Relevant bibliographies by topics / Nerve injury

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Nerve injury'

Author: Grafiati
Published: 4 June 2021
Last updated: 30 January 2023

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Journal articles on the topic "Nerve injury"

1

Stenberg, Lena, Derya Burcu Hazer Rosberg, Sho Kohyama, Seigo Suganuma, and Lars B. Dahlin. "Injury-Induced HSP27 Expression in Peripheral Nervous Tissue Is Not Associated with Any Alteration in Axonal Outgrowth after Immediate or Delayed Nerve Repair." International Journal of Molecular Sciences 22, no. 16 (August 11, 2021): 8624. http://dx.doi.org/10.3390/ijms22168624.

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We investigated injury-induced heat shock protein 27 (HSP27) expression and its association to axonal outgrowth after injury and different nerve repair models in healthy Wistar and diabetic Goto-Kakizaki rats. By immunohistochemistry, expression of HSP27 in sciatic nerves and DRG and axonal outgrowth (neurofilaments) in sciatic nerves were analyzed after no, immediate, and delayed (7-day delay) nerve repairs (7- or 14-day follow-up). An increased HSP27 expression in nerves and in DRG at the uninjured side was associated with diabetes. HSP27 expression in nerves and in DRG increased substantially after the nerve injuries, being higher at the site where axons and Schwann cells interacted. Regression analysis indicated a positive influence of immediate nerve repair compared to an unrepaired injury, but a shortly delayed nerve repair had no impact on axonal outgrowth. Diabetes was associated with a decreased axonal outgrowth. The increased expression of HSP27 in sciatic nerve and DRG did not influence axonal outgrowth. Injured sciatic nerves should appropriately be repaired in healthy and diabetic rats, but a short delay does not influence axonal outgrowth. HSP27 expression in sciatic nerve or DRG, despite an increase after nerve injury with or without a repair, is not associated with any alteration in axonal outgrowth.
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Holland, G. R. "Experimental Trigeminal Nerve Injury." Critical Reviews in Oral Biology & Medicine 7, no. 3 (July 1996): 237–58. http://dx.doi.org/10.1177/10454411960070030301.

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The successful reinnervation of peripheral targets after injury varies with the axonal population of the nerve that is injured and the extent of the dislocation of its central component from the peripheral endoneurial tube. Larger-diameter axons such as those supplying mechanoreceptors recover more readily than narrower axons such as those supplying taste. A complex, bi-directional interaction between lingual epithelium and sprouting nerve results in the redifferentiation of taste buds after denervation. Dentin and the dental pulp provide a strong attraction to sprouting nerves and will become reinnervated from collateral sources if recovery of the original innervation is blocked. The most effective repair technique for transected lingual nerves is one which brings the cut ends together rather than one that provides a temporary bridge. Injuries can result in cell death in the trigeminal ganglion but only if the injury is severe and recovery is prevented. Lesser damage results in chromatolysis and the increased expression of neuropeptides. All nerve injuries bring about changes in the trigeminal nucleus. These occur as changes in receptive field and the incidence of spontaneously active neurons, effects which are consistent with the unmasking of existing afferents. These functional changes are short-lived and reversible. Morphologically, nerve injury results in terminal degeneration in the nuclei and an increased expression of the c-Fos gene and some neuropeptides. Only a chronic constriction injury induces behavioral changes. The adult trigeminal system retains considerable plasticity that permits it to respond successfully to nerve injury. Much remains to be learned about this response, particularly of the trophic factors that control peripheral recovery and the central response to more severe injuries.
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Tode, Jan, Irina Kirillova-Woytke, Vanessa H. Rausch, Ralf Baron, and Wilfrid Jänig. "Mechano- and thermosensitivity of injured muscle afferents 20 to 80 days after nerve injury." Journal of Neurophysiology 119, no. 5 (May 1, 2018): 1889–901. http://dx.doi.org/10.1152/jn.00894.2017.

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Chronic injury of limb nerves leading to neuropathic pain affects deep somatic nerves. Here the functional properties of injured afferent fibers in the lateral gastrocnemius-soleus nerve were investigated 20 and 80 days after suturing the central stump of this muscle nerve to the distal stump of the sural nerve in anesthetized rats. Neurophysiological recordings were made from afferent axons identified in either the sciatic nerve (87 A-, 63 C-fibers) or the dorsal root L4/L5 (52 A-, 26 C-fibers) by electrical stimulation of the injured nerve. About 70% of the functionally identified A-fibers had regenerated into skin by 80 days after nerve suture; the remaining A-fibers could be activated only from the injured nerve. In contrast, 93% of the functionally identified C-fibers could only be activated from the injured sural nerve after 80 days. Nearly half of the injured A- (45%) and C-fibers (44%) exhibited ongoing and/or mechanically or thermally evoked activity. Because ~50% of the A- and C-fibers are somatomotor or sympathetic postganglionic axons, respectively, probably all injured muscle afferent A- and C-fibers developed ectopic activity. Ongoing activity was present in 17% of the A- and 46% of the C-fibers. Mechanosensitivity was present in most injured A- (99%) and C-fibers (85%), whereas thermosensitivity was more common in C-fibers (cold 46%, heat 47%) than in A-fibers (cold 18%, heat 12%). Practically all thermosensitive A-fibers and C-fibers were also mechanosensitive. Thus, unlike cutaneous axons, almost all A- and C-fibers afferents in injured muscle nerves demonstrate ectopic activity, even chronically after nerve injury. NEW & NOTEWORTHY After chronic injury of a muscle nerve, allowing the nerve fibers to regenerate to the target tissue, 1) most afferent A-fibers are mechanosensitive and regenerate to the target tissue; 2) ectopic ongoing activity, cold sensitivity, and heat sensitivity significantly decrease with time after injury in A-afferents; 3) most afferent C-fibers do not regenerate to the target tissue; and 4) injured C-afferents maintain the patterns of ectopic discharge properties they already show soon after nerve injury.
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Ahmadian, Amir, Naomi Abel, and Juan S. Uribe. "Functional recovery of severe obturator and femoral nerve injuries after lateral retroperitoneal transpsoas surgery." Journal of Neurosurgery: Spine 18, no. 4 (April 2013): 409–14. http://dx.doi.org/10.3171/2013.1.spine12958.

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The minimally invasive lateral retroperitoneal transpsoas approach is a popular fusion technique. However, potential complications include injury to the lumbar plexus nerves, bowel, and vasculature, the most common of which are injuries to the lumbar plexus. The femoral nerve is particularly vulnerable because of its size and location; injury to the femoral nerve has significant clinical implications because of its extensive sensory and motor innervation of the lower extremities. The authors present an interesting case of a 49-year-old male patient in whom femoral and obturator nerve functional recovery unexpectedly occurred 364 days after the nerves had been injured during lateral retroperitoneal transpsoas surgery. Chronological video and electrodiagnostic findings demonstrate evidence of recovery. Classification and mechanisms of nerve injury and nerve regeneration are discussed.
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Zochodne, D. W. "Epineurial Peptides: A Role in Neuropathic Pain?" Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 20, no. 1 (February 1993): 69–72. http://dx.doi.org/10.1017/s0317167100047466.

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ABSTRACT:Neuropathic pain is not well understood. Although central dorsal horn remodelling is likely important in maintaining chronic neuropathic pain, afferent activity from injured nerves or ganglia may initiate these changes. It is suggested, in this review that the peripheral nerve trunk is capable of sustaining a “flare” response as observed in injured skin and other tissues. The injury response may be associated with local vasodilatation, plasma extravasation and the generation of painful local afferent activity sustained by locally originating peptidergic fibers (nervi nervorum). These fibers contain substance P, calcitonin gene-related peptide and other peptides that have been linked to nociceptive transmission. Manipulation of the local injury response of the nerve trunk by pharmacologic means may provide one strategy in the treatment of neuropathic pain.
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RAYAN, G. M., S. I. SAID, S. L. CAHILL, and J. DUKE. "Vasoactive Intestinal Peptide and Nerve Regeneration." Journal of Hand Surgery 16, no. 5 (October 1991): 515–18. http://dx.doi.org/10.1016/0266-7681(91)90106-x.

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The role of vasoactive intestinal peptide (V.I.P.) in nerve regeneration was investigated by assessing the changes in immunoreactive V.I.P. levels in rat sciatic nerves following injury and repair. 60 rats were divided into three surgical groups and one control group: In group I (primary repair), sciatic nerves were divided and immediately repaired; in group II (secondary repair), sciatic nerves were divided and repaired two weeks later; in group III (no repair), sciatic nerves were divided and not repaired; and in group IV (controls), sciatic nerves were exposed but not divided. Animals were sacrificed at three days and at weekly intervals. Their sciatic nerves were extracted and assayed for V.I.P. concentrations by a specific radioimmunoassay. The mean V.I.P. concentration varied between 22 and 46 pg./mg. protein in the control nerves and between 60 and 529 pg./mg. protein in all other groups. In the three surgical groups the levels were significantly higher in proximal than in distal stumps. Following nerve injury, there was an increase in V.I.P. concentration in the injured and repaired areas. This increase was greater in injured non-repaired areas and was highest in the first 48 hours, but continued during regeneration. The accumulation of V.I.P. in divided nerves occurred in response to nerve injury.
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Cha, Myeoung Hoon, Taick Sang Nam, Yongho Kwak, Hyejung Lee, and Bae Hwan Lee. "Changes in Cytokine Expression after Electroacupuncture in Neuropathic Rats." Evidence-Based Complementary and Alternative Medicine 2012 (2012): 1–6. http://dx.doi.org/10.1155/2012/792765.

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The production of proinflammatory cytokines including interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor-α(TNF-α) plays a key role in chronic pain such as neuropathic pain. We investigated changes in cytokine expression in injured peripheral nerves and dorsal root ganglia (DRG) following electroacupuncture (EA) treatment. Neuropathic pain was induced by peripheral nerve injury to the left hind limb of Sprague-Dawley rats under pentobarbital anesthesia. Two weeks later, the nerve-injured rats were treated by EA for 10 minutes. The expression levels of IL-1β, IL-6, and TNF-αin peripheral nerves and DRG of neuropathic rats were significantly increased in nerve-injured rats. However, after EA, the cytokine expression levels were noticeably decreased in peripheral nerves and DRG. These results suggest that EA stimulation can reduce the levels of proinflamtory cytokines elevated after nerve injury.
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Seckel, Brooke R. "Facial Danger Zones: Avoiding Nerve Injury in Facial Plastic Surgery." Canadian Journal of Plastic Surgery 2, no. 2 (June 1994): 59–66. http://dx.doi.org/10.1177/229255039400200207.

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BR Seckel. Facial danger zones: Avoiding nerve injury in facial plastic surgery. Can J Plast Surg 1994;2(2):59-66. with today's new emphasis on more aggressive and deeper facial dissection during rhytidectomy, the peripheral nerve branches of cranial nerves V and VII in the face are more often exposed closer to the plane of dissection and more likely to be injured in the course of composite, extended sub-submuscular aponeurotic system (sub-SMAS), and subperiosteal rhytidectomy. It is important to have a keen and thorough understanding of the location of these nerves to avoid injury. I divide the face into seven facial danger zones based on known anatomic locations of the branches of the peripheral nerves of the face and the location in which they are most easily injured in the course of facial dissection. A description of the nerve and consequence of injury, the anatomic location of the zone, and the technique for safe surgical dissection for each facial danger zone is presented.
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Teodori, Rosana Macher, Joice Betini, Larissa Salgado de Oliveira, Luciane Lobato Sobral, Sibele Yoko Mattozo Takeda, and Maria Imaculada de Lima Montebelo. "Swimming Exercise in the Acute or Late Phase after Sciatic Nerve Crush Accelerates Nerve Regeneration." Neural Plasticity 2011 (2011): 1–8. http://dx.doi.org/10.1155/2011/783901.

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There is no consensus about the best time to start exercise after peripheral nerve injury. We evaluated the morphological and functional characteristics of the sciatic nerves of rats that began to swim immediately after crush nerve injury (CS1), those that began to swim 14 days after injury (CS14), injured rats not submitted to swimming (C), and uninjured rats submitted to swimming (S). After 30 days the number of axons in CS1 and CS14 was lower than in C (P<0.01). The diameter of axons and nerve fibers was larger in CS1 (P<0.01) and CS14 (P<0.05) than in C, and myelin sheath thickness was lower in all crushed groups (P<0.05). There was no functional difference between CS1 and CS14 (P>0.05). Swimming exercise applied during the acute or late phase of nerve injury accelerated nerve regeneration and synaptic elimination after axonotmesis, suggesting that exercise may be initiated immediately after injury.
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Boyer, Richard B., Nathaniel D. Kelm, D. Colton Riley, Kevin W. Sexton, Alonda C. Pollins, R. Bruce Shack, Richard D. Dortch, Lillian B. Nanney, Mark D. Does, and Wesley P. Thayer. "4.7-T diffusion tensor imaging of acute traumatic peripheral nerve injury." Neurosurgical Focus 39, no. 3 (September 2015): E9. http://dx.doi.org/10.3171/2015.6.focus1590.

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Diagnosis and management of peripheral nerve injury is complicated by the inability to assess microstructural features of injured nerve fibers via clinical examination and electrophysiology. Diffusion tensor imaging (DTI) has been shown to accurately detect nerve injury and regeneration in crush models of peripheral nerve injury, but no prior studies have been conducted on nerve transection, a surgical emergency that can lead to permanent weakness or paralysis. Acute sciatic nerve injuries were performed microsurgically to produce multiple grades of nerve transection in rats that were harvested 1 hour after surgery. High-resolution diffusion tensor images from ex vivo sciatic nerves were obtained using diffusion-weighted spin-echo acquisitions at 4.7 T. Fractional anisotropy was significantly reduced at the injury sites of transected rats compared with sham rats. Additionally, minor eigenvalues and radial diffusivity were profoundly elevated at all injury sites and were negatively correlated to the degree of injury. Diffusion tensor tractography showed discontinuities at all injury sites and significantly reduced continuous tract counts. These findings demonstrate that high-resolution DTI is a promising tool for acute diagnosis and grading of traumatic peripheral nerve injuries.
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Dissertations / Theses on the topic "Nerve injury"

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Hart, Andrew McKay. "Peripheral nerve injury : primary sensory neuronal death & regeneration after chronic nerve injury." Thesis, University of Glasgow, 2001. http://theses.gla.ac.uk/4472/.

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After a defined unilateral sciatic nerve transection in the rat, a novel triple staining technique was employed in order to enable the detection of neuronal death in L4 & L5 dorsal root ganglia by light microscopic morphology, and TdT Uptake Nick-End Labelling (TUNEL). Optical dissection was then used to quantify neuronal loss from statistically unbiased estimates of the number of surviving neurons. Neuronal death was demonstrated to begin within 24 hours of injury and to peak 2 weeks later, while neuronal loss plateaued 2 months after axotomy, and 39.2% of neurons died overall. Thus the most relevant experimental timepoints at which to examine the effects of putative neuroprotective strategies are 2 weeks and 2 months after axotomy, until which time a window of opportunity exists for therapeutic intervention. The principal that sensory outcome might be related to the delay between injury and nerve repair was confined by the fact that although surgical nerve repair reduced neuronal death 2 weeks after axotomy, the neuroprotective benefit depended upon how soon after injury the nerve was repaired. Even immediate repair did not entirely eliminate neuronal loss, confirming the need for an adjuvent therapy. Hence the effect of two promising agents with established clinical safety records was examined. N-acetyl-cysteine (NAC) is a clinically proven glutathione substrate antioxidant, and anti-mitotic properties. Systemic treatment caused a dose-dependent improvement in neuronal morphology, a significant reduction in the number of TUNEL positive neurons 2 weeks after axotomy (p<0.05), and 2 months after axotomy it was found to have reduced neuronal loss from 35% to only 3% (p<0.001). L-acetyl-carnitine (LAC) is a physiological peptide integral to mitochondrial aerobic glycolysis that was found to be even more neuroprotective than NAC, since after LAC treatment no neuronal loss was detected 2 months after axotomy (no treatment 35% loss; high-dose LAC -4% loss, p<0.001).
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Baillie, Andrew G. S. "Skeletal muscle metabolism after nerve crush injury." Thesis, University of Aberdeen, 1994. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU059079.

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A model was developed in the rat using a nerve crush procedure, as a form of temporary denervation, to block neural input to the hindlimb muscle of one leg. The nerve crush has the advantage of allowing self-reinnervation of the muscles after regrowth of the damaged nerve, which occurred (in this study) after approximately 14 days. The initial denervation-like phase resulted in a large loss of muscle mass over the subsequent few days which was mostly through a loss of muscle protein. The results demonstrate the correlation between the concentration of glutamine in the muscles and the rate of protein synthesis over the first 3 days after the nerve crush, but other metabolites (alanine, lactate, and glutamate) were seen to react much more rapidly, with significant changes recorded in the first hour after injury. Further studies were undertaken in an attempt to find a link between these acute changes and the later changes in protein and glutamine metabolism. It was demonstrated that these rapid changes were not as a result of a local hypoglycemia, although a reduction in the rate of in vivo glucose uptake was reduced within 4 hours of the nerve crush. Similarly, measurement of activities of key glycolytic enzymes suggested that there were no acute changes in flux through the glycolytic pathway. Finally, a difference in regional blood flow was demonstrated in the experimental muscles and it was concluded that the acute changes in metabolite concentrations might result from simple physiological changes, in response to the anaesthesia and/or the surgical procedure, which subsequently resolved in the innervated, but not the nerve-deprived, muscles.
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Rosenthal, Oren D. "Peripheral nerve repair using biomaterial nerve guides containing guidance channels." [Tampa, Fla.] : University of South Florida, 2004. http://purl.fcla.edu/fcla/etd/SFE0000467.

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Welin, Dag. "Neuroprotection and axonal regeneration after peripheral nerve injury." Doctoral thesis, Umeå : Umeå university, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-32819.

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Fitton, Anthony Robert. "Muscle recovery following peripheral nerve injury and repair." Thesis, Imperial College London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.418071.

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Lidman, Olle. "Genetics and inflammation in nerve injury-induced neurodegeneration /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-654-5/.

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Wallin, Johan. "Experimental nerve injury-induced pain : mechanisms and modulation/." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-849-1/.

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Bridges, Daniel Robert. "Cannabinoid receptors and pain following peripheral nerve injury." Thesis, Imperial College London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.407774.

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Qudairat, E. "Thermographic evaluation of nerve injury following facial fracture." Thesis, Queen's University Belfast, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.479394.

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Archer, D. R. "Axonal transport and related responses to nerve injury." Thesis, University of Liverpool, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.234835.

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Books on the topic "Nerve injury"

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Lundborg, Göran. Nerve injury and repair. Edinburgh: Churchill Livingstone, 1988.

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Hirasawa, Yasusuke, ed. Treatment of Nerve Injury and Entrapment Neuropathy. Tokyo: Springer Japan, 2002. http://dx.doi.org/10.1007/978-4-431-67883-0.

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Facial danger zones: Avoiding nerve injury in facial plastic surgery. St. Louis, Mo: Quality Medical Pub., 1994.

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Seckel, Brooke R. Facial danger zones: Avoiding nerve injury in facial plastic surgery. 2nd ed. St. Louis, Mo: Quality Medical Pub., 2010.

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Skouras, Emmanouil, Stoyan Pavlov, Habib Bendella, and Doychin N. Angelov. Stimulation of Trigeminal Afferents Improves Motor Recovery After Facial Nerve Injury. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-662-45789-4.

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Skouras, Emmanouil, Stoyan Pavlov, Habib Bendella, and Doychin N. Angelov. Stimulation of Trigeminal Afferents Improves Motor Recovery After Facial Nerve Injury. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-33311-8.

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1952-, Marwah J., Teitelbaum Herman, and Prasad Kedar N, eds. Neural transplantation, CNS neuronal injury, and regeneration: Recent advances. Boca Raton: CRC Press, 1994.

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Skouras, Emmanouil. Stimulation of trigeminal afferents improves motor recovery after facial nerve injury: Functional, electrophysiological and morphological proofs. Heidelberg: Springer, 2013.

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Enescu, Cristina. Methods of enhancing mechanical properties of hydrogel tubes used as nerve guidance channels in rat spinal cord injury. Ottawa: National Library of Canada, 2003.

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Steve, Parker. Nerves & spinal cord: Injury, illness and health. Oxford: Heinemann Library, 2003.

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Book chapters on the topic "Nerve injury"

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Pannu, Neesh, Xiaoyan Wen, John A. Kellum, John Fildes, N. Al-Subaie, Mark Hamilton, Susan M. Lareau, et al. "Nerve Injury." In Encyclopedia of Intensive Care Medicine, 1519–24. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_478.

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Ficke, Brooks W., and Nileshkumar M. Chaudhari. "Nerve Injury." In Orthopedic Surgery Clerkship, 229–32. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-52567-9_52.

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Winterton, Robert I. S., and Simon P. J. Kay. "Nerve Injury." In Disorders of the Hand, 23–43. London: Springer London, 2014. http://dx.doi.org/10.1007/978-1-4471-6554-5_2.

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Feller, Ross. "Nerve Injury." In Essential Orthopedic Review, 111–13. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-78387-1_53.

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Allen, Shawn, and Roberta Sengelmann. "Nerve Injury." In Complications in Cutaneous Surgery, 21–35. New York, NY: Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-73152-0_3.

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Wang, Angela. "Ulnar Nerve Injury." In The Pediatric Upper Extremity, 529–42. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4614-8515-5_24.

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Peljovich, Allan, and Felicity Fishman. "Median Nerve Injury." In The Pediatric Upper Extremity, 543–62. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4614-8515-5_25.

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Kaushik, Anjan P., and Warren C. Hammert. "Radial Nerve Injury." In The Pediatric Upper Extremity, 563–86. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4614-8515-5_26.

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Wang, Angela. "Ulnar Nerve Injury." In The Pediatric Upper Extremity, 1–17. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-8758-6_24-1.

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Peljovich, Allan, and Felicity Fishman. "Median Nerve Injury." In The Pediatric Upper Extremity, 1–22. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-8758-6_25-1.

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Conference papers on the topic "Nerve injury"

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Bitenc Zore, Sara, Domen Vozel, and Saba Battelino. "Facial Nerve Reconstructive Surgery in Otorhinolaryngology and its Enhancement by Platelet- and Extracellular Vesicle-Rich Plasma Therapy." In Socratic Lectures 7. University of Lubljana Press, 2022. http://dx.doi.org/10.55295/psl.2022.d5.

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The facial nerve and its reconstructive surgical procedures are complex and challenging. The main function of facial nerve is namely motor innervation of facial muscles and its dysfunction presents as facial paralysis. Depending on the extent of facial nerve injury (neurapraxia, axonotmesis, neurotmesis) and consequently a physiological phenomenon of Wallerian degeneration, mechanism, location of the injury, time course of the paralysis and medical condition we decide about the type of the reconstructive surgery. Generally, possible surgical interventions to improve facial nerve functioning are mainly nerve decompression, neurorrhaphy/end-to-end anastomosis, interposition (cable) grafts and nerve rerouting. Moreover, most commonly nerves undergoing facial reconstruction are great auricular and sural nerves. In addition, nerve rehabilitation can be improved by using platelet-rich plasma (PRP/PVRP), applied directly to nerve. There are many roles of PVRP, described in the literature such as neuroprotective, neurogenic, neuroinflammatory, angiogenic role and improving hemostasis. Also, its neoplastic and proliferative effects were not reported. Considering all these features implementing PVRP in the facial nerve regenerative treatment has strong potential in the future. Keywords: Facial nerve; Reeconstructive surgery; Platelet and extracellular vesicle rich plasma; Nerve regeneration
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Bain, Allison C., and David F. Meaney. "Microstructural Kinematics During Elongation of Central Nervous System Tissue: Implications for Traumatic Axonal Injury." In ASME 1998 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1998. http://dx.doi.org/10.1115/imece1998-0076.

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Abstract Diffuse axonal injury (DAI) is the most common form of closed head injury and is responsible for over a third of all head injury deaths. Axons are the primary constituent of the white matter in the brain, and frequently form aligned tracts in the brain. Research has indicated that traumatic axonal injury occurs when these axons experience tensile strains above a critical level. Our laboratory is currently working toward identifying injurious strain levels for axons using the optic nerve stretch model. The optic nerve is an isolated bundle of aligned central nervous system (CNS) axons, thus, dynamic elongation of the optic nerve is an in vivo approximation of the process by which axons are injured in the brain.
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Winkelstein, Beth A., Raymond D. Hubbard, and Joyce A. DeLeo. "Biomechanics and Painful Injuries: Tissue and CNS Responses for Nerve Root Mechanical Injuries." In ASME 2003 International Mechanical Engineering Congress and Exposition. ASMEDC, 2003. http://dx.doi.org/10.1115/imece2003-43117.

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Pain affects as many as 50 million Americans, with annual costs estimated as high as $90 billion. Unfortunately, the mechanism of injuries leading to persistent pain syndromes remain largely uncharacterized. A common painful injury results due from mechanical loading of nerve roots, which can occur for spinal injuries in both the low back and neck. Relationships have been demonstrated between tissue compression and behavioral hypersensitivity responses in animal models, with differential patterns of sensitivity depending on the nature of the mechanical insult (Colburn et al., 1999). Mechanical allodynia (MA) is an increased behavioral sensitivity to a non-noxious stimulus and is observed in the dermatome of the injured tissue. It can be measured by the frequency of paw withdrawals elicited by stimulation with normally non-noxious von Frey filaments. Allodynia is a clinical measure of sensitivity and, therefore, provides a useful gauge of nociceptive responses. Animal studies have shown that compression of neural structures initiates a variety of physiologic responses, including decreased electrical activity, increased edema formation, and increased endoneurial pressure in the region of compression (Lundborg et al., 1983; Olmarker et al., 1989, 1990; Pedowitz et al., 1992). While these studies document physiologic changes immediately following injury, they do not describe the temporal nature of these changes following tissue loading as they relate to pain behaviors. Moreover, despite this evidence of edema formation and increased endoneurial pressure locally in the nerve roots, no study has simultaneously documented local changes in nerve root geometry following compressive injury and how these changes may be linked to the onset and/or maintenance of pain-associated behaviors. Therefore, this study examines injury biomechanics for pain-behaviors in a radiculopathy (nerve root injury) model and temporally characterizes the local geometric changes in the nerve root for a series of postsurgical time points following compressive injury. While these results indicate that compression magnitude clearly modulates pain responses, the local nerve root swelling does not appear to directly drive behavioral changes. This suggests a complicated physiology for injury which likely contributes to the manifestation of pain. Findings are also presented for preliminary investigations into tissue rebound/recovery responses for varied mechanical insult magnitudes to begin to understand potential injury mechanisms leading to pain.
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Chen, Xiaoming, Garrett W. Astary, Thomas H. Mareci, and Malisa Sarntinoranont. "In Vivo Contrast-Enhanced MR Imaging for Direct Infusion Into Rat Peripheral Nerve." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192919.

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Direct infusion of therapeutic agents into the spinal cord provides a promising way to treat traumatic injury and intrinsic diseases of the spinal cord, which may cause paralysis and other neurological deficits. Direct infusion into the spinal cord involves complex invasive surgery since the spinal cord is well protected by the vertebral bone. Instead, infusion directly into peripheral nerves is of interest since it provides a remote delivery site to the spinal cord, requiring less invasive surgery and reducing the risk of spinal cord injury during surgery. It may also allow targeting of specific neurons at nerve root entry. Previous studies have shown [1, 2] that transport in peripheral nerves is anisotropic with a preferred direction parallel to the fiber tracts. A large-scale longitudinal spread of molecular agents may be obtained and spread of molecular agents into the spinal cord may be possible.
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Whitehead, Tonya J., and Harini G. Sundararaghavan. "Electrospun Hyaluronic Acid Scaffolds Containing Microspheres for Protein Delivery to Support Peripheral Nerve Growth." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14630.

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Peripheral nerve injury can cause lifelong pain, loss of function, and decreased quality of life. The gold standard of repair is a nerve autograft; however this requires additional surgeries and can cause donor site morbidity. As an alternative, nerve growth conduits are being developed to guide he existing nerves to cross these injured gaps. Electrospinning has emerged as a popular method to produce fibrous scaffolds for use in tissue engineering applications. However, limited work has been done electrospinning Hyaluronic Acid (HA) a major component of the extra cellular matrix. Cells respond to several factors in their environment including chemical, mechanical, topographical and adhesion cues.1 Using electrospinning along with microspheres allows us to control mechanical, topographical, and chemical signals within our scaffold. Axons are known to respond to topographical cues, prefer ‘soft’ substrates and grow faster in the presence of Nerve Growth Factor (NGF). We can precisely control the mechanics of our scaffold by conjugating methacrylates to the HA backbone and crosslinking under UV light. We also use the rotation speed of the collection mandrel to create fibers that are aligned along one axis. Adhesivity is achieved by coating the finished scaffold with fibronectin. Microspheres are included to release protein and create a chemical signal. These characteristics combined mimic the natural environment of nervous tissue.
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Sheng, Shulei, Lifei Sun, Hongmin Zhou, Fengchen Ren, and Hailong Liu. "Nerve injury detection by means of conducting velocity distribution." In 2014 7th International Conference on Biomedical Engineering and Informatics (BMEI). IEEE, 2014. http://dx.doi.org/10.1109/bmei.2014.7002825.

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Zhang Guang-Hao, Huo Xiao-Lin, Wang Ai-Hua, Zhang Cheng, and Wu Chang-Zhe. "A model of injury potential for myelinated nerve fiber." In 2015 37th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2015. http://dx.doi.org/10.1109/embc.2015.7319255.

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Popova, Nadezhda. "COMPLEX RECOVERY OF THE UPPER LIMB AFTER NERVE TRANSFERS IN PATIENTS WITH ADULT BRACHIAL PLEXUS INJURIES." In INTERNATIONAL SCIENTIFIC CONGRESS “APPLIED SPORTS SCIENCES”. Scientific Publishing House NSA Press, 2022. http://dx.doi.org/10.37393/icass2022/147.

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ABSTRACT Introduction. Adult brachial plexus injuries may lead to a permanent physical impairment in the affected upper extremity. One of the most successful operative methods of treating these injuries is nerve transfer. Depending on the extent of the injury, one or more nerve transfers are usually done for better functional recovery. That is why the aim of our study is to present the results of a two-year postoperative follow-up of the complex upper limb function in patients with different nerve transfers after adult brachial plexus injuries. Methods: All of our 14 patients (mean age of 35.0 years) had one or more nerves in the shoulder and the elbow. The average time between injury and the first surgery was 7.1 months, and the average time between surgeries was 3.4 months. All patients underwent a physiotherapy program with electrostimulation, donor nerve activation exercises, and training activities for daily living. Some patients had also individual hand splints. The complex function of the upper extremity was assessed on the 12th and 24th postoperative month (POM) by the Bulgarian version of the questionnaire Disabilities of Arm, Shoulder, and Hand (DASH). Results: On the 12th POM the average total score of DASH was 49.3 points, and on the 24th POM it decreased to 27.6 points (α≤0.000) which shows an improvement in the complex function of the upper extremity. By the end of the 24th POM almost all of the patients have returned to their job before the accident. Six of our patients have also been practicing sports without serious difficulties in the end of the second postoperative year. Conclusion: The studied patients showed good recovery of the complex function of the upper limb after the nerve transfers. This led to both returning to work after the injury and practicing sports. Although the sample is small, it gives us valuable information about what function of the upper extremity could be expected in these patients.
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Bradeanu, Andrei Vlad, Loredana Pascu, Alexandru Bogdan Ciubara, and Dragos Cristian Voicu. "COMPLICATIONS OF HIP HEMIARTHROPLASTY IN PATIENTS WITH DEMENTIA." In The European Conference of Psychiatry and Mental Health "Galatia". Archiv Euromedica, 2023. http://dx.doi.org/10.35630/2022/12/psy.ro.8.

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ge is one of the most important parameters influencing the occurrence of hip fractures in patients over the age of 65, whereas their mental state is a decisive factor. Older adults have eight times higher risk of dying of a hip fracture if we compared to those people without a hip fracture. The risk of death is very high in the first three months and it remains in first ten years. High incidence of hip fracture and dementia worldwide includes Europe and Middle East part of Europe, South America, Canada, United States and Asia. There is a very high probability that patients with hip fractures and dementia may develop delirium that will result in prolonged hospitalization and poor mobility. Death is a rare complication of hip arthroplasty. Less than 1% patients in United States died, however in the first 90 days the postoperative mortality rate is somewhat higher than 1%. Otherwise, after revision surgery this rate increases. The most common complications of hip hemiarthroplasty that can be avoided by surgeons are: dislocation (posterior approach), and infection (the most common are Gram-positive Staphylococcus aureus- MRSA and Gram-negative bacillus). In one year the mortality rates will be over than half in the patients with deep infection and approximately 65% of patients with dislocation prosthesis in 6 months but also depends by type of prosthesis: monobloc (Austin Moore) or bipolar, cemented or uncemented. Other patient-related complications in the order in which they appear are pulmonary embolism, hematoma formation, unusual ossification, thromboembolism, nerve injury, fracture (periprosthetic). In patients who receive antiplatelet, anti-inflammatory, or anticoagulant therapy, it is necessary to stop the preoperative medication and to perform intraoperative hemostasis. During surgery, there is a risk to damage obturator vessels, perforating branch of femoralis artery and injury iliac vessels when drilling medial acetabular wall. In the last two decades thromboembolism has been prevented by physical therapy and socks with gradual compression. Depending on the type of surgeon's preferred type of proceedings, the following nerves may be injured: femoral nerve, sciatic nerve, and superior gluteal nerves.
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Smith, Jenell R., Sarah M. Rothman, Paul A. Janmey, and Beth A. Winkelstein. "Spinal PAR1 RNA Levels Are Regulated by Mechanical and Inflammatory Cues in Painful Nerve Root Compression." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53084.

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Radicular pain can be caused by a disc herniation that can compress the spinal nerve roots as they exit the spinal canal [1]. Pain models in the rat mimic both the mechanical and chemical components of a disc herniation, either individually or in combination, and have demonstrated that the specific injury inputs (i.e. mechanics, inflammation) modulate the pain responses [2,3]. For both types of nerve root injuries, allodynia (i.e. pain) is elevated as early as 1 day after injury but its temporal responses vary over time according to the type of injury insult [3]. Painful nerve root injuries also induce a host of inflammatory cascades in the spinal cord that promote neuronal healing [2–4]. Although inflammatory responses have been shown to relate to the onset and maintenance of pain following injury, the specific biochemical processes and their relationship to inflammation and pain symptoms are not yet fully defined.
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Reports on the topic "Nerve injury"

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Cao, Siyang, Yihao Wei, Tiantian Qi, Peng Liu, Yingqi Chen, Fei Yu, Hui Zeng, and Jian Weng. Stem cell therapy for peripheral nerve injury: An up-to-date meta-analysis of 55 preclinical researches. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2022. http://dx.doi.org/10.37766/inplasy2022.10.0083.

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Review question / Objective: It has been the gold standard for decades to reconstruct a large peripheral nerve injury with a nerve autograft, and this remains true today as well. In addition to nerve autografts, biological conduits and vessels can also be applied. A fair amount of studies have examined the benefits of adding stem cells to the lumen of a nerve conduit. The aim of this meta-analysis was to summarize animal experiments related to the utilization of stem cells as a luminal additive when rebuilding a peripheral nerve injury using nerve grafts. Eligibility criteria: The inclusion criteria were as following: 1.Reconstruction of peripheral nerve injury; 2.Complete nerve transection with gap defect created; 3.Animal in-vivo models; 4.Experimental comparisons between nerve conduits containing and not containing one type of stem cell; 5.Functional testing and electrophysiology evaluations are performed. The exclusion criteria were as following: 1.Repair of central nervous system; 2.Nerve repair is accomplished by end-to-end anastomosis; 3.Animal models of entrapment injuries, frostbite, traction injuries and electric injuries; 4.Nerve conduits made from autologous epineurium; 5.Clinical trials, reviews, letters, conference papers, meta-analyses or commentaries; 6.Same studies have been published in different journals under the same or a different title.
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Goeckeritz, Joel, Nathan Schank, Ryan L Wood, Beverly L Roeder, and Alonzo D Cook. Use of Urinary Bladder Matrix Conduits in a Rat Model of Sciatic Nerve Regeneration after Nerve Transection Injury. Science Repository, December 2022. http://dx.doi.org/10.31487/j.rgm.2022.03.01.

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Previous research has demonstrated the use of single-channel porcine-derived urinary bladder matrix (UBM) conduits in segmental-loss, peripheral nerve repairs as comparable to criterion-standard nerve autografts. This study aimed to replicate and expand upon this research with additional novel UBM conduits and coupled therapies. Fifty-four Wistar Albino rats were divided into 6 groups, and each underwent a surgical neurectomy to remove a 7-millimeter section of the sciatic nerve. Bridging of this nerve gap and treatment for each group was as follows: i) reverse autograft—the segmented nerve was reversed 180 degrees and used to reconnect the proximal and distal nerve stumps; ii) the nerve gap was bridged via a silicone conduit; iii) a single-channel UBM conduit; iv) a multi-channel UBM conduit; v) a single-channel UBM conduit identical to group 3 coupled with fortnightly transcutaneous electrical nerve stimulation (TENS); vi) or, a multi-channel UBM conduit identical to group 4 coupled with fortnightly TENS. The extent of nerve recovery was assessed by behavioural parameters: foot fault asymmetry scoring measured weekly for six weeks; electrophysiological parameters: compound muscle action potential (CMAP) amplitudes, measured at weeks 0 and 6; and morphological parameters: total fascicle areas, myelinated fiber counts, fiber densities, and fiber sizes measured at week 6. All the above parameters demonstrated recovery of the test groups (3-6) as being either comparable or less than that of reverse autograft, but none were shown to outperform reverse autograft. As such, UBM conduits may yet prove to be an effective treatment to repair relatively short segmental peripheral nerve injuries, but further research is required to demonstrate greater efficacy over nerve autografts.
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Goeckeritz, Joel, Nathan Schank, Ryan L Wood, Beverly L Roeder, and Alonzo D Cook. Use of Urinary Bladder Matrix Conduits in a Rat Model of Sciatic Nerve Regeneration after Nerve Transection Injury. Science Repository, December 2022. http://dx.doi.org/10.31487/j.rgm.2022.03.01.sup.

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Previous research has demonstrated the use of single-channel porcine-derived urinary bladder matrix (UBM) conduits in segmental-loss, peripheral nerve repairs as comparable to criterion-standard nerve autografts. This study aimed to replicate and expand upon this research with additional novel UBM conduits and coupled therapies. Fifty-four Wistar Albino rats were divided into 6 groups, and each underwent a surgical neurectomy to remove a 7-millimeter section of the sciatic nerve. Bridging of this nerve gap and treatment for each group was as follows: i) reverse autograft—the segmented nerve was reversed 180 degrees and used to reconnect the proximal and distal nerve stumps; ii) the nerve gap was bridged via a silicone conduit; iii) a single-channel UBM conduit; iv) a multi-channel UBM conduit; v) a single-channel UBM conduit identical to group 3 coupled with fortnightly transcutaneous electrical nerve stimulation (TENS); vi) or, a multi-channel UBM conduit identical to group 4 coupled with fortnightly TENS. The extent of nerve recovery was assessed by behavioural parameters: foot fault asymmetry scoring measured weekly for six weeks; electrophysiological parameters: compound muscle action potential (CMAP) amplitudes, measured at weeks 0 and 6; and morphological parameters: total fascicle areas, myelinated fiber counts, fiber densities, and fiber sizes measured at week 6. All the above parameters demonstrated recovery of the test groups (3-6) as being either comparable or less than that of reverse autograft, but none were shown to outperform reverse autograft. As such, UBM conduits may yet prove to be an effective treatment to repair relatively short segmental peripheral nerve injuries, but further research is required to demonstrate greater efficacy over nerve autografts.
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Lauer, Henrik, Cosima Prahm, Johannes T. Thiel, Jonas Kolbenschlag, Adrien Daigeler, David Hercher, and Johannes C. Heinzel. The grasping test revisited: A systematic review of functional recovery in rat models of median nerve injury. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2022. http://dx.doi.org/10.37766/inplasy2022.7.0074.

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Review question / Objective: This work aims to report and summarize the course of functional recovery following crush injuries, transections and segmental resection of the rat median nerve. Condition being studied: Peripheral nerve injuries. Eligibility criteria: Only such studies were included which featured at least two postoperative time points at in which functional recovery was evaluated. Main outcome(s): Functional recovery as assessed by the grasping test.
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Hoke, Ahmet, and Hai-Quan Mao. Use of GDNF-Releasing Nanofiber Nerve Guide Conduits for the Repair of Conus Medullaris/Cauda Equina Injury in the Nonhuman Primate. Fort Belvoir, VA: Defense Technical Information Center, December 2013. http://dx.doi.org/10.21236/ada613645.

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Hoke, Ahmet, and Hai-Quan Mao. Use of GDNF-Releasing Nanofiber Nerve Guide Conduits for the Repair of Conus Medullaris/Cauda Equina Injury in the Nonhuman Primate. Fort Belvoir, VA: Defense Technical Information Center, October 2012. http://dx.doi.org/10.21236/ada581474.

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Christe, Kari. Use of GDNF-Releasing Nanofiber Nerve Guide Conduits for the Repair of Conus Medullaris/Cauda Equina Injury in the Nonhuman Primate. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada599060.

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Christe, Kari, Leif Havton, and Ahmet Hoke. Use of GDNF-Releasing Nanofiber Nerve Guide Conduits for the Repair of Conus Medullaris/Cauda Equina Injury in the Non-Human Primate. Fort Belvoir, VA: Defense Technical Information Center, October 2012. http://dx.doi.org/10.21236/ada581480.

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Wang, Zilan, Xiaoxiao Wu, Xiaolong Liang, Youjia Qiu, Huiru Chen, Minjia Xie, Zhouqing Chen, Zhong Wang, and Gang Chen. Efficacy and safety of contralateral C7 nerve transfer for cerebral injury induced upper limb spastic paralysis: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2022. http://dx.doi.org/10.37766/inplasy2022.6.0016.

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