Ultrasound and Magnetic Resonance Imaging in Evaluating the Peripheral Nerves in Patients with Clinically Detected Leprosy Having Peripheral Neuropathy

Introduction:

Hansen's disease remains a leading treatable cause of peripheral neuropathy in endemic regions, with nerve damage often persisting despite bacteriological cure due to under-recognized peripheral neuritis. Clinical palpation and electrodiagnostic testing have limited sensitivity and reproducibility, whereas high-resolution ultrasonography (HRUS) and MRI/MR neurography enable direct visualization of nerve morphology, thickening, and inflammation. This study examines the spectrum of nerve alterations detected by HRUS and MRI in patients with clinically established leprosy and compares the diagnostic utility of the two modalities in assessing nerve involvement.

Objective:

To describe the spectrum of peripheral-nerve alterations demonstrated by high-resolution ultrasonography (HRUS) and magnetic resonance neurography (MRN) in patients with clinically detected leprosy neuropathy, and to compare the two modalities in detecting nerve involvement.

Methods:

In this hospital-based, prospective cross-sectional observational study, 40 consecutive patients with clinically or microbiologically diagnosed leprosy and clinical evidence of peripheral neuropathy underwent HRUS (high-frequency 10–18 MHz linear probes) and 1.5-Tesla MRN of the ulnar, median and posterior tibial nerves. Cross-sectional area (CSA), echotexture, fascicular architecture, endoneural Doppler flow, T1/T2/STIR and fat-suppressed signal, post-contrast enhancement and osteofibrous tunnel compression were assessed. Data were analysed with Student’s t-test, the McNemar test, kappa statistics and receiver operating characteristic (ROC) analysis; a p-value ≤ 0.05 was considered significant.

Results:

The mean age was 39.42 ± 14.488 years with an equal sex distribution (50% female, 50% male). Lepromatous (45%) and borderline (35%) forms predominated. The ulnar and posterior tibial nerves were most frequently involved (35% each), followed by the median nerve (30%). Mean CSA was 20.58 ± 5.272 mm² for the ulnar, 19.73 ± 4.788 mm² for the posterior tibial and 17.18 ± 4.557 mm² for the median nerve. HRUS commonly demonstrated loss of fascicular architecture and heterogeneous echotexture, while MRN showed T2/STIR hyperintensity, nerve enlargement and post-contrast enhancement. HRUS and MRN detected nerve compression at comparable rates (McNemar p = 0.167–0.815) but agreement was only slight to poor (κ = −0.133 to 0.093). Posterior tibial CSA was significantly higher in patients without a history of reversal reaction (21.25 vs 18.2 mm²; p = 0.042). ROC analysis showed fair discrimination of CSA for MRI-detected compression (median AUC 0.701, p = 0.019; ulnar AUC 0.682, p = 0.042).

Conclusion:

HRUS is an effective, accessible screening tool for detecting structural nerve changes, whereas MRN provides additional information on neuritis and deep-nerve involvement. The two modalities are complementary rather than interchangeable, and their combined use improves diagnostic accuracy in leprosy-related neuropathy.