Demyelination secondary to chronic nerve compression injury alters Schmidt–Lanterman incisures

Abstract The role of Schmidt–Lanterman incisures (SLIs) within the myelin sheath remains the subject of much debate. Previous studies have shown a positive correlation between the number of SLIs per internode and internodal width for both normal and pathological myelin internodes. As chronic nerve compression (CNC) injury induces demyelination, we sought to evaluate if CNC injury altered the occurrence of SLIs using nerve‐teasing techniques and light microscopy. Rigorous examination of the teased axons from nerves subjected to CNC injury for 1 month, 2 months or 8 months revealed that there is indeed a positive correlation between the number of SLIs per internode and the internodal width. However, unlike previous studies, the degree of positive correlation between these two parameters was greater in the internodes that had undergone remyelination in response to CNC injury as compared with the internodes from control nerves. These findings support the theory that SLIs are likely to assist in the metabolic processes of the myelin sheath, including growth and maintenance of the myelin sheath.