Younger Multiple Sclerosis Age Onset Could Mean Accelerated NAWM Changes
SEPTEMBER 16, 2016
Are patients worse off if they are diagnosed with multiple sclerosis at a younger age? That’s what Italian researchers aimed to make more clear at the 32nd Congress of the European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS 2016) in London, England.
Clinicians have suspected that the age of multiple sclerosis onset influences the time to reach and level of disability once patients hit adulthood. The team looked at magnetic resonance imaging (MRI) results to determine how maturational effects and pathophysiological mechanisms may be able to help explain disease course.
“Here, we explored brain gray matter (GM) atrophy and white matter (WM) microstructural abnormalities in adult patients according to their age of multiple sclerosis onset,” the researchers explained.
This study was carried out by examining 3D T1-weighted and DT MRI scans from 58 pediatric-onset multiple sclerosis (POMS), 58 age-matched (AOA), 58 disease duration-matched (AODD) adult-onset patients with multiple sclerosis, and 58 healthy controls. Tract-based spatial statistics (TBSS) and voxel-based morphometry (VBM) were used to identify regional distribution of damage in the brain GM and WM.
Patients with multiple sclerosis, as compared to the healthy controls, had the expected regional GM and WM alterations. Those in the AOA group had reduced fractional anisotropy (FA), compared to POMS. But POMS had reduced FA in the previous WM tracts when compared to AODD.
“Compared to POMS, AOA patients had a widespread pattern of regional GM atrophy, whereas AODD patients had atrophy of the right fusiform gyrus,” the team found. “POMS patients showed atrophy of the right superior temporal gyrus (STG) in comparison to AODD.” In addition, older age of onset in POMS cases was associated with right STG and left putamen atrophy.
The POMS patients had less extensive GM and normal-appearing (NA) WM involvement than the AOA. This indicates that younger age results in less pronounced neurodegenerative and inflammatory-demyelinating processes. Based on the outcomes, the researchers think that accelerated NAWM changes occur in POMS as the disease progresses. This could mean impaired reserve of structural plasticity with disease duration.
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