A Cadaveric Study on the Utility of the Levator Scapulae Motor Nerve as a Donor for Brachial Plexus Reconstruction

AUTHORS

Eliana B.Saltzman, Karthik Krishnan, Mark J.Winston, Soumen Das DeM, Steve K.Lee, Scott W. Wolfe

ABSTRACT

Purpose

The purpose of the study was to evaluate the utility of the levator scapulae motor nerve (LSN) as a donor nerve for brachial plexus nerve transfer. We hypothesized that the LSN could be transferred to the suprascapular nerve (SSN) or long thoracic nerve (LTN) with a reliable tension-free coaptation and appropriate donor-to-recipient axon count ratio.

Methods

Twelve brachial plexus dissections were performed on 6 adult cadavers, bilaterally. We identified the LSN, spinal accessory nerve (SAN), SSN, and LTN. Each nerve was prepared for transfer and nerve redundancies were calculated. Cross-sections of each nerve were examined histologically, and axons counted. We transferred the LSN to target first the SSN and then the LTN, in a tension-free coaptation. For reference, we transferred the distal SAN to target the SSN and LTN and compared transfer parameters.

Results

Three cadavers demonstrated 2 LSN branches supplying the levator scapulae. The axon count ratio of donor-to-recipient nerve was 1:4.0 (LSN:SSN) and 1:2.1 (LSN:LTN) for a single LSN branch and 1:3.0 (LSN:SSN) and 1:1.6 (LSN:LTN) when 2 LSN branches were available. Comparatively, the axon count ratio of donor-to-recipient nerve was 1:2.5 and 1:1.3 for the SAN to the SSN and the LTN, respectively. The mean redundancy from the LSN to the SSN and the LTN was 1.7 cm (SD, 3.1 cm) and 2.9 cm (SD, 2.8 cm), and the redundancy from the SAN to the SSN and the LTN was 4.5 (SD, 0.7 cm) and 0.75 cm (SD, 1.0 cm).

Conclusions

These data support the use of the LSN as a potential donor for direct nerve transfer to the SSN and LTN, given its adequate redundancy and size match.

Ultrastructural effects of nerve growth factor and betamethasone on nerve regeneration after experimental nerve injury

AUTHORS

Leman Sencar, Mustafa Güven, Dilek Şaker, Tuğçe Sapmaz, Abdullah Tuli, and Sait Polat

ABSTRACT

Peripheral nerve injuries (PNI) are an important health problem in the world. In this study, the effects of nerve growth factor (NGF) and betamethasone on nerve regeneration after sciatic nerve crush injury were examined by footprint analysis, electron microscopic, histomorphometric, and biochemical methods. Fifty Wistar rats were divided into five groups as intact control, experimental control, NGF, betamethasone, and NGF+betamethasone combined treatment groups. After the injury, betamethasone was subcutaneously injected into the lesion area of the treatment groups three times during the first day. NGF was subcutaneously injected into the lesion area of treatment groups for 14 days. Footprint analysis was made on 7, 14, 21, 28, and 35 days and after 6 weeks, tissue samples were obtained from all groups. In the experimental control group, there were severe degenerative changes in most of the axons and myelin sheaths of the nerve fibers. Moreover, an increase of MDA levels and a decrease in SOD activities were found in this group. On the other hand, malondialdehyde (MDA) levels decreased, superoxide dismutase (SOD) activities increased and significant motor functional recovery were found in the combined treatment group. The number of axons, axon diameters, and myelin thickness were significantly greater in the combined treatment group when compared with experimental control and other treatment groups. It was thought that nerve regenerative effects of NGF and anti-inflammatory and/or anti-edematous effects of betamethasone could induce functional recovery in the combined treatment group. In conclusion, combined therapy of NGF and betamethasone may be an effective approach for the treatment of PNI.

Ferroptosis Mediates Cuprizone-Induced Loss of Oligodendrocytes and Demyelination

AUTHORS

Priya Jhelum, Eva Santos-Nogueira, Wulin Teo, Alice Haumont, Isadora Lenoël, Peter K. Stys and Samuel David

ABSTRACT

Multiple sclerosis (MS) is a chronic demyelinating disease of the CNS. Cuprizone (CZ), a copper chelator, is widely used to study demyelination and remyelination in the CNS, in the context of MS. However, the mechanisms underlying oligodendrocyte (OL) cell loss and demyelination are not known. As copper-containing enzymes play important roles in iron homeostasis and controlling oxidative stress, we examined whether chelating copper leads to disruption of molecules involved in iron homeostasis that can trigger iron-mediated OL loss. We show that giving mice (male) CZ in the diet induces rapid loss of OL in the corpus callosum by 2 d, accompanied by expression of several markers for ferroptosis, a relatively newly described form of iron-mediated cell death. In ferroptosis, iron-mediated free radicals trigger lipid peroxidation under conditions of glutathione insufficiency, and a reduced capacity to repair lipid damage. This was further confirmed using a small-molecule inhibitor of ferroptosis that prevents CZ-induced loss of OL and demyelination, providing clear evidence of a copper-iron connection in CZ-induced neurotoxicity. This work has wider implications for disorders, such as multiple sclerosis and CNS injury.