Highlights
- •Vascular comorbidities are very common in general population as in MS patients.
- •Our results indicated vascular comorbidities as negative prognostic factors for brain atrophy.
- •These conditions should be carefully monitored in patients with MS with a focus on limiting brain damage.
Abstract
Background
Some studies have indicated the importance of considering the presence of vascular
comorbidities as negative prognostic factors for MRI outcomes in multiple sclerosis
(MS). This study aimed to evaluate the possible influence of the most frequent vascular
risk factors on brain volume in MS, also exploring the burden of their combined effects.
Methods
MS patients with at least one vascular risk factor and a control group of MS patients
were enrolled. Patients underwent brain MRI and the volumes of the whole brain (WB),
white matter (WM), grey matter (GM), and cortical GM were estimated by SIENAX. Longitudinal
atrophy was assessed by SIENA.
Results
The sample included 326 MS patients, of these 49 (15%) had diabetes mellitus, 44 (13.4%)
hypertension and 50 (15.3%) were active smokers. Multiple regression analyses revealed
that diabetes mellitus was associated with significant reductions in WB (p = 0.03), GM and cortical GM (p = 0.01) volumes. Similarly, reduced cortical GM volume was associated with hypertension
(p < 0.05). A strong relationship between the co-occurrence of multiple vascular risk
factors and lower cortical GM volume (p = 0.007) was also identified. Ninety patients were included in the longitudinal study
and a greater annualized brain volume loss was found in those with at least one vascular
risk factor than in the control group (−1.05% vs. −0.58%, p = 0.005).
Conclusions
Our results show that the vascular comorbidities affect brain atrophy, indicating
that these conditions should be carefully monitored in patients with MS with a focus
on limiting brain damage.
Keywords
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Article info
Publication history
Published online: October 15, 2018
Accepted:
October 14,
2018
Received in revised form:
October 10,
2018
Received:
August 9,
2018
Identification
Copyright
© 2018 Elsevier B.V. All rights reserved.