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Hippocampal sclerosis in refractory temporal lobe epilepsy is associated with gluten sensitivity
  1. Maria Peltola
  1. Medical school, University of Tampere, Finland
    1. Katri Kaukinen
    1. Department of Gastroenterology and Alimentary Tract Surgery, Tampere University Hospital, Finland
      1. Prasun Dastidar
      1. Department of Radiology, Tampere University Hospital, Finland
        1. Katri Haimila
        1. Department of Tissue Typing Laboratory, Finnish Red Cross Blood Transfusion Service, Finland
          1. Jukka Partanen
          1. Department of Tissue Typing Laboratory, Finnish Red Cross Blood Transfusion Service, Finland
            1. Anna-Maija Haapala
            1. Department of Clinical Microbiology, Center for Laboratory Medicine, Tampere University Hospital, Finland
              1. Markku Mäki
              1. Department of Pediatrics, Tampere University Hospital, Finland
                1. Tapani Keränen
                1. Department of Neurology and Rehabilitation, Tampere University Hospital, Finland
                  1. Jukka Peltola (jukka.peltola{at}
                  1. Tampere University Hospital, Finland


                    Previously coeliac disease (CD) and gluten sensitivity (defined as the presence of anti-gliadin antibodies and positive immunogenetics) has been associated with cerebellar degeneration and epilepsy with occipital calcifications. Hippocampal sclerosis (HS) in temporal lobe epilepsy (TLE) is a potentially progressive disorder with unknown aetiology, and autoimmunity has been implicated in TLE+HS as one of the possible mechanism leading to HS.The purpose of this study is to analyze CD associated antibodies and gluten sensitivity in well characterized group of patients with refractory focal epilepsy.

                    We measured anti-gliadin, anti-tTG and anti-EMA and celiac type HLA (DQ2 and DQ8) in 48 consecutive patients with therapy resistant localisation-related epilepsy. The patients were categorised TLE+HS (N=16), TLE-HS (N=16) and extratemporal epilepsy (N=16) based on ictal eletro-clinical characteristics and high resolution MRI. Patients with suspected CD or gluten sensitivity underwent duodenal biopsies.

                    Seven patients were gluten sensitive, all of these patients had TLE+HS whereas none of the patients without HS were gluten sensitive (p< 0.0002). In duodenal biopsies three of the patients had histological evidence of CD and four had inflammatory changes consistent with early developing CD without villous atrophy. Four of the patients with gluten sensitivity had evidence of dual pathology (HS + another brain lesion) whereas none of the rest of patients did (p< 0.0002).

                    The present study demonstrates a previously unrecognized association between gluten sensitivity and TLE with hippocampal sclerosis. The association was very robust in this well characterised group of patients; thus gluten sensitivity should be added to the list of potential mechanism leading to intractable epilepsy and HS.

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