Contributions
Abstract: P646
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - 25 Biomarkers
Background: Cortical grey matter (GM) atrophy correlates with worsening physical and cognitive disability in patients with relapsing-remitting multiple sclerosis (RRMS). While transcranial magnetic stimulation (TMS) provides evidence of cortical dysfunction in patients with motor disability and progressive MS, this technique has not been explored extensively in patients with RRMS.
Objective: To perform cortical structure-function correlations in a cohort of real-world patients with RRMS.
Methods: Sixteen RRMS patients were prospectively recruited. Magnetic resonance imaging (MRI), threshold tracking-TMS (TT-TMS), neuropsychological testing (Minimal Assessment of Cognitive Function in MS [MACFIMS]) and clinical assessment (including the Expanded Disability Status Scale [EDSS]) were performed. Lesion masks were semi-automatically delineated with JIM and volumetrics obtained using Freesurfer. The worse affected hemisphere (defined as larger T2 lesion volume) was used for comparisons. Pearson correlations were used to compare cortical structure and function measures, and the Benjamini-Hochberg procedure applied for multiple comparisons.
Results: The cohort was mostly female (11 female, 5 male) with mean age (SD) 42.83(10.74) years, mean disease duration 5.96(5.16) years and mean EDSS 2.25(1.45). Statistical significance was considered at p < 0.05 (corrected for age, disease duration and multiple comparisons). Normalised brain volume (NBV) significantly correlated with normalised cortical GM (cGM) volume (r=0.959) and cGM thickness (r=0.869); normalised cGM volume and cGM thickness correlated significantly (r=0.842). Resting motor threshold (RMT) negatively correlated with NBV (r=-0.838) and normalised cGM volume (r=-0.828). No significant correlations were found between brain volumetric data (NBV, normalised cGM volume, cGM thickness) and other measures, including T2 lesion volume, paired-pulse TMS variables, EDSS, and components of the MACFIMS cognitive battery.
Conclusions: Strong negative correlations between resting motor threshold and normalised cortical GM volume link cortical structure and function in this real-world RRMS patient cohort. Furthermore, the correlation of RMT with NBV; and between cortical GM and NBV, supports further investigation of threshold tracking-TMS as a potential biomarker of neurodegeneration in RRMS.
Disclosure: This study was funded by Biogen.
Heidi N Beadnall has received compensation for education travel, speaker honoraria and consultant fees from Biogen, Novartis, Merck and Sanofi-Genzyme.
Chenyu Wang has nothing to disclose.
Jose M Matamala has nothing to disclose.
Todd A Hardy has received honoraria for talks and advisory boards, and support for scientific meetings from Novartis, Biogen Idec, Merck-Serono and Genzyme.
James Howells has nothing to disclose.
Caitlin Dawes has nothing to disclose.
Justin Garber has nothing to disclose.
Joshua Barton has received support for education travel and speaker honoraria from TEVA, Biogen, Novartis, Merck and Sanofi-Genzyme.
Stephen Reddel has received payments for grant support from Biogen, CSL, Novartis and Sanofi-Genzyme, travel support from Merck, Sanofi-Genzyme and Teva, membership on advisory councils from Biogen, Merck, Sanofi-Genzyme and Teva, speaker's bureau from Biogen, Novartis, and Sanofi-Genzyme.
Matthew C Kiernan is the Editor-in-Chief of the Journal of Neurology, Neurosurgery & Psychiatry.
Michael H Barnett has received institutional support for research, speaking and/or participation in advisory boards (Biogen, Novartis, and Sanofi Genzyme); research consultant (Medical Safety Systems).
Abstract: P646
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - 25 Biomarkers
Background: Cortical grey matter (GM) atrophy correlates with worsening physical and cognitive disability in patients with relapsing-remitting multiple sclerosis (RRMS). While transcranial magnetic stimulation (TMS) provides evidence of cortical dysfunction in patients with motor disability and progressive MS, this technique has not been explored extensively in patients with RRMS.
Objective: To perform cortical structure-function correlations in a cohort of real-world patients with RRMS.
Methods: Sixteen RRMS patients were prospectively recruited. Magnetic resonance imaging (MRI), threshold tracking-TMS (TT-TMS), neuropsychological testing (Minimal Assessment of Cognitive Function in MS [MACFIMS]) and clinical assessment (including the Expanded Disability Status Scale [EDSS]) were performed. Lesion masks were semi-automatically delineated with JIM and volumetrics obtained using Freesurfer. The worse affected hemisphere (defined as larger T2 lesion volume) was used for comparisons. Pearson correlations were used to compare cortical structure and function measures, and the Benjamini-Hochberg procedure applied for multiple comparisons.
Results: The cohort was mostly female (11 female, 5 male) with mean age (SD) 42.83(10.74) years, mean disease duration 5.96(5.16) years and mean EDSS 2.25(1.45). Statistical significance was considered at p < 0.05 (corrected for age, disease duration and multiple comparisons). Normalised brain volume (NBV) significantly correlated with normalised cortical GM (cGM) volume (r=0.959) and cGM thickness (r=0.869); normalised cGM volume and cGM thickness correlated significantly (r=0.842). Resting motor threshold (RMT) negatively correlated with NBV (r=-0.838) and normalised cGM volume (r=-0.828). No significant correlations were found between brain volumetric data (NBV, normalised cGM volume, cGM thickness) and other measures, including T2 lesion volume, paired-pulse TMS variables, EDSS, and components of the MACFIMS cognitive battery.
Conclusions: Strong negative correlations between resting motor threshold and normalised cortical GM volume link cortical structure and function in this real-world RRMS patient cohort. Furthermore, the correlation of RMT with NBV; and between cortical GM and NBV, supports further investigation of threshold tracking-TMS as a potential biomarker of neurodegeneration in RRMS.
Disclosure: This study was funded by Biogen.
Heidi N Beadnall has received compensation for education travel, speaker honoraria and consultant fees from Biogen, Novartis, Merck and Sanofi-Genzyme.
Chenyu Wang has nothing to disclose.
Jose M Matamala has nothing to disclose.
Todd A Hardy has received honoraria for talks and advisory boards, and support for scientific meetings from Novartis, Biogen Idec, Merck-Serono and Genzyme.
James Howells has nothing to disclose.
Caitlin Dawes has nothing to disclose.
Justin Garber has nothing to disclose.
Joshua Barton has received support for education travel and speaker honoraria from TEVA, Biogen, Novartis, Merck and Sanofi-Genzyme.
Stephen Reddel has received payments for grant support from Biogen, CSL, Novartis and Sanofi-Genzyme, travel support from Merck, Sanofi-Genzyme and Teva, membership on advisory councils from Biogen, Merck, Sanofi-Genzyme and Teva, speaker's bureau from Biogen, Novartis, and Sanofi-Genzyme.
Matthew C Kiernan is the Editor-in-Chief of the Journal of Neurology, Neurosurgery & Psychiatry.
Michael H Barnett has received institutional support for research, speaking and/or participation in advisory boards (Biogen, Novartis, and Sanofi Genzyme); research consultant (Medical Safety Systems).