Synopsis

Vascular suppression is critical to facilitate confident identification and pathologic changes of small caliber peripheral nerves, many of great clinical importance, that run alongside slow-flowing veins. In our experience, non-contrast flow suppression techniques are suboptimal for complete venous suppression. Previous studies describe the efficacy of intravenous gadolinium for vascular suppression and visualization of the plexus proper using a three-dimensional STIR pulse, but its use for visualizing small plexus branch nerves has not been reported. This study demonstrated that post-STIR imaging significantly improved vascular suppression and visualization of branch nerves compared to non-contrast techniques, with high inter- and intra-rater agreement.

Disclosures

Target Audience

Introduction

MRI plays an important role in diagnosing peripheral neuropathies.^1-4 In our experience, conventional, T2-weighted Dixon or short tau inversion recovery (STIR) techniques facilitate reliable identification of the brachial plexus proper (i.e. roots to cords). However, commonly pathologic pre-terminal and terminal branch nerves arising from the plexus can be difficult to confidently visualize due to adjacent vasculature.⁵

Previous reports describe the efficacy of intravenous gadolinium (IV-gad) for vascular suppression and visualization of the plexus proper using a three-dimensional (3-D) STIR pulse.^6,7 Our aim was to determine the utility of 3-D STIR with IV-gad (‘post-STIR’) to evaluate branch nerves and compare its efficacy to a 3-D, 2-point Dixon sequence (CUBE-Flex) with motion-sensitized driven equilibrium (MSDE), our current vascular suppression technique.⁸ We hypothesized that post-STIR imaging would optimize vascular suppression for nerve visualization.

Methods

Results

Post-STIR imaging improved vascular suppression (OR_MSDE=24.2, 95% CI: 6.9–85, p<0.001; OR_PRE=52.6, 95% CI: 8.4–329.0, p<0.001). For all nerves, post-STIR increased diagnostic confidence (OR_MSDE=17.4, 95% CI: 7.0–43.3, p<0.001; OR_PRE=5.6, 95% CI: 1.5–20.4, p=0.010). Post-STIR also improved nerve visualization (OR_MSDE=7.3, 95% CI: 2.8–18.7, p<0.001; OR_PRE=4.7, 95% CI: 1.7–12.9, p=0.003), especially for the suprascapular nerve distal segment (OR_MSDE=14.8, 95% CI: 3.4–65.3, p<0.001; OR_PRE =23.2, CI: 4.5–121.2, p<0.001).

Inter-rater agreement for vascular suppression was almost perfect (AC_MSDE=1, AC_PRE=0.92, AC_POST=0.9) and for nerve visualization and diagnostic confidence moderate to almost perfect in the post-STIR group (AC: 0.41–1.0). Intra-rater agreement for all criteria post-STIR was similarly high (AC: 0.72–1). Mean scan time was comparable among all sequences.

Discussion

Post-STIR imaging significantly improved vascular suppression and particularly signal arising from small caliber, slow-flowing veins. Post-STIR imaging also improved visualization of all nerves compared to MSDE and pre-STIR, with high inter- and intra-rater agreement. The most dramatic post-STIR effect was improved visualization of the distal segment of the suprascapular nerve, which innervates critical rotator cuff muscles (supraspinatus, infraspinatus) and is commonly involved in inflammatory and traumatic neuropathies.

STIR employs a recovery pulse with short inversion time (TI ~180-220 ms at 3.0T) to suppress fat at its null point. IV-gad causes shortening of blood’s T1 signal as it approaches the T1 of fat, allowing it to be simultaneously suppressed with the IR pulse (Fig. 1). In our experience, maximal vascular suppression occurs ~6-8 min. following IV-gad, and thus T1-weighted imaging can be obtained with the same contrast bolus.

Limitations of this study include variance in fat suppression techniques (STIR vs. Dixon) and acquired spatial resolution of MSDE and STIR, although our goal was to compare with our standard of care MSDE sequence. Strengths include the application of a clinical cohort, all scanned with the same magnet and surface coils.

We have since adopted post-STIR imaging in our plexus protocol for select clinical pathologies. In particular, we have found the technique helpful in identifying intrinsic nerve constrictions (Figs. 2-3), a hallmark pathologic finding in neuralgic amyotrophy, which is a syndrome that causes severe weakness in otherwise healthy individuals.^9,10

Acknowledgements

References

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