Schizotypy

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.

Contents
Development of the concept
The relationship between schizotypy
, mental health and mental illness
Quasi-dimensional approach
Dimensional approach
Fully dimensional approach
Relationship to personality traits
Possible biological bases of schizotypy
Anhedonia
Weakness of inhibitory mechanisms
Negative priming
SAWCI
Attention, working memory, and executive functions
Abnormalities of arousal
Dissociation of different arousal systems
Hyperarousal
Aberrant salience hypothesis

See also
References
Further reading

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 insanityand non-psychotic states. Modern diagnostic systems used in psychiatry (such as the DSM)
maintain this categorical view.[1]

In contrast, psychiatristEugen Bleuler did not believe there was a clear separation betweensanity 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]

Claridge named his concept 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
[4][5]
than had been previously thought and could be broken down into four factors.
 1. Unusual experiences: The disposition to have unusualperceptual and other cognitive experiences, such as
hallucinations, magical or superstitious belief and interpretation of events (see alsodelusions).
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, 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.

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
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 premonitorysymptoms of the disease or merely indications of apredisposition 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
[10]
the combinations of symptoms which are present in the manifest types of the disease.’

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
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
[13]
simply someone occupying the extreme upper end of his ‘psychoticism’ dimension.

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 asschizophrenia, 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

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

Many research studies have examined the relationship between schizotypy and various 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
.[16]
and that there is a continuum between normal personality and schizotypy

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
[19]
cooperativeness and self-directedness may protect against the schizotypal tendencies associated with high self-transcendence.

Possible biological bases of schizotypy

Anhedonia
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 m
ight act as a protecting one.

Weakness of inhibitory mechanisms

Negative priming
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
[27]
schizotypes as a sign that ‘inhibition of distracting information is reduced in schizophrenia and high schizotypes’.

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
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

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
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

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 andautonomic 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
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 1sleep 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

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. 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.[47]

See also
Apparitional experience
Hallucinations
Hallucinations in the sane
Pareidolia
Psychosis
 Psychoticism
Schizoaffective disorder
Schizophrenia
Schizotypal personality disorder
Transliminality

References
1. American Psychiatric Association (1994).DSM IV: Diagnostic and Statistical Manual ofMental Disorders, 4th
Edition. Washington: APA.
2. 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. 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. 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 (http://www.staff.ncl.ac.uk/daniel.nettle/jrp.p
df)
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). Morewords, 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. 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 chronicschizophrenia: 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. 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(ht
tps://doi.org/10.1016/j.psychres.2009.07.018). PMID 20537405 (https://www.ncbi.nlm.nih.gov/pubmed/20537405).
17. 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(https://doi.org/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(https://doi.org/
10.1016/j.comppsych.2004.07.010). PMID 15714195 (https://www.ncbi.nlm.nih.gov/pubmed/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"(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC
2565802). Schizophrenia Research. 104 (1–3): 198–205. doi:10.1016/j.schres.2008.06.025(https://doi.org/10.1016/
j.schres.2008.06.025). PMC 2565802 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2565802) . PMID 18718739
(https://www.ncbi.nlm.nih.gov/pubmed/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 dif ferences 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 Dif
ferences, 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 ef
fects 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 (http://www.celiagreen.com/charlesmccreery/dreams-a
nd-psychosis.pdf)
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, visualpop-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
Lenzenweger, M.F. (2010)" Schizotypy and Schizophrenia: The V iew from Experimental Psychopathology". Guilford
Press, New York. ISBN 978-1-60623-865-3

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