Purpose of Review Traumatic spinal cord injury (SCI) is a life-changing event with drastic implications for patients due to sensorimotor impairment and autonomous dysfunction. Current clinical evaluations focus on the assessment of injury level and severity using standardized neurological examinations. However, they fail to predict individual trajectories of recovery, which highlights the need for the development of advanced diagnostics. This narrative review identifies recent advances in the search of clinically relevant biomarkers in the field of SCI. Recent Findings Advanced neuroimaging and molecular biomarkers sensitive to the disease processes initiated by the SCI have been identified. These biomarkers range from advanced neuroimaging techniques, neurophysiological readouts, and molecular biomarkers identifying the concentrations of several proteins in blood and CSF samples. Some of these biomarkers improve current prediction models based on clinical readouts. Validation with larger patient cohorts is warranted. Summary Several biomarkers have been identified—ranging from imaging to molecular markers—that could serve as advanced diagnostic and hence supplement current clinical assessments.

G-ratio weighted imaging is a non-invasive, in-vivo MRI-based technique that aims at estimating an aggregated measure of relative myelination of axons across the entire brain white matter. The MR g-ratio and its constituents (axonal and myelin volume fraction) are more specific to the tissue microstructure than conventional MRI metrics targeting either the myelin or axonal compartment. To calculate the MR g-ratio, an MRI-based myelin-mapping technique is combined with an axon-sensitive MR technique (such as diffusion MRI). Correction for radio-frequency transmit (B1+) field inhomogeneities is crucial for myelin mapping techniques such as magnetization transfer saturation. Here we assessed the effect of B1+ correction on g-ratio weighted imaging. To this end, the B1+ field was measured and the B1+ corrected MR g-ratio was used as the reference in a Bland-Altman analysis. We found a substantial bias (≈-89%) and error (≈37%) relative to the dynamic range of g-ratio values in the white matter if the B1+ correction was not applied. Moreover, we tested the efficiency of a data-driven B1+ correction approach that was applied retrospectively without additional reference measurements. We found that it reduced the bias and error in the MR g-ratio by a factor of three. The data-driven correction is readily available in the open-source hMRI toolbox (www.hmri.info) which is embedded in the statistical parameter mapping (SPM) framework.

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Traumatic spinal cord injury (SCI) triggers a cascade of neurodegenerative events across the neuroaxis. The trajectories of lesion characteristics and brain and spinal cord macro-and microstructural changes were analysed over five years in 23 SCI patients and 21 healthy controls. Initially, SCI patients showed higher volume and iron content in the spinal cord which decreased over time. They showed lower myelin-sensitive MTsat values in the dorsal column and cortex which also decreased over time and were associated with acute lesion characteristics. These observations illustrate the widespread and progressive neuroplastic processes after SCI, its magnitude being predicted by acute lesion characteristics.

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We tracked remote neurodegenerative changes in the cervical cord following spinal cord injury over 2 years using macrostructural readouts (cross-sectional area, left-right width, anterior-posterior width) derived from T1-weighted MPRAGE images. Thereby, we evaluated the dependency of the magnitude of atrophy on the distance to the lesion. Over time, differences in atrophy rates along the cervical cord rostral to the lesion gradually formed a lesion gradient. Using anterior-posterior width and left-right width as surrogates for investigating anterograde and retrograde degeneration separately, our results suggest that these two types exhibit different spatiotemporal dynamics. A lesion gradient was only observable for retrograde degeneration.