Ultrashort echo time (UTE) magnetic resonance imaging of myelin: technical developments and challenges.

Myelin is a concentrically laminated membranous structure consisting of alternating protein and lipid layers, and contains approximately 20% protein and 80% lipid (1). It is formed by two different types of support cells, oligodendrocytes in the central nervous system (CNS) and Schwann cells in the peripheral nervous system (PNS). Myelin is a major component of the CNS and PNS, and accounts for about 14% of the wet mass and 50% of the dry mass of the white matter of the brain (1). It is present in the form of a sheath surrounding the axons of some neurons, and insulates axons from electrically charged ions and molecules. It helps increase nerve conduction velocity. Loss of myelin is the hallmark of numerous inflammatory and neurodegenerative disorders, including multiple sclerosis (MS) and other demyelinating diseases such as optic neuritis, neuromyelitis optica, transverse myelitis, and acute disseminated encephalomyelitis (1). Magnetic resonance imaging (MRI) is the current gold standard imaging modality for diagnosis of disease of the brain (2-10). Conventional clinical MRI sequences are very sensitive to the presence of white matter disease including MS. Clinical T1and T2-weighted fast spin echo (FSE) imaging (2), gadolinium enhancement (3), diffusion tensor imaging (DTI) (4), and Magnetization Transfer (MT) (5), all show high sensitivity for abnormalities in patients with MS. However, conventional clinical MRI only correlates modestly with disability assessed by the expanded disability status scale (EDSS) (6), also T2-hyperintense lesion load in MS is poorly correlated with disability (r=0.2–0.5) in crosssectional studies (7-11). Contrast-enhanced lesions are only moderately correlated with disability in the first six months, and are not predictive of changes in the EDSS in the subsequent 12 or 24 months (12). A recent large scale multicenter study reported a poor correlation between EDSS and normalized brain volume (r=−0.18), cross section area (r=−0.26), MT ratio (MTR) of whole brain tissue (r=−0.16) and MTR of gray matter (GM) (r=−0.17), and no significant correlation between other MR metrics and patients EDSS scores (13). It is commonly accepted that conventional clinical MRI sequences lack specificity for evaluation of the heterogeneous pathologic substrates of MS as well as the ability to provide accurate estimates of damage in areas of the brain apart from focal lesions (6). Most conventional clinical MRI sequences cannot distinguish the different cardinal pathological substrates of MS, namely demyelination, remyelination, inflammation, edema, axonal loss and gliosis (14-16). The inability of conventional MRI sequences to distinguish demyelination and remyelination may be a major factor accounting for the poor correlation between regular MRI metrics and disability. Editorial