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Barriers to Epineural Scarring: Role in Treatment of Traumatic Nerve Injury and Chronic Compressive Neuropathy.

ABSTRACT: The physiological limitations of neural regeneration make peripheral nerve surgery challenging to both the surgeon and the patient. Presence of nerve gaps and local wound factors may all influence outcome, suggesting that barriers to reduce perineural scarring, minimize fibrosis, and avoid ischemia would be beneficial. To examine the evidence supporting their use, we reviewed the autologous and commercially-available options for barriers against scarring around a nerve. Numerous clinical case series demonstrated the effectiveness and safety of local/rotational flaps and autologous vein wrapping when used in the presence of recurrent compressive neuropathy. Translational research in animal models supports the biocompatibility of commercially available nerve wraps following nerve repair. To date, there are no reports of clinical use of commercially available nerve wraps in acute nerve repair, but a growing number of case series demonstrate their effectiveness and safety in chronic compressive neuropathy. Limited clinical evidence exists to support the efficacy of vein or flap coverage in acute nerve repairs.

SUBMITTER: Dy CJ

PROVIDER: S-EPMC5886816 | biostudies-literature | 2018 Apr

REPOSITORIES: biostudies-literature

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Barriers to Epineural Scarring: Role in Treatment of Traumatic Nerve Injury and Chronic Compressive Neuropathy.

Dy Christopher J CJ Aunins Benjamin B Brogan David M DM

The Journal of hand surgery 20180224 4

The physiological limitations of neural regeneration make peripheral nerve surgery challenging to both the surgeon and the patient. Presence of nerve gaps and local wound factors may all influence outcome, suggesting that barriers to reduce perineural scarring, minimize fibrosis, and avoid ischemia would be beneficial. To examine the evidence supporting their use, we reviewed the autologous and commercially-available options for barriers against scarring around a nerve. Numerous clinical case se ...[more]

PMID: 29482956

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Project description:PurposeThe treatment strategy is different for acute traumatic peripheral nerve injury and acute compressive neuropathy. This study aimed to compare magnetic resonance imaging (MRI) features of acute traumatic peripheral nerve injury and acute compressive neuropathy in a rat model.Materials and methodsTwenty female Sprague-Dawley rats were divided into two groups. In the crush injury group (n = 10), the unilateral sciatic nerve was crushed using forceps to represent acute traumatic peripheral nerve injury. In the compression injury group (n = 10), the unilateral sciatic nerve was ligated using silk to represent acute compressive neuropathy. The MRI of eight rats from each group were acquired on postoperative days 3 and 10. Fat-suppressed T2-weighted images were acquired. Changes in the injured nerve were divided into three grades. A Fisher's exact test was used to compare the changes in the nerves of the two groups. Histological staining and a western blot analysis were performed on one rat in each group on day 3. Neurofilament, myelin basic protein (MBP), and p75NTR staining were performed. Expression of neurofilament, MBP, p75NTR, and c-jun was evaluated by western blot analysis.ResultsMR neurography revealed substantial nerve changes in the compression injury group compared with the crush injury group at two-time points (p = 0.001 on day 3, p = 0.026 on day 10). The histopathological analysis indicated the destruction of the axon and myelin, mainly at the injury site and the distal portion of the injury in the crush injury group. It was prominent in the proximal portion, the injury site, and the distal portion of the injury in the compression injury group. The degree of axonal and myelin destruction was more pronounced in the compression injury group than in the crush injury group.ConclusionMR neurography showed prominent and long-segmental changes associated with the injured nerve in acute compressive neuropathy compared with acute traumatic peripheral nerve injury.

Project description:Traumatic axonal injury (TAI), thought to be caused by rotational acceleration of the head, is a prevalent neuropathology in traumatic brain injury (TBI). TAI in the optic nerve is a common finding in multiple blunt-force TBI models and hence a great model to study mechanisms and treatments for TAI, especially in view of the compartmentalized anatomy of the visual system. We have previously shown that the somata and the proximal, but not distal, axons of retinal ganglion cells (RGC) respond to DLK/LZK blockade after impact acceleration of the head (IA-TBI). Here, we explored the role of the sterile alpha and TIR-motif containing 1 (SARM1), the key driver of Wallerian degeneration (WD), in the progressive breakdown of distal and proximal segments of the optic nerve following IA-TBI with high-resolution morphological and classical neuropathological approaches. Wild type and Sarm1 knockout (KO) mice received IA-TBI or sham injury and were allowed to survive for 3, 7, 14, and 21 days. Ultrastructural and microscopic analyses revealed that TAI in the optic nerve is characterized by variable involvement of individual axons, ranging from apparent early disconnection of a subpopulation of axons to a range of ongoing axonal and myelin perturbations. Traumatic axonal injury resulted in the degeneration of a population of axons distal and proximal to the injury, along with retrograde death of a subpopulation of RGCs. Quantitative analyses on proximal and distal axons and RGC somata revealed that different neuronal domains exhibit differential vulnerability, with distal axon segments showing more severe degeneration compared with proximal segments and RGC somata. Importantly, we found that Sarm1 KO had a profound effect in the distal optic nerve by suppressing axonal degeneration by up to 50% in the first 2 weeks after IA-TBI, with a continued but lower effect at 3 weeks, while also suppressing microglial activation. Sarm1 KO had no evident effect on the initial traumatic disconnection and did not ameliorate the proximal optic axonopathy or the subsequent attrition of RGCs, indicating that the fate of different axonal segments in the course of TAI may depend on distinct molecular programs within axons.

Dataset Information

Barriers to Epineural Scarring: Role in Treatment of Traumatic Nerve Injury and Chronic Compressive Neuropathy.

Publications

Barriers to Epineural Scarring: Role in Treatment of Traumatic Nerve Injury and Chronic Compressive Neuropathy.

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