Skip to main content

Aberrant salience correlates with psychotic dimensions in outpatients with schizophrenia spectrum disorders



Aberrant salience is a well-known construct associated with the development and maintenance of psychotic symptoms in schizophrenia. However, only a few studies have investigated aberrance salience as a trait, with no study investigating the association between the five aberrant salience domains and psychotic symptoms. We aimed to explore the role of aberrant salience and its domains on psychotic dimensions in both clinically remitted and non-remitted patients.


A sample of 102 patients diagnosed with schizophrenia spectrum disorders was divided according to the Positive and Negative Syndrome Scale (PANSS) remission criteria into two groups: remitted and non-remitted. Differences regarding psychotic symptomatology assessed by the PANSS and aberrant salience measured by the Aberrant Salience Inventory (ASI) were explored. Finally, a correlation analysis between the PANSS and the ASI was run.


Significantly higher ASI scores were evident among non-remitted patients. Positive symptoms (i.e. delusions, conceptual disorganization, and hallucinatory behaviour) and general psychopathology (i.e. postural mannerisms, unusual thought content) were correlated to the aberrant salience subscales ‘sharpening of senses’, ‘heightened emotionality’ and ‘heightened cognition’ and with the ASI total score. Significant correlations emerged between negative symptoms (blunted affect and social withdrawal) and ‘heightened cognition'. Finally, lack of spontaneity of conversation was related to the subscales ‘heightened emotionality’ and ‘heightened cognition’, as well as to the ASI total score.


These preliminary results support the hypothesis of an association between aberrant salience and psychotic symptoms in schizophrenia. Further research is needed, especially into the mechanisms underlying salience processing, in addition to social and environmental factors and cognitive variables.


Aberrant salience is a well-known construct associated with the development and maintenance of psychotic symptoms [1]. Much has been speculated about the origin of delusions; current knowledge considers that delusions are caused and maintained by dysregulated discharges of dopaminergic neurons that force patients to focus their attention to otherwise irrelevant external stimuli, thus attributing a pathological and wrong meaning. This phenomenon is known as ‘aberrant salience attribution’ [2,3,4]. This aberrant relevance causes a conflict that could be cognitively resolved with the creation of the first delusional thought and, eventually, end in complete delusion with a self-sustaining course [4, 5]. Thus, delusions might represent a cognitive strain to sort out confusing and unintelligible stimuli that make sense of subsequent aberrant salient experiences, whereas hallucinations may reflect a direct experience of aberrant salience [4]. Indeed, according to the original Kapur’s conceptualization, hallucinations are aberrant perceptions belonging to the wide model of psychosis, also defined as exaggerated, amplified, and aberrantly recognized internal percepts. In this framework, hallucinations arise from the internal representations of percepts and memories, with a huge gradation of severity, ranging from stimuli similar to own “internal thoughts” up to clear “voices” coming from without [4].

There is some evidence on the role of aberrant salience in schizophrenia, even if the results are somewhat inconsistent and inconclusive [6]. Data from measures of aberrant salience, such as the Salience Attribution Task (SAT) [7] and the Aberrant Salience Inventory (ASI) [8], which measure implicit (behavioural) and explicit (self-report) aberrant and adaptive salience, respectively, show increased aberrant salience in patients with schizophrenia compared to controls [8, 9]. Additionally, aberrant salience is associated with abnormal beliefs [10], perceptual aberration and magical ideation [8, 11] in individuals with no history of psychosis, as well as in individuals at ultra-high risk (UHR) to develop psychosis and first-episode psychosis (FEP) patients [12,13,14], suggesting also a link between aberrant salience and the risk of developing psychosis.

Conversely, data from other studies with the SAT suggest that salience is normal in schizophrenia [7, 15] and several studies did not find any direct relationship between the ASI and the SAT [6].

The aberrant salience hypothesis of schizophrenia may also be extended to explain social cognition impairments and negative symptoms [16]. Indeed, findings suggest that the degree of salience coding in the prefrontal cortex could be inversely correlated with anhedonia [17]. Disrupted salience processing, including the salience network and a disconnection of the salience and reward networks, may account for the lack of motivation in patients with schizophrenia [18]; nevertheless, only a few studies have supported the relationship between the salience network and negative symptoms [19].

To date, only one study has evaluated the association between the aberrant salience ‘trait’ and psychotic symptoms, in a mixed sample that also included patients with schizophrenia [20]. However, the authors only found an association between first rank symptoms and aberrant salience, regardless of the diagnosis, and found no correlation between aberrant salience and positive/negative symptoms or general psychopathology assessed by the Positive and Negative Syndrome Scale (PANSS).

To the best of our knowledge, no studies have investigated the association between the five aberrant salience domains—feelings of increased significance, sense sharpening, impending understanding, heightened emotionality and heightened cognition—according to Kapur’s conceptualization [4] and psychotic symptoms in patients affected by schizophrenia spectrum disorders (SSD).

We hypothesize that the aberrant salience trait and its domains are related to more severe general psychopathology as well as positive and negative symptoms. Therefore, the goal of this study was to investigate the relationship between aberrant salience and psychotic symptoms in a sample of SSD patients, according to clinical remission state. In particular, we aimed to study the correlation between each aberrant salience subdomain and psychosis, to better understand their relationships.


Participants and procedures

This cross-sectional study was carried out at the Psychiatry Unit of the University Hospital Mater Domini of Catanzaro (Italy) in accordance with the latest version of the Declaration of Helsinki [21]. The study protocol was approved by the local research ethics committee. All patients signed written informed consent before any data were collected.

A total of 122 outpatients aged 18–65 years were consecutively recruited from August 2019 to August 2020. Following current definition of SSD [22, 23], we included all patients with a diagnosis of schizophrenia or schizoaffective disorder according to Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) criteria [24], formulated through the Structured Clinical Interview for DSM-5 (SCID-5-CV) [25] by experienced psychiatrists who used these tools in their daily clinical practice, after a minimum follow-up period of 12 months in our unit. The daily dose of prescribed antipsychotic drugs was expressed as the equivalent daily dose of chlorpromazine, based on the international consensus study [26].

We settled on the following exclusion criteria: (1) patients with schizotypal personality disorder, brief limited intermittent psychotic symptoms (BLIPS), delusional disorder, or acute psychotic episode (according to clinical evaluation); (2) patients diagnosed with dementia, intellectual disability or other severe medical conditions associated with psychiatric symptoms potentially biasing assessment; (3) patients with active substance abuse in the last 6 months; (4) patients affected by conditions that did not allow them to complete the assessment, such as language problems, dyslexia or lack of knowledge of Italian language; and (5) those who have not provided valid informed consent.

Of the 122 patients initially enrolled in the study, 20 were excluded. Seven patients (5.7%) dropped out before the end of the assessment and thus were excluded from the study, and 13 (10.7%) were not eligible for various reasons: five patients were not interested in participating and eight met the exclusion criteria (i.e. intellectual disability, active substance use). Thus, the final sample was made up of 102 participants (dropout rate 16.4%) who completed the study, including:

  • • 78 patients diagnosed with schizophrenia

  • • 24 patients diagnosed with schizoaffective disorder

Then, the sample was divided into two groups according to the current clinical remission state as defined by the PANSS remission criteria elaborated by Andreasen et al. [27] and set up by the Remission in Schizophrenia Working Group [28]. The eight items considered include delusions (P1), conceptual disorganization (P2), hallucinatory behaviour (P3), blunted affect (N1), social withdrawal passive/apathetic (N4), lack of spontaneity of conversation (N6), mannerisms and posturing (G5) and unusual content of thought (G9); symptomatic remission is defined as a score of 3 (‘mild’) or lower, on all items considered.


Clinical and sociodemographic characteristics

An ad hoc schedule was administered in order to assess the demographic and clinical characteristics of the sample. Collected data included general medical information, psychiatric familial and personal history, age at onset of illness, duration of untreated psychosis (DUP), previous psychiatric hospitalizations and antipsychotic therapy.


The Aberrant Salience Inventory (ASI) [8] is a self-administered test, consisting of 29 items with a dichotomous yes/no response, that assesses individual aberrant salience and psychotic proneness. The scale investigates the presence of five factors correlated with each other and in line with Kapur’s conceptualization [4]: feelings of increased significance (7 items), sense sharpening (5 items), impending understanding (5 items), heightened emotionality (6 items) and heightened cognition (6 items). The Italian version of the ASI used in this study confirmed the good psychometric properties of the scale, with gold standard values of internal coherence and stability at retest [29].

The Positive and Negative Symptom Scale (PANSS) [28] is a standardized clinical interview that rates the presence and severity of positive and negative symptoms, as well as general psychopathology, for patients with schizophrenia within the past week. The instrument consists of 30 items evaluated on a seven-point Likert scale (1 = absent to 7 = extreme): the positive and negative subscales consist of seven items each (score: 7–49), whereas the general psychopathology subscale consists of 16 items (score: 16–122).

In this study, with the aim of considering the sample based on remission state [30], we applied the eight items of the PANSS remission criteria: delusions (P1), conceptual disorganization (P2), hallucinatory behaviour (P3), blunted affect (N1), social withdrawal passive/apathetic (N4), lack of spontaneity of conversation (N6), mannerisms and posturing (G5) and unusual content of thought (G9).

Statistical analyses

Data were analysed using the Social Sciences Statistical Package, Version 26.0 (SPSS Inc., Chicago, IL, USA). In order to select appropriate methods of statistical analysis, the normal distribution was checked using the Shapiro–Wilk test.

The variables of the PANSS and ASI were not normally distributed; therefore, the Mann–Whitney U test was used for group comparison. Additionally, effect size r was calculated for significant results. Values of 0.2, 0.5 and > 0.8 can be categorized into small, moderate and large effect size, respectively [31].

Pearson’s correlation was used to assess the correlation between psychotic symptomatology (PANSS) and aberrant salience (ASI). The statistical significance level was set at p < 0.05.


Table 1 summarizes the demographic and clinical characteristics of the sample. Most patients (77%) reported no familial history of SSD. The age of onset of the disorder was, on average, 23.2 ± 6.3 years, while the mean DUP was 1.6 ± 2.1 years. The average dose of antipsychotics was 467.7 ± 185.6 mg/day (chlorpromazine equivalents). Almost 60% of patients were not clinically remitted.

Table 1 Socio-demographic and clinical characteristics

Patients who were not in remission scored significantly higher than remitted patients on the ASI subscales ‘sharpening of senses’ (SS: p = 0.002), ‘heightened emotionality’ (HE; p = 0.036), ‘heightened cognition’ (HC: p = 0.007) and the total score (p = 0.010), with an ES that ranged from small to moderate (0.21–0.63) (Table 2).

Table 2 Comparison of scores obtained at PANSS and ASI according to the remission

Table 3 shows the correlation between psychotic symptoms (PANSS) and aberrant salience (ASI). Positive symptomatology (P1, P2, P3) and general psychopathology (G5, G9) were correlated with the subscales ‘sharpening of senses’, ‘heightened emotionality’ and ‘heightened cognition’, and with the total ASI score. Regarding negative symptomatology, we found a significant correlation between N1 and N4 and the subscale ‘heightened cognition’; N6 was related to the subscales ‘heightened emotionality’ and ‘heightened cognition’, as well as with the total ASI score.

Table 3 Correlations between psychotic symptoms and ASI subscales


The aim of this study was to assess the association between the aberrant salience trait and the severity of psychotic symptoms. The results of data analysis showed not only significantly higher ASI scores among non-remitted patients, but also an association between aberrant salience and positive symptoms (i.e. delusions, conceptual disorganization, hallucinatory behaviour) and general psychopathology (i.e. postural mannerisms, unusual thought content), as well as with negative symptoms (i.e. blunted affect, social withdrawal, lack of spontaneity of conversation).

This result is consistent with previous research that assessed the interplay of momentary aberrant salience in the development of paranoid [32] and psychotic experiences [33] in patients with SSD.

However, to our knowledge, this was the first study to examine the association between psychotic symptoms and aberrant salience domains in patients with SSD.

Dopaminergic dysfunction may contribute to a misattribution of salience involving both rewarding and aversive signalling; this could lead to the world seeming loaded with significance, generating feelings of apprehension and a sense that the world has changed in some, as yet, uncertain way [34].

According to this model of impaired processing capability, the dysfunction of the attribution of meaning leads to a “defective filter” where dopamine mediates a flood of stimuli together with aberrant significance from a neutral information into a positive or noxious entity [4, 35].

These experiences are characteristic of the prodromal phase of schizophrenia [34]. From this perspective, primary delusions can derive from the prodromal state, such as the individual's explanation of the experience of aberrant salience [36]. Moreover, it is possible that social environmental factors interact with the neurocognitive processes involved in the early stage of psychotic symptoms [37]. In fact, in our previous study, we found that emotional abuse during childhood can be associated with a higher level of aberrant salience in SSD patients [38].

The measurement of aberrant salience as a lifetime condition (trait) and as an episodic element (state) is essential for both a dimensional understanding of psychosis and the management of therapy [32].

In this regard, we hypothesize that aberrant salience differentiation could be explained by different variables, including psychosis severity and phase [10], medication confounding bias [7], or still to the different assessment sensibility [6]. Indeed, the SAT has shown good construct and concurrent validity when used in non-psychotic populations [9, 39], while the ASI better identifies psychotic-like experiences, such as magical ideation, regardless of the diagnosis, discriminating schizophrenia from other major disorders, such as bipolar disorder [8]. Therefore, some authors have speculated that the ASI may be able to identify the aberrant salience as a trait [40], and this could be of particular interest especially when studying non-psychotic populations.

In line with previous findings, we found stronger correlations between aberrant salience and positive symptoms than with negative symptoms [11, 41]. Kapur [4] proposed that antipsychotic drugs, which block the D2 dopamine receptors, can reduce positive symptoms by mitigating aberrant motivational salience. A consequence of this hypothesis is that antipsychotic drugs will essentially also reduce adaptive motivational salience, that is, the correct allocation of salience. Unfortunately, this can result both in remission of positive symptoms and increasing negative symptoms as a side effect, mainly related to loss of motivation, such as apathy and anhedonia [4].

Previous research found that schizophrenia patients with florid delusions exhibited significantly more momentary aberrant salience than those without [7]. However, there is a positive relationship between explicit aberrant salience and delusion-like symptoms in people at ultra-high risk of psychosis [10]. Also, a significant association between cannabis-induced psychotic symptom severity (accounting for 37% of the variance in psychotic symptom severity) and aberrant salience processing has been found [42].

On the other hand, to date, the correlation between aberrant salience and negative symptoms has been less investigated. In our study, a relationship emerged between aberrant salience and both expressive deficits (i.e. blunted affect, alogia) and the motivational domain (i.e. asociality).

Motivation impairment, underlying avolition, asociality and potentially anhedonia can derive from different dopamine pathophysiological mechanisms involving the salience system [43]. Indeed, several imaging studies found an association between alterations of the dopamine-dependent response of the ventral striatum to reward anticipation and negative symptoms in patients with schizophrenia [44]. However, in other studies the same alterations were not found to be correlated with negative symptoms [45], thus maintaining uncertainty on the subject.

Schizophrenia is characterized by well-known deficits in the comprehension and production of speech, as well as impairments in the perception and production of gestures [46]. A functional network connectivity analysis conducted on patients with schizophrenia found disrupted communication between the anterior default mode network and the salience network that was positively associated with the severity of blunted affect [47]. In this regard, impaired processing of emotional salience has been proposed as a primary antecedent to the development of psychosis [48] and may be affected according to illness stage [49].

In our study, we found a significant correlation between the subscale ‘heightened cognition’ and positive symptomatology (i.e. delusions, conceptual disorganization, hallucinatory behaviour), postural mannerisms, unusual thought content and both expressive deficits and asociality. Heightened cognition denotes experiences in which individuals feel as if they are part of something important that may not be readily apparent. These perceptual experiences are often accompanied by the feeling that some important understanding may be forthcoming, as a revelation or a sensation of unknown and uncontrolled changes [8]. The presence of elevated levels of heightened cognition was found to be positively correlated to unusual thought content [50] and studies have shown that this dimension of aberrant salience is able to distinguish patients with psychosis from other psychiatric patients, suggesting it may be the most specific for psychosis [51]. Speaking about heightened cognition, the role of neurocognition and intelligence quotient (IQ) prognosis of severe psychiatric diseases is still far from being completely understood [52]. Indeed, there are some emerging data about the correlation between higher IQ and a different prognosis in severe psychiatric conditions, which deserves more future research [53, 54].

Moreover, the subscale ‘heightened emotionality’ was associated with positive symptomatology, postural mannerisms, unusual thought content and alogia. Heightened emotionality represents increased levels of anxiety during the early stages of a psychotic episode in which an individual is trying to make sense of the increased importance of stimuli [4, 8]. Significantly, this dimension is one of the components identified by classical European psychopathology as determining the transition from a pre-delirious state to fully articulated delirious experiences [55].

Finally, the subscale ‘sharpening of senses’ correlated with positive symptomatology, postural mannerisms and unusual thought content. This dimension of aberrant salience involves anomalies of perception in the form of subjective feelings of sharpening of the senses. The experience of aberrant salience may cause a subjective feeling of the senses sharpening as previously non-salient stimuli become salient [4, 8].

Although the preliminary results presented in this study pave the way for a new conceptualization of salience as a trait, and not just as a trigger for psychosis, these findings should be considered in light of several limitations. Firstly, the assessment was conducted through a self-report tool and we could not cross-test aberrant salience with convergent clinician-related tasks (e.g. the SAT) [7]. On the other hand, self-report measures allow the enrolment of large samples; in addition, at present, the ASI is the only available test to measure the aberrant salience trait [8, 56] and it has shown high reliability among patients with a history of psychosis [8]. ASI scores correlate with psychotic-like experiences and discriminate schizophrenia from other psychopathologies, such as bipolar disorder [8], while the SAT shows good construct validity in unaffected individuals [39]. Second, we must acknowledge that our sample included patients taking antipsychotic treatments. While this reflects the naturalistic design of the study, it can clearly affect the relationships between aberrant salience and positive symptoms, considering the antipsychotic medications block the underlying aberrant dopaminergic drive, and given the critical role of dopamine in salience, with a consequential mitigation of the aberrantly salient ideas and perceptions [4]. Therefore, our results must be replicated in a drug-naive sample, preferably at the onset of the disorder, to mitigate this bias. Finally, the association that we found between aberrant salience and positive symptoms may be potentially influenced by their conceptual overlapping. Indeed, we should consider that aberrant salience and psychosis (i.e. experience of delusions, hallucinations, and the secondary related behaviour) are relatively close concepts, even difficult to clinically discriminate from each other. Therefore, although ASI and PANSS are two well-established and solid tools to evaluate aberrant salience and psychosis, this limitation should be considered.


Our preliminary results seem to support the hypothesis of a dopaminergic regulation of salience that is essential to the pathogenesis of SSD [34]. Indeed, a salience network dysfunction may also play a critical role in explaining the positive, negative and cognitive symptoms of SSD [57].

We found a correlation between the aberrant salience trait and psychotic symptoms. At the beginning of the twentieth century the study of phenomenology seemed destined to never link to the neurobiology, as if they were two irreconcilable aspects of psychiatry. Instead, the application of a more recent dimensional research approach, which aimed to understand salience alterations, allowed to relate neurobiological phenomena (such as dopaminergic alterations) to psychopathological experiences (such as delusions and other psychotic symptoms), thus overcoming this gap [36]. The measurement of aberrant salience could enrich the characterization of genesis and the maintenance of psychotic experiences in patients with schizophrenia. However, the mechanisms underlying salience processing remain unclear and further consideration of social factors and cognitive variables is recommended for future studies.

Availability of data and materials

Data are available on request due to privacy restrictions.



Aberrant salience inventory


Brief limited intermittent psychotic symptoms


Diagnostic and statistical manual of mental disorders, fifth edition


Duration of untreated psychosis


First-episode psychosis


Intelligence quotient


Positive and Negative Symptom Scale


Salience Attribution Task


Structured Clinical Interview for DSM-5


Social sciences statistical package


Schizophrenia spectrum disorders


Ultra-high risk


  1. Chun C, Gross G, Mielock A, Kwapil T. Aberrant salience predicts psychotic-like experiences in daily life: an experience sampling study. Schizophr Res. 2020;220:218–24.

    Article  Google Scholar 

  2. Heinz A, Murray GK, Schlagenhauf F, Sterzer P, Grace AA, Waltz JA. Towards a unifying cognitive, neurophysiological, and computational neuroscience account of schizophrenia. Schizophr Bull. 2019.

    Article  PubMed  PubMed Central  Google Scholar 

  3. Howes OD, Kapur S. The dopamine hypothesis of schizophrenia: version III--the final common pathway. Schizophr Bull. 2009;35(3):549–62.

    Article  Google Scholar 

  4. Kapur S. Psychosis as a state of aberrant salience: a framework linking biology, phenomenology, and pharmacology in schizophrenia. Am J Psychiatry. 2003 Jan;160(1):13–23. 10 Apr 2020.

  5. Kapur S, Mizrahi R, Li M. From dopamine to salience to psychosis-linking biology, pharmacology and phenomenology of psychosis. In: Schizophrenia Research. Schizophr Res. 2005;79:59–68.

    Article  Google Scholar 

  6. Neumann SR, Glue P, Linscott RJ. Aberrant salience and reward processing: a comparison of measures in schizophrenia and anxiety. Psychol Med. 2021;51(9):1507–15.

    Article  Google Scholar 

  7. Roiser JP, Stephan KE, Den Ouden HEM, Barnes TRE, Friston KJ, Joyce EM. Do patients with schizophrenia exhibit aberrant salience? Psychol Med. 2009;39(2):199–209.

    Article  CAS  Google Scholar 

  8. Cicero DC, Kerns JG, McCarthy DM. The aberrant salience inventory: a new measure of psychosis proneness. Psychol Assess. 2010;22(3):688–701.

    Article  Google Scholar 

  9. Katthagen T, Dammering F, Kathmann N, Kaminski J, Walter H, Heinz A, et al. Validating the construct of aberrant salience in schizophrenia—Behavioral evidence for an automatic process. Schizophr Res Cogn. 2016;6:22–7.

    Article  Google Scholar 

  10. Roiser JP, Howes OD, Chaddock CA, Joyce EM, McGuire P. Neural and behavioral correlates of aberrant salience in individuals at risk for psychosis. Schizophr Bull. 2013;39(6):1328–36.

    Article  Google Scholar 

  11. Cicero DC, Becker TM, Martin EA, Docherty AR, Kerns JG. The role of aberrant salience and self-concept clarity in psychotic-like experiences. Personal Disord. 2013;4(1):33–42.

    Article  Google Scholar 

  12. Poletti M, Pelizza L, Azzali S, Garlassi S, Scazza I, Paterlini F, et al. Subjective experience of aberrant salience in young people at Ultra-High Risk (UHR) for psychosis: a cross-sectional study. Nord J Psychiatr. 2022;76(2):129–37.

    Article  Google Scholar 

  13. Scazza I, Pelizza L, Azzali S, Garlassi S, Paterlini F, Chiri LR, et al. Aberrant salience in first-episode psychosis: longitudinal stability and treatment-response. Early Interv Psychiatry. 2021.

    Article  PubMed  Google Scholar 

  14. Azzali S, Pelizza L, Scazza I, Paterlini F, Garlassi S, Chiri LR, et al. Examining subjective experience of aberrant salience in young individuals at ultra-high risk (UHR) of psychosis: A 1-year longitudinal study. Schizophr Res. 2022; 241:52–8.

  15. Abboud R, Roiser JP, Khalifeh H, Ali S, Harrison I, Killaspy HT, et al. Are persistent delusions in schizophrenia associated with aberrant salience? Schizophr Res Cogn. 2016;4:32–8.

    Article  Google Scholar 

  16. Schmidt SNL, Fenske SC, Kirsch P, Mier D. Nucleus accumbens activation is linked to salience in social decision making. Eur Arch Psychiatry Clin Neurosci. 2019;269(6):701–12.

    Article  Google Scholar 

  17. Walter H, Heckers S, Kassubek J, Erk S, Frasch K, Abler B. Further evidence for aberrant prefrontal salience coding in schizophrenia. Front Behav Neurosci. 2010.

    Article  PubMed  PubMed Central  Google Scholar 

  18. Kim BH, Shin Bin Y, Kyeong S, Lee SK, Kim JJ. Disrupted salience processing involved in motivational deficits for real-life activities in patients with schizophrenia. Schizophr Res. 2018;197:407–13.

    Article  Google Scholar 

  19. Cicero DC, Docherty AR, Becker TM, Martin EA, Kerns JG. Aberrant salience, self-concept clarity, and interview-rated psychotic-like experiences. J Pers Disord. 2015;29(1):79.

    Article  Google Scholar 

  20. Ballerini A, Tortorelli M, Marino P, Appignanesi C, Baschirotto C, Mallardo L, et al. Aberrant salience relationship with first rank symptoms. Ann Gen Psychiatry. 2022;21(1):8.

    Article  Google Scholar 

  21. World Medical Association. World medical association declaration of Helsinki: ethical principles for medical research involving human subjects. JAMA. 2013;310(20):2191.

    Article  Google Scholar 

  22. Bhati MT. Defining psychosis: the evolution of DSM-5 schizophrenia spectrum disorders. Curr Psychiatry Rep. 2013;15(11):409.

    Article  PubMed  Google Scholar 

  23. Lewine R, Hart M. Schizophrenia spectrum and other psychotic disorders. In 2020. 315–33.

  24. American Psychiatric Association. Diagnostic and statistical manual of mental disorders (5th ed.). Washington, D.C.: American Psychiatric Publishing. 2013.

    Google Scholar 

  25. First MB, Williams JBW, Karg RS, Spitzer RL: Structured Clinical Interview for DSM-5 Disorders, Clinician Version (SCID-5-CV). Arlington, VA, American Psychiatric Association, 2016.

    Google Scholar 

  26. Gardner DM, Murphy AL, O’Donnell H, Centorrino F, Baldessarini RJ. International consensus study of antipsychotic dosing. Am J Psychiatry. 2010;167(6):686–93.

    Article  Google Scholar 

  27. Andreasen NC, Carpenter WT, Kane JM, Lasser RA, Marder SR, Weinberger DR. Remission in Schizophrenia: proposed criteria and rationale for consensus. Am J Psychiatry. 2005;162(3):441–9. Accessed 2 Feb 2019.

  28. Kay SR, Fiszbein A, Opler LA. The positive and negative syndrome scale (PANSS) for schizophrenia. Schizophr Bull. 1987;13(2):261–76. Accessed 10 Apr 2020.

  29. Raballo A, Scanu R, Petretto DR, Preti A. Aberrant salience and psychosis risk symptoms in Italian undergraduate students: further validation of the Aberrant Salience Inventory. Early Interv Psychiatr. 2014;8(Supplementary 1):134.

    Google Scholar 

  30. Mosolov SN, Potapov AV, Ushakov UV. Remission in schizophrenia: results of cross-sectional with 6-month follow-up period and 1-year observational therapeutic studies in an outpatient population. Ann Gen Psychiatr. 2012;11(1):1.

    Article  Google Scholar 

  31. Cohen J. Statistical power analysis for the behavioral sciences. 2nd ed. Statistical power analysis for the behavioral sciences. Hillsdale NJ: L Erlbaum Associates; 1988.

    Google Scholar 

  32. So SHW, Chau AKC, Peters ER, Swendsen J, Garety PA, Kapur S. Moment-to-moment associations between negative affect, aberrant salience, and paranoia. Cogn Neuropsychiatr. 2018;23(5):299–306.

    Article  Google Scholar 

  33. Reininghaus U, Kempton MJ, Valmaggia L, Craig TKJ, Garety P, Onyejiaka A, et al. Stress sensitivity, aberrant salience, and threat anticipation in early psychosis: an experience sampling study. Schizophr Bull. 2016;42(3):712–22.

    Article  Google Scholar 

  34. Howes OD, Nour MM. Dopamine and the aberrant salience hypothesis of schizophrenia. 15, World Psychiatry. Hoboken: Blackwell Publishing Ltd; 2016.

    Google Scholar 

  35. Berridge KC, Robinson TE. What is the role of dopamine in reward: hedonic impact, reward learning, or incentive salience? Brain Res Rev. 1998;28(3):309–69.

  36. Mishara AL, Fusar-Poli P. The phenomenology and neurobiology of delusion formation during psychosis onset: jaspers, truman symptoms, and aberrant salience. Schizophr Bull. 2013;39(2):278–86.

    Article  Google Scholar 

  37. Gawęda Ł, Göritz AS, Moritz S. Mediating role of aberrant salience and self-disturbances for the relationship between childhood trauma and psychotic-like experiences in the general population. Schizophr Res. 2019;206:149–56.

    Article  Google Scholar 

  38. De Fazio P, Pugliese V, Cattolico M, Aloi M, Segura-Garcia C. The relationship between childhood trauma and aberrant salience: a preliminary study in patients with Schizophrenia. J Psychopathol. 2020;26:28–35.

    Google Scholar 

  39. Schmidt K, Roiser JP. Assessing the construct validity of aberrant salience. Front Behav Neurosci. 2009.

    Article  PubMed  PubMed Central  Google Scholar 

  40. Mezquida G, Savulich G, Atkinson S, Bernardo M, Fernandez-Egea E. Aberrant salience: a comparison of different measures in anxiety and schizophrenia. Schizophr Bull. 2018;44(suppl_1):S351–S351.

    Article  Google Scholar 

  41. Chun CA, Brugger P, Kwapil TR. Aberrant salience across levels of processing in positive and negative schizotypy. Front Psychol. 2019.

    Article  PubMed  PubMed Central  Google Scholar 

  42. Bloomfield MAP, Mouchlianitis E, Morgan CJA, Freeman TP, Curran HV, Roiser JP, et al. Salience attribution and its relationship to cannabis-induced psychotic symptoms. Psychol Med. 2016;46(16):3383–95.

    Article  CAS  Google Scholar 

  43. Galderisi S, Mucci A, Buchanan RW, Arango C. Negative symptoms of schizophrenia: new developments and unanswered research questions Vol. 5, the Lancet psychiatry, vol. 5. Amsterdam: Elsevier Ltd; 2018. p. 664–77.

    Google Scholar 

  44. Radua J, Schmidt A, Borgwardt S, Heinz A, Schlagenhauf F, McGuire P, et al. Ventral striatal activation during reward processing in psychosis a neurofunctional meta-analysis. JAMA Psychiat. 2015;72(12):1243–51.

    Article  Google Scholar 

  45. Nielsen MØ, Rostrup E, Wulff S, Bak N, Lublin H, Kapur S, et al. Alterations of the brain reward system in antipsychotic nave schizophrenia patients. Biol Psychiatry. 2012;71(10):898–905.

    Article  Google Scholar 

  46. Meyer L, Lakatos P, He Y. Language dysfunction in schizophrenia: assessing neural tracking to characterize the underlying disorder(s)? Front Neurosci. 2021;15:22.

    Google Scholar 

  47. Hare SM, Ford JM, Mathalon DH, Damaraju E, Bustillo J, Belger A, et al. Salience-default mode functional network connectivity linked to positive and negative symptoms of schizophrenia. Schizophr Bull. 2019;45(4):892–901.

    Article  Google Scholar 

  48. Anticevic A, Van Snellenberg JX, Cohen RE, Repovs G, Dowd EC, Barch DM. Amygdala recruitment in schizophrenia in response to aversive emotional material: a meta-analysis of neuroimaging studies. Schizophr Bull. 2012;38(3):608–21.

    Article  Google Scholar 

  49. Modinos G, Tseng HH, Falkenberg I, Samson C, Mcguire P, Allen P. Neural correlates of aberrant emotional salience predict psychotic symptoms and global functioning in high-risk and first-episode psychosis. Soc Cogn Affect Neurosci. 2015;10(10):1429–36.

    Article  Google Scholar 

  50. Comparelli A, Corigliano V, Montalbani B, Bargagna P, Forcina F, Cocco G, et al. Relationship between aberrant salience and positive emotion misrecognition in acute relapse of schizophrenia. Asian J Psychiatr. 2020.

    Article  PubMed  Google Scholar 

  51. Golay P, Laloyaux J, Moga M, Della Libera C, Larøi F, Bonsack C. Psychometric investigation of the French version of the Aberrant Salience Inventory (ASI): Differentiating patients with psychosis, patients with other psychiatric diagnoses and non-clinical participants. Ann Gen Psychiatry. 2020;19(58).

    Article  Google Scholar 

  52. Greenwald DF, Harder DW, Gift TE, Strauss JS, Ritzler BA, Kokes RF. IQ as a prognostic indicator in adult psychiatric first-admissions. J Clin Psychol. 1989;45(1):37–50.;2-4.

    Article  CAS  PubMed  Google Scholar 

  53. Karpinski RI, Kinase Kolb AM, Tetreault NA, Borowski TB. High intelligence: a risk factor for psychological and physiological overexcitabilities. Intelligence. 2018; 66:8–23.

  54. Ohi K, Sumiyoshi C, Fujino H, Yasuda Y, Yamamori H, Fujimoto M, et al. A brief assessment of intelligence decline in schizophrenia as represented by the difference between current and premorbid intellectual quotient. Front Psychiatr. 2017;22:8.

    Article  Google Scholar 

  55. Bovet P, Parnas J. Schizophrenic delusions: a phenomenological approach. Schizophr Bull. 1993;19(3):579–97.

    Article  CAS  Google Scholar 

  56. Raballo A, Cicero DC, Kerns JG, Sanna S, Pintus M, Agartz I, et al. Tracking salience in young people: a psychometric field test of the Aberrant Salience Inventory (ASI). Early Interv Psychiatry. 2019;13(1):64–72.

    Article  Google Scholar 

  57. Palaniyappan L, Liddle PF. Does the salience network play a cardinal role in psychosis? An emerging hypothesis of insular dysfunction. J Psychiatry Neurosci. 2012;37(1):17–27.

    Google Scholar 

Download references


Authors are grateful to participants for the time they have given to this study.


This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sector.

Author information

Authors and Affiliations



PDF designed the study. VP, MA, RdF, EAC, PR and RG collected the data. MA performed the statistical analyses. VP, RdF and MA wrote the first draft of the manuscript. PDF made the first critical review and participated in writing the final manuscript. All authors read and approved the final manuscript.

Corresponding author

Correspondence to Pasquale De Fazio.

Ethics declarations

Ethics approval and consent to participate

This study was conducted in accordance with the latest version of the Declaration of Helsinki. The study protocol was approved by the local research ethics committee. All patients signed a written informed consent according to the Ethical Committee’s guidelines before any data were collected.

Consent for publication

All authors have read and agree to its content to be published on Annals of General Psychiatry.

Competing interests

The authors declare that they have no competing interests.

Additional information

Publisher's Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Rights and permissions

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit The Creative Commons Public Domain Dedication waiver ( applies to the data made available in this article, unless otherwise stated in a credit line to the data.

Reprints and Permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Pugliese, V., de Filippis, R., Aloi, M. et al. Aberrant salience correlates with psychotic dimensions in outpatients with schizophrenia spectrum disorders. Ann Gen Psychiatry 21, 25 (2022).

Download citation

  • Received:

  • Accepted:

  • Published:

  • DOI:


  • Aberrant salience
  • Negative symptoms
  • Positive symptoms
  • Postural mannerisms
  • Social withdrawal
  • Alogia
  • Blunted affect
  • Delusions
  • Disorganization
  • Schizophrenia