• Clinical Pain
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• v.20 no.1
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• pp.43-48
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• 2021

Sciatic nerve can be injured by various mechanism such as compression, traction during surgery, and direct trauma. This case reports a sciatic neuropathy caused by compression due to hematoma occurring after intramuscular injection in the gluteus medius muscle far from the nerve. In order to avoid occurrence of sciatic neuropathy after buttock injection, the injection was made in the upper outer quadrant of the buttock, but sciatic neuropathy occurred. Sciatic neuropathy can be confused with lumbar radiculopathy, so differential diagnosis is important.

• Environmental Analysis Health and Toxicology
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• v.9 no.1_2
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• pp.1-8
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• 1994

Nerve conduction impairment in lead neuropathy has been empirically linked to altered nerve myo-inositol metabolism. In most cases of neuropathy, abnormal myo-inositol metabolism is associated with abnormal $Na^+/K^+$ATPase provides a potential mechanism to relate defects of the myo-inositol metabolism in the peripheral nerve treated with lead. Therefore, the effect of lead on the rat sciatic nerve $Na^+/K^+$ATPase and other ATPase of sciatic nerve was studied. ATPase activity was measured enzymatically in sciatic nerve homogenates from 2-wk lead treated neuropathy rats and age-mached controls administered myo-inositol. $Na^+/K^+$ATPase components were assessed by ouabain inhibition or the omission of sodium and potassium ions. Lead reduced 50% reduction in the $Na^+/K^+$ATPase activity in homogenates of sciatic nerve. The 50% reduction in the $Na^+/K^+$ ATPase activity was selectively prevented by myo-inositol treatment. This study suggests that the toxic mechanism of the lead on peripheral nerve may be through reduction in $Na^+/K^+$ATPase activity which has been linked to axonal transport slowing in the rat model of lead neuropathy, via direct changes by the perturbation of the intracelluar sodium or potasium level.

• Journal of Electrodiagnosis and Neuromuscular Diseases
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• v.20 no.2
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• pp.139-143
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• 2018

Rhabdomyolysis is a syndrome caused by injury to skeletal muscles and involves leakage of large quantities of potentially toxic intracellular contents into the plasma. It is known that rhabdomyolysis results in peripheral nerve injury, however, reports of bilateral sciatic neuropathy following rhabdomyolysis are rare. We report a case involving a 42-year-old female patient with no past medical history, who presented with sudden bilateral calf pain, redness, and burning sensation with weakness of both lower extremities after sleeping on an electric heating pad following alcohol drinking. Lower extremity magnetic resonance angiography (MRA) revealed multifocal edema with enhancement of bilateral lower extremity muscles. Clinical and electrodiagnostic tests were consistent with the diagnosis of bilateral sciatic neuropathy following rhabdomyolysis. This is a rare case of bilateral sciatic neuropathy following rhabdomyolysis.

• Journal of Korean Neurosurgical Society
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• v.57 no.2
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• pp.123-126
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• 2015

A rare case of chronic pain of entrapment neuropathy of the sciatic nerve successfully relieved by surgical decompression is presented. A 71-year-old male suffered a chronic right buttock pain of duration of 7 years which radiating to the right distal leg and foot. His pain developed gradually over one year after underwenting drainage for the gluteal abscess seven years ago. A cramping buttock and intermittently radiating pain to his right foot on sitting, walking, and voiding did not respond to conventional treatment. An MRI suggested a post-inflammatory adhesion encroaching the proximal course of the sciatic nerve beneath the piriformis as it emerges from the sciatic notch. Upon exploration of the sciatic nerve, a fibrotic tendinous scar beneath the piriformis was found and released proximally to the sciatic notch. His chronic intractable pain was completely relieved within days after the decompression. However, thigh weakness and hypesthesia of the foot did not improve. This case suggest a need for of more prompt investigation and decompression of the chronic sciatic entrapment neuropathy which does not improve clinically or electrically over several months.

• Annals of Clinical Neurophysiology
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• v.7 no.1
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• pp.55-57
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• 2005

Two different unusual cases of acute sciatic neuropathy are described. They appeared to have been caused by complications from a procedure performed on a patient in the lithotomy position, and an uncertain etiology associated with either a previous femur fracture or a recent blunt trauma to the buttock. Comprehensive histories of weakness, with radiographic or electrophysiological studies, or even exploratory surgery are important in order to understand the etiologies of the sciatic neuropathies.

• The Journal of Korean Obstetrics and Gynecology
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• v.23 no.1
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• pp.124-135
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• 2010

Purpose: To report the patient with sciatic neuropathy after gynecologic laparoscopy, who improved by Traditional Korean Medical treatment and to study Traditional Korean Medicine(TKM) management of complications of gynecologic laparoscopy. Methods: A patient with sciatic neuropathy after gynecologic laparoscopy was managed with herbal medicine, acupuncture and moxibustion treatment. Results: After about 2 months treatment, patient's symptoms and signs were improved. TKM management was effective in recovery of neurologic complication after gynecologic laparoscopy. Conclusion: We need to actively participate in management of complications of gynecologic laparoscopy as primary or adjuvant therapy. And more study is needed for developing Traditional Korean Medical indication of complications of Gynecologic Laparoscopy.

• Investigative Magnetic Resonance Imaging
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• v.20 no.3
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• pp.175-180
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• 2016

Carbon monoxide (CO) intoxication is a leading cause of the variable neuropsychiatric impairment. Despite of widely known central nerve system complications after CO intoxication, peripheral neuropathy due to CO poisoning is rare and has been under-recognized. We report interesting case of a 29-year-old male who suffered from motor weakness and sensory abnormalities in his lower extremity following acute CO intoxication. The patient revealed direct and indirect signs of peripheral neuropathy of the left inferior gluteal and sciatic nerve on magnetic resonance imaging.

• The Korean Journal of Food And Nutrition
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• v.21 no.4
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• pp.430-435
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• 2008

The main cause of diabetic neuropathy, one of the most debilitating complications, is the chronic hyperglycemia, the increase sorbitol or the decrease of nerve growth factor(NGF). NGF, a protein, plays a major role in the development and maintenance of peripheral nervous system. Systemic administration of NGF prevents manifestations of neuropathy in rodent models of diabetic neuropathy. In the previous investigation, we report the hypoglycemia effect of Dioscorea rhizoma extract(DRE) in diabetic mice. The present study shows protective effect of DRE on diabetic neuropathy by induction of NGF protein. We investigated the NGF level in salivary gland and sciatic nerve of normal mouse and the effect of DRE on sciatic nerve conductivity and thermal hyperalgesia test in Type 2 db/db mouse. DRE increased endogenous NGF level in salivary gland and sciatic nerve of mouse. And sensory nerve conductivity velocity(SNCV), motor nerve conductivity velocity(MNCV) and thermal hyperalgesia increased in DRE treatment mice compared with control group. On the basis of our results, we conclude that DRE increase induction of endogenous NGF level and have protective effect on diabetic neuropathy by induction of NGF. Therefore, we propose that long-term use of DRE might help prevention of diabetes-associated complication; diabetic neuropathy.

• Parasites, Hosts and Diseases
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• v.60 no.4
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• pp.247-254
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• 2022

Vincristine (VCR) is a chemotherapeutic agent widely used in treatment of malignancies. However, VCR has a limitation in use since it commonly causes a painful neuropathy (VCR-induced peripheral neuropathy, VIPN). Inflammatory cytokines secreted by immune cells such as macrophages can exacerbate allodynia and hyperalgesia, because inhibiting the inflammatory response is a treatment target for VIPN. In this study, we investigated whether Trichinella spiralis, a widely studied helminth for its immunomodulatory abilities, can alleviate VCR-induced allodynia. Von Frey test showed that T. spiralis infection improved mechanical allodynia at 10 days after VCR injection. We further observed whether the difference was due to mitigated axon degeneration, but no significant difference between the groups in axonal degeneration in sciatic nerves and intra-epidermal nerve fibers was found. Conversely, we observed that number of infiltrated macrophages was decreased in the sciatic nerves of the T. spiralis infected mice. Moreover, treatment of T. spiralis excretory-secretory products caused peritoneal macrophages to secrete decreased level of IL-1β. This study suggests that T. spiralis can relieve VCR-induced mechanical allodynia by suppressing neuroinflammation and that application of controllable degree of helminth may prove beneficial for VIPN treatment.

• Journal of Environmental Science International
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• v.9 no.3
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• pp.209-214
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• 2000

The preventive effects of sodium molybdate on the acute toxicity of lead were studied by investigating tissue accumulation of lead, changes of nerve conduction velocity and concentrations of metabolites related to function of sciatic nerve in rats treated with lead, sodium molybdate and both, respectively. In lead-intoxicated rat, the conduction velocity, myo-inositol concentration and $Na^{+}/K^{+}$ ATPase activity of sciatic nerve were decreased by about 33 %, 48 % and 58 %, respectively. However, sodium molybdate treatment significantly normalized the conduction velocity, $Na^{+}/K^{+}$ ATPase activity and myo-inositol concentration of sciatic nerve in lead-intoxicated rat. Also, sodium molybdate treatment decreased the contents of lead in blood and sciatic nerve through promotion of urinary excretion of lead. But sodium molybdate treatment did not affect the glucose concentration in sciatic nerve. These results suggest that sodium molybdate prevented peripheral neuropathy not only by reducing lead contents in sciatic nerve and blood, but also by enhancing $Na^{+}/K^{+}$ ATPase activity in sciatic nerve.