Clinical Features of Conduction Block in Ulnar Neuropathy at the Elbow: Surgery of the Ulnar Nerve Multicenter Clinical Trial.

BACKGROUND

In ulnar neuropathy at the elbow, weakness is classically a sign of severe disease. Weakness is associated with motor axonal loss as measured by decreased distal compound muscle action potential (CMAP) amplitude. Conduction block, a demyelinating phenomenon that recovers readily, can also cause weakness, creating ambiguity for the treating clinician.

METHODS

This cross-sectional study evaluated baseline blinded data collected from 2020 through 2023 from the Surgery of the Ulnar Nerve randomized controlled trial comparing in situ decompression versus transposition procedures. Adult patients underwent electrodiagnostic testing and clinical motor and sensory testing, and completed the Michigan Hand Questionnaire and Carpal Tunnel Questionnaire.

RESULTS

A total of 177 patients were categorized into 3 distinct groups based on normal distal CMAP amplitudes (77 patients), presence of conduction block with or without distal CMAP amplitude loss (37 patients), or pure axonal loss with distal CMAP amplitude loss in the absence of conduction block (63 patients). Compared with the normal group, patients with conduction block had significantly decreased pinch strength and worse function domain scores on the Michigan Hand Questionnaire and Carpal Tunnel Questionnaire, but shorter duration of disease. Patients with pure axonal loss had decreased pinch strength, worse 2-point discrimination, and worse overall, function, and aesthetics domain scores on the Michigan Hand Questionnaire. There was a significant interaction between the effects of conduction block and distal CMAP amplitude on pinch strength, indicating that higher degrees of conduction block resulted in more pronounced loss of pinch strength in patients with relatively preserved distal CMAP amplitude.

CONCLUSION

These findings support the paradigm that ulnar neuropathy at the elbow presenting with conduction block represents a distinct and intermediate pathophysiology, distinguished by quicker onset with less advanced neurologic deficits.

CLINICAL QUESTION/LEVEL OF EVIDENCE: Risk, II.