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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: Actins, Action Potentials, Analysis of Variance, Animals, Axons, Carpal Tunnel Syndrome, Cytoskeleton, Disease Models, Animal, Electromyography, Intercellular Signaling Peptides and Proteins, Male, Mice, Mice, Inbred C57BL, Mice, Neurologic Mutants, Myelin Sheath, Nerve Tissue Proteins, Neural Conduction, Schwann Cells, Sciatic Nerve, Statistics, Nonparametric, Time Factors.
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Does chronic nerve compression alter Schwann cell myelin architecture in a murine model? Context: Myelinating Schwann cells compartmentalize their outermost layer to form actin-rich 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. Chronic nerve compression (CNC) injury was created in wild-type and slow-Wallerian degeneration (Wld(S) ) mice. Over 12 weeks, nerves were electrodiagnostically assessed, and Schwann cell morphology was thoroughly evaluated. A decline in nerve conduction velocity and increase in g-ratio 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.
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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. Final Decision: yes