Cognitive Impairment, Associated Clinical Factors, and MR Volumetric Measures in Myelin Oligodendrocyte Glycoprotein-IgG-Associated Disease

Abstract

Background and objectives: Cognitive impairment is a common and challenging symptom in multiple sclerosis and neuromyelitis optica spectrum disease; however, data in myelin oligodendrocyte glycoprotein-IgG-associated disease (MOGAD) remain scarce. In this cross-sectional study, we investigated the frequency of cognitive impairment, associated clinical factors, and MRI volumetric measures in MOGAD.

Methods: Participants were investigated in a single center by certified psychologists and underwent a standardized 3-T-MRI protocol. MRI data were processed with FreeSurfer for gray and white matter volume estimation, presented as a fraction of total intracranial volume. Sera screening for antineural antibodies has been conducted using cell-based assays. The following clinical factors were included in the multivariate logistic regression analysis: sex, age, overall number of previous relapses, and specifically the history of acute disseminated encephalomyelitis (ADEM)/ADEM-like episodes and other brain relapses.

Results: Thirty-two patients with MOGAD (19 female, median age 29.4 years) after a median of 2 relapses with a median EDSS of 1.0 were recruited. Seven patients (21.9%) demonstrated cognitive impairment with the most prevalent deficits in mental flexibility (16.7%), attention (11.1%-14.8%), and verbal working memory (10.3%). 72.4% suffered from fatigue and 42.9% from signs of depression, moderate to severe in 28.6%. The overall number of previous relapses (odds ratio [OR] 1.789, 95% CI 1.041-3.074) and specifically ADEM/ADEM-like episodes (OR 16.929, 95% CI 1.228-233.427) were the only clinical factors associated with cognitive impairment in a multivariate logistic regression model. Screening for antineuronal antibodies remained negative. Cerebral white matter (WM) (0.300 vs 0.317, p = 0.003) and deep gray matter (DGM) (0.036 vs 0.038, p = 0.002) volumes were reduced in patients with MOGAD compared with healthy controls (n = 32). Both cognitive impairment (0.031 vs 0.036, p = 0.003) and history of ADEM/ADEM-like episodes (0.032 vs 0.036, p = 0.006) were associated with reduced DGM volume compared with unaffected patients with MOGAD.

Discussion: Despite a low overall disability, every 5th patient with MOGAD experiences cognitive impairment. Cognitive impairment is associated with a higher number of relapses and particularly ADEM/ADEM-like attacks. Although both WM and DGM atrophies are apparent in MOGAD, the latter only seems to have an association with cognitive impairment.