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Neuropathies tend to be associated with late onset celiac disease. Dementia and ataxia appear to be more common. A recent study of children with neuropathies revealed no increase of CD in early onset neuropathies.. Although many studies link CD to various neuropathies such as migraine, encephalopathy, chorea, brain stem dysfunction, myelopathy, mononeuritis multiplex, Guillain-Barre-like syndrome, and antiganglioside-positive neuropathy with antibodies, strong associations remain largely unconfirmed in epidemiologic studies. A recent study looking for changes in the physiology of the brain found regional cerebral hypoperfusion in 73% of untreated CD The calcification of channels at the surface of the brain appear to be a leading

phenomena associated with Migrane, Visual, Auditory, Schizophrenia, Epilepsy, Dementia. The problem is that while these are found increased in GSE the cause of these calcifications

is unclear and this may extend beyond GSE to other immunological or allergic phenomena.

A recent study in Sweden of 14,000 GSE patients revealed no association of CD with

multiple sclerosis, Parkinson's disease, Alzheimer's disease, hereditary ataxia, ataxia(the symptom), Huntington's disease, myasthenia gravis, or spinal muscular atrophy, but prior polyneuropathy was associated with subsequent CD. However, a 2009 study of myasthenics revealed that 1 in 23 had high levels of anti-transglutaminase.

Peripheral neuropathies

Peripheral neuropathies are greatly increased in people who have GSE. In clinical CD there is on obvious reason, Avitaminosis and the inability to adsorb essential fatty acids and vitamins can lead to nervous system problems, including sensitivity of the peripheral nervous system. In addition to these problems there are a number or rare autoimmune conditions, secondary autoimmunities, such as fibromyalgia that are more frequent in GSE than in the normal population. Gulliane-Barre syndrome is associated with peripheral neuropathies, and it has been found that anti-ganglioside autoantibodies take part in the binding to axons and schwann cells. Antibodies to these gangliosides have been found elevated in coeliac disease

Ataxia

A sizable fraction of individuals who have gluten-sensitive ataxia have signs of GSE (either CD or elevated intraepitheal lymphocytes) and ataxia is a common symptom in GSE. Studies of clinically undefinable ataxia generally had higher proportion of late onset gait ataxia, mild upper limb symptoms, and evidence of peripheral neuropathy, questions were raised about the specificity of testing and false positives. Patients with ataxia and CD have antibodies that react with Purkinje fibers but is restricted to the anti-gliadin IgA/IgG. A recent Swedish study of 14,000 registered celiacs showed no association of GSE with Ataxia.

Dementia, epilepsy

Epilepsy has been noticed in a sampling of Coeliac Disease patients. One prime example is calcium channel obstruction in the brain and dementia. There is a growing body of evidence suggesting that subclinical cases in older adults will typically progress toward dementia, a large number of studies in Italy and Spain have documented earlier onset cases, though the autoimmune condition is not known, folic acid malabsorption may be the cause.

Visual and auditory disturbances

According to recent studies calcifications of channels seen in dementia can also occur in specific brain areas such as the visual complex in the occipital lobe. Such calcium channel blockages can cause visual problems or partial field hallucinations (Paroxysmal visual manifestations).. Other papers show a link between migrane, visual aura and cerebral calcifications. Disturbances may be followed by

convulsions and associated with gastrointestinal phenomena.

White matter lesions

Ten (of 75) young patients had neurologic findings such as febrile seizures, single generalized seizures, mild ataxia, and muscular hypotonia with retarded motor development, but magnetic resonance imaging detected unilateral and bilateral T2-hyperintensive white-matter lesions in 15 patients (20%)

Depression

Depression in GSE has several causes, in the more severe CD depression can be the result of lower vitamin adsorption and essential fatty acid adsorption (see section on autism). Depression and anger may also be the result of lower quality of life issues as a result of gluten-free diet. Depression appears to persist on gluten free diet in a sizable fraction of GSE. Elevated anger has been noted also with GSE.

Anxiety

Anxiety is a common feature of GSE, treatment on a gluten-free diet is effective at reducing anxiety, some aspect of which may be due to maladsorption phenomena

and cytokine activity (i.e. constant stress).

Fibromyalgia

Fibromyalgia was found in 9% of adult patients relative to 0.03% in the general population with a link common to IBD. Concurrent IBS is found in 30% to 70%. Small intestinal bacterial overgrowth is associated is common with a transient response to antimicrobial therapy.

Chronic fatigue

Chronic fatigue associated with GSE is a systemic disorder, however there are neurological components that are especially manifest in blood deficiencies like avitaminosis, amineralosis and anemia. Reduced iron and the lack of vitamins folate, B6, B12 and maladsorption of essential fatty acids can cause depression and chronic fatigue. Anti-gliadin antibodies correlate with higher risk for chronic-fatique when no clinical finding of CD is present.

While fatigue is reduced on gluten-free diet, bouts of depression can become worse.


Adapted from the Wikipedia article Gluten-sensitive enteropathy associated conditions, under the G. N. U. Free Documentation License. Please also see http://en.wikipedia.org/wiki