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Gluten sensitivity as a neurological illness
  1. M Hadjivassiliou,
  2. R A Grünewald,
  3. G A B Davies-Jones
  1. Department of Neurology, The Royal Hallamshire Hospital, Glossop Road, Sheffield, S10 2JF, UK
  1. Correspondence to:
 Dr M Hadjivassiliou, Department of Neurology, The Royal Hallamshire Hospital, Glossop Road, Sheffield, S10 2JF, UK;
 m.hadjivassiliou{at}sheffield.ac.uk

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From gut to brain

It has taken nearly 2000 years to appreciate that a common dietary protein introduced to the human diet relatively late in evolutionary terms (some 10 000 years ago), can produce human disease not only of the gut but also the skin and the nervous system. The protean neurological manifestations of gluten sensitivity can occur without gut involvement and neurologists must therefore become familiar with the common neurological presentations and means of diagnosis of this disease.

COELIAC DISEASE THROUGH THE AGES: FROM GUT TO SKIN

” . . .the stomach being the digestive organ, labours in digestion, when diarrhoea seizes the patient . . .and if in addition, the patient's general system be debilitated by atrophy of the body, the coeliac disease of a chronic nature is formed”.1

This extract is from the book on chronic diseases by Aretaeus the Cappadocian, one of the most distinguished ancient Greek doctors of the first century AD. This chapter, entitled “on the coeliac diathesis”, was the first description of coeliac disease (from the greek word κ⊝ιλιακη meaning abdominal). Aretaeus' books were first published in Latin in 1500 and the new Latin word coeliac was used to translate κ⊝ιλιακη. Coeliac disease (CD) remained obscure until 1887 when Samuel Gee gave a lecture entitled On the coeliac affection2 at the Hospital for Sick Children, Great Ormond Street, London. In it he acknowledged Areteaus' contribution and went on to give an accurate description of CD based on his own clinical observations.

With clinical manifestations primarily confined to the gastrointestinal tract or attributable to malabsorption, it was logical to assume that the target organ and hence the key to the pathogenesis of this disease was the gut. The first report of neurological manifestations associated with CD was by Carnegie Brown in 1908.3 In his book entitled Sprue and its treatment …

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