Conventional Magnetic Resonance Imaging (MRI) has a high sensitivity for detecting inflammatory disease activity of the brain, but is time-consuming, only semi-quantitative and rely on subjective assessments. On the contrary, the technique called ‘synthetic MRI’ (SyMRI) uses a single pulse sequence, can create contrast-weighted images from quantitative maps based on relaxometry and simultaneously provides automatic brain volume and myelin measurements. All this information is delivered after a single 6-minute scan and software with post-processing time less than 1 minute. Measuring the change in brain volume and myelin content in vivo could provide new insights into the relationship between two main pathological processes in multiple sclerosis (MS), demyelination and neurodegeneration and the impact of disease modifying treatments (DMTs) on these processes.
The aim was to assess brain volume and myelin content over time in patients with newly diagnosed MS and in healthy control persons.
We prospectively included 116 patients newly diagnosed with relapsing-remitting (RR) MS, and 51 healthy control subjects (HC). All patients initiated DMT and were dichotomized into those with disease activity (relapse and/or new or enlarging lesions on MRI) (n=74) and those without disease activity (n=42) at follow up. The MRI was performed at baseline in both groups and in patients at 6, 12, 24 and 36 months, and in HC only at 24 months. Brain parenchymal fraction (BPF) and myelin parenchymal fraction (MyPF) of the brain were calculated via SyMRI software.
At baseline, there was no significant difference between HC and newly diagnosed MS in BPF (89% and 89.1%, respectively, p=0.97), but HC had significantly lower MyPF than patients (14.1% and 14.9%, respectively, p<0.001). At 36 months follow-up, the mean change of BPF and MyPF in patients was -0.9% (±1.6) p<0.001 and 0.3 % (±1.3) p=0.022, respectively. Patients without disease activity had significantly higher MyPF compared with patients with disease activity during follow-up time (15.7% and 14.9%, respectively, p=0.009). At 24 month follow-up, BPF and MyPF were unchanged in HC compared to baseline (p=0.94 and p=0.44, respectively).
SyMRI showed the development of significant brain atrophy in RRMS after 3 years of follow-up and signs of increased demyelination in patients with disease activity. However, patients had unexpectedly higher MyPF than controls at baseline and the MyPF increased in stable RRMS at follow-up. This might indicate increased remyelination. However, the sensitivity of SyMRI to quantify the myelin fraction of the brain deserves further validation.