Direct MRI Detection of Impending Plaque Development in MS (S44.002)

OBJECTIVE. To detect and localize MRI signal changes prior to contrast enhancement. BACKGROUND. A few longitudinal studies, using group-level statistics on conventional and non-conventional MRI data, have described abnormalities that precede gadolinium (Gad)-enhancement in acute multiple sclerosis (MS) lesions. However, the pathological origin of these changes and their localization relative to features of the developing lesion (including its central vein) are not completely understood. METHODS. We retrospectively evaluated 286 scans in 28 MS patients selected from our database for the presence of enhancing lesions and the availability of at least one 3T or 7T scan before lesion enhancement. Pre-enhancement features were detected on high-resolution (≤1mm3 voxels) T2-FLAIR, T1-MPRAGE, and T2* (when available), and were classified according their temporal relationship with Gad-enhancement. RESULTS. In 25/178 enhancing lesions (14%), pre-enhancement changes were noted. Up to two months before focal Gad-enhancement within the parenchyma, linear enhancement of the central vein and/or fluffy, hyperintense signal on T2-FLAIR or T2* around the central vein, not present in previous scans, were discerned in 12/104 lesions (12%) with a previous scan acquired within two months. In the other 13 lesions, longstanding small nodules (hyperintense on T2-FLAIR and occasionally hypointense on T1-MPRAGE), with a cylindrical configuration on T2* (available in 6 cases), were seen to be centered on the central vein months to years before enhancement. CONCLUSION. In some lesions, the abrupt opening of the blood-brain barrier, detected by Gad-enhancement on MRI, can have directly visible antecedent MRI changes centered on the central vein. We propose that these findings are the basis for prior reports of pre-lesional changes in quantitative MRI indices. Furthermore, prospective detection of the short-term (<2 months) changes may open the possibility of testing whether prophylactic treatment can prevent subsequent lesion formation and ensuing disability accumulation and brain atrophy.