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Published on: February 19, 2021
Comparison of MRI T2-lesion evolution in pediatric MOGAD, NMOSD, and MS
Vyanka Redenbaugh1, Nicholas H Chia1, Laura Cacciaguerra2
1Department of Neurology, Mayo Clinic College of Medicine, Rochester, MN, USA.
Background:
Magnetic resonance imaging (MRI) T2-lesions resolve more often in myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD) than aquaporin-4 IgG-positive neuromyelitis optica spectrum disorder (AQP4 + NMOSD) and multiple sclerosis (MS) in adults but few studies analyzed children.
Objective:
The main objective of this study is to investigate MRI T2-lesion evolution in pediatric MOGAD, AQP4 + NMOSD, and MS.
Methods:
Inclusion criteria were as follows: (1) first clinical attack; (2) abnormal MRI (⩽6 weeks); (3) follow-up MRI beyond 6 months without relapses in that region; and (4) age < 18 years. An index T2-lesion (symptomatic/largest) was identified, and T2-lesion resolution or persistence on follow-up MRI was determined.
Results:
We included 56 patients (MOGAD, 21; AQP4 + NMOSD, 8; MS, 27) with 69 attacks. Index T2-lesion resolution was more frequent in MOGAD (brain 9 of 15 [60%]; spine 8 of 12 [67%]) than AQP4 + NMOSD (brain 1 of 4 [25%]; spine 0 of 7 [0%]) and MS (brain 0 of 18 [0%]; spine 1 of 13 [8%]), p < 0.01. Resolution of all T2-lesions occurred more often in MOGAD (brain 6 of 15 [40%]; spine 7 of 12 [58%]) than AQP4 + NMOSD (brain 1 of 4 [25%]; spine 0 of 7 [0%]), and MS (brain 0 of 18 [0%]; spine 1 of 13 [8%]), p < 0.01. Reductions in median index T2-lesion area were greater in MOGAD (brain, 305 mm; spine, 23 mm) than MS (brain, 42 mm [p<0.001]; spine, 10 mm [p<0.001]) without differing from AQP4 + NMOSD (brain, 133 mm [p=0.42]; spine, 19.5 mm [p=0.69]).
Conclusion:
In children, MRI T2-lesions resolved more often in MOGAD than AQP4 + NMOSD and MS which is similar to adults suggesting these differences are related to pathogenesis rather than age.
Insights
Pediatric myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) shows more frequent MRI T2-lesion resolution than aquaporin-4 IgG-positive neuromyelitis optica spectrum disorder (AQP4+NMOSD) and multiple sclerosis (MS). These findings suggest age-independent pathogenic differences in lesion evolution.
Area of Science:
- Neuroimmunology
- Pediatric Neurology
- Radiology
Background:
- Magnetic resonance imaging (MRI) T2-lesions resolve more frequently in myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) compared to aquaporin-4 IgG-positive neuromyelitis optica spectrum disorder (AQP4+NMOSD) and multiple sclerosis (MS) in adults.
- Limited research exists on T2-lesion evolution in pediatric cases of these neuroinflammatory conditions.
Purpose of the Study:
- To investigate and compare the evolution of MRI T2-lesions in children diagnosed with MOGAD, AQP4+NMOSD, and MS.
- To determine if lesion resolution patterns differ significantly across these pediatric autoimmune neurological diseases.
Main Methods:
- A cohort of pediatric patients (<18 years) with a first clinical attack and abnormal MRI (within 6 weeks) were included.
- Follow-up MRIs were obtained >6 months post-attack, ensuring no relapses in the evaluated regions.
- The resolution or persistence of an index T2-lesion (symptomatic/largest) was assessed, along with the resolution of all T2-lesions and changes in lesion area.
Main Results:
- Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) demonstrated significantly higher rates of index T2-lesion resolution (brain 60%, spine 67%) and complete T2-lesion resolution (brain 40%, spine 58%) compared to AQP4+NMOSD and MS (p < 0.01).
- Reductions in median index T2-lesion area were greater in MOGAD compared to MS, with no significant difference from AQP4+NMOSD.
- No index T2-lesion resolution was observed in pediatric MS, and very limited resolution occurred in AQP4+NMOSD.
Conclusions:
- In pediatric patients, MRI T2-lesions resolve more frequently in MOGAD than in AQP4+NMOSD and MS.
- These findings in children mirror adult observations, suggesting that the observed differences in lesion evolution are primarily driven by underlying disease pathogenesis rather than patient age.
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