{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,23]],"date-time":"2026-01-23T08:11:02Z","timestamp":1769155862792,"version":"3.49.0"},"reference-count":36,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2012,1,12]],"date-time":"2012-01-12T00:00:00Z","timestamp":1326326400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Muscle and Nerve"],"published-print":{"date-parts":[[2012,2]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Introduction: Myelinating Schwann cells compartmentalize their outermost layer to form actin\u2010rich channels known as Cajal bands. Herein we investigate changes in Schwann cell architecture and cytoplasmic morphology in a novel mouse model of carpal tunnel syndrome. Methods: Chronic nerve compression (CNC) injury was created in wild\u2010type and slow\u2010Wallerian degeneration (<jats:italic>Wld<\/jats:italic><jats:sup><jats:italic>S<\/jats:italic><\/jats:sup>) mice. Over 12 weeks, nerves were electrodiagnostically assessed, and Schwann cell morphology was thoroughly evaluated. Results: A decline in nerve conduction velocity and increase in g\u2010ratio is observed without early axonal damage. Schwann cells display shortened internodal lengths and severely disrupted Cajal bands. Quite surprisingly, the latter is reconstituted without improvements to nerve conduction velocity. Conclusions: Chronic entrapment injuries like carpal tunnel syndrome are primarily mediated by the Schwann cell response, where decreases in internodal length and myelin thickness disrupt the efficiency of impulse propagation. Restitution of Cajal bands is not sufficient for remyelination after CNC injury. 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