The British Journal of Psychiatry (2008)

193, 426427

Correspondence
Edited by Kiriakos Xenitidis and
Colin Campbell

Contents
&

Treatment of antisocial personality disorder

&

Symptoms do not helpfully distinguish unipolar

and bipolar depression

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

Treatment of antisocial personality disorder

Although Professor Madens 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
treatability.
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.

426

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: 123548.

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.

Symptoms do not helpfully distinguish unipolar

and bipolar depression
Forty et als 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: 3889.

Martin P. Lock, address supplied. Email: dr.martinlock@tiscali.co.uk

Bernard J. Carroll, Pacific Behavioral Research Foundation, PO Box 223040, Carmel,

CA 93922-3040, USA. Email: bcarroll@redshift.com

doi: 10.1192/bjp.193.5.426

doi: 10.1192/bjp.193.5.426b

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.

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.

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.

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

Treatment of antisocial personality disorder

Martin P. Lock
BJP 2008, 193:426.
Access the most recent version at DOI: 10.1192/bjp.193.5.426

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