Technical harmonization?

Theoretically, revisions of a diagnostic classification system should be driven by solid scientific evidence for introducing necessary changes that improve the core functions of a classificatory system. For example, changes should improve communication in research and practice and improve utility in terms of treatment, intervention and prognosis. In reality, however, revisions are strongly driven by additional motivations, such as the drive to be different from the past, political concerns, and technical reasons. Bearing this in mind, the meaning of the proposed meta-structure is not entirely clear. Is it simply meant to simplify the grouping of the disorders by significantly reducing the number of major classes? This might indeed be a worthwhile goal if it were simply for technical/pragmatic reasons. The alphanumeric system of ICD chapters, for example, only allows for 10 major groups and it would be desirable if there was a greater concordance with the current DSM-IV-TR classification, which currently specifies 17. Such concordance would reduce the potential for problems between the classificatory systems. Harmonization between the two systems could simply occur by reducing the number of DSM categories by a more or less arbitrary or ‘technical’ procedure that combined major DSM groups; in fact the current ICD-10 provides an example, though imperfect, for this. Alternatively, a more radical approach could be used, such as the one suggested with the meta-structure proposal. If such a ‘technical harmonization’ is the primary intention, then the meta-structure proposal would not do any major harm because it allows individual diagnoses to be retained, albeit under different umbrellas within the meta-structures five clusters.

However, the current proposition mentions five clusters, leaving open how the remaining slots will be filled. This opens the dangerous possibility that additional clusters will be added with other groups of disorders, but without a similarly rigorous approach used to derive the five meta-structure clusters suggested in this issue. Alternatively, it is possible that there will be only one residual class. Having been involved in some of the ‘political negotiations’ of past DSM and ICD revisions, we assume the former will happen, resulting in a mixed bag of classificatory structures.

Deeper theoretical meaning and implication?

We struggled with the fact that the meta-structure proposition was obviously intended to have a ‘deeper’ meaning. All papers emphasize repeatedly that the proposition ‘is a step away from a classification based on symptom picture alone’ (Andrews et al. Reference Andrews, Goldberg, Krueger, Carpenter, Hyman, Sachdev and Pine2009a) towards ‘a classification based on etiological risk factors’ (Andrews et al. Reference Andrews, Goldberg, Krueger, Carpenter, Hyman, Sachdev and Pine2009a). Across variations in terminology, all papers emphasize the role of ‘causal risk’ factors or ‘spectrum's phenotypic coherence’ (Krueger & South, Reference Krueger and South2009) and suggest that the findings move us towards a deeper aetiological meaning. Within this context, the authors claim that the emotional cluster disorders, for example, share ‘emotional dysregulation and negative emotionality’ as core defining features whereas the externalizing cluster disorders share ‘disinhibition’. To the degree that this is the case, significant concerns arise.

(a) Given that the evidence presented in favour of the proposed clusters is selective and ‘biased’ towards the similarities rather than the differences between disorders, we question the claim that the meta-structure will be helpful. How significant and substantial is the danger that the guiding principles will misguide future research or even negatively impact our clinical practice?

(b) The proposal is strongly driven by one theoretically and methodologically problematic approach, namely explorations of higher-order factor analytic methods. Based largely on studies of co-morbidity patterns in the community, these studies suggest that symptom and diagnostic data might be best grouped into an internalizing factor (i.e. panic disorder, generalized anxiety disorder, agoraphobia, specific and social phobia in addition to major depression and dysthymia) and an externalizing factor (i.e. substance dependence, conduct and antisocial personality disorders). However, the authors of the meta-structure papers should have also acknowledged the severe limitations of this methodological approach and the data upon which it is based (Wittchen et al. Reference Wittchen, Höfler and Merikangas1999, Reference Wittchen, Beesdo and Gloster2009). The most relevant limitations are the statistical method, the lack of developmental stability, and the lack of structural stability when additional disorders are considered. In fact, these factor analytic studies have been based on only some (maximum 12 disorders) of the disorders considered for the five clusters and only a minority of all DSM disorders. Therefore, the rationale and designation of additional disorders above and beyond the factor analytic evidence remains unclear in many sections.

(c) Alternative meta-structure approaches exclusively based on single risk factor domains (e.g. neurobiological, familiality, shared specific environmental factors), course and outcome or other perspectives such as ‘staging of disorder progression’ (Shear et al. Reference Shear, Bjelland, Beesdo, Gloster and Wittchen2007), or functional–behavioural or linguistic concepts (Hayes et al. Reference Hayes, Barnes-Holmes and Roche2001) were neither considered nor explored systematically. The scientific evidence presented in the meta-structure papers was always ‘forced to fit’ the top-down derived meta-structure emphasizing similarities and ‘downplaying’ differences. How heavily should we weight the danger that this strategy misses or discards important and meaningful signals for core psychopathological mechanisms and processes?

(d) In many papers, we struggled with the authors' use of the term ‘causal’ risk factors. The overemphasis on ‘causal’ risk factors occurred to the exclusion of other factors. Furthermore, the authors seem to assume that the availability of family-genetic and neurobiological evidence in many domains is tantamount to causal proof for a mental disorder. This seems to be overly optimistic. To date, for almost all disorders there is little evidence for any causal factor or mechanism that is both necessary and sufficient for a specific mental disorder and even the status of many measures as reliable ‘markers’ is typically controversial. Throughout the papers, the authors only poorly address the degree to which these ‘neurobiological’ measures are merely correlates of disturbances in cognition, emotion and behaviour inherent in the respective condition considered and across all mental disorders. Clearly, all mental disorders must be associated with disturbances in neural mechanisms but, with a few diagnostic exceptions, a core causal role as precipitant is as questionable as it is for psychological and environmental factors (see, for example, Andrews et al. Reference Andrews, Pine, Hobbs, Anderson and Sunderland2009b). It might be more appropriate to assume that all these factors interact dynamically and might all be responsible in a probabilistic way at all times for all disorders in some way or another. This, of course, is difficult to capture in a structural appraisal of a diagnostic classification system.

(e) Some of the major limitations of the meta-structure proposal are addressed in the introductory paper. These include the ‘top-down’ approach, lack of systematic reviews, lack of coherent and comprehensive data supporting the proposed clusters, incomplete and partly contradictory evidence in terms of the 11 criteria, largely lacking proof-of-concept information, lack of systematic exploration and testing of alternative grouping, and the partly assumed cluster membership of a diagnosis without data and research evidence. Despite these understandable but considerable limitations, the papers frequently seem to overstate what they found in many places. Claims that the data ‘validate’ the clusters (Andrews et al. Reference Andrews, Goldberg, Krueger, Carpenter, Hyman, Sachdev and Pine2009a) or that the meta-structure proposition relied on (causal) risk factors and clinical factors and is thus ‘more parsimonious’ (Andrews et al. Reference Andrews, Goldberg, Krueger, Carpenter, Hyman, Sachdev and Pine2009a) seem to go much too far.

‘Deeper’ practical implications?

Is the proposition meant to suggest or would its implementation result in the deletion of certain groups of disorders or even certain diagnoses from our research and clinical practice agenda? To what degree is the meta-structure meant to replace current diagnostic practice by allowing the cluster labels to be used as a sufficient global diagnostic substitute? To what degree is it meant to reduce spurious co-morbidity, by assuming that ‘relevant’ co-morbidity only exists between the five clusters? Although it is prominently emphasized several times that the meta-structure is not meant to delete disorders nor should the clusters be seen as mutually exclusive, inconsistent claims and suggestions for each of these aims can be found across all papers. Given that these questions are not considered systematically, nor are the potential dangers explored, we feel uncomfortable about the ultimate goal, namely the actual use of the proposed meta-structure and its implications for the field. And given the very limited and exploratory evidence for the clusters, adoption of the proposed meta-structure seems premature. It is therefore disconcerting that Andrews et al. (Reference Andrews, Goldberg, Krueger, Carpenter, Hyman, Sachdev and Pine2009a) strongly advocate a major broad-range research programme not only to explicate the neurobiological and other cluster risk factors but also to use the proposed meta-structure as a base for research on treatment, prognosis, and even practice.

In terms of increased clinical utility, there is no explanation of why the proposition would be expected to have greater utility and validity compared to the current DSM grouping. This is especially concerning in that this ‘fact’ is explicitly stated in several papers. For example, Andrews et al. (Reference Andrews, Goldberg, Krueger, Carpenter, Hyman, Sachdev and Pine2009a) state that, for internists and general practitioners, ‘the clustering will simplify an otherwise confusing system’. Yet the papers do not specify how and why a simplification will work, even when a specific diagnostic category still needs to be reliably ascertained before deciding on cluster membership. To be fair, the authors admit this problem indirectly in other places when they state that the utility should be tested and that primary proof of concept studies are needed.

Harmful effects?

The authors of this proposition fail to reflect on the potentially significant negative side-effects. Leaving aside the substantial gaps with regard to supporting data, might the lumping of anxiety, somatoform and depressive disorders under the very broad umbrella of ‘emotional cluster’ revive the stigmatizing and otherwise controversial concept of neurosis? The initial beauty and simplicity of grouping mental disorders into conditions that could be mainly characterized by ‘emotional dysregulation’, as in the emotional cluster, and ‘disinhibition’, as in the externalizing cluster, does not protect against the revival of potentially stigmatizing diagnostic group labels. Even worse, such an organization carries an increased risk of losing sight of research-based distinctions and considerably different intervention needs of the specific anxiety, depressive, somatoform and other ‘emotional cluster’ disorders. It took two decades to communicate, albeit sometimes too subtly, that diagnosing specific mental disorder matters. For example, it is true that the cross-sectional picture of a person with panic disorder with past uncued panic attacks might not be that different from agoraphobia, severe specific phobia, generalized anxiety disorder or even depression with anxiety features when considering presenting symptoms, distress, and associated neurobiological and behavioural correlates. However, doesn't the occurrence of initial spontaneous panic attacks tell us something extremely useful with regard to prognosis (Wittchen & Gloster, Reference Wittchen, Beesdo and Gloster2009; Wittchen et al. Reference Wittchen, Beesdo and Gloster2009) and to treatment? Isn't there persuasive evidence that panic disorder without agoraphobia is a quite different ‘animal’ from panic disorder with agoraphobia (Wittchen et al. Reference Wittchen, Beesdo and Gloster2009) ? How damaging will a broad cluster proposition be in this respect if a ‘deeper’ meaning is involved?

In addition, just as these authors suggest that progress is impeded by the current system's failure to use meta-structures, we must ask what progress might be impeded if these meta-structures are incomplete or incorrect. Intended or not, the diagnostic system will always influence the field's thinking about psychopathology and treatment. Is it therefore wise to adopt a meta-structure with a ‘deeper meaning’ that has not been adequately tested?