Due to the observation, lipid disorder and AT III, PS, PC factors having an important role in the formation of clots in blood vessels, cerebral infarction. This study was carried out on 123 patients with cerebral infarction and 52 normal persons. Results: The normal values of AT III, PS, PC were equal to the normal values of foreigners: AT III: 115.88719.129%; PC: 108.36019.767%; PS: 109.93725.108%. The reduction of AT III, PS, and PC had the important role in cerebral infarction, especially the reduction of PS. This relationship had statistical meaning. There was relationship between AT III and triglyceride; PS and cholesterol; PS and LDL-C in patients with cerebral infarction
Cerebral Infarction ; Lipid Metabolism Disorders

BACKGROUND AND OBJECTIVES: Stroke onset is known to vary by several factors. Although it has been known that stroke may develop most frequently in the morning, its association with the type of activity has quite rarely been described. METHODS: We prospectively investigated by interview the time of and the activity during or before the onset of stroke in patients with acute cerebral infarction from Aug. 1995 to Mar. 1996. The activities were subdivided into basal metabolic rate state, sedentary, light, moderate, and heavy movements based on the caloric expenditure. RESULTS: One hundred-twenty five patients were enrolled. The time of day when ischemic stroke most frequently occurred was from 8:00 AM to noon. The type of activity was significantly associated with stroke onset in that it developed most commonly during and just after sleep or resting. The relationship between the onset of stroke and such patterns of onset time and the activity was found only in the atherothrombotic infarction, but not in the other stroke types. CONCLUSION: We demonstrated that stroke has clear diurnal variation. Our observations also suggested that the activity may be significantly associated with stroke onset. These findings may be useful for better understanding of the pathogenesis and prevention of ischemic stroke.
Basal Metabolism ; Cerebral Infarction* ; Health Expenditures ; Humans ; Infarction ; Prospective Studies ; Stroke

PURPOSE: This study was done to identify whether pre-conditioning exercise has neuroprotective effects against cerebral ischemia, through enhance brain microvascular integrity. METHODS: Adult male Sprague-Dawley rats were randomly divided into four groups: 1) Normal (n=10); 2) Exercise (n=10); 3) Middle cerebral artery occlusion (MCAo), n=10); 4) Exercise+MCAo (n=10). Both exercise groups ran on a treadmill at a speed of 15 m/min, 30 min/day for 4 weeks, then, MCAo was performed for 90 min. Brain infarction was measured by Nissl staining. Examination of the remaining neuronal cell after MCAo, and microvascular protein expression on the motor cortex, showed the expression of Neuronal Nuclei (NeuN), Vascular endothelial growth factor (VEGF) & laminin. RESULTS: After 48 hr of MCAo, the infarct volume was significantly reduced in the Ex+MCAo group (15.6+/-2.7%) compared to the MCAo group (44.9+/-3.8%) (p<.05), and many neuronal cells were detected in the Ex+MCAo group (70.8+/-3.9%) compared to the MCAo group (43.4+/-5.1%) (p<.05). The immunoreactivity of laminin, as a marker of microvessels and Vascular endothelial growth factor (VEGF) were intensively increased in the Ex+MCAo group compared to the MCAo group. CONCLUSION: These findings suggest that the neuroprotective effects of exercise pre-conditioning reduce ischemic brain injury through strengthening the microvascular integrity after cerebral ischemia.
Animals ; Brain Infarction/pathology ; Disease Models, Animal ; Infarction, Middle Cerebral Artery/metabolism/pathology/*prevention & control ; Laminin/metabolism ; Male ; Microvessels/metabolism ; Neurons/metabolism ; *Physical Conditioning, Animal ; Rats ; Rats, Sprague-Dawley ; Stroke/prevention & control ; Vascular Endothelial Growth Factor A/metabolism

C677T mutation in the gene encoding 5,10-methylenetetrahydrofolate reductase (MTHFR) predisposes to hyperhomocysteinemia in vivo and is known to be one of the causes of perinatal ischemic stroke. As MTHFR plays a role in the metabolism of homocysteine, C677T mutation may account for reduced enzymatic activity resulting in hyperhomocysteinemia. This may be prevented by introducing activity-enhancing coenzymes such as folic acid, vitamin B6, and B12. Though C677T mutation is known as a significant risk factor for cerebral infarction, reported cases of cerebral infarction among affected neonates are scarce. This report describes a case of a neonate homozygous for C677T mutation who had a perinatal ischemic stroke, born in a mother whose folic acid and nutritional consumption had been reduced during pregnancy.
Cerebral Infarction* ; Coenzymes ; Folic Acid ; Homocysteine ; Humans ; Hyperhomocysteinemia ; Infant, Newborn ; Metabolism ; Mothers ; Oxidoreductases ; Pregnancy ; Risk Factors ; Stroke ; Vitamin B 6

Although the mechanism has not been clearly understood, it has been reported that various altered gene expressions are induced by cerebral ischemia. In order to investigate the effects of transient cerebral ischemia on the amyloid precursor protein(APP) metabolism, the 3 isoforms of APP mRNA and the APP were examined. Rats were given ischemic insult through middle cerebral artery occlusion and reperfusions using blunted 4-0 nylon thread after exposure of cervical region. Groups were assigned with each being 1 hour occlusion and 1hr, 3hrs, 8hrs, 1day, 3days, 7days after reperfusion. The rats were then sacrificed and cerebral cortex of each animal was dissected. The mRNA level of APP770, 751, 695 was investigated by reverse transcription coupled polymerase chain reaction (RT-PCR) and the protein amount of APP was investigated by Western blotting method. The results showed that transient ischemia induced the change of APP mRNA. The APP mRNA which encodes the KPI(Kunitz-type protease inhibitor) domain began to increase after 1 day, reaching a maximun at 3 days, and then decreased to control level in the 7 days. The protein level of APP was same until 7 days. We conclude that transient cerebral ischemia alters the gene expression of APP isoforms. Therefore, we speculate that some factors regulating the splicing of APP gene transcript may also undergo ischemia-induced changes and the increase in levels of KPI-APP following ischemia might be associated with pathological changes during the ischemic process.
Amyloid* ; Animals ; Blotting, Western ; Brain Ischemia ; Cerebral Cortex ; Gene Expression ; Infarction, Middle Cerebral Artery ; Ischemia* ; Ischemic Attack, Transient ; Metabolism ; Middle Cerebral Artery ; Nylons ; Polymerase Chain Reaction ; Protein Isoforms ; Rats ; Reperfusion ; Reverse Transcription ; RNA, Messenger*

BACKGROUND: The thalamus has multiple connections with areas of the cerebral cortex involved in arousal and cognition. Thalamic damage has been reported to be associated with variable neuropsychological dysfunctions and dementia. This study investigates the changes of regional cerebral blood flow (rCBF) by using SPM analysis of 99mTc-ECD SPECT and examining the neuropsychological abnormalities of 4 patients with anterior thalamic infarctions. METHODS: Four patients with left anterior thalamic infarctions and eleven normal controls were evaluated. K-MMSE and the Seoul Neuropsychological Screening Battery were performed within 2 days after stroke. The normalized SPECT data of 4 patients were compared to those of 11 controls for the detection of areas with decreased rCBF by SPM analysis. RESULTS: All 4 patients showed anterograde amnesia in their verbal memory, which was not improved by recognition. Dysexecutive features were occasionally present, such as decreased word fluency and impaired Stroop test results. SPM analysis revealed decreased rCBF in the left supramarginal gyrus, the superior temporal gyrus, the middle and inferior frontal gyrus, the medial dorsal and anterior nucleus of the left thalamus. CONCLUSIONS: The changes of rCBF in patients with left anterior thalamic infarctions may be due to the remote suppression on metabolism by the interruption of the cortico-subcortial circuit, which connects the anterior thalamic nucleus and various cortical areas. The executive dysfunction and dysnomia may be caused by the left dorsolateral frontal dysfunction of the thalamocortical circuit. Anterograde amnesia with storage deficit may be caused by the disruption of mamillothalamic tract.
Amnesia, Anterograde ; Anomia ; Arousal ; Cerebral Cortex ; Cognition ; Dementia ; Humans ; Infarction* ; Mass Screening ; Memory ; Metabolism ; Seoul ; Stroke ; Stroop Test ; Thalamus ; Tomography, Emission-Computed, Single-Photon*

Phospholipase C (PLC) and related enzymes in signal transduction system are closely linked to cellular damage in ischemic encephalopathy. This study was undertaken to elucidate the time sequential changes of PLC isoenzymes (beta and gamma) in vulnerable areas of hippocampus in global ischemia and infarcted area in focal infarction. Mongolian gerbils were used because of their susceptibility to ischemic encephalopathy and divided into the following groups: the bilateral ischemia with various reperfusion periods group, unilateral progressive ischemia group, and focal ischemia group induced by infusion of iron particles through the femoral artery. The changes of PLC isoenzymes were observed immunohistochemically and matched with morphological changes. In the global ischemia with reperfusion group, the changes were most significant in hippocampus. Sequential changes of neurons such as red neurons at an early stage progressed to pknotic neurons at a later stage were noted with typical delayed neuronal damage in the corns ammonis (CA) 1 subfield of hippocampus. Red neurons and pyknotic neurons as well as intracytoplasmic inclusion in 3 to 24 hours of reperfusion showed loss of PLC isoenzymes as well as tubulin. The changes of PLC expression were corresponding to the degeneration of neurons with no discernible time sequential changes in remaining neurons. In the unilateral hemispheric progressive ischemia group, ischemic damage was far more marked and extensive with no selective injury pattern according to time and location. At 1 day, there was diffuse vacuolization and necrosis of neuropil with a loss of neuron. Admixed surviving neurons and vacuolated neuropil showed increased reaction to anti-PLC antibodies, which could be either an evidence of protein synthesis responding to ischemic insult or an artifactual change. Focal ischemia group showed time sequential changes of blood vessels and white blood cells with necrosis of surrounding tissue. Degenerating hippocampal neurons in infarction also showed a strong positive reaction to anti-PLC antibody, which was most likely due to condensation of cytoplasm rather than increased synthesis. This study showed different changes of PLC expression in global ischemic encephalopathy with reperfusion, progressive ischemia, and focal infarction, which suggested different pathophysiologic mechanism between these conditions.
Animal ; Brain Ischemia/*metabolism/pathology ; Cerebral Infarction/metabolism/pathology ; Female ; Gene Expression ; Gerbillinae ; Hippocampus/*enzymology ; Immunoenzyme Techniques ; Isoenzymes/*biosynthesis ; Male ; Neurons/enzymology/ultrastructure ; Phospholipase C/*biosynthesis ; Support, Non-U.S. Gov't ; Time Factors