Gluten Ataxia and Post-Streptococcal Central Nervo

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Curr Treat Options Neurol. 2005 May;7(3):183-189. Related Articles,

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Gluten Ataxia and Post-Streptococcal Central Nervous System

Syndromes: Emerging Immune-mediated Disorders of the Central Nervous

System?

 

Wills A, Dale R, Giovannoni G.

 

Institute of Neurology, Queen Square, London WC1 3BG, United Kingdom.

G.Giovannoni@ion.ucl.ac.uk.

 

There is an "emerging concept" that central nervous system

dysfunction can be caused by an aberrant immune response triggered by

exogenous antigens such as the food allergen gluten or streptococcal

infection. The hypothesis of a gluten sensitive ataxia remains

unproven, but is worthy of consideration. The data in support of this

hypothesis require critical review before any treatment

recommendations can be formulated. The idea that anti-gliadin

antibody seropositivity per se justifies the term "gluten

sensitivity" is important because it offers potential therapeutic

possibilities, including simple exclusion diets, for patients with

anti-gliadin antibody-associated ataxia. Post-streptococcal basal

ganglia dysfunction has various manifestations, all of which fall

into a relatively well-defined symptom complex or syndrome. Anti-

basal ganglia antibodies that are associated with serologic evidence

of recent streptococcal infection are a potential diagnostic marker

for this group of disorders, which includes Sydenham's chorea (SC) as

the prototype. More recently subjects with pediatric autoimmune

neuropsychiatric disorders associated with streptococcal infection,

Tourette's syndrome, obsessive-compulsive disorder and other movement

disorders have been described in association with anti-basal ganglia

antibodies. The apparent overlap between the clinical phenotype of

SC, pediatric autoimmune neuropsychiatric disorders associated with

streptococcal infections, Tourette's syndrome, and obsessive-

compulsive disorder suggests that they may represent one disease

entity. The current working hypothesis is that antibodies induced in

response to streptococcal infection cross-react with antigenic

determinants in the basal ganglia resulting in basal ganglia

dysfunction. Although the experimental evidence is incomplete, there

is sufficient evidence to support immune-mediated basal ganglia

dysfunction as an emerging clinical entity. This has important

implications for the diagnosis and treatment of subjects with these

disorders. The latter includes the judicious use of antibiotic

prophylaxis and immunomodulatory therapies. Apart from the diagnosis

and management of SC, no consensus exists regarding the diagnosis and

management of the other clinical entities within this group of

disorders.