section, the FES patients were divided into four subgroups of high and low negative and positive SANS and SAPS scores. Combined High Levels of Negative and Positive Symptoms -6 This document is copyrighted by the American Psychological Association or one of its allied publishers. This article is intended solely for the personal use of the individual user and is not to be disseminated broadly. Measure Z_VeMeTo Z_Token Z_SymCod Z_comp Z_Digit Z_VFIuTo Z_ToLTot Figure 1. Brief Assessment of Cognition in Schizophrenia (BACS) box and whiskers plot. Performance of first episode schizophrenia patients on the Danish BACS subtests and composite score standardized to healthy controls. All differences between patients and controls were statistically significant (p ⬍ 0.0003). See the online article for the color version of this figure. BLIKSTED, VIDEBECH, FAGERLUND, AND FRITH -10 This document is copyrighted by the American Psychological Association or one of its allied publishers. This article is intended solely for the personal use of the individual user and is not to be disseminated broadly. -5 0 5 214 Z_TASSin Z_InteToM Z_NoejTot Z_TarRan Z_TASSim Z_invInteRan Z_TarToM Z_socomp Figure 2. Social cognitive composite score. Performance of first episode schizophrenia patients on the social cognitive subtests and composite score standardized to healthy controls. All differences between patients and controls were statistically significant (p ⬍ 0.01). The Awareness of Social Inference Test (TASIT) Bias scores were inverted so that higher scores indicated better performances as for all other tests. See the online article for the color version of this figure. social perception and ToM, while those with high levels of positive symptoms and low levels of negative symptoms had the least severe deficits, and in fact did not differ from their matched controls. In general, patients with many negative symptoms also had more severe social– cognitive and neurocognitive deficits. Patients with low levels of positive and negative symptoms (resembling remission) had more severe deficits in composite scores of neurocognition and social cognition compared to their matched controls. A majority of results remained significant when data were adjusted for multiple comparisons via the Bonferroni methods (see Table 4). Comparison of Clinical Subgroups We compared the four clinical subgroups by Wilcoxon’s rank sum test (see Table 5). Patients dominated by many negative symptoms had more severe social– cognitive and neurocognitive deficits than the other subgroups. It did not make a difference whether the high level of negative symptoms were accompanied by high levels of positive symptoms or not. On the contrary, patients dominated by many positive symptoms and few negative symptoms had better social– cognitive and neuro- Table 3 Spearman’s Rank Correlations Between Clinical Symptoms, IQ, Social Cognition, and Composite Scores in First-Episode Schizophrenia Patients Measure Intelligence DART (estimated premorbid IQ) WAIS-III (estimated functional IQ) Animated triangles Appropriateness, total score Appropriateness, random TASIT Sincere Simple sarcasm Sensitivity Composite scores BACS composite score Social cognitive composite score Delusion (SAPS) Affective flattening (SANS) Alogia (SANS) Avolition-Apathy (SANS) Anhedonia-Asociality (SANS) ⫺.20 ⫺.33ⴱⴱ ⫺.14 ⫺.44ⴱⴱ† .16 ⫺.20 .04 ⫺.36ⴱⴱ† ⫺.19 ⫺.22 ⫺.30ⴱ ⫺.33ⴱⴱ ⫺.32ⴱⴱ ⫺.25 ⫺.07 ⫺.07 ⫺.24 ⫺.23 ⫺.04 ⫺.09 ⫺.08 ⫺.03 ⫺.16 ⫺.09 ⫺.27ⴱ ⫺.29ⴱ ⫺.32ⴱⴱ .02 ⫺.12 ⫺.04 ⫺.19 ⫺.32ⴱⴱ ⫺.31ⴱ ⫺.25 ⫺.29ⴱ ⫺.21 ⫺.28ⴱ ⫺.30ⴱ ⫺.26 ⫺.38ⴱ† ⫺.39ⴱⴱ† .32ⴱ .11 .09 .06 Note. N ⫽ 59. TASIT ⫽ The Awareness of Social Inference Test; SAPS ⫽ Scale for Assessment of Positive Symptoms; SANS ⫽ Scale for Assessment of Negative Symptoms; DART ⫽ Danish Adult Reading Test; WAIS-III ⫽ Wechsler Adult Intelligence Scale-III (Matrix Reasoning, Block Design, Vocabulary, and Similarities); BACS ⫽ Brief Assessment of Cognition in Schizophrenia. † Bonferroni corrected p-values (p ⬍ .0056) adjusted for nine tests. ⴱ p ⱕ .05. ⴱⴱ p ⱕ .01. 11.5 [10.7; 12.3] 11.4 [10.6; 12.2] .46 [.16; .75] 18.2 [16.7; 19.6] 18.0 [16.5; 19.5] .46 [.12; .81] 15.8 [14.0; 17.7] 15.7 [13.5; 17.8] .47 [.13; .81] ⫺.8 [⫺1.8; .1]ⴱ ⫺.1 [⫺.9; .8] .69 [.38; 1.0] ⫺.6 [⫺1.5; .4]ⴱ .2 [⫺.6; 1.0] .71 [.40; 1.0] 15.7 [13.4; 18.0]ⴱ 18.1 [17.0; 19.2] .71 [.45; .96] 11.1 [7.7; 14.4]ⴱ 14.9 [11.9; 18.0] .75 [.51; 1.0] ⫺1.7 [⫺2.7; ⫺.7]ⴱⴱⴱ .1 [⫺.6; .9] .86 [.69; 1.0] ⫺1.7 [⫺2.9; ⫺.5]ⴱⴱⴱ .5 [⫺.3; 1.3] .85 [.67; 1.0] 98.1 [86.9; 109.2] 104.4 [94.8; 114.1] .67 [.35; .99] (NFES 10.9 [9.8; 12.0] 11.6 [11.0; 12.3] .65 [.42; .88] 89.8 [75.3; 104.4]ⴱ 104.1 [94.1; 114.0] .71 [.46; .97] (NFES Low SANS High SAPS ⫽ 13; NCON ⫽ 12) ⫺2.4 [⫺4.0; ⫺.9]ⴱⴱ .2 [⫺1.0; 1.3] .88 [.67; 1.0] ⫺2.4 [⫺3.9; ⫺.9]ⴱⴱ ⫺.3 [⫺1.5; 1.0] .83 [.58; 1.0] 12.2 [7.8; 16.6] 14.7 [11.8; 17.6] .66 [.32; 1.0] 15.8 [13.0; 18.7]ⴱⴱ 18.9 [17.3; 20.5] .83 [.57; 1.0] 10.4 [8.4; 12.4] 11.3 [10.1; 12.4] .61 [.30; .91] 80.1 [62.1; 98.1] 92.7 [81.1; 104.2] .69 [.35; 1.0] (NFES High SANS Low SAPS ⫽ 12; NCON ⫽ 12) ⫺2.6 [⫺4.1; ⫺1.1]ⴱⴱⴱ .4 [⫺.1; 1.0] .97 [.90; 1.0] ⫺2.2 [⫺3.5; ⫺1.0]ⴱⴱⴱ .1 [⫺.5; .6] .91 [.78; 1.0] 9.4 [4.4; 14.5]ⴱⴱ 16.8 [14.4; 19.1] .82 [.62; 1.0] 13.2 [9.2; 17.1]ⴱⴱⴱ 18.7 [17.3; 20.1] .85 [.67;1.0] 10.1 [9.5; 10.8]ⴱ 11.7 [11.3; 12.1] .71 [.48; .95] 83.1 [70.1; 96.1]ⴱⴱⴱ 108.2 [97.1; 119.2] .87 [.70; 1.0] (NFES High SANS High SAPS ⫽ 17; NCON ⫽ 16) .03 (.15) .72 (1.0) .041 (.21) .57 (1.0) .012 (.062) .29 (1.0) .024 (.12) .20 (1.0) .31 (1.0) .69 (1.0) .058 (.35) .043 (.26) Kruskal-Wallis p value (adj. p) Note. Comparison within SANS/SAPS subgroups was done by Wilcoxon Rank-Sum Test and the effect size is given in terms of Harrell’s C (HC). To account for multiple testing we adjusted p values for five tests with the Bonferroni Method and correspondingly 99% confidence intervals (CIs) are used. The two composite scores are highly correlated and adjusting for six tests would be too conservative. comparison by Kruskal-Wallis Rank Test between subgroups within patients and controls, respectively. These p values are from 3 df ␹2 tests corrected for ties. SANS ⫽ Scale for Assessment of Negative Symptoms; SAPS ⫽ Scale for Assessment of Positive Symptoms. Wechsler Adult Intelligence Scale-III (Matrix Reasoning; Block Design, Vocabulary, and Similarities). TASIT ⫽ The Awareness of Social Inference Test; BACS ⫽ Brief Assessment of Cognition in Schizophrenia. Wilcoxon rank-sum test: ⴱ p ⬍ .05. ⴱⴱ p ⬍ .01. ⴱⴱⴱ p ⬍ .001; Bonferroni corrected p-values adjusted for five tests p ⬍ .01. Animated triangles Appropriateness, random FES CON HC TASIT Simple sarcasm FES CON HC Sensitivity FES CON HC Composite scores BACS composite score FES CON HC Social cognitive composite score FES CON HC Intelligence WAIS-III (estimated functional IQ) FES CON HC Mean (99% CI) Low SANS Low SAPS ⫽ 17; NCON ⫽ 17) Sysptom subgroups versus CON Table 4 Clinical First-Episode Schizophrenia (FES) SANS/SAPS Subgroups Compared With Healthy Controls (CON) This document is copyrighted by the American Psychological Association or one of its allied publishers. This article is intended solely for the personal use of the individual user and is not to be disseminated broadly. SOCIAL COGNITIVE SUBGROUPS IN SCHIZOPHRENIA 215 .21 1.00 .36 [.05; .67] .67 1.00 .46 [.15; .76] .79 1.00 .53 [.21; .84] .58 1.00 .56 [.24; .88] .23 1.00 .37 [.06; .68] .22 1.00 .36 [.06; .66] .19 .97 .64 [.34; .94] .37 1.00 .59 [.32; .85] .042 .21 .72 [.45; .98] .0025 .013 .82 [.59; 1.00] .075 .38 .69 [.42; .97] .057 .28 .71 [.43; .98] Subgroups LNLP vs HNLP .46 1.00 .43 [.14; .71] .40 1.00 .42 [.13; .70] .52 1.00 .44 [.15; .72] .23 1.00 .38 [.11; .65] .30 1.00 .40 [.14; .66] .22 1.00 .38 [.10; .65] .0077 .038 .19 [.00; .45] .011 .053 .20 [.00; .46] .029 .14 .24 [.00; .56] .038 .19 .26 [.00; .56] .21 1.00 .37 [.07; .66] .022 .11 .23 [.00; .52] Subgroups LNHP vs HNLP Comparison of symptoms subgroups Subgroups LNLP vs HNHP .018 .090 .24 [.00; .50] .025 .13 .26 [.00; .51] .0098 .049 .22 [.00; .48] .0049 .025 .20 [.00; .43] .062 .31 .31 [.07; .56] .024 .12 .26 [.00; .53] Subgroups LNHP vs HNHP .89 1.00 .51 [.18; .85] .69 1.00 .54 [.22; .87] .30 1.00 .38 [.08; .68] .27 1.00 .38 [.08; .68] .71 1.00 .46 [.23;.69] .64 1.00 .55 [.21; .89] Subgroups HNLP vs HNHP Note. Comparison within SANS/SAPS subgroups was done by Wilcoxon Rank-Sum Test and the effect size is given in terms of Harrell’s C (HC). To account for multiple testing we adjusted p values for five tests with the Bonferroni method and correspondingly 99% confidence intervals (CIs) are used. The two composite scores are highly correlated and adjusting for six tests would be too conservative. Clinical subgroups: LNLP ⫽ Low SANSa ⫹ Low SAPSb (N ⫽ 17); LNHP ⫽ Low SANS ⫹ High SAPS (N ⫽ 13); HNLP ⫽ High SANS ⫹ Low SAPS (N ⫽ 12); HNHP ⫽ High SANS ⫹ High SAPS (N ⫽ 17). SANS ⫽ Scale for Assessment of Negative Symptoms; SAPS ⫽ Scale for Assessment of Positive Symptoms; WAIS-III ⫽ Wechsler Adult Intelligence Scale-III (Matrix Reasoning; Block Design, Vocabulary, and Similarities); BACS ⫽ Brief Assessment of Cognition in Schizophrenia; TASIT ⫽ The Awareness of Social Inference Test. Intelligence WAIS-III (estimated functional IQ) p Adj. p HC Animated triangles Appropriateness, random p Adj. p HC TASIT Simple sarcasm p Adj. p HC Sensitivity p Adj. p HC Composite scores BACS composite score p Adj. p HC Social cognitive composite score p Adj. p HC Mean (99% CI) Subgroups LNLP vs LNHP Table 5 Comparison of the Clinical First-Episode Schizophrenia (FES) SANS/SAPS Subgroups This document is copyrighted by the American Psychological Association or one of its allied publishers. This article is intended solely for the personal use of the individual user and is not to be disseminated broadly. 216 BLIKSTED, VIDEBECH, FAGERLUND, AND FRITH SOCIAL COGNITIVE SUBGROUPS IN SCHIZOPHRENIA cognitive functioning even than the subgroup with few positive and negative symptoms. This document is copyrighted by the American Psychological Association or one of its allied publishers. This article is intended solely for the personal use of the individual user and is not to be disseminated broadly. Discussion In this study, we found significant differences in social cognition and neurocognition between clinical subgroups of patients with FES based on the level of their negative and positive symptoms. The results showed that patients with high levels of negative symptoms had significant cognitive and social– cognitive deficits irrespective of their level of positive symptoms compared to the other subgroups of FES patients. FES patients with high levels of negative symptoms combined with high levels of positive symptoms had the most pronounced difficulties perceiving sarcasm and discriminating between sincerity and sarcasm. In the presence of low levels of negative symptoms, high levels of positive symptoms were associated with the least impairment of all the subgroups. In fact, the patients dominated by high levels of positive symptoms and low levels of negative symptoms did not differ from their matched healthy controls. These results could imply that premorbid social– cognitive and neurocognitive deficits could be a predictor of future development of schizophrenia dominated by negative symptoms but not necessarily accompanied by high levels of positive symptoms. Patients with high levels of alogia (e.g., poverty of content of speech, blocking, and increased latency of response) and anhedonia-asociality (e.g., problems regarding ability to feel intimacy and closeness and have relationships with friends and peers) had greater deficits in social perception. Alogia and affective flattening (e.g., unchanging facial expression, poor eye contact, affective nonresponsivity, inappropriate affect, and lack of vocal inflections) were associated with the most inaccurate descriptions of the Animated triangles film clips. This could imply that expressive linguistic difficulties impair the ability to analyze input from the surroundings correctly. However, we did not find any correlation between affective flattening and social perception which is surprising as it is reasonable to presume that the items measured in the affective flattening subscale are involved in expressing aspects of social perception, for example, sarcasm. Our results are in accordance with the findings of Bell et al. (Bell et al., 2013) who made a principal component analysis based on subscales of negative symptoms and five social– cognitive tests. They found that patients could be divided into three subgroups: One group dominated by high levels of overall negative symptoms and two groups with low levels of negative symptoms combined with high versus low social– cognitive functioning. Bell et al. suggested that patients with high social– cognitive functioning combined with few negative symptoms had the best community functioning compared to the other subgroups. The findings in our study are also consistent with Friths ToM subgroups (Frith, 1992) where the most affected subgroup of patients with schizophrenia was thought to be patients dominated by negative symptoms. However, our results could not confirm the hierarchical structure of the Frith model since the most remitted patients (low SANS and low SAPS scores) in fact had more social– cognitive deficits than the patients dominated by positive symptoms (high SAPS and low SANS scores). Our findings regarding the relationship between high levels of negative symptoms and severe deficits in IQ imply that these 217 patients could be comparable with deficit schizophrenia, which is a subgroup of patients with poor prognosis (Carpenter, Heinrichs, & Wagman, 1988; Galderisi, Bucci, et al., 2013). Aspects of negative symptoms such as affective flattening, alogia, and anhedonia might be connected to deficits in ToM and social perception or perhaps even be a result of such social– cognitive deficits. In line with this assumption a recent multicenter study found that blunted affect was the most persistent negative symptom in firstepisode schizophrenia at 12 month follow-up (Galderisi, Mucci, et al., 2013). Lin et al. (Lin et al., 2013) suggest that negative symptoms mediate the influence of neurocognition and social cognition on functional outcome. Moreover, they suggest that negative symptoms impair neuro- and social cognition by lowering the motivation to attend to psychological tasks. They also hypothesize that negative symptoms decrease the motivation to participate in social activities and thereby influence functional outcome. A similar hypothesis regarding a mediating effect of negative symptoms with respect to the correlation between second-order ToM and social functioning was suggested by Mehta et al. (Mehta, Thirthalli, Kumar, Kumar, & Gangadhar, 2014). Because we did not measure social functioning in our study, we were not able to test if the same mediating effect was found in our sample. However, research has shown that ultra-high risk (UHR) subjects who later develop psychosis have more pronounced social– cognitive deficits compared with the other UHR subjects (Cornblatt et al., 2012; Kim et al., 2011). These results are in accordance with our findings that FES subjects with the most pronounced social– cognitive and neurocognitive had the most severe levels of negative and positive symptoms. Similar results were found in a recent study by Ventura et al. (Ventura, Wood, & Hellemann, 2013). These results could imply that prodromal social– cognitive and neurocognitive deficits enhances the risk of later development of psychosis and/or schizophrenia. It is of note that Galderisi et al.(Galderisi, Mucci, et al., 2013) did not find any difference in neurocognition between FES subgroups dominated by persistent negative symptoms (deficit schizophrenia) and remitted negative symptoms. The effects of positive symptoms depended upon the context in which they occurred. Regarding detection of sarcasm in TASIT (sensitivity), the FES patients with high levels of positive symptoms had the best social perception skills (regarding perception of sarcasm and discriminating sarcasm from sincerity) in the presence of low levels of negative symptoms, but the worst social perception in the presence of high negative symptoms. In other words, patients with many negative symptoms had poor social perception, but the presence of positive symptoms made their performance even worse. These results suggest that the understanding of social– cognitive deficits in schizophrenia is closely linked to a detailed account of symptomatology. A significant positive correlation was found between the global SAPS Delusion subscale score and functional IQ. Our results contradict the notion that patients become increasingly paranoid because of deficits in ToM and social perception. Recent studies have suggested that instead of ToM deficits (hypomentalizing) paranoid patients may in fact be hypermentalizing attributing too much idiosyncratic meaning to social interactions (Abu-Akel & Bailey, 2000; Ciaramidaro et al., 2015; Crespi & Badcock, 2008; Fretland et al., 2015; Frith, 2004; Montag et al., 2011). Patients dominated by negative symptoms have been hypothesized to have ToM deficits (hypomentalizing) resem- BLIKSTED, VIDEBECH, FAGERLUND, AND FRITH This document is copyrighted by the American Psychological Association or one of its allied publishers. This article is intended solely for the personal use of the individual user and is not to be disseminated broadly. 218 bling patients with autism spectrum disorder (Abu-Akel & Bailey, 2000; Bliksted et al., 2016; Crespi & Badcock, 2008; Frith, 2004; Kästner et al., 2015). The results of the present study imply that patients with FES is not a clinically homogeneous group in terms of neurocognitive and social– cognitive deficits, and that subtypes are differentially related to clinical symptoms. If the present results are replicated in a larger sample of FES subjects (with more statistical power), this would imply that there is no such thing as an average FES patient with regard to social– cognitive and neurocognitive deficits. The results of the present study indicate that a careful evaluation of social– cognitive and neurocognitive skills is needed in subjects with UHR and first-episode psychosis because such deficits tend to make the subject more vulnerable to a future development of psychotic and negative symptoms. Strengths and Limitations All patients were tested by the same psychologist and patients were recruited from the same mental health clinic on both occasions. The two patient populations did not differ regarding age (t(57) ⫽ ⫺0.73), gender (␹2(1) ⫽ 2.64, p ⫽ .10) or years of education, t(57) ⫽ 0.06, p ⫽ .95. The patients from time period two had only received medication for a few weeks or were antipsychotic-naïve. The patients from the first time period had been medicated for a longer period of time. However, given the limited effects of antipsychotics on neurocognition, and the relative stability of social– cognitive deficits across illness phases in schizophrenia (Green et al., 2012; Horan et al., 2012), we do not expect this difference between previous antipsychotic medication to have affected our results. The fact that sample one had received antipsychotic medication for a longer period of time than sample two probably explains why sample one had significantly fewer positive symptoms, t(57) ⫽ 0.03, p ⫽ .0009 than study two. No significant difference in negative symptoms, t(57) ⫽ 0.03, p ⫽ .98 was found between the two samples. Clinical Implications of the Results In this study, we found that FES patients by no means are alike regarding cognitive and social– cognitive deficits. Our results imply that cognitive and social– cognitive training must be tailored to different subgroups of patients with a particular focus on FES patients with high levels of negative symptoms while also taking into account the presence of positive symptoms. References Abell, F., Happé, F., & Frith, U. (2000). Do triangles play tricks? Attribution of mental states to animated shapes in normal and abnormal development. Cognitive Development, 15, 1–16. http://dx.doi.org/10 .1016/S0885-2014(00)00014-9 Abu-Akel, A., & Bailey, A. L. (2000). The possibility of different forms of theory of mind impairment in psychiatric and developmental disorders. Psychological Medicine, 30, 735–738. http://dx.doi.org/10.1017/ S0033291799002123 Andreasen, N. C. (1984a). Scale for the assessment of negative symptoms. Iowa City, IA: University of Iowa. Andreasen, N. C. (1984b). Scale for the assessment of positive symptoms. Iowa City, IA: University of Iowa. Bell, M. D., Corbera, S., Johannesen, J. K., Fiszdon, J. M., & Wexler, B. E. (2013). Social cognitive impairments and negative symptoms in schizophrenia: Are there subtypes with distinct functional correlates? Schizophrenia Bulletin, 39, 186 –196. http://dx.doi.org/10.1093/schbul/sbr125 Bertelsen, M., Jeppesen, P., Petersen, L., Thorup, A., Øhlenschlaeger, J., leq Uach, P., . . . Nordentoft, M. (2008). Five-year follow-up of a randomized multicenter trial of intensive early intervention vs standard treatment for patients with a first episode of psychotic illness: The OPUS trial. Archives of General Psychiatry, 65, 762–771. http://dx.doi.org/10 .1001/archpsyc.65.7.762 Bliksted, V., Fagerlund, B., Weed, E., Frith, C., & Videbech, P. (2014). Social cognition and neurocognitive deficits in first-episode schizophrenia. Schizophrenia Research, 153, 9 –17. http://dx.doi.org/10.1016/j .schres.2014.01.010 Bliksted, V., Ubukata, S., & Koelkebeck, K. (2016). Discriminating autism spectrum disorders from schizophrenia by investigation of mental state attribution on an on-line mentalizing task: A review and meta-analysis. Schizophrenia Research, 171, 16 –26. http://dx.doi.org/10.1016/j.schres .2016.01.037 Bora, E., & Pantelis, C. (2013). Theory of mind impairments in firstepisode psychosis, individuals at ultra-high risk for psychosis and in first-degree relatives of schizophrenia: Systematic review and metaanalysis. Schizophrenia Research, 144, 31–36. http://dx.doi.org/10 .1016/j.schres.2012.12.013 Bora, E., Yucel, M., & Pantelis, C. (2009). Theory of mind impairment in schizophrenia: Meta-analysis. Schizophrenia Research, 109, 1–9. http:// dx.doi.org/10.1016/j.schres.2008.12.020 Carpenter, W. T., Jr., Heinrichs, D. W., & Wagman, A. M. (1988). Deficit and nondeficit forms of schizophrenia: The concept. The American Journal of Psychiatry, 145, 578 –583. http://dx.doi.org/10.1176/ajp.145 .5.578 Castelli, F., Happé, F., Frith, U., & Frith, C. (2000). Movement and mind: A functional imaging study of perception and interpretation of complex intentional movement patterns. NeuroImage, 12, 314 –325. http://dx.doi .org/10.1006/nimg.2000.0612 Ciaramidaro, A., Bölte, S., Schlitt, S., Hainz, D., Poustka, F., Weber, B., . . . Walter, H. (2015). Schizophrenia and autism as contrasting minds: Neural evidence for the hypo-hyper-intentionality hypothesis. Schizophrenia Bulletin, 41, 171–179. Corcoran, R., Cahill, C., & Frith, C. D. (1997). The appreciation of visual jokes in people with schizophrenia: A study of ‘mentalizing’ ability. Schizophrenia Research, 24, 319 –327. Retrieved from. http://www.ncbi. nlm.nih.gov/pubmed/9134592 Cornblatt, B. A., Carrión, R. E., Addington, J., Seidman, L., Walker, E. F., Cannon, T. D., . . . Tsuang, M. T. (2012). Risk factors for psychosis: Impaired social and role functioning. Schizophrenia Bulletin, 38, 1247–1257. Crespi, B., & Badcock, C. (2008). Psychosis and autism as diametrical disorders of the social brain. Behavioral and Brain Sciences, 31, 241– 261. http://dx.doi.org/10.1017/S0140525X08004214 Fletcher, P. C., & Frith, C. D. (2009). Perceiving is believing: A Bayesian approach to explaining the positive symptoms of schizophrenia. Nature Reviews Neuroscience, 10, 48 –58. http://dx.doi.org/10.1038/nrn2536 Fretland, R. A., Andersson, S., Sundet, K., Andreassen, O. A., Melle, I., & Vaskinn, A. (2015). Theory of mind in schizophrenia: Error types and associations with symptoms. Schizophrenia Research, 162, 42– 46. http://dx.doi.org/10.1016/j.schres.2015.01.024 Frith, C. D. (1992). The cognitive neuropsychology of schizophrenia. New York, NY: Routledge Taylor & Francis Group. Frith, C. D. (2004). Schizophrenia and theory of mind. Psychological Medicine, 34, 385–389. http://dx.doi.org/10.1017/S0033291703001326 Frith, C. D., & Corcoran, R. (1996). Exploring ‘theory of mind’ in people with schizophrenia. Psychological Medicine, 26, 521–530. http://dx.doi .org/10.1017/S0033291700035601 This document is copyrighted by the American Psychological Association or one of its allied publishers. This article is intended solely for the personal use of the individual user and is not to be disseminated broadly. SOCIAL COGNITIVE SUBGROUPS IN SCHIZOPHRENIA Galderisi, S., Bucci, P., Mucci, A., Kirkpatrick, B., P...
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Running Head: SCHIZOPHRENIA STUDIES

Schizophrenia Studies

Name
Institution:
Date:

1

SCHIZOPHRENIA STUDIES

2

Directions:
In the library, using Academic Search Premiere and PsycArticles (and relevant advanced search
options), find five research articles (NOT meta-analyses, literature reviews, commentaries, or
book reviews) on a topic of interest to you and complete the table below.
Article #1
APA Reference of

Christina, J. H., Lena, A. S., Marc, M. L., Ulrich S., & Johannes, S.

Article

(2005). Germany, Cognitive Performance in Patients with Chronic
Schizophrenia Across the Lifespan, Psychiatric Rehabilitation Journal.

Subjects/Participants The study aimed at patients who had psychiatric health conditions for
used in study

both young and old people. The data was the hypothesized for the
patients who were affected with Schizophrenia at a young age and the
old age. After this hypothesis the expected results were supposed to
show whether schizophrenia differed with age.

Method used

Methods used while performing the cognitive test were drawn from
healthy participants and the ones with chronic schizophrenia between
the ages of 18 and 82 years of age. The data was later divided into three
groups. That is, below 34 years, between 35 and 49 years, and the last
group was above 54 years of age. Out of the 94 patients with chronic or
subchronic Schizophrenia according to DSM-IV, were recruited from
three long-term psychiatric units.

Summary of main

After these tests, it was clearly shown that there were broad deficits in

findings (2-3

different phases of life in regards from the young to the old. It also

sentences)

showed that cognitive disorders are mostly associated with the old age.

Article #2
APA Reference of

Vibeke, B., Poul, V., Birgitte, F., & Chris, F. (2016, November 3). The

Article

Effect of Positive Symptoms on Social Cognition in First-Episode
Schizophrenia Is Modified by the Presence of Negative Symptoms;
Journal of Neuropsychology Vol. 31, No. 2, 209–219.

SCHIZOPHRENIA STUDIES

3

Subjects/Participants The first study of schizophrenia involved patients between ages of 18
used in study

and 34 years. In 2010, the study included 36 patients and from the 36
no patient had ever received the antipsychotic medication for more than
three months. During the year 2012 and 2011, 23 patients were
included. The patients never had psychopharmacological treatment
before for six weeks.

Method used

The first phase came from OPUS. This community was treated as the
treatment group of schizophrenia. These patients had already been
treated with this disease and had an experience with a psychiatrist. This
was according to ICD-10 criteria. These patients were further recorded
within two periods. The first period lasted for one year (January, 2009
to February 2010) while the second phase lasted for another one year
(August 2011 to August 2012).

Summary of main

It was found that there were major differences in social cognition and

findings (2-3

neurocognition. From the two different categories of patients. Patients

senten...


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