Spinal cord injuries (SCIs) are a leading cause of disability and can lead to devastating consequences for patients. Traumatic lesions (including primary and secondary lesions) not only can induce a physical discontinuity of the tracts but also anterograde Wallerian demyelination as well as some retrograde degeneration. After SCI, some pathways may be preserved and contribute to recovery of function. This could be achieved by regeneration of pathways or sprouting of undamaged pathways. Whereas in the first case, pathways are replaced by regenerated fibres, in the second case, new connections are either made or strengthened through existing structures. Thus, damage to the corticospinal tract can be in part offset by sprouting new connections through propriospinal or reticulospinal pathways, which then act more or less as a new (or enhanced relay) between the cortex and the spinal cord. It is thus important to develop prognostic imaging tools that will allow the characterization of the damaged tracts and the state of residual tracts.

Injury may disrupt the normal functions of the spinal cord, and lead to severe sensory and motor behavioural deficits. Over time, the impaired functions may recover through different mechanisms at both the Spinal Cord and brain levels. Regeneration of injured Spinal Cord is a key process during functional recovery, and has been a major topic of research for developing improved therapies. SCI can induce cell death and create tissue cavities, while subsequent reactions including inflammation can stimulate both destructive and reparative processes, and lead to edema and cysts and demyelination. SCI also culminates in glial scarring, and the scar tissue may contain secreted and transmembrane molecular inhibitors of axon growth.  To be able to evaluate potential new treatments, it is important to understand the temporal changes and recovery of injured SC tissue from structural, functional and molecular perspectives. Non-invasive quantitative magnetic resonance imaging (MRI) methods are well suited for monitoring the recovery process in a comprehensive way. Furthermore, validation of MRI measures of compositional and structural changes that occur at and around spinal lesion sites is crucial for the interpretation of MRI findings.

Magnetization transfer (MT) is the spin exchange between proton pools in different environments, and can be used to evaluate macromolecular content of tissue.  There are two main approaches to measure MT effects: semiquantitative magnetization transfer ratio (MTR) and Quantitative magnetization transfer (qMT) methods that extract numerical parameters based on a specific model. To date, simpler metrics such as MTR have been the major approach to assess changes in macromolecular composition in neurological disorders. MTR has also been shown to be sensitive to changes in protein content and has been used previously in studies of SC. The sensitivity and reproducibility of MTR measure can be influenced by various experimental parameters. To increase specificity and sensitivity, qMT methods have been developed to measure intrinsic MT parameters, and to isolate the pool size ratio (PSR, the ratio of the macromolecular proton pool to the free water pool) from relaxation rates and exchange rates.

Free water protons are observed with conventional MRI, there are additional protons residing on immobile macromolecules in tissue. Conventional MRI cannot image these protons directly because their T₂ relaxation times are too short (≈10 μs) to be captured by typical readout schemes. However, these macromolecular protons communicate with the surrounding water and, thus, can be indirectly imaged by exploiting this exchange, which is referred to as the MT effect. Importantly, MT imaging can serve as a surrogate marker for white matter myelin density in nervous system tissue and, therefore, may be a more specific biomarker of disease evolution.