Human Studies

Pain is the primary symptom of chronic pancreatitis (CP), but methods for sensory testing and pain characterization have not previously been validated for clinical use. We present a clinically feasible method for the assessment and characterization of pain mechanisms in patients with CP based on quantitative sensory testing (QST).

The trigeminal nerve (TGN) is the largest cranial nerve and can be involved in multiple inflammatory, compressive, ischemic or other pathologies. Currently, imaging-based approaches to identify the TGN mostly rely on T2-weighted magnetic resonance imaging (MRI), which provides localization of the cisternal portion of the TGN where the contrast between nerve and cerebrospinal fluid (CSF) is high enough to allow differentiation. The course of the TGN within the brainstem as well as anterior to the cisternal portion, however, is more difficult to display on traditional imaging sequences. An advanced imaging technique, diffusion MRI (dMRI), enables tracking of the trajectory of TGN fibers and has the potential to visualize anatomical regions of the TGN not seen on T2-weighted imaging. This may allow a more comprehensive assessment of the nerve in the context of pathology. To date, most work in TGN tracking has used clinical dMRI acquisitions with a b-value of 1000 s/mm and conventional diffusion tensor MRI (DTI) tractography methods. Though higher b-value acquisitions and multi-tensor tractography methods are known to be beneficial for tracking brain white matter fiber tracts, there have been no studies conducted to evaluate the performance of these advanced approaches on nerve tracking of the TGN, in particular on tracking different anatomical regions of the TGN.

Diabetic neuropathy (DPN) is one of the most severe and yet most poorly understood complications of diabetes mellitus. imaging of dorsal root ganglia (DRG), a key structure for the understanding of DPN, has been restricted to animal studies. These have shown a correlation of decreased DRG volume with neuropathic symptom severity. Our objective was to investigate correlations of DRG morphology and signal characteristics at 3 Tesla (3T) magnetic resonance neurography (MRN) with clinical and serological data in diabetic patients with and without DPN. In this cross-sectional study, participants underwent 3T MRN of both L5 DRG using an isotropic 3D T2-weighted, fat-suppressed sequence with subsequent segmentation of DRG volume and analysis of normalized signal properties. Overall, 55 diabetes patients (66 ± 9 years; 32 men; 30 with DPN) took part in this study. DRG volume was smaller in patients with severe DPN when compared to patients with mild or moderate DPN (134.7 ± 21.86 vs 170.1 ± 49.22; = 0.040). In DPN patients, DRG volume was negatively correlated with the neuropathy disability score ( = -0.43; 95%CI = -0.66 to -0.14; = 0.02), a measure of neuropathy severity. DRG volume showed negative correlations with triglycerides ( = -0.40; 95%CI = -0.57 to -0.19; = 0.006), and LDL cholesterol ( = -0.33; 95%CI = -0.51 to -0.11; = 0.04). There was a strong positive correlation of normalized MR signal intensity (SI) with the neuropathy symptom score in the subgroup of patients with painful DPN ( = 0.80; 95%CI = 0.46 to 0.93; = 0.005). DRG SI was positively correlated with HbA1c levels ( = 0.30; 95%CI = 0.09 to 0.50; = 0.03) and the triglyceride/HDL ratio ( = 0.40; 95%CI = 0.19 to 0.57; = 0.007). In this first study, we found DRG morphological degeneration and signal increase in correlation with neuropathy severity. This elucidates the potential importance of MR-based DRG assessments in studying structural and functional changes in DPN.

Post-herpetic neuralgia (PHN) is a common herpes zoster (HZ) complication, where pain persists 90 days after the initial HZ diagnosis. Evaluating PHN risk is essential for determining the burden on patients and health-care systems, but research shows variable estimates. The extent to which these differences are related to the assessment method has not been examined. The purpose of this study is to compare the proportion of PHN among HZ patients measured by medical chart review and self-report surveys.

Small fiber polyneuropathy (SFN) involves ectopic firing and degeneration of small-diameter, somatic/autonomic peripheral axons. Causes include diabetes, inflammation and rare pathogenic mutations, including in genes that encode small fiber sodium channels.