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MR properties of rat sciatic nerve following trauma
Author(s) -
Stanisz Greg J.,
Midha Rajiv,
Munro Catherine A.,
Henkelman R. Mark
Publication year - 2001
Publication title -
magnetic resonance in medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.696
H-Index - 225
eISSN - 1522-2594
pISSN - 0740-3194
DOI - 10.1002/1522-2594(200103)45:3<415::aid-mrm1054>3.0.co;2-m
Subject(s) - sciatic nerve , fractional anisotropy , magnetization transfer , medicine , histopathology , degeneration (medical) , anatomy , regeneration (biology) , t2 relaxation , nerve injury , diffusion mri , axonal degeneration , pathology , magnetic resonance imaging , anesthesia , radiology , biology , microbiology and biotechnology
T 1 and T 2 relaxation times, magnetization transfer (MT), and diffusion anisotropy of rat sciatic nerve were measured at different time intervals following trauma. The nerve injury was induced by either cutting (irreversible nerve degeneration) or crushing (degeneration followed by regeneration). The MR properties were measured for proximal and distal portions of the injured nerve. The portions of the nerve proximal to the induced injury exhibited MR characteristics similar to those of normal nerves, whereas the distal portions showed significant differences in all MR parameters. These differences diminished in the regenerating nerves within approximately 4 weeks post injury. In the case of irreversible nerve damage, the differences in the distal nerves were slightly larger and did not resolve even 6 weeks after induced trauma. The MR measurements were correlated with histopathology exams. Observed changes in tissue microstructure, such as demyelination, inflammation, and axonal loss, can result in a significant increase in the average T 1 and T 2 relaxation times, reduction in the MT effect, and decrease in diffusion anisotropy. MR parameters, therefore, are very good indicators of nerve damage and may be useful in monitoring therapies that assist nerve regeneration. Magn Reson Med 45:415–420, 2001. © 2001 Wiley‐Liss, Inc.