Abstract
This study explored the effect of glatiramer acetate (GA, 20 mg) on lesion activity using the 1.5 T standard MRI protocol (single dose gadolinium [Gd] and 5-min delay) or optimized 3 T protocol (triple dose of Gd, 20-min delay and application of an off-resonance saturated magnetization transfer pulse). A 15-month, phase IV, open-label, single-blinded, prospective, observational study included 12 patients with relapsing-remitting multiple sclerosis who underwent serial MRI scans (Days −45, −20, 0; the minus ign indicates the number of days before GA treatment; and on Days 30, 60, 90, 120, 150, 180, 270 and 360 during GA treatment) on 1.5 T and 3 T protocols. Cumulative number and volume of Gd enhancing (Gd-E) and T2 lesions were calculated. At Days −45 and 0, there were higher number (p < 0.01) and volume (p < 0.05) of Gd-E lesions on 3 T optimized compared to 1.5 T standard protocol. However, at 180 and 360 days of the study, no significant differences in total and cumulative number of new Gd-E and T 2 lesions were found between the two protocols. Compared to pre-treatment period, at Days 180 and 360 a significantly greater decrease in the cumulative number of Gd-E lesions (p = 0.03 and 0.021, respectively) was found using the 3 T vs. the 1.5 T protocol (p = NS for both time points). This MRI mechanistic study suggests that GA may exert a greater effect on decreasing lesion activity as measured on 3 T optimized compared to 1.5 T standard protocol.
Highlights
Gadolinium (Gd) enhancement in multiple sclerosis (MS) lesions correlates with histopathologic findings of blood-brain barrier (BBB) breakdown and active inflammation. [1,2,3,4] Gd-enhancing (Gd-E)lesions on post-contrast T 1-weighted images (WI) usually correspond to areas of high signal intensity on T2-WI and low signal intensity on unenhanced T1-WI, probably due to edema and demyelination [5].Gd-enhancement is a transient phenomenon in MS that usually disappears after several weeks [6]
These strategies, which maximize the information that can be obtained by Gd-enhancement, include [2]: (1) frequent serial monthly scanning; (2) a delay longer than 5 min between Gd injection and scanning; (3) using doses of higher contrast; (4) acquiring thinner tomographic slices; (5) coregistration; (6) reducing the background signal by the application of off-resonance saturation magnetization transfer (MT) pulses to T1-WI and (7) use of high-field strength scanners [7,8,9]
120 due to an inability to adhere to the MRI schedule; and 1 discontinued the study at Day 150 due to incarceration
Summary
Gadolinium (Gd) enhancement in multiple sclerosis (MS) lesions correlates with histopathologic findings of blood-brain barrier (BBB) breakdown and active inflammation. [1,2,3,4] Gd-enhancing (Gd-E)lesions on post-contrast T 1-weighted images (WI) usually correspond to areas of high signal intensity on T2-WI and low signal intensity on unenhanced T1-WI, probably due to edema and demyelination [5].Gd-enhancement is a transient phenomenon in MS that usually disappears after several weeks [6]. Lesions on post-contrast T 1-weighted images (WI) usually correspond to areas of high signal intensity on T2-WI and low signal intensity on unenhanced T1-WI, probably due to edema and demyelination [5]. Various strategies have been proposed to increase the sensitivity of Gd-enhanced MRI for the detection of active MS lesions. These strategies, which maximize the information that can be obtained by Gd-enhancement, include [2]:. (3) using doses of higher contrast (e.g., a double or triple dose instead of a standard 0.1 mmoL/kg dose);. A number of studies used the standard protocol at 1.5 T (a single dose of Gd, with a 5-min scanning time delay after Gd injection) to compare with the optimized protocols at 1.5 T or 3 T (4) acquiring thinner tomographic slices; (5) coregistration; (6) reducing the background signal by the application of off-resonance saturation magnetization transfer (MT) pulses to T1-WI and (7) use of high-field strength scanners [7,8,9].
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