NeuroTalk Support Groups - Hippocampal scelerosis in refractory temporal lobe epilepsy associated with gluten

NeuroTalk Support Groups (https://www.neurotalk.org/)

- Epilepsy (https://www.neurotalk.org/epilepsy/)

- - Hippocampal scelerosis in refractory temporal lobe epilepsy associated with gluten (https://www.neurotalk.org/epilepsy/79113-hippocampal-scelerosis-refractory-temporal-lobe-epilepsy-associated-gluten.html)

Hippocampal scelerosis in refractory temporal lobe epilepsy associated with gluten

Quote:

Feb 2009

Hippocampal sclerosis in refractory temporal lobe epilepsy is associated with gluten sensitivity.

Medical school, University of Tampere, 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.
PMID: 19244266

Gluten is the protein found in wheat, barely, and rye. Celiac disease is an autoimmune disease that occurs in those with an adverse immunological response to gluten when autoantibodies form and attack the intestinal villi. Neurological problems, including seizures, have been associated with celiac disease for decades. However because celiac disease is a GI disease, and used to be considered rare (its not, its common)... it has not been on the radar screens of neurologists.

This study is really significant because it is one of the first to broaden the search to include gluten sensitivity that isn't celiac disease. It is only in the last decade that researchers have begun to show that gluten sensitivity can cause neurological and other disease without showing as "celiac disease". I've been posting about this most of that time.

I honestly believe that every new seizure patient, of any type, should be screened for antigliadin antibodies associated with gluten sensitivity. And, because this has not been on the radar screen for neurologists, "old" seizure patients should also follow up on this...particularly if there is any family history of autoimmune disease or GI problems. Gluten has been implicated in many different seizure types, and frankly, they haven't looked enough. Kudos to those who put together this study.

BTW... if gluten sensitivity IS the underlying factor in seizures, in some cases a gluten free diet alone is enough to resolve the seizures...if instituted before permanent damage is done.

For more info on gluten sensitivity/ celiac disease see The Gluten File:
http://jccglutenfree.googlepages.com/seizuresepilepsy

Cara

Here are some pertinent excerpts from the study above:

Quote:

Evidence suggests that gluten sensitivity/ celiac disease clearly exist beyond small bowel
mucosal villous atrophy (25). Even if AGA is regarded unspecific for classic small bowel
lesion that defines celiac disease (26), it has been useful in detecting diverse neurological
manifestations of gluten sensitivity (8 ). Gluten sensitivity has been implicated in cerebellar
degeneration (11), where there is emerging data addressing the epidemiology,
pathogenetic mechanisms and genetic background of gluten sensitivity and cerebellar
degeneration. Interestingly, the findings in the duodenal biopsies from patients with gluten
ataxia are similar to our patients with gluten sensitivity and TLE+HS; inflammatory
changes are consistent with early developing CD without villus atrophy (27). Furthermore,
the presence of class IgA tTG deposits were recently demonstrated both in jejunal tissue
and in the brain of patients with gluten ataxia without an enteropathy (28 ). In the present
study the definition of gluten sensitivity included AGA positivity and classical celiac type
HLA. However in cerebellar degeneration patients with AGA positivity without the presence
of HLA DQ2/8 have been described and in future studies also this group of patients would
be interesting to address in patients with epilepsy.

Quote:

There are several studies suggesting that autoimmunity is involved in refractory
localization-related epilepsy, especially in TLE+HS patients (30). Increased prevalence of
anti-GluR3 antibodies (31) and anti-GAD antibodies (15) have been observed in refractory
TLE.

Quote:

Our findings open a possibility for prevention of progression of HS in TLE. In CD gluten
free diet (GFD) produces clinical and symptomatic improvement and also decreases the
possibility of developing complications of CFD such as lymphoma and osteoporosis (5).
Gluten ataxia responds to GFD even in the absence of an enteropathy (35). In the epileptic
syndrome with occipital calcifications the chances of seizure control after GFD seem to be
significantly inversely related to the duration of epilepsy before GFD and to the age at the
beginning of GFD (36). Thus in temporal lobe epilepsy GFD should most probably to be
initiated early in the course of epilepsy to be effective, our patients had a long duration of
epilepsy with established HS where GFD is very unlikely to be effective.

Early identification and gluten free diet may halt the progression of certain types of epilepsy. This is all especially important to those with family history of any autoimmune disease.