Hippocampal sclerosis in refractory temporal lobe epilepsy is associated with gluten sensitivity
- M Peltola1,
- K Kaukinen2,
- P Dastidar3,
- K Haimila4,
- J Partanen4,
- A-M Haapala5,
- M Mäki6,
- T Keränen7,
- J Peltola7
- 1Medical school, University of Tampere, Tampere, Finland
- 2Department of Gastroenterology and Alimentary Tract Surgery, Tampere University Hospital, Tampere, Finland
- 3Department of Radiology, Tampere University Hospital, Tampere, Finland
- 4Tissue Typing Laboratory, Finnish Red Cross Blood Transfusion Service, Helsinki, Finland
- 5Department of Clinical Microbiology, Center for Laboratory Medicine, Tampere University Hospital, Tampere, Finland
- 6Department of Pediatrics, Tampere University Hospital, University of Tampere, Tampere, Finland
- 7Department of Neurology and Rehabilitation, Tampere University Hospital, Tampere, Finland
- Dr Jukka Peltola, Tampere University Hospital, PO Box 2000,Tampere, 33521 TRE, Finland; jukka.peltola{at}pshp.fi; nekujupe{at}yahoo.com
- Received 27 February 2008
- Revised 13 January 2009
- Accepted 27 January 2009
- Published Online First 24 February 2009
Abstract
Background: Previous studies have associated coeliac disease (CD) and gluten sensitivity (defined as the presence of anti-gliadin antibodies and positive immunogenetics) with cerebellar degeneration and epilepsy with occipital calcifications. Hippocampal sclerosis (HS) in temporal lobe epilepsy (TLE) is a potentially progressive disorder with unknown aetiology; however, autoimmunity has been implicated as one of the possible mechanisms leading to HS. The purpose of this study is to analyze CD-associated antibodies and gluten sensitivity in a well-characterised group of patients with refractory focal epilepsy.
Methods: We measured anti-gliadin, anti-tissue-transglutaminase and anti-endomysium antibodies, and coeliac-type human leukocyte antigen (DQ2 and DQ8), in 48 consecutive patients with therapy-resistant, localisation-related epilepsy. The patients were categorised into the following three groups on the basis of ictal electro–clinical characteristics and the findings of high resolution MRI: TLE with HS (n = 16), TLE without HS (n = 16) and extratemporal epilepsy (n = 16). Patients with suspected CD or gluten sensitivity underwent duodenal biopsies.
Results: Seven patients in total were gluten sensitive; all of these patients fell in the TLE with HS group. On the other hand, none of the TLE without HS patients or those with extratemporal epilepsy were gluten sensitive (p<0.0002). The results of duodenal biopsies showed that three of the seven gluten-sensitive patients had histological evidence of CD and four had inflammatory changes consistent with early CD without villous atrophy. Four of the patients with gluten sensitivity had evidence of dual pathology (HS+another brain lesion), whereas none of the remaining patients did (p<0.0002).
Conclusions: The present study demonstrates a previously unrecognised link between gluten sensitivity and TLE with HS. This association was very robust in this well-characterised group of patients; thus gluten sensitivity should be added to the list of potential mechanisms leading to intractable epilepsy and HS.
Footnotes
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Competing interests: None.
