Contributions
Abstract: EP1528
Type: ePoster
Abstract Category: Pathology and pathogenesis of MS - 21 Imaging
Background: Cognitive dysfunction is associated with brain atrophy in multiple sclerosis (MS). The brain and lesion volumetric measurements are time and resource consuming and they are still not available in routine practice. The corpus callosum index (CCI) is measured using conventional magnetic resonance imaging (MRI) and it may be a surrogate marker of brain atrophy in MS. However, no study evaluated the correlation between cognitive dysfunction and CCI.
Objective: To assess the correlation between the cognitive dysfunction and the CCI, brain and MS lesion volumes in MS.
Methods: This study was a cross-sectional, exploratory study with relapsing-remitting MS using clinical and neuropsychological assessments and MRI scans using a GE 3T scanner. The CCI is calculated measuring anterior, medium and posterior segments of CC adjusted to its greatest anteroposterior diameter. Automated total and segmented brain volumetric measurements were performed with the FreeSurfer software. MS lesion load volume was calculated using Freesurfer. The correlations were adjusted for age, disease duration and educational level as appropriate.
Results: Twenty-four patients were included. They were in their majority women (58.3%) and Caucasians (87.5%). The mean age was 28.8 (SD 7.9) years and the median disease duration was 17.5 months (IQR 7 - 79.5). The median EDSS score was 2.5 (range 0 - 5). The CCI correlated with the scores on the MS Functional Composite - MSFC (R=0.457, p=0.037). The CCI correlated with individual scores from 9-Hole Peg Test (R=-0.463, p=0.030), Paced Auditory Serial Addition Test - PASAT (R=0.461, p=0.035), but has no correlation with the Timed 25-Foot Walk test. The CCI correlated well with the corpus callosum volume - CCV (R=0.798, p< 0.001), white matter fraction - WMF (R=0.615, p< 0.003), brain parenchymal fraction - BPF (R=0.489, p=0.024) and MS lesions volume (R=-0.704, p< 0.001). There were no correlations between the CCI and gray matter fraction, as well as with the Expanded Disability Status Scale scores.
Conclusion: The cognitive dysfunction tests requiring hand function and auditory processing correlates with the CCI. The CCI correlates with brain volumetric measurements (CCV, WMF, BPF) and MS lesion load. The CCI is a practical surrogate marker of neurodegeneration in patients with MS.
Disclosure:
LI Gonçalves: nothing to disclose.
GR Passos: nothing to disclose.
LP Conzatti: nothing to disclose.
JLP Burger: nothing to disclose.
GH Tomasi: nothing to disclose.
ME Zandona: nothing to disclose.
LS Azambuja: nothing to disclose.
I Gomes: nothing to disclose.
A Franco: nothing to disclose.
DK Sato has received scholarship from the Ministry of Education, Culture, Sports, Science and Technology (MEXT) of Japan, grant-in-aid for scientific research from the Japan Society for the Promotion of Science (JSPS KAKENHI 15K19472), research support from CAPES/Brazil (CSF-PAJT 88887.091277/2014-00), and speaker honoraria / advisory board from Novartis, Genzyme, Merck-Serono, Teva, Shire, and Biogen.
J Becker has received speaking honoraria and research or travel grants from Bayer Healthcare, Biogen, Genzyme, Merck Serono, Novartis, Roche, and Teva.
This academic study is financially supported by Novartis. The authors do not receive any reimbursement or financial benefits and declare that they have no competing interests. Novartis played no role in the design, methods, data management or analysis or in the decision to publish.
Abstract: EP1528
Type: ePoster
Abstract Category: Pathology and pathogenesis of MS - 21 Imaging
Background: Cognitive dysfunction is associated with brain atrophy in multiple sclerosis (MS). The brain and lesion volumetric measurements are time and resource consuming and they are still not available in routine practice. The corpus callosum index (CCI) is measured using conventional magnetic resonance imaging (MRI) and it may be a surrogate marker of brain atrophy in MS. However, no study evaluated the correlation between cognitive dysfunction and CCI.
Objective: To assess the correlation between the cognitive dysfunction and the CCI, brain and MS lesion volumes in MS.
Methods: This study was a cross-sectional, exploratory study with relapsing-remitting MS using clinical and neuropsychological assessments and MRI scans using a GE 3T scanner. The CCI is calculated measuring anterior, medium and posterior segments of CC adjusted to its greatest anteroposterior diameter. Automated total and segmented brain volumetric measurements were performed with the FreeSurfer software. MS lesion load volume was calculated using Freesurfer. The correlations were adjusted for age, disease duration and educational level as appropriate.
Results: Twenty-four patients were included. They were in their majority women (58.3%) and Caucasians (87.5%). The mean age was 28.8 (SD 7.9) years and the median disease duration was 17.5 months (IQR 7 - 79.5). The median EDSS score was 2.5 (range 0 - 5). The CCI correlated with the scores on the MS Functional Composite - MSFC (R=0.457, p=0.037). The CCI correlated with individual scores from 9-Hole Peg Test (R=-0.463, p=0.030), Paced Auditory Serial Addition Test - PASAT (R=0.461, p=0.035), but has no correlation with the Timed 25-Foot Walk test. The CCI correlated well with the corpus callosum volume - CCV (R=0.798, p< 0.001), white matter fraction - WMF (R=0.615, p< 0.003), brain parenchymal fraction - BPF (R=0.489, p=0.024) and MS lesions volume (R=-0.704, p< 0.001). There were no correlations between the CCI and gray matter fraction, as well as with the Expanded Disability Status Scale scores.
Conclusion: The cognitive dysfunction tests requiring hand function and auditory processing correlates with the CCI. The CCI correlates with brain volumetric measurements (CCV, WMF, BPF) and MS lesion load. The CCI is a practical surrogate marker of neurodegeneration in patients with MS.
Disclosure:
LI Gonçalves: nothing to disclose.
GR Passos: nothing to disclose.
LP Conzatti: nothing to disclose.
JLP Burger: nothing to disclose.
GH Tomasi: nothing to disclose.
ME Zandona: nothing to disclose.
LS Azambuja: nothing to disclose.
I Gomes: nothing to disclose.
A Franco: nothing to disclose.
DK Sato has received scholarship from the Ministry of Education, Culture, Sports, Science and Technology (MEXT) of Japan, grant-in-aid for scientific research from the Japan Society for the Promotion of Science (JSPS KAKENHI 15K19472), research support from CAPES/Brazil (CSF-PAJT 88887.091277/2014-00), and speaker honoraria / advisory board from Novartis, Genzyme, Merck-Serono, Teva, Shire, and Biogen.
J Becker has received speaking honoraria and research or travel grants from Bayer Healthcare, Biogen, Genzyme, Merck Serono, Novartis, Roche, and Teva.
This academic study is financially supported by Novartis. The authors do not receive any reimbursement or financial benefits and declare that they have no competing interests. Novartis played no role in the design, methods, data management or analysis or in the decision to publish.