Objectives The purpose of this study was to provide clinical evidence of the use of contrast-enhanced sonography in detecting and quantifying changes in intraneural vascularity due to median mononeuropathy. Methods Five Macaca fascicularis monkeys were exposed to 20 weeks of repetitive work to increase their risk of developing median mononeuropathy. Contrast-enhanced sonograms were obtained in 30-second increments for 7 minutes while a contrast agent was being delivered. Data were collected immediately at the conclusion of the 20-week work exposure and then again during a recovery phase approximately 3 months after the completion of work. Quantitative analysis and trend graphs were used to analyze median nerve perfusion intensity. This study also compared the use of both manual counting of pixels and semiautomatic measurement using specialized software. Results Based on the average data, maximum intensity values were identified as the best indicators of nerve hyperemia. Paired t tests demonstrated significantly higher maximum intensities in the working stage for 4 of the 5 subjects (P < .01). Conclusions This study provides preliminary evidence that (1) in a controlled exposure model, a change in intraneural vascularity of the median nerve between working and recovery can be observed; (2) this vascular change can be measured using an objective technique that quantifies the intensity of vascularity; and (3) contrast-enhanced sonography may improve the ability to reliably capture and measure low-flow microvascularity.

A preclinical study of 15 Macaca fascicularis monkeys was conducted to determine (1) the ability of detecting median mononeuropathy (MMN) within the median nerve after a work intervention and (2) the relationship between the layers of the median nerve during an acute inflammatory process by using sonography in conjunction with magnetic resonance imaging (MRI). Cross-sectional areas (CSAs) were imaged using MRI and sonography proximal to the carpal tunnel inlet (defined by the most distal portion of the radius) and further distal into the carpal tunnel (defined by the most proximal portion of the pisiform) at the prework exposure stage. CSAs measured on the outer edge of the median nerve were obtained from both modalities, at both anatomical locations. An intermodality t test demonstrated no statistical differences between the two sets of measurements (radius, P ≤ .15; pisiform, P ≤ .46). At the postwork exposure stage, sonographic measurements were obtained on the outer and inner borders of the median nerve at both anatomical levels. A two-tailed t test showed statistically significant differences within the carpal tunnel comparing pre- and postwork CSA measurements (radius, P ≤ .01; pisiform, P ≤ .297). The epineurial layer area was then determined as the difference between outer-border and inner-border CSAs. Pearson correlations between the epineurial layer and overall median nerve CSA within the carpal tunnel demonstrated a strong positive correlation that was statistically significant ( r = 0.97; P ≤ .01) after postwork exposure. Possible factors contributing to this acute phase of MMN could be hyperemia within the layers of the nerve and the development of Renault bodies. This work would need to be translated to human studies for further confirmation of the anatomic and clinical significance of this effect.