In vivo determination of multiexponential T2 relaxation in the brain of patients with multiple sclerosis

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.…”

Investigating the effect of exchange and multicomponent T1 relaxation on the short repetition time spoiled steady‐state signal and the DESPOT1 T1 quantification method

“…In biological systems, however, relaxation can rarely be fully characterized by single relaxation times (13,14). Observation of multicomponent T 2 relaxation, for instance, has been well documented in several biological tissues, most notably in white and gray matter (15)(16)(17), articular cartilage (18), and skeletal muscle (19). In human white and gray matter, short (less than 50 msec) and long (50 -200 msec) T 2 species have been consistently observed and attributed to water protons bound within the myelin layer and the less restricted intra-and extracellular water pools, respectively (16).…”

MRS in MS, With and Without Interferon Beta 1a Treatment, to Define the Dynamic Changes of Metabolites in the Brain, and to Monitor Disease Progression

“…Many studies (Arnold et al, 1992;Arnold et al, 1994;Davie et al, 1997;De Stefano et al, 1995;Husted et al, 1994;Narayana et al, 1998,( Allen & McKeown, 1979De Stefano et al, 1995;Fu et al, 1998;Husted et al, 1994;Narayana et al, 1998) have shown a reduction in the absolute concentration of NAA or the NAA/Cr ratio in MS lesions. However, pathological (Allen & McKeown, 1979) and quantitative MRSI studies (Armspach, Gounot, Rumbach, & Chambron, 1991;Filippi et al, 1995;Gasperini et al, 1996;Loevner et al, 1995) have shown that in patients with clinically definite MS, abnormalities also occur in the NAWM (Arnold et al, 1992;Davie et al, 1997;Davie et al, 1994;Fu et al, 1998;Husted et al, 1994;Narayana et al, 1998). Although the principal finding of MRS studies in patients with MS was a decrease in the NAA peak area, opposite results were obtained for other metabolites (Davie et al, 1994;Davies, Newcombe, Williams, McDonald, & Clark, 1995;De Stefano et al, 1995;Husted et al, 1994;Larsson et al, 1991).…”