Skip to main content Accessibility help
×
×
Home

Information:

  • Access
  • Cited by 39
  • Cited by
    This article has been cited by the following publications. This list is generated based on data provided by CrossRef.

    Altamura, A. Carlo Serati, Marta Albano, Alessandra Paoli, Riccardo A. Glick, Ira D. and Dell’Osso, Bernardo 2011. An epidemiologic and clinical overview of medical and psychopathological comorbidities in major psychoses. European Archives of Psychiatry and Clinical Neuroscience, Vol. 261, Issue. 7, p. 489.

    Hohwy, Jakob and Rajan, Vivek 2012. Delusions as Forensically Disturbing Perceptual Inferences. Neuroethics, Vol. 5, Issue. 1, p. 5.

    Coghill, David and Sonuga-Barke, Edmund J.S. 2012. Annual Research Review: Categories versus dimensions in the classification and conceptualisation of child and adolescent mental disorders - implications of recent empirical study. Journal of Child Psychology and Psychiatry, Vol. 53, Issue. 5, p. 469.

    Ahmed, A. O. Buckley, P. F. and Mabe, P. A. 2012. Latent structure of psychotic experiences in the general population. Acta Psychiatrica Scandinavica, Vol. 125, Issue. 1, p. 54.

    Laurens, K. R. Hobbs, M. J. Sunderland, M. Green, M. J. and Mould, G. L. 2012. Psychotic-like experiences in a community sample of 8000 children aged 9 to 11 years: an item response theory analysis. Psychological Medicine, Vol. 42, Issue. 07, p. 1495.

    Palm, Ulrich 2012. Centenary of schizophrenia: Should the term survive “togo shicchou sho” and “salience syndrome”?. Asia-Pacific Psychiatry, Vol. 4, Issue. 4, p. 228.

    Brambilla, P. Perlini, C. Bellani, M. Tomelleri, L. Ferro, A. Cerruti, S. Marinelli, V. Rambaldelli, G. Christodoulou, T. Jogia, J. Dima, D. Tansella, M. Balestrieri, M. and Frangou, S. 2013. Increased salience of gains versus decreased associative learning differentiate bipolar disorder from schizophrenia during incentive decision making. Psychological Medicine, Vol. 43, Issue. 03, p. 571.

    Delvecchio, G. Sugranyes, G. and Frangou, S. 2013. Evidence of diagnostic specificity in the neural correlates of facial affect processing in bipolar disorder and schizophrenia: a meta-analysis of functional imaging studies. Psychological Medicine, Vol. 43, Issue. 03, p. 553.

    Linscott, Richard J. 2013. The taxonicity of schizotypy: Does the same taxonic class structure emerge from analyses of different attributes of schizotypy and from fundamentally different statistical methods?. Psychiatry Research, Vol. 210, Issue. 2, p. 414.

    Pearlson, G. D. and Ford, J. M. 2014. Distinguishing Between Schizophrenia and Other Psychotic Disorders. Schizophrenia Bulletin, Vol. 40, Issue. 3, p. 501.

    Johns, Louise C. Kompus, Kristiina Connell, Melissa Humpston, Clara Lincoln, Tania M. Longden, Eleanor Preti, Antonio Alderson-Day, Ben Badcock, Johanna C. Cella, Matteo Fernyhough, Charles McCarthy-Jones, Simon Peters, Emmanuelle Raballo, Andrea Scott, James Siddi, Sara Sommer, Iris E. and Larøi, Frank 2014. Auditory Verbal Hallucinations in Persons With and Without a Need for Care. Schizophrenia Bulletin, Vol. 40, Issue. Suppl_4, p. S255.

    Córdova-Palomera, Aldo Calati, Raffaella Arias, Bárbara Ibáñez, Manuel-Ignacio Moya, Jorge Ortet, Generós Crespo-Facorro, Benedicto and Fañanás, Lourdes 2015. Season of birth and subclinical psychosis: Systematic review and meta-analysis of new and existing data. Psychiatry Research, Vol. 225, Issue. 3, p. 227.

    Ronald, Angelica 2015. Recent quantitative genetic research on psychotic experiences: new approaches to old questions. Current Opinion in Behavioral Sciences, Vol. 2, Issue. , p. 81.

    DeRosse, Pamela and Karlsgodt, Katherine H. 2015. Examining the Psychosis Continuum. Current Behavioral Neuroscience Reports, Vol. 2, Issue. 2, p. 80.

    Melville, C.A. Johnson, P.C.D. Smiley, E. Simpson, N. McConnachie, A. Purves, D. Osugo, M. and Cooper, S.-A. 2016. Statistical modelling studies examining the dimensional structure of psychopathology experienced by adults with intellectual disabilities: Systematic review. Research in Developmental Disabilities, Vol. 53-54, Issue. , p. 1.

    Prudent, Cécile Evrard, Renaud Claude, Nina Laurent, Mélanie and De Tychey, Claude 2016. DSM-5, trouble de la personnalité schizotypique et nosographie psychanalytique structurale française. L'Évolution Psychiatrique, Vol. 81, Issue. 1, p. 176.

    Lawrie, Stephen M O’Donovan, Michael C Saks, Elyn Burns, Tom and Lieberman, Jeffrey A 2016. Improving classification of psychoses. The Lancet Psychiatry, Vol. 3, Issue. 4, p. 367.

    Quintana, D. S. Westlye, L. T. Kaufmann, T. Rustan, Ø. G. Brandt, C. L. Haatveit, B. Steen, N. E. and Andreassen, O. A. 2016. Reduced heart rate variability in schizophrenia and bipolar disorder compared to healthy controls. Acta Psychiatrica Scandinavica, Vol. 133, Issue. 1, p. 44.

    Lawrie, Stephen M. 2016. Whether “psychosis” is best conceptualized as a continuum or in categories is an empirical, practical and political question. World Psychiatry, Vol. 15, Issue. 2, p. 125.

    Morris, Sarah E. Vaidyanathan, Uma and Cuthbert, Bruce N. 2016. The Neuropsychopathology of Schizophrenia. Vol. 63, Issue. , p. 225.

    ×

Actions:

      • Send article to Kindle

        To send this article to your Kindle, first ensure no-reply@cambridge.org is added to your Approved Personal Document E-mail List under your Personal Document Settings on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part of your Kindle email address below. Find out more about sending to your Kindle. Find out more about sending to your Kindle.

        Note you can select to send to either the @free.kindle.com or @kindle.com variations. ‘@free.kindle.com’ emails are free but can only be sent to your device when it is connected to wi-fi. ‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.

        Find out more about the Kindle Personal Document Service.

        The ‘continuum of psychosis’: scientifically unproven and clinically impractical
        Available formats
        ×

        Send article to Dropbox

        To send this article to your Dropbox account, please select one or more formats and confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your <service> account. Find out more about sending content to Dropbox.

        The ‘continuum of psychosis’: scientifically unproven and clinically impractical
        Available formats
        ×

        Send article to Google Drive

        To send this article to your Google Drive account, please select one or more formats and confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your <service> account. Find out more about sending content to Google Drive.

        The ‘continuum of psychosis’: scientifically unproven and clinically impractical
        Available formats
        ×
Export citation

Summary

The limitations of current diagnostic categories are well recognised but their rationale, advantages and utility are often ignored. The scientific support for a ‘continuum of psychosis' is limited, and the examination of whether categories, a continuum or more than one continua, and alternatives such as subtypes or hybrid models, best account for the distributions of symptoms in populations has simply not been done. There is a lack of discussion, let alone consensus, about the critical aspects of psychosis to measure, the best ways to quantify those and how these would be applied in clinical practice. Systematic studies are needed to evaluate which of a range of plausible approaches to the classification of psychosis is most useful before change could be justified.

Footnotes

Declaration of interest

None.

The DSM–V and ICD–11 planning processes have re-ignited the debate about the definition and validity of concepts such as schizophrenia. 1 Many commentators criticise the current categorical diagnostic systems and favour a ‘continuum of psychosis’. 2,3 They do so however without any specific proposals, while neglecting the limitations of what could be several continua and ignoring alternative approaches to classifying psychotic disorders. We argue here that rejecting time-tested and progressively refined clinical concepts is at best premature and at worst wrong scientifically, and that a continuous approach to psychosis would be time consuming and quite possibly disastrous in clinical practice.

The known value and limitations of categories

The limitations of current categorical diagnostic systems are well recognised – principally, their uncertain validity, the lack of clear ‘zones of rarity’ between disorders, the heterogeneity observed between individuals within categories and that individuals often meet multiple diagnostic criteria. The rationale and advantages of diagnostic categories are however in danger of being forgotten. 4,5 Diagnosis is a preliminary to treatment and prognostication. The current criteria for the psychoses are neither arbitrary nor fixed – they consist of symptoms that tend to aggregate in patient groups and have evolved over decades of clinical observations. Critically, extant categories of psychosis have enabled reliable diagnosis around the world, definite advances in our understanding of aetiology and pathogenesis, based on highly replicable neurobiological differences between people with psychoses and healthy controls, and improvements in management. 6 From a genetic perspective, they identify relatively stable concepts of high heritability – certainly more stable over time than any symptom and as heritable as many proposed endophenotypes. A number of plausible candidate genes for schizophrenia and bipolar disorder have been identified in recent years, and the pace of progress appears to be increasing – apparently not fatally hindered by clinical heterogeneity. 7

We acknowledge that there is overlap in genetic susceptibility, symptoms, treatments and prognoses between schizophrenia and bipolar disorder. Indeed, perhaps the most striking finding of recent genetic association and genome-wide association studies has been the degree of shared genetic susceptibility to schizophrenia and bipolar disorder. 7 However, shared polygenic vulnerability does not necessarily imply that the resultant conditions lie on one continuum or even several continua. Indeed, there is considerable evidence for differences between the disorders in terms of risk factors, pathology and treatment response. Thus urban birth, abnormal neurodevelopment and premorbid cognitive impairment are strongly associated with schizophrenia but not with bipolar disorder. 8 Schizophrenia is associated with an increased burden of large and rare chromosomal abnormalities (copy number variants) not seen in bipolar disorder. 9 In addition there are replicated differences in brain structure and function between the disorders, which although primarily quantitative allow for considerable separation of the disorders. 1012 Most importantly, there are clearly established differences in responsiveness to lithium and other treatments. 13

The putative value of a continuous approach

The main arguments used to support the adoption of one or more continua – and it is usually unclear whether it is one or more – tend to revolve around the fact that psychotic symptoms are continuously distributed in general populations. It is asserted that psychosis is therefore on a continuum, that continua are more valid and easier to dissect biologically than heterogeneous categories, and that such an approach would lead to faster scientific and clinical progress. None of these speculations necessarily follow and each can be challenged on theoretical grounds.

Just because psychotic symptoms are continuously distributed in the general population does not mean that schizophrenia and other psychoses are qualitatively indistinct from normal experience, or each other; nor does it exclude the possibilities of distinct underlying latent categories or several subtypes of psychosis. Phenotypic or symptomatic heterogeneity may be a particularly common, even intrinsic, feature of disruptions in complex systems such as the brain/mind. Indeed, as Paul Meehl observed, the very phenotypic heterogeneity of schizophrenia and the fact that the symptoms of schizophrenia are more highly intercorrelated in mixed than in pure clinical population samples are indicative of underlying categories and inconsistent with a continuous model. 14 It may even be that psychotic symptoms are epiphenomenal to the true nature of psychosis as Bleuler 15 argued and could be considered the case when psychotic symptoms complicate Alzheimer's disease. Crucially, the research to evaluate whether categories, subtypes, continua or hybrid models of psychosis best account for the distribution of symptoms in general or patient populations has simply not been done.

It is not just that there is no guarantee that a continuum of psychosis is more valid and will aid scientific progress – there are in fact good reasons to question some of the implicit assumptions underlying the view that symptoms will be easier to dissect than diagnoses. 16 Individual symptoms are less reliably elicited than a multidimensional diagnosis, they vary in severity over time and may differ in different environmental contexts. In line with traditional teaching, passivity, grandiose and depressive delusions appear to be qualitatively distinct, and a mood congruent delusion or hallucination may have more in common biologically with other features of mood disturbance than with other delusions or hallucinations. On the other hand, cutting-edge functional brain imaging studies have shown that counterintuitive combinations of hallucinations or delusions can have distinct pathophysiologies at a neuronal systems level. 17 The possibility to examine these aetiopathogenetic similarities and differences would be lost in a single delusional rating, let alone a ‘positive psychosis’ severity scale. The bottom line is that a continuous model may be scientifically better than a categorical approach, but we just do not know. Why jeopardise the advances we have made for something of unknown value? This is even more true clinically.

Clinical utility and practical concerns

Above all, established diagnostic categories for psychosis are useful clinically – essential now and for the foreseeable future if we are to regulate and prescribe treatments based on the currently available replicated clinical trial evidence (which is all from studies in diagnostic groups), make dichotomous decisions such as whether or not to legally detain people, and in some health systems to approve insurance and other payments. Categories are also more easily used and communicated than continua. Although there are studies that suggest that symptom types are better predictors of treatment response than disorders, some of the same studies show better overall outcome prediction with categories, and in any case specific replications are rare. 3 Different tasks may require different solutions.

From a practical perspective, major questions are yet to be addressed, let alone answered. Which symptom and outcome continua should be rated, and how are they to be reliably elicited and measured, recorded and available for reference? How are busy clinicians going to find the time to do the ratings and establish reliability over time and between colleagues? Most cogently, how are clinicians going to use complex multidimensional information in clinical practice – which continuous measurements would be used, when and what would be the necessary cut-offs for actions such as initiating treatment or detention? Critically, how will clinicians know when to apply these assessments at all? They would, ironically, have to first make the categorical judgement as to whether or not someone was ‘psychotic’ before applying these assessments. This begs a definition of ‘psychosis’, and if there truly is a ‘continuum of psychosis’ – or even several continua – this decision will be completely arbitrary.

Prima facie, there are equally valid claims for spectra of schizophrenia and bipolar disorder, 18 merging respectively into the apparently distinctive schizotypy and cyclothymia and ultimately into the eccentricities and moodiness of everyday life. There are also symptomatic overlaps between the schizophrenia and autistic spectra, whereas the bipolarity spectrum merges into depression and then anxiety, with their associated mild variants and personality types. 19 Where then are the boundaries of psychosis? Would conditions with occasional psychotic symptoms qualify, and if so when? Would bipolar II disorder, which is rarely associated with psychotic symptoms, no longer be a psychotic disorder?

Worse, individuals with more or less equivalent scores on putative depression and psychosis dimensions could for example have prodromal schizophrenia, acute schizoaffective psychosis, drug-induced psychosis, post-schizophrenic depression or psychotic depression – all of which would currently and with good justification from clinical trials be treated differently. If several continua were required to characterise individuals with psychosis – e.g. positive, negative, disorganised, depression, euphoria, anxiety, obsessionality, cognitive function, personality – how would clinicians decide when to treat? By returning to arbitrary categories of mild, moderate and severe? With respect to arbitrary cut-offs on scale severity scores? Continuous measures could thus reduce evidence-based practice, while exacerbating medicalisation, overdiagnosis, comorbidity, excessive treatment and polypharmacy.

Conclusions and future directions

Our principal concern is that an overenthusiastic and undercritical acceptance of ‘the continuum of psychosis’ will throw away something scientifically serviceable and clinically useful. Clinical definitions may have limited validity but categories that can account for a range of observations cannot just be dismissed until we have something better to put in their place. This drive towards what seems new and exciting might be borne of frustration with the slow pace of progress in psychosis, but that might be better attributed to insufficient resources and the lack of a research culture in psychiatry generally. Although it is true that ‘facts’ about psychiatric disorders have been difficult to accumulate, we no longer have to argue that schizophrenia and other disorders have neurobiological correlates. The focus is now rightly on explaining these findings and using objective measures to distinguish disorders and inform clinical decisions.

Above all, we need consistent evidence that any change in our approach to the classification of psychosis would benefit patients and thereby justify the time and effort involved. We need systematic studies to establish the essential measures for particular purposes, whether available neurocognitive examinations, blood tests and neuroimaging indices add any value, and in which patients, and when they could usefully be applied. We also need clinical trials to determine the therapeutic implications of different approaches and different cut-offs on putative continua – to establish, for example, what levels of symptom severity predict therapeutic responses, the degrees of clinical benefits at certain thresholds and whether comorbidities required additional treatments. Alternative approaches, including hybrids such as categories with stratification for key traits, potentially including relevant biological assays, should also be considered in these studies. We are pleased that two other articles that have been published since we submitted the present editorial have come to similar conclusions. 20,21 One of these has usefully highlighted that extant studies can support both a continuous and categorical view of schizophrenia, 20 but the additional possibilities described above have received little or no study. The research agenda we describe requires large studies of reliably rated and diagnosed and measured patients across many settings, but this would pave the way for any new initiative and would be a welcome opportunity for many clinicians to participate in research that directly addresses their concerns about diagnostic practice. It would also foster more research experience and capability generally. It is a complex and daunting series of tasks but we psychiatrists need to handle that complexity in research before we can translate any changes required into routine clinical practice.

References

1 Tamminga, CA, Sirovatka, PJ, Regier, DA, van Os, J. Deconstructing Psychosis: Refining the Research Agenda for DSM–V. American Psychiatric Association, 2006.
2 Craddock, N, Owen, MJ. The beginning of the end for the Kraepelinian dichotomy. Br J Psychiatry 2005; 186: 364–6.
3 van Os, J, Linscott, RJ, Myin-Germeys, I, Delespaul, P, Krabbendam, L. A systematic review and meta-analysis of the psychosis continuum: evidence for a psychosis proneness-persistence-impairment model of psychotic disorder. Psychol Med 2009; 39: 179–95.
4 Kendell, RE. The Role of Diagnosis in Psychiatry. Blackwell, 1975.
5 Johnstone, EC, Lawrie, SM. An introduction to psychiatry. In Companion to Psychiatric Studies (eds Johnstone, EC, Owens, DGC, Lawrie, SM, Sharpe, M, McIntosh, A). Churchill Livingstone, 2010.
6 Tandon, R, Keshavan, MS, Nasrallah, HA. Schizophrenia, ‘just the fact’: what we know in 2008. Part 1: Overview. Schizophr Res 2008; 100; 419.
7 The International Schizophrenia Consortium. Common polygenic variation contributes to risk of schizophrenia and bipolar disorder. Nature 2009; 460: 748–52.
8 Kirkbride, JB, Fearon, P, Morgan, C, Dazzan, P, Morgan, K, Tarrant, J, et al. Heterogeneity in incidence rates of schizophrenia and other psychotic syndromes: findings from the 3-center AeSOP study. Arch Gen Psychiatry 2006; 63: 250–8.
9 Grozeva, D, Kirov, G, Ivanov, D, Jones, IR, Jones, L, Green, EK, et al. Rare copy number variants: a point of rarity in genetic risk for bipolar disorder and schizophrenia. Arch Gen Psychiatry 2010; 67: 318–27.
10 McIntosh, AM, Whalley, HC, McKirdy, J, Hall, J, Sussmann, JE, Shankar, P, et al. Prefrontal function and activation in bipolar disorder and schizophrenia. Am J Psychiatry 2008; 165: 378–84.
11 Hall, J, Whalley, HC, Marwick, K, McKirdy, J, Sussmann, J, Romaniuk, L, et al. Hippocampal function in schizophrenia and bipolar disorder. Psychol Med 2010; 40: 761–70.
12 Arnone, D, Cavanagh, J, Gerber, D, Lawrie, SM, Ebmeier, KP, McIntosh, AM. Magnetic resonance imaging studies in bipolar disorder and schizophrenia: meta-analysis. Br J Psychiatry 2009; 195: 194201.
13 Leucht, S, Kissling, W, McGrath, J. Lithium for schizophrenia. Cochrane Database Syst Rev 2007; 3: CD003834.
14 Waller, NG. Carving nature at its joints: Paul Meehl's development of taxometrics. J Abn Psychol 2006; 115: 210–5.
15 Bleuler, E. Dementia Praecox, or the Group of Schizophrenias. International University Press, 1911.
16 Mojtabai, R, Rieder, RO. Limitations of the symptom-oriented approach to psychiatric research. Br J Psychiatry 1998; 173: 198202.
17 Fletcher, PC, Frith, CD. Perceiving is believing: a Bayesian approach to explaining the positive symptoms of schizophrenia. Nat Rev Neurosci 2009; 10: 4858.
18 Angst, J. The bipolar spectrum. Br J Psychiatry 2007; 190: 189–91.
19 Blacker, D, Tsuang, MT. Contested boundaries of bipolar disorder and the limits of categorical diagnosis in psychiatry. Am J Psychiatry 1992; 149: 1473–83.
20 Linscott, RJ, van Os, J. Systematic reviews of categorical versus continuum models in psychosis: evidence for discontinuous subpopulations underlying a psychometric continuum. Implications for DSM–V, DSM–VI, and DSM–VII. Annu Rev Clin Psychol 2010; 6: 391419.
21 David, AS. Why we need more debate on whether psychotic symptoms lie on a continuum with normality. Psychol Med 2010; Feb 11: 18 (Epub ahead of print).