Ataxia, peripheral neuropathy, and anti-gliadin antibody. Guilt by association?

Some authors contend that patients with idiopathic neurological disease who are also anti-gliadin antibody seropositive are gluten sensitive. However, anti-gliadin antibodies lack disease specificity being found in 10% of healthy blood donors. We report a study comparing anti-gliadin antibody with other food antibodies in patients with idiopathic ataxia (20), hereditary ataxias (seven), or idiopathic peripheral neuropathy (32). Patients were HLA typed. IgA anti-tissue transglutaminase antibodies (tTG) were measured. No case was positive for IgA anti-tTG making occult coeliac disease unlikely. HLA DQ2 and HLA DQ8 were found distributed equally across all patient groups and unrelated to gliadin antibody status. HLA DQ2 expressing, anti-gliadin antibody positive cases (so called "gluten ataxia") were rare in our clinics (four cases in 2 years from a population of 2 million). We conclude that coeliac disease per se is not commonly associated with either idiopathic ataxia or idiopathic peripheral neuropathy. Our study also casts doubt on the nosological status of "gluten ataxia" as a discreet disease entity. All food antibodies tested, particularly IgG, were a common finding in both ataxia and peripheral neuropathy groups. No particular food antibody was associated with any patient group. Food antibodies were equally common in hereditary ataxias. We conclude they are a non-specific finding.

Urgent 2-week referrals for CNS/brain tumours: a retrospective audit.

OBJECTIVE: To assess the effectiveness of the 2-week referral system for CNS/brain tumours and to contrast this with the number of patients with neurological cancers identified independently of this system. METHOD: Retrospective casenote review of patients referred to emergency neurology clinics pre-implementation of the 2-week referral system. Retrospective review of GP referral letters via this system and comparison to Department of Health referral guidelines. Review of corresponding casenotes to determine the actual neurological diagnosis. Identification of patients with CNS/brain tumours diagnosed independently of this system from a local CNS cancer register. RESULTS: Over a 3-month period pre-implementation of the referral system, of 12 patients referred as emergencies, none had CNS/brain cancer. Forty-three patients were referred via this system over a 9-month period to neurology departments of a teaching hospital and a district general hospital. Thirty per cent of the referrals did not follow the Department of Health guidelines. Only 9% actually had CNS tumours (two astrocytomas, two cerebral metastases). The remainder were diagnosed with chronic daily headache (10), epilepsy (5), migraine (3), demyelination (2), essential tremor (2), other (17). During this period at least 69 neurological cancers were identified independently of the 2-week system. CONCLUSION: These guidelines may increase diagnostic precision if adhered to rigidly. Inappropriate referrals have extended already lengthy outpatient waiting times in other specialities. We suggest early re-consideration of these guidelines and further study for earlier identification of CNS cancer.

Neurological complications of coeliac disease.

A variety of neurological disorders have been reported in association with coeliac disease including epilepsy, ataxia, neuropathy, and myelopathy. The nature of this association is unclear and whether a specific neurological complication occurs in coeliac disease remains unproved. Malabsorption may lead to vitamin and trace element deficiencies. Therefore, patients who develop neurological dysfunction should be carefully screened for these. However, malabsorption does not satisfactorily explain the pathophysiology and clinical course of many of the associated neurological disorders. Other mechanisms proposed include altered autoimmunity, heredity, and gluten toxicity. This review attempts to summarise the literature and suggests directions for future research.