TY - JOUR
T1 - Myelin oligodendrocyte glycoprotein antibody-associated demyelination
T2 - comparison between onset phenotypes
AU - Zhou, Y.
AU - Jia, X.
AU - Yang, H.
AU - Chen, C.
AU - Sun, X.
AU - Peng, L.
AU - Kermode, A. G.
AU - Qiu, W.
PY - 2019/1
Y1 - 2019/1
N2 - Background and purpose The aim of this study was to analyse the clinical and prognostic features of myelin oligodendrocyte glycoprotein (MOG) antibody-associated demyelination with different onset phenotypes. Methods A total of 52 MOG-IgG-seropositive patients were divided into four groups: (i) optic neuritis (ON) at onset (MOG-ON+, n = 23), (ii) transverse myelitis (TM) at onset (MOG-TM+, n = 12), (iii) pure brain symptoms at onset (MOG-ON--TM-, n = 14) and (iv) both ON and TM at onset (n = 3). This final group was not included in further analyses. Data were collected through medical records and regular follow-up. Results Median age at presentation was 24 (range, 3-63) years in the whole cohort (50% female). MOG-ON--TM- patients had the youngest age of onset across the three groups. Patients with MOG-TM+ tended to relapse more frequently and had a longer interval to first relapse than was observed in MOG-ON+ and MOG-ON--TM- patients. High MOG-IgG titres were associated with increased cerebrospinal fluid leukocytes. The likelihood of harbouring transient, low MOG-IgG titres was higher in the MOG-TM+ group than in the other groups. After a median disease duration of 20 months, most but not all cases had a favourable outcome, with 8% developing severe visual deficit, 2% becoming wheelchair-dependent and 6% developing cognitive impairment. The onset phenotype appeared to be an important predictor of disability type. Having high MOG-IgG titres (odds ratio, 0.168, P = 0.027) or female gender (odds ratio, 0.270, P = 0.067) was associated with a lower likelihood of complete recovery.Conclusions Onset phenotype may influence long-term presentation, MOG-IgG status as well as outcome. Further large and prospective studies are needed to better clarify the clinical implications of the first demyelinating event.
AB - Background and purpose The aim of this study was to analyse the clinical and prognostic features of myelin oligodendrocyte glycoprotein (MOG) antibody-associated demyelination with different onset phenotypes. Methods A total of 52 MOG-IgG-seropositive patients were divided into four groups: (i) optic neuritis (ON) at onset (MOG-ON+, n = 23), (ii) transverse myelitis (TM) at onset (MOG-TM+, n = 12), (iii) pure brain symptoms at onset (MOG-ON--TM-, n = 14) and (iv) both ON and TM at onset (n = 3). This final group was not included in further analyses. Data were collected through medical records and regular follow-up. Results Median age at presentation was 24 (range, 3-63) years in the whole cohort (50% female). MOG-ON--TM- patients had the youngest age of onset across the three groups. Patients with MOG-TM+ tended to relapse more frequently and had a longer interval to first relapse than was observed in MOG-ON+ and MOG-ON--TM- patients. High MOG-IgG titres were associated with increased cerebrospinal fluid leukocytes. The likelihood of harbouring transient, low MOG-IgG titres was higher in the MOG-TM+ group than in the other groups. After a median disease duration of 20 months, most but not all cases had a favourable outcome, with 8% developing severe visual deficit, 2% becoming wheelchair-dependent and 6% developing cognitive impairment. The onset phenotype appeared to be an important predictor of disability type. Having high MOG-IgG titres (odds ratio, 0.168, P = 0.027) or female gender (odds ratio, 0.270, P = 0.067) was associated with a lower likelihood of complete recovery.Conclusions Onset phenotype may influence long-term presentation, MOG-IgG status as well as outcome. Further large and prospective studies are needed to better clarify the clinical implications of the first demyelinating event.
KW - demyelinating disorder
KW - myelin oligodendrocyte glycoprotein antibody-associated demyelination
KW - prognosis
KW - TREATMENT RESPONSES
KW - CNS
KW - CHILDREN
KW - DISEASE
U2 - 10.1111/ene.13791
DO - 10.1111/ene.13791
M3 - Article
C2 - 30153357
VL - 26
SP - 175
EP - 183
JO - European Journal of Neurology
JF - European Journal of Neurology
SN - 1351-5101
IS - 1
ER -