Well Written Medical Explanation Of Nuerological Celiac

[marciab]

I thought some of you might be interested in this.

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marcia

[Ursa Major]

Marcia, that is an amazing article. SOMEBODY obviously gets it and completely understands! And they even cite the gluten sensitivity gene, HLA DQ1, as causing especially neurological manifestations of celiac disease. Meaning, not only Dr. Fine recognizes it.

[marciab]

This article was written back in 2002 in the UK, but ... I copied this is in ...

"The introduction of the small bowel biopsy in 1950

[marciab]

I woke up this morning remembering that my labs over the years (the ones I have found to date anyway) did not reflect a low B12 or iron deficiency. 17 years of being sick this month ...

This article explains how a person can have nuerological celiac and little or no damage to the villi ... So, I would have been absorbing B12 and iron.

I know getting the gluten out of my diet got rid of my ataxia and myoclonus, I was just looking for an explanation .... This article says that the nerves have to heal, so that is probably why it took 1 year to get rid of the ataxia ....

ARTICLE --------------------------------------------------------------------------------------------------------

RECENT ADVANCES: PREVALENCE, SMALL BOWEL HISTOLOGY AND GENETIC SUSCEPTIBILITY

Some studies looking at normal populations have shown that the prevalence of celiac disease is much higher than previously thought (approximating to 1 in 100).

Most of such patients have no gastrointestinal symptoms. In addition, experimental data in patients with gluten sensitivity suggest that there is a range of mucosal abnormalities affecting the small bowel ranging from preinfiltrative (histologically normal) to infiltrative, to hyperplastic to flat destructive (seen in celiac disease), and finally to the irreversible hypoplastic atrophic lesions.

Increasing the gluten load may result in progression of the severity of the lesion. In those patients where the histology is normal, staining of the T cell subpopulations of the intraepithelium of the small bowel biopsies shows alteration of T cell subpopulations of the intraepithelial lymphocytes (increase of the / T cells).

This finding is said to be a marker of potential celiac disease. This procedure is only available in a very few pathology laboratories, rendering its use limited.

Finally, celiac disease has a very strong association with the human lymphocyte antigen (HLA) of the major histocompatibility complex. Ninety per cent of patients with celiac disease have the HLA DQ2; the rest have DQ8.

These advances suggest that gastrointestinal symptoms are absent in most patients with celiac disease, that the definition of gluten sensitivity can no longer be solely based on the presence of an enteropathy and that genetic susceptibility may be an important additional marker for gluten sensitivity.

Given the knowledge of these advances and approaching gluten sensitivity from a neurological perspective we set up to address the following question: Does cryptic gluten sensitivity play a part in neurological illness?

THE NEUROLOGY OF GLUTEN SENSITIVITY

Over the past 8 years we have used antigliadin antibodies to screen patients with neurological dysfunction of unknown aetiology.

Our original study concluded that gluten sensitivity played an important part in neurological illness.

The evidence was statistical: Patients with neurological disease of unknown aetiology were found to have a much higher prevalence of circulating antigliadin antibodies (57%) in their blood than either healthy control subjects (12%) or those with neurological disorders of known aetiology (5%).

Since then we have identified 131 patients with gluten sensitivity and neurological disorders of unknown aetiology. Table 2 shows the neurological diagnoses we have encountered. Perhaps not surprisingly the commonest manifestations are ataxia (also known as gluten ataxia18) and peripheral neuropathy.

GLUTEN ATAXIA

Systematic screening of 143 patients with so-called "idiopathic sporadic ataxia" showed that 41% had gluten sensitivity as defined by the presence of circulating antigliadin antibodies20 (IgG with or without IgA).

The prevalence of antigliadin antibodies in 51 patients with familial ataxia did not differ from that found in normal healthy control subjects (13%).

The mean age of onset of the ataxia was 54 but we have recently seen three patients with early onset (under 20 years of age) sporadic idiopathic ataxia and gluten sensitivity.

Recently four patients have been described with celiac disease presenting as gait disturbance and ataxia in infancy.

Alhough the ataxia tends to be slowly progressive, in some cases it can take a very rapid course with the development of cerebellar atrophy within a year of the onset of the illness (fig 1).

Ataxia and myoclonus is a much less common presentation (only four patients in these series). We have encountered two patients who in addition to ataxia had evidence of chorea but normal genetic testing for Huntington's disease.

Gluten ataxia primarily affects the lower limbs and gait. Extrapyramidal or autonomic features are rarely apparent and these features distinguish it from the cerebellar variant of multisystem atrophy (MSA).

Screening of patients with clinically probable MSA (cerebellar variant) for the presence of antigliadin antibodies showed the prevalence to be similar to the normal population.

Brain MRI usually shows cerebellar atrophy; sometimes with evidence of white matter abnormalities. Up to 40% of patients also have a sensorimotor axonal peripheral neuropathy that can often be subclinical. In a few cases oligoclonal bands are present in the CSF.

Marcia

[Sophiekins]

Three cheers for our darling Dr. H! (Doing his part to convince the medical community we're not all crazy!)

[happygirl]

Thanks for sharing this article...it really is great!

[darlindeb25]

A B12 deficiency is only one symptom of neuropathy. And, remember, B12 levels are only as good as the person reading them. A person with neuropathy needs much higher levels of B12. The doctor told me that my B12 level is good, yet I take 2400mcg of B12 daily just to keep it at that level. 2400mcg is 40,000% of the daily allowance for a normal person.