© 2005 The Royal College of Psychiatrists
Correspondence |
Kraepelinian dichotomy
Scottish Centre for Autism, Royal Hospital for Sick Children, Glasgow G3 8SJ, UK.
Correspondence: E-mail: Val.Murray{at}yorkhill.scot.nhs.uk
Craddock & Owen (2005) attribute the proposed demise of the Kraepelinian dichotomy to advances in genetic epidemiology, and rightly emphasise the need to integrate data across multiple domains in large numbers of people. However, it may also be important to use a population-based approach. This involves extra effort but avoids being misled by convenience samples which may not be representative of the population. This is illustrated by Fig. 1 in the editorial of Craddock & Owen which suggests that prototypical schizophrenia and prototypical bipolar disorder are relatively rare in clinical populations. Work in population-based samples suggests that there is an early, insidious-onset psychosis with a poor outcome affecting predominantly men – a ‘neurodevelopmental’ form of schizophrenia which is very close to dementia praecox (Castle et al, 1998). This prototypical form of schizophrenia together with protoypical bipolar disorder accounts for 50% of people with psychosis in a treated prevalence sample, demonstrating the utility of Kraepelin’s division. In our experience affective and non-affective psychoses can be accounted for by these prototypical forms and a further two latent classes which appear to be valid (Murray et al, 2005). Whether such empirically derived classes might provide better phenotypes for genetic studies is as yet undetermined.
Until biological markers are identified there is perhaps only one way to improve our classification. Large-scale, empirical, population-based studies of psychiatric symptoms, demography, course, treatment response and outcomes are suggested to reclassify these disorders from first principles and provide an atheoretical framework which may capture underlying pathophysiological substrates. Such studies should, as described by Craddock & Owen, integrate both dimensional and categorical approaches but also require a developmental perspective across the life span. The debate about the Kraepelinian dichotomy illustrates the lack of evidence-based diagnostic classification in psychiatry as a discipline. It would be fitting if psychiatric genetics, which has been severely impeded by the lack of a robust nosology, focused the collective will of practitioners to establish the evidence base required for a psychiatric classification which at last reflects nature.
EDITED BY KIRIAKOS XENITIDIS and COLIN CAMPBELL
REFERENCES
- Castle, D. J., Wessely, S., van Os, J., et al (1998) Subtypes of schizophrenia. In Psychosis in the Inner City: The Camberwell First Episode Study, pp. 37 –49. Hove: Psychology Press.
- Craddock, N. & Owen, M. J. (2005) The
beginning of the end of the Kraepelinian dichotomy. British Journal
of Psychiatry, 186, 364
–366.
[Free Full Text] - Murray, V., McKee, I., Miller, P. M., et al (2005) Dimensions and classes of psychosis in a population cohort: a four class, four dimension model of schizophrenia and affective psychoses. Psychological Medicine, 35, 499 –510.[CrossRef][Medline]
Authors’ reply
Department of Psychological Medicine, Henry Wellcome Building, School of Medicine, Cardiff University, Heath Park, Cardiff CF14 4XN, UK.
Correspondence: E-mail: craddockn{at}Cardiff.ac.uk
EDITED BY KIRIAKOS XENITIDIS and COLIN CAMPBELL
N.C. and M.J.O. are consultants to GlaxoSmithKline and have received grant funding and honoraria from GlaxoSmithKline, AstraZeneca and Lilly.
We are in full agreement with Dr Murray regarding the utility of large-scale, population-based studies. These are highly desirable and will, we hope, be facilitated by the recent establishment of the Mental Health Research Network (http://www.mhrn.info) under the auspices of the UK Clinical Research Collaboration (http://www.ukcrc.org). We also agree that longitudinal variables such as course, outcome and treatment response might be key to classification, as Kraepelin supposed. However, although we have not undertaken relevant population studies ourselves, we are not convinced that Kraepelinian dichotomous categories are any more useful in population-based samples than in clinical samples. We find the studies of Van Os and colleagues (e.g. Krabbendam et al, 2004) persuasive that dimensional measures are useful in describing psychosis-related morbidity in the general population and, contrary to the proposition of Dr Murray, we would expect dimensions to be more useful than categories in populations unselected for severe illness.
Finally, we would like to restate and further emphasise our optimism about the likely rate of progress in identifying biological markers that can validate psychiatric diagnoses. Markers (in the form of genetic polymorphisms) have already been identified that challenge current nosology. For example, using the Bipolar Affective Disorder Dimension Scale (which rates affective and psychotic dimensions; Craddock et al, 2004) in a study of over 600 cases each of schizophrenia and bipolar disorder, we have demonstrated that a risk variant within the Neuregulin 1 gene, which has been associated with risk of schizophrenia in several samples (reviewed in Craddock et al, 2005), may confer specific risk for a form of psychotic illness characterised by features of both mania and mood-incongruent psychosis (Green et al, 2005). Other findings of a similar nature are currently emerging from our own studies and those of other groups, and we anticipate that we are entering a period during which psychiatric research and practice will be placed on much firmer nosological foundations than has been possible in the past.
REFERENCES
- Craddock, N., Jones, I., Kirov, G., et al (2004) The Bipolar Affective Disorder Dimension Scale (BADDS) – a dimensional scale for rating lifetime psychopathology in bipolar spectrum disorder. BMC Psychiatry, 4, 19.[CrossRef][Medline]
- Craddock, N., O’Donovan, M. C. & Owen, M. J.
(2005) The genetics of schizophrenia and bipolar disorder:
dissecting psychosis. Journal of Medical Genetics,
42, 288
–299.
[Free Full Text] - Green, F. K., Raybould, R., Macgregor, S., et al
(2005) Operation of the schizophrenia susceptibility gene,
neuregulin 1, across traditional diagnostic boundaries to increase risk for
bipolar disorder. Archives of General Psychiatry,
62, 642
–648.
[Abstract/Free Full Text] - Krabbendam, L., Myin-Germeys, I., De Graaf, R., et al (2004) Dimensions of depression, mania and psychosis in the general population. Psychological Medicine, 34, 1177 –1186.[CrossRef][Medline]
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