Schizotypy

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.

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).

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.

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]

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]

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]

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]

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, 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.

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]

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.

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]

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.

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.

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.

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]