Contributions
Abstract: P597
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - 22 OCT
Purpose: To evaluate the association between retinal layer volumes as measured by optical coherence tomography (OCT), and cognitive and affective disorders in patients with early multiple sclerosis (MS).
Methods: A total of 82 patients with early relapsing-remitting MS (RRMS) and eight patients with clinically isolated syndrome (CIS) (both groups: age 33 ± 0.9 years, disease duration 5.8 ± 6.7 months) were enrolled into the study and prospectively followed over 26.4 ± 8.3 months. At baseline, patients underwent clinical assessment and OCT examination, eyes with a history of optic neuritis before baseline or during follow-up were excluded. Every 12 months, Beck's depression inventory (BDI), fatigue scale for motor and cognitive functions (FSMC) and multiple sclerosis inventory cognition (MUSIC cognition) were evaluated. Kaplan Meyer survival analysis for worsening within the respective disease scores corrected for age, sex, diagnosis, disease duration, disease modifying therapy and other medications were performed.
Results: We found continuous and sustained worsening in BDI in 10% of patients during follow-up. Increased values of peripapillary nerve fibre layer (pRNFL >101.8 µm; p= 0.04) and total macular volume (TMV > 8.8 mm3, p=0.03) at baseline were associated with a higher risk for depression worsening. Similarly, thicker pRNFL (pRNFL > 105.5 µm; p< 0.001) and TMV (TMV > 8.835 mm3, p= 0.01) were linked to a higher chance of developing fatigue, as measured by the FSMC score, during follow-up. In contrast, lower volumes of the common ganglion cell and inner plexiform layer at baseline (GCIPL< 1.98 mm3) were associated with an increased risk for sustained cognitive decline (hazard ratio HR=5.7, p=0.04) during follow-up as measured by MUSIC cognition test.
Conclusion: MS-associated comorbidities might be associated with changes in retinal architecture in early MS. Atrophy patterns of inner retinal layers seem to be linked to an increased risk for developing cognitive deficits but decreased risk of fatigue or depression. Further studies are required to address whether the retinal architecture can predict long-term cognitive decline and the occurrence of depression and fatigue in the context of CNS autoimmunity.
Disclosure:
C. Wetzlmair: has nothing to disclose
G. Leppenetier: has nothing to disclose
T. Daltrozzo: has nothing to disclose
V. Biberacher: has nothing to disclose
A. Berthele: reports grants from Bayer Healthcare, personal fees from Biogen, Merck Serono, Teva, Novartis, and Genzyme, and compensations for clinical trials from Biogen, Novartis, Genzyme, Roche, Teva, and Alexion Pharmaceuticals - outside the submitted work.
M. Hoshi: reports grants from Bayer Healthcare and personal fees from Novartis and Biogen Idec outside the submitted work.
B. Hemmer: has served on scientific advisory boards for F. Hoffmann-La Roche Ltd, Novartis, Bayer AG, and Genentech; he has served as DMSC member for AllergyCare; he or his institution have received speaker honoraria from Biogen Idec, Teva Neuroscience, Merck Serono, Medimmune, Novartis, Desitin, and F. Hoffmann-La Roche Ltd; his institution has received research support from Chugai Pharmaceuticals and Hoffmann-La-Roche; holds part of two patents; one for the detection of antibodies and T cells against KIR4.1 in a subpopulation of MS patients and one for genetic determinants of neutralizing antibodies to interferon β.
T. Korn: has nothing to disclose
B. Knier: has nothing to disclose
Abstract: P597
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - 22 OCT
Purpose: To evaluate the association between retinal layer volumes as measured by optical coherence tomography (OCT), and cognitive and affective disorders in patients with early multiple sclerosis (MS).
Methods: A total of 82 patients with early relapsing-remitting MS (RRMS) and eight patients with clinically isolated syndrome (CIS) (both groups: age 33 ± 0.9 years, disease duration 5.8 ± 6.7 months) were enrolled into the study and prospectively followed over 26.4 ± 8.3 months. At baseline, patients underwent clinical assessment and OCT examination, eyes with a history of optic neuritis before baseline or during follow-up were excluded. Every 12 months, Beck's depression inventory (BDI), fatigue scale for motor and cognitive functions (FSMC) and multiple sclerosis inventory cognition (MUSIC cognition) were evaluated. Kaplan Meyer survival analysis for worsening within the respective disease scores corrected for age, sex, diagnosis, disease duration, disease modifying therapy and other medications were performed.
Results: We found continuous and sustained worsening in BDI in 10% of patients during follow-up. Increased values of peripapillary nerve fibre layer (pRNFL >101.8 µm; p= 0.04) and total macular volume (TMV > 8.8 mm3, p=0.03) at baseline were associated with a higher risk for depression worsening. Similarly, thicker pRNFL (pRNFL > 105.5 µm; p< 0.001) and TMV (TMV > 8.835 mm3, p= 0.01) were linked to a higher chance of developing fatigue, as measured by the FSMC score, during follow-up. In contrast, lower volumes of the common ganglion cell and inner plexiform layer at baseline (GCIPL< 1.98 mm3) were associated with an increased risk for sustained cognitive decline (hazard ratio HR=5.7, p=0.04) during follow-up as measured by MUSIC cognition test.
Conclusion: MS-associated comorbidities might be associated with changes in retinal architecture in early MS. Atrophy patterns of inner retinal layers seem to be linked to an increased risk for developing cognitive deficits but decreased risk of fatigue or depression. Further studies are required to address whether the retinal architecture can predict long-term cognitive decline and the occurrence of depression and fatigue in the context of CNS autoimmunity.
Disclosure:
C. Wetzlmair: has nothing to disclose
G. Leppenetier: has nothing to disclose
T. Daltrozzo: has nothing to disclose
V. Biberacher: has nothing to disclose
A. Berthele: reports grants from Bayer Healthcare, personal fees from Biogen, Merck Serono, Teva, Novartis, and Genzyme, and compensations for clinical trials from Biogen, Novartis, Genzyme, Roche, Teva, and Alexion Pharmaceuticals - outside the submitted work.
M. Hoshi: reports grants from Bayer Healthcare and personal fees from Novartis and Biogen Idec outside the submitted work.
B. Hemmer: has served on scientific advisory boards for F. Hoffmann-La Roche Ltd, Novartis, Bayer AG, and Genentech; he has served as DMSC member for AllergyCare; he or his institution have received speaker honoraria from Biogen Idec, Teva Neuroscience, Merck Serono, Medimmune, Novartis, Desitin, and F. Hoffmann-La Roche Ltd; his institution has received research support from Chugai Pharmaceuticals and Hoffmann-La-Roche; holds part of two patents; one for the detection of antibodies and T cells against KIR4.1 in a subpopulation of MS patients and one for genetic determinants of neutralizing antibodies to interferon β.
T. Korn: has nothing to disclose
B. Knier: has nothing to disclose