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Overview and Description

The peripheral nervous system includes all nerves and ganglia located outside of the brain and spinal cord and is divided into the somatic and autonomic nervous systems. The somatic nervous system is made up of both motor and sensory nerves. The cell bodies of the motor nerves are located in the brainstem and ventral horn of the spinal cord while those of the sensory nerves are located outside of the spinal cord in the dorsal root ganglia (Fig 1).1 Disrupting the peripheral nervous system interferes with the body’s ability to move and sense the environment.

Fig 1. Diagram of Central and Peripheral Nervous System

Common signs and symptoms of peripheral nerve injuries include:

  • Hyperesthesia
  • Hypesthesia
  • Paresthesia
  • Dysesthesia
  • Weakness
  • Pain
  • Muscular atrophy
  • Dystrophic changes
  • Hyporeflexia or areflexia
  • Bowel or bladder incontinence


  • A combination of clinical assessment and electrodiagnostic studies are the standard to assess the location and severity of peripheral nerve injuries.  Injuries to the myelin are usually the least severe, while injuries to the axons and supporting structures are more severe (Fig 2).2
  • Pathologic findings, specifically neurapraxia, axonotmesis, and neurotmesis, are used to classify the severity of nerve damage according to the Seddon Classification.3 It is sometimes difficult to differentiate the severity by clinical findings, because all three lesion types have common neurologic impairments—motor and/or sensory loss—distal to the lesion.
  • Sunderland Classification expands Seddon Classification by introducing five grades of nerve injuries.
  • In neuropraxia (Sunderland grade 1) there is focal demyelination with impaired sensory and motor function distal to the lesion but preserved axonal continuity.
  • Axonotmesis (Sunderland grades 2, 3, and 4) develops when axons are damaged.
    • Sunderland grade 2 is only axon damage; Sunderland grade 3 is axon and endoneurium damage; and Sunderland grade 4 is axon, endoneurium, and perineurium damage.
    • As the Sunderland-grade increases, regeneration becomes less optimal and recovery time becomes longer.
  • In neurotmesis (Sunderland grade 5), the axon and all surrounding connective tissue (endoneurium, perineurium, and epineurium) are damaged (i.e., transected nerve). Spontaneous recovery is not possible.

Fig 2. An example of a peripheral nerve structure

Table 1 Classification of Peripheral Nerve Injury

Relevance to Clinical Practice

Natural history of peripheral nerve injury

  • In neurapraxia, diminished muscle strength and/or sensation develop acutely, but the axon continuity and nerve conduction of the distal segment remains intact regardless of the time following injury.
  • Both axonotmesis and neurotmesis involve axonal degeneration but there are differences in the process and prognosis of axonal recovery.
    • Degeneration usually proceeds proximally up one to several nodes of Ranvier.
    • Distal axon degeneration (Wallerian degeneration) involves motor and sensory fiber deterioration immediately within 24-36 hours.
    • Paralysis and sensory loss develop acutely, but nerve conduction of the distal segment remains intact until the distal segment is consumed by Wallerian degeneration.
    • During Wallerian degeneration, Schwann cells both phagocytose the axonal and myelin debris and help regenerate myelin.

Electrodiagnostic findings4

  • Injury and electrodiagnostic findings are time-dependent. Therefore, it is suggested to delay these studies for several weeks to assess for specific findings better and delineate injury severity.
  •  Most peripheral nerve injuries are initially managed conservatively, with nerve function evaluation at three weeks via a nerve conduction study and electromyography (NCS/EMG). 
  • Neuropraxia
    • Nerve conduction studies (NCS): Delayed conduction (prolonged distal latency, conduction block, and/or slow conduction velocity) across the lesion but normal conduction distal to the lesion.
    • Needle electromyography (EMG): normal spontaneous activity but may show decreased motor unit action potential (MUAP) recruitment due to conduction block.
    • With recovery, conduction is re-established across the lesion and electrodiagnostic findings will normalize.
  • Axonotmesis
    • NCS: In the first few days after the injury, there will be reduced conduction across the lesion. However, conduction may be normal above and below the lesion until Wallerian degeneration occurs.  With time, the partial axonal loss may result in reduced amplitude and slowed conduction, while complete axonal injury results in loss of action potentials.   
    • Needle EMG: Effective immediately, there will be decreased recruitment in partial lesions and unobtainable MUAPs/absent recruitment in complete lesions. Within weeks, fibrillations and positive sharp waves appear in affected muscles.
    • As axon sprouting and regeneration progress, abnormal spontaneous potentials decrease and MUAPs may appear variable.
    • In the first weeks to months, re-innervation by collaterals may result in polyphasic MUAPs and/or satellite potentials, while the slower axonal re-growth will eventually result in larger amplitude, longer duration potentials.
  • Neurotmesis
    • NCS: Loss of NCS waveforms below the lesion once distal axon degeneration (Wallerian degeneration) is complete.
  • EMG: Diffuse positive sharp waves and fibrillation potentials will appear in about three weeks in affected muscles, with no observable MUAPs. The amplitudes of the spontaneous potentials will diminish over time as the denervated muscle fibers atrophy.  As in axonotmesis, if there is any re-innervation by collaterals, EMG may reveal polyphasic MUAPs and/or satellite potentials, while the slower axonal re-growth will eventually result in larger amplitude, longer duration potentials.
  • Extensive axonotmesis cannot be differentiated initially from neurotmesis by either clinical or electrodiagnostic examination.
  • Sequential electrodiagnostic examinations may help predict recovery:
    • As noted above, reinnervation by collaterals may result in polyphasic MUAPs and/or satellite potentials, while the slower axonal re-growth will eventually result in larger amplitude, longer duration potentials.

Table 2: Electrodiagnostic Findings at 1 Month following Peripheral Nerve Injury

Table Assumptions and Key

  • This table lists general electrodiagnostic findings.
  • In the setting of neuropraxia, this chart assumes that the conduction block is persisting across the lesion and EMG findings listed are distal to the lesion in the relevant nerve territory.
  • For axonotmesis and neurotmesis, the EMG findings listed are distal to the lesion in the relevant nerve territory.
  • Key
    • WNL = Within normal limits
    • Abnl = Abnormal
    • NR = No response


  • Imaging studies are not the standard of care for peripheral nerve injuries. However, studies such as magnetic resonance imaging (MRI) and ultrasound (US) can be used assess injury to adjacent structures, localize the site of injury, grade severity of injury, and identify treatable causes for the peripheral nerve injury.5
  • Ultrasound (US) – can accurately diagnose various nerve injuries, especially superficial nerves (digital nerves, superficial sensory branches of radial and median nerves), but it can be limited by anatomy, body habitus, edema, and architectural distortions with deeper structures.5,6
    • Generalized findings indicative of injury on ultrasound include hypoechogenicity, nerve enlargement, fascicular changes, hyperechogenicity (intraneural and perineural) as well as indirect changes such as muscular atrophy.
    • Specific types of injuries with US findings6
      • Contusion
        • Edema within the nerve bundle
        • Increased distance between hyperechoic lines
      • Stretching
        • Edema over a long segment
        • Multiple branches involved with the loss of fascicular pattern
      • Laceration
        • Proximal end terminal neuroma, homogenous hypoechoic echotexture
        • May see muscle atrophy (especially in chronic injuries)
      • Edema
        • Echogenic
        • Heterogeneous echotexture of muscles5
    • US Advantages5
      • Time: very quick to do, faster than EMG or MRI6
      • Dynamic:  real-time assessment, visualize anatomy with anatomical manipulation and doppler feature
      • Cost: relatively low cost compared to other modalities
      • Comparison with contralateral side is easy
      • Better assessment of superficial nerves
    • US Disadvantages5
      • Cannot assess the physiological functioning of the nerve
      • Prognosis: cannot distinguish between neurotmesis and neuropraxic lesions
      • Operator-dependent, limiting reproducibility
      • Evaluation difficult for deep nerves and in obese patients
      • Anisotropy in long axis may lead to interpretation errors
  • MRI – demonstrating promise in diagnosing and monitoring injury, especially in the surgical setting. 
    • MR neurography can identify nerve discontinuity of a nerve, but over 50% of high-grade nerve transections have minimal to no gap present.7
    • Nerves have a honeycomb appearance with multiple alternating hyperechoic and hypoechoic bands at baseline. Loss of this “fascicular pattern” often indicates nerve injury.
      • T2-weighted images are more helpful than T1. During injury, nerves become more hyperintense and larger on T2 and, given the chronicity, muscle atrophy may be present and localized edema can be seen. 
      • Additionally, high-resolution MRI (1.5 and 3 Tesla) can further enhance injury detection. 
    • T2-weighted images can detect axonotmesis and neurotmesis but not neuropraxia.7
      • Axonotmesis – presents as enlarged hyperintensity with loss of fascicular structure and edema 
      • Neurotmesis – terminal neuroma, muscle atrophy, fatty replacement8
    • MRI Advantages5
      • Time: provider may be able to have a study done sooner if a timely EMG is difficult to obtain.
      • Site: if the muscle is very deep or limited by body habitus, MRI could be a better option than EMG. 
      •  If the patient cannot tolerate an NCS/EMG
      • Can detect muscle denervation changes through indirect findings
      • Identify osseous edema and fractures surrounding peripheral nerve injury
      • Objective assessment with less variation between operators
    • MRI Disadvantages5
      • Cost: expensive with regional limitations
      • Contraindications: pacemaker, metal implants, aneurysm clips
      • Setup: may be difficult to obtain if the patient is claustrophobic or morbidly obese

 Recovery and prognosis

  • The prognosis, in general, is more favorable for a demyelinating lesion than for a lesion producing axonal loss.
  • In addition, recovery of an injury is highly dependent on the severity of the injury. For instance, the less severe injuries (i.e., neuropraxia) recover in a shorter amount of time and to a better degree. On the contrary, axonotmesis and neurotmesis take longer to recover and may not recover as well or at all.
  • Two mechanisms of nerve recovery resulting in re-innervation of end-organs occur simultaneously:
    • Collateral branching/sprouting of intact axons
      • Primary mechanism when 20-30% of axons injured
      • Starts within four days of injury and proceeds for 3-6 months
      • Mechanism involves the process of surviving axons in the region around an injured nerve to “branch” or “sprout” towards the associated denervated muscle in an attempt to re-innervate the muscle and thus restore its function.
      • The clinical effectiveness of collateral branching/sprouting is determined by the extent of the number of axons injured in a region
    • Axonal regeneration
      • Primary method when greater than 90% of axons injured
      • Mechanism essentially involves a complex array of growth factors at the molecular level and glial cells at the cellular level, which coordinate degeneration, repair, and growth of the distal portion of an axon to grow and thus reinnervate their corresponding muscle.
      • Begins within hours of injury and takes months to years to complete.
      • Requires an intact endoneurial tube to re-establish continuity between the cell body and the distal terminal nerve segment.9 An axon has approximately 24 months to reach the target before the endoneurial tube is closed off by fibrosis
      • Axons re-grow at the rate of 1 mm/day (i.e. approximately one inch per month), but individual nerves may have different speeds (ulnar, 1.5 mm/day; median, 2-4.5 mm/day; and radial, 4-5 mm/day).3
      •  Sensory nerve regeneration is often less successful than motor-nerve regeneration due to the difference in structural architecture of these nerves.10 
      • Axonal regeneration is faster in the initial stages of nerve injury and becomes slower as it reaches the nerve end.
      • If neural regeneration is successful, the conduction velocity of the injury returns to 60% to 90% of the pre-injury level (but this does not usually adversely affect clinical recovery).
      • Scar formation at the injury site will block axonal regeneration. If the axons fail to cross over the injury site, the distal segment is permanently denervated and the axonal growth from the proximal segment forms a neuroma.
  • NCS can demonstrate the resolution of conduction block or remyelination
  • EMG can demonstrate reinnervation via collateral sprouting and axonal regrowth.
  • Functional Imaging like DWI and DTI can evaluate peripheral nerve regeneration following nerve repair or nerve reconstruction.

Rehabilitation management of peripheral nerve injury

  • Peripheral neuropathy most frequently results from a specific disease or damage of the nerve, or as a consequence of generalized systemic illness, the most fundamental treatment involves prevention and control of the primary disease.
  • Rehabilitation for nerve injury includes various treatments:
    • Discomfort and swelling relief
    • Personalized or pre-made braces
    • Adaptive techniques for daily activities, relearning motor skills, and regaining sensory awareness.
    • Contractures and deformities can be prevented through a combination of exercises, stretching, and biofeedback20
    • Sensory re-education techniques improve sensory function after reinnervation, but evidence of their effectiveness is limited20.
  • Post-nerve injury promptly treats all pain components for rehabilitation, especially neuropathic pain which is linked to poor results and high disability11. Essential pain management and psychological aid impact patient satisfaction, pain, and disability outcomes11.
  • If surgery is warranted for the nerve injury, the type of surgery could influence healing and outcomes.12 Risks include:
    • Muscle and tendon transfers: potential for adhesive scarring, impaired tendon function.
    • Graft repairs: fibrosis, endplate degeneration may compromise functionality.
  • After undergoing surgery for peripheral nerve injury, swelling is a typical occurrence managed similarly to how one would treat any other surgical injury. This involves utilizing methods such as positioning, elevating, manual edema mobilization, and compression.11
  • It is advisable to have a period of initial protection after the nerve has been surgically repaired.11 Early therapy includes bandages or splints to secure the repaired nerve. Protection duration depends on injury location and stress on the repaired area. Minimizing joint and soft tissue immobilization, while preserving repair integrity, is critical11.
  • Scar management for nerve injury: massages, taping, silicone/compression dressing11. Daily massages can be self-performed. Avoid silicone dressings in hyperesthesia, hyperalgesia, allodynia11
  • Muscle fatigue, or the decline of performance during an exercise or task, after muscle reinnervation is one limiting factor in the rehabilitation process.12
    • Post-nerve injury, muscle atrophy and fibrosis occur without reinnervation11. Reinnervated fibers, predominantly type II, fatigue faster, affecting therapy and daily activities.
    • The initial phase of treatment focuses on passive range of motion exercises, followed by active exercises to encourage muscle function.11
    • Functional electrical stimulation may prevent muscle atrophy, but the evidence is limited.
    • Custom-made or prefabricated splints can support motor function recovery.11

Surgical repair of peripheral nerve injury

  • Surgical repair criteria are based on open or closed injuries and nerve continuity.14
  • Open versus closed injuries:
    • Open injuries with complete nerve transection are repaired based on the laceration type.
      • Open injuries with sharp lacerations are managed with immediate repair within 3-7 days.
      • Open injuries with dirty, blunt lacerations are delayed for surgical repair to better allow demarcation of injury and avoid complications such as infection.
    • Open injuries with nerve discontinuity (epineurium intact) and all closed injuries initially are managed conservatively with nerve function evaluation at three weeks via nerve conduction studies and electromyography (NCS/EMG).  This testing can further determine Sunderland grade. Sunderland grades 1-3 are treated with conservative measures while grades 4-5 usually require surgical repair.13-15 Sunderland Grade III lesions have the potential to undergo incomplete regeneration, leading to spontaneous recovery, and as a result, this may result in improved functional recovery compared to nerve reconstruction.11
    • If clinical or electrical recovery is not evident within three months, surgical intervention is usually recommended. Surgical procedures are typically performed for three main reasons11:
      • Firstly, to diagnose or confirm a medical condition.
      • Secondly, to restore the continuity of a severed or ruptured nerve.
      • Thirdly, to release any obstruction caused by compression, distortion, or external agents that are occupying the nerve.
    • Factors that may contraindicate surgical intervention include poor patient health, risk of sepsis, and uncertainty about the nature and extent of the injury.11 In some cases, nerve reconstruction may not be feasible due to a lack of equipment or an experienced surgical team. Primary muscle or tendon transfer may be a better option for irreparable motor nerve damage, such as to the radial and common peroneal nerves.11
  • Surgical repair is further classified based on the size of the nerve gap and includes primary repair, conduits, allografts, and autografts.16,17
  • The type of surgery can be guided by the size of the gap of injury:
    • <1 cm: End-to-end neurorrhaphy.17,18
    • >1 cm:
      • Autologous graft to provide a conduit for axonal regrowth
      • Donor’s nerve is usually a sensory nerve

Cutting Edge/Unique Concepts/Emerging Issues

Pharmacological Agents

  • Currently, there are no FDA-approved pharmacological treatments for nerve regeneration.
  • Various possibilities have been studied to improve/accelerate nerve repair/regeneration via neuronal-death reduction and axonal-growth enhancement.
  • All agents have been tested only in cell-culture or animal models. Some of the agents include erythropoietin, tacrolimus, acetyl-L-carnitine, N-acetylcysteine, testosterone, chondroitinase ABC, dimethylsulfoxide, transthyretin (pre-albumin), ibuprofen, melatonin, and polyethylene glycol.
  • Polyethylene glycol (PEG) has proven successful in animal models and was applied to human trials.18
    • PEG helps fuse cells, develop desired cell lines, remove water at the injured lipid bilayer, and increase the fusion of axolemmal ends.
    • One study found that during a surgical repair of a sharp, complete resection, the application of PEG for 2 minutes after surgical connection of the injured ends, helps to decrease inappropriate calcium-mediated vesicle formation, promote fusion, enhance axonal continuity with nerve healing, and improve sensory recovery, based on static two-point discrimination.18
    • Benefits: affordable, readily available, low risk of toxicity
    • Limitations: not been tested in mixed nerves, motor nerves, or jagged injuries
  • Agents that inhibit inflammation, oxidative stress, excitotoxicity, and apoptosis are believed to be beneficial for peripheral nerve regeneration. However, the positive or negative effects can vary greatly based on dosage, types of injury, route of administration, and a variety of other factors.25
    • Glucocorticoids (Dexamethasone, methylprednisolone) are found to be neuroprotective and improves functional recovery after peripheral nerve injury
    • Atorvastatin has neuroprotective effects, attributed to its anti-inflammatory, anti-excitotoxic, antioxidant properties. Furthermore, atorvastatin upregulates proteins and collagens associated with growth, such as myelin basic protein, growth-associated protein 43.
      • In mice models with nerve crush injury, pretreatment with atorvastatin is associated with an improved outcome.
      • However, long-term use of statins has been associated with peripheral neuropathy. More studies need to be conducted on the long-term effect of atorvastatin use in peripheral nerve injury.
    • Citicoline and its endogenous metabolites are associated with improved nerve regeneration and functional recovery in rat models.
    • L-Carnitine has neuroprotective effects and is associated with improved nerve regeneration and functional recovery in rat models.
    • Memantine and Riluzole: NMDA antagonists that prevent excitotoxicity. However, studies on mice models show no significant benefits. In fact, Riluzole treatment demonstrated reduced functional and electrophysiological outcome after nerve injury.
  • Combined Therapy (stem cells + pharmacological treatment)
    • Stem cell therapy provides cell-seeded scaffolds that help bridge the nerve gap in injuries.
    • In combination with pharmacological agents discussed above (such as glucocorticoids, statins, L-carnitine) this treatment demonstrates improved functional and electrophysiological outcome. Stem cells in combination with L-Carnitine led to regeneration across a 10 mm sciatic nerve gap. Treating stem cells with statins upregulates Schwann cell markers and lipogenic genes that play a role in myelin formation

Artificial Nerve Conduits

  • An artificial nerve conduit is a biodegradable, bridge-like structure that guides axonal regrowth during nerve regeneration. Current nerve conduits on the market are synthesized from biodegradable polymers, such as Type 1 collagen, polysaccharides, polyglycolic acid, polycaprolactone (PCL).
  • An ideal nerve conduit consists of favorable physical structure and a regenerative biomaterial. Progress in 3D bioprinting enables the manufacturing of nerve conduits and customized spatial structures to enhance the efficacy of peripheral nerve regeneration.22
    • Advanced 3D bioprinting uses biological polymers and even living cells to mimic the topological shape, biocompatibility, and mechanical properties of nerve tissue ECM. The biochemical substrates and living cells provide an environment that allows for continued nutrient supply and accelerated nerve regeneration.23
    • In in-vivo studies on rats, biomimetic nerve conduit showed complete regeneration of a bifurcated nerve injury across a 10 mm gap.24
    • In 2022, a novel 3D printing approach using nanoparticles that can release drugs to further facilitate nerve regeneration appeared.


  • Acute, brief, low-frequency electric stimulation following post-operative peripheral nerve repair has been shown in human models to improve motor and sensory reinnervation. This is thought to be due to increased production of neurotrophic factors by Schwann cells, as well as increased production of cytoskeletal proteins.10,19

Gaps in Knowledge/Evidence Base

The current standards of care for peripheral nerve injury is based on serial examinations and/or electrodiagnostics. There is significant room for improvement in the development of more formal diagnostic tools, aiding prognostication for these difficult and severe injuries. In addition, cost-effective approaches to following progress to recovery are needed.  For the treatment of traumatic nerve injuries, research in pharmacologic interventions, gene therapy, stem cell therapy, and biochemical nerve conduits have shown great promise in clinical application. However, the research needs to be expanded to human subjects.


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  3. Dumitru D, Amato A, Machiel Z. Electrodiagnostic Medicine. 2nd ed. 2001.
  4. Preston D, Shapiro B. Electromyography and Neuromuscular Disorders: Clinical-Electrophysiologic Correlations. 2013.
  5. Goyal, Ankur, et al. “Imaging of Traumatic Peripheral Nerve Injuries.” Journal of Clinical Orthopaedics and Trauma, vol. 21, July 2021, p.101-51.
  6. Visalli C, Cavallaro M, Concerto A et al. Ultrasonography of traumatic injuries to limb peripheral nerves: technical aspects and spectrum of features. Jpn J Radiol 2018;36:592-602.
  7. Marquez Neto OR, Leite MS, Freitas T, Mendelovitz P, Villela EA, Kessler IM. The role of magnetic resonance imaging in the evaluation of peripheral nerves following traumatic lesion: where do we stand? Acta Neurochir (Wien ) 2017;159:281-290.
  8. Boyer RB, Kelm ND, Riley DC et al. 4.7-T diffusion tensor imaging of acute traumatic peripheral nerve injury. Neurosurg Focus 2015;39:E9.
  9. Rodrigues MC, Rodrigues AA, Jr., Glover LE, Voltarelli J, Borlongan CV. Peripheral nerve repair with cultured schwann cells: getting closer to the clinics. ScientificWorldJournal 2012;2012:413091.
  10. Gordon T, English AW. Strategies to promote peripheral nerve regeneration: electrical stimulation and/or exercise. Eur J Neurosci 2016;43:336-350.
  11. Haastert-Talini, Kirsten., Hans. Assmus, and Gregor. Antoniadis. Modern Concepts of Peripheral Nerve Repair. Ed. Kirsten. Haastert-Talini, Hans. Assmus, and Gregor. Antoniadis. 1st ed. 2017. Cham: Springer International Publishing, 2017. Web.
  12. Wilcox M, Brown H, Johnson K, Sinisi M, Quick TJ. An assessment of fatigability following nerve transfer to reinnervate elbow flexor muscles. Bone Joint J 2019;101-B:867-871.
  13. Grinsell D, Keating CP. Peripheral nerve reconstruction after injury: a review of clinical and experimental therapies. Biomed Res Int 2014;2014:698256.
  14. Panagopoulos GN, Megaloikonomos PD, Mavrogenis AF. The Present and Future for Peripheral Nerve Regeneration. Orthopedics 2017;40:e141-e156.
  15. Sullivan R, Dailey T, Duncan K, Abel N, Borlongan CV. Peripheral Nerve Injury: Stem Cell Therapy and Peripheral Nerve Transfer. Int J Mol Sci 2016;17.
  16. Bassilios HS, Bond G, Jing XL, Kostopoulos E, Wallace RD, Konofaos P. The Surgical Management of Nerve Gaps: Present and Future. Ann Plast Surg 2018;80:252-261.
  17. Ducic I, Fu R, Iorio ML. Innovative treatment of peripheral nerve injuries: combined reconstructive concepts. Ann Plast Surg 2012;68:180-187.
  18. Bamba R, Waitayawinyu T, Nookala R et al. A novel therapy to promote axonal fusion in human digital nerves. J Trauma Acute Care Surg 2016;81:S177-S183.
  19. Willand MP, Nguyen MA, Borschel GH, Gordon T. Electrical Stimulation to Promote Peripheral Nerve Regeneration. Neurorehabil Neural Repair 2016;30:490-496.
  20. Simon, Neil G et al. “Advances in the Neurological and Neurosurgical Management of Peripheral Nerve Trauma.” Journal of Neurology, Neurosurgery and Psychiatry 87.2 (2016): 198–208. Web.
  21. Radtke, Prof Dr et al. “Abstract 66: Single Treatment with Alpha-1-Antitrypsin Enhances Nerve Regeneration After Peripheral Nerve Injury.” Plastic and reconstructive surgery (1963) 133.3 Suppl (2014): 77–77. Web.
  22.  Han, Ying, and Jun Yin. “Industry News: The Additive Manufacturing of Nerve Conduits for the Treatment of Peripheral Nerve Injury.” Bio-design and manufacturing 5.1 (2022): 6–8. Web.
  23. Tao J, Zhang JM, Du T et al (2019) Rapid 3D printing of functional nanoparticle-enhanced conduits for efective nerve repair. Acta Biomater 90:49–59
  24. Singh A, Asikainen S, Teotia AK et al (2018) Biomimetic photocurable three-dimensional printed nerve guidance channels with aligned cryomatrix lumen for peripheral nerve regeneration. ACS Appl Mater Interf 10(50):43327–43342.
  25. Bolandghamat S, Behnam-Rassouli M. Recent Findings on the Effects of Pharmacological Agents on the Nerve Regeneration after Peripheral Nerve Injury. Curr Neuropharmacol. 2020;18(11):1154-1163. doi: 10.2174/1570159X18666200507084024. PMID: 32379588; PMCID: PMC7709152.

Original Version of the Topic

Chong Tae Kim, MD, Jung Sun Yoo, MD. Peripheral neurological recovery and regeneration. 9/20/2013.

Previous Revision(s) of the Topic

David Haustein, MD, Mariko Kubinec, MD, Douglas Stevens, MD, Clinton Johnson, DO. Peripheral neurological recovery and regeneration. 8/03/2017.

David Haustein, MD, C. Alex Carrasquer, MD, Stephanie M. Green, DO, Michael J. Del Busto, MD. Peripheral neurological recovery and regeneration. 6/1/2020

Author Disclosure

Loc Lam, DO
Nothing to Disclose

Colton Reeh, MD
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Royce Copeland, DO
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Gaibo Yan, BS/BA
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Cody Richards, BS/BA
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Emanuel Narcis Husu, MD
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