• Journal of Korean Neurosurgical Society
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• v.65 no.5
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• pp.640-651
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• 2022

Clinical studies on neuromodulation intervention for trigeminal neuralgia have not yet shown promising results. This might be due to the fact that the pathophysiology of chronic trigeminal neuropathy is not yet fully understood. Chronic trigeminal neuropathy includes trigeminal autonomic neuropathy, painful trigeminal neuropathy, and persistent idiopathic facial pain. This disorder is caused by complex abnormalities in the pain processing system, which is comprised of the affective, emotional, and sensory components, rather than mere abnormal sensation. Therefore, integrative understanding of the pain system is necessary for appropriate neuromodulation of chronic trigeminal neuropathy. The possible neuromodulation targets that participate in complex pain processing are as follows : the ventral posterior medial nucleus, periaqueductal gray, motor cortex, nucleus accumbens, subthalamic nucleus, globus pallidus internus, anterior cingulate cortex, hypothalamus, sphenopalatine ganglion, and occipital nerve. In conclusion, neuromodulation interventions for trigeminal neuralgia is yet to be elucidated; future advancements in this area are required.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.17
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• pp.7603-7606
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• 2015

Background: The chemotherapeutic agent oxaliplatin can cause acute and chronic forms of peripheral neuropathy. The aim of this study was to evaluate the incidence of chronic neuropathy and its risk factors in colorectal cancer (CRC) patients treated with FOLFOX or XELOX regimens in the Oncology Ward of Hazrate-Rasoul Hospital in Tehran. Materials and Methods: A total of 130 patients with CRC were entered into our study, aged over 18 years, without history of receiving other neurotoxic agents or other predisposing factors such as diabetes or neurologic diseases and kidney and liver dysfunction. For the FOLFOX regimen, patients received oxaliplatin, 85mg/m2, every 2 weeks for 12 courses and with the XELOX regimen, oxaliplatin was $130mg/m^2$, every 3 weeks for 8 courses. Based on Common Toxicity Criteria (CTC or NCI-CTC v.3), the patients were divided into 5 groups (grades) based on the severity of their symptoms. Results: Fifty-seven patients (43.8%) were male and 73(56.2%) female. Some 19 patients (14.7%) had BMI<20, 97(74.6%) were between 20-25 and 14 (10.8%) ${\geq}25$. In 105 patients (80.7%) neuropathy was found. There was significant correlation between BMI, hypomagnesaemia and especially, severity of anemia in patients with neuropathy compared to those without. Conclusions: Oxaliplatin regimens can induce chronic neuropathy in CRC patients, with anemia, high BMI and hypomagnesaemia as risk factors that can predispose to this kind of neurotoxicity.

• Annals of Clinical Neurophysiology
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• v.8 no.1
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• pp.6-15
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• 2006

Intravenous immunoglobulin (IVIg) is the treatment of choice for many autoimmune neuropathic disorders such as Guillain-Barre syndrome (GBS), chronic inflammatory Demyelinating neuropathy (CIDP), and multifocal motor neuropathy (MMN). IVIg is preferred because the adverse reactions are milder and fewer than the other immune-modulating methods such as steroid, other immunosuppressant such as azathioprine, and plasmapheresis. IVIg also has been used in other autoimmune neuromuscular disorders (inflammatory myopathy, myasthenia gravis, and Lambert-Eaton myasthenic syndrome) and has been known as safe and efficient agent in these disorders. Since IVIg would get more indications and be used more commonly, clinicians need to know the detailed mechanism of action, side effects, and practical points of IVIg.

• Journal of Haehwa Medicine
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• v.13 no.1
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• pp.47-59
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• 2004

Objectives & Methods: We investigated 28 books to study etiology and pathology of Son-Bal Jeorim. Result and Conclusion 1. The eiology of Son-Bal Jeorim is same as it of Bee Jeung(痺症). 2. Generally speaking, the cause of Bee Jeung was distributed Wind(風), Coldness(寒), Wetness (濕) of meridian. Bee Jeung can be devided into SilBi(實痺) and HeoBi(虛痺). In SilBi(實痺) there are PungHanSeupBi(風寒濕痺) and YeolBi(熱痺). In HeoBi(虛痺), there are GiHyeolHeoBi(氣血虛痺), EumheoBi(陰虛痺) and YangHeoBi(陽虛痺). 3. Son-Bal Jeorim belong to peripheral neuropathy in western medicine. 4. Syndrome of acute motor paralysis with variable disturbance of sensory and autonomic function, subacute sensorymotor paralysis, syndrome of chronic sensorimotor polyneuropathy, neuropathy with mitochondrial disease, syndrome of mononeuropathy or nerve plexusopathy. 5. Peripheral neuropathy is caused by carpal tunnel syndrome, diabetic neuropathy, uremic neuropathy, hepatic neuropathy, hypothyroid neuropathy, hyperthyroid neuropathy, neuropathy due to malnutrition, neuropathy due to toxic material, neuropathy due to drug, paraneoplastic neuropathy, hereditary neuropathy, etc. 6. Cerebral apoplexy, myelopathy, peripheral circulatory disturbance, anxiety syndrome cause symptoms of peripheral neuropathy

• 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.

• Journal of Korean Neurosurgical Society
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• v.66 no.4
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• pp.344-355
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• 2023

Chronic lower back pain is a leading cause of disability in musculoskeletal system. Degenerative disc disease is one of the main contributing factor of chronic back pain in the aging population in the world. It is postulated that sinuvertebral nerve and basivertebral nerve main mediator of the nociceptive response in degenerative disc disease as a result of neurotization of sinuvertebral and basivertebral nerve. A review in literature is done on the pathoanatomy, pathophysiology and pain generation pathway in degenerative disc disease and chronic back pain and management strategy is discussed in this review to aid understanding of sinuvertebral and basivertebral neuropathy treatment strategies.

• Annals of Clinical Neurophysiology
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• v.4 no.2
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• pp.98-107
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• 2002

Multifocal motor neuropathy (MMN) is a chronic immune-mediated peripheral myelinopathy. The major clinical features include slowly progressive, painless, and asymmetric weakness, usually of distal limb muscle. Early in the course of the disease, weakness is not necessarily associated with muscle atrophy, owing to the initial primary involvement of peripheral myelin. Chronic progressive weakness is often associated with some degree of concurrent axonal loss and subsequent muscle atrophy. Sensory symptoms are usually mild or absent, and involvement of cranial and respiratory muscles is rare. The findings of multifocal motor conduction block, abnormal temporal dispersion, and focal conduction slowing at segments not at risk for common entrapment or compression injury, associated with normal sensory conduction studies along the same segments, are the hallmark electrophysiologic features of MMN. The slow progression and absence of upper motor neuron signs are the major clinical points that separate MMN from amyotrophic lateral sclerosis. The role of GM1 antibodies, found in high titers in 22~84% of MMN patients, remains uncertain. The contention that MMN is an autoimmune disorder is largely based on the often dramatic improvement in symptoms following the administration of intravenuos immunoglobulin or cyclophosphamide.

• Annals of Clinical Neurophysiology
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• v.20 no.2
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• pp.101-104
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• 2018

Multifocal acquired demyelinating sensory and motor (MADSAM) neuropathy is a variant of chronic acquired demyelinating polyneuropathy. A 65-year-old women presented with upper arm weakness. A nerve conduction study showed conduction blocks over intermediate segments with sparing of distal compound action potentials. Magnetic resonance imaging revealed asymmetric hypertrophy of the brachial plexus on the affected side. These findings represent important electrophysiological and radiological evidence of MADSAM neuropathy. The condition of the patient began to improve after starting intravenous immunoglobulin administration.

• Annals of Clinical Neurophysiology
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• v.15 no.1
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• pp.19-23
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• 2013

Some patients with leprosy may present with atypical features, such as isolated peripheral neuropathy without skin lesions, or marked proprioceptive dysfunction. We report a 56-year-old female who presented with predominant proprioceptive loss without skin lesion, but was finally confirmed as leprous neuropathy by sural nerve biopsy. It is postulated that large myelinated fibers were affected by chronic immunological reactions triggered by inactive bacterial particles, producing a peripheral neuropathy presenting as predominant proprioceptive sensory loss without typical skin lesions.

• Annals of Clinical Neurophysiology
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• v.19 no.1
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• pp.54-57
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• 2017

Distal acquired demyelinating symmetric (DADS) neuropathy is a variant form of chronic inflammatory demyelinating polyradiculoneuropathy. A 54-year-old man presented with gait disturbance owing to weakness in both legs. Nerve conduction studies showed demyelinating sensorimotor polyneuropathy, and laboratory studies demonstrated anti-GM1 and anti-GD1b IgG antibodies, but no anti-myelin associated glycoprotein activity. We suggest that an antiganglioside antibodies assay needs to be applied when DADS neuropathy is suspected in order to improve the classification of dysimmune neuropathies.