Introduction. When using the double interval slide technique for arthroscopic repair of chronic large or massive rotator cuff tears, the posterior interval release is directed toward the scapular spine until the fat pad that protects the suprascapular nerve is reached. Injury to the suprascapular nerve can occur due to the nerve's proximity to the operative field. This study aimed to identify safe margins for avoiding injury to the suprascapular nerve. Materials and Methods. For 20 shoulders in ten cadavers, the distance was measured from the suprascapular notch to the glenoid rim, the articular margin of the rotator cuff footprint, and the lateral border of the acromion. Results. From the suprascapular notch, the suprascapular nerve coursed an average of 3.42 cm to the glenoid rim, 5.34 cm to the articular margin of the rotator cuff footprint, and 6.09 cm to the lateral border of the acromion. Conclusions. The results of this study define a safe zone, using anatomic landmarks, to help surgeons avoid iatrogenic injury to the suprascapular nerve when employing the double interval slide technique in arthroscopic repair of the rotator cuff.

Objectives Describe the histopathology of the temporal bones in MELAS (myopathy, encephalopathy, lactic acidosis, and stroke‐like episodes) syndrome. The syndrome results from a known point mutation in mitochondrial DNA. Methods Histopathology analysis of a pair of temporal bones from the oldest surviving MELAS syndrome temporal bone donor. Histopathologic findings were correlated with known premortem clinical data. Results The inner ears showed severe but incomplete atrophy of the stria vascularis for the length of the cochleae. In contrast, the organ of Corti and inner hair cells appeared intact with some loss of outer hair cells. Other than moderate loss at the basal turn, spiral ganglion cells numbers were normal. The vestibular neuroepithelium was mostly normal with the exception of moderate degeneration of the macula sacculi and partial collapse of the saccular wall on the right. The cerebral cortex had infarct‐like lesions with adjacent gliosis. Conclusion This is an analysis of the oldest patient with MELAS syndrome to date, an addition to only two previously published patients. It supports the notion that hearing loss is a result of dysfunction of the stria vascularis and not loss of hair cells or neurons. Patterns of vestibular pathology are in agreement to in‐vivo measurements. These findings support auditory rehabilitation with cochlear implants and may be relevant to hearing loss due to other mitochondrial mutations. Level of evidence 4