Schizotypy

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In psychology, schizotypy is a theory stating that there is a continuum of personality characteristics and experiences ranging from normal dissociative, imaginative states to more extreme states related to psychosis and in particular, schizophrenia. This is in contrast to a categorical view of psychosis, where psychosis is considered to be a particular (usually pathological) state, that someone either has, or has not.

Development of the concept[edit]

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]

This was picked up by psychologists such as Hans Eysenck and Gordon Claridge who sought to understand this variation in unusual thought and behaviour in terms of personality theory. This was conceptualised by Eysenck as a single personality trait named psychoticism.[3]

Claridge named his concept schizotypy and by examining unusual experiences in the general population and the clustering of symptoms in diagnosed schizophrenia, Claridge's work suggested that this personality trait was much more complex, and could break 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).
  2. Cognitive disorganization: A tendency for thoughts to become derailed, disorganised or tangential (see also formal thought disorder).
  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.
  4. Impulsive nonconformity: The disposition to unstable mood and behaviour particularly with regard to rules and social conventions.

The relationship between schizotypy and mental illness[edit]

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 academic 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.

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’.[9]

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[edit]

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.’[10]

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.’[10]

Later advocates of the quasi-dimensional view of schizotypy are Rado[11] and Meehl,[12] 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[edit]

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.[13]

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[14] (although they are typically present in much less intense forms).

Fully dimensional approach[edit]

Claridge calls the latest version of his model ‘the fully dimensional approach’.[15] 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 personality traits[edit]

Many research studies have examined the relationship between schizotypy and standard models of personality such as the Five factor model.[16] Research has linked the unusual experiences factor to high neuroticism and openness to experience. The introvertive anhedonia factor has been linked to high neuroticism and low extraversion. The cognitive disorganisation factor has 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.[16] Relationships between schizotypy and the Temperament and Character Inventory have also been examined.[17] 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"[17] and research has found that this specific combination of traits is associated with a high "risk" of schizotypy.[18] 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.[17] On the other hand, high levels of cooperativeness and self-directedness may protect against the schizotypal tendencies associated with high self-transcendence.[19]

Possible biological bases of schizotypy[edit]

Anhedonia[edit]

Anhedonia, or a reduced ability to experience pleasure, is a feature of full-blown schizophrenia that was commented on by both Kraepelin[20] 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[21] 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[22] 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[23] 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[24] and L.J. and J.P. Chapman[25] 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[edit]

Various lines of evidence from experimental psychology have suggested a relative weakness of inhibitory mechanisms may be a characteristic of the schizotypal nervous system.

Negative priming[edit]

A number of studies have found that high schizotypes, as measured by questionnaire, show less negative priming than controls.[26] Negative priming is said to occur when a person reacts more slowly than usual to a stimulus which has previously been presented as a distractor and which has therefore had to be ignored. Beech interprets the relative weakness of the negative priming effect in schizotypes as a sign that ‘inhibition of distracting information is reduced in schizophrenia and high schizotypes’.[27]

The reduced negative priming shown by high schizotypes has the interesting effect that they actually perform better on certain tasks (those that require them to respond to previously ignored stimuli) than low schizotypes. This phenomenon may be of significance in the relation to the question of why schizotypy, and indeed schizophrenia itself, is not progressively ‘weeded out’ by the process of natural selection.

SAWCI[edit]

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[28] 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[edit]

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.[29] 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[30]

Many studies have also shown that individuals who exhibit schizotypy features demonstrate deficits in Attention and Working memory.[31][32][33][34]

Abnormalities of arousal[edit]

Claridge[35] 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. This, it was proposed, could lead, both to lability of arousal, and to dissociation of arousal in different parts of the nervous system.

Dissociation of different arousal systems[edit]

Claridge and co-workers[36][37][38] 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[39] 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[edit]

A failure of homeostasis in the central nervous system could lead to episodes of hyper-arousal. Oswald[40] has pointed out that extreme stress and hyper-arousal can lead to sleep as a provoked reaction. McCreery[41][42] 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,[43] which measures proneness to perceptual anomalies such as hallucinations, and the Chapmans’ Hypomania scale,[44] 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,[45] 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[edit]

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.[46] 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 [4]. Symptoms of schizophrenia and schizotypy may arise out of ‘the aberrant assignment of salience to external objects and internal representations’, and antipsychotic medications 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.[47]

See also[edit]

References[edit]

  1. ^ American Psychiatric Association (1994). DSM IV: Diagnostic and Statistical Manual of Mental Disorders, 4th Edition. Washington: APA.
  2. ^ a b c 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. ^ a b 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. ^ a b 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
  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. ^ 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.
  10. ^ a b Bleuler, E. (1911). Dementia Praecox or the Group of Schizophrenias. Translated by J. Zinkin. New York: International Universities Press, Inc. (1950), p. 238.
  11. ^ Rado, S. (1953). Dynamics and classification of disordered behaviour. American Journal of Psychiatry, 110, 406 416.
  12. ^ Meehl, P.E. (1962). Schizotaxia, schizotypy, schizophrenia. American Psychologist, 17, 827 838.
  13. ^ Eysenck, H.J. (1960). Classification and the problems of diagnosis. In H.J. Eysenck, ed., Handbook of Abnormal Psychology. London: Pitman. Pp.1-31.
  14. ^ Liddle, P.F. (1987). The symptoms of chronic schizophrenia: A re-examination of the positive negative dichotomy. British Journal of Psychology, 151, 145 151.
  15. ^ 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.
  16. ^ a b 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. 
  17. ^ a b c 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. 
  18. ^ 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. 
  19. ^ 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. 
  20. ^ Kraepelin, E. (1913). Dementia Praecox and Paraphrenia. Translated by R.M. Barclay. Edinburgh: Livingston, (1919).
  21. ^ Rado, S. (1953). Dynamics and classification of disordered behaviour. American Journal of Psychiatry, 110, 406 416.
  22. ^ Meehl, P.E. (1962). Schizotaxia, schizotypy, schizophrenia. American Psychologist, 17, 827 838.
  23. ^ McCreery, C. and Claridge, G. (2002). Healthy schizotypy: the case of out-of-the-body experiences. Personality and Individual Differences, 32, 141-154.
  24. ^ Kelley, M.P. and Coursey, R.D. (1992). Factor structure of schizotypy scales. Personality and Invividual Differences, 13, 723-731.
  25. ^ 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.
  26. ^ See, for example, 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.
  27. ^ Beech, A.R. (1987). Cognitive Differences and Schizophrenia. Unpublished DPhil thesis, University of Oxford.
  28. ^ Evans, J.L. (1992). Schizotypy and Preconscious Processing. Unpublished D.Phil. thesis, University of Oxford.
  29. ^ 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.
  30. ^ Tsakanikos, E. & Claridge, G. (2005). Less words, more words: psychometric schizotypy and verbal fluency. Personality and Individual Differences, 39, 705-713.
  31. ^ ^ 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.
  32. ^ Tsakanikos, E. (2004). Logical reasoning in schizotypal personality. Personality and Individual Differences, 37, 1717-1726.
  33. ^ 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.
  34. ^ Tsakanikos, E. & Reed, P. (2005). Dimensional approaches to experimental psychopathology: shift learning and schizotypic traits in college students. Journal of Behavior Therapy & Experimental Psychiatry, 36, 300-312.
  35. ^ Claridge, G.S. (1967). Personality and Arousal. Oxford: Pergamon.
  36. ^ 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.
  37. ^ Claridge, G.S. and Birchall, P.M.A. (1978). Bishop, Eysenck, Block and psychoticism. Journal of Abnormal Psychology, 87, 664 668.
  38. ^ 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.
  39. ^ McCreery, C., and Claridge, G. (1996). ‘A study of hallucination in normal subjects – II. Electrophysiological data’. Personality and Individual Differences, 21, 749-758.
  40. ^ Oswald, I. (1962). Sleeping and Waking: Physiology and Psychology. Amsterdam: Elsevier.
  41. ^ 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.
  42. ^ 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
  43. ^ Chapman, L.J., Chapman, J.P. and Raulin, M.L. (1978). Body image aberration in schizophrenia. Journal of Abnormal Psychology, 87, 399 407.
  44. ^ Eckblad, M. and Chapman, L.J. (1986). Development and validation of a scale for hypomanic personality. Journal of Abnormal Personality, 95, 217 233.
  45. ^ 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.
  46. ^ 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.
  47. ^ 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[edit]

  • Claridge, G. (1997) Schizotypy: Implications for Illness and Health. Oxford University Press. ISBN 0-19-852353-X
  • Lenzenweger, M.F. (2010)" Schizotypy and Schizophrenia: The View from Experimental Psychopathology". Guilford Press, New York. ISBN 978-1-60623-865-3