ABSTRACT
<p><b>OBJECTIVE</b>To investigate the features of glutamate activity in the limbic system and the effects of glutamate on the activation of the hypothalamus-pituitary-adrenal (HPA) axis throughout both acute cerebral ischemia and reperfusion.</p><p><b>METHODS</b>The changes in glutamate content in the nervous cell gap, in corticotrophin releasing hormone (CHR) mRNA expression level in brain tissue, and in adrenocorticotropic hormone in blood plasma at different time-points after middle cerebral artery occlusion (MCAO) in rats were determined respectively with high-performance liquid chomatography (HPLC) and in situ hybridization.</p><p><b>RESULTS</b>Glutamate content in the hippocampus and the hypothalamus increased rapidly at ischemia 15 minutes, and reached peak value (the averages were 21.05 mg/g +/- 2.88 mg/g and 14.20 mg/g +/- 2.58 mg/g, respectively) at 1 hour after middle cerebral artery occlusion. During recirculation, it returned rapidly to the baseline level. At 24 hours after reperfusion, it went up once more, and remained at a relative high level until 48 hours after reperfusion, and then declined gradually. CRH mRNA expression levels in the temporal cortex, hippocampus and hypothalamus were enhanced markedly at 1 hour ischemia and were maintained until 96 hours after reperfusion. At the same time, adrenocorticotropic hormone level in plasma was relatively increased. In the peak stage of reperfusion injury, there was a significantly positive correlation (n = 15, r = 0.566, P < 0.05) of the glutamate contents in the hypothalamus with the number of cells positive for CRH mRNA expression level in the hypothalamus.</p><p><b>CONCLUSION</b>It is probable that the CRH system in the central nervous system is mainly distributed in the limbic system, and glutamate might be one of the trigger factors to induce excessive stress response in the HPA axis.</p>
Subject(s)
Animals , Male , Rats , Glutamic Acid , Hypothalamo-Hypophyseal System , Chemistry , Infarction, Middle Cerebral Artery , Metabolism , Limbic System , Chemistry , Pituitary-Adrenal System , Chemistry , Rats, Wistar , Reperfusion Injury , MetabolismABSTRACT
Objective To study the relationship between atherosclerotic plaques in carotid artery and ischemic cerebrovascular diseases. Methods The extracranial carotid arteries (ECA) and middle cerebral artery (MCA) of 54 patients with transient ischemic attack (TIA) or cerebral infarction (CI) were examined with doppler ultrasound. The distribution of atherosclerotic plaque, degree of stenosis and ultrasounic classification of ECA and the mean velocity of blood flow in MCA were examined. Results ①Stenosis over middle-grade on asymptomatic side in extracranial internal carotid artery (EICA) in group of patients with TIA was significantly higher than symptomatic side(P<0.01). Stenosis over high-grade on asymptomatic side in ELCA in group of patients with CI was significantly higher than symptomatic side (P<0.01). ②Flat and soft plaque are most common in group of patients with TIA or CI, then are hard and ulcerative plaques. Incidence of soft plaques on asymptomatic side in group of patients with TIA or CI are significantly higher than symptomatic side (P<0.01); ③Among the group of patients with CI, mean velocity of MCA decreased on asymptomatic side in 31 cases (68.9%), and significantly higher than symptomatic side (P<0.01). Conclusion Atheroclerotic plaques in carotid artery and intracranial hemodynamic characteristics are the important risk factors for ischemic cerebrovascular diseases. These findings have important values in predicting subsequent TIA or CI in asymptomatic subjects.
ABSTRACT
Objective To study the relationship between atherosclerotic plaques in carotid artery and ischemic cerebrovascular diseases. Methods The extracranial carotid arteries (ECA) and middle cerebral artery (MCA) of 54 patients with transient ischemic attack (TIA) or cerebral infarction (CI) were examined with doppler ultrasound. The distribution of atherosclerotic plaque, degree of stenosis and ultrasounic classification of ECA and the mean velocity of blood flow in MCA were examined. Results ①Stenosis over middle-grade on asymptomatic side in extracranial internal carotid artery (EICA) in group of patients with TIA was significantly higher than symptomatic side(P<0.01). Stenosis over high-grade on asymptomatic side in ELCA in group of patients with CI was significantly higher than symptomatic side (P<0.01). ②Flat and soft plaque are most common in group of patients with TIA or CI, then are hard and ulcerative plaques. Incidence of soft plaques on asymptomatic side in group of patients with TIA or CI are significantly higher than symptomatic side (P<0.01); ③Among the group of patients with CI, mean velocity of MCA decreased on asymptomatic side in 31 cases (68.9%), and significantly higher than symptomatic side (P<0.01). Conclusion Atheroclerotic plaques in carotid artery and intracranial hemodynamic characteristics are the important risk factors for ischemic cerebrovascular diseases. These findings have important values in predicting subsequent TIA or CI in asymptomatic subjects.
ABSTRACT
To explore the cause and pathology of hemifacial spasm and evaluate the therapeutic efficacy of butulin A, 240 HFS patients were studied for therapeutic efficacy of multifocal facial injections with botulin A. Symptomatic alleviations after the injection were graded in comparison with the symptoms in the pre-treatment stage. Electromyography (EMG) was performed in 68 patients at random. Following the treatment, 96% of the patients were relieved of symptomes, but in 80% of the patients the symptom relapsed about one half a year later. The results showed that the latent period of EMG was longer than normal facial muscle, and the amplitude of evoked movement potential of EMG of orbiticularis occuli muscle and orbiticularis oris muscle was decreased. The cause of hemifacial spasm was resulted from pathological stimulation of the facial nerve, producing abnormal nervous conduction. The therapeutic hemifacial spasm with botulin A is an easy and effective method.