scholarly journals Underlying histopathology of peripheral nerve injury and the classical nerve repair techniques

2019 ◽  
pp. 17-22
Author(s):  
Marin Andrei ◽  
Mihai Ruxandra Ioana ◽  
Enescu Dan Mircea

A much-debated subject in the last 20 years, the recovery after peripheral nerve injury still remains one of the most researched themes of our days. Although the central nervous system has not exhibited any ground-breaking discoveries in matters of healing through surgical procedures, this is not the case for the peripheral nervous system (PNS). The PNS recovery after injury has improved over the years so we now speak of time and percentage of rehabilitation. The increased interest for this subject is a result in the development of the medical technique, that allowed the creation of new molecules capable to improve the regeneration rate. Furthermore, the evolution in diagnostic parameters, as well as the possibility of a thorough follow-up, contributed to the ascending research of this field.  One must not forget that all experimental studies have as endpoint obtaining safe and reproducible solutions which can be applied in treating patients with peripheral nerve injury. We will briefly present the microscopic events that occur following a peripheral nerve injury, the key factors which influence their regeneration as well as the classical techniques used to repair them. However, the most intriguing topic in nerve regeneration is not related to the surgical procedure (considered to be the Gold Standard in whole nerve injury), but rather the helping substances that facilitate a faster and better recovery.

2016 ◽  
Vol 2016 ◽  
pp. 1-18 ◽  
Author(s):  
Kulraj Singh Bhangra ◽  
Francesca Busuttil ◽  
James B. Phillips ◽  
Ahad A. Rahim

Peripheral nerve injury continues to pose a clinical hurdle despite its frequency and advances in treatment. Unlike the central nervous system, neurons of the peripheral nervous system have a greater ability to regenerate. However, due to a number of confounding factors, this is often both incomplete and inadequate. The lack of supportive Schwann cells or their inability to maintain a regenerative phenotype is a major factor. Advances in nervous system tissue engineering technology have led to efforts to build Schwann cell scaffolds to overcome this and enhance the regenerative capacity of neurons following injury. Stem cells that can differentiate along a neural lineage represent an essential resource and starting material for this process. In this review, we discuss the different stem cell types that are showing promise for nervous system tissue engineering in the context of peripheral nerve injury. We also discuss some of the biological, practical, ethical, and commercial considerations in using these different stem cells for future clinical application.


2002 ◽  
Vol 87 (4) ◽  
pp. 1763-1771 ◽  
Author(s):  
Antoni Valero-Cabré ◽  
Xavier Navarro

We investigated the changes induced in crossed extensor reflex responses after peripheral nerve injury and repair in the rat. Adults rats were submitted to non repaired sciatic nerve crush (CRH, n = 9), section repaired by either aligned epineurial suture (CS, n = 11) or silicone tube (SIL4, n = 13), and 8 mm resection repaired by tubulization (SIL8, n = 12). To assess reinnervation, the sciatic nerve was stimulated proximal to the injury site, and the evoked compound muscle action potential (M and H waves) from tibialis anterior and plantar muscles and nerve action potential (CNAP) from the tibial nerve and the 4th digital nerve were recorded at monthly intervals for 3 mo postoperation. Nociceptive reinnervation to the hindpaw was also assessed by plantar algesimetry. Crossed extensor reflexes were evoked by stimulation of the tibial nerve at the ankle and recorded from the contralateral tibialis anterior muscle. Reinnervation of the hindpaw increased progressively with time during the 3 mo after lesion. The degree of muscle and sensory target reinnervation was dependent on the severity of the injury and the nerve gap created. The crossed extensor reflex consisted of three bursts of activity (C1, C2, and C3) of gradually longer latency, lower amplitude, and higher threshold in control rats. During follow-up after sciatic nerve injury, all animals in the operated groups showed recovery of components C1 and C2 and of the reflex H wave, whereas component C3 was detected in a significantly lower proportion of animals in groups with tube repair. The maximal amplitude of components C1 and C2 recovered to values higher than preoperative values, reaching final levels between 150 and 245% at the end of the follow-up in groups CRH, CS, and SIL4. When reflex amplitude was normalized by the CNAP amplitude of the regenerated tibial nerve, components C1 (300–400%) and C2 (150–350%) showed highly increased responses, while C3 was similar to baseline levels. In conclusion, reflexes mediated by myelinated sensory afferents showed, after nerve injuries, a higher degree of facilitation than those mediated by unmyelinated fibers. These changes tended to decline toward baseline values with progressive reinnervation but still remained significant 3 mo after injury.


2019 ◽  
Vol 20 (1) ◽  
pp. 33-37 ◽  
Author(s):  
Marzia Malcangio

AbstractBackgroundAcute pain is a warning mechanism that exists to prevent tissue damage, however pain can outlast its protective purpose and persist beyond injury, becoming chronic. Chronic Pain is maladaptive and needs addressing as available medicines are only partially effective and cause severe side effects. There are profound differences between acute and chronic pain. Dramatic changes occur in both peripheral and central pathways resulting in the pain system being sensitised, thereby leading to exaggerated responses to noxious stimuli (hyperalgesia) and responses to non-noxious stimuli (allodynia).Critical role for immune system cells in chronic painPreclinical models of neuropathic pain provide evidence for a critical mechanistic role for immune cells in the chronicity of pain. Importantly, human imaging studies are consistent with preclinical findings, with glial activation evident in the brain of patients experiencing chronic pain. Indeed, immune cells are no longer considered to be passive bystanders in the nervous system; a consensus is emerging that, through their communication with neurons, they can both propagate and maintain disease states, including neuropathic pain. The focus of this review is on the plastic changes that occur under neuropathic pain conditions at the site of nerve injury, the dorsal root ganglia (DRG) and the dorsal horn of the spinal cord. At these sites both endothelial damage and increased neuronal activity result in recruitment of monocytes/macrophages (peripherally) and activation of microglia (centrally), which release mediators that lead to sensitisation of neurons thereby enabling positive feedback that sustains chronic pain.Immune system reactions to peripheral nerve injuriesAt the site of peripheral nerve injury following chemotherapy treatment for cancer for example, the occurrence of endothelial activation results in recruitment of CX3C chemokine receptor 1 (CX3CR1)-expressing monocytes/macrophages, which sensitise nociceptive neurons through the release of reactive oxygen species (ROS) that activate transient receptor potential ankyrin 1 (TRPA1) channels to evoke a pain response. In the DRG, neuro-immune cross talk following peripheral nerve injury is accomplished through the release of extracellular vesicles by neurons, which are engulfed by nearby macrophages. These vesicles deliver several determinants including microRNAs (miRs), with the potential to afford long-term alterations in macrophages that impact pain mechanisms. On one hand the delivery of neuron-derived miR-21 to macrophages for example, polarises these cells towards a pro-inflammatory/pro-nociceptive phenotype; on the other hand, silencing miR-21 expression in sensory neurons prevents both development of neuropathic allodynia and recruitment of macrophages in the DRG.Immune system mechanisms in the central nervous systemIn the dorsal horn of the spinal cord, growing evidence over the last two decades has delineated signalling pathways that mediate neuron-microglia communication such as P2X4/BDNF/GABAA, P2X7/Cathepsin S/Fractalkine/CX3CR1, and CSF-1/CSF-1R/DAP12 pathway-dependent mechanisms.Conclusions and implicationsDefinition of the modalities by which neuron and immune cells communicate at different locations of the pain pathway under neuropathic pain states constitutes innovative biology that takes the pain field in a different direction and provides opportunities for novel approaches for the treatment of chronic pain.


RSC Advances ◽  
2019 ◽  
Vol 9 (49) ◽  
pp. 28627-28635 ◽  
Author(s):  
Zhiqiang Huang ◽  
Zhenzhao Guo ◽  
Manman Sun ◽  
Shaomao Fang ◽  
Hong Li

Electrical stimulation (ES) provides an effective alternative to peripheral nerve repair via conductive scaffolds.


Hand Surgery ◽  
2002 ◽  
Vol 07 (01) ◽  
pp. 83-100 ◽  
Author(s):  
Judith A. Bell Krotoski

Any restoration of hand function following tendon and nerve injury has to include the repair or replacement of the hand's ability to perform a great many tasks. It is hard at first to appreciate fully the loss that occurs with flexor tendon injury. With loss of flexor tendons operating at the fingers or thumb, they cannot be fully closed and the hand is impaired for grasp and release as it interfaces with objects. But, sensibility can also be compromised from tendon injury even without direct injury to nerve, as object recognition in the absence of vision requires finger movement. When peripheral nerve injury is combined with flexor tendon injury, sensibility is directly impaired. There is a loss in the sense of finger or thumb position, pain, temperature, and touch/pressure recognition, in addition to the tendon injury.


2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Yongsong Guo ◽  
Ke Zhu ◽  
Jing Guo ◽  
Yongbing Kuang ◽  
Zhihui Zhao ◽  
...  

The electric shock has been proposed as one of the new needling sensations in recent years. In acupuncture sensation scales, the electric shock is included by ASS and SNQS, but not SASS, MASS, and C-MMASS. Some scholars argue that the electric shock is a normal needling sensation, but some researchers do not agree with this view. This problem has not been resolved due to a lack of evidence from basic research. Literature and research point out that the electric shock is caused by inserting a needle into the nerve directly. A question of considerable scientific and practical interest is whether the electric shock should be a normal needling sensation. In this article, we review the historical documentation of the needling sensation and the process of formulating and improving acupuncture sensation scales to suggest that the electric shock may not be a normal needling sensation. Secondly, we collected and analyzed cases of nerve injury caused by acupuncture accompanied by the electric shock and why acupuncture caused the electric shock without nerve injury. It suggests that there may be a correlation between the electric shock and peripheral nerve injury, and acupuncture manipulation is an essential factor in adverse acupuncture events. Finally, we put forward that the electric shock during acupuncture is a warning sign that the peripheral nerve may be injured, rather than a normal needling sensation. In the future, we hope to have experimental studies on the mechanism of the electric shock or observational studies on the correlation between the electric shock and peripheral nerve injury to verify.


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