AbstractAlthough superior gluteal nerve (SGN) injury can have significant morbidity, to date, surgical strategies for its repair are scant in the literature. Specifically, neurotization options have not been explored. To address this deficiency in the literature, the current cadaveric feasibility study was performed. Via a transgluteal approach on 16 cadaveric sides, the proximal sciatic nerve and the entrance of the SGN into the gluteus medius and minimus were identified. Additionally, branches from the sciatic nerve to the hamstring muscles were traced proximally to confirm their position in relation to the sciatic nerve as a whole. These branches were cut at the level of the ischial tuberosity and teased away from the sciatic nerve proximally to the greater sciatic foramen and transferred superolateral to the SGN. The diameter of each nerve branch was measured as well as its available length for reaching the SGN. All branches of the sciatic nerve to the hamstring muscles arose from the anteromedial part of the nerve. The mean diameters of the branches to the semimembranosus, semitendinosus, and biceps femoris muscles were 2.1, 1.9, and 1.5 mm, respectively. The mean diameter of the SGN was 3.1 mm and the mean distance from this entrance point to the ischial spine was 7.2 cm. The mean length of the donor nerve was 8.5 cm. Based on our study, use of a tibial‐innervated hamstring branch as a donor for nerve transfer to the SGN is feasible.
Expanding the phenotypic spectrum of lipomatosis of the sciatic nerve: Early‐onset colonic diverticular disease
AbstractBackgroundLipomatosis of nerve (LN) is a complex peripheral nerve disorder characterized by fibrofatty nerve enlargement. MRI of this pathology is pathognomonic and obviates a diagnostic biopsy. Mutation in PIK3CA has been associated with LN cases with nerve‐territory overgrowth which may occur in some cases. We evaluate an association of LN of the sciatic nerve and early‐onset colonic diverticular disease and discuss the potential pathogenesis.MethodsOur institutional database was searched for LN cases. Available information of identified cases was reviewed, and cases with a confirmed diagnosis of LN affecting the lumbosacral plexus and/or sciatic nerve; available MRI of the affected nerve(s); and diverticular disease occurring in the area supplied by the nerve(s) affected by LN were further analyzed. PIK3CA mutation testing was performed on available tissue samples.ResultsWe identified 10 LN cases of lumbosacral plexus and/or sciatic nerve. Of these, three fulfilled our inclusion criteria. All three patients had concomitant colonic diverticular disease, diagnosed at a relatively young age. MRI studies of these cases showed LN involvement of the sacral nerves innervating the sigmoid colon. All three also had abnormal diagnostic workup including various GI tests and evidence of associated nerve‐territory overgrowth. Colonic tissue samples for PIK3CA mutation were negative.ConclusionWhile the pathogenesis of the colonic diverticular disease is increasingly recognized as being multifactorial, our observations are consistent with the potential role of autonomic nervous system dysfunction affecting either the pelvic floor musculature, or the colon itself (or both) in a subset of patients with early‐onset diverticular disease.
Proposed surgical technique to facilitate targeted reinnervation of the infraspinatus: A cadaveric feasibility study