Assessment of demyelination, edema, and gliosis by in vivo determination of T1 and T2 in the brain of patients with acute attack of multiple sclerosis

Abstract

This study intended to investigate the possibility of magnetic resonance (MR) to characterize the acute plaque due to multiple sclerosis (MS). To obtain information, in vivo measurements of relaxation processes were performed in 10 patients with known acute MS plaques, using a whole-body superconductive MR-scanner, operating at 1.5 T. The measurements were repeated several times, from onset of the disease and during remission by use of six-point partial saturation inversion recovery and 32-echo multiple spin-echo sequences, giving T1 and T2, respectively. We also focused on the issue, whether T1 and T2 relaxation processes in fact were monoexponential. The results of the first T1 and T2 measurements of the acute plaques were not clearly different from T1 and T2 of presumably chronic plaques obtained in a group of chronic MS patients previously (H.B.W. Larsson, J. Frederiksen, L. Kjär, O. Hendriksen, and J. Olesen, Magn. Reson. Med. 7, 43 (1988)). In some of the acute plaques a slight initial increase in T1 and T2 was seen, when the measurement was repeated in about 10 days. Thereafter T1 decreased slowly in all but one patient as a function of days. In all cases the T1 relaxation process followed a monoexponential course. The T2 relaxation process was a monoexponential function in the acute plaques, when measured within 20 days from onset of disease. After an average of 78 days, however, the T2 relaxation process clearly became biexponential in all but two patients. Later some of the relaxation curves changed back toward monoexponentiality. Thus, the study shows that it is possible to detect significant changes in MR parameters during the evolution of the disease, and these changes are discussed in relation to knowledge of pathoanatomical events in MS.

Evaluation of Delayed Neuronal and Axonal Damage Secondary to Moderate and Severe Traumatic Brain Injury Using Quantitative MR Imaging Techniques

“…The main etiologies of increased water concentration in central nervous parenchyma are inflammatory processes, edema, demyelination, gliosis, or neuronal loss. [10][11][12] A higher mean value of T2 relaxation time was observed in the NAWM and CC of the test group in our study, compared with the control group, demonstrating higher water concentration in these regions. The cause of this increased water concentration is thought to be axonal loss (with concomitant myelin sheath loss) and gliosis, secondary to TBI.…”

Quantitative MRI‐pathology correlations of brain white matter lesions developing in a non‐human primate model of multiple sclerosis

“…The latter techniques have been shown to be sensitive in detecting pathogenic processes that contribute to lesion formation in MS, i.e. inflammation and edema, demyelination, axonal destruction and gliosis (8)(9)(10). We compared the presentation of end stage lesions on in vivo MRI with quantitative ex vivo MRI and with histo-pathological characterization, including quantitation of axonal injury (11) and the presence and activity of macrophages (12), which have been recognized as important pathophysiological features of lesion development.…”

Quantitative Magnetic Resonance Imaging of the Brain : Applications for Tissue Segmentation and Multiple Sclerosis

“…The initial increase in T2 of the lesion has also been attributed to increased water content due to the oedema (84,168). Over time, T2 decreases to that of chronic lesions (84,139,170), similar to the behaviour of T1.…”

“…In acute WM lesions T1, T2 and PD are all substantially increased (73,84,(167)(168)(169) which, during the following months, decreases towards slightly elevated T1, T2 and PD seen in chronic lesions (84,170). The main pathological process in the initial increase is attributed to inflammatory oedema, causing increases in both T1 and T2, as well as PD.…”

“…Over time, T2 decreases to that of chronic lesions (84,139,170), similar to the behaviour of T1. One study detected monoexponential relaxation in acute WM lesions, which became bi-exponential during remission, and finally returned to mono-exponential as the lesion turned into a chronic lesion (168). This suggests that the free water pool is the main source of T2 relaxation during the initial increase, whereas during the remission the water trapped between the myelin sheets remains for some time, resulting in biexponential relaxation.…”