Quantitative MRI in a non‐surgical model of cervical spinal cord injury

Abstract

Quantitative T2 (qT2), diffusion tensor imaging (DTI), and histology were used to investigate a cervical model of spinal cord injury (SCI) in the rat. While quantitative MRI can significantly increase the specificity in the presence of pathology, it must be validated for each type of injury or disease. In the case of traumatic SCI most models are difficult to image, either due to the location of the injury, or as a result of damage to surrounding tissues resulting from invasive surgical procedures. In this study a non-surgical cervical model of SCI, produced using a combination of focused ultrasound and microbubbles, was used to produce pathology similar to that seen in models of contusive and compressive injuries. qT2 and DTI were performed at 24 h and 1 and 2 weeks following injury, and compared with H&E and luxol fast blue histology. In the injured spinal cord, in addition to intra/extracellular (I/E) water and myelin water in white matter, qT2 revealed a large component with very short T2 of about 3 ms, which was highly correlated with the presence of hemorrhage in both gray and white matter at 24 h, and with the presence of hemosiderin in gray matter at 2 weeks following injury. The T2 of the I/E water peak was also elevated at 24 h in both gray and white matter, which was correlated with the presence of vacuolation/edema on histology. Cystic cavities were only seen at the 1 or 2 week timepoints, and were correlated with the presence of a water peak with T2 > 250 ms. No significant changes in diffusivity parameters were observed. Pathologies were often co-occurring, with opposite effects on the average T2 in a given voxel, reducing the visibility of injured tissue on standard T2 -weighted MR images.

The Role of Astrogliosis in Formation of the Syrinx in Spinal Cord Injury

“…The rat injured spinal cord reacts by forming a cavity of injury (COI) within the first week post-SCI [ 6 - 11 ] which encompasses the site of hemorrhage and necrosis, and a severe inflammatory infiltration mainly represented by active, phagocytic, CD68+/CD163-, pro-inflammatory macrophages [ 6 , 11 ]. Since the severe inflammation progresses in the aqueous environment in the COI, it apparently serves as a reservoir of the edema fluid from the surrouding CNS tissue with the concurrent decrease in the tissue water content as determined in MRI studies involving SCI [ 6 , 9 , 10 ]. The formation of the COI is unique to the CNS and does not occur in other organs after trauma.…”

Myxoma virus derived immune modulating proteins, M-T7 and Serp-1, reduce early inflammation after spinal cord injury in the rat model

“…Trauma to the spinal cord initiates a complex disease which is dominated by severe, destructive and prolonged inflammation. This destructive inflammation is characterized by an infiltration of phagocytic macrophages [21][22][23][24]37,38]. Macrophages continue to phagocytize myelin, persisting for more than 8 weeks post-spinal cord injury (SCI) [21].…”

Differences in iron and manganese concentration may confound the measurement of myelin fromR1andR2relaxation rates in studies of dysmyelination

“…In general, the transverse relaxation is field independent (115,117), although the observed, apparent rate R 2 may increase because of an increase in R 2 * caused by diffusion within inhomogeneous tissue. This may lead to a slight increase in r 2 relaxivity; however, it has been noted that the observed T 2 spectrum of WM does not change significantly with field (115,118), therefore indicating that the r 2 of 8.7 ± 1.8 s À1 /myelin fraction should, at a first approximation, be constant.…”