In psychology, schizotypy is a theoretical concept that posits a continuum of personality characteristics and experiences, ranging from normal dissociative, imaginative states to extreme states of mind related to psychosis, especially schizophrenia. The continuum of personality proposed in schizotypy is in contrast to a categorical view of psychosis, wherein psychosis is considered a particular (usually pathological) state of mind, which the person either has or does not have.

Development of the concept

The categorical view of psychosis is most associated with Emil Kraepelin, who created criteria for the medical diagnosis and classification of different forms of psychotic illness. Particularly, he made the distinction between dementia praecox (now called schizophrenia), manic depressive insanity and non-psychotic states. Modern diagnostic systems used in psychiatry (such as the DSM) maintain this categorical view.[1]

In contrast, psychiatrist Eugen Bleuler did not believe there was a clear separation between sanity and madness, believing instead that psychosis was simply an extreme expression of thoughts and behaviours that could be present to varying degrees throughout the population.[2]

The concept of psychosis as a spectrum was further developed by psychologists such as Hans Eysenck and Gordon Claridge, who sought to understand unusual variations in thought and behaviour in terms of personality theory. Eysenck conceptualised cognitive and behavioral variations as all together forming a single personality trait, psychoticism.[3]

Meehl et al. 1964 first coined the term 'schizotypy,' and through examination of unusual experiences in the general population and clustering of symptoms in individuals diagnosed with schizophrenia. The work of Claridge suggested that this personality trait was more complex than had been previously thought and could be broken down into four factors.[4][5]

  1. Unusual experiences: The disposition to have unusual perceptual and other cognitive experiences, such as hallucinations, magical or superstitious belief and interpretation of events (see also delusions). This factor is also often referred to as "positive schizotypy" and "cognitive-perceptual" schizotypy
  2. Cognitive disorganization: A tendency for thoughts to become derailed, disorganised or tangential (see also formal thought disorder). This factor is also often referred to as "disorganized schizotypy"
  3. Introverted anhedonia: A tendency to introverted, emotionally flat and asocial behaviour, associated with a deficiency in the ability to feel pleasure from social and physical stimulation. This factor is also often referred to as "negative schizotypy" and "schizoidia"
  4. Impulsive nonconformity: The disposition to unstable mood and behaviour particularly with regard to rules and social conventions.

The relationship between schizotypy, mental health and mental illness

Although aiming to reflect some of the features present in diagnosable mental illness, schizotypy does not necessarily imply that someone who is more schizotypal than someone else is more ill. For example, certain aspects of schizotypy may be beneficial. Both the unusual experiences and cognitive disorganisation aspects have been linked to creativity and artistic achievement.[6] Jackson[7] proposed the concept of 'benign schizotypy' in relation to certain classes of religious experience, which he suggested might be regarded as a form of problem-solving and therefore of adaptive value. The link between positive schizotypy and certain facets of creativity[8] is consistent with the notion of a "healthy schizotypy", which may account for the persistence of schizophrenia-related genes in the population despite their many dysfunctional aspects. The extent of schizotypy can be measured using certain diagnostic tests, such as the O-LIFE.[9]

However, the exact nature of the relationship between schizotypy and diagnosable psychotic illness is still controversial. One of the key concerns that researchers have had is that questionnaire-based measures of schizotypy, when analysed using factor analysis, do not suggest that schizotypy is a unified, homogeneous concept. The three main approaches have been labelled as 'quasi-dimensional', 'dimensional' and 'fully dimensional'.[10]

Each approach is sometimes used to imply that schizotypy reflects a cognitive or biological vulnerability to psychosis, although this may remain dormant and never express itself, unless triggered by appropriate environmental events or conditions (such as certain doses of drugs or high levels of stress).

Quasi-dimensional approach

The quasi-dimensional model may be traced back to Bleuler[2] (the inventor of the term 'schizophrenia'), who commented on two types of continuity between normality and psychosis: that between the schizophrenic and his or her relatives, and that between the patient's premorbid and post-morbid personalities (i.e. their personality before and after the onset of overt psychosis).

On the first score he commented: 'If one observes the relatives of our patients, one often finds in them peculiarities which are qualitatively identical with those of the patients themselves, so that the disease appears to be only a quantitative increase of the anomalies seen in the parents and siblings.'[11]

On the second point, Bleuler discusses in a number of places whether peculiarities displayed by the patient before admission to hospital should be regarded as premonitory symptoms of the disease or merely indications of a predisposition to develop it.

Despite these observations of continuity Bleuler himself remained an advocate of the disease model of schizophrenia. To this end he invoked a concept of latent schizophrenia, writing: 'In [the latent] form, we can see in nuce [in a nutshell] all the symptoms and all the combinations of symptoms which are present in the manifest types of the disease.'[11]

Later advocates of the quasi-dimensional view of schizotypy are Rado[12] and Meehl,[13] according to both of whom schizotypal symptoms merely represent less explicitly expressed manifestations of the underlying disease process which is schizophrenia. Rado proposed the term 'schizotype' to describe the person whose genetic make-up gave him or her a lifelong predisposition to schizophrenia.

The quasi-dimensional model is so called because the only dimension it postulates is that of gradations of severity or explicitness in relation to the symptoms of a disease process: namely schizophrenia.

Dimensional approach

The dimensional approach, influenced by personality theory, argues that full blown psychotic illness is just the most extreme end of the schizotypy spectrum and there is a natural continuum between people with low and high levels of schizotypy. This model is most closely associated with the work of Hans Eysenck, who regarded the person exhibiting the full-blown manifestations of psychosis as simply someone occupying the extreme upper end of his 'psychoticism' dimension.[14]

Support for the dimensional model comes from the fact that high-scorers on measures of schizotypy may meet, or partially fulfill, the diagnostic criteria for schizophrenia spectrum disorders, such as schizophrenia, schizoaffective disorder, schizoid personality disorder and schizotypal personality disorder. Similarly, when analyzed, schizotypy traits often break down into similar groups as do symptoms from schizophrenia[15] (although they are typically present in much less intense forms).

Fully dimensional approach

Claridge calls the latest version of his model 'the fully dimensional approach'.[16] However, it might also be characterised as the hybrid or composite approach, as it incorporates elements of both the disease model and the dimensional one.

On this latest Claridge model, schizotypy is regarded as a dimension of personality, normally distributed throughout the population, as in the Eysenck model. However, schizophrenia itself is regarded as a breakdown process, quite distinct from the continuously distributed trait of schizotypy, and forming a second, graded continuum, ranging from schizotypal personality disorder to full-blown schizophrenic psychosis.

The model is characterised as fully dimensional because, not only is the personality trait of schizotypy continuously graded, but the independent continuum of the breakdown processes is also graded rather than categorical.

The fully dimensional approach argues that full blown psychosis is not just high schizotypy, but must involve other factors that make it qualitatively different and pathological.

Relationship to other personality traits and sociodemographics

Many research studies have examined the relationship between schizotypy and various standard models of personality, such as the five factor model.[17] Research has linked the unusual experiences factor to high neuroticism and openness to experience. Unusual experience in combination with positive affectivity also appears to predict religiosity/spirituality.[18] One study found that a moderate level of unusual experiences predicted increased religiosity, but a high level of unusual experiences predicted lower religiosity, and that impulsive non-conformity was associated with lower religiosity, as well as lower values of tradition and conformity.[19] The introvertive anhedonia factor has been linked to high neuroticism and low extraversion. The cognitive disorganisation factor as well as the impulsive non-conformity factor have been linked to low conscientiousness. It has been argued that these findings provide evidence for a fully dimensional model of schizotypy and that there is a continuum between normal personality and schizotypy.[17]

Relationships between schizotypy and the Temperament and Character Inventory have also been examined.[20] Self-transcendence, a trait associated with openness to "spiritual" ideas and experiences, has moderate positive associations with schizotypy, particularly with unusual experiences. Cloninger described the specific combination of high self-transcendence, low cooperativeness, and low self-directedness as a "schizotypal personality style"[20] and research has found that this specific combination of traits is associated with a "high risk" of schizotypy.[21] Low cooperativeness and self-directedness combined with high self-transcendence may result in openness to odd or unusual ideas and behaviours associated with distorted perceptions of reality.[20] On the other hand, high levels of cooperativeness and self-directedness may protect against the schizotypal tendencies associated with high self-transcendence.[22]

One study examined the relationship between the dimensional MBTI scales, and found that schizotypy was associated with a tendency toward introversion, intuition (as opposed to sensing), thinking (as opposed to feeling), and prospecting (as opposed to judging), which can be represented by the "INTP" personality type in the MBTI model.[23] Intuition is conceptually similar to the Big Five "openness to experience" trait which is thought to be increased in schizotypy, thinking represents the tendency to prefer objectivity and evidence in making decisions and forming beliefs and is conceptually similar to the lower level "intellect" factor of openness in the Big Five, and prospecting is conceptually similar to low conscientiousness in the Big Five.

Schizotypy shows positive associations with traits that are associated with fast life history strategies, including increased sociosexuality (characterized by increased effort for short term sexual relationships, lower effort for long term sexual relationships, increased total amount of sexual partners, and lower sexual disgust) and impulsivity.[24][25]

Personality disorders

Schizotypy shows positive associations with overall psychopathy, however when considering the primary and secondary factors of psychopathy, schizotypy is associated with lower primary psychopathy (also called fearless dominance) and higher secondary psychopathy (also called self-centered impulsivity, or disinhibition).[26] Narcissism is negatively associated with schizotypy,[27] (though persons high in schizotypy may experience grandiose delusions[28] and a sense of deviance and enlightenment (idionomia),[29] which may be mistaken for narcissism) and borderline personality traits are positively associated with schizotypy [30] as well hypomanic personality traits.[31] Schizotypy also shows positive relationships with schizoid, paranoid, and avoidant personality traits,[32] and a negative relationship with obsessive-compulsive personality traits (particularly with disorganized schizotypy).[33] In contrast to obsessive-compulsive personality disorder, obsessive-compulsive disorder shows a positive relationship with schizotypy.[34]

Cognitive function

There is evidence that schizotypy correlates with differentially enhanced and impaired aspects of cognitive function. These findings include schizotypy being positively associated with enhanced global processing over local processing,[35][36] lower latent inhibition,[37][38][39] attention & memory deficits,[40] enhanced creativity & imagination,[41] and enhanced associative thinking.[42]

Autism

Correlational studies of schizotypy and autistic traits tend to find positive correlations, most strongly with negative schizotypy, to a lesser extent disorganized schizotypy, and weak, absent, or negative correlations with positive schizotypy.[43][34][44] Diagnosed schizophrenia and autism spectrum disorder (ASD) also overlap statistically.

However, several researchers have suggested that positive correlations between schizotypy and autism are not necessarily evidence of overlap, but rather are due to a lack of specificity of measurements for autistic and schizotypal traits, and the confounding variable of social difficulties and social-cognitive dysfunction which occur in both autism and schizotypy.[45][46][47][48][49] Researchers have suggested that high comorbidity between diagnosed ASD and schizophrenia are highly unreliable and misleading due to a severe inadequacy of the DSM and diagnostic interviews for differential diagnosis.[50][51][52][53][54][55][56][57][58][59] Studies which show apparent overlap between the causes of autism and the causes of schizotypy also have significant methodological issues.[60][45][61]

Multiple evolutionary theories of schizotypy place schizotypy and autistic traits at opposite poles of a continuum, with relation to traits such as theory of mind,[47][62] life history and mating strategies,[46] "mentalistic" or creative cognition and "mechanistic" cognition,[63][53] and predictive processing.[64] In agreement with this, schizotypy (particularly positive, impulsive, and disorganized schizotypy) shows a negative association with autistic traits when controlling for social difficulty, which has been well replicated across different countries, scales, methods, and independent research teams, and a diametric autism-schizotypy continuum factor emerges through factor analysis.[44][65][25][66][67][68][69] Notably, some studies find a direct negative association with positive schizotypy and autistic traits even when social difficulty is not controlled for.[70][34]

Some researchers have interpreted these findings as indicating that autistic and schizotypal traits are both overlapping and diametrical in different aspects, with autistic social difficulties and negative schizotypal symptoms being a shared dimension, and positive, disorganized, and impulsive schizotypy as a dimension that is diametrically opposed to autism.[67][71]

Possible biological bases of schizotypy

Cognitive imbalances and tradeoffs

Predictive processing

Andersen (2022) put forth a model of schizotypy based on the predictive processing framework, where lower importance is attributed to sensory prediction errors for updating beliefs in individuals with high schizotypy.[64] Essentially, this means that schizotypy is a cognitive-perceptual specialization for processing chaotic and noisy data, where patterns and relationships exist but can only be detected if minor inconsistencies are ignored (i.e., focusing on the 'big picture'). Andersen suggests that a tradeoff exists in predictive processing, where giving higher weight to prediction errors prevents the detection of false patterns (i.e. apophenia) at the cost of being unable to detect higher level patterns, and giving lower weight to prediction errors allows for the detection of higher level patterns at the cost of occasionally detecting patterns that don't exist, as in delusions and hallucinations that occur in schizotypy. This model explains features of schizotypy and previous models of schizotypy, such as the hyper-mentalizing model originally proposed by Abu-Akel (1999),[47] hyper-associative cognition,[72] the hyper-imagination model by Crespi (2016),[73] antagonomia (acting in ways directly opposing societal values) and idiosyncratic worldviews,[29] attentional differences such as latent inhibition,[74] hyper-openness,[75] increased exploratory behavior,[76] and enhanced cognitive abilities in insight problem solving, creativity, and global processing.[77]

Hormone abnormalities

Oxytocin & testosterone

There is some evidence to suggest that abnormalities in the regulation of oxytocin & testosterone are related to schizotypy. Crespi (2015) provides evidence that schizophrenia and related disorders may involve increased or dysregulated oxytocin, and relatively decreased testosterone, leading to "hyper-developed" social cognition,[78] although Crespi's model of schizotypy has been criticized.[79] Evidence for oxytocin's role in schizotypy includes genes associated with higher oxytocin levels being associated with higher levels of positive schizotypy,[80] blood oxytocin levels positively associated with schizotypy in females,[81] ratio of genes associated with low testosterone and high oxytocin positively associated with schizotypy and negatively with autistic traits,[82] oxytocin levels being associated with higher social anxiety,[83] and oxytocin being associated with global processing, divergent thinking, and creativity,[84] which are also strongly associated with schizotypy.[42]

Anhedonia

Anhedonia, or a reduced ability to experience pleasure, is a feature of full-blown schizophrenia that was commented on by both Kraepelin[85] and Bleuler.[2] However, they regarded it as just one among a number of features that tended to characterise the ‘deterioration’, as they saw it, of the schizophrenic's emotional life. In other words, it was an effect, rather than a cause, of the disease process.

Rado[86] reversed this way of thinking, and ascribed anhedonia a causal role. He considered that the crucial neural deficit in the schizotype was an ‘integrative pleasure deficiency’, i.e. an innate deficiency in the ability to experience pleasure. Meehl[87] took on this view, and attempted to relate this deficiency to abnormality in the dopamine system in the brain, which is implicated in the human reward system.

Questionnaire research on schizotypy in normal subjects is ambiguous with regard to the causal role, if any, of anhedonia. Nettle[6] and McCreery and Claridge[88] found that high schizotypes as measured by factor 1 (above) scored lower than controls on the introverted anhedonia factor, as if they were particularly enjoying life.

Various writers, including Kelley and Coursey[89] and L.J. and J.P. Chapman[90] suggest that anhedonia, if present as a pre-existent trait in a person, may act as a potentiating factor, whereas a high capacity for hedonic enjoyment might act as a protecting one.

Weakness of inhibitory mechanisms

Negative priming

Negative priming is "the ability of a preceding stimulus to inhibit the response to a subsequent stimulus."[91] Individuals diagnosed with schizophrenia or schizotypy exhibit “reduced or abolished NP [negative priming], especially in the presence of positive symptomatology, acute psychosis, high severity of symptoms, and/or lack of medication.”[92]

SAWCI

The phenomenon of semantic activation without conscious identification (SAWCI) is said to be displayed when a person shows a priming effect from the processing of consciously undetectable words. For example, a person who has just been shown the word ‘giraffe’, but at a speed at which he or she was not able consciously to report what it was, may nevertheless identify more quickly than usual another animal word on the next trial. Evans[93] found that high schizotypes showed a greater priming effect than controls in such a situation. She argued that this could be accounted for by a relative weakness of inhibitory mechanisms in the semantic networks of high schizotypes.

Attention, working memory, and executive functions

Schizotypy symptoms have been related to deficits in executive functions, which entails the psychological processes that supersede habitual inclinations with novel responses and behaviors to fulfill important goals. In particular, when schizotypy is elevated, the ability to filter out task-irrelevant stimuli may be impaired.[74] That is, participants who score highly on schizotypy tend to fail to ignore a previously preexposed, non-reinforced stimulus as compared to a non-preexposed, novel and potentially important event.

Enhanced performance on verbal fluency has been associated with high levels of positive schizotypy, i.e. increased reports of hallucination-like experiences, delusional ideation, and perceptual aberrations. However, decreased performance was associated with negative schizotypy, such as anhedonia.[94]

Many studies have also shown that individuals who exhibit schizotypy features demonstrate deficits in attention and working memory.[95][96][97][98]

Abnormalities of arousal

Claridge[99] suggested that one consequence of a weakness of inhibitory mechanisms in high schizotypes and schizophrenics might be a relative failure of homeostasis in the central nervous system. It was proposed that this could lead to both lability of arousal and dissociation of arousal in different parts of the nervous system.

Dissociation of different arousal systems

Claridge and co-workers[100][101][102] have found various types of abnormal co-variation between different psychophysiological variables in schizotypes, including between measures of cortical and autonomic arousal.

McCreery and Claridge[103] found evidence of a relative activation of the right cerebral hemisphere as compared with the left in high schizotypes attempting to induce a hallucinatory episode in the laboratory. This suggested a relative dissociation of arousal between the two hemispheres in such people as compared with controls.

Hyperarousal

A failure of homeostasis in the central nervous system could lead to episodes of hyper-arousal. Oswald[104] has pointed out that extreme stress and hyper-arousal can lead to sleep as a provoked reaction. McCreery[105][106] has suggested that this could account for the phenomenological similarities between Stage 1 sleep and psychosis, which include hallucinations, delusions, and flattened or inappropriate affect (emotions). On this model, high schizotypes and schizophrenics are people who are liable to what Oswald calls 'micro-sleeps', or intrusions of Stage 1 sleep phenomena into waking consciousness, on account of their tendency to high arousal.

In support of this view McCreery points to the high correlation that has been found to exist[5] between scores on the Chapmans' Perceptual Aberration scale,[107] which measures proneness to perceptual anomalies such as hallucinations, and the Chapmans' Hypomania scale,[108] which measures a tendency to episodes of heightened arousal. This correlation is found despite the fact that there is no overlap of item content between the two scales.

In the clinical field there is also the paradoxical finding of Stevens and Darbyshire,[109] that schizophrenic patients exhibiting the symptom of catatonia can be aroused from their apparent stupor by the administration of sedative rather than stimulant drugs. They wrote: 'The psychic state in catatonic schizophrenia can be described as one of great excitement (i.e., hyperalertness)[…] The inhibition of activity apparently does not alter the inner seething excitement.'

It is argued that such a view would be consistent with the model that suggests schizophrenics and high schizotypes are people with a tendency to hyper-arousal.

Aberrant salience hypothesis

Kapur (2003) proposed that a hyperdopaminergic state, at a "brain" level of description, leads to an aberrant assignment of salience to the elements of one's experience, at a "mind" level.[110] Dopamine mediates the conversion of the neural representation of an external stimulus from a neutral bit of information into an attractive or aversive entity, i.e. a salient event. Symptoms of schizophrenia and schizotypy may arise out of ‘the aberrant assignment of salience to external objects and internal representations’; and antipsychotic medications may reduce positive symptoms by attenuating aberrant motivational salience, via blockade of the Dopamine D2 receptors (Kapur, 2003). There is no evidence however on a link between attentional irregularities and enhanced stimulus salience in schizotypy.[111]

See also

References

  1. ↑ American Psychiatric Association (1994). DSM IV: Diagnostic and Statistical Manual of Mental Disorders, 4th Edition. Washington: APA.
  2. 1 2 3 Bleuler, E. (1911). Dementia Praecox or the Group of Schizophrenias. Translated by J. Zinkin. New York: International Universities Press, Inc. (1950).
  3. ↑ See, for example, Eysenck, H.J. (1992). The Definition and Meaning of Psychoticism. Personality and Individual Differences, 13, 757-785.
  4. ↑ Bentall, R.P., Claridge, G. and Slade, P.D. (1989). The multi dimensional nature of schizotypal traits: a factor analytic study with normal subjects. British Journal of Clinical Psychology, 28, 363-375.
  5. 1 2 Claridge, G., McCreery, C., Mason, O., Bentall, R., Boyle, G., Slade, P., & Popplewell, D. (1996). The factor structure of 'schizotypal' traits: A large replication study. British Journal of Clinical Psychology, 35, 103-115.
  6. 1 2 Nettle, D. (2006). Schizotypy and mental health amongst poets, visual artist, and mathematicians. Journal of Research in Personality, 40, 876-890. Also available online: Nettle, 2006 Archived 2019-10-14 at the Wayback Machine
  7. ↑ Jackson, M. (1997). Benign schizotypy? The case of religious experience. In G. Claridge, ed., Schizotypy, implications for illness and health. Oxford: Oxford University Press. Pp. 227-250
  8. ↑ ^ Tsakanikos, E. & Claridge, G. (2005). More words, less words: Verbal fluency as a function of 'positive' and 'negative' schizotypy. Personality and Individual Differences, 39, 705-713
  9. ↑ Mason, Oliver; Claridge, Gordon (2006-02-28). "The Oxford-Liverpool Inventory of Feelings and Experiences (O-LIFE): Further description and extended norms". Schizophrenia Research. 82 (2): 203–211. doi:10.1016/j.schres.2005.12.845. ISSN 0920-9964. PMID 16417985. S2CID 24021218. Archived from the original on 2012-04-23. Retrieved 2020-08-10.
  10. ↑ For a discussion of these three variant models, see McCreery, C. and Claridge, G. (2002). Healthy schizotypy: the case of out-of-the-body experiences. Personality and Individual Differences, 32, 141-154.
  11. 1 2 Bleuler, E. (1911). Dementia Praecox or the Group of Schizophrenias. Translated by J. Zinkin. New York: International Universities Press, Inc. (1950), p. 238.
  12. ↑ Rado, S. (1953). Dynamics and classification of disordered behaviour. American Journal of Psychiatry, 110, 406 416.
  13. ↑ Meehl, P.E. (1962). Schizotaxia, schizotypy, schizophrenia. American Psychologist, 17, 827 838.
  14. ↑ Eysenck, H.J. (1960). Classification and the problems of diagnosis. In H.J. Eysenck, ed., Handbook of Abnormal Psychology. London: Pitman. Pp.1-31.
  15. ↑ Liddle, P.F. (1987). The symptoms of chronic schizophrenia: A re-examination of the positive negative dichotomy. British Journal of Psychology, 151, 145 151.
  16. ↑ See, for example, Claridge, G. and Beech, T. (1995). Fully and quasi-dimensional constructions of schizotypy. In Raine, A., Lencz, T., and Mednick, S.A., Schizotypal Personality. Cambridge: Cambridge University Press.
  17. 1 2 Asai, Tomohisa; Sugimori, Eriko; Bando, Naoko; Tanno, Yoshihiko (2011). "The hierarchic structure in schizotypy and the five-factor model of personality". Psychiatry Research. 185 (1–2): 78–83. doi:10.1016/j.psychres.2009.07.018. PMID 20537405. S2CID 27852689.
  18. ↑ Schuurmans‐Stekhoven, James Benjamin (2013). "Is God's call more than audible? A preliminary exploration using a two‐dimensional model of theistic/Spiritual beliefs and experiences". Australian Journal of Psychology. 65 (3): 146–155. doi:10.1111/ajpy.12015. S2CID 143149239.
  19. ↑ Hanel, Paul; Demmrich, Sarah; Uwe, Wolfradt (April 2019). "Centrality of Religiosity, Schizotypy, and Human Values: The Impact of Religious Affiliation". {{cite journal}}: Cite journal requires |journal= (help)
  20. 1 2 3 Laidlaw, Tannis M.; Dwivedi, Prabudha; Naito, Akira; Gruzelier, John H. (2005). "Low self-directedness (TCI), mood, schizotypy and hypnotic susceptibility". Personality and Individual Differences. 39 (2): 469. doi:10.1016/j.paid.2005.01.025.
  21. ↑ Danelluzo, E.; Stratta, P.; Rossi, A. (Jan–Feb 2005). "The contribution of temperament and character to schizotypy multidimensionality". Comprehensive Psychiatry. 46 (1): 50–5. doi:10.1016/j.comppsych.2004.07.010. PMID 15714195.
  22. ↑ Smith, Matthew J.; Cloninger, C.R.; Harms, M.P.; Csernansky, J.G. (September 2008). "Temperament and character as schizophrenia-related endophenotypes in non-psychotic siblings". Schizophrenia Research. 104 (1–3): 198–205. doi:10.1016/j.schres.2008.06.025. PMC 2565802. PMID 18718739.
  23. ↑ Coolidge, Frederick L.; Segal, Daniel L.; Hook, Julie; Yamazaki, T. G.; Ellett, Julie (2001-04-05). "An empirical investigation of Jung's psychological types and personality disorder features". ResearchGate. pp. 33–36. Retrieved 2023-05-07.
  24. ↑ Jonason, Peter; Zeigler-Hill, Virgil; Hashmani, Talia (2018). "Love, Sex, and Personality Pathology: A Life History View of Personality Pathologies and Sociosexuality". The Journal of Sex Research. 56 (2): 239–248. doi:10.1080/00224499.2018.1471444. PMID 29792522. S2CID 43933601.
  25. 1 2 Del Giudice, Marco; Klimczuk, Amanda; Traficonte, Daniel; Maestripieri, Dario (September 2014). "Autistic-like and schizotypal traits in a life history perspective: diametrical associations with impulsivity, sensation seeking, and sociosexual behavior". Evolution and Human Behavior. 35 (5): 415–424. doi:10.1016/j.evolhumbehav.2014.05.007. hdl:2318/1852742. S2CID 15222379.
  26. ↑ Ragsdale, Katie; Bedwell, Jeffrey (July 2013). "Relationships between dimensional factors of psychopathy and schizotypy". Frontiers in Psychology. 4: 482. doi:10.3389/fpsyg.2013.00482. PMC 3724119. PMID 23898320.
  27. ↑ Lang, Andras; Birkas, Bela; Laszlo, Martin; Nagy, Tunde; Kallai, Janos (December 2018). "Schizotypal Traits and the Dark Triad From an Ecological Perspective: A Nonclinical Sample Study". Psychological Reports. 121 (6): 996–1012. doi:10.1177/0033294117742655. PMID 29298579. S2CID 25933710.
  28. ↑ Peters, Emmanuelle; Joseph, Stephen; Day, Samantha; Garety, Philippa (2004). "Measuring delusional ideation: the 21-item Peters et al. Delusions Inventory (PDI)". Schizophrenia Bulletin. 30 (4): 1005–1022. doi:10.1093/oxfordjournals.schbul.a007116. PMID 15954204.
  29. 1 2 Stanghellini, Giovanni; Ballerini, Massimo (2007). "Values in persons with schizophrenia". Schizophrenia Bulletin. 33: 131–141. doi:10.1093/schbul/sbl036. PMC 2632282. PMID 16940339.
  30. ↑ Baryshnikov, I; Suvisaari, J; Aaltonen, K; Koivisto, M; Naatanen, P; Karpov, B; Melartin, T; Oksanen, J; Suominen, K; Heikkinen, M; Paunio, T; Joffe, G; Isometsa, E (March 2016). "Self-reported symptoms of schizotypal and borderline personality disorder in patients with mood disorders". European Psychiatry. 33: 37–44. doi:10.1016/j.eurpsy.2015.12.006. hdl:10138/223888. PMID 26854985. S2CID 5528433.
  31. ↑ Kemp, Kathryn; Gross, Georgina; Barrantes-Vidal, Neus; Kwapil, Thomas (October 2018). "Association of Positive, Negative, and Disorganized Schizotypy Dimensions with Affective Symptoms and Experiences" (PDF). Psychiatry Research. 270: 1143–1149. doi:10.1016/j.psychres.2018.10.031. PMID 30366639. S2CID 53096126.
  32. ↑ Kwapil, Thomas; Clark, Haley; Rbeiz, Katrina; Kemp, Kathryn; Barramtes-Vidal, Neu (2022). "Association of positive, negative, and disorganized schizotypy with cluster a, borderline, and avoidant personality disorders and traits". Personality Disorders: Theory, Research, and Treatment. 13 (2): 182–191. doi:10.1037/per0000488. PMID 33856836. S2CID 233258410.
  33. ↑ Kemp, Kathryn; Kaczorowski, Jessica; Burgin, Christopher; Raulin, Michael; Lynam, Donald; Sleep, Chelsea; Miller, Joshua; Barrantes-Vidal, Neus; Kwapil, Thomas (December 2022). "Association of Multidimensional Schizotypy with PID-5 Domains and Facets". Journal of Personality Disorders. 36 (6): 680–700. doi:10.1521/pedi.2022.36.6.680. PMID 36454161. S2CID 254123754.
  34. 1 2 3 Wakabayashi, Akio; Baron-Cohen, Simon; Ashwin, Chris (September 2011). "Do the traits of autism-spectrum overlap with those of schizophrenia or obsessive-compulsive disorder in the general population?". Research in Autism Spectrum Disorders. 6 (2): 717–725. doi:10.1016/j.rasd.2011.09.008.
  35. ↑ Russell-Smith, Suzanna; Maybery, Murray; Bayliss, Donna (August 2010). "Are the autism and positive schizotypy spectra diametrically opposed in local versus global processing?". Journal of Autism and Developmental Disorders. 40 (8): 968–77. doi:10.1007/s10803-010-0945-7. PMID 20108115. S2CID 22836209.
  36. ↑ Panton, Kirsten; Badcock, Johanna; Dickinson, J; Badcock, David (October 2018). "Poorer Integration of Local Orientation Information Occurs in Students With High Schizotypal Personality Traits". Frontiers in Psychiatry. 9: 518. doi:10.3389/fpsyt.2018.00518. PMC 6207847. PMID 30405458.
  37. ↑ Gray, Nicola; Fernandez, Michelle; Williams, Jayne; Ruddle, Roy; Snowden, Robert (September 2002). "Which schizotypal dimensions abolish latent inhibition?". The British Journal of Clinical Psychology. 41 (Pt 3): 271–84. doi:10.1348/014466502760379136. PMID 12396255.
  38. ↑ Schmidt-Hansen, Mia; Killcross, A; Honey, R (January 2009). "Latent inhibition, learned irrelevance, and schizotypy: assessing their relationship". Cognitive Neuropsychiatry. 14 (1): 11–29. doi:10.1080/13546800802664539. PMID 19214840. S2CID 12303331.
  39. ↑ Kraus, Michael; Rapisarda, Attilio; Lam, Max; Thong, Jamie; Lee, Jimmy; Subramaniam, Mythily; Collinson, Simon; Chong, Siow; Keefe, Richard (August 2016). "Disrupted latent inhibition in individuals at ultra high-risk for developing psychosis". Schizophrenia Research. Cognition. 6: 1–8. doi:10.1016/j.scog.2016.07.003. PMC 5514297. PMID 28740818.
  40. ↑ Ettinger, Ulrich; Mohr, Christine; Gooding, Diane; Cohen, Alex (March 2015). "Cognition and Brain Function in Schizotypy: A Selective Review". Schizophrenia Bulletin. 41 (Suppl 2): S417-26. doi:10.1093/schbul/sbu190. PMC 4373634. PMID 25810056.
  41. ↑ Crespi, Bernard; Leach, Emma; Dinsdale, Natalie; Mokkonen, Mikael; Hurd, Peter (May 2016). "Imagination in human social cognition, autism, and psychotic-affective conditions" (PDF). Cognition. 150: 181–99. doi:10.1016/j.cognition.2016.02.001. PMID 26896903. S2CID 12026641.
  42. 1 2 Mohr, Christine; Claridge, Gordon (March 2015). "Schizotypy—Do Not Worry, It Is Not All Worrisome". Schizophrenia Bulletin. 41 (Suppl 2): S436-43. doi:10.1093/schbul/sbu185. PMC 4373632. PMID 25810058.
  43. ↑ Russell-Smith, Suzanna; Maybery, Murray; Bayliss (2011). "Relationships between autistic-like and schizotypy traits: An analysis using the Autism Spectrum Quotient and Oxford-Liverpool Inventory of Feelings and Experiences". Personality and Individual Differences. 51 (2): 128–132. doi:10.1016/j.paid.2011.03.027.
  44. 1 2 Sierro, Guillaume; Rossier, Jerome; Mohr, Christine (2016). "Validation of the French Autism Spectrum Quotient Scale and its relationships with schizotypy and Eysenckian personality traits". Comprehensive Psychiatry. 68: 147–155. doi:10.1016/j.comppsych.2016.03.011. PMID 27234196.
  45. 1 2 Crespi, Bernard (February 2020). "How is quantification of social deficits useful for studying autism and schizophrenia?". Psychological Medicine. 50 (3): 523–525. doi:10.1017/S0033291719003180. PMID 31753058. S2CID 208229316.
  46. 1 2 Del Giudice, Marco (2018). "Evolutionary psychopathology: A unified approach". doi:10.1093/med-psych/9780190246846.001.0001. ISBN 978-0-19-024684-6. {{cite journal}}: Cite journal requires |journal= (help)
  47. 1 2 3 Abu-Akel, Ahmad (1999). "Impaired theory of mind in schizophrenia". Pragmatics & Cognition. 7 (2): 247–282. doi:10.1075/pc.7.2.02abu.
  48. ↑ Kaufman, Scott. "A Call for New Measures of Asperger's and Schizotypy". Scientific American.
  49. ↑ Parvais, Rizwan; Vindbjerg, Erik; Crespi, Bernard; Happe, Francesca; Schalbroeck, Rik; Al-Sayegh, Zainab; Danielsen, Ida-Marie; Tonge, Bruce; Videbech, Poul; Abu-Akel, Ahmad (March 2023). "Protocol for the development and testing of the schiZotypy Autism Questionnaire (ZAQ) in adults: a new screening tool to discriminate autism spectrum disorder from schizotypal disorder". BMC Psychiatry. 23 (1): 200. doi:10.1186/s12888-023-04690-3. PMC 10044373. PMID 36978026.
  50. ↑ Parnas, Josef; Bovet, Pierre (October 2014). Psychiatry made easy: operation(al)ism and some of its consequences. Oxford University Press. pp. 190–212. doi:10.1093/med/9780198725978.003.0023. {{cite book}}: |work= ignored (help)
  51. ↑ Zandersen, Maja; Parnas, Josef (January 2018). "Identity Disturbance, Feelings of Emptiness, and the Boundaries of the Schizophrenia Spectrum". Schizophrenia Bulletin. 45: 106–113. doi:10.1093/schbul/sbx183. PMC 6293220. PMID 29373752.
  52. ↑ Borsboom, Denny; Cramer, Angelique; Schmittmann, Verena; Epskamp, Sacha; Waldorp, Lourens (November 2011). "The Small World of Psychopathology". PLOS ONE. 6 (11): e27407. Bibcode:2011PLoSO...627407B. doi:10.1371/journal.pone.0027407. PMC 3219664. PMID 22114671.
  53. 1 2 Crespi, Bernard (May 2016). "The Evolutionary Etiologies of Autism Spectrum and Psychotic Affective Spectrum Disorders". Evolutionary Thinking in Medicine. pp. 299–327. doi:10.1007/978-3-319-29716-3_20. ISBN 978-3-319-29714-9.
  54. ↑ Kinghorn, Warren (November 2020). "Crisis in Psychiatric Diagnosis? Epistemological Humility in the DSM Era". The Journal of Medicine and Philosophy: A Forum for Bioethics and Philosophy of Medicine. 45 (6): 581–597. doi:10.1093/jmp/jhaa026.
  55. ↑ Del Giudice, Marco (2014). "A Tower Unto Heaven: Toward an Expanded Framework for Psychopathology". Psychological Inquiry. 25 (3–4): 394–413. doi:10.1080/1047840X.2014.925339. hdl:2318/1852747. S2CID 219727698.
  56. ↑ Poletti, Michele; Raballo, Andrea (2020). "Childhood schizotypal features vs. high-functioning autism spectrum disorder: Developmental overlaps and phenomenological differences". Schizophrenia Research. 223: 53–58. doi:10.1016/j.schres.2020.09.027. PMID 33046336. S2CID 222211985.
  57. ↑ Nilsson, Maria; Arnfred, Sidse; Carlsson, Jessica; Nylander, Lena; Pedersen, Lennart; Lykke Mortensen, Erik; Handest, Peter (May 2019). "Self-Disorders in Asperger Syndrome Compared to Schizotypal Disorder: A Clinical Study". Schizophrenia Bulletin. 46: 121–129. doi:10.1093/schbul/sbz036. PMC 6942161. PMID 31050761.
  58. ↑ Perlman, Lawrence (2000). "Adults with Asperger disorder misdiagnosed as schizophrenic". Professional Psychology: Research and Practice. 31 (2): 221–225. doi:10.1037/0735-7028.31.2.221.
  59. ↑ Parnas, Josef (October 2015). "Differential diagnosis and current polythetic classification". World Psychiatry. 14 (3): 284–287. doi:10.1002/wps.20239. PMC 4592642. PMID 26407775.
  60. ↑ Konstantin, Grace E.; Nordgaard, Julie; Henriksen, Mads Gram (2023-05-10). "Methodological issues in social cognition research in autism spectrum disorder and schizophrenia spectrum disorder: a systematic review". Psychological Medicine. Cambridge University Press. 53 (8): 3281–3292. doi:10.1017/s0033291723001095. ISSN 0033-2917. PMC 10277762. PMID 37161884. S2CID 258590475.
  61. ↑ Stanghellini, Giovanni; Ballerini, Massimo (2011). "What Is It like to Be a Person with Schizophrenia in the Social World? A First-Person Perspective Study on Schizophrenic Dissociality – Part 2: Methodological Issues and Empirical Findings". Psychopathology. S. Karger AG. 44 (3): 183–192. doi:10.1159/000322638. ISSN 0254-4962. PMID 21412032. S2CID 41205817.
  62. ↑ Crespi, Bernard; Badcock, Christopher (June 2008). "Psychosis and autism as diametrical disorders of the social brain". The Behavioral and Brain Sciences. 31 (3): 241–61, discussion 261-320. doi:10.1017/S0140525X08004214. PMID 18578904.
  63. ↑ Nettle, Daniel (October 2005). "Schizotypy and mental health amongst poets, visual artists, and mathematicians". Journal of Research in Personality. 40 (6): 876–890. doi:10.1016/j.jrp.2005.09.004.
  64. 1 2 Andersen, Brett (November 2022). "Autistic-Like Traits and Positive Schizotypy as Diametric Specializations of the Predictive Mind". Perspectives on Psychological Science (Preprint). 17 (6): 1653–1672. doi:10.1177/17456916221075252. PMID 35816687. S2CID 242788588.
  65. ↑ Dinsdale, Natalie; Hurd, Peter; Wakabayashi, Akio; Elliot, Mick; Crespi, Bernard (2013). "How Are Autism and Schizotypy Related? Evidence from a Non-Clinical Population". PLOS ONE. 8 (5): e63316. Bibcode:2013PLoSO...863316D. doi:10.1371/journal.pone.0063316. PMC 3655150. PMID 23691021.
  66. ↑ Luca, Tarasi; Borgomaneri, Sara; Romei, Vincenzo (April 2023). "Antivax attitude in the general population along the autism-schizophrenia continuum and the impact of socio-demographic factors". Frontiers in Psychology. 14. doi:10.3389/fpsyg.2023.1059676. PMC 10161933. PMID 37151316.
  67. 1 2 Nenadic, Igor; Meller, Tina; Evermann, Ulrika; Schmitt, Simon; Pfarr, Julia-Katharina; Abu-Akel, Ahmad; Grezellschak, Sarah (May 2021). "Subclinical schizotypal vs. autistic traits show overlapping and diametrically opposed facets in a non-clinical population". Schizophrenia Research. 231: 32–41. doi:10.1016/j.schres.2021.02.018. PMID 33744683. S2CID 232272664.
  68. ↑ Zhang, Rui-ting; Zhou, Han-yu; Wang, Yong-ming; Yang, Zhuo-ya; Wang, Yi; So, Suzanne H.; Chiu, Chui-De; Leung, Patrick W.L.; Cheung, Eric F.C.; Chan, Raymond C.K. (August 2019). "Network analysis of schizotypal personality traits and their association with other subclinical psychiatric features". Asian Journal of Psychiatry. 44: 209–216. doi:10.1016/j.ajp.2019.08.005. ISSN 1876-2018. PMID 31419738. S2CID 201041246.
  69. ↑ Zhou, Han-yu; Yang, Han-xue; Gong, Jing-bo; Cheung, Eric F.C.; Gooding, Diane C.; Park, Sohee; Chan, Raymond C.K. (October 2019). "Revisiting the overlap between autistic and schizotypal traits in the non-clinical population using meta-analysis and network analysis". Schizophrenia Research. 212: 6–14. doi:10.1016/j.schres.2019.07.050. ISSN 0920-9964. PMID 31387828. S2CID 199467413.
  70. ↑ Hudson, Matthew; Santavirta, Severi; Putkinen, Vesa; Seppälä, Kerttu; Sun, Lihua; Karjalainen, Tomi; Karlsson, Henry K.; Hirvonen, Jussi; Nummenmaa, Lauri (26 March 2022), Neural responses to biological motion distinguish autistic and schizotypal traits in the general population, Cold Spring Harbor Laboratory, doi:10.1101/2022.03.24.485704
  71. ↑ Masters, Julia; Kaufman, Scott. "How is creativity differentially related to autism spectrum and schizotypy?" (PDF).
  72. ↑ Fyfe, Sophie; Williams, Claire; Mason, Oliver; Pickup, Graham (2008). "Apophenia, theory of mind and schizotypy: Perceiving meaning and intentionality in randomness". Cortex. 44 (10): 1316–1325. doi:10.1016/j.cortex.2007.07.009. PMID 18635161. S2CID 5711711.
  73. ↑ Crespi, Bernard; Leach, Emma; Dinsdale, Natalie; Mokkonen, Mikael; Hurd, Peter (February 2016). "Imagination in human social cognition, autism, and psychotic-affective conditions". Cognition. 150: 181–199. doi:10.1016/j.cognition.2016.02.001. PMID 26896903. S2CID 12026641.
  74. 1 2 Shrira, A. & Tsakanikos, E. (2009). Latent inhibition as a function of schizotypal symptoms: evidence for a bi-directional model. Personality and Individual Differences, 47, 922-927.
  75. ↑ DeYoung, Colin; Grazioplene, Rachael; Peterson, Jordan (February 2012). "From madness to genius: The Openness/Intellect trait domain as a paradoxical simplex". Journal of Research in Personality. 46: 63–78. doi:10.1016/j.jrp.2011.12.003.
  76. ↑ Andersen, Brett; Al-Shawaf, Laith; Bearden, Rachel (November 2021). "Positive schizotypy predicts migration intentions and desires". Personality and Individual Differences. 182: 111096. doi:10.1016/j.paid.2021.111096.
  77. ↑ Mohr, Christine; Claridge, Gordon (March 2015). "Schizotypy—do not worry, it is not all worrisome". Schizophrenia Bulletin. 41 (Suppl 2): S436–S443. doi:10.1093/schbul/sbu185. PMC 4373632. PMID 25810058.
  78. ↑ Crespi, Bernard (2015). "Oxytocin, testosterone, and human social cognition" (PDF). Biological Reviews. 91 (2): 390–408. doi:10.1111/brv.12175. PMID 25631363. S2CID 24096994.
  79. ↑ Ragsdale, Gillian; Foley, Robert (July 2012). "Testing the imprinted brain: parent-of-origin effects on empathy and systemizing". Evolution and Human Behavior. 33 (4): 402–410. doi:10.1016/j.evolhumbehav.2011.12.002.
  80. ↑ Crespi, Bernard; Summers, Kyle (February 2014). "Inclusive fitness theory for the evolution of religion" (PDF). Animal Behaviour. 92: 313–323. doi:10.1016/j.anbehav.2014.02.013. S2CID 53199549.
  81. ↑ Tseng, Hsiu; Chi, Mei; Lee, Lan-Ting; Tsai, Hsin; Lee, I; Chen, Kao; Yang, Yen; Chen, Po (April 2014). "Sex-specific associations between plasma oxytocin levels and schizotypal personality features in healthy individuals". Journal of Psychiatric Research. 51: 37–41. doi:10.1016/j.jpsychires.2013.12.011. PMID 24411593.
  82. ↑ Crespi, Bernard; Hurd, Peter (June 2015). "Genetically based correlates of serum oxytocin and testosterone in autism and schizotypy". Personality and Individual Differences. 79: 39–43. doi:10.1016/j.paid.2015.01.052.
  83. ↑ Hoge, Elizabeth; Pollack, Mark; Kaufman, Rebecca; Zak, Paul; Simon, Naomi (August 2008). "Oxytocin Levels in Social Anxiety Disorder". CNS Neuroscience & Therapeutics. 14 (3): 165–170. doi:10.1111/j.1755-5949.2008.00051.x. PMC 6494012. PMID 18801109.
  84. ↑ De Dreu, Carsten; Baas, Matthijs; Roskes, Marieke; Sligte, Daniel; Ebstein, Richard; Chew, Soo; Jiang, Yushi; Mayseless, Naama; Shamay-Tsoory, Simone (August 2014). "Oxytonergic circuitry sustains and enables creative cognition in humans". Social Cognitive and Affective Neuroscience. 9 (8): 1159–65. doi:10.1093/scan/nst094. PMC 4127019. PMID 23863476.
  85. ↑ Kraepelin, E. (1913). Dementia Praecox and Paraphrenia. Translated by R.M. Barclay. Edinburgh: Livingston, (1919).
  86. ↑ Rado, S. (1953). Dynamics and classification of disordered behaviour. American Journal of Psychiatry, 110, 406 416.
  87. ↑ Meehl, P.E. (1962). Schizotaxia, schizotypy, schizophrenia. American Psychologist, 17, 827 838.
  88. ↑ McCreery, C. and Claridge, G. (2002). Healthy schizotypy: the case of out-of-the-body experiences. Personality and Individual Differences, 32, 141-154.
  89. ↑ Kelley, M.P. and Coursey, R.D. (1992). Factor structure of schizotypy scales. Personality and Individual Differences, 13, 723-731.
  90. ↑ Chapman, L.J., Chapman, J.P., Kwapil, T.R, Eckblad, M., & Zinser, M.C. (1994). Putatively psychosis-prone subjects 10 years later. Journal of Abnormal Psychology, 103, 171 183.
  91. ↑ "APA Dictionary of Psychology". dictionary.apa.org. Retrieved 2022-01-21.
  92. ↑ Frings, Christian; Schneider, Katja Kerstin; Fox, Elaine (2015-12-01). "The negative priming paradigm: An update and implications for selective attention". Psychonomic Bulletin & Review. 22 (6): 1577–1597. doi:10.3758/s13423-015-0841-4. ISSN 1531-5320. PMID 25917144.
  93. ↑ Evans, J.L. (1992). Schizotypy and Preconscious Processing. Unpublished D.Phil. thesis, University of Oxford.
  94. ↑ Tsakanikos, E. & Claridge, G. (2005). Less words, more words: psychometric schizotypy and verbal fluency. Personality and Individual Differences, 39, 705-713.
  95. ↑ ^ Beech, A.R. and Claridge, G.S. (1987). Individual differences in negative priming: Relations with schizotypal personality traits. British Journal of Clinical Psychology, 78, 349-356.
  96. ↑ Tsakanikos, E. (2004). Logical reasoning in schizotypal personality. Personality and Individual Differences, 37, 1717-1726.
  97. ↑ Tsakanikos, E., & Reed, P. (2003). Visuo-spatial processing and dimensions of schizotypy: figure-ground segregation as a function of psychotic-like features. Personality and Individual Differences, 35, 703-712.
  98. ↑ Tsakanikos, E. & Reed, P. (2005). Dimensional approaches to experimental psychopathology: shift learning and schizotypic traits in college students. Journal of Behavior Therapy and Experimental Psychiatry, 36, 300-312.
  99. ↑ Claridge, G.S. (1967). Personality and Arousal. Oxford: Pergamon.
  100. ↑ Claridge, G.S. and Clark, K.H. (1982). Covariation between two flash threshold and skin conductance level in first breakdown schizophrenics: Relationships in drug free patients and effects of treatment. Psychiatry Research, 6, 371 380.
  101. ↑ Claridge, G.S. and Birchall, P.M.A. (1978). Bishop, Eysenck, Block and psychoticism. Journal of Abnormal Psychology, 87, 664 668.
  102. ↑ Claridge, G.S., Robinson, D.L. and Birchall, P.M.A. (1985). Psychophysiological evidence of `psychoticism' in schizophrenics' relatives. Personality and Individual Differences, 6, 1 10.
  103. ↑ McCreery, C., and Claridge, G. (1996). ‘A study of hallucination in normal subjects – II. Electrophysiological data’. Personality and Individual Differences, 21, 749-758.
  104. ↑ Oswald, I. (1962). Sleeping and Waking: Physiology and Psychology. Amsterdam: Elsevier.
  105. ↑ McCreery, C. (1997). Hallucinations and arousability: pointers to a theory of psychosis. In Claridge, G. (ed.): Schizotypy, Implications for Illness and Health. Oxford: Oxford University Press.
  106. ↑ McCreery, C. (2008). Dreams and psychosis: a new look at an old hypothesis. Psychological Paper No. 2008-1. Oxford: Oxford Forum. Also available online: McCreery 2008 Archived 2019-02-04 at the Wayback Machine
  107. ↑ Chapman, L.J., Chapman, J.P. and Raulin, M.L. (1978). Body image aberration in schizophrenia. Journal of Abnormal Psychology, 87, 399 407.
  108. ↑ Eckblad, M. and Chapman, L.J. (1986). Development and validation of a scale for hypomanic personality. Journal of Abnormal Personality, 95, 217 233.
  109. ↑ Stevens, J.M. and Darbyshire, A.J. (1958). Shifts along the alert-repose continuum during remission of catatonic 'stupor' with amobarbitol. Psychosomatic Medicine, 20, 99-107.
  110. ↑ Kapur, S. (2003). Psychosis as a state of aberrant salience: a framework linking biology, phenomenology, and pharmacology in schizophrenia. American Journal of Psychiatry,160, 13–23.
  111. ↑ Tsakanikos, E. (2004). Latent inhibition, visual pop-out and schizotypy: is disruption of latent inhibition due to enhanced stimulus salience?Personality and Individual Differences, 37, 1347-1358.

Further reading

  • Claridge, G. (1997) Schizotypy: Implications for Illness and Health. Oxford University Press. ISBN 0-19-852353-X
This article is issued from Wikipedia. The text is licensed under Creative Commons - Attribution - Sharealike. Additional terms may apply for the media files.