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PubMed2001

Effect of Rhizoma Corydalis on focal cerebral infarct in ischemia-reperfusion injured rats.

AIM: To investigate the effect of Rhizoma Corydalis (RC) on focal cerebral infarct. METHODS: A total of 30 Sprague-Dawley (SD) rats were studied. Focal cerebral infarct was established b y occluding the bilateral common carotid arteries and the right middle cerebral artery for 90 min. After 24 h reperfusion, the neurological status was evaluated and then the rats were killed and the brain tissue was stained with 2,3,5-triphenyl-tetrazolium chloride. The neurological status and the changes in the area of cerebral infarct were used as an index to evaluate the effect of RC on cerebral infarct. In addition, the whole blood was examined 24 h after RC treatment in the other 24 SD rats. RESULTS: Pretreatment with RC 100 mg/kg can improve neurological status and also can reduce the area of cerebral infarct in ischemia-reperfusion injured rats. The counts of erythrocyte and the amount of hematocrit increased in whole blood of RC-treated rats. CONCLUSION: RC can improve neurological status and reduce the area of cerebral infarct in ischemia-reperfusion injured rats.

Animals↗
PubMedDate not supplied

Regional cerebral blood flow correlates of aphasia outcome in cerebral hemorrhage and cerebral infarction.

The relationship between recovery from aphasia and regional cerebral blood flow (CBF) was compared in 87 patients, 44 with cerebral hemorrhage and 43 with non-embolic cerebral infarction. CBF values correlated poorly with aphasia outcome in patients with cerebral hemorrhage whereas a tight correlation was demonstrated in patients with non-embolic cerebral infarction. A marked variability of CBF values in the acute and subacute stage might account for the poor correlation between CBF and aphasia outcome in patients with cerebral hemorrhage. On the other hand, a sharp discrimination was achieved between those with a good recovery from aphasia and those with a poor recovery by the dimensions of the hematoma on CT. In non-embolic cerebral infarction, a relative frontal ischemia was associated with motor aphasia while a relative temporal ischemia was associated with sensory aphasia. This dichotomy was not demonstrated in the regional CBF values in patients with cerebral hemorrhage.

Adult↗
PubMed1994

[Protein-losing enteropathy and cerebral infarction associated with systemic lupus erythematosus].

A 26-year old woman, who was diagnosed as having systemic lupus erythematosus at the age of 23 year old, presented diarrhea and headache. She showed severe hypoproteinemia (serum total protein 3.7 g/dl, serum albumin 1.4 g/dl) and hyperlipidemia. She revealed to have protein-losing enteropathy with the result of alpha-1-antitrypsin clearance test using stool. Increase of prednisolone improved the loss of albumin into the bowel and abnormal laboratory findings. She also showed watershed infarction in the area of middle cerebral artery and posterior cerebral artery. Protein-losing enteropathy is a rare complication of SLE, only 18 cases are available on literature. No case is found to have cerebral infarction in patients with protein-losing enteropathy associated with SLE. It is known that blood levels of anticoagulation factors decrease in protein-losing enteropathy due to the leakage of plasma protein into intestinal lumen. Serum antithrombin III was decreased in this case. Hyperlipidemia found in this case seems to be caused by same mechanism in nephrotic syndrome. Lupus anticoagulant was also positive in this patient. These factors seems to be related to the occurrence of cerebral infarction. This case suggests the possibility of cerebral infarction in patients with protein-losing enteropathy in SLE.

Adult↗
PubMed1979

[Classification and course of cerebral infarcts on computer tomography (author's transl)].

The typical computer tomographic signs of ischaemic cerebral infarct are discussed on the basis of 631 cases. Infarcts have three typical stages. Stage I, one week, fresh infarct with signs of oedema (space-occupying lesion with an unsharp margin, slightly reduced density, lack of contrast uptake). Stage II, second to fourth week, reduction in the oedema. Frequently very marked contrast enhancement of the cortex and basal nuclei. Stage III, later than four weeks. Development of malacic cysts, with further reduction in density and size. Development of homolateral atrophy. The computer tomographic diagnosis of cerebral infarcts during Stage I is often very difficult. Distinction from infiltrating tumour is often possible only after further observation. The diagnosis of cerebral infarcts in stages II and III is possible in most cases. Haemorrhagic cerebral infarcts do not follow a temporal pattern as accurately as anaemic infarcts. They show circular increase in contrast of slowly diminishing size. The increased contrast persists considerably longer and is clearly distinguished from that in an anaemic cerebral infarct.

Adolescent↗
PubMed2005

Silent cerebral infarction in heart failure: vascular or thromboembolic?

Silent cerebral infarction in heart failure as reported by Siachos et al is significantly higher than reports of symptomatic cerebral infarction. Are we underestimating the occurrence of silent cerebral infarction, or can this finding be accounted for by concomitant conditions?

Fibrinolytic Agents↗
PubMed1998

[Clinical study on buyang huanwu decoction to the metabolic imbalance of endothelin and calcitonin gene related peptide in patients with early cerebral infarction].

OBJECTIVE: To explore the mechanism of Buyang Huanwu Decoction (BHD) in treating early cerebral infarction. METHODS: Seventy cases with early cerebral infarction were randomly divided into two groups. Chinese medicine group (CMG, n = 35) was treated with BHD; western medicine group (WMG, n = 35) was treated with hydroxyethyl starch injection and enteric coated aspirin tablets. The levels of endothelin (ET) and calcitonin gene related peptide (CGRP) in plasma before and after treatment and the results of clinical treatment were observed, and also controlled with healthy subjects. RESULTS: The levels of ET before treatment in both patient groups were significantly higher than that of the healthy subjects (P < 0.001), and the levels of CGRP were significantly lower (P < 0.001). After treatment the metabolic imbalance of ET and CGRP improved significantly in both treatment groups (in CMG P < 0.001; in WMG (P < 0.01), but the ET and CGRP in CMG improved more obviously than those in WMG (P < 0.01, P < 0.05). The marked effective and cure rate of CMG was higher than that of WMG (68.6% vs 31.4%; chi 2 = 9.65, P < 0.01). CONCLUSIONS: BHD could improve the metabolic imbalance of ET and CGRP in patients with early cerebral infarction and by this mechanism it was able to treat cerebral infarction.

Adult↗
PubMed2001

[The relationship between angiotensin converting enzyme gene polymorphism and risk factors for cerebral infarct].

OBJECTIVE: To explore the relationship between angiotensin converting enzyme (ACE) gene polymorphism and risk factors of cerebral infarct (CI) in Chinese Han nationality. METHODS: One hundred and sixty-five cases with cerebral infarct, 101 cases of essential hypertension patients with 106 normal persons in Chinese Han serving as controls were detected using polymorase chain reaction (PCR) and genetic methods. ACE contents in serum were measured by colorimetric method. Risk factors of cerebral infarct were assessed by standard questionnaire, physical examination and blood tests. RESULTS: ACE DD genotype appeared more common in patients of cerebral infarct when comparing with essential hypertension groups (0.43 versus 0.31, chi 2 = 4.03, P < 0.05) and normal controls (0.43 versus 0.17, chi 2 = 19.86, P < 0.01). D:I allele frequency appeared to be 0.66:0.34 in cerebral infarct patients and 0.41:0.59 in controls (chi 2 = 32.85, P < 0.01). In basal ganglia infarct and thalamus infarct groups, ACE DD genotype and allele ratio distribution were remarkably different to that in normal subjects (chi 2 = 18.30, 12.41, P < 0.01). The mean levels of serum in cerebral and hypertension were higher than in normal controls (F = 2,240.06, P < 0.01), and serum ACE activity in ACE DD genotype was significantly higher than that in ACE DI and II genotype in cerebral group (F = 8.83, P < 0.01). CONCLUSIONS: The ACE gene deletion polymorphism might serve as an independent risk factor for cerebral infarct in Chinese Han nationality while circulation ACE activity might be related to gene deletion polymorphism.

Adult↗
PubMed1984

The correlation between carotid plaque ulceration and cerebral infarction seen on CT scan.

The purpose of the study was to determine the association between cerebral infarction seen on CT scan and macroscopic ulceration of atheromatous carotid plaques in patients undergoing carotid endarterectomy. Following carotid endarterectomy in 65 patients, specimens were examined for the presence of ulceration without knowing the result of the preoperative CT brain scan. The 65 patients thus investigated underwent 68 carotid endarterectomies: 36 for a history of transient ischemic attacks (TIAs), 13 for amaurosis fugax, and six for prior strokes; 13 asymptomatic patients had prophylactic carotid endarterectomy prior to coronary bypass. A macroscopic ulcer was present in 42 specimens. Twenty-six (62%) of the patients with ulceration had one or more ipsilateral cerebral infarcts on CT scan. Only two (8%) of the 26 patients without an ulcer had cerebral infarcts. Of the 36 patients who presented with TIAs, 26 (72%) had carotid plaque ulcers and 23 (88%) of these had cerebral infarcts on CT scan also. In contrast, only three of 13 asymptomatic patients had plaque ulcers and only one of these had a cerebral infarct. There is a high incidence of cerebral infarction seen on CT scan in patients presenting with TIAs. These infarcts occur predominantly in patients with ulcerated atheromatous carotid lesions.

Aged↗
PubMed2005

Serial measurement of serum basic fibroblast growth factor in patients with acute cerebral infarction.

Basic fibroblast growth factor (bFGF) has been reported to be involved in the pathophysiological changes following cerebral infarction. Basic fibroblast growth factor is upregulated in the brain and conduces to neuroprotection and angiogenesis in experimental brain ischemia, but the change of serum bFGF in cerebral infarction patients has not been reported. In the present study, we investigated the dynamic changes of serum bFGF in 30 patients with acute cerebral infarction and found that serum bFGF increased significantly after cerebral infarction compared with the control group (p<0.05). Serum bFGF peaked on day 3 (15.46 +/- 5.58 pg/ml; p<0.01) and remained significantly elevated on day 14 following cerebral infarction. In this study, it was also found that the levels of bFGF with large infarction were higher at each time point than those with moderate or small infarction (p<0.05). There was a positive correlation between the peak level of bFGF and improvement of clinical neurological deficits scored by Scandinavian Stroke Scale (SSS) (r=0.596; p<0.05). These results suggest that the serum bFGF level increased significantly after cerebral infarction and the level of serum bFGF could be of value to estimate the infarction size and clinical prognosis.

Acute Disease↗
PubMed2005

[Observation on therapeutic effect of "Shandong Xiaoying" needling method for treatment of cerebral infarction].

OBJECTIVE: To search for an effective method for treatment of cerebral infarction. METHODS: Sixty cases of cerebral infarction were randomly divided into an observation group and a control group, 30 cases in each group. All of them were treated with routine needling method, and "Shandong Xiaoying" needling was added to the observation group. The therapeutic effects, recovery of myodynamia and daily living ability were compared in the two groups. RESULTS: There was no significant difference between the two groups in the total effective rate for recovery of upper limb myodynamia (P > 0.05), but there was a very significant difference in the total effective rate for recovery of lower limb myodynamia and increase of daily living ability between the two groups (P < 0.01). CONCLUSION: "Shandong Xiaoying" needling has markedly therapeutic effect on cerebral infarction.

Acupuncture Points↗
PubMedDate not supplied

Cerebral infarction in newborns: report of two cases.

Neonates with cerebral infarction do not present with specific symptoms and the condition is usually insidious, so many atypical cases are not diagnosed properly during the neonatal stage. Normal neurological examination results may be found in newborns who have actually had a cerebral infarction insidiously. We present two newborns with cerebral infarction. One had clinical symptoms of seizures. Brain computed tomography showed a low-attenuated area and magnetic resonance angiography showed a decreased caliber and number of cerebral artery branches. The other had normal neurological examination results. He was referred to our hospital due to cyanosis. Brain sonography revealed a focal hyperechoic area and T2 weighted magnetic resonance image showed an increased signal intensity area. The incidence, etiologies, clinical and radiographic findings are also reviewed.

Brain↗
PubMed2004

[Matrix metalloproteinase-9 expression by endothelial cells incubated with peripheral blood leukocytes from patients with cerebral infarction].

OBJECTIVE: Matrix metalloproteinase-9 (MMP-9) have been implicatedin the development of cerebral infarction. In a prospective study we investigated whether the MMP-9 expression are increased by endothelial cells incubated with peripheral blood Leukocytes from patients with acute cerebral infarctions. METHODS: Using Immuno-fluorescence technique, Human umbilical vein endothelial cells were cocultured with leucocytes for 24 hours in vitro before used for detecting the MMP-9 expression. The leucocytes were purified from peripheral blood in 6 patients with acute cerebral infarction and in 6 age- and sex-matched healthy subjects. the smears of endothelial cells were stained with MMP-9 monoclonal antibodies, and detected using the ABC ELITE kit. RESULTS: Laser-Confocus confirmed the presence of MMP-9 within endothelial cells incubated with peripheral blood Leukocytes from patients with acute cerebral infarctions. Compared with the control group, MMP-9 expressions were significantly higher in the stroke group (P < 0.001). CONCLUSION: Our study demonstrated that the leukocytes from acute cerebral infarction patients were Activated, and could stimulate vessel endothelial cells excrete MMP-9. Activated leukocytes and MMP-9 expression by endothelial cells may have an important role in acute cerebrovascular ischemia and its consequences.

Aged↗
PubMed2006

[Study on plasma antibodies against heat shock protein 70 in the hypertensive patients with cerebral infarction].

OBJECTIVE: To determine the level of heat shock protein 70 (HSP70) antibody in the hypertensive patients with cerebral infarction and explore the role of plasma antibody against HSP70 in the pathogenesis of cerebral infarction and its relationship to the brain tissue damage. METHODS: One hundred patients with CT or MRI confirmed cerebral infarction were enrolled in the study, in whom 64 were male, and 36 female. Among them, 67 patients were having hypertension and 33 with normal blood pressure. One hundred healthy individuals, including 58 male and 42 female, served as the control group. The level of plasma HSP70 antibody was determined with Western blot-enzyme linked immunoadsorbent assay (ELISA) technique. RESULTS: Patients with cerebral infarction had a significantly higher incidence (69%) of antibodies to HSP70 compared to the low incidence (13%) of antibodies to HSP70 in the controls. Patients with hypertension had a high incidence (57%) of antibodies to HSP70 compared to the low incidence (12%) of antibodies to HSP70 in patients with normal blood pressure in cerebral infarction group. Patients with hypertension in the control group had a higher incidence (11%) of antibodies to HSP70 compared to the low incidence (2%) of antibodies to HSP70 in the same group. CONCLUSION: There is a significant difference in the level of antibodies to HSP70 between patients with cerebral infarction and controls. Elevation in the level of antibodies to HSP70 may reflect the degree of brain tissue damage.

Aged↗
PubMed2001

Expression of neural plasticity related gene in the pontine tegmental area of rats with overactive bladder after cerebral infarction.

PURPOSE: We investigated the expression of the neural plasticity related genes c-fos, zif268, c-jun, brain-derived neurotrophic factor and tissue plasminogen activator in the pontine tegmental area in rats with overactive bladder induced by cerebral infarction. MATERIALS AND METHODS: Cerebral infarction was induced by left middle cerebral artery occlusion in female Sprague-Dawley rats. Bladder activity was monitored by continuous infusion cystometrography in awake rats. Specimens were obtained from the pontine tegmental area 1, 3, 5, 12 and 24 hours after cerebral infarction or sham operation. The effect of 0.1 mg./kg. intravenously of the N-methyl-d-aspartate glutamatergic receptor antagonist MK-801 on bladder activity, and c-fos and zif268 expression after middle cerebral artery occlusion were studied. Real-time reverse transcriptase-polymerase chain reaction was performed with the LightCycler system (Roche Diagnostics, Mannheim, Germany) to evaluate cerebral infarction influences on gene expression in the pontine tegmental area. RESULTS: Bladder capacity in cerebral infarcted rats was significantly reduced 1 to 24 hours after middle cerebral artery occlusion compared with that of sham operated rats (p <0.05 to 0.01). One hour after occlusion mean c-fos messenger (m)RNA expression plus or minus standard error had significantly increased to 18.9 +/- 4.0 in terms of its density relative to the outer control in a sample obtained immediately after occlusion compared with that in sham operated rats (p <0.05). It returned to the control level within 3 hours after occlusion. Mean zif268 mRNA expression significantly increased to a relative density of 3.2 +/- 1.4 3 hours after middle cerebral artery occlusion (p <0.01) and returned to the control level within 5 hours after occlusion. The expressions of c-jun, brain-derived neurotrophic factor and tissue plasminogen activator was not influenced by occlusion. Pretreatment with MK-801 inhibited bladder overactivity and significantly reduced the expression of c-fos and zif268 mRNA in the pontine tegmental area. CONCLUSIONS: These results indicate that the development of bladder overactivity after middle cerebral artery occlusion is mediated by activation of an N-methyl-d-aspartate receptor and accompanied by an increase in c-fos and zif268 mRNA expression in the pontine tegmental area.

Animals↗
PubMed1993

[Acute prognosis and differentiation of various cerebral infarct groups in comparison with cerebral hemorrhage].

For clinical trials classification of stroke should be possible at the bedside by simple methods that are available every where. In this study are 1105 patients with every first ischaemic strokes and 130 patients with intracerebral haemorrhages. The differences between severity of clinical symptoms, outcome and risk factors of intracerebral haemorrhages, ischaemic stroke caused by cerebral microangiopathy, ischaemic stroke combined with extracranial carotid stenosis, cardiogenic brain embolism and atherothrombotic stroke, were analysed. Intracerebral haemorrhages show the poorest outcome of all groups (mortality 23.8%), due to increased intracranial pressure. Cardiogenic brain embolism is more frequent in older women (mean age 77.8 y.). Main risk factor is atrial fibrillation with absolute arrhythmia. The outcome of this group is the worst of all subgroups of ischaemic stroke and survivors most often in need of institutionalization. Patients with ischaemic stroke combined with extracranial carotid stenosis are significantly younger (mean age 67.6 y.), predominantly male, and smokers. Their mortality is low (0.63%), but recovery of paresis is slower than in other subgroups. Ischaemic strokes caused by cerebral microangiopathy with hypertension as main risk factor recover most quickly but acute mortality is higher than in ischaemic stroke combined with extracranial carotid stenosis because of higher age (mean age 74.5 y.). Institutionalization is more frequent too because of higher incidence of dementia in this subgroup. The main prognostic factors of all groups are age and severity of clinical symptoms. A special subgroup are infratentorial ischaemic strokes.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗