Part III
9
John G. Kerns
People with Cluster A personality disorders are often characterized as odd and eccentric (American Psychiatric Association, 2013). There are three Cluster A disorders in the DSM-5: schizotypal personality disorder (PD), schizoid PD, and paranoid PD. Research on schizoid and paranoid PD is rare and some researchers argued that these disorders should be dropped from DSM-5 (e.g., Triebwasser, Chemerinski, Roussos, & Siever, 2012, 2013). By far most of the research on Cluster A disorders involves research on schizotypal PD. There are at least two different but potentially complementary views of schizotypal PD. One view is that it is a schizophrenia-spectrum disorder, meaning a disorder less severe than schizophrenia but genetically related to it (Siever & Davis, 2004). A second view is that it reflects variation of normal personality traits (Widiger, Crego, Rojas, & Oltmanns, 2018).
Cluster A Disorders and the Schizophrenia-Spectrum
Again, one conceptualization of schizotypal PD is that it reflects a schizophrenia-spectrum disorder. Schizotypal, meaning “like schizophrenia,” PD was first introduced in DSM-III and it arose out of the concept of borderline schizophrenia or stable characteristics thought to be genetically related to schizophrenia (Spitzer, Endicott, & Gibbon, 1979). If schizotypal PD was genetically related to schizophrenia, then it would be expected that relatives of people with schizophrenia would be more likely to have schizotypal PD. This hypothesis has been strongly supported in previous research (Kendler & Walsh, 1995). For instance, Kendler and colleagues (Kendler, McGuire, Gruenberg, & Walsh, 1995) reported that rates of schizotypal PD were higher in relatives of people with schizophrenia than in either relatives of controls or in relatives of people with mood disorders. Further, among Cluster A disorders, there is stronger evidence that schizotypal PD is familially related to schizophrenia than there is for the other Cluster A disorders; and with stronger evidence that paranoid PD is familially related to schizophrenia than schizoid PD (Kendler et al., 2006). There is also some research finding that avoidant PD is familially related to schizophrenia (Triebwasser et al., 2012).
If schizotypal PD was genetically related to schizophrenia, then it would also be expected that relatives of people with schizotypal PD would be more likely to have schizophrenia. Consistent with this, Kendler and Walsh (1995) found that for probands with schizophrenia, also having a parent with schizotypal PD increased risk for schizophrenia in the proband’s siblings, but parental schizotypal PD did not increase sibling risk for mood or anxiety disorders. However, finding elevated rates of schizophrenia in relatives of people with schizotypal PD has not been consistently reported (Siever & Davis, 2004), possibly due to the small numbers of probands with schizotypal PD in these studies (Kendler & Walsh, 1995).
If schizotypal PD was genetically related to schizophrenia, then it might also be expected that schizotypal PD might often be a precursor to developing schizophrenia. Consistent with this, there is evidence that about 20–50 percent of people with schizotypal PD go on to develop schizophrenia. For instance, recently in a nationwide Danish registry study it was reported that risk of 20-year schizophrenia diagnosis in those initially diagnosed with ICD-10 schizotypal disorder was 33 percent (Hjorthøj, Albert, & Nordentoft, 2018). Hence, this suggests that an incident diagnosis of schizotypal PD may be more predictive of future onset of schizophrenia than having two parents with schizophrenia (Gottesman, Laursen, Bertelsen, & Mortensen, 2010). Therefore, there is strong evidence that schizotypal PD is a schizophrenia-spectrum disorder, with schizotypal PD indicating a markedly increased risk for schizophrenia.
Schizotypal PD (SPD) and Schizotypy
The term schizotypy is often used interchangeably with the term schizotypal (Raine, 2006), but there are distinctions between schizotypy and schizotypal PD (Lenzenweger, 2018). Schizotypy has been defined as a latent personality organization reflecting liability for schizophrenia (Lenzenweger, 2018). There has been an extensive amount of research on schizotypy, with a decent amount of schizotypy research involving the use of questionnaires to assess schizotypy. On average, people with extremely elevated questionnaire measured schizotypy are rated as having more interview measured schizotypal/Cluster A symptoms than people with average or lower schizotypy (Kwapil, Gross, Silvia, & Barrantes-Vidal, 2013). However, most people with markedly elevated questionnaire measured schizotypy would not meet criteria for schizotypal PD (Chapman, Chapman, Kwapil, Eckblad, & Zinser, 1994).
SPD and Relation to Schizophrenia Premorbid and Prodromal Phases
As a schizophrenia-spectrum disorder, one can view schizotypal PD as possibly reflecting the premorbid phase of schizophrenia, the prodromal phase of schizophrenia, or both (Raine, 2006). The years before developing schizophrenia are often divided into premorbid and prodromal phases (Tandon, Nasrallah, & Keshavan, 2009). The premorbid phase is from birth until the onset of the prodromal phase (e.g., in one person, from birth until let’s say age 20). The premorbid phase is often associated with enduring deficits (e.g., poorer cognition and social problems). Hence, one can imagine someone first meeting criteria for schizotypal PD in the premorbid phase, with schizotypal PD reflecting enduring deficits developing in childhood and adolescence. Consistent with this, Esterberg and colleagues (Esterberg, Ousley, Cubells, & Walker, 2013) found that adolescents with schizotypal PD were rated by their parents as more socially impaired and with more repetitive interests and behaviors beginning in childhood. These deficits were even more pronounced than in people with 22q11 deletion syndrome who also have markedly elevated schizophrenia risk.
The prodromal phase (e.g., in one person, let’s say from age 20 until age 22) reflects an increase of symptoms and functional disability, sometimes ending in the onset of schizophrenia (Tandon et al., 2009). In most people with schizophrenia, this putative prodromal phase appears to last for more than a year, with the median prodromal phase being more than two years in length. In addition, there is evidence that people can recover from a prodromal phase and become less symptomatic, perhaps to never develop schizophrenia. Hence, someone could also potentially first meet criteria for schizotypal PD in the prodromal phase. Consistent with this, in the NAPLS study attempting to identify people in the prodromal phase at imminent risk for psychotic disorder onset, over 30 percent of the sample was diagnosed with schizotypal PD (Esterberg, Goulding, & Walker, 2010). Further, Esterberg et al. (2013) reported increased positive attenuated psychotic symptoms, thought to be of prodromal intensity, in adolescents with schizotypal PD compared to both a control group and to people with 22q11 deletion syndrome. Given that some people recover from the prodromal phase, this suggests that some temporal instability in schizotypal PD might reflect recovery from the prodromal phase. Importantly, the period of greatest risk for schizophrenia ends in middle adulthood (Tandon et al., 2009). Hence, after that time, it would be expected that few people with schizotypal PD would develop schizophrenia. Consistent with this, in the recent Danish registry study, rate of conversion from schizotypal disorder to schizophrenia decreased through the follow-up period, with conversion rate being 11.7 percent by year 1, 16.3 percent by year 2, and again being 33 percent by year 20 (Hjorthøj et al., 2018). Hence, for people with schizotypal PD who do not develop schizophrenia, it is thought that some protective factors could be present that prevent the onset of schizophrenia (Chemerinski, Triebwasser, Roussos, & Siever, 2013).
SPD Heterogeneity
It has long been argued that a key feature of schizophrenia is its heterogeneity, with any two people with schizophrenia potentially varying widely in types of symptoms, cognitive functioning, and outcome (Tandon et al., 2009). Schizophrenia is thought to involve multiple symptom factors, with at least three commonly identified: positive (e.g., delusions and hallucinations), disorganized (disorganized speech and behavior, inappropriate affect), and negative (decreased verbal and emotional expression; and decreased motivation and pleasure and increased social withdrawal). Given the conceptualization of schizotypal PD as a schizophrenia-spectrum disorder, then it would be expected that schizotypal PD would be similarly very heterogeneous. In fact, it might be argued that schizotypal PD could even be more heterogeneous than schizophrenia, as it has been argued that some people might meet criteria for schizotypal PD without actually having increased genetic risk for schizophrenia, labeled pseudoschizotypy by Raine (2006).
Schizotypal PD does appear to reflect a multidimensional array of symptoms and deficits. This includes symptoms that appear at least somewhat similar to the positive symptoms of schizophrenia, specifically ideas of reference, odd beliefs/magical thinking, unusual perceptual experiences, and paranoia (American Psychiatric Association, 2013). Schizotypal PD also includes excessive social anxiety that appears at least somewhat related to paranoia (i.e., does not abate and reflects paranoid fears), although this has also often been viewed as a negative, or interpersonal, symptom. Schizotypal PD also includes three symptoms that appear most similar to the disorganized symptoms of schizophrenia, specifically odd thinking and speech, odd/eccentric behavior, and inappropriate affect. Schizotypal PD also includes at least two symptoms that appear perhaps most similar to the negative symptoms of schizophrenia, specifically lack of close friends and constricted affect. However, Rosell and colleagues (Rosell, Futterman, McMaster, & Siever, 2014) noted that interview (rather than self-report) measures of constricted affect are more likely to load with disorganized schizotypal symptoms.
Research on schizotypal symptoms has often found a three-factor structure that appears roughly similar to the three-factor symptom structure of schizophrenia. For instance, in a factor analysis of the nine schizotypal symptoms rated using semi-structured interviews, Bergman and colleagues (Bergman, Silverman, Harvey, Smith, & Siever, 2000) found three factors: cognitive/perceptual (i.e., positive), disorganization, and interpersonal (i.e., negative). For the commonly used schizotypal personality questionnaire (SPQ; Raine, 1991), Fonseca-Pedrero et al. (2018) examined the factor structure across 12 countries (n = 27,001) using confirmatory factor analysis. They found support for previously examined three- or four-factor models: a three-factor model with paranoia loading on both the positive/cognitive perceptual and negative/interpersonal factors and with excessive social anxiety loading on the negative/interpersonal factor; and a four-factor model with a separate suspiciousness factor comprised of ideas of references, paranoia, and excessive social anxiety, with both paranoia and excessive social anxiety cross-loading on the negative/interpersonal factor. However, some research has observed more complex schizotypal factor structures. For instance, in an SPQ item-level factor analysis, Chmielewski and Watson (2008) found at least five factors: unusual beliefs and experiences, mistrust, eccentricity/oddity (i.e., disorganized), social anhedonia, and social anxiety. Further, Kendler et al. (1995; n = 1272) found six different factors using the Structured Interview for Schizotypy that includes 20 signs and symptoms. All six factors were more common in the first-degree relatives of people with schizophrenia, which were labeled positive schizotypy, suspicious behavior, odd speech, negative schizotypy (e.g., poor rapport, aloofness), social dysfunction (i.e., amotivation and poor occupational functioning), and avoidant symptoms (including social isolation and social anxiety).
SPD Negative Symptom Coverage
From the perspective of schizophrenia, one could question how well DSM-5 schizotypal PD criteria reflect symptoms that are like the negative symptoms of schizophrenia. Negative-like symptoms have often been most emphasized in descriptions of the relatives of people with schizophrenia (Raine, 2006). Further, negative symptoms were also argued to be neglected in the DSM-III diagnostic criteria of schizophrenia, which could potentially account for their relative neglect in the diagnostic criteria of schizotypal PD, which have not changed much since DSM-III. At the same time, in the schizophrenia literature there has been a continued refinement in the conceptualization and assessment of negative symptoms (e.g., Kring, Gur, Blanchard, Horan, & Reise, 2013). Hence, it could be argued that the negative symptoms of schizotypal PD (again, often labeled interpersonal symptoms) do not reflect the broad range of the negative symptoms of schizophrenia.
Negative symptoms in schizophrenia appear to fall into at least two dimensions (Kring et al., 2013). One negative symptom dimension involves decreased expression, specifically decreased amount of speech, or alogia, and blunted affect. Poverty of speech has been found to predict risk of schizophrenia-spectrum disorders when assessed in mid-childhood (Gooding, Ott, Roberts, & Erlenmeyer-Kimling, 2013). However, decreased amount of speech does not appear among schizotypal criteria. The schizotypal criterion of constricted affect does have some similarity to the schizophrenia negative symptom blunted affect. In schizophrenia, blunted affect has been consistently found to reflect a deficit in emotional expression but not in experience. For instance, decreased emotional facial expressions have been consistently found in schizophrenia in response to standardized stimuli such as film clips (e.g., Mote, Stuart, & Kring, 2014). In contrast, in schizotypal PD there is emphasis on restricted affective expression as being disruptive in interpersonal contexts rather than it reflecting a more primary deficit in emotional expression. Hence, DSM-5 schizotypal PD does not appear to reflect negative symptoms of decreased verbal expression and may not clearly reflect decreased emotional expression.
Although at least somewhat absent in DSM-5, there is some evidence that suggests that people with schizotypal PD, or people with elevated Cluster A symptomatology more broadly, do exhibit decreased verbal and emotional expression. This includes decreased emotion in speech, increased pauses in speech (Dickey et al., 2012), and decreased communicative gestures during speech, which could reflect a similar type of expressive deficit (Mittal et al., 2006). Kosson and colleagues (Kosson et al., 2008) developed the Interpersonal Measure of Schizoid Personality Disorder (IM-SZ) to make behavioral ratings thought to capture signs of schizoid PD, with these ratings strongly correlated with interview-rated schizoid PD symptoms and moderately correlated with schizotypal PD symptoms. Many of the IM-SZ items, especially those with the highest item-total correlations, reflect decreased verbal and emotional expression. Other research on decreased verbal and emotional expression in the schizophrenia-spectrum has focused on social anhedonia. Social anhedonia is associated with Cluster A symptoms, predicts increased risk for schizophrenia-spectrum PDs, and has been associated with increased Cluster A disorders in biological parents (specifically being found in fathers; Cohen, Emmerson, Mann, Forbes, & Blanchard, 2010). Social anhedonia is associated with increased IM-SZ scores, especially items reflecting decreased verbal and emotional expression (Collins, Blanchard, & Biondo, 2005), and with fewer positive facial expressions to positive and neutral film clips (Leung, Couture, Blanchard, Lin, & Llerena, 2010). Hence, overall there is evidence suggesting that people with schizotypal PD or with elevated Cluster A symptoms do exhibit decreased verbal and facial expression. However, it is interesting that the one instance where this was not found was in a study where people with social anhedonia did not display decreased facial expressions specifically in a social interaction task (Llerena, Park, Couture, & Blanchard, 2012), whereas again DSM-5 criteria emphasize rating constricted affect specifically in interpersonal contexts (although people with social anhedonia in Llerena et al. were rated as less socially skilled and affiliative during the task). Overall, decreased verbal and emotional expression seems to reflect schizophrenia-spectrum conditions and could potentially be further emphasized either in schizotypal PD or in attempts to more directly assess risk for schizophrenia (Kendler, Lieberman, & Walsh, 1989).
In addition to decreased verbal and emotional expression, a second schizophrenia negative symptom dimension involves decreased motivation and pleasure and increased social withdrawal. The schizotypal criterion of no close friends appears similar to social withdrawal in schizophrenia. However, a broader focus on decreased motivation, goal-directed activity, and pleasure is missing from the schizotypal PD criteria. Hence, here again, schizotypal PD appears limited in attempting to capture negative symptoms that might be related to schizophrenia.
Schizoid PD and Negative Symptoms of Schizophrenia
In contrast to schizotypal PD, diagnostic criteria for schizoid PD appear to more strongly capture some of the decreased motivation and pleasure and increased social withdrawal symptoms of schizophrenia. This includes lack of social interaction (i.e., lacking close friends; preference for solitary tasks) as well as decreased social motivation (i.e., not desiring close relationships) and decreased social and other types of pleasure (i.e., enjoys few activities; little interest in sexual experiences with another person). Schizoid PD also includes flattened affectivity (and indifference to praise and criticism). However, schizoid PD criteria do not include decreased verbal expression. Further, they do not explicitly involve a broader decrease in motivation and lack of goal-directed activity as is found in schizophrenia (Gard et al., 2014). Another issue for schizoid PD is how well these decreased motivation and pleasure symptoms are assessed. In schizophrenia research, recent negative symptom assessments have been developed to more accurately assess these symptoms (Kring et al., 2013), including using ecological momentary and behavioral task assessment (Gard et al., 2014; Moran, Culbreth, & Barch, 2017). An issue for future research might be whether more valid assessment of these decreased motivation and pleasure symptoms, perhaps specifically in the context of schizoid PD, would increase their sensitivity to detecting genetic risk for schizophrenia, with again schizoid PD being the Cluster A PD least clearly associated with schizophrenia liability. In addition, given that recent research on negative symptoms in schizophrenia has made progress in clarifying potential mechanisms (Strauss & Cohen, 2017), this suggests that research on Cluster A disorders would benefit from testing similar negative symptom mechanisms.
Paranoid PD Symptoms and Factor Structure
Although paranoid PD has rarely been studied, it is thought to be fairly common in clinical and general population samples (Triebwasser et al., 2013). Paranoid PD appears to reflect delusion-like persecutory beliefs. In schizophrenia, the most common type of delusion is persecutory (e.g., thinking others are out to harm them; Appelbaum, Robbins, & Roth, 1999). Paranoid PD symptoms bear some similarity to this type of delusion. There is also evidence suggesting that paranoid PD might be closely related to delusional disorder (Triebwasser et al., 2013).
In a large interview study (n = 903 with PDs; n = 114 with paranoid PD), Falkum and colleagues (Falkum, Pedersen, & Karterud, 2009) found that a two-factor symptom structure for DSM-IV paranoid PD fit better than a one-factor structure using confirmatory factor analysis. One factor was labeled suspiciousness, including doubts about loyalty of friends, suspecting harm from others, reading hidden meanings, and reluctance to confide. The second factor was labeled hostility and included reacting angrily to perceived attacks, persistently bearing grudges, and recurrent suspicions about partner. However, the item recurrent suspicions about partner had the lowest factor loading of any item and it also had the lowest item-total correlation when analyzing all paranoid PD symptoms.
Cluster A Disorders and Relation to Normal Personality
Again, in addition to being a schizophrenia-spectrum disorder, a potentially complementary view of schizotypal PD conceptualizes it as an extreme manifestation of normal personality traits (Widiger et al., 2018). This is also consistent with attempts to view all mental disorders, including psychotic disorders, as variations on traits that occur in the general population (Forbes et al., 2017). Alternatively, one could imagine that both schizophrenia and schizotypal PD reflect some disorder-specific risk that is not shared with the general population. This also seems to echo debates about whether liability for schizophrenia is dimensional in the general population or whether it is taxonic (Lenzenweger, 1999; Linscott, Morton, & GROUP, 2018).
Research from the perspective that schizotypal PD reflects variation of normal personality traits has found that schizotypal PD and other Cluster A disorders have some moderate to large associations with normal personality traits. For instance, in a meta-analysis, Samuel and Widiger (2008) reported that among Five-Factor Model traits schizotypal PD was most associated with increased neuroticism, r = .38, followed by decreased extraversion, r = ‒.28. In a recent large interview study that involved joint analyses of clinical and personality disorders (Forbes et al., 2017), schizotypal PD had a single large loading (.77) on detachment (i.e., low extraversion). Schizotypal PD also had a smaller loading (.32) on a core thought disorder factor (highest loadings on this factor for mania and psychosis). Research on specific schizotypal symptom dimensions has found that the negative symptoms tend to be most associated with decreased extraversion (Cicero & Kerns, 2010). Further, disorganized schizotypal symptoms have been most associated with increased neuroticism as well as decreased conscientiousness. However, much of this research has involved self-report measures and it is not clear whether research using observational ratings of disorganized symptoms would find similar results (see below). In contrast, Samuel and Widiger (2008) found that schizotypal PD was not strongly associated with openness to experience, r = .09. However, it is still debated whether and how schizotypal PD might be associated with openness to experience.
In a recent study, Czajkowski et al. (2018) examined how much PD genetic variance was shared with Big Five traits. They found that only 47.3 percent of schizotypal PD variance was shared with Big Five traits, suggesting a sizable amount of disorder-specific variance not shared with normal personality. However, other research has assessed normal personality (or maladaptive extremes of the Five-Factor Model) using the Personality Inventory for DSM-5 (PID-5), which includes the construct psychoticism as a dimension of normal personality. Using the PID-5, Reichborn-Kjennerud et al. (2017) found that 100 percent of the genetic variance for schizotypal PD was shared with normal personality. Further, this study found genetic correlations between schizotypal PD and psychoticism ≥ .80. Hence, it appears that how normal personality is conceptualized and whether it includes openness to experience or psychoticism can have large consequences for how well schizotypal PD appears to be related to normal personality (more on openness below).
In their meta-analytic review, Samuel and Widiger (2008) also found that both schizoid and paranoid PD were associated with extraversion and neuroticism, although they varied in the strength of these associations. Specifically, schizoid PD was most associated with decreased extraversion, r = ‒.46, and also associated with increased neuroticism, r = .22. In a recent study, Forbes et al. (2017) found that schizoid PD loaded .85 on a detachment factor. For paranoid PD, Samuel and Widiger found it was associated with increased neuroticism, r = .40 and decreased extraversion, r = ‒.21. Further, paranoid PD was also negatively associated with agreeableness, r = ‒.34. Forbes et al. (2017) found that paranoid PD had its highest loadings on antagonism (.42) and detachment (.41). Recently, Czajkowski et al. (2018) reported that paranoid PD shared much more genetic variance with Big Five traits (79.4 percent) than schizotypal PD (47.3 percent). There was also evidence in this study that schizoid PD might share even more genetic variance with Big Five traits than paranoid PD. Hence, there is some evidence that schizoid and paranoid PD are, if anything, perhaps more strongly related to maladaptive levels of normal personality traits than is schizotypal PD.
Prevalence of Cluster A Disorders
The prevalence of Cluster A disorders is still at least somewhat unclear. There has been an impression that Cluster A disorders are rare (Triebwasser et al., 2012). Research on the prevalence of Cluster A disorders in representative community samples has produced some conflicting results. Discrepant results might be due to the use of different assessment instruments, including whether there is reliance on structured versus semi-structured interviews, or differences in sampling methods, or other reasons (Quirk et al., 2016). Across five studies, the average Cluster A prevalence is 4.0 percent, ranging from 1.6 percent to 7.1 percent (reviewed in Quirk et al., 2016). Average rate for schizotypal PD across four studies is 1.29 percent, ranging from 0.06 percent to 3.9 percent. In the National Comorbidity Survey Replication (NCS-R; Lenzenweger, Lane, Loranger, & Kessler, 2007), rate of schizotypal PD was not directly measured, but it was estimated at 3.3 percent, although the authors note that this is expected to be at least a slight overestimate. For schizoid PD across four studies the average is 1.55 percent, ranging from 0.6 percent to 3.1 percent; and for paranoid PD, across four studies the average is 2.35 percent, ranging from 0.7 percent to 4.4 percent. Estimated rates of schizoid PD and paranoid PD in the NCS-R were 4.9 percent and 2.3 percent (again, at least slight overestimates; Lenzenweger et al., 2007). Overall, there is some evidence that prevalence of Cluster A disorders might be higher than often assumed, although again the variability in results across studies also makes this conclusion somewhat tentative.
Socio-demographic correlates of Cluster A disorders have also been found to vary across studies. It is often assumed that the rates of these disorders are higher in males. Consistent with this, in a cross-national study, Huang et al. (2009) reported that the odds ratio for males (relative to females) for Cluster A PDs was 5.0 (with younger age and lower education also associated with Cluster A PDs). In contrast, in the NCS-R, prevalence of Cluster A disorders did not vary by sex or by any other socio-demographic variable (Lenzenweger et al., 2007). Overall, if anything rates might be higher in males, but whether and the extent to which this is true is still unclear.
Another area where these studies have produced some conflicting results concerns relationships with other personality disorders. For instance, in the NCS-R, among Cluster A disorders, schizotypal and schizoid were most highly correlated (tetrachoric correlation = .96), whereas schizotypal and paranoid PD were more modestly associated. Instead, paranoid PD was more highly correlated with Cluster B disorders than with schizotypal PD. In contrast, schizotypal PD was not strongly correlated with Cluster B disorders (tetrachoric correlation = .27), including with borderline PD (tetrachoric correlation = .34). Using NESARC data, Lentz and colleagues (Lentz, Robinson, & Bolton, 2010) also reported that schizotypal and paranoid PD were not strongly (in fact, not significantly) associated. However, Lentz et al. also reported that schizotypal PD was more strongly associated with borderline and narcissistic PDs than with schizoid PD. Again, this seems to suggest marked differences in what some of these interview instruments are assessing.
The NCS-R also reported some other important results for Cluster A disorders. It was found that 41 percent of people with Cluster A disorders had a comorbid Axis I disorder in the past year, with 25 percent of people with Cluster A disorders seeking treatment in the past year (Lenzenweger et al., 2007). These rates were much lower than the rates in Cluster B disorders. This seems to confirm the impression that these Cluster A disorders are less likely to be seen in clinical settings relative to Cluster B PDs. This also suggests that which people with Cluster A disorders are seen in clinical contexts could have an effect on perceptions of these disorders.
SPD and Cognitive and Neural Deficits
A prominent characteristic of schizophrenia is cognitive deficits, with these deficits being fairly generalized across domains and with these deficits related to poorer real-world functioning (Tandon et al., 2009). This suggests that as a schizophrenia-spectrum disorder schizotypal PD should also be related to poorer cognition. As expected, evidence for poorer cognition in schizotypal PD has been found in a large number of studies (Raine, 2006). As in schizophrenia, there is evidence that cognitive deficits in schizotypal PD are fairly general and found across a range of cognitive domains, although perhaps the most examined cognitive domains have been cognitive control, working memory, and processing speed. For instance, McClure and colleagues (McClure, Harvey, Bowie, Iacoviello, & Siever, 2013) found that people with schizotypal PD (n = 46) were impaired on a broad cognitive battery compared both to healthy controls (n = 55), d = .96, and to people with avoidant PD (n = 38), d = .70. Hazlett et al. (2014) found that people with schizotypal PD (n = 51) were impaired on a verbal memory and learning task, d = .57, compared to healthy controls. Dickey et al. (2010) found impairments in verbal fluency tasks ranging from small (d = .37) to medium (d = .52) in effect size in people with schizotypal PD (ns > 120) versus healthy controls (ns > 130). As one final example, McClure and colleagues (McClure, Flory, Barch, Harvey, & Siever, 2008) found that people with schizotypal PD (n = 63) were impaired on the AX-CPT task, d = .92, compared to healthy controls (n = 42). Overall, evidence of broad cognitive deficits in schizotypal PD appears to be well-established, although some examples of potentially intact functioning in some domains have also been observed (Maróthi & Kéri, 2018). There has also been some evidence that it might be possible to improve cognition in schizotypal PD pharmacologically (Rosell et al., 2014).
As might be expected given that schizotypal PD presumably reflects a less severe disorder than schizophrenia, cognitive deficits in schizotypal PD do not appear to be as severe as in schizophrenia (Chemerinski, Triebwasser, et al., 2013; Rosell et al., 2014). Hence, it is possible that one reason why people with schizotypal PD do not develop schizophrenia is that they have less severe cognitive deficits than in schizophrenia. Note that finding less severe cognitive deficits in people with schizotypal PD is also consistent with research on people considered at clinical high risk for psychosis (i.e., prodromal phase) which has also found that these individuals exhibit broad cognitive deficits that are not as severe as found in schizophrenia (e.g., across broad range of cognitive tasks, median effect size d = .49; Seidman et al., 2016). Furthermore, there is also evidence of cognitive deficits being associated with schizotypy. Moreover, given that the vast majority of the people in these studies who have elevated schizotypy would not be expected to meet criteria for schizotypal PD, then it might be expected that cognitive deficits in people with elevated schizotypy would be smaller than in people with schizotypal PD. This appears to be the case (Chun, Minor, & Cohen, 2013), with a recent meta-analysis reporting that effect sizes for associations between schizotypy and most cognitive domains were small (Siddi, Petretto, & Preti, 2017).
Given broad cognitive deficits in both schizophrenia and schizotypal PD, one might expect evidence of fairly broad neural deficits as well. For instance, in schizophrenia there is evidence of widespread decreased gray matter throughout the cortex (Ivleva et al., 2013). Consistent with this, there is also some evidence of widespread decreased gray matter in schizotypal PD (Asami et al., 2013). For instance, in a study of women with schizotypal PD (n = 31), Koo and colleagues (Koo, Dickey, et al., 2006) reported overall decreased cortical gray matter compared to healthy control women (n = 29), with deficits found across temporal, frontal, and parietal regions. Similarly, in a study of men with schizotypal PD (n = 54), Asami et al. (2013) also found globally decreased cortical gray matter compared to healthy control men (n = 54), with decreased gray matter specifically found across a broad range of cortical regions. Hence, as in schizophrenia, neural deficits in schizotypal PD also appear to be potentially broad. One brain area that has been investigated perhaps the most in schizotypal PD is the superior temporal lobe, with frequent evidence of decreased gray matter in the temporal lobe (Rosell et al., 2014), although again deficits do not appear restricted only to this region. There is also evidence of decreased white matter integrity in schizotypal PD. For instance, Lener et al. (2015) reported that fractional anisotropy (thought to reflect white matter integrity) values were intermediate in schizotypal PD (n = 49) relative to people with schizophrenia (n = 22) and healthy controls (n = 55). There are also isolated neural results that could be potentially very important if further established. This includes evidence of preserved volume in one part of the frontal lobe (BA 10; Rosell et al., 2014), decreased caudate volume (Koo, Levitt, et al., 2006), increased putamen volume (Chemerinski, Byne, et al., 2013), and decreased white matter integrity in the genu of the corpus callosum (Lener et al., 2015; Zhang et al., 2017).
A number of studies have found that people with schizotypal PD also exhibit a number of psychophysiological deficits that are also observed in schizophrenia (Chemerinski, Triebwasser, et al., 2013). This includes reduced prepulse inhibition and impaired P50 suppression. It also includes eye tracking impairment as well as reduced P300 amplitude. As in schizophrenia, there is also some evidence suggesting that decreased ventral striatal dopamine (Thompson et al., 2014) and decreased cortical dopamine (Siever & Davis, 2004) might be associated with cognitive deficits and negative symptoms in schizotypal PD (Rosell et al., 2015; more on increased dorsal striatum dopamine below). In addition, based on schizophrenia research, there are a number of other potential neurobiological mechanisms that might be relevant for schizotypal PD (e.g., neurotransmitters GABA and glutamate).
Cluster A PDs and Functional Impairment
In schizophrenia, two predictors of functional impairment are negative symptoms, especially symptoms of decreased motivation and pleasure (Kring et al., 2013), and cognitive deficits (Tandon et al., 2009). Hence, given elevated negative symptoms and cognitive deficits in schizotypal PD, it would be expected that schizotypal PD would also be associated with evidence of functional impairment. McGurk et al. (2013) examined vocational functioning in people with schizotypal PD (n = 38), paranoid PD (n = 17), both PDs (n = 37), or controls (n = 82). They found that people with these Cluster A PDs were less likely to be currently working. For those who were working, they were less likely to have jobs involving cognitive complexity. Both lack of work and lack of work complexity were associated with poor cognition. For people with schizotypal PD, they were less likely to have a job with much social contact. For people with paranoid PD, they were less likely to have a history of work. Hence, as expected, these disorders do appear to be associated with evidence of functional impairment, with some evidence that this is related to cognitive deficits and perhaps to interpersonal deficits.
Other research has also reported functional impairment in schizotypal PD samples, with evidence that this disorder is one of the most functionally impairing of PDs (Chemerinski, Triebwasser, et al., 2013b). Generally consistent with McGurk et al. (2013), Dickey et al. (2005) reported that people with schizotypal PD (n = 104) were more likely to have a period of time unable to work than healthy controls (n = 110). McClure et al. (2013) found that people with schizotypal PD (n = 46; average age = 38) were less likely be living independently (44 percent) than healthy controls (n = 55; 72 percent). In a recent study with adolescents, Verbeke and colleagues (Verbeke, De Clercq, Van der Heijden, Hutsebaut, & van Aken, 2017) found that different schizotypal symptom dimensions were related to impaired interpersonal functioning. Finally, in the NCS-R study, Lenzenweger et al. (2007) found that Cluster A disorders were associated with both instrumental role functioning disability and cognitive disability. However, Cluster A disorders were no longer associated with disability after statistically adjusting for Axis I disorders. Hence, it is still unclear how much disability in Cluster A disorders is not due to other comorbid disorders.
Schizotypal PD has also been associated with substance use disorders (Hjorthøj et al., 2018). In a twin study, Gillespie et al. (2018) reported that although schizotypal PD symptoms were associated with cannabis use and cannabis use disorder, when statistically adjusting for other PD symptoms this was no longer the case. However, in a Danish registry study, Toftdahl and colleagues (Toftdahl, Nordentoft, & Hjorthøj, 2016) found that 35 percent of people with ICD-10 schizotypal disorder had a substance use disorder, with the most common being alcohol (25 percent) and cannabis (11.6 percent). Rates of cannabis use disorders in schizotypal disorder were more than double the rate for all disorders other than schizophrenia (with all PDs examined as a single category). Further, cannabis use disorder and substance abuse more broadly has been found to predict conversion from schizotypal disorder to schizophrenia (Hjorthøj et al., 2018). For other Cluster A disorders, Gillespie et al. (2018) found that paranoid PD symptoms were associated with cannabis use regardless of statistically adjusting for other PD symptoms. Interestingly, schizoid PD was one of the few PDs where its symptoms were not associated with increased cannabis use, with schizoid PD symptoms significantly negatively associated with cannabis when statistically adjusting for other PD symptoms.
SPD Positive Symptoms and SZ Genetic Risk
Another potential issue with the diagnostic criteria of schizotypal PD that has been raised is that they are heavily weighted towards the symptoms that are more like the positive symptoms of schizophrenia. Raine (2006) argued that this is in contrast to the descriptions of negative symptoms that tend to predominate historic descriptions of relatives of people with schizophrenia. Similarly, Kendler et al. (1995) argued that especially negative schizotypy, social dysfunction, and odd speech strongly identify relatives of people with schizophrenia, with, in contrast, positive schizotypy, suspicious behavior, and avoidant symptoms more weakly related to familial risk. Hence, there are some concerns about whether positive schizotypal symptoms are overly weighted in the schizotypal PD diagnostic criteria and even whether positive schizotypal symptoms are strongly related to genetic risk for schizophrenia (Raine, 2006).
For instance, in a review of studies of relatives of people with schizophrenia, Tarbox and Pogue-Geile (2011) found that there was only a small effect size increase (d = .37) in positive schizotypal symptoms among first-degree relatives, found in both questionnaire and interview studies. If anything, this small effect size increase might be an overestimate, as these authors also noted some potentially relevant negative evidence from questionnaire schizotypy studies that they did not include in the overall effect size estimate. Further, a more recent study by Tarbox and colleagues found if anything a negative association between positive schizotypal symptoms and genetic risk (Tarbox, Almasy, Gur, Nimgaonkar, & Pogue-Geile, 2012). Moreover, overall positive schizotypal symptoms have not been found to differentiate those with a first-degree relative with schizophrenia versus those with a first-degree relative with mood disorders (Tarbox & Pogue-Geile, 2011). One possible suggested explanation for these results is that relatives of people with schizophrenia might have a tendency to underreport psychotic-like symptoms. Although possible, other evidence does not clearly support a general underreporting of symptoms (e.g., MMPI K-scale scores; Tarbox et al., 2012). At the same time, people with schizophrenia themselves may not report a very high level of positive schizotypy (Horan, Reise, Subotnik, Ventura, & Nuechterlein, 2008), with these positive schizotypy measures being highly correlated with positive schizotypal symptoms. Further, positive schizotypy has been found to be very strongly related to, and perhaps even indistinguishable from, dissociation (Cicero & Kerns, 2010). And similar to positive schizotypy, people with schizophrenia are not markedly elevated on dissociation (Lyssenko et al., 2018). However, perhaps people with schizophrenia are not markedly elevated on positive schizotypy measures that are highly correlated with positive schizotypal symptoms because of antipsychotic medication and illness chronicity. But on the whole, previous evidence does raise questions about whether positive schizotypal symptoms are highly prevalent in schizophrenia and whether they are strongly related to genetic risk for schizophrenia.
Other evidence suggesting that positive schizotypal symptoms may not strongly reflect genetic risk for schizophrenia comes from research on schizophrenia polygenic risk scores (SPRS). These scores reflect genetic loci each at least weakly statistically associated with schizophrenia in genome-wide association studies and that collectively have a sizable relation to schizophrenia genetic risk (e.g., highest 10 percent with odds ratio for SZ between 7.8 and 20.3 relative to the lowest 10 percent; Schizophrenia Working Group of the Psychiatric Genomics Consortium, 2014). SPRS have been associated with a number of other variables, including being strongly related to risk for bipolar disorder, as well as increased nicotine use, symptoms and family history of depression and anxiety, increased neuroticism, family history of drug and alcohol use disorders, and increased interpersonal trauma (Docherty et al., 2018; Duncan et al., 2018). However, despite these other associations, as of yet, no study has reported that self-reported positive schizotypal symptoms, or self-reported psychotic-like experiences more broadly, are positively associated with SPRS (Ronald & Pain, 2018). In fact, one recent study in a high stress (recent conscript) sample reported that positive schizotypal symptoms were significantly negatively associated with SPRS (Hatzimanolis et al., 2018). Another study only found a significant positive association between SPRS with hallucinations and paranoia after removing people with scores of zero on the hallucinations and paranoia measures (Pain et al., 2018). This study also reported a negative association between self-reported hallucinations and paranoia with bipolar polygenic risk score, which is surprising given a strong positive correlation between schizophrenia and bipolar polygenic risk scores (Lo et al., 2017). Overall, this potentially absent association between positive schizotypal symptoms and SPRS seems consistent with Raine’s concept of pseudoschizotypy, meaning some people with positive schizotypal symptoms are not at increased genetic risk for schizophrenia.
One factor in research on whether positive schizotypal symptoms reflect genetic risk for schizophrenia might be the mode of assessment. Again, self-report studies have not found a significant positive association with SPRS. However, one study that used a semi-structured interview measure of positive schizotypal symptoms (the Structured Interview for Schizotypy) did report a significant positive association with SPRS (van Os et al., 2017). In addition, two other related studies (Jones et al., 2016; Zammit et al., 2014) using semi-structured interviews found near significant positive associations between SPRS and psychotic-like symptoms that presumably would be highly correlated with measures of positive schizotypal symptoms. This suggests that perhaps semi-structured interview measures of positive schizotypal symptoms might be more associated with SPRS than self-report studies. This is also consistent with other evidence indicating the difficulty of measuring psychotic-like symptomatology with questionnaire or fully structured interview (Kendler, Gallagher, Abelson, & Kessler, 1996).
Also relevant for interpreting the general lack of significant associations between SPRS and positive schizotypal symptoms is that associations have also been inconsistent with measures of negative schizotypal symptoms. Again, relatives of people with schizophrenia do exhibit increased negative schizotypal symptoms (Kendler et al., 1995). For instance, in their review, Tarbox and Pogue-Geile (2011) reported that the effect size increase in negative symptoms in first-degree relatives was d = .67 across studies, d = .74 in interview studies, and d = .46 in questionnaire studies, with this also increased compared to first-degree relatives of people with affective disorder. However, five self-report studies did not find a significant positive association between SPRS and negative schizotypal symptoms (Ronald & Pain, 2018). In contrast, three studies, one interview-based, have found that negative schizotypal symptoms are positively associated with SPRS. Hence, there is seemingly more evidence that negative schizotypal symptoms are associated with polygenic risk scores than positive schizotypal scores, but neither appears to be clearly and strongly related thus far.
In addition to whether schizotypal symptoms have been assessed using semi-structured interviews or not, there might be other methodological issues with these polygenic risk studies. It has been suggested that these studies might be affected by collider bias, with people with both high genetic risk and increased schizotypal symptoms being less likely to participate, thereby decreasing what might otherwise be a stronger positive association between schizophrenia genetic risk and schizotypal symptoms (Munafò, Tilling, Taylor, Evans, & Davey Smith, 2018). Further, Ronald and Pain (2018) argued that studies with larger sample sizes and that used more recently developed polygenic risk scores (i.e., based on PGC2) might be more likely to report significant associations. Hence, perhaps these methodological factors could account for the weak to inconsistent evidence associating schizophrenia polygenic risk scores and schizotypal symptoms.
SPD Disorganized Symptoms: Observational Rating Versus Self-Report
As previously noted, there is some evidence that interview measures of schizotypal symptoms might be more strongly related to schizophrenia genetic risk than self-report measures. This might be particularly relevant for assessing disorganized schizotypal symptoms. In particular, there is evidence that only observational ratings of disorganized schizotypal symptoms are clearly related to familial risk of schizophrenia. Kendler et al. (1995) found that disorganized schizotypal symptoms measured observationally were the schizotypal symptom most associated with having a first-degree relative with schizophrenia (effect size d = .96; Tarbox & Pogue-Geile, 2011). There is also a long line of research on disorganized speech (i.e., thought disorder; communication deviance) consistently finding increased disorganized speech in the relatives of people with schizophrenia (Gooding et al., 2012). This is also consistent with some evidence that disorganization symptoms in people with schizophrenia also might be the schizophrenia symptom factor most associated with increased familial risk (Rietkerk et al., 2008). In contrast, using self-report measures of disorganization, there is at best a small increase of disorganization in first-degree relatives of people with schizophrenia (across five studies, effect size d = .22; Tarbox & Pogue-Geile, 2011). Hence, observational ratings of disorganization appear to be much more strongly related to familial risk than self-reported disorganization.
Importantly, disorganized speech in schizophrenia has been consistently associated with poor cognitive control (Becker, Cicero, Cowan, & Kerns, 2012). Further, cognitive control deficits are associated with impaired self-monitoring. Hence, given cognitive control deficits in schizophrenia and in schizotypal PD (McClure et al., 2008), people with schizophrenia-spectrum disorders may be poor at monitoring and identifying their own disorganization. Consistent with this, people with schizophrenia have not been found to give valid self-reports of their own cognitive deficits (Medalia, Thysen, & Freilich, 2008) or of their level of disorganization (Becker et al., 2012). At the same time, although objectively rated disorganization is associated with cognitive deficits in schizophrenia, it is still unclear whether and how strongly self-reported disorganized schizotypal symptoms is associated with cognitive deficits (e.g., Kane et al., 2016). Hence, it is not clear to what extent observed versus self-reported disorganized schizotypal symptoms are measuring the same construct. This is consistent with concerns raised by Kendler et al. (1995) and by Rosell et al. (2014) that interview and observational schizotypal measures are more valid than self-report measures.
SPD and Striatal Dopamine
Psychotic disorders are strongly associated with increased striatal dopamine, especially in the dorsal striatum, with dopamine thought to be specifically related to psychotic symptoms in this disorder (i.e., positive and to some extent disorganized symptoms; Howes, McCutcheon, Owen, & Murray, 2017). Hence, it might then be expected that schizotypal PD, perhaps especially the positive schizotypal symptoms, would be associated with increased striatal dopamine. Consistent with increased striatal dopamine in schizotypal PD, two studies have found increased dopamine metabolites in schizotypal PD, with this correlated with their level of positive schizotypal symptoms (Siever & Davis, 2004). Moreover, at least one study has examined dopamine levels specifically in the striatum in schizotypal PD, finding that schizotypal PD is associated with increased dysregulated release of striatal dopamine (Abi-Dargham et al., 2004). At the same time, this increase in striatal dopamine in schizotypal PD was not as elevated as typically found in psychotic disorders. However, in psychotic disorders, dopamine is especially increased while in an acute psychotic phase (Laruelle, Abi-Dargham, Gil, Kegeles, & Innis, 1999). Further, fluctuations in the intensity of sub-psychotic, or attenuated, symptoms are thought to also occur in schizotypal PD (Stone, 1985). However, it is not clear whether people with schizotypal PD in the study by Abi-Dargham and colleagues were all in a commensurate acute phase. Hence, on the whole, perhaps the results of Abi-Dargham et al. do seem consistent with the idea that people with schizotypal PD can experience marked elevations in dorsal striatal dopamine. It is also possible that one protective factor that prevents some people with schizotypal PD from developing schizophrenia is that their levels of striatal dopamine do not get as dysregulated as in schizophrenia (Chemerinski, Triebwasser, et al., 2013). Hence, on the whole, there is evidence of increased striatal dopamine in schizotypal PD, but there is certainly a need for further research on this.
The fact that dopamine levels are thought to episodically fluctuate in psychotic disorders seemingly correlated with episodic changes in psychotic symptoms also might have implications for understanding positive schizotypal symptoms. As noted by Spitzer et al. (1979), original schizotypal PD diagnostic criteria were selected to be stable and not to episodically fluctuate. However, this does raise some conceptual issues about the nature of positive schizotypal symptoms. If these symptoms are stable, then this makes it less clear whether they are caused by the same mechanism(s) that cause psychotic symptoms in schizophrenia that tend to be very episodic (Appelbaum et al., 1999). The possibility that positive schizotypal symptoms may reflect different mechanisms than those that cause psychotic symptoms in schizophrenia might also be consistent with earlier reviewed evidence questioning how strongly these symptoms are related to schizophrenia familial risk and be consistent with Raine’s concept of pseudoschizotypy.
However, although psychotic symptoms do fluctuate episodically in psychotic disorder, they can also often remain in a residual form in the chronic phase, even in the face of antipsychotic medication (Appelbaum et al., 1999). This suggests that in some people positive schizotypal symptoms might also reflect in part a residual form of perhaps an attenuated psychotic symptom that arose in a period of increased striatal dopamine. Therefore, speculatively, there might be at least two different forms of positive schizotypal symptoms. One form might be related in part to increased striatal dopamine that might episodically fluctuate in intensity, and perhaps at times reflects a residual attenuated psychotic symptom. A second form might be unrelated to increased striatal dopamine and might be less likely to be familially related to schizophrenia (Raine, 2006). Potentially generally consistent with this is the evidence from Chapman et al. (1994) who found that only people with extremely elevated positive schizotypy with interview evidence of attenuated psychotic symptoms had increased risk for psychotic disorder. In contrast, people with elevated positive schizotypy but without a history of attenuated psychotic symptoms, and potentially without increased striatal dopamine, did not have increased risk of psychotic disorder.
SPD and Cognitive Biases
Another factor related to persistence and severity of psychotic symptoms in schizophrenia is cognitive biases (Moritz et al., 2014). For instance, there is a long line of evidence finding that delusions in psychotic disorders are related to a jumping to conclusions bias whereby people make confident decisions on the basis of limited evidence. This bias also does not appear related to striatal dopamine (So, Peters, Swendsen, Garety, & Kapur, 2014). Hence, one reason why someone might adopt a delusional belief when in a high dopamine state, or why someone might maintain a delusion when in a low dopamine state, is due to cognitive biases that result in faulty inferences. Importantly, although the jumping to conclusions bias is more common in psychotic disorder, it is also present in a sizable minority of people without psychotic disorder (Ross, McKay, Coltheart, & Langdon, 2015). In fact, there is evidence that cognitive biases like this and a tendency to make faulty inferences can be quite common (Risen, 2016). Other research suggests that cognitive biases might also play a role in positive schizotypal symptoms. For instance, psychotic-like beliefs, which are correlated with positive schizotypal symptoms, have also been associated with a jumping to conclusions bias, although it should be noted that the average effect size might be small (Ross et al., 2015).
Consistent with an association between cognitive biases and positive schizotypal symptoms, research on magical and superstitious thinking in the general population also supports a role for cognitive biases. In particular, Risen (2016) has argued that magical thinking often arises from cognitive biases due to increased influence of intuitive and implicit cognitive processes, such as a reliance on heuristics. Moreover, magical thinking is also thought to reflect an inability or unwillingness for people to use controlled and effortful cognition in order to override the often flawed conclusions that arise from the use of heuristics. This suggests the possibility that in people with schizotypal PD that they also might entertain and adopt odd and magical beliefs because they are overly reliant on biased cognitive heuristics and are unable or unwilling to override these conclusions. Hence, in addition to positive schizotypal symptoms reflecting increased striatal dopamine, it is possible that these symptoms can also reflect, or perhaps in some people perhaps only reflect, an overreliance on biased heuristic processing.
SPD and Trauma
In addition to research on whether schizotypal symptoms are related to familial risk for schizophrenia, many studies have examined whether they are also related to experiences of trauma. There is now a wealth of evidence that schizotypal symptoms are fairly strongly associated with childhood abuse and trauma. For instance, in a recent review, Velikonja and colleagues (Velikonja, Fisher, Mason, & Johnson, 2015) found that odds ratios for overall trauma and schizotypal symptoms across 25 studies ranged from 2.01 to 4.15, with all studies supporting the association. This association was especially strong for positive schizotypal symptoms. However, associations with trauma have been reported for other schizotypal dimensions too, making it difficult to conclude whether the association is particularly specific to positive schizotypal symptoms. Similarly, associations with types of trauma are also broad and it is not clear whether associations are particularly specific to a certain type of trauma.
The association between trauma and schizotypal symptoms, especially positive schizotypal symptoms, is also consistent with other research on psychosis. For instance, self-reported psychotic-like symptoms have been consistently associated with stress and trauma (Kelleher et al., 2013). In addition, again the most established neurobiological correlate of psychosis is increased striatal dopamine. Both animal and human research supports an influence of stress on striatal dopamine, including in people with schizophrenia and in people at clinical high risk for psychosis (Howes et al., 2017). Further, there is also evidence that stress and trauma are associated with increased risk for psychotic disorders, with a host of psychosocial adversity variables associated with increased rate of psychotic disorder. At the same time, there is also evidence that genetic risk for schizophrenia is itself associated with increased risk of experiencing interpersonal trauma (Docherty et al., 2018). Hence, the association between stress and trauma with positive schizotypal symptoms seems consistent with other research on psychosis.
Among psychotic symptoms, perhaps the one symptom most clearly associated with trauma is hallucinations. This has even been found in people who experience hallucinations without a clinical need for care (Longden, Madill, & Waterman, 2012). Further, in people with PTSD without a psychotic disorder diagnosis the occurrence of hallucinations has also been found to be relatively common (Waters, Blom, Jardri, Hugdahl, & Sommer, 2018). This suggests that trauma might be especially associated with unusual perceptual experiences in schizotypal PD. There is also research on the experimental inducement of anomalous experiences in the general population that suggests that our normal perceptual and bodily experience might be constructed from the integration of multiple streams of information (Lenggenhager, Tadi, Metzinger, & Blanke, 2007). When this normal integration is disrupted, it appears surprisingly easy to induce perceptual and bodily distortions (Botvinick & Cohen, 1998). Speculatively, it might be that the experience of trauma induces a less integrated, dissociative processing style which then increases the chance of experiencing future perceptual distortions. At least generally consistent with this, dissociation as a construct is thought to reflect disruption in integrated processing (Lyssenko et al., 2018). Further, both dissociation and trauma have been strongly associated with hallucinations in people with psychotic disorder (Longden et al., 2012). Moreover, dissociation is also strongly associated with positive schizotypy (Cicero & Kerns, 2010). Hence, a potential issue for future research might be to further examine integration of perceptual and bodily experiences and their relation to unusual perceptual experiences in schizotypal PD.
Positive Schizotypal Symptoms and Openness to Experience
As noted earlier, an important question about the nature of schizotypal symptoms, perhaps especially positive and to some extent disorganized schizotypal symptoms, is whether these symptoms are related to increased openness to experience (Widiger et al., 2018). In general, correlations between self-reported positive schizotypal symptoms and broad measures of openness to experience tend to be only weakly to moderately associated (Widiger et al., 2018). A number of different explanations have been proposed to account for why this association is not stronger. One is that openness and positive schizotypal symptoms (or psychoticism; Reichborn-Kjennerud et al., 2017) are distinct, with psychoticism forming a sixth personality factor (Crego & Widiger, 2017; Watson, Clark, & Chmielewski, 2008). Another explanation is that some openness measures may not effectively assess the maladaptive high end of the trait, which might truncate associations with positive schizotypal symptoms (Haigler & Widiger, 2001).
It has also been suggested that positive schizotypal symptoms are only associated with just one or more particular sub-facets of openness (Crego & Widiger, 2017; Sutin, 2017). For instance, some facets of openness reflect adventurousness and liberal values. It is possible that these facets may not be strongly related to positive schizotypal symptoms (DeYoung, Grazioplene, & Peterson, 2012). In contrast, openness facets reflecting imagination and fantasy appear to be more strongly related to positive schizotypal symptoms (Moorman & Samuel, 2018). Further, some conceptualizations of openness or of related constructs include facets such as unconventionality or oddity/eccentricity and these facets might have higher associations with positive schizotypal symptoms (Crego & Widiger, 2017).
A related possibility is that the broader construct of openness reflects both openness and intellect (DeYoung et al., 2012). However, positive schizotypal PD might reflect elevation on only openness and might be associated with decreased intellect (Chmielewski, Bagby, Markon, Ring, & Ryder, 2014; DeYoung, Carey, Krueger, & Ross, 2016). An association with decreased intellect also seems consistent with evidence that schizotypal PD does involve cognitive deficits. And it also seems consistent with the general explanation for magical thinking offered by Risen (2016) that this reflects being high on intuitive and implicit cognition (possibly reflected by increased openness) while being unwilling or unable to use systematic and effortful cognition (possibly reflected by decreased intellect) to counteract the illogical conclusions made by intuitive cognition. Furthermore, openness has been associated with better implicit learning (Kaufman et al., 2010), potentially consistent with an increased reliance on intuitive cognition in people high on openness. However, on the whole, it does not appear that whether and how positive schizotypal symptoms are associated with openness to experience has been resolved. Some tentative conclusions are that positive schizotypal symptoms are not strongly correlated with broad measures of openness, but that some positive schizotypal symptoms are more strongly correlated with particular facets of openness.
Although possible relations between positive schizotypal symptoms and openness are still unclear, there is other converging evidence that does support a relationship between these two constructs. First, openness is associated with some measures of creativity (Sutin, 2017). Further, positive schizotypal symptoms are also associated with measures of creativity, although effect sizes are small in magnitude (Baas, Nijstad, Boot, & De Dreu, 2016). There is also evidence that people who pursue artistic education have an increased risk of schizophrenia (MacCabe et al., 2018). In addition, first-degree relatives of people with schizophrenia might have increased creativity (Kyaga et al., 2011). In particular, first-degree relatives of people with schizophrenia have been found to be more likely to pursue occupations that involve artistic creativity (although perhaps another interpretation of this association is being more likely to pursue less social professions; McGurk et al., 2013). Hence, there is some evidence consistent with links between openness, schizotypal PD, and schizophrenia.
Further, like positive schizotypal symptoms, openness is also associated with increased childhood trauma and abuse; this is specifically true for openness measured in adults but not when measured in children (Sutin, 2017). Moreover, both schizotypal PD and openness have been associated with increased use of cannabis. Schizotypal PD includes odd and eccentric appearance whereas openness is associated with a more distinctive and more messy appearance. In addition, there are theoretical and empirical links between both positive schizotypal symptoms and openness with increased striatal dopamine (Allen & DeYoung, 2017).
And perhaps most importantly, increased openness has been associated with increased genetic risk for schizophrenia based on polygenic risk scores. For instance, Lo et al. (2017) found relations between openness with both schizophrenia and bipolar disorder, with an openness–schizophrenia genetic correlation of .36. In a follow-up study, Smeland et al. (2017) found six genetic loci that overlap between schizophrenia and openness. Finally, Duncan et al. (2018) reported that the genetic correlation between schizophrenia and openness was .21. Hence, it appears that people with increased genetic risk for schizophrenia also tend to score more highly on measures of openness. There is also evidence that increased schizophrenia polygenic risk score, even in people without a family history of schizophrenia, is associated with increased creativity and creative success (Power et al., 2015), again suggesting a genetic association between openness and schizophrenia.
It should be noted that people with schizophrenia actually report decreased openness (Ohi et al., 2016). Perhaps this decrease in openness could reflect the chronic use of antipsychotic medications that block striatal dopamine. It could also reflect pervasive cognitive deficits in schizophrenia that decrease the intellect component of openness. There is also recent evidence suggesting that the cognitive deficits of schizophrenia appear to be strongly related to non-familial risk factors (Kendler, Ohlsson, Mezuk, Sundquist, & Sundquist, 2016). Hence, it is possible that schizophrenia is genetically associated with increased openness yet this relation is somewhat obscured by non-familial cognitive deficits. However, another potential issue with the genetic association between openness and schizophrenia could be possible collider bias (Munafò et al., 2018). For instance, if people with increased genetic risk for schizophrenia are less likely to participate in research and people with increased openness are more likely to participate in research, then this could result in a spuriously more positive polygenic association between openness and schizophrenia (because people with both high schizophrenia genetic risk and low openness would be less likely to be in research samples). On the whole, there are intriguing empirical connections between openness with both schizotypal PD and schizophrenia. However, whether and how these constructs are related is still unresolved.
SPD Treatment
There are few high quality treatment studies of schizotypal PD. For instance, there have been no RCTs for psychotherapy of schizotypal PD (Dixon-Gordon, Turner, & Chapman, 2011). In a non-experimental study, Bartak et al. (2011) did report some evidence that people with Cluster A personality disorders (n = 57, most with paranoid PD) benefited from psychotherapy. Rosell et al. (2014) noted that a still recommended source for information on psychotherapy on schizotypal PD is the paper by Stone (1985).
There have been some pharmacotherapy studies that have examined the use of antipsychotic medication in people with schizotypal PD or with schizotypal symptoms (Raine, 2006). In recent reviews of antipsychotic medication in schizotypal PD, it has been noted that few studies meet standards for high quality, with recommendations that this evidence should be viewed with caution and that no firm clinical recommendations can be made (Jakobsen et al., 2017; Koch et al., 2016). Rosell et al. (2014) also suggested caution because positive schizotypal symptoms may not be the most disturbing or problematic symptoms for people with schizotypal PD. Given the high proportion of people with schizotypal PD who develop schizophrenia, treatment recommendations for people at clinical high risk for schizophrenia might also be relevant.
Rosell et al. (2014) suggested that stimulants might be useful for cognitive deficits in schizotypal PD, although that they need to be closely monitored given risk for psychosis. In contrast, research on antidepressant medication in schizotypal PD has generally not found evidence that supports its efficacy (Chemerinski, Triebwasser, et al., 2013). A source now or in the future for schizotypal PD treatment might be research attempting to treat cognitive deficits (e.g., Bowie, McGurk, Mausbach, Patterson, & Harvey, 2012) and negative symptoms (Grant, Huh, Perivoliotis, Stolar, & Beck, 2012) in schizophrenia. In addition, meta-cognitive training for positive schizotypal symptoms might also prove useful (Moritz et al., 2014).
Conclusions
There is strong evidence that schizotypal PD is a schizophrenia-spectrum disorder and an initial diagnosis of schizotypal PD is a strong predictor of future onset of schizophrenia. Despite this evidence, there are questions about whether schizotypal PD or the other Cluster A disorders as currently diagnosed best reflect traits indicating risk for schizophrenia. Further, it is still not empirically resolved to what extent positive schizotypal symptoms reflect genetic risk for schizophrenia. There is strong evidence that schizotypal PD is related to psychological trauma. At the same time, there is evidence that some schizotypal symptoms do appear to reflect variation on normal personality traits, but it is still unresolved whether and how schizotypal symptoms reflect high levels of openness to experience. Cluster A disorders appear to be more common than often assumed and have been associated with poor functioning, but there is a lack of treatment research on these disorders.
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