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At least 487 records · Page 27Linked to original sources
PubMed2000

Incidence and risk factors for subtypes of cerebral infarction in a general population: the Hisayama study.

BACKGROUND AND PURPOSE: We estimated the incidence of first-ever cerebral infarction in regard to its subtypes and analyzed their risk factors separately in a community-based prospective cohort study in Japan. METHODS: Stroke-free subjects (n=1621) aged >/=40 years were followed up for 32 years from 1961. During this period, 298 cerebral infarctions occurred and were divided into 167 lacunar, 62 atherothrombotic, 56 cardioembolic, and 13 undetermined subtypes of infarction on the basis of clinical information including brain imaging and autopsy findings. RESULTS: The age-adjusted incidence of lacunar infarction (3.8 per 1000 person-years for men and 2.0 for women) was higher than that of atherothrombotic infarction (1.2, 0. 7) and cardioembolic infarction (1.3, 0.5) in both sexes. Time-dependent Cox's proportional hazard analysis revealed systolic blood pressure as well as age to be independent risk factors for all subtypes of cerebral infarction except for cardioembolic infarction in men. Additionally, ST depression on ECG, glucose intolerance, and smoking in men and left ventricular hypertrophy on ECG and body mass index in women remained significant risk factors for lacunar infarction. ST depression was also significantly related to events of atherothrombotic infarction in women. The risk of atrial fibrillation for cardioembolic infarction was outstandingly high in both sexes, and left ventricular hypertrophy and lower total cholesterol were additional risk factors for cardioembolic infarction in women. CONCLUSIONS: In this Japanese population, lacunar infarction was the most common subtype of cerebral infarction and had a greater variety of risk factors, including not only hypertension but also ECG abnormalities, diabetes, obesity, and smoking, than did atherothrombotic infarction or cardioembolic infarction.

Adult↗
PubMed2004

Hemihyperhidrosis in cerebral infarction.

Increased sweating on the hemiparetic side in cerebral infarcts is not a common clinical finding. The onset, severity and duration of symptoms can vary. The structural lesion responsible for this is a subject of conjecture. We present the case of a 66-year-old man who developed hemihyperhidrosis secondary to a cerebral infarct.

Aged↗
PubMed1998

[Evaluation of patients with cerebral infarction using transesophageal echocardiography: atherosclerotic changes in the thoracic aorta and the branches of the aortic arch].

Atherosclerotic disease of the aortic arch is thought to be a potential source of cerebral emboli, but this disease in the branch of the aortic arch has not been extensively explored. This study assessed atherosclerotic lesions in the thoracic aorta and the branches of the aortic arch using transesophageal echocardiography in patients with cerebral infarction, and simultaneously searched for potential cardiac sources for emboli. Thrombi were detected in the left atrial appendage in nine of 54 patients with cerebral infarction and these patients were excluded. The remaining 45 patients with cerebral infarction (31 males and 14 females aged 68.5 +/- 7.4 years) and 35 normal subjects (21 males and 14 females aged 69.2 +/- 9.5 years) were evaluated. The thickness of the wall was measured in the branches of the aortic arch (brachiocephalic trunk, left common carotid artery and left subclavian artery) as well as the thoracic aorta (ascending aorta, aortic arch and descending aorta). Atherosclerotic lesions were defined as increased echogenicity of the intima (intimal thickening), calcification, protruded plaque, ulceration or plaque with cystic lesion. The thicknesses of the wall in the aortic arch (3.84 +/- 1.25 vs 2.71 +/- 1.33 mm, p < 0.01), left common carotid artery (2.67 +/- 1.10 vs 2.16 +/- 0.91 mm, p < 0.05) and the left subclavian artery (2.52 +/- 0.67 vs 2.15 +/- 0.88 mm, p < 0.05) were significantly greater in patients than in the normal subjects. The incidence of plaque or ulceration was significantly increased in patients with cerebral infarction compared with the normal subjects in the aortic arch (76% vs 43%, p < 0.05) and left common carotid artery (44% vs 17%, p < 0.05). Transesophageal echocardiography can detect possible sources of emboli in the branches of the aortic arch as well as the thoracic arch in patients with cerebral infarction.

Aged↗
PubMed2005

[Influence of beginning time of hypothermia treatment on prognosis of extensive cerebral infarction].

OBJECTIVE: To study the influence of beginning time of cranial hypothermia treatment on the prognosis of extensive cerebral infarction(ECI) so as to establish the optimum time for such treatment. METHODS: Ninety-two ECI patients were divided into three groups. In group A hypothermia treatment was begun within 6 hours after cerebral infarction in 31 patients. In another 31 cases in group B it was begun in 7-10 hours, and in 30 cases in group C it was begun in 11-14 hours after the attack. The mortality rate, the volume of cerebral infarction, neurological deficiency score(NDS) and quality of life in survivors were determined respectively in three groups. RESULTS: The volume of cerebral infarction in group A and B was obviously smaller than that of group C after hypothermia treatment(P<0.01). The mortality rate was higher in group C (26.67% in group C, 3.23% in group A and 6.45% in group B, both P<0.05) The mortality rate was highest in cases with high body temperature in group C(P<0.05). NDS was significantly lower in survivors of groups A and B compared with group C (both P<0.05), groups A and B compared with group C(P<0.05). The NDS and quality of life of the survivors with high body temperature(P<0.05 or P<0.01). CONCLUSION: Cranial hypothermia treatment should be begun with 10 hours after illness to obtain best effect.

Cerebral Infarction↗
PubMed2003

[The protection of seed oil of Hippophae rharmnoides on ischemic cerebral infarction in rats].

OBJECTIVE: To study the protection of seed oil of Hippophae rhamnoides on ischemic cerebral infarction in rats and the mechanism of the action. METHOD: Focal cerebral ischemia model was made by middle cerebral artery occlusion(MCAO) in rats. Behavior obstacles of rats were observed. Cerebral infarction volume was determined by Megnetic Resonance Imaging(MRI). RESULT: Seed oil of Hippophae rhamnides 0.7 and 0.35 g.kg-1 could markedly reduce infarction volume after occlusion of middle cerebral artery in rats and also could ameliorate the behavior obstacles of rats. CONCLUSION: These results suggested that seed oil of Hippophae rhamnoides had distinct protection to ischemic cerebral infarction in rats.

Animals↗
PubMed2004

Reversible dementia in systemic lupus erythematosus without antiphospholipid antibodies or cerebral infarction.

Dementia is a very rare neurological manifestation of systemic lupus erythematosus (SLE) and has a deep link with antiphospholipid antibodies (APL) and cerebral infarction in its development. However, nonvascular dementia irrelevant to APL or cerebral infarction has not been reported in patients with SLE until now. We describe a case of reversible dementia in an SLE patient without APL or cerebral infarction which was successfully treated with corticosteroid and cyclophosphamide. There are two significant points in this case. One is that humoral factors other than APL might be involved in the development of dementia. Secondly, reversible dementia without APL or cerebral infarction may respond more favorably to immunosuppressive therapy.

Adrenal Cortex Hormones↗
PubMed1995

Effects of bifemelane hydrochloride on plasma neuropeptide Y, 3-methoxy-4-hydroxyphenylethylene glycol and 5-hydroxy-indole acetic acid concentrations in patients with cerebral infarction.

Bifemelane hydrochloride (BH) is widely employed in Japan in the treatment of cerebral infarction patients with depressive symptoms and its antidepressant action is considered to be caused by the normalizing effects of neurotransmitters. The relationship between the normalizing effects of neurotransmitters of BH and the depressive state of patients with cerebral infarction was examined. BH 150 mg/day was administered for three months to 13 cerebral infarction patients with depressive state. We measured the plasma neuropeptide Y (NPY), 3-methoxy-4-hydroxyphenylethylene glycol (MHPG) and 5-hydroxy-indole acetic acid (5-HIAA), and assessed the depressive symptoms using the 21-item Hamilton's Rating Scale for Depression (HRSD) before and after administration of BH. After treatment, the plasma NPY concentration was significantly increased, the plasma MHPG concentration and total score of HRSD were significantly decreased, and the plasma 5-HIAA concentration showed no changes. These findings suggest that the antidepressant effect of BH is caused by the normalizing effects of NPY and noradrenalinergic neurons.

Aged↗
PubMedDate not supplied

High-dose acetylsalicylic acid after cerebral infarction. A Swedish Cooperative Study.

Within 3 weeks of the event, 505 patients with cerebral infarction, minor or major stroke, were randomly assigned to treatment with acetylsalicylic acid (ASA) 1.5 g/day or placebo in a double-blind clinical trial with a follow-up of 2 years in all patients. Primary events were considered to be recurrent stroke or death; secondary events, myocardial infarction and transient ischemic attack. There was no difference in stroke recurrence rate in the ASA and placebo groups (12 and 13%, respectively), nor was there any significant difference in the rate of recurrent stroke or death, first event counted (23% in the ASA and 22% in the placebo group). The risk of transient ischemic attack and myocardial infarction was not reduced in the ASA group. In the present study there was no prophylactic effect of high-dose ASA after cerebral infarction. A compilation of the major trials of ASA after transient ischemic attack and cerebral infarction is presented.

Adult↗
PubMed1992

Cerebral infarction in young men with nephrotic syndrome.

BACKGROUND AND PURPOSE: Thrombosis is one of the main complications of nephrotic syndrome; however, cerebral infarction associated with nephrotic syndrome has been rarely reported. SUMMARY OF REPORT: We describe acute cerebral infarction in two young men with nephrotic syndrome. Both had a hypercoagulable state based on hemostatic studies. By retrospectively reviewing the medical records of the past 10 years at our hospital, we found an additional five cases of cerebral infarction with nephrotic syndrome. Two of the patients were found to have nephrotic syndrome during admission for stroke. CONCLUSIONS: Hypercoagulability may be the major contributing factor of cerebral infarction in patients with nephrotic syndrome.

Acute Disease↗
PubMed2005

Retinal microvascular abnormalities and MRI-defined subclinical cerebral infarction: the Atherosclerosis Risk in Communities Study.

BACKGROUND AND PURPOSE: Retinal microvascular abnormalities reflect cumulative small vessel damage from elevated blood pressure and may reflect subclinical cerebral microvascular changes. We examined their associations with MRI-defined cerebral infarcts. METHODS: Population-based, cross-sectional study of 1684 persons 55 to 74 years of age without a history of clinical stroke, sampled from 2 US southeastern communities. Retinal photographs were obtained and graded for presence of retinal microvascular abnormalities, including arteriovenous nicking, focal arteriolar narrowing, retinal hemorrhages, soft exudates and microaneurysms. Photographs were also digitized, and retinal vessel diameters were measured and summarized as the arteriole-to-venule ratio (AVR). Cerebral MRI scans were graded for presence of cerebral infarct, defined as a lesion > or =3 mm diameter in a vascular distribution with typical imaging characteristics. RESULTS: There were a total of 183 MRI cerebral infarcts. After adjustment for age, gender, race, 6-year mean arterial blood pressure, diabetes, and other stroke risk factors, cerebral infarcts were associated with retinal microvascular abnormalities, with odds ratios 1.90 (95% CI, 1.25 to 2.88) for arteriovenous nicking, 1.89 (95% CI, 1.22 to 2.92) for focal arteriolar narrowing, 2.95 (95% CI, 1.30 to 6.71) for blot hemorrhages, 2.08 (95% CI, 0.69, 6.31) for soft exudates, 3.17 (95% CI, 1.05 to 9.64) for microaneurysms, and 1.74 (95% CI, 0.95 to 3.21) for smallest compared with largest AVR. In stratified analyses, these associations were only present in persons with hypertension. CONCLUSIONS: Retinal microvascular abnormalities are associated with MRI-defined subclinical cerebral infarcts independent of stroke risk factors. These data suggest that retinal photography may be useful for studying subclinical cerebrovascular disease in population-based studies.

Aged↗
PubMed1999

[Influence of nitric oxide upon cerebral infarction in 15 cases].

To study the role of the nitric oxide(NO) in patients with cerebral infarction, NO in cerebrospinal fluid was determined in cerebral infarction group(15 cases) and control group(10 cases). Infarct volume was determined by CT between the second and the 7th day after the onset of symptoms. The severity of neurological deficits was assessed with the stroke scale of Ministry of Public Healthy(China). The results showed that NO was higher in cerebral infarction group (3.12 +/- 1.60) than that in control group(1.19 +/- 1.01) (P < 0.01). The concentration of NO was positively correlated with infarction volume(r = 0.57, P < 0.05) and severity of neurological of deficits(r = 0.54, P < 0.05), respectively. The results support the conclusion that NO produced in large amounts in the postischemic tissue contributes to the progression of the brain damage, which was demonstrated in animal models of focal cerebral ischemia.

Adult↗
PubMed2006

[A linkage between beta-fibrinogen gene -148C/T polymorphism and cerebral infarction].

OBJECTIVE: To study the linkage between -148C/T polymorphism of beta-fibrinogen gene and plasma fibrinogen levels in patients with acute cerebral infarction. METHODS: One hundred and fifty-one patients with cerebral infarction and 101 healthy individuals were enrolled in this trial. The beta-fibrinogen gene -148C/T polymorphism was analyzed by PCR-restriction fragment length polymorphism, and plasma fibrinogen levels were obtained from prothrombin time assay. RESULTS: Plasma fibrinogen levels of patients were significantly higher than those of controls (P<0.01). In both groups, T allele carriers had higher plasma fibrinogen levels than other those did (P<0.01); and the fibrinogen level difference was still significant if both groups was based on their sex (P<0.05). Divided by age, each group of the study cases has significant difference between two genotypes (P<0.05). T -148 allele frequency of the middle age case in study group was higher than that in control group (P<0.05). CONCLUSION: High plasma fibrinogen level is a risk factor to cerebral infarction. Plasma fibrinogen level is affected by -148C/T polymorphism of beta-fibrinogen gene. With or without other risk factors and environmental factors affecting, T allele increases plasma fibrinogen level and may be a heritable risk factor to cerebral infarction.

Adult↗
PubMed2003

Administration of melatonin after onset of ischemia reduces the volume of cerebral infarction in a rat middle cerebral artery occlusion stroke model.

BACKGROUND AND PURPOSE: In both permanent and transient 3-hour middle cerebral artery occlusion rat stroke models, a single intraperitoneal injection of melatonin at 5 or 15 mg/kg given before ischemia was shown to reduce infarct volume at 72 hours. The present study was conducted to examine the treatment time window when melatonin was commenced after onset of ischemia. METHODS: Adult male Sprague-Dawley rats were anesthetized to undergo right-sided middle cerebral artery occlusion for 3 hours. A single intraperitoneal injection of vehicle or melatonin at 5 mg/kg was given at 0, 1, or 3 hours after onset of ischemia. Other groups received multiple injections of vehicle or melatonin at 5 mg/kg with the first injection given at 1, 2, or 3 hours after onset of ischemia and the second and third injections at 24 and 48 hours, respectively. Multiple injections of melatonin at 15 mg/kg with the first injection given at 3 hours were also made. The infarct volume was determined at 72 hours. RESULTS: A single dose of melatonin at 5 mg/kg given at 0 or 1 but not 3 hours after onset of ischemia reduced the infarct volume. Multiple doses of melatonin at 5 mg/kg also reduced the infarct volume when the first dose was given at 1 or 2 but not 3 hours after onset. Significant hemodynamic effects were not observed. CONCLUSIONS: Our results indicate that melatonin at 5 mg/kg given as a single injection or multiple injections protects against focal cerebral ischemia when commenced within 2 hours of onset.

Animals↗
PubMed2001

Cerebrovascular reactivity to acetazolamide in alert patients with cerebral infarction: usefulness of first-pass radionuclide angiography using 99m Tc-HMPAO in monitoring cerebral haemodynamics.

Cerebral blood flow (CBF) and cerebrovascular reactivity (CVR) were studied in 75 patients with cerebral infarction. All patients were alert with the symptoms of hemiparesis and/or aphasia, and were divided into two groups: 42 patients had occlusion or stenosis of >75% at the internal carotid artery or main trunk of middle cerebral artery; and 33 patients did not. Hemispheric mean CBF was measured by performing first-pass radionuclide angiography using 99mTc-hexamethylpropylene amine oxime. CVR was measured as the percentage change from the baseline mean CBF value after the administration of 500 mg acetazolamide. The CVR in both groups was significantly impaired (5.2+/-6.3%, P<0.001 and 7.7+/-6.1%, P<0.01, respectively) compared with normal controls (14.7+/-3.3%), although the mean CBF was not significantly reduced compared with age-matched controls. In the 12 patients with unilateral carotid occlusion, five patients with good collateral flow via the anterior communicating artery showed preserved CVR (11.0+/-7.8%), but those without did not (1.6+/-7.0%). CVR is impaired in alert patients with cerebral infarction, although the mean CBF is not reduced, and good collateral flow via the anterior communicating artery in patients with carotid occlusion may be a sign of well-preserved haemodynamic status.

Acetazolamide↗
PubMed1997

Suppressed cardiac and electroencephalographic arousal on apnea/hypopnea termination in elderly patients with cerebral infarction.

The goal of the present investigation is to show the clinical significance of arousal response at termination of apnea/hypopnea in patients with sleep apnea syndrome (SAS) after cerebral infarction. We polygraphically assessed "cardiac arousal," which is defined as an abrupt increase in heart rate at a termination of sleep apnea/hypopnea, and electroencephalographic (EEG) arousal. There were six elderly subjects, bedridden after cerebral infarction, with SAS aged 71-87 years (mean 72.3 years) and 11 age-matched patients with SAS aged 61-78 years (mean 62.3 years) as controls. The following sleep parameters were measured: number of apneas per hour (apnea index [AI]), number of hypopneas per hour (hypopnea index [HI]), summation of the two (apnea/hypopnea index [AHI]), and duration in which nocturnal oxygen saturation was decreased below 90% (duration of SaO2 < 90%). We calculated the ratio of apnea/hypopnea per hour with cardiac arousal to total apnea/hypopneas (XI) (% cardiac arousal [XI/AHI x 100]) and the ratio of that with EEG arousal (YI) (% EEG arousal [YI/AHI x 100]). Between the two groups, we found no significant difference in body mass index, the ratio of central apnea to total apnea/hypopnea, AHI, duration of apnea/hypopnea, lowest SaO2, and duration of SaO2 < 90%. Compared with controls, % cardiac and % EEG arousals were significantly lower in patients with cerebral infarction. In contrast, the ratio of HI to AHI was significantly higher in patients with cerebral infarction than in control subjects. Our findings indicate that cardiac and EEG arousals at termination of apnea/hypopnea are significantly suppressed in elderly patients with SAS after cerebral infarction, which may provide useful information on the pathophysiology of SAS in patients with cerebrovascular disease.

Aged↗
PubMedDate not supplied

[Glucose, pyruvate and lactate concentrations in the cerebrospinal fluid in patients with cerebral infarction].

The determinations were performed in cerebrospinal fluid of 50 patients with recent cerebral infarction in the 1-st, 3-rd and 10-th day of disease. Spectrophotometrie methods were used for the determination of lactate and pyruvate and a colorimetric method for glucose determination. A statistically significant increase of glucose in the cerebrospinal fluid on the 1-st day after cerebral infarction and of pyruvate, lactate and lactate: pyruvate index on 1-st and 3-rd day after cerebral infarction was found. The results obtained point to intensification of the anaerobic pathway of glucose metabolism.

Adult↗
PubMed2005

Body temperature and mortality in acute cerebral infarction.

BACKGROUND AND OBJECTIVE: In animal models, a rise in body temperature after cerebral ischemia consistently produces more extensive brain damage. In humans, however the relationship between body temperature and stroke outcome has been far less extensively investigated, providing conflicting results. The objective of the present study is to determine whether body temperature recorded during the first 72 hours after admission is an independent predictor of mortality in acute cerebral infarction. MATERIAL AND METHOD: The medical records of patients admitted within 48 hours of onset of symptoms to Prasat Neurological Institute between 1 January 2002 and 31 December 2003, with a diagnosis of cerebral infarction, confirmed by CT or MRI of the brain were retrospectively studied. The relationship between the highest temperature recorded during the first 72 hours after admission and mortality during hospital stay was evaluated. Multiple logistic regression analysis included relevant confounders and potential predictors such as gender, age, hypertension, diabetes, smoking, previous stroke, ischemic heart disease, atrial fibrillation, consciousness and infections was performed. RESULTS: There were 332 patients included in the present study. During the first 72 hours after admission, 88 (26.5%) patients had fever (> 37.5 degrees C). The highest temperature recorded during the first 72 hours after admission was a significant predictor of in hospital mortality in the final multivariate logistic regression model. For each 1 degree C increase in body temperature the odd ratio of mortality rose by 3.95 (OR, 3.95; 95%CI, 1.84 - 8.45). CONCLUSION: In the present study, the highest body temperature recorded during the first 72 hours after admission was shown to be a significant predictor of mortality in acute cerebral infarct patients.

Acute Disease↗
PubMed1989

Dental infections in association with cerebral infarction in young and middle-aged men.

The association between dental infections and cerebral infarction was investigated in a case-control study involving 40 patients with ischaemic cerebral infarction under the age of 50, and 40 randomly selected community controls matched for sex and age. Poor oral health, as assessed by two indices measuring the severity of infections of teeth and periodontium, or by the presence of subgingival calculus or the presence of suppuration in the gingival pockets, were more common in male patients than in male controls, but no difference was observed in females. If severe dental infections were combined with other probable bacterial infections there were altogether 16 patients (40%) but only two controls (5%) who had suffered from a probable bacterial infection within 1 month or at the time of the stroke or when examined as a control (P less than 0.01). Our results suggest an association between bacterial infection and ischaemic cerebrovascular disease in patients under 50 years of age. Severe chronic dental infection seems to be an important type of infection associated with cerebral infarction in males.

Adolescent↗