Reply to: Gluten ataxia 'in perspective'

We note Dr Wills’ and Dr Unsworth’s continued scepticism at the concept of gluten ataxia in the face of overwhelming evidence in its support. We have proposed that IgG antigliadin antibodies are currently the best marker of the whole spectrum of gluten sensitivity although they are not specific for gluten‐sensitive enteropathy. We hope that a better marker of neurological manifestations of gluten sensitivity will come with the identification of the antibodies recognizing neuronal epitopes, such as those on Purkinje cells identified by antibodies in patients with gluten ataxia. This would be analogous to the antiendomysium antibody in cases with gluten‐sensitive enteropathy or epidermal transglutaminase antibodies in patients with Dermatitis Harpetiformis. We have long recognized that the final test of the hypothesis that gluten ataxia as an entity comes with the demonstration of response to treatment. The benefit of a gluten‐free diet in patients with gluten ataxia has been demonstrated in our study of 43 patients (so far) (Hadjivassiliou et al., 2003). The response in the treatment group was independent of the presence of an enteropathy, confirming that gluten ataxia is part of a spectrum of gluten sensitivity. It is not, unfortunately, feasible to conduct a blinded study because of the nature of the intervention (gluten‐free diet).