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Symptoms do not helpfully distinguish unipolar and bipolar depression
- Bernard J. Carroll (11 June 2008)
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Re: Symptoms do not helpfully distinguish unipolar and bipolar depression
- Nick Craddock, Liz Forty , Daniel Smith, Lisa Jones, Ian Jones, Sian Caesar , Carly Cooper, Christine Fraser, Katherine Gordon-Smith, Sally Hyde, Anne Farmer, Peter McGuffin (27 August 2008)
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Bernard J. Carroll, psychiatry Pacific Behavioral Research Foundation
Send letter to journal:
bcarroll{at}redshift.com Bernard J. Carroll
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8 June, 2008 LETTER TO EDITOR, BRITISH JOURNAL OF PSYCHIATRY Word count 339. References 1. In response to 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. British Journal of Psychiatry 2008; 192: 388-389.1 This study1 revisits a familiar question and reports some statistically significant differences in the frequency of clinical features between unipolar and bipolar depressions. The report then moves beyond description to emphasize the clinical importance of these differences. The 3 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 3 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 3 “important clinical differences” were present. When all 3 features are required, beginning with the highest PPV (psychotic features), then the middle PPV (hypersomnia), then the lowest PPV (diurnal variation), and assuming the 3 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. Reference 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. British Journal of Psychiatry 2008; 192: 388-389. Bernard J. Carroll, MBBS, PhD, FRCPsych Pacific Behavioral Research Foundation P.O. Box 223040 Carmel, CA 93922-3040 Phone 831-626-1467 Fax 831-626-6963 E-mail bcarroll@redshift.com Courier deliveries: 100 Del Mesa Carmel Carmel, CA 93923-7950 |
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Nick Craddock, Professor of Psychiatry Cardiff University, Liz Forty , Daniel Smith, Lisa Jones, Ian Jones, Sian Caesar , Carly Cooper, Christine Fraser, Katherine Gordon-Smith, Sally Hyde, Anne Farmer, Peter McGuffin
Send letter to journal:
craddockn{at}cardiff.ac.uk Nick Craddock, et al.
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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 (1-4). 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.” Declaration of interest: None. Liz Forty a,b, Daniel Smith a, Lisa Jones b, Ian Jones a, b, Sian Caesar b, Carly Cooper b, Christine Fraser a, Katherine Gordon-Smith a, b, Sally Hyde b, Anne Farmer c, Peter McGuffin c, Nick Craddock a, b*. a Department of Psychological Medicine, School of Medicine, Cardiff University, Cardiff, UK. b Department of Psychiatry, Division of Neuroscience, University of Birmingham, Birmingham, UK. c MRC SGDP Research Centre, Institute of Psychiatry, London, UK. References 1. Green E, Raybould R, McGregor S, et al, (2005) The schizophrenia susceptibility gene, Neuregulin 1 (NRG1) operates across traditional diagnostic boundaries to increase risk for bipolar disorder. Archives of General Psychiatry 62(6): 642-6. 2. Williams NM, Green E, Macgregor S, et al. (2006) Variation at the DAOA/G30 locus influences susceptibility to major mood episodes but not psychosis in schizophrenia and bipolar disorder. Arch Gen Psychiatry 63: 366-373. 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; 447:661-78. 4. Craddock N, Jones L, Jones IR et al. Strong genetic evidence for a selective influence of GABAA receptors on a component of the bipolar disorder phenotype. Molecular Psychiatry. 2008. advance online publication, 1 July 2008; doi:10.1038/mp.2008.66 5. Craddock N, Owen MJ. Rethinking psychosis: the disadvantages of a dichotomous classification now outweigh the advantages. World Psychiatry. 2007 Jun;6(2):84-91. |
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