The British Journal of Psychiatry (2008

193, 426–427

Edited by Kiriakos Xenitidis and
Colin Campbell


Treatment of antisocial personality disorder


Symptoms do not helpfully distinguish unipolar
and bipolar depression

Author’s 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 don’t discharge them and stretch the
definition of treatment in so far it makes sense only to lawyers.
I don’t 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:
doi: 10.1192/bjp.193.5.426a

Treatment of antisocial personality disorder
Although Professor Maden’s article was only 100 words long,1 it
contained some profound and, I think, unfair and unsubstantiated, 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 Coid2 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
The Canadians and Americans are concerned that psychological 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.



Maden T. Can personality disorder be treated? 100 words. Br J Psychiatry
2008; 192: 457.


Dolan B, Coid J. Psychopathic and Antisocial Personality Disorders:
Treatment and Research Issues. Gaskell, 1993.


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.


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.


Seto MC, Barbaree HE. Psychopathy, treatment behaviour, and sex offender
recidivism. J Interpers Violence 1999; 14: 1235–48.


Seto MC, Quinsey VL. Toward the future: translating basic research into
prevention and strategies. In Handbook of Psychopathy (ed CJ Patrick):
589–601. Guilford Press, 2006.

Symptoms do not helpfully distinguish unipolar
and bipolar depression
Forty et al’s study1 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: 388–9.

Martin P. Lock, address supplied. Email:

Bernard J. Carroll, Pacific Behavioral Research Foundation, PO Box 223040, Carmel,
CA 93922-3040, USA. Email:

doi: 10.1192/bjp.193.5.426

doi: 10.1192/bjp.193.5.426b

Ian Jones. Williams N. Cardiff University. Hamshere ML. Owen MJ. Carly Cooper. of course. Owen MJ. Jones L. Vukcevic D. Dwyer S. Kirov G. Grozeva D. MRC SGDP Research Centre.000 shared controls. 4 Craddock N. School of Medicine. Grozeva D. Farmer A. Jones I. Jones IR. Macgregor S. Department of Psychiatry. Russell E. Norton N. we have a keen interest in using findings to provide biological validators for psychiatric nosology. Department of Psychiatry. Gordon-Smith K. but wrongly. Cardiff University. 63: 366–73. Craddock N. Sian Caesar. School of Medicine. School of Medicine. Norton N. the main focus of our research is molecular genetic epidemiological investigation of mood disorders and psychoses that has precisely this aim. 2 Williams NM. classification and clinical diagnosis.5. Liz Forty. Rethinking psychosis: the disadvantages of a dichotomous classification now outweigh the advantages. Green EK. Arch Gen Psychiatry 2006. School of Medicine. neuregulin 1. in press. Department of Psychological Medicine. Donnelly P. Sally Hyde. and Department of Psychiatry. Division of Neuroscience. Christine Fraser. University of Birmingham. Kirov G. Lisa Jones. School of Medicine. University of Birmingham. Mol Psychiatry 2008.1192/bjp. Department of Psychiatry. In fact. University of Birmingham. Department of Psychological Medicine. The clinical features of depression are not. London. assumed that there are no important differences in the clinical presentation of unipolar and bipolar depression . Institute of Psychiatry. Gordon-Smith K. Anne Farmer. University of Birmingham. . Hyde S. and Department of Psychiatry. Raybould R. Genome-wide association study of 14. Owen MJ. for the moment. Green E. Macgregor S. Nature 2007. across traditional diagnostic boundaries to increase risk for bipolar disorder. Department of Psychological Medicine. Division of Neuroscience. Breen G. St Clair D.193. University of Birmingham. McGuffin P. 62: 642–6. Peter McGuffin.5 However. School of Medicine. Hamshere M. Cardiff University. Williams H.’ 1 Green EK. Cardiff University. Division of Neuroscience. Arch Gen Psychiatry 2005. Email: craddockn@cardiff. Zammit S. Katherine Gordon-Smith. Owen MJ. Operation of the schizophrenia susceptibility gene. Fraser C. Variation at the DAOA/G30 locus influences susceptibility to major mood episodes but not psychosis in schizophrenia and bipolar disorder. and Department of Psychiatry. Craddock N. Nikolov I. Grozeva D. Jones L. O’Donovan MC. Strong genetic evidence for a selective influence of GABA-A receptors on a component of the bipolar disorder phenotype. Holmans PA.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. University of Birmingham. O’Donovan MC. 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. Department of Psychological Medicine. Jones L. 6: 84–91. Division of Neuroscience. Kirov G. a definitive guide to diagnosis but can help alert the clinician to a possible bipolar course . Young AH. Caesar S. O’Donovan doi: 10. Cardiff University. . .427 427 . Nick Craddock. Cardiff University. Department of Psychological Medicine. 447: 661–78. 5 Craddock cases of seven common diseases and 3. Division of Neuroscience. This is important because optimal management varies between bipolar and unipolar depression. World Psychiatry 2007. Hamshere M. Collier DA. Department of Psychological Medicine. Cardiff CF14 4XN. Raybould R. We stand by the statements in our paper: ‘It is commonly. Division of Neuroscience. Cardno A. endophenotypes or genetic markers. 3 Wellcome Trust Case Control Consortium. Jones I. Heron J.1–4 Further. Ferrier IN. . Moskvina V. Daniel Smith.

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