Gluten ataxia

  title={Gluten ataxia},
  author={Marios Hadjivassiliou and David S. Sanders and Nicola Woodroofe and Clare Alice Williamson and Richard A Gr{\"u}newald},
  journal={The Cerebellum},
Gluten ataxia is an immune-mediated disease triggered by the ingestion of gluten in genetically susceptible individuals. It should be considered in the differential diagnosis of all patients with idiopathic sporadic ataxia. Early diagnosis and treatment with a gluten free diet can improve ataxia and prevent its progression. Readily available and sensitive markers of gluten ataxia include antigliadin antibodies. IgA deposits against TG2 in the small bowel and at extraintestinal sites are proving… 

Gluten Ataxia: An Important Treatable Etiology of Sporadic Ataxia

The case of a patient with imbalance and no abdominal symptoms diagnosed with gluten ataxia and her neurological symptoms responded to gluten-free diet is reported, indicating early diagnosis and treatment may result in neurological improvement.

Autoantibodies in gluten ataxia recognize a novel neuronal transglutaminase

This work has identified a novel neuronal transglutaminase isozyme and investigated whether this enzyme is the target of the immune response in patients with neurological dysfunction, and identified an autoimmunity directed toward different members of the transglutsin gene family.

Progressive Ataxia Revealing Gluten Sensitivity

The clinical, radiological, and neurophysiological features of ataxia are described, which are the commonest neurological manifestation of coeliac disease.

Gluten sensitivity: associated sporadic cerebellar ataxia in Taiwan.

Gluten sensitivity-related sporadic ataxia exists in Taiwan with linkage to autoimmune events and anti-gliadin IgG still is a very powerful indicator to implicate the immune-related autoimmune disease.

The neuroimmunology of gluten intolerance

The recent concept of extraintestinal manifestations without enteropathy (termed non-coeliac gluten sensitivity (NCGS)) has become accepted as part of the same spectrum.

Guidelines for treatment of immune-mediated cerebellar ataxias

Evaluated the efficacies of immunotherapies in reported cases using a common scale of daily activity and highlighted the importance of removal of autoimmune triggering factors and the need for immunotherapy evaluation according to each subtype.

Cerebellar Ataxia, Celiac Disease and Non-Celiac Gluten Sensitivity

Cerebellar Ataxia is equally responsive to GFD in CD and NCGS patients and the increased recognition of the whole spectrum of Gluten related disorders (GRD) is the best way to improve the time of the diagnosis and to avoid patients with neurological manifestation remaining untreated if duodenal biopsy does not reveal an enteropathy.

Gluten-related disorders: an evolving story

  • G. Holmes
  • Medicine
    Gluten-Related Disorders
  • 2022

exploring non coeliac gluten sensitivity a neuropsychiatric disorder

Case reports and retrospective questionnaires highlight a potential link between gluten and mental health effects, however mechanisms will only be established with carefully conducted double-blind placebo-controlled cross-over designs which reveal re-producible findings.



Antigliadin antibodies in Huntington’s disease

The authors found high antigliadin antibody titers in 23 of 52 patients with Huntington’s disease (HD), suggesting a previously unrecognized association between HD and gluten sensitivity, and raises the possibility that antIGliadin antibodies in ataxia and other neurodegenerative diseases may be an epiphenomenon.

Dietary treatment of gluten ataxia

Gluten ataxia responds to a strict gluten-free diet even in the absence of an enteropathy, which is vital as it is one of the very few treatable causes of sporadicAtaxia.

Gluten sensitivity in sporadic and hereditary cerebellar ataxia

A high prevalence of gluten sensitivity was found in patients with sporadic and autosomal dominant ataxias, including patients with known ataxia genotypes indicating a hitherto unrecognized association between hereditary ataxians and gluten sensitivity.

Gluten ataxia in perspective: epidemiology, genetic susceptibility and clinical characteristics.

The prevalence of gluten sensitivity amongst a large cohort of patients with sporadic and familial ataxia was investigated and possible genetic predisposition to gluten sensitivity among these groups was looked at.

The immunology of gluten sensitivity: beyond the gut.

Cerebellar ataxia associated with subclinical celiac disease responding to gluten-free diet.

Clinical and electrophysiologic improvement in a patient with ataxia and peripheral neuropathy associated with subclinical CD after 2 years of a gluten-free diet is described.

Sporadic cerebellar ataxia associated with gluten sensitivity.

The fact that the disease is strongly associated with the same HLA haplotypes found in coeliac disease not only demonstrates coeliasis disease and ataxia with gluten sensitivity to be part of the same disease entity but supports the hypothesis of an immunological pathogenesis of cerebellar degeneration.

Gluten sensitivity in Japanese patients with adult-onset cerebellar ataxia.

Gluten sensitivity is involved in at least some of the unexplained neurological symptoms of Japanese patients with adult-onset, sporadic cerebellar ataxia, and a gluten-free diet had positive effects on neurological symptoms and nutritional status.

The humoral response in the pathogenesis of gluten ataxia

Patients with gluten ataxia have antibodies against Purkinje cells, and adsorption of the antigliadin antibodies using crude gliadin abolished the staining in patients with celiac disease without neurologic dysfunction, but not in those with glutenAtaxia.

Autoantibody targeting of brain and intestinal transglutaminase in gluten ataxia

Anti–tissue transglutaminase IgA antibodies are present in the gut and brain of patients with gluten ataxia with or without an enteropathy in a similar fashion to patients with celiac disease, latent celiac Disease, and dermatitis herpetiformis but not in ataxIA control subjects.