The Gluten File - Seizures / Epilepsy The Gluten File

CELIAC DISEASE ~ GLUTEN SENSITIVITY

The relationship between celiac disease and epilepsy has been documented in medical journals for decades. Unfortunately, it is something our neurologists rarely consider as an underlying possibility in cases of idiopathic epilepsy.

Recent research is also showing that gluten sensitivity can manifest outside of intestinal celiac disease, and present solely as neurological disease in the form of ataxia, peripheral neuropathy, and seizures. This means that ruling out "celiac disease" does not absolutely rule out gluten related neurological disease. This is an important distinction to keep in mind should you decide to pursue testing. See the Diagnostic Testing page for more detailed information.

Particularly those with a family history of autoimmune disease or gastrointestinal problems or vitamin deficiency should give consideration to gluten being a potential cause for seizures.

Excerpts From:

Hippocampal sclerosis in refractory temporal lobe epilepsy is associated with gluten sensitivity. Feb 2009

Peltola M, Kaukinen K, Dastidar P, Haimila K, Partanen J, Haapala AM, Mäki M, Keränen T, Peltola J.
Medical school, University of Tampere, Finland.

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.

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.

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

From:

Is the prevalence of celiac disease increased among epileptic patients?
June 2003
PRATESI, Riccardo, GANDOLFI, Lenora, MARTINS, Rita C. et al. Is the prevalence of celiac disease increased among epileptic patients?. Arq. Neuro-Psiquiatr. [online]. 2003, vol. 61, no. 2B [cited 2006-08-23], pp. 330-334. Available from: <http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0004-282X2003000300002&lng=en&nrm=iso>. ISSN 0004-282X. doi: 10.1590/S0004-282X2003000300002.

"Taking our findings into account and reviewing previously published studies, some general observations concerning the association between epilepsy and CD can be brought forward:

(a) in many epileptic patients CD is asymptomatic or disclose only mild or atypical features14,15;

(b) epilepsy without cerebral calcifications, may be an early manifestation of CD, with calcifications developing later30;

(c) early identification and treatment of CD may reverse the tendency to epilepsy and probably to the development of calcifications16;

(d) seizures seen in association with CD are frequently difficult to control and, at least in some cases, this is due to poor AEDs absorption resulting from the concurrent enteropathy17;

(e) if CD is not precociously diagnosed, epilepsy will have propensity to progress in severity, evolving to a degree in which, even the introduction of GFD will fail to ameliorate the clinical picture17;

(f) although generalized forms of epilepsy are seen that, at times, rapidly evolve to a severe and progressive encephalopathy suggestive of Lennox-Gastaut syndrome31, partial complex seizures with involvement of the occipital lobes are more frequent16.

In conclusion, a greater attention is needed to the possible coexistence of CD in epileptic patients. Although a systematic screening for CD in all epileptic patients seems to be, at the present time, neither practical nor cost-effective, it seems reasonable to screen at least all patients with complex partial seizures, especially when associated with occipital paroxysms and resistance to drug therapy."

PubMed Abstracts

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.

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

PMID: 19244266 Feb 2009

CONCLUSION. Prevalence of CD was increased among patients with epilepsy of unknown etiology. It is important to investigate CD in any patient with idiopathic epilepsy even in the absence of digestive symptoms.

How frequent is celiac disease among epileptic patients?

PMID: 19104696 Dec 2008

Neurological complications of coeliac disease: what is the evidence?

PMID: 18344378 April 2008

Whole-brain histogram and voxel-based analyses of apparent diffusion coefficient and magnetization transfer ratio in celiac disease, epilepsy, and cerebral calcifications syndrome.
PMID: 17353316 Mar 2007

Increased prevalence of silent celiac disease among greek epileptic children.
PMID: 17352949 Mar 2007

Occult celiac disease presenting as epilepsy and MRI changes that responded to gluten-free diet.

PMID: 17296923 Feb 2007

Epilepsy and Celiac Disease: Favorable Outcome With a Gluten-Free Diet in a Patient Refractory to Antiepileptic Drugs.

PMID: 17122729 Nov 2006

Celiac disease-related antibodies in an epilepsy cohort and matched reference population.
PMID: 15820348 May 2005

Coeliac disease, epilepsy and cerebral calcifications.
PMID: 15737700 April 2005

Neurologic presentation of celiac disease.
PMID: 15825133 April 2005