Correlation Between MRI T2 Hyperintensity, Apoptosis, and Neuroinflammation in Chronic Cervical Spinal Cord...

Experimental animal study using a rabbit model of chronic cervical spinal cord compression.

To investigate the relationship between MRI T2-weighted signal intensity changes in the spinal cord and underlying apoptotic and neuroinflammatory mechanisms in chronic cervical spinal cord compression.

T2-weighted MRI hyperintensity in degenerative cervical myelopathy (DCM) patients is commonly observed, but its pathological significance remains incompletely understood. Apoptosis and neuroinflammation are key pathophysiological mechanisms, yet their correlation with MRI signal changes lacks systematic investigation.

Twenty-four rabbits were randomized into control, mild compression, and severe compression groups (n=8/group). Chronic cervical spinal cord compression was induced at C3 using radiopaque resin pins. Motor function (Tarlov scores, Rivlin inclined plane test), somatosensory evoked potentials (SEPs), and MRI signal intensity ratios (SCR) were assessed at 1 week, 3 months, and 6 months. At 6 months, spinal cord tissues were analyzed via hematoxylin-eosin staining, TUNEL assay, immunofluorescence, and Western blotting for apoptotic (Bax, Bcl-2, Caspase-3) and neuroinflammatory markers (NLRP3, ASC, NF-κB).

Compression severity correlated with functional decline and prolonged SEP latency (P<0.05). At 6 months, SCR was significantly elevated in severe compression group (1.16 vs. 1.00 in controls, P<0.001). TUNEL-positive cells increased proportionally with compression severity (3.2±0.8% control vs. 19.8±2.4% severe compression, P<0.001). Bax/Bcl-2 ratio and NLRP3 expression escalated with compression intensity. Spearman analysis revealed strong positive correlations between SCR and both Bax/Bcl-2 ratio (rs=0.817, P<0.001) and NLRP3 expression (rs=0.849, P<0.001).

In chronic cervical spinal cord compression, MRI T2 hyperintensity correlates significantly with the severity of neuronal apoptosis and NLRP3-mediated neuroinflammation, suggesting that SCR may serve as a quantitative imaging biomarker for underlying pathological changes in DCM.