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Depression severity measurement in primary care: "What is already known on this topic", and why GPs should remain cautious
- Isobel M Cameron, Ian C Reid, Professor of Mental Health (23 March 2009)
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And it's a good thing!
- David J Reinhardt (25 March 2009)
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All that weeps is not depression
- Petre T C Jones (26 March 2009)
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NOT All that weeps is depression
- L Sam Lewis (27 March 2009)
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Can the management of depression be discussed adequately without reference to its pathophysiology ?
- Leslie O Simpson (30 March 2009)
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Depression scores are valuable in outcome assessments
- Gnanie Panch (30 March 2009)
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23 years of undertreatment
- Conor Maguire, Tara Coughlan, Des O'Neill, Ronan Collins (2 April 2009)
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Authors' reply
- Tony Kendrick, Chris Dowrick (9 April 2009)
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Depression severity measurement in primary care
- Isobel M Cameron, Ian C Reid (11 April 2009)
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Isobel M Cameron, Research Fellow Applied Clinical Sciences (Mental Health), University of Aberdeen, AB25 2ZH, Ian C Reid, Professor of Mental Health
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Kendrick and colleagues confirm our finding that the PHQ-9 and HADS depression subscale (HAD-D) classify patients' depression severity differently (1). They found that practices using the PHQ-9 recorded larger proportions of patients with moderate to severe depression than those using the HAD-D (2). In light of this, it is perhaps fortunate that the proportion of patients receiving antidepressant prescriptions and referrals to specialist services were similar for both groups: after all, it is entirely appropriate that GPs should treat cautiously the results of assessments over which questions of validity remain (1), however much patients like them (3). The authors propose that a cut-off greater than or equal to 12 in the PHQ-9 and greater than or equal to 9 in HAD-D might be "more valid". In their study, this would have led to a similar proportion of patients being classified as moderately to severely depressed. However, observing similar proportions of cases does not mean that, had the same patients been assessed with both measures, then the same individuals would fit within the same cut-offs for both measures. To test this notion, we re- analysed our sample of patients referred to primary care mental health workers who had completed both PHQ-9 and HAD-D (1) using the cut-offs suggested by Kendrick and colleagues. Cases for PHQ-9 and HAD-D remained significantly different, with PHQ-9 classifying more patients as cases (McNemar test chi square=6.509, p=0.011). Clearly, altering the threshold along the lines proposed by Kendrick and colleagues does not lead to a concordance between the PHQ-9 and HAD-D in our sample. Rather than modifying the scales "on the hoof", surely it would be more appropriate to compare the psychometric properties of the HAD-D and PHQ-9 with the Hamilton Rating Scale for Depression (4). After all, most of what is known about treatment effectiveness for depression in relation to severity is based on this last assessment (5). Should the PHQ- 9 and HAD-D fall at this hurdle, then the QOF depression measures will simply have to be reconsidered if we wish to keep faith with the evidence base. For now, GPs should continue to exercise circumspection when interpreting depression severity measure scores - and their clinical judgement when treating people with depression. References 1. Cameron IM, Crawford JR, Lawton K, Reid IC. Psychometric comparison of the PHQ-9 and HADS for measuring depression severity in primary care. Br J Gen Pract 2008;58:32-6. 2. Kendrick T, Dowrick C, McBride A, Howe A, Clarke P, Maisey S, et al. Management of depression in UK general practice in relation to scores on depression severity questionnaires: analysis of medical record data. BMJ 2009;338: b750. 3. Dowrick C, Leydon GM, McBride A, Howe A, Burgess H, Clarke P, et al. Patients' and doctors' views on depression severity questionnaires incentivised in UK quality and outcomes framework: qualitative study. BMJ 2009;338: b663. 4. Cameron IM, Crawford JR, Lawton K, Sharma S, DuToit S, Hay S, et al. Assessing the validity of the PHQ-9, HADS, BDI-II and QIDS-SR16 in measuring the severity of depression in a UK sample of primary care patients with a diagnosis of depression: study protocol. Primary Care and Community Psychiatry 2008;13(2):67-71. 5. NHS National Institute for Clinical Excellence. Depression: Management of depression in primary and secondary care 2004. Report No 23. Competing interests: None declared |
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David J Reinhardt, Clinical Director Center for Health Science 90808
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The general practitioners who did not prescribe antidepressants to 21% of patients in response to these two simple self assessments are to be applauded for their circumspection. Those that failed to refer the 77% to specialized services are not. As noted in this journal, in February 2007 Kirsch and colleagues concluded, "there seems little evidence to support the prescription of antidepressant medication to any but the most severely depressed patients." Your editorial giving the chemicals the benefit of the doubt (as opposed to a demand for scientific rigor)also did not give a rousing endorsement of a chemical only approach. (March 4, 2008) The value of supportive therapy has been well documented. The failure to refer more patients to supportive services needs to be explained. Competing interests: None declared |
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Petre T C Jones, GP The Project Surgery , Plaistow Newham London E13 0LN
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Doctors listening to the chests of patients with left ventricular failure will remember that 'All that wheezes is not asthma'. Similarly when low mood stikes our patients we need to remember that 'All that weeps is not depression'. Ajustment disorders, bereavement, dysthymia and borderline personality traits can all present in low mood, and are not depression, but are easily mislabeled. The HADS BDI and PHQ9 are all markers of severity of depression, and for PHQ9 and HADs secreening tools to judge the probability that depression is present. They are not diagnostic tools. In particular the fragile labile mood and need for instant relief because of low frustration tolerance that feature in borderline personality traits can give very odd results with theses tools. Often the score is heavily shifted to the severe end. In the study no attempt seems to have been made to establish the actual diagnosis for the patients given the tools, other than that they were given them. We need to use diagnostic labels carefully, and certainly avoid the easy trap of low mood is depression needs counselling. Competing interests: None declared |
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L Sam Lewis, GP Surgery, Newport, Pembrokeshire, SA42 0TJ
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actually, on a point of pedantry, the phrase was "not all that wheezes is Asthma " hence 'Not all that weeps is depression..' But of course I do agree , the order of events, and their relation one to another, makes all the difference of meaning in the world. Sadness and Grief are not the same as Depression in need of drug treatment, but often do share the same pervasive space in human understanding. Competing interests: None declared |
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Leslie O Simpson, retired experimental pathologist Dunedin, New Zealand 9077
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This and its associated paper discussed the importance of depression severity questionnaires to provide guidance to general practitioners with the aim of improving patient management. Although amongst other things, it was noted that GPs take account of age and physical illness, but there was no comment about why such factors are important. What is important is that both increasing age and physical illnesses such as cardiovascular and cerebrovascular disorders and type 1 diabetes, for example, share the common features of having impaired blood flow because of increased blood viscosity and reduced red cell deformability. Such changes are well documented in the medical literature. So it is not surprising that depressive illness has been shown to be associated with reduced rates of cerebral blood flow. Perhaps the most informative study was that of Bench et al (1) who reported, "Thus, recovery from depression is associated with increases in regional cerebral blood flow in the same area in which focal decreases in regional cerebral blood flow are described in the depressed state, in comparison with normal subjects." Therefore it is not surprising that during the systemic impairment of blood flow associated with heart disease, stroke and diabetes, that depression should develop. More recently, Navarro et al (2) reported that the reduced rate of blood flow which had been observed in the left anterior frontal region of the brain in elderly subjects suffering from depression, returned to normal during remission. As low intensity physical activity has been shown to lower blood viscosity, it could be anticipated that physical activity would be helpful in depression and this has been shown in several studies. For example, in a randomised, controlled study of exercise on depressive symptoms, Mather et al (3) stated, "Although anti-depressants may facilitate a more rapid therapeutic response than exercise, after 16 weeks of treatment exercise was equally effective in reducing depression among patients with major depressive disorders." It is relevant also that among the various risk factors, at least three of those factors (stressful events, inactivity and cigarette smoking) are also associated with increased blood viscosity. Therefore, if impaired cerebral blood flow is a primary factor in depressive illness, the most important question is, "Can the blood viscosity problem be treated ?" If it is legitimate to extrapolate from the observations in other studies, the answer would be in the affirmative. Kromhout et al (4) reported in 1985 that in a 20-year follow-up study it was found that a daily intake of 35 grams of oily fish was associated with a 50% decrease in coronary heart disease. In 1986, Kamada et al (5) reported the use of spin label technology to show that the poor deformability of diabetic red cells was improved by sardine oil as a dietary supplement which increased the fluidity of the lipid bilayer of the red cell membrane and improved cell deformability. Those findings suggest that in adequate doses, fish oil rich in omega-3 fatty acids could be helpful in conditions with impaired blood flow, including depressive illness. Although there have been investigations into the effectiveness of omega-3 fatty acids in depression the results have been variable and no study was located which studied the effects of the oil on blood flow. A 2004 report from Finland stated that a low intake of fish was associated with depression in women but not in men. A study from Ireland of the association of depressed mood and fish intake in 10,602 men, reported that, "These findings suggest that depressed mood is associated with fish intake both directly and indirectly, etc." It should be noted that in the Northern Hemisphere the common food fish are oily fish, but in the Southern Hemisphere there are no common food fish which are good sources of omega-3 fatty acids. Two epub 2009 papers also comment on the benefits of a diet rich in oily fish. The first paper concluded, "Our findings suggest that dietary intakes of fish and long-chain omega-3 fatty acids may be inversely asssociated with chronic depressive symptoms in women." The abstract of the second paper commenced, "The unsatisfactory results of the monoamine-based anti-depressant therapy and the high occurrence of somatic symptoms and physical illness in patients with depression imply that the serotonin hypothesis is insufficient to approach the aetiology of depression." It seems reasonable to conclude from the foregoing that depression is the consequence of inadequate rates of regional cerebral blood flow. For that reason alone, GPs should consider the potential benefits of suggesting a daily dietary supplement of 6 grams daily of fish oil to any patient presenting with the symptom of depression. We have found that 4 grams daily of fish oil was inadequate to maintain the resulting benefits. References. 1. Bench CJ, Frackowiak RS, Dolan RJ. Changes in regional cerebral blood flow on recovery from depression. Psychol Med 1995; 25: 247-61. 2. Navarro V, Gasto C, Lomena F, et al. Normalisation of frontal cerebral perfusion in remitted elderly major depression: a 12-month follow -up SPECT study. Neuroimage 2002; 16: 781-7. 3. Mather AS, Rodriguez C, Guthrie ME, et al. Effects of exercise on depressive symptoms in older adults with poorly responsive depressive disorder: randomised, controlled trial. Br J Psychiatry 2002; 180: 411-5. 4. Kromhout D, Bosschieter IH, Coulander C, et al. The inverse relation between fish consumption and 20 year mortality from coronary heart disease. N Engl J Med 1985; 312: 1205-9. 5. Kamada T, Yamashita T, Baba Y, et al. Dietary sardine oil increased erythrocyte fluidity in diabetic patients. Diabetes 1986; 35: 604-11. Competing interests: None declared |
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Gnanie Panch, Consultant- Chronic pain service. Whittington Hospital London N19 5NF
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A comparison of the questionnaire scores and their relationship with the rate of referral to the psychiatric services and antidepressant prescription was conducted. At face value it appears that PHQ9 responders may have falsely alerted the clinicians to act in a more aggressive manner. It may be a false assumption. It is probably likely that the incidence is in fact higher among those who responded to the PHQ9. The comparison at baseline shows a higher preponderance in chronic physical illnesses among this group. The percentage of chronic physical illness PHQ 9 group is in fact 50% higher than in the HAD group. This alone could be the reason for the disparity in severity assessment performed in this investigations. The suitability of questionnaire debate is not new and may probably never be settled as more new questionnaires are produced for depression assessment. The ideal use of the questionnaire, however, is in the measurement of progress. For assessment of improvement the use of any of the three validated questionnaires is acceptable. Competing interests: None declared |
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Conor Maguire, Senior House Officer, ARHC, Tallaght hospital AMNCH, Tallaght Hospital, Tara Coughlan, Des O'Neill, Ronan Collins
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Dear Editor- It is disappointing to read the results of Kendrick’s study on the management of depression particularly in relation to older adults and to realise that little has changed since MacDonald published his paper in this journal over 23 years ago (1). In 1986 he found that although depression was being recognised in older people they were less likely to be prescribed antidepressant medication or referred to specialist mental health care. Despite the medical advances of two decades, the developments of new antidepressant medications and increasing availability of psychological interventions it would appear that older adults are still underdiagnosed and undertreated. Depression is the most common mental health disorder in older adults. One in four older people living in the community have symptoms of depression that are severe enough to warrant intervention (2). Older people themselves are often slow to recognise and seek help for depression in the mistaken belief that this is a normal part of ageing and that treatment is not needed, a view unfortunately shared by some health care professionals. Although depression in older adults may be more prolonged than in younger people it responds equally well to therapeutic intervention (3).Untreated, it may cause needless suffering for many individuals and their families. It is sobering to remember that depression is the leading risk factor for suicide(4)and that older adults have a suicide risk of almost twice that of the general population. Studies such as this, highlighting the inequalities which exist in the treatment of depression, serve as a timely reminder to constantly and vigorously challenge attitudes that create barriers to the equitable treatment of older people. 1. MacDonald AJ. Do general practitioners ‘miss’ depression in elderly patients? BMJ 1996; 282: 1365-6 2. Age Concern Policy Publication. 13th August 2008. 3. G. Alexopoulos. Depression in the elderly. The Lancet; 365: 1961-1970 4. Fiske A et al. Depression in older adults. Annual Review Clinical Psychology. 2009; 5: 363-89 Dr Conor Maguire, Dr T Coughlan, Dr R Collins, Prof D O’Neill, Age Related Health Care, Adelaide and Meath, National Children Hospital, Tallaght, Dublin 24, Ireland. Competing interests: None declared |
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Tony Kendrick, Profesor of Primary Medical Care University of Southampton, Aldermoor Health Centre, Southampton SO16 5ST, Chris Dowrick
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We thank Cameron and colleagues for their thoughtful response. We don’t agree however that we’re proposing modifying scales ‘on the hoof’ in suggesting that practitioners might adopt slightly different threshold scores for considering intervention. We suggest this not on the basis of our study alone but in light of the results of validation studies against more extensive ‘gold standard’ diagnostic assessments, along the lines of the suggestion made by Cameron and colleagues in fact. It is these studies which have suggested that the validity of the measures in terms of identifying major depressive disorder could be improved by using a more conservative cut-off score of 12 rather than 10 on the PHQ-9[1,2], and a less conservative cut-off of 10 rather than 11 on the HAD-D.[1] However, notwithstanding that point, it is important to emphasise that the validity of a symptom questionnaire score in identifying significant depression is always going to be questionable in any individual person. Validity is expressed in terms of the ability of an instrument to identify cases at the group level, and there will always be false positives and false negatives. This has two implications for clinical practice. Firstly, when assessing patients, practitioners should not be guided entirely by the symptom score alone, but should consider the severity of symptoms in terms of significant effects on work and daily activities, their duration, and whether there is a past history of more severe symptoms. The need to take these factors into account is stressed in the quality and outcomes framework (QOF) guidance for the GP contract[3] and it seems likely that the GPs in our study were doing just that, given our findings. Secondly, what’s more important in any individual patient is the trajectory of scores rather than the absolute value at any given point in time. We thank Panch for making that point above. This is the basis of a new indicator in the QOF for 2009/10, DEP3, which awards practices additional points for carrying out a follow-up questionnaire measure of severity recorded 5-12 weeks (inclusive) after the initial recording of the assessment of severity.[3] The PHQ-9 has been shown to be a responsive and reliable measure for gauging response to treatment in individual patient care,[4] and there is on-line guidance available on using it to assess response to treatment.[5] [1] Lowe B, Spitzer RL, Grafe K, Kroenke K, Quenter A, Zipfel S et al. Comparative validity of three screening questionnaires for DSM-IV depressive disorders and physicians' diagnoses. J Affective Disorders 2004; 78:131-140. [2] Gilbody SM, Richards D, Barkham M. Diagnosing depression in primary care using self-completed instruments: UK validation of PHQ-9 and CORE-OM. Br J General Practice 2007; 57:650-652. [3] BMA, NHS Employers. Quality and Outcomes Framework guidance for GMS contract 2009/10. Delivering investment in general practice. London: 2009. [4] Lowe B, Unutzer J, Callahan CM, Perkins AJ, Kroenke K. Monitoring depression treatment outcomes with the Patient Health Questionnaire-9. Medical Care 2004; 42:1194-1201. [5] The MacArthur Initiative on Depression in Primary Care. Using the PHQ-9 to assess patient response to treatment. www.depression- primarycare.org/clinicians/toolkits/materials/forms/phq9/treatment_response. Competing interests: I am the lead author on the paper to which this rapid response is being made. I was a member of the mental health expert reference group for the quality and outcomes framework.the |
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Isobel M Cameron, Research Fellow University of Aberdeen AB25 2ZH, Ian C Reid
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Kendrick & Dowrick justify their suggestion that the cut offs for depression severity measures should be altered by appealing to studies which have assessed the scales’ validity as case finders for major depression 1, 2. We believe that making a change on this basis would be premature. It is important to be clear about which aspect of the scales’ validity is under scrutiny. They might be used in three rather different ways: to identify cases; to determine severity as a guide to treatment selection; and to measure outcome. The weight of the validation lies with identification1, 2, and we have no quarrel with that (though one study is very small (n=96) and the other is conducted on a non-UK population). But it is as a guide to selection of treatment that the PHQ-9 scale limitations in particular are most important. QOF guidance states that “assessment of severity is essential to decide on appropriate interventions and improve the quality of care”3, and goes on to link this statement with NICE recommendations. However, reading beyond the “Summary of Recommendations” in the NICE guidance, we learn: “a key issue is whether severity of illness can guide the use of antidepressant medication. Unfortunately there is little data to help with this point.”4. Importantly, such data that do exist are certainly not based on the PHQ-9: most research has utilised the Hamilton Depression Rating Scale. Indeed, Kendrick & Dowrick use exactly this outcome measure in their THREAD study5. If the PHQ-9 fails to map onto the measures used to derive the evidence base, then it cannot be used sensibly to make treatment decisions which are framed by that evidence base. Kendrick and colleagues emphasise that practitioners are taking into account other factors in their treatment decisions in their linked papers 6, 7. One could just as easily conclude that practitioners are basing their decisions entirely on other factors. Perhaps this is just as well - in our view, the scales are not measuring the same constructs. Snaith warned in 1993 that “unwary researchers will assume that all depression scales assess more or less the same state”8. Clinicians should continue to be wary when interpreting the scores of the HADS-D or the PHQ-9 - regardless of the cut-off applied. References 1. Gilbody S, Richards D, Barkham M. Diagnosing depression in primary care using self-completed instruments: UK validation of PHQ-9 and CORE-OM. Br J Gen Pract 2007;57:650-2. 2. Lowe B, Spitzer RL, Grafe K, Kroenke K, Quenter A, Zipfel S, et al. Comparative validity of three screening questionnaires for DSM-IV depressive disorders and physicians' diagnoses. J Affect Disord 2004;78:131-40. 3. NHS Employers and the General Practitioners' Committee. Quality and Outcome Frameworks: guidance for GMS contract 2009/10. 2009. 4. NHS National Institute for Clinical Excellence. Depression: Management of depression in primary and secondary care; 2004. Report No.23. 5. Chatwin J, Kendrick T, THREAD Study G. Protocol for the THREAD (THREshold for AntiDepressants) study: a randomised controlled trial to determine the clinical and cost-effectiveness of antidepressants plus supportive care, versus supportive care alone, for mild to moderate depression in UK general practice. BMC Family Practice 2007;8:2. 6. Kendrick T, Dowrick C, McBride A, Howe A, Clarke P, Maisey S, et al. Management of depression in UK general practice in relation to scores on depression severity questionnaires: analysis of medical record data. BMJ 2009;338. 7. Dowrick C, Leydon GM, McBride A, Howe A, Burgess H, Clarke P, et al. Patients' and doctors' views on depression severity questionnaires incentivised in UK quality and outcomes framework: qualitative study. BMJ 2009;338. 8. Snaith P. What Do Depression Rating Scales Measure?. British Journal of Psychiatry 1993;163:293-8. Competing interests: None declared |
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