Murthy, Nikhil K.

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.

OBJECTIVE Neurolymphomatosis (NL) is a rare manifestation of lymphoma confined to the peripheral nervous system that is poorly understood. It can be found in the cauda equina, but extraspinal disease can be underappreciated. The authors describe how extraspinal NL progresses to the cauda equina by perineural spread and the implications of this on timely and safe diagnostic options. METHODS The authors used the Mayo Clinic medical records database to find cases of cauda equina NL with sufficient imaging to characterize the lumbosacral plexus diagnosed from tissue biopsy. Demographics (sex, age), clinical data (initial symptoms, cerebrospinal fluid, evidence of CNS involvement, biopsy location, primary or secondary disease), and imaging findings were reviewed. RESULTS Ten patients met inclusion and exclusion criteria, and only 2 of 10 patients presented with cauda equina symptoms at the time of biopsy, with 1 patient undergoing a cauda equina biopsy. Eight patients were diagnosed with diffuse large B-cell lymphoma, 1 with low-grade B-cell lymphoma, and 1 with mantle cell lymphoma. Isolated spinal nerve involvement was identified in 5 of 10 cases, providing compelling evidence regarding the pathophysiology of NL. The conus medullaris was not radiologically involved in any case. Lumbosacral plexus MRI was able to identify extraspinal disease and offered diagnostically useful biopsy targets. FDG PET/CT was relatively insensitive for detecting disease in the cauda equina but was helpful in identifying extraspinal NL. CONCLUSIONS The authors propose that perineural spread of extraspinal NL to infiltrate the cauda equina occurs in two phases. 1) There is proximal and distal spread along a peripheral nerve, with eventual spread to anatomically connected nerves via junction and branch points. 2) The tumor cells enter the spinal canal through corresponding neural foramina and propagate along the spinal nerves composing the cauda equina. To diffusely infiltrate the cauda equina, a third phase occurs in which tumor cells can spread circumdurally to the opposite side of the spinal canal and enter contralateral nerve roots extending proximally and distally. This spread of disease can lead to diffuse bilateral spinal nerve disease without diffuse leptomeningeal spread. Recognition of this phasic mechanism can lead to identification of safer extraspinal biopsy targets that could allow for greater functional recovery after appropriate treatment.