between patients with GA and patients with ACAA (with and without serological evidence of sensitivity to gluten). Methods Subjects and Controls A retrospective review of all patients attending the ataxia clinic, Royal Hallamshire Hospital, Sheffield, UK was performed. Patients with a diagnosis of GA and ACAA were sought (see Chapter 3 for details). All patients from the two groups that had undergone the exact same MR imaging protocol of the brain were selected for MR imaging analysis. The clinical notes of these patients were assessed to obtain the duration and severity of ataxia symptoms at the time of MR imaging (as outlined in Chapter 3). Evidence of CD (in the form of positive duodenal biopsies) was also sought in both patient groups. Age- and sex-matched control data were acquired from a group of 55 healthy volunteers as detailed in Chapter 4.() All controls and subjects underwent the exact same imaging protocol. MR imaging outcome measures Outcome measures comprised of: (a) CV:TIV; (b) NAA/Cr and Cho/Cr ratios in the cerebellar vermis and hemisphere and (c) grey matter ‘density’ as indicated by VBM. In each case, subjects’ data were compared to control data matched for age and sex. Imaging protocol and analysis Details of structural MR imaging and 1H MR spectroscopy, as well as imaging analysis can be found in Chapter 3. %CV:TIV was estimated using the modified method. Results Over a 15-year period, 904 patients with progressive cerebellar ataxia attended the specialist ataxia clinic at the Royal Hallamshire Hospital, Sheffield, UK. Of these, 104 patients were diagnosed with ACAA and 159 patients with GA. 61% of the ACAA group and 70% of the GA group had the HLA DQ2/DQ8 genotype, compared to 30% in healthy local blood donors.() 44% of patients
between patients with GA and patients with ACAA (with and without serological evidence of sensitivity to gluten). Methods Subjects and Controls A retrospective review of all patients attending the ataxia clinic, Royal Hallamshire Hospital, Sheffield, UK was performed. Patients with a diagnosis of GA and ACAA were sought (see Chapter 3 for details). All patients from the two groups that had undergone the exact same MR imaging protocol of the brain were selected for MR imaging analysis. The clinical notes of these patients were assessed to obtain the duration and severity of ataxia symptoms at the time of MR imaging (as outlined in Chapter 3). Evidence of CD (in the form of positive duodenal biopsies) was also sought in both patient groups. Age- and sex-matched control data were acquired from a group of 55 healthy volunteers as detailed in Chapter 4.() All controls and subjects underwent the exact same imaging protocol. MR imaging outcome measures Outcome measures comprised of: (a) CV:TIV; (b) NAA/Cr and Cho/Cr ratios in the cerebellar vermis and hemisphere and (c) grey matter ‘density’ as indicated by VBM. In each case, subjects’ data were compared to control data matched for age and sex. Imaging protocol and analysis Details of structural MR imaging and 1H MR spectroscopy, as well as imaging analysis can be found in Chapter 3. %CV:TIV was estimated using the modified method. Results Over a 15-year period, 904 patients with progressive cerebellar ataxia attended the specialist ataxia clinic at the Royal Hallamshire Hospital, Sheffield, UK. Of these, 104 patients were diagnosed with ACAA and 159 patients with GA. 61% of the ACAA group and 70% of the GA group had the HLA DQ2/DQ8 genotype, compared to 30% in healthy local blood donors.() 44% of patients
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