Initial evaluation of nerve compression involves determining longevity and severity of symptoms prior to proceeding down a treatment path. The surgeon must differentiate whether the presenting condition involves a transient onset of symptoms affecting a normal nerve, in which case relief of the compression should allow return to a normal physiologic state; or a nerve with an altered physiology resulting from a slowly developing subclinical, and possibly intermittent, chronic compression, that has a lower threshold of tolerance for nonphysiologic pressure changes. The latter nerve may return to its baseline condition once the offending agent is removed, yet remain physiologically abnormal and susceptible to subsequent pressure changes. A third category involves nerves in a symptomatic state of static chronic compression. Thus, the clinical question arises: Should a nerve with new-onset symptoms undergo surgical decompression acutely, or should it be allowed a trial of nonoperative treatment such as bracing, anti-inflammatory medications, and injections?

The study by Jung et al. has attempted to shed light on this clinical question involving chronic compression by means of a laboratory animal model. The authors conducted an elegant study investigating neurovascular changes utilizing a previously published murine model of chronic nerve compression, comparing the effects of early surgical decompression (at two weeks) and late decompression (at six weeks). They demonstrated an injury response within the nerve after the time of compression. Interestingly, they identified evidence of irreversible physiologic changes seen after late decompression but not after early decompression at two weeks. This study demonstrates that decompression of an otherwise physiologically normal nerve can return the nerve to its previous normal physiologic state if performed within a certain early time period.