• The Korean Journal of Pain
• /
• v.7 no.1
• /
• pp.69-73
• /
• 1994

A 37 years old man who suffered from right facial palsy was treated successfully with the application of both magnetic resonance diagnostic analyser(MRA) and stellate Ganglion block(SGB). SGB is effective in treatment of facial palsy resulting from abolishing cerebral vascular spasm and increasing cerebral blood flow. Short daily period of exposure to appropriate MRA can also modulate the balance of autonomic nervous system that are responsible for sympathetic overflow resulting the edema and poor circulation on the course of the facial nerve. It was seemed that recovery of facial palsy by application of both MRA and SGB was faster than by SGB only.

• Journal of Physiology & Pathology in Korean Medicine
• /
• v.20 no.4
• /
• pp.1014-1020
• /
• 2006

This study was intended to examine the effects of electroacupuncture(EA) and therapeutic exercise on the improvement of exercise function, BNDF, and HSP70 protein expression in an ischemic stroke model induced by MCA occlusion. Experiments were conducted for 1, 3 days, 1, 8 weeks respectively. Group I was a group of EA and therapeutic exercise; Group II was a group of therapeutic exercise; Group III was a group of EA; Group IV was a sham group of EA; Group V was a control group; and Group VI was a sham group without ischemic stroke. In each group, neurologic motor behavior test, histologic observations, BDNF, and HSP70 expression were observed and analyzed. The following results were obtained. The results of behavior test suggest that 8 weeks after ischemic stroke was induced, Group I improved in degeneration and inflammation of muscle fiber and decreased in destruction of nerve cells and cerebral infarction, indicating a similar state of muscle fiber and brain to Group VI. In immunohistochemical observations, Group I showed increase in BDNF and decrease in HSP70. Based on these results, EA and therapeutic exercise may improve muscle atrophy and change in BDNF and HSP70 expression of ischemic stroke rats and contribute to the improvement of exercise function.

• Korean Journal of Veterinary Research
• /
• v.48 no.4
• /
• pp.463-467
• /
• 2008

Granulomatous meningoencephalomyelitis (GME) is a sporadic, idiopathic, non suppurative inflammatory disease of the canine central nervous system. GME appears to have a worldwide distribution and to occur mostly in young to middle-age dogs of small breeds. A 6-year-old female mixed dog with wry neck, ataxia and rolling was submitted to the Cheju National University for diagnosis. Grossly, in the brain, cerebrospinal fluid was mildly increased and dilatation of the subarachnoid blood vessels was observed. Histopathologically, the lesions were characterized by perivascular cuffs of lymphocytes, various numbers of macrophages and plasma cells in the brainstem and cerebral white matter. Numerous granuloma composed of lymphocytes and histiocytes were scattered throughout the brainstem. Two malacic foci characterized by axonal swelling and gitter cell infiltration with hemorrhage were noted in the medulla oblongata and cerebellum. Special stains failed to demonstrate any infectious agents. Immunohistochemically, the infiltrated cells demonstrated strong positive reactions for CD3, a marker for T lymphocytes origin. Based on the clinical signs, histopathology, and immunohistochemistry, this case was diagnosed as GME in a mixed dog.

• Journal of Korean Neurosurgical Society
• /
• v.30 no.5
• /
• pp.622-626
• /
• 2001

Acute disseminated encephalomyelitis(ADEM) is an uncommon immune-mediated inflammatory demyelinating disorder that typically affects the white matter of the central nervous system. Radiologic findings of acute disseminated encephalomyelitis are not pathognomomic. The differential diagnosis is always difficult. Occasionally, the clinical features, radiological and histopathological findings of patients with acute disseminated encephalomyelitis mimic the brain tumor or other space occupying lesions. The authors report a 6-year-old girl who presented with right hemiparesis two days after nausea and vomiting. Brain MRI of the patient revealed non-enhanced multiple cystic lesions in subcortical white matter of both cerebral hemisphere with prominent edema. One of the cystic lesions was resected to differentiate with metastatic tumor or inflammatory disease such as abscess and confirmed as the acute disseminated encephalomyelitis via various immunohistochemical stains. Pertinent literature is reviewed with discussion on this uncommon ADEM associated with multiple cystic lesions.

• Journal of Korean Neurosurgical Society
• /
• v.46 no.6
• /
• pp.588-591
• /
• 2009

Radiologic findings of Bing-Neel syndrome, which is an extremely uncommon complication resulting from malignant lymphocyte infiltration into the central nervous system (CNS) in patients with Waldenstr$\ddot{o}$m's macroglobulinemia (WM), have been infrequently reported due to extreme rarity of the case. A 75-year-old man with WM presented at a neurology clinic with progressive gait and memory disturbances, and dysarthria of 2 months duration. Cerebrospinal fluid and serum protein electrophoresis and immunofixation electrophoresis showed IgM kappa-type monoclonal gammopathy. Brain magnetic resonance imaging revealed multifocal, hyperintense lesions on T2 weighted-images. Brain diffusion-weighted imaging (DWI) demonstrated hyperintensities in cerebral and cerebellar lesions that appeared isointense on apparent diffusion coefficient maps, which were compatible with vasogenic edema. Although histologic analysis is a confirmative study to prove direct cell infiltration into the brain, brain MRI with DWI may be a good supportive study to diagnose Bing-Neel syndrome.

• Journal of Chest Surgery
• /
• v.13 no.2
• /
• pp.149-153
• /
• 1980

Von Recklinghausen's disease is a systemic hereditary disorder with varied manifestations in bone, soft tissue, nervous system, and skin, the most common of which is the developement of multiple, small, cutaneous tumors with a characteristic histologic picture. Tumors develop after birth and before puberty in most cases, and they increase in number until old age. Malignant neoplasms that complicate multiple neurofibromatosis include gliomas of the optic nerve, astrocytomaas of the cerebral and cerebellar hemispheres, and sarcomas of peripheral nerves (femoral, tibial and intercostal nerves) and somatic soft tissues. Little attention has been paid to the presence of cystic lung disease in association with neurofibromatosis. Currently, most think of thoracic involvement in neurofibromatosis in terms of posterior mediastinal neuroma, pheochrocytoma, meningocele or, less commonly parenchymal pulmonary neurofibromas. Author have experienced 2 cases of Von Recklinghausen's disease. One case developed a hyge malignant Schwannoma in the parietal pleura of left 4th intercostal space and multiple benign neurofibromas (two in intercostal spacees and one in the neck) , and the other has several episodes of pneumothorax resulting from diffuse cystic lung disease which required closed thoracotomy drainage.

• Journal of Korean Neurosurgical Society
• /
• v.48 no.1
• /
• pp.91-93
• /
• 2010

Neurocysticercosis (NCC) is the most common parasitic infestation of the central nervous system. Most cases of NCC are to related and/or associated with inflammation within the cerebral parenchyma. A 71-year-old woman presented with a 4-year history of visual disturbance. This symptom had become aggravated 4 weeks earlier. Her visual acuity gradually decreased and superior hemianopsia was noted. Magnetic resonance imaging (MRI) revealed an enhanced and thickened pituitary stalk accompanying a suspicious mass. The provisional diagnoses were lymphoma, glioma, or other inflammatory conditions. Laboratory studies, including blood and hormonal studies, showed normal findings. Surgical resection was performed. In the pathological examination, degenerated parasitic wall structure was seen and its contents were composed of completely degenerated focal globular structures suggesting the scolex of cysticercus. We report an unusual case of NCC involving the pituitary stalk which was presented with a juxtasellar tumor. The possible underlying mechanisms are discussed with a review of pertinent literature.

• Journal of Integrative Natural Science
• /
• v.6 no.3
• /
• pp.125-137
• /
• 2013

Promising evidence suggests that amyloid beta peptide ($A{\beta}$), a key mediator in age-dependent neuronal and cerebrovascular degeneration, activates death signalling processes leading to neuronal as well as non-neuronal cell death in the central nervous system. A major cellular event in $A{\beta}$-induced apoptosis of non-neuronal cells, including cerebral endothelial cells, astrocytes and oligodendrocytes, is mitochondrial dysfunction. The apoptosis signalling cascade upstream of mitochondria entails $A{\beta}$ activation of neutral sphingomyelinase, resulting in the release of ceramide from membrane sphingomyelin. Ceramide then activates protein phosphatase 2A (PP2A), a member in the ceramide-activated protein phosphatase (CAPP) family. PP2A dephosphorylation of Akt and FKHRL1 plays a pivotal role in $A{\beta}$-induced Bad translocation to mitochondria and transactivation of Bim. Bad and Bim are pro-apoptotic proteins that cause mitochondrial dysfunction characterized by excessive ROS formation, mitochondrial DNA (mtDNA) damage, and release of mitochondrial apoptotic proteins including cytochrome c, apoptosis inducing factor (AIF), endonuclease G and Smac. The cellular events activated by $A{\beta}$ to induce death of non-neuronal cells are complex. Understanding these apoptosis signalling processes will aid in the development of more effective strategies to slow down age-dependent cerebrovascular degeneration caused by progressive cerebrovascular $A{\beta}$ deposition.

• Journal of The Korean Dental Society of Anesthesiology
• /
• v.7 no.1
• /
• pp.18-21
• /
• 2007

Pelizaeus-Merzbacher disease (PMD) can be defined as an X-linked recessive leukodystrophy that is caused by a mutation in the proteolipid protein gene on chromosome Xq22. PMD is one of a group of progressive, degenerative disorders of the cerebral white matter known as the leukodystrophies. Due to the progressive nature of the disorders and their devastating effects on the central nervous system, these children frequently require anesthesia during imaging procedures such as MRI or during various surgical procedures. Anesthetic concerns in theses cases include high prevalence of seizure disorders, gastroesophageal reflux with the risk of aspiration, airway complications related to poor pharyngeal muscle control and copious oral secretions, and mental retardation. We report a successful anesthetic management in a patient with PMD for dental procedures.

• Journal of Dental Rehabilitation and Applied Science
• /
• v.23 no.2
• /
• pp.179-186
• /
• 2007

The decrease of masticatory function caused by tooth loss leads to a decrease of cerebral blood flow volume resulting in impairment of cognitive function and learning memory disorder. However, the reduced mastication-mediated morphological alteration in the central nervous system (CNS) responsible for senile deficit of cognition, learning and memory has not been well documented. In this study, the effect of the loss of the molar teeth (molarless condition) on the hippocampal expression of glial fibrillary acidic protein (GFAP) protein was studied by immunohistochemical techniques. The results were as follows : 1. The molarless mice showed a lower density of pyramidal cells in the cornu ammonis 1 (CA1) and dentate gyrus (DG) region of the hippocampus than control mice. 2. Immunohistochemical analysis showed that the molarless condition enhanced the time-dependent increase in the cell density and hypertrophy of GFAP immunoreactivity in the CA1 region of the hippocampus. The molarless condition enhanced an time-dependent decrease in the number of neurons in the hippocampal formation and the time-dependent increase in the number and hypertrophy of GFAP-labeled cells in the same region. The data suggest a possible link between reduced mastication and histological changes in hippocampal formation that may be one risk factor for senile impairment of cognitive function and spatial learning memory.