See Morrow and Reilly (doi:) for a scientific commentary on this article.Transthyretin familial amyloid polyneuropathy is a rare, autosomal-dominant multisystem disorder. Kollmer et al. show that high-resolution MR-neurography can quantify and localize lower limb nerve injury in vivo, both in symptomatic patients and in asymptomatic mutation carriers. Lesions appear at thigh-level and are predominantly proximal, although symptoms start and prevail distally.

ObjectiveThe aim of this work was to localize and quantify alterations of nerve microstructure in diabetic polyneuropathy (DPN) by magnetic resonance (MR) neurography with large anatomical coverage.MethodsPatients (N = 25) with mild‐to‐moderate (Neuropathy‐Symptom‐Score [NSS]/Neuropathy Deficit Score [NDS] 3.8 ± 0.3/2.6 ± 0.5) and patients (n = 10) with severe DPN (6.2 ± 0.6/7.4 ± 0.5) were compared to patients (n = 15) with diabetes but no DPN and to age‐/sex‐matched nondiabetic controls (n = 25). All subjects underwent MR neurography with large spatial coverage and high resolution from spinal nerve to ankle level: four slabs per leg, each with 35 axial slices (T2‐ and proton‐density–weighted two dimensional turbo‐spin‐echo sequences; voxel size: 0.4 × 0.3 × 3.5 mm3) and a three‐dimensional T2‐weighted sequence to cover spinal nerves and plexus. Nerve segmentation was performed on a total of 280 slices per subject. Nerve lesion voxels were determined independently from operator input by statistical classification against the nondiabetic cohort. At the site with highest lesion‐voxel burden, signal quantification was performed by calculating nerve proton spin density and T2 relaxation time.ResultsTotal burden of nerve lesion voxels was significantly increased in DPN (p = 0.003) with strong spatial predominance at thigh level, where average lesion voxel load was significantly higher in severe (57 ± 18.4; p = 0.0022) and in mild‐to‐moderate DPN (35 ± 4.0; p < 0.001) than in controls (18 ± 3.6). Signal quantification at the site of predominant lesion burden (thigh) revealed a significant increase of nerve proton spin density in severe (360 ± 22.9; p = 0.043) and in mild‐to‐moderate DPN (365 ± 15.2; p = 0.001) versus controls (288 ± 13.4), but not of T2 relaxation time (p = 0.49). Nerve proton spin density predicted severity of DPN with an odds ratio of 2.9 (95% confidence interval: 2.4–3.5; p < 0.001) per 100 proton spins.InterpretationIn DPN, the predominant site of microstructural nerve alteration is at the thigh level with a strong proximal‐to‐distal gradient. Nerve proton spin density at the thigh level is a novel quantitative imaging biomarker of early DPN and increases with neuropathy severity. Ann Neurol 2015;78:939–948

For novice trainees, in-class didactic teaching enables significantly better recognition of the pCLE features of Barrett's esophagus than self-directed teaching. The in-class didactic group had a shorter learning curve and were able to achieve 90 % accuracy for their high confidence predictions.

Using a standardized educational tool, the accuracy of distinguishing adenomatous versus hyperplastic colon polyps using NBI between the in-class teaching and self-directed learning were similar. This suggests that both training methods can be utilized for the education of medical trainees in the use of NICE criteria.