2008, 193:426. BJP Martin P. Lock Treatment of antisocial personality disorder References http://bjp.rcpsych.org/content/193/5/426.1#BIBL This article cites 0 articles, 0 of which you can access for free at: permissions Reprints/ permissions@rcpsych.ac.uk write to To obtain reprints or permission to reproduce material from this paper, please to this article at You can respond http://bjp.rcpsych.org/cgi/eletter-submit/193/5/426 from Downloaded The Royal College of Psychiatrists Published by on January 19, 2014 http://bjp.rcpsych.org/ http://bjp.rcpsych.org/site/subscriptions/ go to: The British Journal of Psychiatry To subscribe to Treatment of antisocial personality disorder Although Professor Madens article was only 100 words long, 1 it contained some profound and, I think, unfair and unsubstan- tiated, statements. Where is the evidence that patients with severe antisocial personality disorders who do not want to be treated, like many of those detained in the dangerous and severe personality disorder (DSPD) unit at Broadmoor Hospital, where Professor Maden is the clinical director, can be effectively treated? Professor Maden criticises lawyers and independent experts but both he and others researching in the field have not produced independently verified evidence of efficacy. Professors Coid 2 and Duggan, 3,4 with others, have carried out meta-analyses and concluded that there was no evidence or that the evidence was very weak. Professor Duggan went as far as to suggest that this situation was ultimately unsustainable and would inevitably lead to legal challenges by those detained on the basis of their treatability. The Canadians and Americans are concerned that psycho- logical therapy with individuals with high scores on the Hare Psychopathy Checklist Revised is making the situation worse and leading to increases in recidivism. 5 They appear to have moved on and are investigating biological treatments such as hormone treatment for sex offenders or even addressing the putative causes with gene mapping. 6 Is it really justifiable to blame lawyers and independent experts for pointing out this lack of evidence and that the DSPD project might not only be an expensive waste of time but it could be making the situation worse? Declaration of interest M.P.L. provides independent psychiatric reports to solicitors of patients in DSPD units. He is also a member of the Mental Health Review Tribunal and sometimes sits on DSPD units. 1 Maden T. Can personality disorder be treated? 100 words. Br J Psychiatry 2008; 192: 457. 2 Dolan B, Coid J. Psychopathic and Antisocial Personality Disorders: Treatment and Research Issues. Gaskell, 1993. 3 Binks CA, Fenton M, McCarthy L, Lee T, Adams CE, Duggan C. Pharmacological interventions for people with borderline personality disorder. Cochrane Database Syst Rev 2006; 1: CD005653. 4 Binks CA, Fenton M, McCarthy L, Lee T, Adams CE, Duggan C. Psychological therapies for people with borderline personality disorder. Cochrane Database Syst Rev 2006; 1: CD005652. 5 Seto MC, Barbaree HE. Psychopathy, treatment behaviour, and sex offender recidivism. J Interpers Violence 1999; 14: 123548. 6 Seto MC, Quinsey VL. Toward the future: translating basic research into prevention and strategies. In Handbook of Psychopathy (ed CJ Patrick): 589601. Guilford Press, 2006. Martin P. Lock, address supplied. Email: dr.martinlock@tiscali.co.uk doi: 10.1192/bjp.193.5.426 Authors reply: Article, 100; response, 300+. Is this a metaphor for the medico-legal contribution to psychiatric knowledge, i.e. more words? The evidence for treatability of detained patients is the case law: tribunals dont discharge them and stretch the definition of treatment in so far it makes sense only to lawyers. I dont criticise the players for making a living, but the waste of public money from asking the wrong people the wrong question. Still, the profession could do more by ensuring independent experts in psychiatry (as in other branches of medicine) have clinical or research expertise rather than just an opinion (100). Anthony Maden, Division of Neurosciences and Mental Health, Imperial College London. Email: a.maden@imperial.ac.uk doi: 10.1192/bjp.193.5.426a Symptoms do not helpfully distinguish unipolar and bipolar depression Forty et als study 1 revisits a familiar question and reports some statistically significant differences in the frequency of clinical features between unipolar and bipolar depression. The report then moves beyond description to emphasise the clinical importance of these differences. The three symptoms most predictive of bipolar depression were presence of psychosis, diurnal mood variation and hypersomnia. To be considered important, these symptoms when present would need to influence clinical decisions. The sensitivity of these three symptoms for bipolar depression ranged from 0.3 to 0.59. The specificity ranged from 0.5 to 0.9. The positive predictive value (PPV) ranged from 0.55 to 0.69. As the prevalence of bipolar disorder in the sample was 0.43, these PPV results do not greatly increase the probability of bipolar disorder above the base rate. Likewise, the negative predictive value ranged from 0.63 to 0.69, while the base rate of unipolar depression was 0.57. Again, there is little gain of information. Because this differential diagnosis relies on pattern recognition rather than on discrete, pathognomonic symptoms, it may be more helpful to examine cases in which all three important clinical differences were present. When all three features are required, beginning with the highest PPV (psychotic features), then the middle PPV (hypersomnia), then the lowest PPV (diurnal variation), and assuming the three symptoms are independent, then 34 bipolar cases and 7 unipolar cases would stand out. From this result, the sensitivity of the triune pattern would be 0.08 and the specificity 0.99. The PPV is 0.83 and the negative predictive value is 0.59. How important is a clinical symptom pattern that detects only 8% of bona fide bipolar cases and that does not positively rule in unipolar cases? Moreover, there is no guarantee that latent bipolar depression has the same symptom profile as fully expressed bipolar depression. All in all, these results underscore the limitations of parsing clinical symptoms for the purpose of classification. The important clinical differences give little added information to clinicians for treatment planning. That is why efforts continue to discover biomarkers or endophenotypes or genetic markers. 1. Forty L, Smith D, Jones L, Jones I, Caesar S, Cooper C, Fraser C, Gordon-Smith K, Hyde S, Farmer A, McGuffin P, Craddock N. Clinical differences between bipolar and unipolar depression. Br J Psychiatry 2008; 192: 3889. Bernard J. Carroll, Pacific Behavioral Research Foundation, PO Box 223040, Carmel, CA 93922-3040, USA. Email: bcarroll@redshift.com doi: 10.1192/bjp.193.5.426b 426 Edited by Kiriakos Xenitidis and Colin Campbell Contents & Treatment of antisocial personality disorder & Symptoms do not helpfully distinguish unipolar and bipolar depression The British Journal of Psychiatry (2008) 193, 426427 Correspondence Authors reply: We are in full agreement with Carroll about the limited utility of clinical symptoms for diagnostic tests and the consequent importance of efforts to discover biomarkers, endophenotypes or genetic markers. In fact, the main focus of our research is molecular genetic epidemiological investigation of mood disorders and psychoses that has precisely this aim. 14 Further, we have a keen interest in using findings to provide biological validators for psychiatric nosology, classification and clinical diagnosis. 5 However, for the moment, psychiatrists have to make do with the clinical tools available and be alert to diagnostic clues that can help in the delivery of optimal care to their patients. We stand by the statements in our paper: It is commonly, but wrongly, assumed that there are no important differences in the clinical presentation of unipolar and bipolar depression . . . The clinical features of depression are not, of course, a definitive guide to diagnosis but can help alert the clinician to a possible bipolar course . . . This is important because optimal management varies between bipolar and unipolar depression. 1 Green EK, Raybould R, Macgregor S, Gordon-Smith K, Heron J, Hyde S, Grozeva D, Hamshere M, Williams N, Owen MJ, ODonovan MC, Jones L, Jones I, Kirov G, Craddock N. Operation of the schizophrenia susceptibility gene, neuregulin 1, across traditional diagnostic boundaries to increase risk for bipolar disorder. Arch Gen Psychiatry 2005; 62: 6426. 2 Williams NM, Green E, Macgregor S, Dwyer S, Norton N, Williams H, Raybould R, Grozeva D, Hamshere M, Zammit S, Jones L, Cardno A, Kirov G, Jones I, ODonovan MC, Owen MJ, Craddock N. Variation at the DAOA/G30 locus influences susceptibility to major mood episodes but not psychosis in schizophrenia and bipolar disorder. Arch Gen Psychiatry 2006; 63: 36673. 3 Wellcome Trust Case Control Consortium. Genome-wide association study of 14,000 cases of seven common diseases and 3,000 shared controls. Nature 2007; 447: 66178. 4 Craddock N, Jones L, Jones IR, Kirov G, Green EK, Grozeva D, Moskvina V, Nikolov I, Hamshere ML, Vukcevic D, Caesar S, Gordon-Smith K, Fraser C, Russell E, Norton N, Breen G, St Clair D, Collier DA, Young AH, Ferrier IN, Farmer A, McGuffin P, Holmans PA, Donnelly P, Owen MJ, ODonovan MC. Strong genetic evidence for a selective influence of GABA-A receptors on a component of the bipolar disorder phenotype. Mol Psychiatry 2008; in press. 5 Craddock N, Owen MJ. Rethinking psychosis: the disadvantages of a dichotomous classification now outweigh the advantages. World Psychiatry 2007; 6: 8491. Liz Forty, Department of Psychological Medicine, School of Medicine, Cardiff University, and Department of Psychiatry, Division of Neuroscience, University of Birmingham; Daniel Smith, Department of Psychological Medicine, School of Medicine, Cardiff University; Lisa Jones, Department of Psychiatry, Division of Neuroscience, University of Birmingham; Ian Jones, Department of Psychological Medicine, School of Medicine, Cardiff University, and Department of Psychiatry, Division of Neuroscience, University of Birmingham; Sian Caesar, Carly Cooper, Department of Psychiatry, Division of Neuroscience, University of Birmingham; Christine Fraser, Department of Psychological Medicine, School of Medicine, Cardiff University; Katherine Gordon-Smith, Department of Psychological Medicine, School of Medicine, Cardiff University, and Department of Psychiatry, Division of Neuroscience, University of Birmingham; Sally Hyde, Department of Psychiatry, Division of Neuroscience, University of Birmingham; Anne Farmer, Peter McGuffin, MRC SGDP Research Centre, Institute of Psychiatry, London; Nick Craddock, Department of Psychological Medicine, School of Medicine, Cardiff University, Cardiff CF14 4XN. Email: craddockn@cardiff.ac.uk doi: 10.1192/bjp.193.5.427 427 Correspondence