‘Salience syndrome’ replaces ‘schizophrenia’ in DSM-V and ICD-11: psychiatry’s evidence-based entry into the 21st century?


  • J. Van Os

    1. Department of Psychiatry and Neuropsychology, South Limburg Mental Health Research and Teaching Network, EURON, Maastricht University Medical Centre, Maastricht, the Netherlands and Division of Psychological Medicine, Institute of Psychiatry, London SE5 8AF, UK
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  • The author is member of the APA DSM-V Psychotic Disorders Work Group. The views expressed are his own. Parts of this article appeared previously in the British Journal of Psychiatry [Van Os, J. (2009) A salience dysregulation syndrome. British Journal of Psychiatry, 194, 101–3]

  • Invited paper

Prof. Dr J. van Os, Department of Psychiatry and Neuropsychology, Maastricht University Medical Centre, P.O. BOX 616 (DRT10) Maastricht, the Netherlands.
E-mail: j.vanos@sp.unimaas.nl


Objective:  Japan was the first country to abandon the 19th century term of ‘mind-splitting disease’ (schizophrenia). Revisions of DSM and ICD are forthcoming. Should the rest of the world follow Japan’s example?

Method:  A comprehensive literature search was carried out in order to review the scientific evidence for the validity, usefulness and acceptability of current concepts of psychotic disorder.

Results:  The discussion about re-classifying and renaming schizophrenia and other psychotic disorders is clouded by conceptual confusion. First, it is often misunderstood as a misguided attempt to change societal stigma instead of an attempt to change iatrogenic stigma occasioned by the use of misleading and mystifying terminology. Second, the debate is misunderstood as purely semantic, whereas in actual fact it is about the core concepts underlying psychiatric nosology. Third, it has been suggested that the debate is political. However, solid scientific evidence pointing to the absence of nosological validity of diagnostic categories lies at the heart of the argument. Fourth, there is confusion about what constitutes a syndrome (a group of symptom dimensions that cluster in different combinations in different people and for which one or more underlying diseases may or may not be found) and a disease (a nosologically valid entity with specific causes, symptoms, treatment and course).

Conclusion:  Scientific evidence favours a syndromal system of classification combining categorical and dimensional representations of psychosis. The concept of ‘salience’ has the potential to make the public recognize psychosis as relating to an aspect of human mentation and experience that is universal. It is proposed to introduce, analogous to the functional-descriptive term ‘Metabolic syndrome’, the diagnosis of ‘Salience syndrome’ to replace all current diagnostic categories of psychotic disorders. Within Salience syndrome, three subcategories may be identified, based on scientific evidence of relatively valid and specific contrasts, named Salience syndrome with affective expression, Salience syndrome with developmental expression and Salience syndrome not otherwise specified.

Clinical recommendations

  •  A 21st century concept of psychotic disorder refers to an experience that can be understood as a variation of normal human mentation.
  •  A 21st century concept of psychotic disorder can be expressed quantitatively, corresponding with the natural phenotype of psychosis.
  •  A 21st century concept of psychotic disorder makes use of scientific evidence of specificity yielding high diagnostic likelihood ratios rather than evidence of weak mean differences yielding low diagnostic likelihood ratios

Additional comments

  •  Insurance systems, scientific journals, professional groups, educational initiatives, regulatory bodies and organization of services are fixed in 19th century tradition providing natural protection against change.
  •  The existence of two separate diagnostic systems in psychiatry, DSM and ICD, produces a bias that is conservative rather than anti-conservative, reducing the probability of non-cosmetic change.
  •  Funding for diagnostic research is very limited – mental health research thus continues to examine the distribution, determinants and treatments for constructs that do not exist.


A diagnosis in psychiatry ideally should combine the following elements. First, it must be shown that the diagnostic construct of disease has some link with a measurable phenotype in Nature. Second, the diagnostic construct ideally is valid in the classic sense of combining aetiological, symptomatic, prognostic and treatment specificity, setting it apart from other disorders (1). Third, the diagnostic construct is useful and fourth, the diagnostic construct is acceptable to those who are invited to carry its label. Previous authors have cogently argued that these four elements do not apply in combination to the diagnostic construct of schizophrenia and, by implication, all other diagnostic categories of psychotic disorder (2–5).

Aims of the study

This article will analyse to what degree the situation depicted above has changed and what the consequences of this might be for DSM-V and ICD-11.

Material and methods

A literature search was conducted focusing on the topic of diagnosis of psychotic disorders, with special reference to the diagnostic category of schizophrenia and focusing on evidence of natural phenotype, validity, usefulness and acceptability.


The current state of diagnosis

It is not very hard to identify the delusions and hallucinations of psychosis. Classifying these psychotic states, however, remains a major challenge. Psychosis is not exclusive to schizophrenia and occurs across a range of diagnostic categories of psychotic disorder as depicted in Box 1.

Table Box 1..   DSM-IV main diagnostic categories of psychotic disorder, based on current principles of diagnosis taking into account duration, dysfunction, associated substance use, ‘bizarreness’ of delusions, co-presence of depression or mania, presence of somatic disorder and other criteria
Non-affective psychotic disorders
 Schizoaffective disorder
 Schizophreniform disorder
 Delusional disorder
 Brief psychotic disorder
 Psychotic disorder not otherwise specified
Affective psychoses
 Bipolar disorder with psychotic features
 Major depressive disorder with psychotic features
Substance-induced psychotic disorder
 Other substance-induced
Psychotic disorder due to a general medical condition

The criteria used to distinguish between these different categories of psychotic disorder are based on duration, dysfunction, associated substance use, ‘bizarreness’ of delusions and presence of depression or mania. It is quite unlikely, however, that the current diagnoses in Box 1 represent discrete nosological entities (6). Indeed, the diagnostic categories of psychotic disorder show overlap in genetic liability amongst themselves (7) and with bipolar disorder (8–10), suggesting a broad underlying liability that is expressed across the different categories.

Within this cluster of psychotic disorders, the term schizophrenia is applied to a syndrome that is characterized by longer duration, bizarre delusions, negative symptoms and few affective symptoms (non-affective psychosis). Patients who present with a psychotic disorder with fewer negative symptoms, but whose psychosis is preceded by longer-standing affective (depression and mania) symptoms usually will be diagnosed as depression with psychosis or bipolar disorder (affective psychosis).

Currently, the Diagnostic and Statistical Manual of Mental Disorders IV (DSM-IV, the US system of classification) and International Classification of Diseases, 10th version (ICD-10) are used to establish a diagnosis of schizophrenia. It is clear, however, that the various workgroups developing the next generation of the DSM and ICD (DSM-V and ICD-11; expected after 2012) have to find solutions for several difficult diagnostic issues. First, how many disorders ought to be carved out of the current cluster of categories in Box 1 and (how) should a specific category of schizophrenia be defined amongst them? Second, does the diagnosis of schizophrenia refer to a categorical illness (like Huntington’s disease, that one either has or not) or is it a continuous or dimensional concept (like the regularly reviewed boundaries of arterial blood pressure above which hypertension is diagnosed). Finally, does a 19th century expression referring to a state of ‘split mind’ represent a suitable term to diagnose patients in the 21st century?

Schizophrenia: natural phenotype?

The various definitions of schizophrenia and related disorders in DSM, ICD, RDC and other classification systems in practice combine a mix of positive, negative, cognitive, depressive and manic symptoms in a context of need for care (11, 12). However, the symptoms that characterize psychotic patients seen in mental health clinics are also prevalent in the community. For example, a recent meta-analysis reported prevalence and incidence rates of positive psychotic experiences of around 8% and 3% respectively, around 10 respectively 100 times greater than reported rates for psychotic disorder (13). Similar data exist for symptoms and experiences pertaining to the bipolar spectrum (14). Subclinical psychotic experiences are typically expressed in adolescence and young adulthood and are transitory in the great majority of cases (15, 16). There is evidence that these attenuated expressions may be conceived as the transitory behavioural expression of the underlying distributed liability for schizophrenia and related disorders, just as higher levels of blood pressure express higher liability for cardiovascular disease in a dose-response fashion (17). They show a degree of epidemiological, psychopathological, longitudinal, familial and aetiological continuity with schizophrenia and related disorders (13) and even display some syndromal continuity with diagnostic constructs such as schizophrenia. For example, subclinical delusional experiences at the level of the general population are strongly associated with subclinical hallucinatory experiences and, similarly, subclinical positive experiences are associated with depressive symptoms and blunting of affect (18). A degree of syndromal continuity therefore appears to exist linking associated subclinical positive and negative experiences of psychosis in the community to the comorbid positive and negative dimensions of the syndrome called schizophrenia in the mental health clinic. There is evidence, however, that at the level of the general population, positive and negative experiences of psychosis are more loosely associated with each other than at the level of clinical disorder due to the phenomenon of morbidity concentration or Berkson’s bias (19). This is the phenomenon that if both positive and negative symptoms each independently contribute to the risk of developing need for care and subsequent receipt of treatment, diagnosed patients in treatment will always display more comorbidity (Fig. 1). A similar phenomenon of relatively inflated comorbidity of mania and depression has been shown to occur in bipolar disorder (20).

Figure 1.

 Berkson’ s or comorbidity bias: the phenomenon that compared to the level of the community, observed comorbidity coefficients of the dimensions that make up psychotic disorders are much higher at the level of mental health services (MH services), due to the fact that each dimension contributes independently to the risk of developing need for care and subsequent receipt of treatment, resulting in a ‘concentration’ of comorbidity at the level of mental health services. Pos: positive symptom dimension; Neg: negative symptom dimension.

What are the implications of this for diagnosis? First, psychotic disorders appear to be fuzzy in that they blur into normality. The evidence suggests a natural representation of psychotic disorders that is dimensional along a continuum from subclinical expression to psychotic disorder. Second, when a ‘first episode’ of psychotic illness is diagnosed, it may in fact be more correct to conceive of this as the poor and unnaturally comorbid outcome of a natural phenotype of subclinical dimensions of psychosis that is transitory in the great majority of cases (13, 16). Third, if psychotic experiences are frequent, their diagnostic value will be low in relation to the rare disorder of schizophrenia. For example, the probability of having a psychotic disorder given the presence of a psychotic experience in the community is not very high at around 0.25 (21); similarly, the probability of developing a psychotic disorder over a 2-year follow-up period given the presence of psychotic experiences is around 0.08 (15). Even if the follow-up period is extended to more than 15 years, the probability of developing a psychotic disorder does not exceed 25% (22). Therefore, understanding the diagnosis of psychotic disorder in part becomes understanding the onset of need for care in the context of subclinical positive psychotic experiences with variable frequency, distress, preoccupation and influence on behaviour (23). For example, it has been suggested that some environmental risk factors cause psychotic experiences in young people to persist over time, thus increasing the risk of onset of clinical impairments and need for care (24).

Schizophrenia and other psychotic disorders: validity?

Validity: where to look?  A recent Finnish study showed that the total lifetime prevalence of psychotic disorders is 3.5%, divided over 12 different diagnostic categories (25). This prevalence estimate is much higher than any previous investigation has suggested. The question that presents itself is whether the diagnostic distinction between these 12 different categories is valid, or whether they merely represent arbitrary cut-offs across clustered dimensional representations of positive, negative, manic, depressive and substance dependence symptoms in the community. If the diagnostic categories are not valid, it may be argued that the myriade of diagnostic categories in DSM and ICD has created scientific blindness for the true morbidity force of psychotic disorders, thus hampering scientific progress in the field of aetiology, treatment and prognosis. As argued before (2, 3, 26), there is no consistent evidence for specificity in terms of symptoms, aetiology, treatment and prognosis between diagnostic categories such as, for example, schizophrenia, bipolar disorder, brief psychotic disorder, schizophreniform disorder, substance-induced psychotic disorder, psychotic disorder NOS, delusional disorder and psychotic depression. A traditional misunderstanding is to suggest that mean differences between traditional categories have diagnostic relevance. For example, first-rank symptoms may be more common in schizophrenia than in bipolar disorder but their diagnostic value is too low to be of diagnostic significance, as indicated by a diagnostic likelihood ratio (LR; the likelihood of being a true positive rather than a false positive) of lower than 2 (27); an LR of 10 is usually considered evidence of diagnostic value (28). Similarly, patients with schizophrenia have more cognitive impairment and greater levels of negative symptoms than patients with bipolar disorder, but these differences similarly do not translate to diagnostic significance (29–32).

Given the diagnostically low discriminative power of positive symptoms and cognitive impairment, more focus on negative symptoms has been advocated (33). Negative symptoms refer to the observation that patients with schizophrenia may have poverty of speech, display restricted affect and diminished emotional range, and show little interest and a diminished sense of purpose and social drive (social indifference). It has been suggested that to the degree that these phenomena are not caused by positive symptoms, affective symptoms, cognitive impairment, antipsychotic extra-pyramidal side effects, experience of stigma, social exclusion, environmental deprivation or other treatment- and illness-related factors (secondary negative symptoms), they may represent primary negative symptoms as expression of a disease entity within the schizophrenia syndrome (the deficit syndrome) (34). It can be argued that there is a good rational for examining the diagnostic value of negative symptoms, given that (i) the negative symptom dimension is associated with neurocognitive alterations whereas positive and affective dimensions of psychopathology are not (35) and (ii) positive and negative symptoms seem to follow independent longitudinal courses (36). However, while of theoretical interest, the hypothesis of primary negative symptoms may not advance diagnosis at this stage, given the fact that a valid and reliable distinction between secondary and primary negative symptoms is difficult to make cross-sectionally (37) as per definition the removal of secondary causes, if possible (38), is required to diagnose the primary aspect of the negative symptom in question. In addition, the primary/secondary distinction may be conceptually incomplete as an interaction between ‘secondary’ factors and ‘primary’ outcome is likely yet remains to be elucidated (39, 40). For example, patients who are genetically predisposed towards social indifference as primary negative symptom may likely also be the ones at risk of developing indifference after exposure to dopamine D2 receptor-blocking drugs. Finally, the iatrogenic component of primary negative symptoms has received relatively little attention. The first randomized experimental study investigating non-motor antipsychotic-induced negative symptoms (such as indifference, apathy, avolition) was only recently published. This study showed that a single dose of antipsychotic medication in well controls may induce prominent non-motor negative symptoms (41). These findings are not unexpected, given the fact that antipsychotics have long been observed to act by creating indifference, thus correcting ‘aberrant salience’ (42). Therefore, more evidence is needed how negative symptoms and the hypothesis of deficit syndrome can currently contribute to diagnosis in terms of valid distinctions. In fact, research to date suggests that of all psychopathological domains, manic symptoms in particular have the highest level of specificity and represent the best diagnostic value (30, 43).

Valdity: specificity?  ‘Points of rarity’ between diagnostic categories of psychotic disorders in terms of symptoms, aetiology, treatment and prognosis are rare. Nevertheless, some prominent differences are apparent. The problem, however, is that not all observed differences may go in the same direction. For example, Cardno et al. (9) showed that in terms of genetics, most of the liability between schizophrenia and bipolar disorder appears to be shared. However, the environmental risk associated with growing up in an urban environment may be specific for schizophrenia (44). Translating these findings to diagnosis would mean that one aetiological factor favours ‘lumping’, whereas the other favours ‘splitting’. A similar phenomenon exists in relation to cognition. Recent meta-analytic work indicates that in schizophrenia, patients and their first-degree relatives display alterations in neurocognition. The cognitive alterations in patients with a diagnosis of schizophrenia are not qualitatively dissimilar from the alterations seen in bipolar patients. The pattern in bipolar relatives, however, is dissimilar as these, contrary to the schizophrenia relatives, display only minimal cognitive alterations (29, 45). Furthermore, the developmental cognitive impairments preceding the onset of schizophrenia are not detectable in bipolar disorder (46). Therefore, cognitive findings also suggest both ‘lumping’ and ‘splitting’.

In addition, discrepancies in validity can occur across domains of validation. For example, in terms of prognosis, brief psychotic disorder and schizophrenia show clear separation (splitting), whilst in terms of genetics and response to antipsychotic treatment they do not (lumping). Finally, one and the same construct can show divergent diagnostic relevance. For example, the nuclear schizophrenia syndrome characterized by first-rank symptoms is not associated with cognitive impairment and does not strongly predict outcome. Nevertheless, it is highly heritable (47).

In conclusion, correlates of current diagnostic categories of psychotic illness are not consistently specific in terms of classic validation criteria (1). Although there are mean differences and some differences that suggest a degree of diagnostic specificity, these are not consistent and categories in reality represent fuzzy sets blending into each other just as the symptoms that make up the categories are fuzzy in terms of being continuous with normal mentation. The challenge for DSM-V and ICD-11 is to make use of the evidence suggesting specificity, such as the relative specificity of manic symptoms and the relative specificity of developmental impairment between bipolar disorder and schizophrenia (48), while at the same time acknowledging that in many other areas of validation no specificity appears to exist.

Schizophrenia and other psychotic disorders: utility?

Although the diagnostic constructs of DSM, ICD or RDC schizophrenia do not appear to be valid, they may nevertheless be useful ‘by virtue of the information about outcome, treatment response, and aetiology that they convey’, as suggested by Kendell and Jablensky (3). Usefulness is also suggested by anecdotal evidence that patients and their families may find it useful to learn that their difficulties are recognized as an illness with the possibility of treatment. Nevertheless, these assumptions may be questioned. Thus, as explained above, the evidence suggests that the natural phenotype for psychosis is dimensional, with different domains of distributed positive, negative, disorganization, depressive, manic and neurocognitive symptoms that are continuous with normal mentation and relatively non-specific with regard to traditional diagnostic constructs, or at least not specific enough to be of diagnostic value, although there is evidence that changes in distinct psychopathological dimensions during treatment independently and differentially influence outcome (49). A growing number of studies suggests that when in samples of patients with a range of psychotic disorders dimensional representations (i.e. scoring patients’ symptoms along continuous axes of positive, negative, disorganization, depressive, manic and cognitive symptoms) and categorical representations of psychosis (i.e. grouping patients in categories of schizophrenia, bipolar disorder, schizo-affective disorder, schizophreniform disorder, etc.) are compared in terms of the utility criterion of how much information about aetiology, treatment needs and outcome they convey, the combination of categorical and dimensional representations of psychosis in patients with psychotic disorders does better than either representation alone (50–53). In other words: expressing patients’ symptoms not only categorically but also dimensionally may be more useful clinically than either one alone.

Schizophrenia: acceptability?

It may be useful to point out that the discussion about renaming schizophrenia is not about an attempt to change societal stigma by changing the name. Rather, it can be conceived as an attempt to change iatrogenic stigma occasioned by the use of misleading, mystifying and, ultimately, stigma-inducing terminology. The term ‘schizophrenia’ may be considered stigma-inducing by itself because it confusingly and mystifyingly refers to a ‘disease’ that is characterized by a ‘split mind’− a psychological state that the public cannot personally relate to. This is different from, for example, depression, given the fact that virtually every member of the public knows that depression is about a negative emotional state that they themselves may also experience on a daily basis, albeit to a lesser degree. The mystifying 19th century term ‘schizophrenia’, however, does not correspond to any generally known human experience − and therefore is likely to induce fear and exclusion.

In addition, the complicated, albeit ultimately meaningless, greek term suggests that schizophrenia really is a ‘thing’, i.e. a ‘brain disease’ that exists as such in Nature. This is a false suggestion, however, as schizophrenia refers to a syndrome of symptom dimensions that for unknown reasons cluster together in different combinations in different people with different contributions of known risk factors and dramatically different outcomes and response to treatment; no knowledge exists that may help decide to what degree schizophrenia, for example, reflects a single or 20 different underlying diseases – or none at all. Nevertheless, the way mental health professionals use the medical diagnosis of schizophrenia in clinical practice and communication inevitably results in its ‘reification’– or becoming a ‘thing’. As pointed out by Brockington (2), this type of behavioural pseudo-validation and psychiatric reification of a construct that does not exist can expose psychiatry to ridicule and hamper scientific progress.

Finally, while it is often assumed that diagnostic categories in routine clinical practice are, if not valid, at least reliable, research suggests that in practice this is not invariably the case for hybrid categories such as schizo-affective disorder (54). Similarly, considerable reductions in interrater agreement have been observed going from a comparison of clinicians working within the same site to a comparison of clinicians working in different sites (55).

What guides the renaming of schizophrenia?

The Japanese experience.  Although criticisms about the diagnostic construct of schizophrenia may be deflected with the argument that it is merely a syndrome (i.e. the association of several clinically recognizable features that often occur together for which one or more specific disorders may or may not be identified as the underlying cause) that has the same status as did ‘dropsy’ in 19th century medicine (56), the problem, described above, is that the way mental health professionals use and communicate about the term inevitably results in medical reification through behavioural pseudo-validation. It may be argued, therefore, that if it is a syndrome, calling it as such may serve to remind professionals, and downstream of these the rest of the world, of the relatively agnostic state of science in this regard. For the same reason, giving it a more modest descriptive name analogous to, for example, the ‘metabolic syndrome’ in internal medicine may reduce the risk of pseudo-validation. In fact, research suggests that clinicians are increasingly reluctant to use the term ‘schizophrenia’ (57). In Japan, the name for schizophrenia was changed in 2002, at the request of patients’ families, in order to reduce stigma and move away from the Kraepelinian ‘dementia praecox’ tradition to a modern stress-vulnerability model. Subsequent research suggests that the change resulted in uptake of the new name in 78% of cases and a doubling of the proportion of patients who were informed about their diagnosis – from 37% to 70% (58). In addition, 86% of psychiatrists found the new term more suitable to inform patients of the diagnosis as well as to explain the modern concept of the disorder (58).

Linking psychosis to normal human mentation.  It may be argued that the potential for a new name for schizophrenia to induce stigma may be inversely proportional to the degree in which the general public can make a ‘translation’ to their own process of mentation and experience. A scientifically valid theory exists that attempts to bridge the gulf between the level of biological alterations and the level of actual experiences reported by patients (42). This theory is based on knowledge that the dopamine system fires in response to novel rewards in the environment and that the released dopamine leads to a switch in attention and behaviour towards the rewarding situation – thus imbuing the stimulus with ‘motivational salience’ (59, 60). It has been proposed (42), with support from some recent fMRI studies (61, 62), that an aberrant firing of the dopamine system would lead to the aberrant assignment of motivational salience to objects, peoples and actions (63). The patient then makes an effort to interpret these aberrant experiences and constructs a seemingly plausible (to them) account to understand the changing world. Thus, a mixture of bottom-up dopamine dysregulation and aberrant assignment of salience to stimuli, coupled with a top-down cognitive scheme that attempts to grapple with these experiences to give them meaning is thought to lead to the development of psychotic symptoms (64). Alterations in affective state (depression or mania) as well as some thinking styles, such as a tendency to ‘jump to conclusions’ may combine with the bottom-up dopamine dysfunction to increase the risk of delusion formation (65). It is proposed that this knowledge may be useful in the discussion about re-conceptualizing schizophrenia and other psychotic disorders as described below.

A Salience syndrome

Many people with impaired glucose regulation also have several other continuous cardiovascular risk factors – they have a tendency to occur together. This disorder is referred to as the ‘metabolic syndrome’. Although the pathogenesis of the metabolic syndrome and each of its dimensional components is not completely understood, central obesity and insulin resistance are now recognized as important factors. If a dimensional component of the metabolic syndrome rises above a certain threshold, a dichotomous need for care may arise. For example, if blood pressure rises, the individual may need treatment for hypertension. Similarly, high values on one or more components of the metabolic syndrome increase the risk for coronary heart disease, diabetes and other disorders.

Analogous to the metabolic syndrome, many people with positive psychotic experiences also display evidence of alterations in other dimensions of psychopathology such as mania, disorganization and information processing deficits. This may be referred to as the ‘Salience syndrome’, reflecting the broad syndromal nature of what is now called schizophrenia and other psychotic disorders (66). If the values of the dimensional components of the Salience syndrome rise above a certain threshold, need for care may arise. Depending on which combinations of dimensional psychopathology are most prominent, and taking into account which elements have been shown to possess the best diagnostic specificity, as discussed above, the categorical representation of the combinations of dimensional psychopathology pertaining to the Salience syndrome may be categorized as Salience syndrome with affective expression (high in mania/depression dimension), Salience syndrome with developmental expression (high in developmental cognitive deficit/negative symptoms) and Salience syndrome not otherwise specified (Fig. 2). The first two subcategories of Salience syndrome (Salience syndrome with affective expression and Salience syndrome with developmental expression) are based on evidence of specificity while the more agnostic category of Salience syndrome not otherwise specified reflects the continuing gap in knowledge.

Figure 2.

 Salience syndrome. Six dimensions that tend to co-occur make up SDS, along which individuals may make the transition from Risk to Need for care if they pass the threshold on one or more dimensions, resulting in subcategories of: With Affective Expression, With Developmental Expression and Not Otherwise Specified. Axis Cat: Categorical Axis; Axis Dim: Dimensional Axis. N.O.S.: Not Otherwise Specified. Patient A: ‘typical’ Salience syndrome with developmental expression; Patient B: ‘typical’ Salience syndrome with affective expression; Patient C: Salience syndrome Not Otherwise Specified. Please note that position of subcategories and dimensions with respect to each other is arbitrary. Reprinted with permission of British Journal of Psychiatry (67).


The term ‘salience’ may appear obscurantist at first glance. However, a more detailed analysis may reveal why it is suitable. As explained earlier, the term ‘schizophrenia’ is stigma-inducing because it confusingly and mystifyingly refers to a disease that is characterized by a ‘split mind’− a psychological state that the public cannot personally relate to. If schizophrenia were to be called ‘reality distortion syndrome’ or ‘integration dysregulation syndrome’, the meaning of the words would certainly be clear to the general public, but these names paradoxically may also have a high potential to induce stigma because the people cannot relate to a universal psychological function of ‘reality’ or ‘integration’. How comfortable would the public be talking to somebody who ‘cannot see reality’ or is ‘not integrated’? In other words: it may not be the degree of immediate and easy recognition that is important for a new name for schizophrenia, but rather (i) the potential of the new name to teach the general public about the experiences the are currently considered psychotic, based on (ii) a scientifically valid model and (iii) an aspect of psychological experience/mentation that everybody can relate to. The reality, of course, is that this is never going to be easy and cannot be resolved by an appealing name alone. Salience is about how internal or external stimuli can become attention-grabbing and how this, if it is not willed, can lead to perplexing experiences that result in a search for an explanation that are subsequently recognized as delusions (42). It is argued that describing this cognitive process requires some effort, but does not constitute an impossible message to convey. Therefore, the focus perhaps should not be on whether or not a new concept of psychotic disorder is immediately clear to the general public, but on whether it has the potential to make people recognize it as relating to an aspect of mentation that is universal. Salience, and by implication the Salience syndrome, may be a vehicle to teach the general public about the experiences we call psychotic.

Declaration of interest