• The Korean Journal of Physiology and Pharmacology
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• v.9 no.3
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• pp.143-147
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• 2005

Following peripheral nerve injury, excessive nociceptive inputs result in diverse physiological alterations in the spinal cord substantia gelatinosa (SG), lamina II of the dorsal horn. Here, I report the alterations of excitatory or inhibitory transmission in the SG of a rat model for neuropathic pain ('spared nerve injury'). Results from whole-cell recordings of SG neurons show that the number of distinct primary afferent fibers, identified by graded intensity of stimulation, is increased at 2 weeks after spared nerve injury. In addition, short-term depression, recognized by paired-pulse ratio of excitatory postsynaptic currents, is significantly increased, indicating the increase of glutamate release probability at primary afferent terminals. The peripheral nerve injury also increases the amplitude, but not the frequency, of spontaneous inhibitory postsynaptic currents. These data support the hypothesis that peripheral nerve injury modifies spinal pain conduction and modulation systems to develop neuropathic pain.

• Korean Journal of Veterinary Research
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• v.44 no.4
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• pp.483-486
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• 2004

The expression of nestin and vimentin in the spinal nerve roots of rats with experimental autoimmune encephalomyelitis (EAE) was studied to ascertain whether Schwann cells in the peripheral nerves respond to acute central nervous system autoimmune injury. Immunohistochemistry demonstrated that nestin was constitutively expressed in the dorsal roots of spinal nerves in control rats; its expression was enhanced in the spinal nerve roots of rats with EAE. Vimentin expression was weak in control rat spinal nerve roots, and it was increased in the dorsal roots of rats with EAE. It is postulated that normal animals have multipotent progenitor cells that constitutively express nestin and vimentin in the spinal nerve roots. In response to an injury of the central nervous system, these multipotent Schwann cells are activated in the spinal nerve roots through the expression of the intermediate filament proteins vimentin and nestin.

• Journal of Korean Neurosurgical Society
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• v.39 no.1
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• pp.52-57
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• 2006

Objective : It has been suggested that the occurrence of persistent pain signal during the early postnatal period may alter an individual's response to pain later in life. The aim of this study is to assess whether neonatal nerve injury resulted in long-lasting consequences on nociceptive system in the rat. Methods : We examined whether neuropathic pain behaviors and the changes of spinal neuropeptides [SP, CGRP, VIP and VIP] induced by peripheral nerve injury within 1 day after birth [Neonate group] were different from those at 8 weeks after birth [Mature group]. Results : The Neonate group showed more robust and long-lasting pain behaviors than the Mature group. Immunohistochemical findings demonstrated that spinal SP- & CGRP-immunoreactivities[ir] of the ipsilateral to the contralateral side increased in the Neonate group, whereas those decreased in the Mature group. In addition, increase in spinal VIP- & NPY-ir of the ipsilateral to the contralateral side was more robust in the Mature group than in the Neonate group. Conclusion : These results suggest that peripheral nerve injury in the early postnatal period may result in long-lasting and potentially detrimental alterations in nociceptive pathways.

• Journal of Korean Biological Nursing Science
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• v.4 no.1
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• pp.101-112
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• 2002

Peripheral nerve injury results in plastic changes in the dorsal ganglia (DRG) and spinal cord, and is often complicated with neuropathic pain. The mechanisms underlying these changes are not known, but these changes seem to be most likely related to the neurotrophic factors. This study investigated the effects of mechanical peripheral nerve injury on expression of brain-derived neurotrophic factor(BDNF) in the DRG and spinal cord in rats. 1) Bennett model and Chung model groups showed significantly increased percentage of small, medium and large BDNF-immunoreactive neurons in the ipsilateral $L_4$ DRG compared with those in the contralateral side at 1 and 2 weeks of the injury. 2) In the ipsilateral $L_5$ DRG of the Chung model, percentage of medium and large BDNF-immunoreactive neurons increased significantly at 1 week, whereas that of large BDNF-immunoreactive neurons decreased at 2 week when compared with those in the contralateral side. The intensity of immunoreactivity of each neuron was lower in the ipsilateral than in the contralateral DRG. 3) In the spinal cord, the Bennett and Chung model groups showed a markedly increased BDNF-immunoreactivity in axonal fibers of both superficial and deeper laminae. The present study demonstrates that peripheral nerve injury in neuropathic models altered the BDNF expression in the DRG and spinal cord. This may suggest important roles of BDNF in sensory abnormalities after nerve injury and in protecting the large-sized neurons in the damaged DRG.

• Archives of Plastic Surgery
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• v.49 no.3
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• pp.440-443
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• 2022

Spinal accessory nerve (SAN) palsy is typically a result of posterior triangle surgery and can present with partial or complete paralysis of the trapezius muscle and severe shoulder dysfunction. We share an atypical case of a patient who presented with SAN palsy following an injury sustained playing competitive volleyball. A 19-year-old right hand dominant competitive volleyball player presented with right shoulder weakness, dyskinesia, and pain. She injured the right shoulder during a volleyball game 2 years prior when diving routinely for a ball. On physical examination she had weakness of shoulder shrug and a pronounced shift of the scapula when abducting or forward flexing her shoulder greater than 90 degrees. Manual stabilization of the scapula eliminated this shift, so we performed scapulopexy to stabilize the inferior angle of the scapula. At 6 months postoperative, she had full active range of motion of the shoulder. SAN palsy can occur following what would seem to be a routine volleyball maneuver. This could be due to a combination of muscle hypertrophy from intensive volleyball training and stretch sustained while diving for a ball. Despite delayed presentation and complete atrophy of the trapezius, a satisfactory outcome was achieved with scapulopexy.

• The Journal of Korean Physical Therapy
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• v.19 no.2
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• pp.41-55
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• 2007

Purpose: This study aimed to compare the effect on nerve regeneration of ultrasound irradiation in rats with peripheral nerve injury. Methods: To investigate alterations of the NCAM immunoreactivity in non-crushed part and crushed part of the spinal cord, the unilateral sciatic nerve of the rats were crushed. The expression of NCAM was used as the marked of peripheral nerve regeneration, and also plays an important role in developing nerve system. Experimental animals were sacrificed by perfusion fixation at post-injury 1, 3, 7, 14 days after ultrasound irradiation. The pulsed US was applied at a frequency of 1MHz and a spatial average-temporal average Intensity of 0.5W/of (20% pulse ratio) for 1 mins. The Luxol fast blue-cresyl violet stain were also done to observe the morphological changes. Results: Alteration of NCAM immunoreactivity in the crushed part and the non-crushed part of lower lumbar spinal cord were observed. NCAM-immunoreactivity cells were some increased in the dorsal horn lamina I, III and cell ventral horn at 1 day after unilateral sciatic nerve injury. However, there was not significant difference in the relationship between crushed part and non-crushed part. NCAM-inmmunoreactivity was remarkably increased at 3 days after unilateral sciatic nerve injuryin the gray matter and white matter. NCAM-immunoreactivity was increased in the ventral horn and post horn of experimental crushed part. Also, NCAM-immunoreactivity in large motor neurons in ventral horns lamina VIII, IX were increased at 7 days after unilateral sciatic nerve injury. At 14 days after sciatic nerve crushed injury, there was no significant difference. All group were decreased for 14 days. In the time course of NCAM expression, all groups showed a significant difference at 3day groups(p<0.05). Whereas, CC group was noted a significant difference between 3day and 7 day group respectively. In NCAM expression, there were significantly increased in all group. In the relationship between CNC group and ENC group, significant difference was detected among 3, 7, 14 day group(p<0.05). The difference between CC group and ENC group were noted in all groups(p<0.05). Conclusion: It is consequently suggested that the effects of the ultrasound irradiation may increase the NCAM immunoreactive neurons and glial cell in the spinal cord after unilateral sciatic nerve crushed injury. Therefore, the increased NCAM immunoreactivity in the spinal cord may reflect the neuronal damage and healing process induced by a ultrasound irradiation after peripheral nerve injury in rat.

• Journal of Korean Neurosurgical Society
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• v.54 no.4
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• pp.359-362
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• 2013

Chronic hypoventilation due to injury to the brain stem respiratory center or high cervical cord (above the C3 level) can result in dependence to prolonged mechanical ventilation with tracheostomy, frequent nosocomial pneumonia, and prolonged hospitalization. Diaphragm pacing through electrical stimulation of the phrenic nerve is an established treatment for central hypoventilation syndrome. We performed chronic phrenic nerve stimulation for diaphragm pacing with the spinal cord stimulator for pain control in a quadriplegic patient with central apnea due to complete spinal cord injury at the level of C2 from cervical epidural hematoma. After diaphragmatic pacing, the patient who was completely dependent on the mechanical ventilator could ambulate up to three hours every day without aid of mechanical ventilation during the 12 months of follow-up. Diaphragm pacing through unilateral phrenic nerve stimulation with spinal cord stimulator was feasible in an apneic patient with complete quadriplegia who was completely dependent on mechanical ventilation. Diaphragm pacing with the spinal cord stimulator is feasible and effective for the treatment of the central hypoventilation syndrome.

• Korean Journal of Medicinal Crop Science
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• v.16 no.3
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• pp.183-187
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• 2008

Nerve injury can lead to neuropathic pain, which is often resistant to current analgesics and interventional therapeutic methods. Extracellular signal-regulated kinase (ERK) plays important role in the induction of neuropathic pain. We explored the antinociceptive effect of curcumin and its effect on ERK in the spinal cord in the neuropathic pain model of rats induced by chronic constriction injury (CCI) of the sciatic nerve. In injured rats, mechanical allodynia, which is one of characteristics of neuropathic pain developed and the activation of ERK in spinal cord significantly increased compared with control group. However, administration of curcumin (50 mg/kg/day p.o) for 7 days started from one day before the injury prevented the development of mechanical allodynia and increase of ERK phosphorylation. These results indicate that curcumin can be a new therapeutic agent in the treatment of neuropathic pain.

• The Korean Journal of Pain
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• v.25 no.4
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• pp.213-220
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• 2012

Background: It has been demonstrated that the expression of tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) and apoptotic cell death in the dorsal root ganglion (DRG) following spinal nerve constriction injury play a role in the initiation and continuation of hyperalgesia and allodynia. The present study was designed to investigate the effects of ethyl pyruvate (EP) on mechanical and cold allodynia, TNF-${\alpha}$ expression, and apoptosis in DRG after spinal nerve ligation injury. Methods: Rats were divided into 3 groups: control, pre-EP, and post-EP. EP (50 mg/kg) was intraperitoneally injected 30 minutes before (pre-EP) or after (post-EP) surgery. Behavioral tests to determine mechanical and cold allodynia were conducted before surgery and 4 and 7 days after surgery. Seven days after surgery, TNF-${\alpha}$ protein levels in DRG were evaluated by enzyme-linked immunosorbent assay, and DRG apoptosis was determined by immunohistochemical detection of activated caspase-3. Results: Treatment with EP significantly reduced mechanical and cold allodynia following spinal nerve ligation injury. TNF-${\alpha}$ protein levels in the pre-EP ($4.7{\pm}1.2$ pg/200 ${\mu}g$; P < 0.001) and post-EP ($6.4{\pm}1.8$ pg/200 ${\mu}g$; P < 0.001) groups were 2-3 times lower than the control group ($14.4{\pm}1.2$ pg/200 ${\mu}g$). The percentages of neurons and satellite cells that co-localized with caspase-3 were also significantly lower in the pre-EP and post-EP groups than the control group. Conclusions: These results demonstrate that EP has a strong anti-allodynic effect that acts through the inhibition of TNF-${\alpha}$ expression and apoptosis in DRG after spinal nerve ligation injury.

• The Korean Journal of Physiology and Pharmacology
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• v.14 no.2
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• pp.59-69
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• 2010

Impairment in spinal inhibition caused by quantitative alteration of GABAergic elements following peripheral nerve injury has been postulated to mediate neuropathic pain. In the present study, we tested whether neuropathic pain could be induced or reversed by pharmacologically modulating spinal GABAergic activity, and whether quantitative alteration of spinal GABAergic elements after peripheral nerve injury was related to the impairment of GABAergic inhibition or neuropathic pain. To these aims, we first analyzed the pain behaviors following the spinal administration of GABA antagonists ($1{\mu}g$ bicuculline/rat and $5{\mu}g$ phaclofen/rat), agonists ($1{\mu}g$ muscimol/rat and $0.5{\mu}g$ baclofen/rat) or GABA transporter (GAT) inhibitors ($20{\mu}g$ NNC-711/rat and $1{\mu}g$ SNAP-5114/rat) into naive or neuropathic animals. Then, using Western blotting, PCR or immunohistochemistry, we compared the quantities of spinal GABA, its synthesizing enzymes (GAD65, 67) and its receptors (GABAA and GABAB) and transporters (GAT-1, and -3) between two groups of rats with different severity of neuropathic pain following partial injury of tail-innervating nerves; the allodynic and non-allodynic groups. Intrathecal administration of GABA antagonists markedly lowered tail-withdrawal threshold in naive animals, and GABA agonists or GAT inhibitors significantly attenuated neuropathic pain in nerve-injured animals. However, any quantitative changes in spinal GABAergic elements were not observed in both the allodynic and non-allodynic groups. These results suggest that although the impairment in spinal GABAergic inhibition may play a role in mediation of neuropathic pain, it is not accomplished by the quantitative change in spinal elements for GABAergic inhibition and therefore these elements are not related to the generation of neuropathic pain following peripheral nerve injury.