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.
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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.
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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.
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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.