Traumatic neuropathic pain caused by traumatic neuroma has long been bothering both doctors and patients, the mechanisms of traumatic neuropathic pain are widely discussed by researchers and the treatment is challenging. Clinical treatment of painful neuroma is unclear. Numerous treatment modalities have been introduced by experts in this field. However, there is still no single standard recognized treatment.Different forms of treatments have been tested in animals and humans, but pharmacotherapies (antidepressants, antiepileptics) remain the basis of traumatic neuropathic pain management. For intractable cases, nerve stump transpositions into a muscle, vein or bone are seen as traditional surgical procedures which provide a certain degree of efficacy. Novel surgical techniques have emerged in recent years, such as tube guided nerve capping, electrical stimulation and adipose autograft have substantially enriched the abundance of the treatment for traumatic neuropathic pain.Several treatments show advantages over the others in terms of pain relief and prevention of neuroma formation, making it difficult to pick out a single modality as the reference. An effective and standardized treatment for traumatic neuropathic pain would provide better choice for researchers and clinical workers.In this review, we summarized current knowledge on the treatment of traumatic neuropathic pain, and found a therapeutic strategy for this intractable pain. We tried to provide a useful guideline for choosing the right modality in management of traumatic neuropathic pain.
Neuropathic pain is a well‐known type of chronic pain caused by damage to the nervous system. Autophagy is involved in the development and/or progression of many diseases, including neuropathic pain. Emerging evidence suggests that metformin relieves neuropathic pain in several neuropathic pain models; however, metformin's cellular and molecular mechanism for pain relief remains unknown. In this study, we investigated the therapeutic effects of metformin on pain relief after spinal nerve ligation (SNL) and its underlying mechanism of autophagy regulation. Behavioural analysis, histological assessment, expression of c‐Fos and molecular biological changes, as well as ultrastructural features, were investigated. Our findings showed that the number of autophagosomes and expression of autophagy markers, such as LC3 and beclin1, were increased, while the autophagy substrate protein p62, as well as the ubiquitinated proteins, were accumulated in the ipsilateral spinal cord. However, metformin enhanced the expression of autophagy markers, while it abrogated the abundance of p62 and ubiquitinated proteins. Blockage of autophagy flux by chloroquine partially abolished the apoptosis inhibition and analgesic effects of metformin on SNL. Taken together, these results illustrated that metformin relieved neuropathic pain through autophagy flux stimulation and provided a new direction for metformin drug development to treat neuropathic pain.
OBJECTIVETraumatic neuromas represent a prevalent source of neuropathic pain. As of yet, there has been no single treatment method that can guarantee permanent relief of symptoms. Although nerve-capping techniques have shown promise, their exact mechanisms remain elusive. The authors’ aim was to examine the role of the RhoA/ROCK signaling pathway in the prevention of neuroma formation after neurectomy utilizing a nerve-capping technique.METHODSAn aligned nanofiber tube was fabricated to cap the sciatic nerve in Sprague Dawley rats. The rats (n = 60) were randomly divided into the aligned SF/P (LLA-CL) capping group (capping group, n = 20), the capping and Y-27632 (ROCK pathway inhibitor) intervention group (intervention group, n = 20), and the no-capping group (control group, n = 20). The authors undertook a comprehensive assessment of the capping group, examining the animals’ behavior, the extent of neuroma development, histology, gene and protein expression, and ultrastructural changes associated with the RhoA/ROCK signaling pathway. These findings were compared with those in the intervention and control groups.RESULTSThe inciting injury resulted in the expression of the RhoA/ROCK signaling pathway, as well as its further upregulation in peripheral neurons. Axon outgrowth was significantly increased when RhoA/ROCK signaling pathway was suppressed. The average autotomy score in the capping group was observed to be much lower than that of the intervention and control groups. At 30 days postneurectomy, the capping group displayed no obvious neuroma formation, while a bulbous neuroma was found in the nerve stumps of both the control and intervention groups. Quantitative real-time polymerase chain reaction and the Western blot analysis demonstrated that the expression of myelin-associated glycoprotein was substantially upregulated in the capping group; in contrast, the expression of NF-200 was significantly downregulated. The expression of myosin light chain was notably lower in the intervention group, but there was no significant difference when compared with the control group (p > 0.05).CONCLUSIONSThe RhoA/ROCK signaling pathway has emerged as a critical player in the process of traumatic neuroma formation after neurectomy. It is possible that the nerve-capping technique could generate a “regenerative brake” based on the regulation of the RhoA/ROCK signaling pathway in this event. These findings may provide concrete evidence that could help develop new strategies for the management of painful neuromas.
Background:Open release of post-traumatic elbow stiffness is effective in restoring elbow function, but there is no guideline on the optimal time point of surgical release so far. The purpose of this article was to summarize the current available literature reporting on the timing of open release of post-traumatic elbow stiffness.Methods:The PubMed, Cochrane Library, and EMBASE were searched with a set of predefined inclusion and exclusion criteria. Manual searches for references were performed to find potential relevant studies. Two authors separately extracted data from all the articles selected.Results:27 articles published between 1989 and 2017 were included with an overall enrollment of 836 patients. We divided all included studies into 3 groups according to the timing of surgical release: group 1 (6–10 months after injury), group 2 (11–20 months after injury), and group 3(>20 months after injury). The mean postoperative Mayo Elbow Performance Score (MEPS) and recurrence rate were similar among the 3 groups; however, the mean gain in arc of motion in group 1 was the highest with the lowest complication rate among the 3 groups.Conclusion:There was a trend toward a shorter waiting time from injury to open arthrolysis from 12 months to 6 months. The shorter waiting period of 6 to 10 months yielded better results. Therefore, early surgical release of stiff elbows is recommended for a shorter rehabilitation time and earlier return to work.Level of evidence: Level IV, Systematic Review.
Enchondroma, reportedly the most common primary tumor of the long bones of the hand, usually develops during the first till fourth decades of life. However, there has no consensus been reached regarding the surgical intervention timing for these patients. We aim to evaluate the optimal surgical intervention timing for the patients with fractures due to enchondromas, investigate the impact of pathological fractures on the treatment and outcomes in these patients.Medical records and X-rays of patients treated for enchondroma of the hand from 2005 to 2015 were retrospectively reviewed. We collected 148 cases in total and 92 of them had complete information including X-rays, medical records, and files of follow up.There were no significant differences in terms of consolidation time after surgery, recurrence rate, and DASH scores between the groups with and without fractures; the treatment costs were higher in the group with fractures than those without fractures; however, patients without fractures were able to resume work earlier than those with fractures.The pathological fractures associated with enchondromas have no significant impact on the treatment outcomes compared to those with simple nonfractured enchondromas. Although the cost was more expensive for patients treated primarily with pathological fractures due to enchondromas, these patients could resume their work normally much earlier than those treated by delayed surgery. Early surgical intervention is recommended for better results and no increased risks for patients with pathological fractures caused by enchondromas.
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