BACKGROUND: In spite of the different pathogenesis and exclusive respect in the diagnosis of Alzheimer's disease (AD) and vascular dementia (VaD), recent epidemiological and pathological studies indicates that ischemic stroke have an important role in the pathogenesis of both VaD and AD. However, the association of ischemic stroke and AD on the cellular and molecular level is still unknown. We evaluated the effect of ischemic neuronal insult on the regulation of amyloid precursor protein (APP) processing. METHODS: We used an in vitro model of cerebral ischemia (oxygen-glucose deprivation, OGD) to evaluate the effect of ischemic insult on the amyloidogenic and non-amyloidogenic pathways using human neuroblastoma cell line, SH-SY5Y, and primary cultured cells of Tg2576 APP transgenic mouse. RESULTS: Ischemic insult significantly increased the beta amyloid (A beta) production in the primary cultured cells of Tg2576 APP transgenic mice (p<0.001). A disintegrin and metalloprotease 10 (ADAM 10), a candidate of alpha-secretase, was markedly increased in the early stage of ischemic insult (up to 2 hours of OGD, p<0.001; 4 hours of OGD, p<0.05), which was followed by the decreased level of ADAM 10 expression in a later stage (p<0.001). However, the protein and mRNA expression of beta-site cleavage enzyme (BACE) and BACE activity were not significantly different between the group of ischemic insult and control. By contrast, the activity of gamma-secretase was significantly increased after 4 hours of ischemic insult, as compared to controls. CONCLUSIONS: This study demonstrates that the ischemic neuronal insults increase the production of A beta via activation of the amyloidogenic pathway, which may link the role of ischemic insults to the pathogenesis of AD.
Alzheimer Disease ; Amyloid Precursor Protein Secretases ; Amyloid* ; Animals ; Brain Ischemia ; Cell Line ; Cells, Cultured ; Dementia, Vascular ; Diagnosis ; Humans ; Mice ; Mice, Transgenic ; Neuroblastoma ; Neurons* ; RNA, Messenger ; Stroke

The mechanism of chorea underlying nonketotic hyperglycemia was controversial. Serial follow up of brain MRI, 99mTc-ECD SPECT, and 18F-FDG PET in conjunction with clinical observation was done to clarify the pathologic localization. From the functional neuroimages, according to the clinical improvement, the relevant pathology was localized on the lentiform nucleus, mainly on the putamen. In caudate, the mismatch between glucose metabolism and blood flow was observed during and after choreoballistic movement which suggested an important cue to understand the pathogenesis of chorea.
Basal Ganglia* ; Brain ; Chorea ; Corpus Striatum ; Cues ; Fluorodeoxyglucose F18 ; Follow-Up Studies* ; Glucose ; Humans ; Hyperglycemia* ; Magnetic Resonance Imaging ; Metabolism ; Pathology* ; Putamen ; Tomography, Emission-Computed, Single-Photon

The clinical cases of 6 patients suffering with chorea after acute carbon monoxide (CO) poisoning were reviewed. There were 2 men and 4 women, and the age at onset ranged from 11 to 60 (mean 33.0) years. All the patients except one were associated with mild delayed CO encephalopathy. The latency period between CO poisoning and the onset of chorea was 10 to 30 (mean 21.7) days. The duration of chorea after CO poisoning was 14 to 90 (mean 39.8) days. The brain CT findings were bilateral low- density lesions in the basal ganglia and/or in the white matter of the cerebral cortex, and there was no correlation between the lesion sites on the imagings and the development of chorea. Neuroleptic agents alleviated the chorea and the patients did not relapse after neuroleptic agents were halted.
Acute Disease ; Adolescent ; Adult ; Brain Diseases/etiology/radiography ; Carbon Monoxide Poisoning/*complications/radiography ; Chorea/*etiology/radiography ; Female ; Human ; Male ; Middle Aged ; Tomography, X-Ray Computed

BACKGROUND: As brain tumor cells are immunologically active, they release various factors like a cytokine, growth factor and express a death domain on their surfaces. Accordingly they support proliferation, vascularity, invasiveness and maintain immune privileged sites. However, the relationship between tumor cells and surrounding neuron cells have been rarely reported in tumor patients with epilepsy that inhibitory neuron cells have been lost around peritumoral sites. This study was designed to address that tumor cells directly damage neuron cells. METHODS: Using LDH assay and special stain, we investigated whether or not cultured supernatants of astrocytoma cells induce the damage of neuron cells. RESULTS: The neuron cells were killed by tumor cells supernatant and increased by pretreatment of neuron cells supernatant and lysates. Protein extracted tumor cells supernatant also damage neuron cells. It was proved by Annexin-PI stain and DNA fragmentation that neuronal death by tumor cells was apoptosis. The more malignant tumor cells, the more neuronal death was induced and the more their cytokines were expressed. In comparison with various cytokine expressions in tumor cells, it can be assumed that the released protein from tumor cells was associated with TNF (tumor necrosis factor)-alpha. CONCLUSIONS: Brain tumor cells are active processing cells that they recognize surrounding normal neuron cells, release death factors and induce apoptosis of neuron cells. Released death factors are related toTNF-alpha. (J Korean Neurol Assoc 19(3):266~277, 2001)
Apoptosis* ; Astrocytoma ; Brain Neoplasms* ; Brain* ; Cytokines ; DNA Fragmentation ; Epilepsy ; Humans ; Necrosis ; Neurons*

Carbon monoxide (CO) has the toxic effects of tissue hypoxia and produces various systemic and neurological complications. The main clinical manifestations of acute CO poisoning consist of symptoms caused by alterations of the cardiovascular system such as initial tachycardia and hypertension, and central nervous system symptoms such as headache, dizziness, paresis, convulsion and unconsciousness. CO poisoning also produces myocardial ischemia, atrial fibrillation, pneumonia, pulmonary edema, erythrocytosis, leucocytosis, hyperglycemia, muscle necrosis, acute renal failure, skin lesion, and changes in perception of the visual and auditory systems. Of considerable chinical interest, severe neurological manifestations may occur days or weekes after acute CO poisoning. Delayed sequelae of CO poisoning are not rare, usually occur in middle or older, and are clinically characterized by symptom triad of mental deterioration, urinary incontinence, and gait disturbance. Occasionally, movement disorders, particularly parkinsonism, are observed. In addition, peripheral neuropathy following CO poisoning usually occurs in young adults.
Animal ; Carbon Monoxide Poisoning/complications/*physiopathology ; Human

BACKGROUND: There is a lack of basic epidemiological information on bacterial meningitis in children and adults in Korea. Therefore, more research is needed to investigate the causative organisms, clinical manifestations, and prognosis in Korean children and adults. METHODS: We analyzed retrospectively 148 medical records with final diagnosis of bacterial meningitis. The diagnosis of bacterial meningitis was based on culture-positive cases. RESULTS: Out of a total 148 patients, 71 were children and 77 were adults. In the children with community acquired meningitis, infection-related meningitis was the most common predisposing factor (23.3%). In adults, otitis media was the most common (21.7%). There were more frequent seizures in children than adults (38.1%, 17.1%, p<0.05). In community-acquired meningitis, Streptococcus pneumoniae was the most common type. However, in nosocomial meningitis, gram-negative bacilli was the most common type. The prognostic factors associated with mortality rate in adults were old age (>50 years), seizure (p<0.05), and mental change (p<0.001). CONCLUSIONS: Although a causative organism is not documented, we believe that our study will help to properly treat acute bacterial meningitis in children and adults regardless if it is community acquired or nosomial.
Adult ; Causality ; Child ; Cross Infection ; Diagnosis ; Epidemiology ; Humans ; Korea ; Medical Records ; Meningitis ; Meningitis, Bacterial* ; Meningitis, Pneumococcal ; Mortality ; Otitis Media ; Prognosis* ; Retrospective Studies ; Seizures

Background: It is important to make the accurate diagnosis of leptomeningeal metastasis(LM) because the institution of appropriate therapy may produce symptomatic improvement, prevent neurologic deterioration, and prolong survival. To evaluate the appropriate diagnostic methods of LM, we conducted the comparison of diagnostic yield in each diagnostic method and analyzed factors influencing the diagnostic results. METHODS: We analyzed 62 patients of LM with following inclusion criteria: positive CSF cytology, or abnormal neuroimaging, or elevated CSF biochemical marker, or characteristic clinical symptom and abnormal routine CSF examination. RESULTS: Primary cancer of LM was following; lung cancer 21, lymphoma 15, stomach cancer 13, breast cancer 9, rhabdomyosarcoma 2, bladder cancer 1, and colon cancer 1. The positive yield in the diagnosis of LM was 54.5% in CSF cytology, 55.9% in neuroimaging, 62.5% in CSF biochemical marker. As each diagnostic method was combined, the positive yield was increased to 86.4-88.5% with the highest in combination of CSF cytology with neuroimaging. The relationship between CSF cytology and neuroimaging is complementary in the diagnosis of LM (p=0.01). In positive group of CSF cytology, the count of CSF WBC was higher than in negative group (p=0.026), and clinical feature revealed a tendency of combined cerebral and cranial symptom than isolated symptom. The interval from the diagnosis of primary cancer to diagnosis of LM was most prolonged in breast cancer with a mean of 38.2 month. CONCLUSIONS: Combination of each diagnostic method increases the diagnostic yield, and CSF cytology and neuroimaging must be performed with each other.
Biomarkers* ; Breast Neoplasms ; Colonic Neoplasms ; Diagnosis ; Humans ; Lung Neoplasms ; Lymphoma ; Neoplasm Metastasis* ; Neuroimaging* ; Rhabdomyosarcoma, Alveolar ; Stomach Neoplasms ; Urinary Bladder Neoplasms

Idiopathic hypertrophic pachymeningitis is a rare inflammatory disease of unknown origin in which the recurrence is frequently observed despite an initial response to steroid therapy. Four patients, two men and two women aged 63 to 67 years, with severe headaches were evaluated by a brain MRI, and two patients were evaluated by follow up MRI receiving azathioprine therapy. All patients were given initial oral prednisolone 60mg or steroid pulse therapy followed by oral prednisolone and azathioprine therapy. Four patients improved with prednisolone but became steroid depen-dent. Azathioprine therapy permitted a reduction of the corticosteroid which may lead to clinical and radiological improvement. At present, high dose corticosteroid therapy is the treatment of choice, followed by immunosuppressive agents, such as azathioprine, if necessary. Further long-term follow-up studies of these patients are needed to clarify the outcome of this rare disease.
Azathioprine* ; Brain ; Female ; Follow-Up Studies ; Headache ; Humans ; Immunosuppressive Agents ; Magnetic Resonance Imaging ; Male ; Meningitis* ; Prednisolone ; Rare Diseases ; Recurrence

Idiopathic hypertrophic pachymeningitis is a rare inflammatory disease of unknown origin in which the recurrence is frequently observed despite an initial response to steroid therapy. Four patients, two men and two women aged 63 to 67 years, with severe headaches were evaluated by a brain MRI, and two patients were evaluated by follow up MRI receiving azathioprine therapy. All patients were given initial oral prednisolone 60mg or steroid pulse therapy followed by oral prednisolone and azathioprine therapy. Four patients improved with prednisolone but became steroid depen-dent. Azathioprine therapy permitted a reduction of the corticosteroid which may lead to clinical and radiological improvement. At present, high dose corticosteroid therapy is the treatment of choice, followed by immunosuppressive agents, such as azathioprine, if necessary. Further long-term follow-up studies of these patients are needed to clarify the outcome of this rare disease.
Azathioprine* ; Brain ; Female ; Follow-Up Studies ; Headache ; Humans ; Immunosuppressive Agents ; Magnetic Resonance Imaging ; Male ; Meningitis* ; Prednisolone ; Rare Diseases ; Recurrence

BACKGROUND: Presently, it is well known that there are neurological and systemic complications after carbon monox-ide (CO) intoxication. Until recently, delayed-onset movement disorders after CO intoxication were rarely reported. We analyzed 32 patients with delayed onset movement disorders after CO intoxication. METHODS: We reviewed the medical records of 242 patients admitted to the Yonsei University Medical Center from January 1986 to December 1996 due to CO intoxication. Patients were analyzed with respect to movement disorders, onset, latency, and radiological findings. RESULTS: Among the 242 patients of CO intoxication, 32 (13.2%) patients had delayed-onset movement disorders. Of these, 23 (71.9%) had parkinsonism, 5 (15.6%) had dystonia, 3 (9.4%) had chorea, and 1 (3.1%) had myoclonus. The mean age of the patients was 46.66 +/-16.91 years. Among the 4 patients with CO intoxication occuring at age 17 or younger (Childhood group), 2 had parkinsonism and 2 had focal dystonia. The mean age of the Childhood group was 1 7 . 7 5 +/-6.99 years. Among the 28 patients with CO intoxication occuring at age 18 or older (Adult group), 21 (75%) had parkinsonism, 3(10.7%) dystonia, 3(10.7%) chorea, and 1(3.6%) myoclonus. Among the 3 patients with dystonia in the Adult group, 1 had focal dystonia and 2 had segmental dystonia. The mean age of the adult group was 50.79 +/-1 3 . 4 6 years. The mean latency between CO intoxication and the onset of movement disorders was 27.20 +/-27.94 weeks in the Childhood group and 9.60 +/-14.97 weeks in the Adult group. The mean latency between CO intoxication and the onset of movement disorders was 6.44 +/-6.76 weeks in parkinsonism, 41.76 +/-27.99 weeks in dystonia, 4.0 weeks in chorea, and 8.0 weeks in myoclonus. The mean latency in dystonia was longer than in the others. Among the 23 patients who underwent brain computed tomography, 12 (52.2%) had abnormal findings. Low density lesions were found in the globus pallidus (13.0%), cerebral white matter (13.0%), and both globus pallidus and cerebral white matter (17.4%). One (14.3%) patient showed cortical atrophy while another patient showed both cortical atrophy and low density in cerebral white matter. CONCLUSIONS: The development of a delayed-onset movement disorder after CO intoxication is not rare. In our research, the radiological findings of patients with delayed-onset movement disorders after CO intoxication were inconsistant. The findings revealed no correlations with the various types of delayed-onset movement disorders.
Academic Medical Centers ; Adult ; Atrophy ; Brain ; Carbon Monoxide* ; Carbon* ; Chorea ; Dystonia ; Dystonic Disorders ; Globus Pallidus ; Humans ; Medical Records ; Movement Disorders* ; Myoclonus ; Parkinsonian Disorders