The diagnosis of art: WH Auden's face
Authors: Jeffrey K Aronson, Manoj Ramachandran
Journal: Journal of the Royal Society of Medicine (2011)

Rene Bouche,1,2 born in Prague in 1905, first came to prominence as an artist for Paris Vogue, to which he contributed fashion drawings. He then settled in Manhattan and painted portraits of the famous. His sitters included Nancy Astor, Jack Benny, Leonard Bernstein, Georges Braque, Alexander Calder, Truman Capote, Jean Cocteau, Isak Dinesen (Karen Blixen), Benny Goodman, Aldous Huxley, Edward Kennedy, Jacqueline Kennedy, J F Kennedy, Willem de Kooning, Anita Loos, Sophia Loren, Elsa Maxwell, Edward R Murrow, Helena Rubinstein, Igor Stravinsky, Gloria Swanson, and the Duchess of Windsor.


Bouche's portrait of WH Auden ( Figure 1) and an accompanying sketch ( Figure 2) shows the famous face, the ‘wedding cake left out in the rain’, of which Auden was so very proud. David Hockney, who also drew Auden, later reported, ‘I kept thinking, if his face looks like this, what must his balls look like?’ Hannah Arendt said that it was ‘as if life itself had delineated a kind of face-scape to make manifest the “heart's invisible furies”’. She was referring to Auden's poem ‘The Capital’: 

Yet with orchestras and glances, O, you betray us
To belief in our infinite powers; and the innocent
Unobservant offender falls in a moment
Victim to the heart's invisible furies.





Figure 1

WH Auden by Rene Bouche (1963, oil on canvas, 90.8 x 61.0 cm, National Portrait Gallery, Smithsonian Institution) (in colour online)





Figure 2

Sketch of WH Auden by Rene Bouche (1963) (in colour online)



The wrinkling on Auden's face in Bouche's portrait is not as pronounced as later portrayals show it, for example the pencil sketch by the author and illustrator Caroline Binch ( Figure 3), but the furrows are already deep. Bouche also shows Auden's tar-stained fingers (he was a lifelong smoker). And look carefully at the index finger. Is there a hint of clubbing? Impossible to tell, but perhaps there should be. Many others have portrayed the poet, including Kenneth Hari, David Hockney, Richard Francis Lahey, Natalia Moroz, Nikki Morris, John Springs and Feliks Topolski. But Auden's fingers do not appear in these portraits and are rarely seen in photographs.



Figure 3

Pencil sketch of WH Auden by Caroline Binch (31.5 x 46.0 cm). Reproduced with permission from the artist (see http://www.carolinebinch.co.uk )



In a letter to Auden's memoirist Charles H Miller, Jacques Barzun, whom Miller described as ‘my Gibraltar of counsel’, wrote that Auden had Touraine‐Solente‐Gole syndrome.3 The syndrome gets its eponym from a 1935 description by Albert Touraine, Gabriel Solente and Laurent Gole,4 and is otherwise known as pachydermoperiostosis or primary hypertrophic osteoarthropathy. Typically, and in accordance with the law of NOMEN (Non-Original Malappropriate Eponymous Nomenclature), which states that no phenomenon is named after its discoverer,5 the three Frenchmen were not the first to describe the condition. That honour belonged to Nikolaus Friedreich (1825–1882), a German neurologist who was Professor of Pathology at Wurzburg (where he succeeded Virchow) and later at Heidelberg, and who gave his name to Friedreich's ataxia,6 subsequently described by Wilhelm Heinrich Erb7 and by Julius Arnold8 and also called Friedreich‐Erb‐Arnold syndrome.9

Other syndromes named after Albert Touraine (1883–1961) that illustrate the same law include: Touraine's syndrome, skin pigmentation and neurofibromatosis, originally described by Virchow;10 Touraine's syndrome, better known as Behcet's disease, first described by Planner and Remenovsky;11 and Christ‐Siemens‐Touraine syndrome, X-linked hypohidrotic ectodermal dysplasia, which was first described in this journal in 1848 by Thurnam, a British psychiatrist, archaeologist and ethnologist.12 There is, however, a Touraine's syndrome that Touraine did describe, facial freckles associated with mental retardation.13

Inherited diseases and their associated genes and functional segments of DNA are assigned unique numbers called MIMs (Mendelian Inheritance in Man);14 the Touraine‐Solente‐Gole syndrome is the autosomal recessive form of pachydermoperiostosis, MIM 259100; the rarer autosomal dominant form is MIM 167100. The main features, apart from the skin changes, are digital clubbing, subperiosteal bone formation, and arthropathy; other features include anaemia, blepharitis, hyperhidrosis, and congenital cardiac defects. There is an excellent description in Rook's Textbook of Dermatology, at times poetic: ‘The pattern of folds and furrows on the forehead and cheeks, and the heavy thickened eye-lids, stamp the patients with a uniform expression of weariness and despair’.15 It is linked to a 9 Mb region on chromosome 4q33-q34 between markers D4S2979 and D4S41516 and has been associated with germ-line mutations of the gene (MIM 601688) that codes for 15-hydroxyprostaglandin dehydrogenase, the main enzyme responsible for prostaglandin breakdown.17 This potentially implicates prostaglandins in the aetiology of clubbing in general.

‘I thought,’ wrote Miller, ‘that [Auden's] furrowed face of later years reflected the agonies of writing; that time totted up the price of poetry on his face, that he pursued life – tried to corner it on squares of paper – until life turned and clawed his face. Yet Wystan had no patent on his geopoetic facial map, for here in high Massachusetts I see a farm woman whose face has identical dermal diagrams, and I see similar anxiety acrostics on the face of Asian refugees.’

In their 1935 paper Touraine and his colleagues described three forms: the classic or complete form, with skin and skeletal changes; an incomplete form, with skeletal changes but no skin changes; and a forme fruste, with skin changes but no skeletal effects. Perhaps Auden had the last of these. The condition does not seem to have contributed to his death in Kirchstetten in Austria in 1973. His death certificate merely says that he died of ‘arteriosclerosis, hypertrophy of the heart, and endocarditis’.18