ECTRIMS eLearning

Retinal ganglion cell loss in clinically isolated syndrome is associated with subsequent MS diagnosis
Author(s): ,
H Zimmermann
Affiliations:
NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin
,
T Oberwahrenbrock
Affiliations:
NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin
,
S Specovius
Affiliations:
NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin
,
J Mikolajczak
Affiliations:
NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin
,
J Bellmann-Strobl
Affiliations:
NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin;Experimental and Clinical Research Center, Max Delbrueck Center for Molecular Medicine and Charité - Universitätsmedizin Berlin
,
K Ruprecht
Affiliations:
Department of Neurology, Charité - Universitätsmedizin Berlin, Berlin, Germany
,
F Paul
Affiliations:
NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin;Experimental and Clinical Research Center, Max Delbrueck Center for Molecular Medicine and Charité - Universitätsmedizin Berlin;Department of Neurology, Charité - Universitätsmedizin Berlin, Berlin, Germany
A.U Brandt
Affiliations:
NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin
ECTRIMS Learn. Zimmermann H. 09/16/16; 145776; P1092
Hanna Gwendolyn Zimmermann
Hanna Gwendolyn Zimmermann
Contributions
Abstract

Abstract: P1092

Type: Poster

Abstract Category: Pathology and pathogenesis of MS - OCT

Introduction: Retinal ganglion cell loss was found in patients with clinically isolated syndrome (CIS) in absence of optic neuritis (ON). The goal of this study was to evaluate whether ganglion cell and inner plexiform layer (GCIP) thickness in patients with CIS is associated with a subsequent MS diagnosis according to the McDonald diagnostic criteria (MDMS) or clinically definite MS (CDMS).

Methods: Forty-nine CIS patients (mean age 33.5±7.9 years, 31 female) were observed over a period of at least one year (mean follow-up period 30.2±8.9 months, range 12-46 months). All patients underwent retinal optical coherence tomography analysis of the combined ganglion cell and inner plexiform layer at baseline visit. MS diagnosis was established based on MRI and clinical presentation according to the revised McDonald 2010 criteria.

Results: Twenty-seven CIS patients were classified as MDMS (n=15) or CDMS (n=12) during follow-up. GCIP thickness at baseline in NON eyes was thinner in patients that were diagnosed with MS by the last follow-up visit (69.3±4.9 vs. 73.6±6.7 µm, p=0.014). Follow-up duration, time since onset, age and sex had no significant influence.

Conclusion: Our results indicate that low GCIP thickness in clinically isolated syndrome without optic neuritis is associated with a later MS diagnosis. However, the predictive information for individual patients is limited by the wide range of inter-individual variety of GCIP measurements.

Disclosure: HZ received speaking fees from Teva and Bayer. TO is supported by EXIST-Forschungstransfer (German Federal Ministry for Economic Affairs and Energy, 03EFEBE079) and received speaker honorary from TEVA and Bayer unrelated to the presented scientific work. SS: nothing to disclose. JM received speaking fees from Teva and Biogen Idec unrelated to the presented scientific work. JBS has received speaking fees and travel grants from Bayer Healthcare, sanofi-aventis/Genzyme, and Teva Pharmaceuticals unrelated to the presented scientific work. KR received research support from Novartis as well as speaking fees or travel grants Bayer Healthcare, Biogen Idec, Merck Serono, Sanofi/Genzyme, Teva, Roche, and Novartis. FP is supported by the Deutsche Forschungsgemeinschaft (DFG EXC257), the Bundesministerium für Bildung und Forschung (BMBF Competence Network Multiple Sclerosis) and the Guthy Jackson Charitable Foundation, he has received travel grants, research support and personal compensation for activities with Alexion, Bayer, MerckSerono, Teva, Sanofi Genzyme, MedImmune, Chugai, BiogenIdec and Novartis and is member of the steering committee of the OCTIMS study (Novartis). AUB s supported by EXIST-Forschungstransfer (German Federal Ministry for Economic Affairs and Energy, 03EFEBE079) and received consulting fees from Biogen, Novartis, Teva, Nexus, and Motognosis and received funding for research from Novartis and Biogen.

Abstract: P1092

Type: Poster

Abstract Category: Pathology and pathogenesis of MS - OCT

Introduction: Retinal ganglion cell loss was found in patients with clinically isolated syndrome (CIS) in absence of optic neuritis (ON). The goal of this study was to evaluate whether ganglion cell and inner plexiform layer (GCIP) thickness in patients with CIS is associated with a subsequent MS diagnosis according to the McDonald diagnostic criteria (MDMS) or clinically definite MS (CDMS).

Methods: Forty-nine CIS patients (mean age 33.5±7.9 years, 31 female) were observed over a period of at least one year (mean follow-up period 30.2±8.9 months, range 12-46 months). All patients underwent retinal optical coherence tomography analysis of the combined ganglion cell and inner plexiform layer at baseline visit. MS diagnosis was established based on MRI and clinical presentation according to the revised McDonald 2010 criteria.

Results: Twenty-seven CIS patients were classified as MDMS (n=15) or CDMS (n=12) during follow-up. GCIP thickness at baseline in NON eyes was thinner in patients that were diagnosed with MS by the last follow-up visit (69.3±4.9 vs. 73.6±6.7 µm, p=0.014). Follow-up duration, time since onset, age and sex had no significant influence.

Conclusion: Our results indicate that low GCIP thickness in clinically isolated syndrome without optic neuritis is associated with a later MS diagnosis. However, the predictive information for individual patients is limited by the wide range of inter-individual variety of GCIP measurements.

Disclosure: HZ received speaking fees from Teva and Bayer. TO is supported by EXIST-Forschungstransfer (German Federal Ministry for Economic Affairs and Energy, 03EFEBE079) and received speaker honorary from TEVA and Bayer unrelated to the presented scientific work. SS: nothing to disclose. JM received speaking fees from Teva and Biogen Idec unrelated to the presented scientific work. JBS has received speaking fees and travel grants from Bayer Healthcare, sanofi-aventis/Genzyme, and Teva Pharmaceuticals unrelated to the presented scientific work. KR received research support from Novartis as well as speaking fees or travel grants Bayer Healthcare, Biogen Idec, Merck Serono, Sanofi/Genzyme, Teva, Roche, and Novartis. FP is supported by the Deutsche Forschungsgemeinschaft (DFG EXC257), the Bundesministerium für Bildung und Forschung (BMBF Competence Network Multiple Sclerosis) and the Guthy Jackson Charitable Foundation, he has received travel grants, research support and personal compensation for activities with Alexion, Bayer, MerckSerono, Teva, Sanofi Genzyme, MedImmune, Chugai, BiogenIdec and Novartis and is member of the steering committee of the OCTIMS study (Novartis). AUB s supported by EXIST-Forschungstransfer (German Federal Ministry for Economic Affairs and Energy, 03EFEBE079) and received consulting fees from Biogen, Novartis, Teva, Nexus, and Motognosis and received funding for research from Novartis and Biogen.

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