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Updated: May 21, 2026

Comprehensive Autopsy Program for Individuals with Multiple Sclerosis
Published on: July 19, 2019
Differences and similarities in the evolution of morphologic brain abnormalities between paediatric and adult-onset
A Pichler1, C Enzinger, S Fuchs
1Department of Neurology, Medical University of Graz, Austria.
Insights
Paediatric-onset multiple sclerosis (pMS) shows more aggressive brain lesion accrual but less clinical disability compared to adult-onset MS (aMS). This suggests children with MS may have a higher compensatory capacity, potentially masking disease severity.
Area of Science:
- Neurology
- Neuroimmunology
- Pediatric Neurology
Background:
- Paediatric-onset multiple sclerosis (pMS) differs from adult-onset MS (aMS) in presentation and development.
- Brain changes in pMS versus aMS are not well understood.
Purpose of the Study:
- To compare the evolution of brain lesions and volume changes in pMS and aMS.
- To correlate MRI findings with clinical disability progression.
Main Methods:
- Compared T2-lesion load (LL), T1-LL, black hole ratio (BHR), and annualised brain volume change (aBVC) in 21 pMS and 21 aMS patients.
- Matched patients for disease duration and followed them for 3-4 years.
- Assessed Expanded Disability Status Scale (EDSS) and annualised relapse rate (ARR).
Main Results:
- pMS patients had lower baseline T2-LL but similar T1-LL and BHR compared to aMS.
- Both groups showed similar changes in T2-LL and T1-LL over time.
- Despite higher BHR (destructive lesions) in pMS, they had lower EDSS scores at follow-up.
Conclusions:
- pMS exhibits a morphologically more aggressive disease course with greater lesion burden.
- Lower disability in pMS suggests a higher compensatory capacity, potentially masking disease severity.
- Clinical assessment alone may underestimate the need for disease-modifying treatments in pMS.
Background:
Paediatric-onset multiple sclerosis (pMS) is multiple sclerosis (MS) occurring before the age of 18 years and may present and develop differently from adult-onset MS (aMS). Whether there are also differences regarding the accrual of brain changes is largely unknown.
Methods:
We compared the evolution of the T2- and T1-lesion load (LL), the black hole ratio (BHR), and annualised brain volume change (aBVC) between 21 pMS patients (age at onset: 14.4±2.3 years) and 21 aMS patients (age at onset: 29.4±6.5 years) matched for disease duration (pMS: 1.0±1.8 years; aMS: 1.6±1.7 years, p=0.27). Follow-up was for 4.2±3.7 years in pMS and 3.1±0.6 years in aMS. Clinical comparisons included the course of disability assessed with the Expanded Disability Status Scale (EDSS) score and annualised relapse rate (ARR).
Results:
At baseline, pMS and aMS had similar EDSS, T1-LL, BHR, whereas T2-LL was higher in aMS (aMS: 9.2±11.6 ccm; pMS: 4.1±6.2 ccm, p=0.02). The change of T2-LL and T1-LL during the observation period was similar in both groups. At follow-up, disability was lower in pMS (EDSS score in pMS: 0.9±0.9; aMS: 1.7±1.3, p=0.04), despite a significantly higher accrual of destructive brain lesions (BHR in pMS: 23.7±23.7%; aMS: 5.9±4.0%, p=0.02) and a similar rate of brain volume loss.
Conclusion:
Our observation of a morphologically more aggressive disease evolution paralleled by less disability in pMS than in aMS (defined using EDSS) suggests a higher compensatory capacity in pMS. This fact may obscure the need for treatment of pMS patients with disease modifying treatments (DMTs) based solely on clinical observation.

