Derek Bolton

What is a mental/psychiatric disorder? From DSM-IV to DSM-V

The distinction between normality and psychopathology has long been subject to debate. DSM-III and DSM-IV provided a definition of mental disorder to help clinicians address this distinction. As part of the process of developing DSM-V, researchers have reviewed the concept of mental disorder and emphasized the need for additional work in this area. Here we review the DSM-IV definition of mental disorder and propose some changes. The approach taken here arguably takes a middle course through some of the relevant conceptual debates. We agree with the view that no definition perfectly specifies precise boundaries for the concept of mental/psychiatric disorder, but in line with a view that the nomenclature can improve over time, we aim here for a more scientifically valid and more clinically useful definition.

What is mental disorder? : an essay in philosophy, science, and values

1. The current diagnostic manuals: aims, methods, and questions 2. The sciences on mental order/disorder and related concepts: normality, meaning, natural and social norms 3. Mental disorder and human nature 4. Clinical definition: distress, disability and the need to treat 5. Boundaries and terminology in flux 6. Some conclusions

Magical thinking in childhood and adolescence: Development and relation to obsessive compulsion

Magical thinking in childhood bears at least superficial similarities to obsessive compulsion, and recent cognitive models of obsessive compulsive disorder implicate forms of thinking akin to the magical. However, there has been little research on the relations between normal magical thinking in childhood and obsessive compulsion. The present study has two aims: to investigate magical thinking in young children and through to late adolescence, and to examine the relation between magical thinking and obsessive compulsion. It was found that children across the age range studied reported some magical thinking, and there was no general decline in the level of magical thinking with age. This overall pattern was complicated, however, by fluctuations in the level of magical thinking in later childhood and early adolescence, and by gender differences. There was a significant correlation between levels of magical thinking and obsessive compulsion. The results are discussed in the light of current theories.

Prevalence and genetic and environmental influences on anxiety disorders in 6 year old twins

BACKGROUND Prevalence of childhood anxiety disorders at specific ages and genetic etiological influences on anxiety disorders in young children have been little studied. The present study reports prevalence estimates in a community sample of 6-year-old twins, and patterns of genetic and environmental influences on these early-onset anxiety disorders. METHOD Using a two-phase design 4,662 twin-pairs were sampled and 854 pairs were assessed in the second phase by maternal-informant diagnostic interview using DSM-IV criteria. RESULTS The most common conditions were separation anxiety disorder (SAD) [2.8%, 95% confidence interval (CI) 2.1-3.8, for current disorder] and specific phobia (10.8%, 95% CI 8.4-13.6, for current disorder). Behavioral genetic modeling was feasible for these two conditions, applied to two phenotypes: symptom syndrome (regardless of impairment) and the narrower one of diagnostic status (symptom syndrome with associated impairment). The heritability estimate for SAD diagnostic status was high, 73%, with remaining variance attributed to non-shared environment. The heritability estimates for specific phobia were also high, 80% for the symptom syndrome and 60% for diagnostic status, with remaining variance attributed in both cases to non-shared environment. CONCLUSIONS Compared with previous epidemiological surveys of children and adolescents in wide age-bands, the current estimates suggest that rates of anxiety disorders assessed in young childhood are generally at least as high and perhaps higher compared with those found in older children. The heritability estimates suggest that the genetic effects on these early-onset anxiety disorders are substantial and more significant than environmental effects, whether shared or non-shared.

Obsessive-compulsive disorder, tics and anxiety in 6-year-old twins

BACKGROUND Previous reports of genetic influences on obsessive-compulsive disorder (OCD) symptoms have suggested moderate heritability. Family history studies of co-morbidity have found familial aggregation with tics, especially for early-onset OCD, and familial aggregation with anxiety disorders. METHOD Heritability of OCD and familial aggregation of OCD, tics and anxiety disorders were investigated in a community sample of 6-year-old twins using a two-phase design in which 4662 twin pairs were sampled and 854 pairs were assessed in the second phase by maternal-informant diagnostic interview using DSM-IV criteria. RESULTS In the multivariate model combined additive genetic and common environmental effects were estimated as 47% for sub-threshold OCD, and the model was unable to distinguish these sources of familial aggregation. There were strong familial aggregations between sub-threshold OCD and tics and between sub-threshold OCD and other anxiety disorders (80% and 97% respectively), although again specific sources could not be distinguished. CONCLUSIONS The findings are consistent with the hypothesis of a tic-related early-onset OCD phenotype, but also with the hypothesis of an anxiety-related early-onset OCD phenotype.

Neurological and neuropsychological signs in obsessive compulsive disorder: interaction with behavioural treatment

The main aim of this study was to test the hypothesis that neurological soft signs and neuropsychological abnormalities associated with obsessive-compulsive disorder (OCD) predict poor response to behavioural treatment. The design permitted investigation of secondary hypotheses, regarding correlations among these neurological markers and levels of symptomatology, and their stability in relation to changes in levels of symptomatology. Thirty-five participants satisfying DSM-IV diagnostic criteria for OCD were assessed pre- and postbehavioural treatment using a scaled measure of symptom severity, and a battery of tests sensitive to neuropsychological deficits associated with OCD. Eighteen of the participants were also assessed on an inventory of neurological soft signs. Neither neuropsychological test deficits nor neurological soft signs pretreatment predicted response to behavioural treatment. Lower performance on neuropsychological tasks and symptom severity were both significantly correlated with levels of soft signs. Some neurological markers were less severe posttreatment, but these changes were not related to treatment response.

Neurological soft signs in obsessive compulsive disorder: standardised assessment and comparison with schizophrenia

While several studies have detected raised levels of neurological soft signs in patients with obsessive compulsive disorder (OCD), the specificity of these abnormalities remains uncertain. This study used a new standardised measure, the Cambridge Neurological Inventory (CNI), to assess soft signs in 51 subjects with OCD. Comparison was made with data on patients with schizophrenia and a non-clinical control group from a previously reported study. Individuals with OCD showed raised levels of soft signs compared with non-clinical controls in many categories of the CNI: Motor Coordination, Sensory Integration, Primitive Reflexes, Extrapyramidal Signs, and Failure of Suppression. Compared with patients with schizophrenia, the OCD group had lower levels of neurological signs in some CNI categories: Hard Signs, Motor Co-ordination, Tardive Dyskinesia, Catatonic Signs, and Extrapyramidal Signs. However, levels of soft signs in the OCD group did not significantly differ from those in the schizophrenia group in other CNI categories: Sensory Integration, Primitive Reflexes and Failure of Suppression. The significance of these patterns of findings is discussed.

Randomized controlled trial of full and brief cognitive-behaviour therapy and wait-list for paediatric obsessive-compulsive disorder

BACKGROUND Reviews and practice guidelines for paediatric obsessive-compulsive disorder (OCD) recommend cognitive-behaviour therapy (CBT) as the psychological treatment of choice, but note that it has not been sufficiently evaluated for children and adolescents and that more randomized controlled trials are needed. The aim of this trial was to evaluate effectiveness and optimal delivery of CBT, emphasizing cognitive interventions. METHODS A total of 96 children and adolescents with OCD were randomly allocated to the three conditions each of approximately 12 weeks duration: full CBT (average therapist contact: 12 sessions) and brief CBT (average contact: 5 sessions, with use of therapist-guided workbooks), and wait-list/delayed treatment. The primary outcome measure was the child version of the semi-structured interviewer-based Yale-Brown Obsessive Compulsive Scale. CLINICAL TRIAL REGISTRATION http://www.controlled-trials.com/ISRCTN/; unique identifier: ISRCTN29092580. RESULTS There was statistically significant symptomatic improvement in both treatment groups compared with the wait-list group, with no significant differences in outcomes between the two treatment groups. Controlled treatment effect sizes in intention-to-treat analyses were 2.2 for full CBT and 1.6 for brief CBT. Improvements were maintained at follow-up an average of 14 weeks later. CONCLUSIONS The findings demonstrate the benefits of CBT emphasizing cognitive interventions for children and adolescents with OCD and suggest that relatively lower therapist intensity delivery with use of therapist-guided workbooks is an efficient mode of delivery.

A multivariate genetic analysis of specific phobia, separation anxiety and social phobia in early childhood.

BackgroundComorbidity amongst anxiety disorders is very common in children as in adults and leads to considerable distress and impairment, yet is poorly understood. Multivariate genetic analyses can shed light on the origins of this comorbidity by revealing whether genetic or environmental risks for one disorder also influence another. We examined the genetic and environmental influences on the comorbidity between three common childhood anxiety disorders: Specific Phobia, Separation Anxiety and Social Phobia.MethodsUsing a two-phase design 4,662 twin-pairs were screened in the first phase and 854 pairs were assessed in the second phase by maternal-informant diagnostic interview using DSM-IV criteria.ResultsMultivariate genetic analysis revealed significant shared environmental over-lap between Specific Phobia and Separation Anxiety and significant familial and non-shared environmental over-lap between Specific Phobia and Social Phobia.ConclusionsFamilial influences, especially shared environment, are central to the comorbidity between Specific Phobia and both Separation Anxiety and Social Phobia.

Should mental disorders be regarded as brain disorders? 21st century mental health sciences and implications for research and training.

Two recent papers focus our attention on developments in mental health sciences and their implications, respectively, for research, by Insel et al 1, and for the psychiatry profession, by White et al 2. Both papers headline the classification problem and both propose to regard mental disorders as brain disorders. While this proposal is not new 3,4, what is striking is that these two recent formulations are plainly not reductionist. By this, I mean that they do not suppose that neural dysfunctions are the only causes of mental disorders, but rather recognize developments in mental health sciences showing that causes or risks of mental disorders may operate at many levels, including the genetic and the neural, the individual, the family environment, and the social context. Crucially, this view of multifactorial or multilevel view of causation (or risk) acknowledges and is intended to accommodate the fact that interventions at these various levels may affect onset and course, playing parts in primary prevention and management and treatment after. This is one aspect of developments in mental health sciences outlined by both papers; another, and the emphasis in both papers, is the massive recent developments in the fields of genetics and neuroscience. There is something of a tension between these two aspects of the new mental health sciences. On the one hand, the importance of genetics and neuroscience can suggest that the important causal pathways are intra-organism, within the brain in particular, pulling toward reductionism, a plausible interpretation of the proposal that mental disorders are brain disorders. On the other hand, if the causal pathways really do run up and down the biopsychosocial system, in and out of the organism, then the brain is part of the system involved, so also may be the mental life of the patient and their life circumstances — a nonreductionist view, not well expressed by the proposal that mental disorders are brain disorders. One way to examine this apparent tension is by considering the “biopsychosocial model” in the context of the new sciences. This model has recently come under criticism from Ghaemi 5 in its original version due to Engel, in which “all three levels, biological, psychological, and social, must be taken into account in every health care task” 6, a proposition which Ghaemi 5 understands as meaning that the three levels “are all, more or less equally, relevant, in all cases, at all times”. Ghaemi rejects the biopsychosocial model in this sense and also rejects its traditional opposite, biological reductionism, proposing to explore other options between these two extremes. In the brief characterization of new developments in the mental health sciences above, the intention was to say that causal pathways and hence interventions may involve all the three “levels” — the biological, the psychological, and the social — but this was not meant to imply that all the three levels were always causally involved, let alone always involved “equally”. The Research Domain Criteria (RDoC) framework proposed by Insel et al 1 has a matrix in which there are columns labeled genetic, molecular, cellular, neural circuitry, individual, family environment, and social context; in the rows, there are conditions that may be diagnostic or trans-diagnostic. The authors say 1(1, p. 749): “Importantly, all of these levels [in the columns] are seen as affecting both the biology and psychology of mental illness. With the RDoC approach, independent variables for classification might be specified from any of these levels of analysis, with dependent variables chosen from one or more other columns”. However, there is no implication here that all these levels of analysis will always have causal relevance, still less equal causal relevance — regardless of what conditions are entered in the rows. Depending on the condition, genetic risk may be more or less important, for example, as may be the potential for psychological therapy to make any sustainable difference to the primary problem, or the causal role of social factors and potential for effective intervention in this domain. To make the point at one extreme: some conditions that might go into the rows of the RDoC framework will have no ticks under any boxes indicating causal processes at levels other than, for instance, the genetic or the neural, such as Huntingtons disease or concussion, that is, no psychological or social factors make any difference (though they may do if the row had “adjustment to”). That is to say, reductionism might be right in some cases and in some cases it is already known to be right; in other cases, the psychosocial might be more important, account for more of the variance in incidence or outcomes, than, for instance, genetic factors. In short, the new sciences for which RDoC provides a framework make discriminations between conditions in these respects. A related aspect of the view of causation in the new sciences is that they emphasize the interplay between the internal biology, the environment, and individual differences. Causal interplay occurs in normative development and in the development and course of health conditions, in psychiatric conditions and in some general medical conditions such as cardiovascular disease. The new sciences of genetics and gene–environment interactions through the life course can be expected to increase this emphasis on interactions, and it will require research attention to be given not only to genes and the brain but also to environmental impacts and their timing in interaction with internal processes. In this context, the research effort needs to span the biological, the psychological/behavioral, and the environmental/social context, and their interactions — not limited to a “brain science” that studies only what is inside the skull. The question of the importance of biological factors in mental disorders and especially the proposition that mental disorders should be regarded and classified as brain disorders is often coupled with challenges facing the psychiatry profession 2,4(e.g., 2,4). Many recent within-psychiatry papers have referred to challenges facing the profession, including clarifying the distinctive task of medical psychiatry within multiprofessional mental health care provision and improving the too low rates of recruitment of medical graduates into psychiatry 2,4,7–10. The new sciences as indicated above generally reaffirm the position of psychiatry as a medical specialty by blurring the differences between mental health and physical health conditions: the same kinds of multifactorial pathways may be operating in both. Nevertheless, while this is correct, the common assumption is that mental health conditions involve much of the psychosocial, evidenced for example in many of the “rapid responses” in the BMJ (see http://www.bmj.com) following the publication of the White et al analysis 2. The RDoC framework 1 actually provides a way in which medical and psychiatric conditions could be compared, and let me make a suggestion: if you put 10 typical physical health conditions in the first 10 rows of the framework and 10 typical mental health conditions in the next 10 rows, and fill in the cells in each column with processes known to be causal and amenable to effective intervention in the condition (after onset) — then the density of the resulting matrix would be greater in the upper left and the lower right quadrants. Once they have onset, physical health conditions are more amenable to internal medical procedures and not much to psychosocial; conversely, mental health conditions are more amenable to psychosocial interventions. My only excuse for flying such a kite without book length examination is that it at least represents common prejudice. In any case, it would all likely look different again — the density patterns would shift — if the rows had “primary prevention of”; and it would shift around again if the rows had “persons attitude to their illness”, or “attitude to risk”, or “adjustment to/quality of life in”, that is, factors relevant to decent health care. Insofar as psychiatry has particular expertise in the management of psychosocial factors as well as internal biological factors, it is somewhat unlike the rest of medicine, in particular, unlike much of internal medicine, and this is probably one of the problems in defining medical psychiatrys distinctive role among the other psychosocial professions — clinical psychology and social work — and in medical graduate recruitment to the profession. However — and this is the main point I wish to make in this connection — these professional divisions and the educational traditions they embody do not make much sense from the point of view of the new mental health sciences. These new sciences do not work with ideological battles between the biological, the psychological, and the social, the old parallel universes with poor communication between them; rather they work with all of these factors and the diversity of interplay between them. Whether our current professional boundaries and trainings are fit for the purpose of accommodating, assimilating, and applying the vast fields and subtleties of these new sciences is seriously open to doubt. Yet this is what we need, I suggest, to align future mental health services with the science. What is to be looked forward to — and I raise this issue as a clinical psychologist, not a psychiatrist — is not so much reestablishing psychiatry as a medical speciality, going over again a 100-year-old problematic, but the construction of a new curriculum covering genetics, neuroscience, psychology, and social determinants of health, for a new profession of consultants in mental health for the 21st century. This might provide better care for patients, relative to expenditure, and might also solve the recruitment problem.