• 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.

• Journal of The Korean Society of Clinical Toxicology
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• v.13 no.1
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• pp.46-49
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• 2015

Carbon monoxide (CO) intoxication is a leading cause of severe neuropsychological impairments. Peripheral nerve injury has rarely been reported. Following are brief statements describing the motor peripheral neuropathy involved bilateral lower extremities of a patient who recovered following acute carbon monoxide poisoning. After inhalation of smoke from a fire, a 60-year-old woman experienced bilateral leg weakness without edema or injury. Neurological examination showed diplegia and deep tendon areflexia in lower limbs. There was no sensory deficit in lower extremities, and no cognitive disturbances were detected. Creatine kinase was normal. Electroneuromyogram patterns were compatible with the diagnosis of bilateral axonal injury. Clinical course after normobaric oxygen and rehabilitation therapy was marked by complete recovery of neurological disorders. Peripheral neuropathy is an unusual complication of CO intoxication. Motor peripheral neuropathy involvement of bilateral lower extremities is exceptional. Various mechanisms have been implicated, including nerve compression secondary to rhabdomyolysis, nerve ischemia due to hypoxia, and direct nerve toxicity of carbon monoxide. Prognosis is commonly excellent without sequelae. Emergency physicians should understand the possible-neurologic presentations of CO intoxication and make a proper decision regarding treatment.

• Journal of Korean Neurosurgical Society
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• v.63 no.2
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• pp.171-177
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• 2020

Objective : To evaluate the neuroprotective effects of lacosamide after experimental peripheral nerve injury in rats. Methods : A total of 28 male wistar albino rats weighing 300-350 g were divided into four groups. In group I, the sciatic nerve exposed and the surgical wound was closed without injury; in group II, peripheral nerve injuries (PNI) was performed after dissection of the nerve; in group III, PNI was performed after dissection and lacosamide was administered, and in group IV, PNI was performed after dissection and physiological saline solution was administered. At 7 days after the injury all animals were sacrificed after walking track analysis. A 5 mL blood sample was drawn for biochemical analysis, and sciatic nerve tissues were removed for histopathological examination. Results : There is low tissue damage in lacosamide treated group and antioxidant anzymes and malondialdehyde levels were higher than non-treated and placebo treated group. However there was no improvement on clinical assessment. Conclusıon : The biochemical and histological analyses revealed that lacosamide has neuroprotective effect in PNI in rats. This neuroprotective capacity depends on its scavenger role for free oxygen radicals by increasing antioxidant enzyme activity.

• The Journal of Korean Physical Therapy
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• v.12 no.3
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• pp.415-432
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• 2000

In mammals. axotomy of peripheral nerve leads to a complex. These events include swelling of cell body, disappearance of Nissl substance. Proximal and distal axon undergoes a variable deriable degree of traumatic degeneration and wallerian degeneration, respectively. Nerve injury may result in cell death or regeneration. Molecular changes include proliferation of Schwann cells, upregulation of neurotropism, neural cell adhesion molecules and cytokine. Also growth cone plays an essential role in axon guidance through interaction of cytoskeleton. We review cellular and molecular events after nerve injury and describe nerve regeneration and associated proteins.

• The Korean Journal of Pain
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• v.21 no.3
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• pp.187-196
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• 2008

Background: Upregulation of one type of the pro-inflammatory chemokine (CCL2) and its receptor (CCR2) following peripheral nerve injury contributes to the induction of neuropathic pain. Here, we examined whether another type of chemokine (CCL3) is involved in neuropathic pain. Methods: We measured changes in mechanical and thermal sensitivity in the hind paws of naïve rats or rats with an L5 spinal nerve ligation (SNL) after intra-plantar injection of CCL3 or met-RANTES, an antagonist of the CCL3 receptor, CCR1. We also measured CCL3 levels in the sciatic nerve and the hind paw skin as well as CCR1 expression in dorsal root ganglion (DRG) cells from the lumbar spinal segments. Results: Intra-plantar injection of CCL3 into the hind paw of naive rats mimicked L5 SNL-produced hyperalgesia. Intra-plantar injection of met-RANTES into the hind paw of rats with L5 SNL attenuated hyperalgesia. L5 SNL increased CCL3 levels in the sciatic nerve and the hind paw skin on the affected side. The number of CCR1-positive DRG cells in the lumbar segments was not changed following L5 SNL. Conclusions: Partial peripheral nerve injury increases local CCL3 levels along the degenerating axons during Wallerian degeneration. This CCL3 binds to its receptor, CCR1, located on adjacent uninjured afferents, presumably nociceptors, to induce hyperalgesia in the neuropathic pain state.

• The Journal of Korean Medicine
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• v.27 no.4
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• pp.116-124
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• 2006

Peripheral nerve injuries are a commonly encountered clinical problem and often result in chronic pain and severe functional deficits. At the Dept. of Oriental Rehab. Medicine, we have used for pain control a herbal bath containing the following herbs: Harpagophytum radix, Atractylodes japonica and Corydalis tuber. In the present study, we investigated the effects of this herbal bath on the recovery rate of the locomotor function and the expression of c-Fos in the ventrolateral periaqueductal gray (vIPAG) region of the brain following sciatic crushed nerve injury in rats. In the present study, characteristic gait change with decreasing of the sciatic function index (SFI) was observed and c-Fos expression in the vIPAG was suppressed following sciatic crushed nerve injury in rats. Immersion into herbal bath enhanced SFI value and restored c-Fos expression in the vIPAG to the control value. These results suggest the herbal bath might activate neurons in the vIPAG, and could facilitate functional recovery from peripheral nerve injury.

• 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.

• The Journal of Internal Korean Medicine
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• v.34 no.4
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• pp.384-404
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• 2013

Objectives : Effects of Bogijetong-tang (BJT) on peripheral nerve regeneration have been reported in a previous study on BJT but additional study on a damaged peripheral neuropathy where its damage level is physically and chemically more severe was needed. Plus, this study was conducted because there haven't been any studies for BJT on central nerve regeneration. Methods : In order to check the effect on central nerve regeneration, the study on cerebellum cells was started and the sciatic nerve was used to observe the effects on a peripheral nerve which was severely damaged both physically and chemically. Nerve recovery effects were observed by analyzing target proteins such as phospho-extracellular signal-regulated kinase, ${\beta}1$ integrin, neurofilament 200, growth-associated protein-43, cyclin-dependent kinase 1, phospho-vimentin, phospho-Smad, and caspase 3. Results : The significant changes of target protein in cerebellum neurons have been observed. The changes of index protein on the axon regeneration and the nerve recovery in the sciatic nerve have been observed and the effects on cell protection were observed, as well. Conclusions : This study confirmed that BJT made a significant influence on nerve protection and recovery of a damaged peripheral neuropathy and it also made a possibility of its regeneration in a damaged central nerve injury.

• The Korean Journal of Pain
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• v.19 no.1
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• pp.33-44
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• 2006

Background: Peripheral nerve injury leads to neuropathic pain, including mechanical hyperalgesia (MH). Nerve discharges produced by an injury to the primary afferents cause the release of glutamate from both central and peripheral terminals. While the role of centrally released glutamate in MH has been well studied, relatively little is known about its peripheral role. This study was carried out to determine if the peripherally conducting nerve impulses and peripheral glutamate receptors contribute to the generation of neuropathic pain. Methods: Rats that had previously received a left L5 dorsal rhizotomy were subjected to a spinal nerve lesion (SNL) or brief electrical stimulation (ES, 4 Hz pulses for 5 min) of the left L5 spinal nerve. The paw withdrawal threshold (PWT) to von Frey filaments was measured. The effects of an intraplantar (i.pl.) injection of a glutamate receptor (GluR) antagonist or agonist on the changes in the SNL- or ES-produced PWT was investigated. Results: SNL produced MH, as evidenced by decrease in the PWT, which lasted for more than 42 days. ES also produced MH lasting for 7 days. MK-801 (NMDAR antagonist), DL-AP3 (group-I mGluR antagonist), and APDC (group-II mGluR agonist) delayed the onset of MH when an i.pl. injection was given before SNL. The same application blocked the onset of ES-induced MH. NBQX (AMPA receptor antagonist) had no effect on either the SNL- or ES-induced onset of MH. When drugs were given after SNL or ES, MK-801 reversed the MH, whereas NBQX, DL-AP3, and APDC had no effect. Conclusions: Peripherally conducting impulses play an important role in the generation of neuropathic pain, which is mediated by the peripheral glutamate receptors.

• Journal of International Academy of Physical Therapy Research
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• v.3 no.1
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• pp.345-355
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• 2012

This study purposed to examine the effect of low power laser on pain response and axonal regeneration. In order to prepare peripheral nerve injury models, we crushed the sciatic nerve of Sprague-Dawley rats and treated them with low power laser for 21 days. The rats were divided into 4 groups: normal group(n=10); control group(n=10) without any treatment after the induction of sciatic nerve crush injury; experimental group I(n=10) treated with low power laser(0.21$mJ/mm^2$) after the induction of sciatic nerve crush injury; and experimental group II(n=10) treated with low power laser(5.25$mJ/mm^2$) after the induction of sciatic nerve crush injury. We measured spontaneous pain behavior(paw withdrawal latency test) and mechanical allodynia(von Frey filament test) for evaluating pain behavioral response, and measured the sciatic function index for evaluating the functional recovery of peripheral nerve before the induction of sciatic nerve crush injury and on day 1, 7, 14 and 21 after the induction. After the experiment was completed, changes in the H & E stain and toluidine blue stain were examined histopathologically, and changes in MAG(myelin associated glycoprotein) and c-fos were examined immunohistologically. According to the results of this study, when low power laser was applied to rat models with sciatic nerve crush injury for 21 days and the results were examined through pain behavior evaluation and neurobehavioral, histopathological and immunohistological analyses, low power laser was found to affect pain response and axonal regeneration in both experimental group I and experimental group II. Moreover, the effect on pain response and axonal regeneration was more positive in experimental group I to which output 0.21$mJ/mm^2$ was applied than in experimental group II to which 5.25$mJ/mm^2$ was applied.