Basic mechanisms of peripheral nerve injury and treatment via electrical stimulation

Chu, Xiao-Lei; Song, Xi-Zi; Li, Qi; Li, Yu-Ru; He, Feng; Gu, Xiao-Song; Ming, Dong

doi:10.4103/1673-5374.335823

Cited by 164Nerve injury and regenerationNerve Injury and RehabilitationNeuroscience and Neural Engineering

Basic mechanisms of peripheral nerve injury and treatment via electrical stimulation

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Chu, Xiao-Lei, Song, Xi-Zi, Li, Qi, Li, Yu-Ru, He, Feng, Gu, Xiao-Song, Ming, Dong·2022·Neural Regeneration Research

DOI 10.4103/1673-5374.335823PMC PMC9083151

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Abstract

Previous studies on the mechanisms of peripheral nerve injury (PNI) have mainly focused on the pathophysiological changes within a single injury site. However, recent studies have indicated that within the central nervous system, PNI can lead to changes in both injury sites and target organs at the cellular and molecular levels. Therefore, the basic mechanisms of PNI have not been comprehensively understood. Although electrical stimulation was found to promote axonal regeneration and functional rehabilitation after PNI, as well as to alleviate neuropathic pain, the specific mechanisms of successful PNI treatment are unclear. We summarize and discuss the basic mechanisms of PNI and of treatment via electrical stimulation. After PNI, activity in the central nervous system (spinal cord) is altered, which can limit regeneration of the damaged nerve. For example, cell apoptosis and synaptic stripping in the anterior horn of the spinal cord can reduce the speed of nerve regeneration. The pathological changes in the posterior horn of the spinal cord can modulate sensory abnormalities after PNI. This can be observed in cases of ectopic discharge of the dorsal root ganglion leading to increased pain signal transmission. The injured site of the peripheral nerve is also an important factor affecting post-PNI repair. After PNI, the proximal end of the injured site sends out axial buds to innervate both the skin and muscle at the injury site. A slow speed of axon regeneration leads to low nerve regeneration. Therefore, it can take a long time for the proximal nerve to reinnervate the skin and muscle at the injured site. From the perspective of target organs, long-term denervation can cause atrophy of the corresponding skeletal muscle, which leads to abnormal sensory perception and hyperalgesia, and finally, the loss of target organ function. The mechanisms underlying the use of electrical stimulation to treat PNI include the inhibition of synaptic stripping, addressing the excessive excitability of the dorsal root ganglion, alleviating neuropathic pain, improving neurological function, and accelerating nerve regeneration. Electrical stimulation of target organs can reduce the atrophy of denervated skeletal muscle and promote the recovery of sensory function. Findings from the included studies confirm that after PNI, a series of physiological and pathological changes occur in the spinal cord, injury site, and target organs, leading to dysfunction. Electrical stimulation may address the pathophysiological changes mentioned above, thus promoting nerve regeneration and ameliorating dysfunction.

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Peripheral nerves have the potential to self-repair and regenerate, aided by conditions such as anatomical continuity of the injured site, myelination, and the extent of the injury.
“However, peripheral nerves have the potential to self-repair and regenerate, aided by conditions such as anatomical continuity of the injured site, myelination, and the extent of the injury [112].”
From Active Neural Interface Circuits and Systems for Selective Control of Peripheral Nerves: A Review (2024) · cites this paper as [112]

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Multifunctional Conductive and Electrogenic Hydrogel Repaired Spinal Cord Injury via Immunoregulation and Enhancement of Neuronal Differentiation
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Morphofunctional Improvement of the Facial Nerve and Muscles with Repair Using Heterologous Fibrin Biopolymer and Photobiomodulation
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Early Intensive Neurorehabilitation in Traumatic Peripheral Nerve Injury—State of the Art
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Advanced nerve regeneration enabled by neural conformal electronic stimulators enhancing mitochondrial transport
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Epigenetic combined with transcriptomic analysis of the m6A methylome after spared nerve injury-induced neuropathic pain in mice
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Graphene oxide-doped chiral dextro-hydrogel promotes peripheral nerve repair through M2 polarization of macrophages
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Functional material-mediated wireless physical stimulation for neuro-modulation and regeneration
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Neural repair and regeneration interfaces: a comprehensive review
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Multilevel analysis of the central–peripheral–target organ pathway: contributing to recovery after peripheral nerve injury
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Authors: Chu, X.-L., Song, X.-Z., Li, Q., Li, Y.-R., He, F., Gu, X.-S., & Ming, D.
Affiliations: Academy of Medical Engineering and Translational Medicine, Tianjin University, Tianjin, China
Tianjin University (CN)
Tianjin University of Sport (CN)
Corresponding author: He, Feng
Gu, Xiao-Song
ORCID: Li, Qi
He, Feng
Gu, Xiao-Song
Venue: Neural Regeneration Research
Publisher: Ovid Technologies (Wolters Kluwer Health)
Published: 2022-02-28
Volume: 17
Issue: 10
Pages: 2185-2193
ISSN: 1673-5374 (ISSN-L)
1876-7958
DOI: 10.4103/1673-5374.335823
PMC: PMC9083151
OpenAlex: W4220934018
Cited by: 164
References: 122
Citations by year: 2026: 46 · 2025: 47 · 2024: 40 · 2023: 20 · 2022: 11
FWCI: 4.21
Type: journal article
Language: en
Open access: gold
doi.org
Licence: cc-by-nc-sa
Locations: Neural Regeneration Research (publishedVersion, cc-by-nc-sa)
PubMed Central (publishedVersion, cc-by-nc-sa)
PubMed (publishedVersion)
DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
Health Sciences › Medicine › Surgery › Nerve Injury and Rehabilitation
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neural Engineering
Keywords: peripheral nerve injury, electrical stimulation, axon regeneration, neuropathic pain, spinal cord, synaptic stripping, dorsal root ganglia, ectopic discharges, denervation, skeletal muscle atrophy, hyperalgesia, functional rehabilitation, target organs

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