PSYCHOTHERAPY: EXPENSIVE PLACEBO?

PSYCHOTHERAPY: EXPENSIVE PLACEBO?

224 SCREENING FOR MENTAL ILLNESS SiR,—Dr Hoeper and his colleagues (Jan 7, p 33) have misunderstood my research, made misleading calculations on thei...

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224 SCREENING FOR MENTAL ILLNESS

SiR,—Dr Hoeper and his colleagues (Jan 7, p 33) have misunderstood my research, made misleading calculations on their own data, and drawn unwarranted conclusions. They are incorrect in asserting that the experimental group in my work with Johnstonel was "not comparable to the control group, which was chosen twelve months later". The two groups were drawn in exactly the same way: they were high scorers on GHQ (general health questionnaire) at the index consultation and were rated as "non-cases" by the general practitioner at that consultation. Both groups were followed up twelve months later. Hoeper et al use their data to compute a positive predictive value of 55 - 3% for the GHQ in primary care. However, 28% of their respondents had high scores, which-even if we accept Hoeper’s validity coefficients-would give a predicted prevalence of 30%. 2,3 The figure of 16% is in fact an estimate of conspicuous psychiatric morbidity", and Hoeper et al have failed to grasp the difference between this and "total psychiatric morbidity". With a prevalence of 30%, the positive predictive value (ie, the probability that a patient with a high score is a "case") is 75%, and the negative predictive value (probability that a low scorer is normal) is 87%. However, there are several reasons for not accepting Hoeper and colleagues’ validity coefficients: they are not to be found in the reference cited, they relate to a version of the GHQ different from the one used in the study under discussion, and 9-33 days (on average) elapsed between the completion of the GHQ and the validation interview, and this would lower the validity coefficients. The case criterion was unsatisfactory in that it was the "lifetime" version of the SADS, and included as cases conditions which the GHQ never set out to identify, such as intermittent depression and various personality disorders. Well-conducted studies4,s have produced higher validity coefficients for the GHQ-28 than those used by Hoeper et al. Hoeper et al complain that clinicians will not have much confidence in a screening test with a low positive predictive value. Everything really depends on the way in which the primary care physicians are briefed about how to interpret an individual’s score. The higher the score, the greater the likelihood that they will find a disorder to be present if they discuss a patient’s symptoms with him. The "threshold score"-which is of such interest to researchers-is, from the clinician’s viewpoint, merely the score for which there is a 50% chance of finding a disorder to be present. It is a simple matter to indicate score levels that give a 75% and a 95% chance for an individual patient. Hoeper et al did not discuss their main finding, which was that giving the fourteen general practitioners information about their patients’ psychiatric symptoms had no impact upon their diagnostic practices. Before one can evaluate such a depressing finding one would need to be given information about the way in which the study was discussed with the participating physicians, the assistance they were given in interpreting an individual’s score, and whether they were encouraged to discuss unexpected high GHQ scores with their patients. If the physicians were not encouraged to use the additional information, what was the point of the study? Department of Psychiatry, University Hospital of South Manchester,

DAVID GOLDBERG

Manchester M20 8LR

SIR,-I am uncertain of the practical benefits of screening for mental illness in general practice. Screening in general practice is becoming popular, and fairly stringent guidelines have been suggested to justify its initiation 6,7 Screening can be seen to be of 1.

Johnstone A, Goldberg DP. Psychiatric screening

in

general practice. Lancet 1976; i:

605-08. 2. 3.

Rogan W, Gladen B. Estimating prevalence from the results ofa screening test. Am J Epidemiol 1978; 107: 71-76. Goldberg DP. Estimating prevalence of psychiatric disorder from the results of a screening test. In: Wing JK, ed. What is a case? London. Grant, McIntyre. 1981: 129-36.

Banks M. Validation of the GHQ in a young community. Psychol Med 1983; 3: 349-54. Bridges K. A study of psychiatric morbidity in patients admitted to an adult neurology ward. MSc thesis, University of Manchester, 1983. 6. Hodgkin K. Towards earlier diagnosis in primary care, 4th ed. Edinburgh: Churchill Livingstone, 1978: 34. 7. Grant IWB. Screening for lung cancer. Br Med J 1982; 284: 1209-10.

4. 5.

benefit in diseases such as diabetes mellitus, hypertension, and lung cancer, but I do not know if, as a general principle, it can be applied to mental illness. The above-mentioned illnesses can be symptomless yet indubitably present, but can the same be said of psychiatric morbidity? Dr Hoeper and coplleagues do not define "mental illness". Where diagnosis is still under debate and where there is no clear "cut-off point" between disease and health, exhaustive screening

justified. In psychiatry we have no easy way to make a diagnosis. There are no blood tests or pathology specimens: in a way symptoms are the disease and not merely a marker of it. The time, money, and energy may be better utilised in public education to allay widespread misconceptions about mental illness.

tests are not

Bethlem

Royal Hospital, Beckenham, Kent BR3 3BX

ALISTAIR BURNS

PSYCHOTHERAPY: EXPENSIVE PLACEBO?

SIR,-Your Jan 14 editorial draws attention to the ignorance about the social and epidemiological context of psychotherapy within medical settings in the UK. Controversy has been raging in the USA for several years-not on scientific grounds but over the issue of payment and the related question of who should provide to raise these matters in the psychotherapy services I-but attempts UK have hitherto fallen on deaf ears.22 Psychotherapy was introduced to the National Health Service as a subspecialty in 1975. Between 1976 and 1982 there was about a 350% increase in the number of consultant psychotherapists3,4-a rise surpassed only by that in audiological medicine, and matched only by endocrinology, forensic psychiatry, and gastroenterology. Why did this happen, in the face of no convincing evidence that psychotherapy is effective? No count has been made of the probably enormous increase in non-medical staff who have assumed the role of individual, group, or family "therapists" or counsellors, in hospital and general practice. A multicentre trial seems unlikely to resolve the issue. A mass of data has already been collected, to little purpose; and there is not much reason to hope for results that are any more conclusive than those already obtained by people with an interest in finding that psychotherapy has a positive outcome. As in the US,the decisions that matter will have to be taken, not by researchers, but by policymakers. Psychotherapy in the NHS is a suitable topic for their urgent consideration, bearing in mind the government’s concern with value for money. .

General Practice Research Unit, Institute of Psychiatry, London SE5 8AF

as

D. G. WILKINSON

SiR,-Manifestly psychotherapy is now a medical discipline and such should be subject to the same objective evaluation as any

other

medical practice. It is most profitable to consider psychotherapy as a methodological rather than a theoretical discipline: it is a set of things put into practice. In this regard, it is like any other method or instrument employed in medicine, whether diagnostic or therapeutic. Last week it was nuclear magnetic resonance; this week it is psychotherapy. Psychotherapy is not one method but many. It has a long and varied set of originators. But it is invariable in one respect: the patient wants to talk and the therapist wants to listen. What emerges is of such complexity that it will take a long time before all significant statements can be refined down to certainties, generally observable and testable. It is no fault of psychotherapists that this is so. As a response to human need, it is slowly fitting into the corpus 1. Wilkinson G. Psychotherapy in the market-place. Psychol Med (in press). 2. Shepherd M. Psychoanalysis, psycho-therapy, and health services. Br Med J 1979; ii: 1557-59. 3. Department of Health and Social Security, Medical Manpower Division. Medical staffing and prospects in the NHS in England and Wales, 1976. Health Trends 1977;

9: 45-47. 4.

Department of Health and Social Security, Medical Manpower Division. Medical and dental staffing prospects in the NHS in England and Wales, 1982 Health Trends 1983; 15: 35-39.

225 of medicine. Chance observations,

inspired hunches,

tentative

hypotheses have emerged, but no general theory. Thus it seems premature to apply to psychotherapy

evaluative methods at their present level of development. Statistical analysis of clinical data became the accepted means of evaluation only since the 1939-45 war. Today the double-blind trial is an article of scientific faith. We have yet to devise the double-deaf trial for doubly deaf doctors. To assume that "science" is all-knowing in its final judgments is to deny the essential humility of the scientific approach. Our ignorance is the true scientific challenge. But it seems to be argued that "just talk" gets us nowhere, or is merely a placebo. Can this be so when there has been no "scientific" evaluation of, for example, editorials in scientific journals or of "discussions", which invariably constitute the last word in every scientific presentation? Is there no significance in editorials or in discussions? So long as the concept "the last word" has any meaning, we must allow our patients to have it. 35

Beechgrove Avenue,

AberdeenAB24HE

W. MALCOLM MILLAR

TEMPORARY TICKET TO AMERICA

SiR,-Dr Bick (Dec 24/31, p 1481) provides an accurate account of the difficulties encountered by doctors intending permanent emigration to the USA. The requirements are only slightly less stringent for those who wish to practise temporarily in the USA during, for example, a senior registrar appointment. Like the permanent visa, the J-1 exchange visitor’s visa also demands a pass in a two-day test of medical knowledge and a test in English. The applicant will also need a certificate of eligibility for exchange visitor status (form IAP-66) to bed provided by the sponsor of the programme and evidence sufficient funding to cover expenses while in the USA. Finally, the applicant must sign a written assurance that the medical skills to be acquired in the USA are needed in the UK and that, on completion of training, he or she will return home. Having obtained a J-1 visa and provided evidence of adequate secondary school education, it is then possible to obtain a limited licence to practise. Foreign graduates intending to do research on a temporary basis in the USA may also use a J-1visa but do not require the visa qualifying or equivalent examination. Memorial Sloan-Kettering Cancer Centre, New York, NY 10021, USA New York

Hospital

MICHAEL J. GREENALL PRISCILLA BURGESS

COLON CANCER AT SITES OF ANASTOMOSIS

SIR, The possibility that unabsorbed suture materials may neoplastic change in the colon, and thus anastomotic

promote

development, has been raised by Mr Stanek and his colleagues (Dec 10, p 1371). We too have considered this possibility, and have examined the effects of using different suture materials on tumour production at colonic anastomotic sites in rats treated preoperatively with azoxymethane.Our experiments confirm that more tumours occur in the region of the anastomotic sites than at other sites in the large bowel.2,3 However, no difference was noted tumour

in the numbers of tumours at anastomoses sutured with silk, ’Dexon’, or chromic catgut. This suggests either that these three differing types of suture material are equally tumour promotive or that some other factor related to the trauma of anastomosis acts as a promoter of oncogenesis. BYRNE B. STEPHENS P. J. HENNESSY B. WEST G. SHEAHAN

P. J. Departments of Surgery and Pathology, St James’s Hospital and Trinity College, Dublin 8, Ireland

1. Ward

R. T. A. D.

JN, Yamamoto RS, Brown CA. Pathology of intestinal neoplasms and other lesions in rats exposed to azoxymethane. J Natl Cancer Inst 1973; 51: 1029-39. 2. Rubio CA, Nylander G, Wallin B. Anastomotic tumors following partial colon resection: an experimental model. Surg Gastroenterol 1982; 1: 63-66. 3. Filipe MI, Scurr JH, Ellis H. Effects of faecal stream on experimental colorectal carcinogenesis. Cancer 1982; 50: 2859-65.

ANGIOTENSIN CONVERTING ENZYME INHIBITION IN RENOVASCULAR HYPERTENSION: FREQUENCY OF REVERSIBLE RENAL FAILURE

SiR,-Acute deterioration in renal function has been reported in patients with renovascular hypertension treated with angiotensin converting enzyme (ACE) inhibitors, suggesting that these drugs are contraindicated in such patients. 1-4 This is an important issue because ACE inhibitors are effective blood-pressure-lowering agents in hypertension due to renovascular disease, a condition often difficult to treat with conventional agents.5-7 ACE inhibition offers considerable promise as an alternative to surgery, especially in patients with renovascular hypertension as part of severe general atheromatous disease. In the kidney with renal artery stenosis glomerular filtration is maintained by efferent arteriolar constriction, mediated by angiotensin 11.8 ACE inhibition might therefore be expected to impair glomerular filtration in most stenotic kidneys, as has been demonstrated experimentally.9,1O Watson and colleagues" have suggested that diuretics also predispose to impairment of renal function in patients with renovascular hypertension. We have monitored renal function in 32 patients with proven renovascular hypertension treated with captopril and a diuretic. Treatment has lasted for 1-212 weeks (mean 49 weeks). 11patients had unilateral renal artery stenosis (group A), 8 had a solitary kidney renal artery stenosis (native kidney and transplant kidney) (B), and 13 had bilateral renal artery stenosis (C). No rise in serum creatinine was observed in group A. In contrast, 3 patients in group B and 3 in group C went into renal failure, as judged by acute rise in serum creatinine to three times basal level or to more than 800 mol/1, on introduction of captopril. In 1 patient from group C renal failure developed on three successive occasions when captopril was introduced. In all cases of acute renal failure the serum creatinine returned to pre-treatment levels within 7 days of captopril withdrawal. Patients in whom acute renal failure developed had higher pretreatment creatinine levels (251±45 Mmol/1) than those whose renal function remained stable (153±21 mol/1; pG0001). The fall in blood pressure with captopril therapy did not appear to be a critical factor in influencing renal function: similar falls in blood pressure were observed in patients whose creatinine levels rose and in patients whose creatinine values remained stable. ,Our experience suggests that certain patients with renovascular hypertension are at risk of deterioration in renal function after treatment with ACE inhibitors. These patients have either a single functioning kidney (natural or transplant) or bilateral renal artery

1. Collste

P, Hagland L, Lunggren G, Magnusson G, Ostman J. Reversible renal failure during treatment with captopril Br MedJ 1979; iii: 612. 2. Woodhouse K, Farrow PR, Wilkinson R. Reversible renal failure during treatment with captopril. Br Med J1979, in: 1146. 3. Hrielk DE, Browning PJ, Kopelman R, et al. Captopril induced functional renal insufficiency in patients with bilateral renal artery stenosis or renal artery stenosis in a solitary kidney. N Engl J Med 1983; 308: 373-76. 4. Curtis JJ, Luke RG, Whelchel JD, et al. Inhibition of angiotensin converting enzyme in renal transplant recipients with hypertension. N Engl J Med 1983; 308: 377-81. 5. Atkinson JB, Brown JJ, Cumming AM, Fraser R, Lever AF, Lechse BJ, Morton JJ, Robertson JIS, Davies DL. Captopril in the management of hypertensives with renal artery stenosis. The long term effect as a prediction of surgical outcome. Am J Cardiol 1982, 49: 1460-66. LP, Brown JJ, Davies DL, Fraser R, Lever AF, Morton JJ, Murray GD, Robertson JIS. Converting enzyme inhibition enalapril (MK421) in treatment of hypertensives with renal artery stenosis. Br Med J 1982; 285: 1697-99. 7. Laragh JJ, Case DB, Atlas SA, Sealey JE. Captopril compared with other anti-renin system agents in hypertensive patents: Its triphasic effects on blood pressure and its use to identify and treat the renin factor. Hypertension 1980; 2: 486-592. 8. Anderson W, Korner PI, Johnston CI. Acute angiotensin II mediated restoration of distal renal artery pressure in renal artery stenosis and its relationship to the development of sustained "one kidney" hypertension in conscious dogs. 6. Hoodsmann

Hypertension 1979; 1: 292-98. U, Gröne HJ, Kirchetz EJ, et al. Contrasting renal effects of different antihypertensive agents in hypertensive rats with bilaterally constricted renal arteries. Kidney Int 1982; 12 (suppl) S198-205. 10. Navar LG, La Grange RA, Bell PD, Thomas CE, Ploth DE. Glomerular and renal haemodynamics during converting enzyme inhibition (SQ20,881) in the dog. Hypertension 1979; 1: 371-77. 11. Watson ML, Bell GM, Muir AL, Brust TAS, Kellett RJ, Padfield PL. Captopril/diuretic combinations in severe renovascular disease: a cautionary note. 9. Helmchen

Lancet

1983;

ii:

404-05.