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simultaneous measurement of regional myocardialperfusion and function to differentiate between

stunning and sustained silent ischaemia.The main candidates for clinical testing against

stunning are the calcium antagonists and free-radicalscavengers. The angiotensin-converting-enzymeinhibitors may also exert some inhibitory effect onstunning.28 The next step will be to compare theeffects of these three types of agents on stunning inlarge animals before selecting the best candidate to tryin man.

1. Poole-Wilson PA. Reperfusion damage in heart muscle: still unexplainedbut with new clinical relevance. Clin Physiol 1987; 7: 439-53.

2. Bolli R. Mechanism of myocardial "stunning". Circulation 1990; 82:723-38.

3. Braunwald E, Kloner RA. The stunned myocardium: prolonged,postischemic ventricular dysfunction. Circulation 1982; 66: 1146-49.

4. Opie LH. Reperfusion injury and its pharmacological modification.Circulation 1989; 80: 1049-62.

5. Hearse DJ. Ischemia, reperfusion, and the determinants of tissue injury.Cardiovasc Drugs Ther 1990; 4: 767-76.

6. Bernier M, Hearse DJ, Manning AS. Reperfusion-induced arrhythmiasand oxygen-derived free radicals. Studies with "anti-free radical"interventions and a free radical-generating system in the isolated

perfused rat heart. Circ Res 1986; 58: 331-40.7. Opie LH, Coetzee WA. Role of calcium ions in reperfusion arrhythmias.

Relevance to pharmacological intervention. Cardiovasc Drugs Ther1988; 2: 623-36.

8. Coetzee WA, Owen P, Dennis SC, Saman S, Opie LH. Reperfusiondamage: free radicals mediate delayed membrane changes rather thanearly ventricular arrhythmias. Cardiovasc Res 1990; 24: 156-64.

9. Yamada M, Hearse DJ, Curtis MJ. Reperfusion and readmission ofoxygen. Pathophysiological relevance of oxygen-derived free radicals toarrhythmogenesis. Circ Res 1990; 67: 1211-24.

10. Hearse DJ, Tosaki A. Free radicals and calcium: simultaneous interactingtriggers as determinants of vulnerability to reperfusion-inducedarrhythmias in the rat heart. J Mol Cell Cardiol 1988; 20: 213-23.

11. Cumming DVE, Holmberg SRM, Kusama Y, et al. Effects of reactiveoxygen species on the structure and function of the calcium-releasechannel from isolated sheep cardiac sarcoplasmic reticulum. J Physiol1990; 420: 88.

12. Taegtmeyer H, Roberts AFC, Raine AEG. Energy metabolism inreperfused heart muscle: metabolic correlates to return of function.JACC 1985; 6: 864-70.

13. Ambrosio G, Jacobus WE, Bergman CA. Preserved high-energyphosphate metabolic reserve in globally "stunned" hearts despitereduction of basal ATP content and contractility. J Mol Cell Cardiol1987; 19: 953-64.

14. Kusuoka H, Koretsune Y, Chacko VP, et al. Excitation-contraction

coupling in postischemic myocardium. Does failure of activator Ca2 +

transients underlie stunning? Circ Res 1990; 66: 1268-76.15. Marban E. Myocardial stunning and hibernation. The physiology behind

the colloquialisms. Circulation 1991; 83: 681-88.16. Przyklenk K, Kloner RA. Effect of verapamil on postischemic "stunned"

myocardium: importance of the timing of treatment. JACC 1988; 11:614-23.

17. Du Toit E, Owen P, Opie LH. Attenuated reperfusion stunning with acalcium channel antagonist or internal calcium blocker in the isolatedperfused rat heart. J Mol Cell Cardiol 1990; 22 (suppl III): S58 (abstr).

18. Bavaria JE, Furukawa S, Kreiner G, et al. Myocardial oxygen utilizationafter reversible global ischemia. J Thorac Cardiovasc Surg 1990; 100:210-20.

19. Mercier JC, Lando U, Kanmatsuse K, et al. Divergent effects of inotropicstimulation on the ischemic and severely depressed reperfusedmyocardium. Circulation 1982; 66: 397-400.

20. Przyklenk K, Ghafari GB, Eitzman DT, Kloner RA. Nifedipineadministered after reperfusion ablates systolic contractile dysfunctionof postischemic "stunned" myocardium. JACC 1989; 13: 1176-83.

21. Mak IT, Boehme P, Weglicki WB. Protection against free radical injuryin endothelial cells by calcium blockers—correlation with antioxidantactivity and glutathione levels. Circulation 1990; 82 (suppl III): 264(abstr).

22. Bolli R, Hartley CT, Rabinovitz RS. Clinical relevance of myocardial"stunning". Cardiovasc Drugs Ther (in press).

23. Wijns W, Serruys PW, Slager CJ, et al. Effect of coronary occlusion

during percutaneous transluminal angioplasty in humans on left

ventricular chamber stiffness and regional diastolic pressure-radiusrelations. JACC 1986; 7: 455-63.

24. Kloner RA, Allen J, Zheng Y, Ruiz C. Myocardial stunning followingexercise treadmill testing in man. JACC 1990; 15: 203 (abstr).

25. Nixon JV, Brown CN, Smitherman TC. Identification of transient andpersistent segmental wall motion abnormalities in patients with

unstable angina by two-dimensional echocardiography. Circulation

1982; 7: 1497-503.26. Schmidt WG, Sheehan FH, von Essen R, et al. Evolution of left

ventricular function after intracoronary thrombolysis for acute

myocardial infarction. Am J Cardiol 1989; 63: 497-502.27. Ferrari R, Alfieri O, Curello S, et al. Occurrence of oxidative stress during

reperfusion of the human heart. Circulation 1990; 81: 201-11.28. Przyklenk K, Kloner RA. Angiotensin converting enzyme inhibitors

enhance contractile function of "stunned" myocardium by differentmechanisms of action. Circulation 1990; 82 (suppl III): 264 (abstr).

Recurrent brief depression andanxiety

In the past ten years there have been many apparentadvances in the classification of psychiatric disorder.In particular, the numerically largest group,sometimes collectively described as "non-psychotic",have been subjected to much tighter diagnosticscrutiny than ever before. The key to the newclassification is provided by operational criteria-these are well-defined characteristics that can berecorded consistently and, when they occur insufficient numbers, cross the threshold for the

diagnosis in question. By use of such criteria the mostprevalent psychiatric conditions, anxiety and

depression, have been separated into adjustmentdisorders, generalised anxiety disorder, panicdisorder, major depressive episode, and dysthymicdisorder.1 Ideally each operational criterion shouldnot be shared or overlap with others from differentdiagnoses. Thus, in the game of diagnostic’Monopoly’, players accumulate houses of operationalcriteria until they have sufficient to purchasediagnostic hotels, which remain on the same site tillsold.

This exercise has stimulated considerable researchand has convinced many sceptics that neuroticdisorder can be classified satisfactorily on the basis ofprimary symptoms without any need to invoketheoretical constructs. However, there is a lessattractive aspect to the making of these new diagnoses.The minimum duration of symptoms necessarybefore making a diagnosis varies between the extremesof panic disorder, in which one panic attack can besufficient to trigger off the diagnostic requirements forthe disorder if it is followed by persistent fear of havingothers, and dysthymic disorder, in which depressivesymptoms have to be present for most of the previoustwo-year period. These temporal elements have notbeen subjected to the same scrutiny as have theindividual symptoms. The reasoning behind the timelimits imposed on different diagnoses is far from clear.The diagnosis of major depressive episode requiresdepressive symptoms to have been present for twoweeks, but for its anxiety equivalent, generalisedanxiety disorder, symptoms have to have been present

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for most of the previous six months to qualify for thediagnosis.Two newcomers are now pressing for inclusion in

the diagnostic system. Angst and his colleagues inZurich2 have described recurrent brief depression-by comparison with major depressive episode thesymptom pattern is identical, together with

occupational impairment, but the condition lasts forless than two weeks and so does not qualify for thatdiagnosis. Recurrent brief depression was fashionedfrom data derived from an epidemiological survey andit could be argued that it is not relevant to clinical

practice. Nevertheless, the population described byAngst et al has been followed over twelve years and therecurrent nature of the symptoms suggests that the

diagnosis is clinically important. The prevalence inyoung adults is about 10% (higher than that of majordepressive disorder at slightly less than under 8%)and there is little overlap between the two conditions.3 3

Angst and co-workers have now identified an

equivalent diagnosis of recurrent brief anxiety, whichhas the same diagnostic requirements as generalisedanxiety disorder (together with work impairment),but a shorter time span. The anxious mood has to be

present for less than two weeks with a recurrence rateof at least once a month in the preceding year. Thereis also some evidence that recurrent but infrequentpanic attacks could be regarded as a separate diagnosissince patients with at least four panic attacks over oneyear comprise a reasonably homogeneous groups

If the existence of these syndromes is supported byclinical studies there should be no reason why theycannot be included among the other diagnoses that arenow commonly used. Alternatively, the temporalcriteria for existing diagnoses could be adjusted toallow inclusion of these newer disorders. To someextent this view has been anticipated in the

preparation of the tenth revision of the InternationalClassification of Disease, in which recurrent

depression is likely to be recognised at three differentdiagnostic levels-mild, moderate, and severe.6 6

Is there any evidence that these conditions are

important clinical entitities rather than immaterial

epidemiological findings? One in six of the patientsidentified in the Zurich study had sought treatment inthe preceding year and nearly a half had done so atsome time since the onset of their condition. Suicide

attempts were twice as frequent in patients withrecurrent brief depression as in those with majordepressive disorders. Recurrent attempted suicide isone of the more serious issues in psychiatry and publichealth and a satisfactory way to deter repeat attemptshas not been found.7,8 If many of these patients wereawarded the diagnosis of recurrent brief depressionand given appropriate antidepressant treatment

prophylactically, more successful prevention might beachieved.9noSome might argue that brief depression is common

but that it does not justify identification as a separate

mental state disorder because it is already part ofanother condition-borderline personality disorder.The operational criteria listed for this conditioninclude brief depression and anxiety as well as

recurrent suicidal acts.1 This view is partly supportedby the evidence that patients with recurrent briefdepression have more childhood emotional andbehavioural problems than those with no depressivedisorder.4 A counter argument is that effective criteriashould not be part of the diagnostic requirements forpersonality disorder. Brief anxiety and depression arebest regarded as primary abnormalities of mentalstate; where these conditions belong in psychiatricclassification is worth further debate. Above all, thisissue highlights the potential drawback of introducingstrict time limits before a diagnosis can be justified;such criteria may be nosologically satisfying butclinically farcical. "Come back tomorrow Mr Smith.Today you fail to qualify for diagnosis, treatment, orinsurance cover. Tomorrow, however, if yoursymptoms persist I will be able to help you".

1. American Psychiatric Association. Diagnostic and statistical manual ofmental disorders, 3rd edn, revised. Washington, DC: AmericanPsychiatric Association, 1987.

2. Angst J, Dobler-Mikola A. The Zurich study-a prospectiveepidemiological study of depressive neurotic and psychosomaticsyndromes. Eur Arch Psychiatry Neurol Sci 1985; 234: 408-16.

3. Angst J, Merikangas K, Scheidegger P, Wicki W. Recurrent briefdepression: a new subtype of affective disorder. J Affect Dis 1990; 19:87-98.

4. Angst J, Wicki W. The epidemiology of frequent and less frequent panicattacks. Br J Psychiatry (in press).

5. Vollrath M, Koch R, Angst J. The Zurich study. IX. Panic disorder andsporadic panic: symptoms, diagnosis, prevalence, and overlap withdepression. Eur Arch Psychiatry Neurol Sci 1985; 239: 221-30.

6. World Health Organisation. International classification of diseases, draftof 10th revision. Geneva: WHO, 1989.

7. Gibbons JS, Butler J, Urwin P, Gibbons JL. Evaluation of a social workservice for self-poisoning patients. Br J Psychiatry 1978; 133: 111-18.

8. Ettlinger R. Evaluation of suicide prevention after attempted suicide.Acta Psychiatr Scand 1975; 260 (suppl).

9. Montgomery S, Montgomery D. Pharmacological prevention of suicidalbehaviour. J Affect Dis 1982; 4: 291-98.

10. Montgomery SA, Roy D, Montgomery DB. The prevention of recurrentsuicidal acts. Br J Clin Pharmacol 1983; 15: 183S-88S.

Brains and vitamins

In January, 1988, The Lancet published a study byBenton and Roberts in 90 Welsh schoolchildren aged12 to 13 that claimed to show an improvement innon-verbal intelligence after eight months ofmultivitamin and mineral supplementation. Twosubsequent studies2,3 failed to confirm the originalfindings although Benton later reported data onBelgian schoolchildren that supported his first study. 4A group from California, London, and Israel havenow distributed the results of another trial, sponsoredby the scientific directorate of the Dietary ResearchFoundation.

Release of the latest research findings, at a pressconference in London last week, coincided with thecommercial launch of the vitamin product given in thetrial (formulated by the senior author, Dr S.