Pathogenesis of rapidly reversible compressive neuropathy: revisiting the classic sphygmomanometer experiment

Using the sequential inflation of 2 sphygmomanometers, Lewis et al. (Heart 16:1-32, 1931) concluded that compressive neuropathy was secondary to ischemia of the compressed nerve segment. Despite subsequent animal studies demonstrating that compressive lesions are more likely the result of mechanical nerve deformation, disagreement remains as to the etiology of rapidly reversible compressive neuropathy. Our hypothesis is that, during the classic sphygmomanometer experiments, the areas of nerve compression at the cuff margins overlapped, so that a region of transient nerve deformation persisted during the second cuff inflation. If true, the original results by Lewis et al. would be consistent with a mechanical pathogenesis.

In our study, 6 patients underwent sequential upper extremity dual-sphygmomanometer inflation with serial assessment by grip-dynamometer and 2-point discrimination. The order of cuff inflation, as well as the distance between cuffs, was varied. Mean grip force and 2-point discrimination values were statistically compared between conditions.

Patients with overlapping cuffs maintained their neurological deficits, whereas those with separated cuffs experienced an improvement in both grip force (P = 0.02) and 2-point discrimination (P < 0.001) when cuff inflation was switched.

Rapidly reversible compressive neuropathy seems to be secondary to mechanical nerve deformation at the margins of the compressive force rather than the result of ischemia of the compressed nerve segment. Overlap of the mechanically deformed nerve segments likely explains why neurological deficits persisted despite sequential cuff inflation in the classic experiments by Lewis et al.