2023 American Academy of Neurology Abstract Website

Ilya Ayzenberg¹, Theodoros Ladopoulos², Carolin Schwake¹, Bianca Teegen⁴, Ingo Kleiter⁵, Nadine Siems¹, Christian Prehn¹, Marius Ringelstein⁶, Orhan Aktas⁶, Refik Pul⁷, Britta Matusche³, Carsten Lukas³, Iris Katharina Penner⁸, Ralf Gold¹, Ruth Schneider², Ann-Katrin Kogel¹
¹Department of Neurology, St.Josef Hospital, ²Department of Neurology & Institute of Neuroradiology, ³Institute of Neuroradiology, St Josef Hospital, Ruhr-Universität Bochum, ⁴Euroimmun Reference Laboratory, ⁵Marianne-Strauß-Klinik, Behandlungszentrum Kempfenhausen für Multiple Sklerose Kranke, ⁶Department of Neurology, Medical Faculty, Heinrich-Heine-University Düsseldorf, ⁷Center for Translational Neuro- and Behavioral Sciences, University Medicine Essen, University of Duisburg-Essen, ⁸COGITO Center & Bern University Hospital, Inselspital, Department of Neurology

Objective:

To identify the prevalence of cognitive impairment (CI) as well as associated clinical factors and MRI-volumetric changes in myelin oligodendrocyte glycoprotein-IgG-associated disease (MOGAD).

Background:

Supratentorial tumefactive ADEM-like lesions are common in MOGAD, however data on a CI and its potential risk factors remain scarce. Despite an almost complete regression of tumefactive lesions there are no data on long-term volumetric changes available.

Design/Methods:

All participants were investigated by certified neuropsychologists and underwent a standardised 3T-MRI at the University of Bochum. Images were processed with FreeSurfer for grey and white matter volume estimation. Sera were tested for a panel of autoantibodies (NMDAR-/CASPR2-/LGI1-/GABA-a/b/DPPX-/mGluR-IgG). The following clinical factors were included into analysis: disease duration, number and type of relapses, presence and type of supratentorial lesions, disability (EDSS), fatigue (FSMC), and depression (BDI-II).

Results:

32 MOGAD patients (19 females, 29.4 years (IQR 21.3-40.6)) were included. Median disease duration was 18 months with a median of two relapses and EDSS of 1.0. 20/32 patients had experienced optic neuritis, 17/32 myelitis and 8/32 ADEM-like episodes in their history. 7/32 patients (22%) suffered from CI with most prevalent deficits in mental flexibility (16.7%), alertness (11.1-14.4%) and verbal working memory (9.4%) in the cohort. 72.4% suffered from fatigue and 42.9% from depression. History of ADEM-like episodes was associated with CI (ExpB 7.333, 95% CI 1.168-46.052, p=0.034). Neither depression, fatigue, nor relapse rate or disability were risk factors. No coexisting antineuronal antibodies were found. Cerebral white and deep grey matter volumes were significantly reduced in MOGAD compared to healthy controls. Both history of ADEM-like lesions and CI were associated with reduced deep grey matter volume compared to unaffected MOGAD patients.

Conclusions:

Every fifth MOGAD patient suffers from significant CI. Despite an almost complete resolution on conventional MRI, ADEM-like lesions in the history seem to be associated with CI and sustained deep grey matter atrophy.