• Applied Microscopy
• /
• v.39 no.3
• /
• pp.261-266
• /
• 2009

This study aim to disclose a possible mechanism for the neuronal cell death induced by peripheral nerve injury following a spinal nerve ligation (SNL) as a neuropathic pain model. Male Sprague-Dawley rats (270~290 g) were used for this study. Pain threshold was evaluated for their response to mechanical (von Frey hairs) stimuli 1, 3, and 7 days after a tight ligation of L5 ventral ramus. In control group, the small ganglion cells were strongly stained with routine toluidine blue (TB), whereas the large ganglion cells showed a little bit weak stainity. Each large ganglion cell is surrounded by perineuronal satellite cells. In experimental groups, small ganglion cells showing apparent degenerative changes increased on 1 day, and showed a peak in degenerative cell number at 3 days group, and decreased gradually at 7 days group. We also found a small number of large-sized ganglion cells showing mild degenerative changes. However their satellite cells ware relatively intact with no typical findings throughout this experiment. Under the electron microscope, small ganglion cells showed various stage and typical features of the dark degeneration including mitochondrial swelling.

• Clinics in Shoulder and Elbow
• /
• v.18 no.2
• /
• pp.102-104
• /
• 2015

In this report, a case of a 70-year-old man with a large ganglion cyst formed after anterior transposition of the left ulnar nerve is presented. Three months after the index surgery, the patient presented with a painless superficial ovoid, soft mass measuring $5{\times}4{\times}2cm$ in size located at the posteromedial aspect of the left elbow, the previously operated site. Magnetic resonance imaging showed a well demarcated cystic mass with a stalk connecting to the elbow joint. Excisional biopsy was performed and pathologic findings showed that the cystic wall had no definite lining cells with myxoid degeneration compatible with findings of ganglion cyst.

• The Korean Journal of Pain
• /
• v.24 no.2
• /
• pp.69-73
• /
• 2011

Although the incidence of partial-thickness rotator cuff tears (PTRCTs) was reported to be from 13% to 32% in cadaveric studies, the actual incidence is not yet known. The causes of PTRCTs can be explained by either extrinsic or intrinsic theories. Studies suggest that intrinsic degeneration within the rotator cuff is the principal factor in the pathogenesis of rotator cuff tears. Extrinsic causes include subacromial impingement, acute traumatic events, and repetitive microtrauma. However, acromially initiated rotator cuff pathology does not occur and extrinsic impingement does not cause pathology on the articular side of the tendon. An arthroscopic classification system has been developed based on the location and depth of the tear. These include the articular, bursal, and intratendinous areas. Both ultrasound and magnetic resonance image are reported with a high accuracy of 87%. Conservative treatment, such as subacromial or intra-articular injections and suprascapular nerve block with or without block of the articular branches of the circumflex nerve, should be considered prior to operative treatment for PTRCTs.

• YAKHAK HOEJI
• /
• v.36 no.3
• /
• pp.269-277
• /
• 1992

The effects of ginseng saponins on the distribution of nerve cells in cerebral cortex of carbon monoxide (CO)-intoxicated mice were studied in the young ($5{\sim}8$ weeks) and aged ($43{\sim}52$ weeks) mice. Mice were exposed to 5000 ppm of CO for 40 minutes (72% HbCO). After that, nerve cells in motor(area 4), somatosensory(area 3) and visual(area 17) area of cerebral cortex was observed. In young mice, the number of nerve cells in each area was significantly decreased on 1st, 7th and 14th day after CO intoxication. In aged mice, that was also decreased after CO intoxication. Especially the number of the nerve cells in motor and somatosensory area was significantly decreased on 1st and 7th day, while that in visual area was decreased only on 1st day. The number of nerve cells in young mice pretreated with ginseng saponins were significantly decreased less on 7th and 14th day than that of untreated mice. The number of nerve cells in each area of normal aged mice was larger than that of normal young mice. The results suggest that CO exposure causes local degeneration or disturbance of nerve cells and delayed neurologic sequelae, while ginseng saponins might play a role of protective action on the nerve cells which were damaged by CO.

• The Korean Journal of Pain
• /
• v.29 no.3
• /
• pp.158-163
• /
• 2016

Background: Phenol and alcohol have been used to ablate nerves to treat pain but are not specific for nerves and can damage surrounding soft tissue. Lidocaine at concentrations > 8% injected intrathecal in the animal model has been shown to be neurotoxic. Tests the hypothesis that 10% lidocaine is neurolytic after a peri-neural blockade in an ex vivo experiment on the canine sciatic nerve. Methods: Under ultrasound, one canine sciatic nerve was injected peri-neurally with 10 cc saline and another with 10 cc of 10% lidocaine. After 20 minutes, the sciatic nerve was dissected with gross inspection. A 3 cm segment was excised and preserved in 10% buffered formalin fixative solution. Both samples underwent progressive dehydration and infusion of paraffin after which they were placed on paraffin blocks. The sections were cut at $4{\mu}m$ and stained with hemoxylin and eosin. Microscopic review was performed by a pathologist from Henry Ford Hospital who was blinded to which experimental group each sample was in. Results: The lidocaine injected nerve demonstrated loss of gross architecture on visual inspection while the saline injected nerve did not. No gross changes were seen in the surrounding soft tissue seen in either group. The lidocaine injected sample showed basophilic degeneration with marked cytoplasmic vacuolation in the nerve fibers with separation of individual fibers and endoneurial edema. The saline injected sample showed normal neural tissue. Conclusions: Ten percent lidocaine causes rapid neurolytic changes with ultrasound guided peri-neural injection. The study was limited by only a single nerve being tested with acute exposure.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
• /
• v.31 no.3
• /
• pp.239-247
• /
• 2005

This study demonstrated that xenogenic human marrow mesenchymal stem cells (hMSCs) could elicit the regeneration of the sensory nerve after axotomy in the adult rats infraorbital nerves without immunosuppression. For this, we evaluated the behavioral testing for functional recovery of the nerve and histological findings at weeks 3 and 5 compared to controls. Xenogenic hMSCs did not evoke any significant inflammatory or immunologic reaction after systemic and local administrations. HMSCs-treated rats exhibited significant improvement on sensory recovery tested with von Frey monofilaments. At 5 postoperative weeks, in the hMSCs treated nerve, expression of myelin basic protein (MBP), neurofilament (NF) at the site of axotomy was higher than control. And mRNA expression of neurotropin receptor Trk precursor (TrkPre), nerve growth factor receptor (NGFR) and neuropeptide (NPY) in trigeminal ganglion were also higher. The number of myelinated nerve at distal stump and cells in trigeminal ganglion were higher in hMSC treated rats. So it was supposed that transplanted MSCs contributed to reducing post-traumatic degeneration and production of neurotrophic factors. Immunofluorescence labeling showed small portion of hMSCs (<10%) expressed a phenotypic marker of Schwann cell (S-100). Xenogenic or allogenic mesenchymal stem cells might have immune privileged characteristics and useful tool for cell based nerve repair.

• Maxillofacial Plastic and Reconstructive Surgery
• /
• v.35 no.6
• /
• pp.376-380
• /
• 2013

Frey syndrome is a disease characterized by abnormal sweating, facial redness, and rare pain by stimulation of taste sense on the limited area dominated by the auriculotemporal nerve and great auricular nerve. Although the developmental mechanism and histopathologic cause of Frey syndrome are still being debated, the most reliable theory is based on injury of the parathympathetic nerve connected to the auriculotemporal nerve continuing to abnormal regeneration. The other theory is that the sweat glands develop an increased sensitivity after degeneration of sympathetic fibers. Therapy of Frey syndrome includes drugs, radiographic treatment, and surgical treatment; however, in most cases, treatment is not satisfactory. This is a case report on a 24-year-old male patient with Frey syndrome caused by the fracture reduction with retromandibular approach after multiple facial traumas and spontaneous healing without any special treatment.

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

• Journal of Korean Neurosurgical Society
• /
• v.58 no.6
• /
• pp.504-507
• /
• 2015

Objective : Our aim was to evaluate the histopathological effects of tissue adhesives on peripheral nerve regeneration after experimental sciatic nerve transection in rats and to search whether these tissue adhesives may possess a therapeutic potential in peripheral nerve injuries. Methods : This experimental study was performed using 42 female Wistar-Albino rats distributed in 6 groups subsequent to transection of right sciatic nerves. Group I underwent external circumferential neurolysis; Group II received suture repair; Group III had local polymeric hydrogel based tissue adhesive administration; Group IV received suture repair and polymeric hydrogel based tissue adhesive application together; Group V had gelatin based tissue adhesive application and Group VI had suture repair and gelatin based tissue adhesive together. After a 6-week follow-up period, biopsies were obtained from site of neural injury and groups were compared with respect to histopathological scoring based on inflammatory, degenerative, necrotic and fibrotic changes. Results : There were remarkable differences between control group and study groups with respect to inflammation (p=0.001), degeneration (p=0.002), necrosis (p=0.007), fibrosis (p<0.001) and vascularity (p=0.001). Histopathological scores were similar between study groups and the only noteworthy difference was that Group V displayed a lower score for necrosis and higher score in terms of vascularization. Conclusion : Our results imply that tissue adhesives can be useful in repair of peripheral nerve injuries by decreasing the surgical trauma and shortening the duration of intervention. Results with gelatin based tissue adhesive are especially promising since more intense vascularity was observed in tissue after application. However, trials on larger series with longer durations of follow-up are essential for reaching more reliable conclusions.

• Journal of Preventive Medicine and Public Health
• /
• v.20 no.2 s.22
• /
• pp.236-246
• /
• 1987

n-Hexane and benzene are organic compounds which have been widely used as industrial solvents. However, they are also increasingly recognized as important pollutants in working environment. The purpose of this study is tp analyze neurotoxicity of benzene and n-hexane. In this study, tibial nerve of Sprague-Dawley rats were observed after exposing them to two different concentrations of these compounds (6000 ppm of n-hexane and 2000 ppm of benzene) which were known to be the levels to cause subacute toxicity for the three different periods; two weeks, four weeks, and six weeks. The following results were obtained from the analysis of variance, Duncan's multiple comparison test, and regression analysis: 1) Myelin sheath thickness of nerve fiber for two n-hexane exposed groups (four weeks and six weeks) were both reduced compared with the control group and the benzene exposed group. 2) There were positive relationships between nerve fiber diameter and myelin sheath thickness for both exposed and control groups. 3) There was no significant difference in myelin sheath thickness from equal diameter nerve fibers between benzene exposed group and control group, but the greater number of thin myelin sheath were observed for n-hexane exposed group compared with control group. Thus, it is concluded that n-hexane tends to reduce the rate of growth of nerve fiber more than the benzene and control group. While these results shed light on understanding the effects of benzene and n-hexane, the duration of exposure was not long enough to apply these results to real working environments. In addition, to further understand the mechanims of nerve degeneration caused by organic solvents, both epidemiological and biochemical studies should accompanied by this kind of study.