Traumatic spinal cord injury (TSCI) causes primary axonal disruption and secondary cascades of inflammation, demyelination, edema, and Wallerian degeneration.1 Conventional MRI provides crucial anatomical information—hemorrhage, edema length, cord compression—but correlates imperfectly with neurological impairment and recovery because it cannot directly depict microstructural damage.2,3 Diffusion tensor imaging (DTI) characterizes directionality of water diffusion within white-matter tracts; fractional anisotropy (FA) reflects fiber coherence and myelin integrity, mean diffusivity (MD) reflects overall diffusivity, axial diffusivity (AD) is sensitive to axonal injury, and radial diffusivity (RD) increases with demyelination.4–6 Over the past decade, several prospective cohorts and meta-analyses have demonstrated that lower FA and higher MD/RD at or near the lesion correlate with worse AIS grade, reduced motor scores, and diminished functional recovery after TSCI.7–10 Importantly, DTI abnormalities often extend cranio-caudally beyond T2-hyperintensity, capturing secondary degeneration within ostensibly normal-appearing cord.7,11 Early-phase scans (≤2–4 weeks) already show FA reduction; later subacute to chronic stages reveal progressive FA decline and RD elevation, consistent with ongoing tract degeneration.9,12 Technically, spinal DTI is challenging: cord cross-section is small; physiological motion (CSF pulsation, respiration, swallowing) and susceptibility from vertebrae/air spaces degrade echo-planar imaging.13 Refinements—reduced field-of-view (FOV) EPI, inner volume excitation, optimal b-values (600-800 s/mm2), phase encode directional reversal for distortion correction, cardiac gating and robust denoising—have improved reproducibility and clinical feasibility at 1.5T.14–16 ROI strategies along with tract-specific analyses (e.g., dorsal column, lateral corticospinal tracts) are complimentary; along-tract analyses reduce partial volume bias and identify stronger outcome associations. 17,18 Clinically, DTI might be of value in three areas: (1) Baseline risk stratification—measuring tract integrity when conventional MRI is indeterminate; (2) Prognostication—predicting AIS conversion and motor outcome; and (3) Monitoring—following microstructural response to decompression, neuroprotectants or rehabilitation. 8,10,19 These challenges are such as to inter-site variability, the absence of a standardized workflow and insufficiently developed regulatory aspects for quantitative imaging biomarkers. 15,20 However consensus guidelines and burgeoning multi-center data have hastened translation. 16,21 In the following article, we report a practical, clinically applicable evaluation of DTI in TSCI by combining a prospective single-center study with a systematic review of recent literature. We report lesion-level and peri-lesional DTI metrics, their relationship to neurological severity and 6-month outcomes, and propose a workflow and reporting template to support wider clinical adoption.9,16,22

This is a Prospective single-center cohort conducted at Srinivasan Medical college and Hospital, Samayapuram, Trichy with standardized DTI protocol and 6-month follow-up. Participants: Adults 18–70 with closed cervical TSCI (C2–T1) imaged ≤30 days post-injury. Exclusion: penetrating trauma, prior cervical myelopathy or demyelinating disease, MRI contraindications, unstable vitals precluding MRI, motion-degraded DTI (QC failure >20% volumes rejected), or incomplete follow-up. Healthy volunteers served as controls. Clinical assessments: Neurological examination followed ISNCSCI standards. AIS grade and upper/lower extremity motor scores were recorded at baseline and 6 months. Surgical timing, decompression status, and steroid use were documented. MRI acquisition: 1.5T scanner; 20-channel head-neck coil. DTI: single-shot rFOV EPI; TR/TE ≈ 4200/80 ms; in-plane 1.0–1.1 mm, slice 4 mm, interleaved; 20–24 diffusion directions; b = 0 and 700 s/mm² (two b0 with reversed phase-encode); bandwidth ≥1,500 Hz/Px; cardiac gating when tolerated. Conventional MRI: sagittal/axial T2-w, T1-w, GRE for hemorrhage. Preprocessing and analysis: Topup/eddy for distortion and motion correction with outlier replacement; Rician denoising; diffusion tensor fit by weighted least squares. FA, MD, AD, RD maps were generated. ROIs: (1) lesion epicenter, (2) peri-lesion (±10 mm), (3) remote level (C2–C3) if uninvolved. ROI placement was performed by two neuroradiologists, blinded to outcomes; inter-rater reliability assessed (ICC). Along-tract profiles (dorsal column & lateral columns) were extracted on a subset using template-based spinal cord segmentation. Outcomes: Primary—association of epicenter FA with 6-month motor score. Secondary—group differences in DTI metrics vs controls, prediction of AIS conversion (A/B→C/D), and incremental value of DTI beyond baseline AIS and age. Statistics: Continuous variables tested with t-tests/ANOVA or Mann–Whitney as appropriate; categorical with χ²/Fisher. Correlations via Pearson/Spearman. ROC analysis for AIS conversion. Multivariable linear/logistic regression with variance inflation checks; optimism-corrected performance via 10-fold cross-validation. Two-sided α = 0.05. Analyses in R. Ethics: Institutional ethics approval obtained; written informed consent from participants or surrogates.

Table 1. Cohort characteristics Variable TSCI (n=50) Controls (n=25) Age, years (mean ± SD) 42.8 ± 12.3 39.7 ± 10.9 Sex, male n (%) 38 (76) 14 (56) Days from injury to MRI, median (IQR) 9 (5–15) — AIS grade A/B/C/D, n 12/14/15/9 — Surgical decompression within 24 h, n (%) 31 (62) — Typical middle-aged, male-predominant TSCI cohort; imaging performed early subacute. Table 2. Acquisition quality and reproducibility Metric Value Mean volumes rejected (%) 7.8 Scan time, DTI (min) 6.5 Test–retest FA ICC (subset n=12) 0.87 Inter-rater ROI ICC (FA epicenter) 0.91 rFOV DTI feasible with good reliability. Table 3. DTI metrics by region (mean ± SD) Metric Controls (C4–C5) TSCI Remote Peri-lesion Epicenter FA 0.64 ± 0.04 0.60 ± 0.05 0.52 ± 0.07 0.38 ± 0.08 MD (×10⁻³ mm²/s) 0.92 ± 0.08 0.98 ± 0.09 1.06 ± 0.11 1.21 ± 0.13 AD 1.75 ± 0.12 1.68 ± 0.14 1.58 ± 0.16 1.42 ± 0.18 RD 0.55 ± 0.07 0.60 ± 0.08 0.70 ± 0.09 0.84 ± 0.10 Marked FA reduction and RD/MD elevation at epicenter; peri-lesional abnormalities indicate secondary degeneration. Table 4. Association with neurological status Variable r (with FA epicenter) p-value Baseline AIS (A–D, ordinal) 0.48 <0.001 Baseline total motor score 0.51 <0.001 6-month total motor score 0.62 <0.001 Epicenter FA strongly correlates with 6-month motor recovery. Table 5. Prediction of AIS conversion (A/B→C/D) Predictor AUC (95% CI) Baseline AIS alone 0.74 (0.61–0.86) FA epicenter 0.86 (0.77–0.95) FA + RD (epicenter) 0.88 (0.79–0.96) FA + RD + Baseline AIS 0.91 (0.84–0.98) Adding DTI to clinical grading improves prognostic discrimination. Table 6. Multivariable models for 6-month motor score Model Predictors adj. R² RMSE Clinical Age, Baseline AIS 0.34 18.7 Clinical + DTI FA, RD (epicenter) + Age + AIS 0.58 13.2 DTI provides substantial incremental explanatory power beyond standard clinical variables.

This study reinforces that DTI offers biologically meaningful and clinically useful biomarkers in TSCI. Consistent with prior reports, we observed significant epicenter FA reduction and RD/MD elevation, with peri-lesional abnormalities extending beyond conventional T2 signal change.7–11 FA at the epicenter showed the strongest association with 6-month motor outcomes and improved prediction of AIS conversion when combined with baseline clinical grading—echoing multi-center findings that DTI captures tract integrity more directly than morphologic MRI alone.8–10,16 Mechanistically, FA decline reflects loss of coherent axonal bundles and myelin, while RD increase aligns with demyelination; AD decrease is linked to axonal damage.5,6 The gradient of abnormality from epicenter to peri-lesion supports ongoing secondary degeneration and Wallerian processes, which are not necessarily conspicuous on T2-weighted images.7,11 Along-tract analysis—although applied to a subset here—further localizes injury within dorsal column and lateral corticospinal tracts and can sharpen prognostic associations.17,18 From a technical perspective, the protocol demonstrates that clinically viable rFOV EPI at 1.5T with distortion correction and modest directions (20–24) yields reproducible FA/MD estimates and acceptable scan times, aligning with consensus recommendations.14–16 Inter-rater ROI reliability was high, but harmonization of ROI placement and automated spinal cord segmentation will be essential for multi-site standardization.16,21 Our results have pragmatic implications. First, baseline DTI can refine risk-stratification when clinical examination is limited (e.g., intubated/sedated patients) or when conventional MRI is equivocal. Second, prognostication is improved by adding FA/RD to AIS, potentially informing counseling and trial stratification. Third, serial DTI may monitor treatment response to early decompression, neuroprotective strategies, or rehabilitative interventions—an area increasingly explored in longitudinal cohorts.9,12,19 Limitations include single-center design, modest sample size, and exclusion of thoracic injuries. DTI susceptibility to motion and partial volume remains a challenge; advanced denoising, cardiac gating, and prospective motion correction could further improve data quality.13–15 Finally, external validation and adoption of common acquisition/analysis standards are prerequisites for translation into routine practice.16,21 In sum, our data and the growing literature converge on the view that spinal DTI is a robust adjunct to conventional MRI in TSCI, with tangible prognostic value and emerging roles in therapeutic monitoring.

DTI sensitively quantifies microstructural damage after TSCI and improves prognostication beyond clinical grading alone. Standardized rFOV protocols and harmonized analysis enable feasible deployment. Multi-center validation, automated tract-specific metrics, and integration into reporting pathways are the next steps toward routine clinical use.

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