ECTRIMS eLearning

Leptomeningeal contrast enhancement correlates with neurodegeneration in multiple sclerosis
Author(s): ,
I. Kalinin
Affiliations:
SBIH City Clinical Hospital #31, City Center of MS and other Autoimmune Diseases
,
G. Makshakov
Affiliations:
SBIH City Clinical Hospital #31, City Center of MS and other Autoimmune Diseases; Neurology Department, FSBEI HE I.P. Pavlov SPbSMU MOH Russia
,
E. Magonov
Affiliations:
`NMC-Tomography` LLC, Saint-Petersburg, Russian Federation
,
T. Trofimova
Affiliations:
`NMC-Tomography` LLC, Saint-Petersburg, Russian Federation
,
N. Totolyan
Affiliations:
Neurology Department, FSBEI HE I.P. Pavlov SPbSMU MOH Russia
,
M. Shumilina
Affiliations:
SBIH City Clinical Hospital #31, City Center of MS and other Autoimmune Diseases; Neurology Department, FSBEI HE I.P. Pavlov SPbSMU MOH Russia
,
A. Skoromets
Affiliations:
Neurology Department, FSBEI HE I.P. Pavlov SPbSMU MOH Russia
E. Evdoshenko
Affiliations:
SBIH City Clinical Hospital #31, City Center of MS and other Autoimmune Diseases
ECTRIMS Learn. Kalinin I. 10/10/18; 228303; P459
Ivan Kalinin
Ivan Kalinin
Contributions
Abstract

Abstract: P459

Type: Poster Sessions

Abstract Category: Pathology and pathogenesis of MS - Neurodegeneration

Background: Leptomeningeal contrast enhancement (LMCE) on magnetic resonance imaging (MRI) is associated with disease progression and neurodegeneration in multiple sclerosis (MS). Studies show that both cortical grey matter (GM) and white matter (WM) lesions correlate with neurodegeneration. It is unknown if LMCE correlate with WM or GM lesions.
Aim: The aim of this study was to assess the relationship between LMCE and lesion burden of the brain white and grey matter in patients with MS.
Objectives: To measure the volume of white and grey matter lesions in patients with and without LMCE and to assess the correlation of lesion load and volumes of brain structures.
Materials and methods: LMCE were detected on 3 Tesla MRI with post-contrast fluid attenuated inversion-recovery (FLAIR) sequence, 10-12 minutes after gadolinium administration. WM and intracortical GM lesion load on FLAIR/T2 and double inversion-recovery (DIR) sequences respectively was manually counted using 3D Slicer. Normalized brain volume (NBV), WM and GM volume were counted using SIENAX software. Cortical thickness, total ventricles, thalamus and hippocampal volumes were assessed with FreeSurfer.
Results: 54 MS patients (20 male and 34 female) were included. LMCE was detected in 23/54 (43%) patients. The median (IQR) age was 36 (25) years in LMCE(-) patients and 43 (22) years in LMCE(+) patients, p=0.0613. The disease duration was significantly lower in LMCE(-) vs LMCE(+) patients - 64 (104) months and 121 (142) months respectively, p=0.0094. LMCE(+) patients revealed some higher WM and GM lesions load, but the difference was not statistically significant. In LMCE(+) patients, volume of WM lesions, but not GM lesions, revealed significant negative correlation with NBV (r=-0.4792, p=0.0207), whole WM volume (r=-0.5158, p=0.0118), cortical WM volume (r=-0.5632, p=0.0051) and significant positive correlation with total ventricles volume (r=0.6423, p=0.001). In LMCE(-) patients, volume of WM and GM lesions showed significant positive correlation only with total ventricles volume (FLAIR: r=0.723, p< 0.0001; DIR: r=0.5458, p=0.0015). WM and GM lesion load didn't correlate with disease duration or age in both groups. In LMCE(-) group GM lesions volume correlated with WM lesions volume (r=0.5543, p=0.0012), but not in LMCE(+) group.
Conclusion: WM lesions in LMCE(+) MS patients are associated with more profound neurodegeneration that is independent from age, disease duration and GM lesions.
Disclosure: Ivan Kalinin: nothing to declare; Gleb Makshakov has received honoraria for lectures and speaking in the past 3 years from Genzyme and Roche; Evgeniy Magonov has received honoraria for lectures in the last 3 years from GE Healthcare; Tatiana Trofimova has received honoraria for lectures in the last 3 years from GE Healthcare, Philips Healthcare, Bayer, Toshiba (Canon Medical); Natalia Totolyan has received honoraria for lectures and speaking from Genzyme, Janssen, Merck and Roche; Maria Shumilina: nothing to declare; Alexander Skoromets: nothing to declare; Evgeniy Evdoshenko has received grants and honoraria for lectures and speaking in the past 3 years from Biogen, Generium, Genzyme, Johnson, Merck, Novartis, Pharmstandard, Pharmsynthez, Roche, Sanofi, SIA-API.

Abstract: P459

Type: Poster Sessions

Abstract Category: Pathology and pathogenesis of MS - Neurodegeneration

Background: Leptomeningeal contrast enhancement (LMCE) on magnetic resonance imaging (MRI) is associated with disease progression and neurodegeneration in multiple sclerosis (MS). Studies show that both cortical grey matter (GM) and white matter (WM) lesions correlate with neurodegeneration. It is unknown if LMCE correlate with WM or GM lesions.
Aim: The aim of this study was to assess the relationship between LMCE and lesion burden of the brain white and grey matter in patients with MS.
Objectives: To measure the volume of white and grey matter lesions in patients with and without LMCE and to assess the correlation of lesion load and volumes of brain structures.
Materials and methods: LMCE were detected on 3 Tesla MRI with post-contrast fluid attenuated inversion-recovery (FLAIR) sequence, 10-12 minutes after gadolinium administration. WM and intracortical GM lesion load on FLAIR/T2 and double inversion-recovery (DIR) sequences respectively was manually counted using 3D Slicer. Normalized brain volume (NBV), WM and GM volume were counted using SIENAX software. Cortical thickness, total ventricles, thalamus and hippocampal volumes were assessed with FreeSurfer.
Results: 54 MS patients (20 male and 34 female) were included. LMCE was detected in 23/54 (43%) patients. The median (IQR) age was 36 (25) years in LMCE(-) patients and 43 (22) years in LMCE(+) patients, p=0.0613. The disease duration was significantly lower in LMCE(-) vs LMCE(+) patients - 64 (104) months and 121 (142) months respectively, p=0.0094. LMCE(+) patients revealed some higher WM and GM lesions load, but the difference was not statistically significant. In LMCE(+) patients, volume of WM lesions, but not GM lesions, revealed significant negative correlation with NBV (r=-0.4792, p=0.0207), whole WM volume (r=-0.5158, p=0.0118), cortical WM volume (r=-0.5632, p=0.0051) and significant positive correlation with total ventricles volume (r=0.6423, p=0.001). In LMCE(-) patients, volume of WM and GM lesions showed significant positive correlation only with total ventricles volume (FLAIR: r=0.723, p< 0.0001; DIR: r=0.5458, p=0.0015). WM and GM lesion load didn't correlate with disease duration or age in both groups. In LMCE(-) group GM lesions volume correlated with WM lesions volume (r=0.5543, p=0.0012), but not in LMCE(+) group.
Conclusion: WM lesions in LMCE(+) MS patients are associated with more profound neurodegeneration that is independent from age, disease duration and GM lesions.
Disclosure: Ivan Kalinin: nothing to declare; Gleb Makshakov has received honoraria for lectures and speaking in the past 3 years from Genzyme and Roche; Evgeniy Magonov has received honoraria for lectures in the last 3 years from GE Healthcare; Tatiana Trofimova has received honoraria for lectures in the last 3 years from GE Healthcare, Philips Healthcare, Bayer, Toshiba (Canon Medical); Natalia Totolyan has received honoraria for lectures and speaking from Genzyme, Janssen, Merck and Roche; Maria Shumilina: nothing to declare; Alexander Skoromets: nothing to declare; Evgeniy Evdoshenko has received grants and honoraria for lectures and speaking in the past 3 years from Biogen, Generium, Genzyme, Johnson, Merck, Novartis, Pharmstandard, Pharmsynthez, Roche, Sanofi, SIA-API.

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