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BACKGROUND: With the deep investigations of pathophysiological mechanism of acute cerebral infarction, it is discovered that inflammation occupies an important stance in the ischemic injuries of central nervous system ( CNS ), in which tumor necrosis factor-αt (TNF-α), interleukin- 1β(IL-1β), and soluble intercellular adhesion molecule(sICAM-1) become hotspots in the researches.OBJECTIVE: To investigate the relationship between the levels of serous inflammatory cell factors and the course of the disease, the severity of the situation in patients with ischemic stroke.DESIGN: A case-control study based on patients and healthy individuals.SETTING: Department of neurology in a university hospital.PARTICIPANTS: Fifty ischemic stroke patients including 23 males and 27 females with an average age of(60.26 ± 8.77) years old were selected from the outpatient and inpatient Departments of Neurology of the Renmin Hospital of Wuhan University between January 2001 and December 2003. Forty healthy controls including 18 males and 22 females with an average age of (61.05 ± 8.09) years old were selected from the subjects who had physical check up at outpatient department during corresponding period.INTERVENTIONS: Serous TNF-α, IL-1 β and sICAM-1 levels were detected by double-antibody-ELISA.MAIN OUTCOME MEASURES: Serous levels of TNF-α, IL-1β and sICAM-1 in patients with ischemic stroke of different stage, with different infarction volume and different neural functional defects.RESULTS: Serous TNF-α, IL-1β and sICAM-1 levels of patients with cerebral infarction during acute phase and convalescence were significant higher than that of control group( P ＜ 0.01 ), and the levels was significantly higher in acute phase than convalescence ( P ＜ 0.05 ) . The elevation was closely correlated with the degree of neural functional defect and the size of infarction volume, and furthermore, the serous content of TNF-α was also correlated with IL-1β and sICAM-1 levels.CONCLUSION: TNF-α, IL-1β and sICAM-1 interact and participate in the inflammation and reperfusion injury of acute cerebral infarction. Surveillance on them can provide experimental indicators for early clinical therapy and rehabilitative intervention, which is good for the control of the development and recurrence of stroke.
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Objective To investigate the effect of m il d hypothermia on the content of Ca 2+、Mg 2+、EAA in rat brain tissue and ET in plasma after acute cerebral infarction. Methods Forty-eight Sprague-Dawley rats were randomly assigned into trial group and control group. Using the method of reformed line-thrombosis,the cerebral in farction models were established. The rats in the trial-group were cooled by mi ld hypothermia for half an hour, while those in the control group were subjected to no disposal. Every group was divided into 4 sub-groups according to the pos t-infarction disposal time. Every sub-group was composed of 6 SD rats and kill ed at the time points of 1 hour,2 hour,4 hour and 8 hour after infarction, respe ctively. Then the content of Ca 2+、Mg 2+、EAA in rat brain tissue an d ET in plasma were measured. ResultsThe post-infar ction content of Ca 2+、EAA and ET of trial-group increased mildly and Mg 2+ reduced very little. There was a significant statistical difference bet ween the trial group and the control group. Conclusion Mild hypothermia may significantly reverse the increase of the content of Ca 2+ and EAA and the fall of Mg 2+ and the increment of ET in plasma as well after acute cerebral infarction in experimental animals. So as a result, m ild hypothermia possesses protective effect on brain.
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Objective To evaluate the effect of mild hypothermia on acute cerebrovascular diseases. Methods Sixty-two cases of severe cerebrovascular diseases were randomized into hypothermia group and control group. In hypothermia group the patients were cooled to 34～35℃ for 48h ,while the patients in the control group treated by routine methods. Median nerve short latency somatosensory evoked potentials (SLSEP) and brain-stem auditory evoked potentials (BAEP) were recorded before cooling and 30 minutes, 24, 72, and 120 hours after cooling. The changes of EP were analyzed statistically. Results After treatment with mild hypothermia, the N13-N20 interpeak latency (IPL) of SLSEP and I-V IPL of BAEP were significantly reduced as compared with those of the control group ( P
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Objective To explore the relationship between the changes of Caspase 3mRNA expression and the injuried nervous cell apoptosis after rat focal cerebral ischemia/reperfusion injury who was then treated by mild hypothermia.Methods The middle cerebral arteries(MCA) of SD rats were occluded for 2 hours,and reperfused for 12 hours.Using FCM and semiquantitative RT-PCR technique,the DNA fragmentation rate and Caspase 3mRNA expression level were detected in the shamoperation group,the control group and the mild hypothermia group,respectively.Results The DNA fragmentaation rate and Caspase 3mRNA expression level in the sham operation group and the mild hypothermia group were obviously lower than those in the control group.Conclusions The significantly decreased level of Caspase-3mRNA expression may be related to the obviously decreased nervous cell apoptosis after rat cerebrall ischemia/reperfusion injury treated by the mild hypothemia.
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AIM: To study the language characteristics and origins of subcortical aphasia. METHODS: One hundred and five patients with unilateral subcortical lesions were confirmed by CT scans. Aphasia examinations, brain electrical activity mapping (BEAM) and CT image standardization were performed at the end of two weeks, one month and two months after onset. RESULTS: Most aphasia patients had lesions in the lateral, front and upper part of basal ganglion. BEAM is largely abnormal in the aphasia patients of lateral type and thalamic aphasia who had serious auditory comprehension disturbance. Prominent dysarthria and dysprosody occurred in aphasia patients with lesions in caudate nucleus. CONCLUSION: Subcortical aphasia has its language characteristics. It is mostly due to the damage of language related zone of hemisphere caused directly or indirectly by subcortical lesions. Thalamus serves as a subcortical center in controlling language and its disturbance causes aphasia in some patients.