Abstract
This study aims to examine a time-extended dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) protocol and report a comparative study with three different pharmacokinetic (PK) models, for accurate determination of subtle blood–brain barrier (BBB) disruption in patients with multiple sclerosis (MS). This time-extended DCE-MRI perfusion protocol, called Snaps, was applied on 24 active demyelinating lesions of 12 MS patients. Statistical analysis was performed for both protocols through three different PK models. The Snaps protocol achieved triple the window time of perfusion observation by extending the magnetic resonance acquisition time by less than 2 min on average for all patients. In addition, the statistical analysis in terms of adj-R 2 goodness of fit demonstrated that the Snaps protocol outperformed the conventional DCE-MRI protocol by detecting 49% more pixels on average. The exclusive pixels identified from the Snaps protocol lie in the low k trans range, potentially reflecting areas with subtle BBB disruption. Finally, the extended Tofts model was found to have the highest fitting accuracy for both analyzed protocols. The previously proposed time-extended DCE protocol, called Snaps, provides additional temporal perfusion information at the expense of a minimal extension of the conventional DCE acquisition time.
Highlights
Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system (CNS) usually affecting young adults
The range of ktrans values for Tofts model (TM) and extended Tofts model (ETM) lies in the same range of values for the same protocol, while the Patlak model returns lower ktrans values (Figure 1)
A systematic decrease of the ktrans values from the NoSnaps protocol to the Snaps protocol can be observed for every threshold, and the distribution of ktrans boxplots on the Snaps protocol is skewed toward the higher ktrans values compared with the NoSnaps protocol (Figure 2)
Summary
Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system (CNS) usually affecting young adults. The etiology of MS is largely unknown, it is considered primarily an autoimmune disease in which activated myelin-specific T-cells migrate from the periphery to the CNS, by crossing the blood–brain barrier (BBB), and induce the formation of new inflammatory demyelinating lesions [1,2]. Recent studies have emphasized the crucial role the BBB dysfunction plays in the inflammatory events that take place in MS [3,4]. Histopathological and magnetic resonance imaging (MRI) studies reported BBB abnormalities in acute active inflammatory MS lesions and in inactive, non-enhancing lesions and the normal appearing white matter (NAWM) as well [5–7]. According to research studies concerning the development of drug therapies in MS, the leukocyte passage across the BBB is very important for disease pathophysiology [8,9] and resolution of inflammation along with the protection of BBB function is the therapeutic target for many proposed MS treatments [1,2].
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