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Cardiovascular Research 1992;26: 1170- 1 171

Commentary Eponyms, priority, and attribution Robert G Richardson, Michael J Curtis

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nevertheless, to learn that Robert Graves was a relative latecomer. Caleb Parry had described the disease in 1786,’’ though the case was not published until 1825, three years after his death, but 10 years before Graves’s account. Sir William Osler championed Parry’s priority to such good effect that Parry’s disease entered the literature; however, the competition was too great for it to replace Graves’ disease. However, we would ask you to spare a thought for Giuseppe Flajani, who was responsible for the first published account in 1802.13 But he really didn’t stand a chance with the description submerged in the third volume of his collected observations. The eponymous naming of diseases and syndromes should, therefore, never be taken to imply priority of description - that would be far too hazardous an assumption. All too often it is a matter of luck, the laurels being awarded to the person, or author of the description (however incomplete), who the world sees as having been in the right place at the right time to create the necessary impact. Should eponym and priority happen to conicide we have cause for rejoicing. Thus the eponym must, sadly, be regarded as nothing more or less than a convenient shorthand to communication. When, however, we move from diseases and syndromes (which usually have been sitting in the wings awaiting discovery) to tests, techniques, and the like (which have to be invented) we find ourselves in an infinitely more perilous part of the minefield. In 1881 Newel1 Martin of Johns Hopkins University devised an isolated working heart model. l4 Although his system was complex, requiring oxygenation of the perfusing blood by the lungs, it did nevertheless antedate the now standard isolated working rat heart model of Neely et all‘ by some 86 years. Neely et a1 did not cite Martin’s paper. There was no direct line of descent from Martin to Neely and his group, so no debt was owed to him. In 1967 it was no longer common practice to write fairly exhaustive historical introductions to scientific papers and, presumably, the group did not include a professional medical historian. Martin’s work, advanced though it was, must therefore be relegated to an honourable place in medical history. (A more detailed account of Martin’s work has been given by Opie,I6 though we have identified an earlier paper than the one he cited.) Langendorffi7 was more fortunate, since his isolated perfused mammalian heart was simple, more suited to metabolic studies, and is still with us, with his name

Apple Tree Cottage, French Street, Westerham, Kent, United Kingdom: R G Richardson; Department of Pharmacology, King’s College, Manresa Road, London SW3 6LX, United Kingdom: M J Curtis. Correspondence to Dr Curtis.

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et us join Michael Rosen on his Paladin0 and ride off with him into the Glomset and there, freed from laboratory cares, consider the vexed (to some) questions of attribution and priority. In flushing the Wolff from his lair, Rosen has stumbled on a Mines field. If we are to be fair to all concerned, the Wolff-Parkinson-White syndrome should be named the Paladino-Kent-MinesGlomset-Glomset (why give credit to only one Glomset?) Wolff-Parkinson-White-Holzman-Scherf syndrome. We make this point because it would be equally ridiculous to give the condition a descriptive title - it is a composite, a syndrome and, as such, needs a manageable name by which it may be readily recognised. Furthermore, despite the depth of Rosen’s research, it is not beyond the bounds of possibility that there were other labourers in the electrophysiological vineyard whose contributions have passed unnoticed. “Who knows”, wrote Sir Thomas Browne in Hydriotaphia, “whether the best of men be known, or whether there be not more remarkable persons forgot, than any that stand remembered in the known account of time.” Perhaps Charcot got it right. In 1884 he prompted his protegC, Gilles de la Tourette, to describe nine patients with compulsive tics.’ One of these was the Marquise de Dampierre who had previously been reported by Jean Marie Gaspard Itard in 1825.* The Marquise lived as a recluse, ticking and blaspheming away until her death at the age of 80. We have thus the possibility of three names for the syndrome (the two physicians and the patient) but Charcot preferred the euphonious eponym of Gilles de la Tourette, and so it was. Remaining in the past, we find that the Stokes-Adams attack which characteristically occurs in patients with heart block was originally (as :ar as we know) described by Marcus Gerbezius in 17 19: He was followed by Giovanni Battista Morga ni4 (1761) and Thomas Spens’ (1793) before Robert Adams (1827) and William Stokes7 (1846) came on the scene, and again, Raymond Vieussens’ in 17 15 described the collapsing pulse of aortic insufficiency more than a century before Dominic Comgan’ himself. Would it be wrong to detect an Anglophone tendency in those days? A national preference is clearly evident in the case of exophthalmic goitre in so far as this is known as Graves’ disease” in English speaking countries, and as von Basedow’s disease“ on the continent of Europe, despite von Basedow’s description having followed that of Graves after an interval of nearly 40 years. It will come as no surprise,

Commentary

progressively easier to detect biases in attribution and misattributions from whatever cause. Received 5 October 1992; accepted 5 October 1992.

1 Guilly P. Gilles de la Tourette. In: Clifford Rose F, Bynum W. eds. Historical aspects of the neurosciences. New York Raven Press, 1982:397. 2 Itard JMG. MCmoire sur quelques fonctions involontaires des appareils de la locomotion, de la prkhension et de la voix. Arch Gen M6d (Paris) 1825:8:385. 3 Gerbezius M. Appendix ad Ephemeridum Academiae CaeseroLeopoldino-Carolinae Naturae Curiosum in Germania. Nuremberg, 1719. Centuriae VII et VIII, p 23. 4 Morgagni JB. De sedibus ef causis morborum per anatomen indagatis libri quinque. Venetiis, ex typog. Remondiniana, 1761. 5 Spens T. History of a case in which there took place a remarkable slowness of the pulse. Medical Commentaries, 1792. Edinburgh, 1793;7:458-65. 6 Adams R. Cases of diseases of the heart accompanied by pathological observations. Dublin Hospital Reports 1827;4: 353453. 7 Stokes W. Observations on some cases of permanently low pulse. Dublin J Med Sci 1846;2:73-85. 8 Vieussens R. Trait6 nouveau de la structure et des cuuses du mouvement nature1 du coeu,: Toulouse: Guillemette, 1715:107. 9 Corrigan DJ. On permanent Datencv of the mouth of the aorta, or inadequacy of ihe aortic- valves. Edinburgh Med Surg J I832;37:22545. 10 Graves RJ. Newly observed affection of the thyroid gland in females. London Med Surg J 1835;7:5 16-7. 11 Basedow CA van. Exophthalmos durch Hypertrophie des Zellgewebes in der Augenhohle. Wochenschriji fur die gesammte Heilkunde, Berlin 1840;6:197-204, 22C8. 12 Parry CH. Diseases of the heart. Enlargement of the thyroid gland in connection with enlargement or palpitation of the heart. In: Collected work, vol 1. London:Underwood, 1825:478-80. 13 Flajani G. Sopra un tumor freddo nell’anterior parte del collo detto broncocele. In: Collezione d’osservaiione e riflessioni di chirurgia. Roma, 1802;3:27&3. 14 Martin HN. On a method of isolating the mammalian heart. Science 1881;2:228. 15 Neely JR, Liebermeister H, Battersby El, Morgan HE. Effect of pressure development on oxygen consumption by isolated rat heart. Am J Physiol 1967;212:804-14. 16 Opie LH. Cardiac metabolism - emergence, decline, and resurgence. Part I . Cardiovasc Res I992;26:72 1-33. 17 Langendorff 0. Untersuchungen am Oberlebenden Saugethierherzen. fJugers Arch 1895;61:29 1-332. 18 Krebs HA, Henseleit Y. Untersuchungen Ober die Harnstoffbildung im Tierkorper. Hoppe-Seylers Z Physiol Chem 1932; 210:33-66. 19 Sandritter W, Jestadt R. Triphenyltetrzoliumchlorid als Reductionsindikator zur makropischen Diagnose des Freschen Herzinfarktes. Verhandl Deutsch Gesellsch fathol 1958;41: 165-71. 20 Nachlas MM, Shnitka TK. Macroscopic identification of early myocardial infarcts by alterations in dehydrogenase activity. Am J Pathol 1963;17:379405. 21 Mullane KM, Read N, Salmon JA, Moncada S. Role of leukocytes in acute myocardial infarction in anesthetized dogs: relationship to myocardial salvage by anti-inflammatory drugs. J fharmacol Exp Ther 1984;510:522. 22 Lie JT, Pairolero PC, Holley KE, Titus JL. Macroscopic enzymemapping verification of large, homogeneous, experimental myocardial infarcts of predictable size and location in dogs. J Thorac Cardiovasc Surg 1975;69:599405.

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attached, as the standard model. Another survivor is the Krebs-Henseleit buffer solution,’8 yet how many of us have read LangendorlT‘ s paper or those of Krebs and Henseleit, let alone understood them? We would argue that, since both model and solution have been in use for a sufficiently long time and no one has questioned the originators’ priority, there is a strong case for ceasing to cite these references in the bibliography. Other considerations apart, it would probably be the honest thing for most of us to do. The situation becomes considerably more complex in the case of our next example. The technique of delineating a myocardial infarct by tetrazolium staining for dehydrogenases was originally described by Sandritter and Jestadt in 1958 - in the German literature. They used triphenyltetrazolium which forms a red formazan product in the presence of dehydrogenases. Five years later Nachlas and Shnitka’” published - in the American literature - a modification in which nitroblue tetrazolium was used to form a blue formazan product to improve the delineation. They acknowledged the German workers, and said that their own work “confirms and extends the findings of the European investigators”. Which paper is to be cited? Unfortunately, the matter does not end there. In 1983, Mullane et al” used Sandritter and Jestadt’s technique, but attributed it to Lie et al.” A clear case of misattribution? Apparently not, since they had used dogs and Lie et a1 had also used dogs, whereas Sandritter and Jestadt had used human and guinea pig tissue. This is splitting hairs. Surely it is the first description (and successful use) of the technique that is important, not the subsequent minor modifications and fine tuning? Thereafter signijicanr modifications should be cited as “Smith’s technique as modified by Jones”. Common sense is obviously necessary, but we should bear in mind that we are in the business of scientific accuracy, not historical pedantry. Finally, we come to a reprehensible aspect of citation what might be termed “political citation”. In our experience, authors are often requested by reviewers to cite further papers in their typescripts. The usual reason is the perfectly valid one that the reviewer considers the citations to be biased in favour of the author’s viewpoint. However, it sometimes happens that the reviewer is anxious to see his own work cited and, if priority is involved, the peer review system then becomes decidedly counterproductive. Misattribution may result from the reverse of this process, when the author has a fairly shrewd idea of who the reviewer will be and proceeds to pack his reference list with citations that he feels will ensure a favourable review, or a successful grant application. Alas, we believe that both of these practices do occur. With the advent of computerised literature searches and the move towards a more concise form in scientific publication, we earnestly hope that controversies over priority will fade into the past, and that it will become

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Eponyms, priority, and attribution.

1170 Cardiovascular Research 1992;26: 1170- 1 171 Commentary Eponyms, priority, and attribution Robert G Richardson, Michael J Curtis L B neverth...
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