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At least 19 recordsLinked to original sources
PubMed1995

[A comparison of risk factors between silent brain infarction and symptomatic brain infarction--clinical significance of hypertension and diabetes mellitus].

We studied a clinical significance of hypertension and diabetes mellitus between silent brain infarction and symptomatic brain infarction. History of hypertension was present in 50% of silent infarction and in 53.3% of symptomatic infarction. Untreated hypertension was more frequent in symptomatic infarction than silent infarction (28.3% vs 16.7%) and the control of the blood pressure was very poor even if the patients with symptomatic infarction was treated with antihypertensive drugs. 66.7% of silent infarction with hypertension was treated with antihypertensive therapy and the control of the blood pressure was also relatively good. In the population with silent infarction, good control of the blood pressure was important for the prevention of symptomatic infarction. Diabetes mellitus with long history was strongly related to symptomatic infarction as compared with silent infarction. The prevalence of both hypertension and diabetes mellitus was high in the population with symptomatic infarction as compared with silent infarction and control individual.

Adult↗
PubMed1997

[Postoperative brain infarction in a patient with the previous asymptomatic brain infarction].

We report a case of a postoperative brain infarction, in which an asymptomatic preoperative brain infarction was also revealed postoperatively. A 63-year-old man with bladder carcinoma was scheduled for the cystoplasty. The patient had no prominent preoperative abnormality. Anesthesia was maintained with isoflurane in N2O/oxygen combined with a spinal block and a continuous epidural block. Anesthesia lasted uneventfully for 16.5 hours. However, emergence from anesthesia was delayed. On the first postoperative day, motor aphasia and right hemiparalysis was confirmed. The computed tomography (CT) of the brain demonstrated a low density area in the frontoparietal region. The magnetic resonance imaging (MRI) indicated the corresponding lesion as the CT had demonstrated, and an old brain infarction in the parietal region. This meant that the patient had a history of asymptomatic brain infarction (ABI). Patients with ABI are considered to be a high-risk group for a brain infarction. It is important to evaluate the risk factors of brain infarction preoperatively and to minimize those risks during the operation. Maintenance of the cerebral perfusion pressure is imperative.

Anesthesia, Epidural↗
PubMed1986

Is there a transitional zone between brain infarcts and the surrounding brain? A histological study.

Twenty-eight recent brain infarcts were studied histologically for the presence of zones of partial tissue destruction between the infarct border and the surrounding normal brain. Such transitional zones have been demonstrated in animals and might be suspected in humans from the broad zones of reduced blood flow that have been demonstrated around brain infarcts. Necrotic neurons were observed outside the infarct borders in 20 of 28 cases. However, the width of the peri-infarct border zone was less than 5 mm in 17 of 20 cases and between 7 and 10 mm in 2 cases. Only one section from one case showed necrotic neurons more than 20 mm from the infarct border. It is concluded that the large majority of the brain infarcts in man are sharply delimited and that the broad zones of reduced flow around the infarcts may be due to functional inactivity following partial denervation of the cortex rather than to true ischemia.

Aged↗
PubMed1995

Neocortical grafts placed in the infarcted brain of adult rats: few or no efferent fibers grow from transplant to host.

The present study examines the capacity of fetal neocortical grafts placed in a brain infarct to exchange axonal projections with the host brain. Five to 7 days after a middle cerebral artery occlusion in adult spontaneously hypertensive rats, dissociated neocortical primordium from fetuses of gestational age 15-16 days was implanted into the infarcted area. Four to 11 months later, the neural tracers Phaseolus vulgaris-leucoagglutinin and Fluoro-Gold were injected in the grafts and host neocortex. An extensive axonal network was present in the transplants but only one of eight rats with appropriate placed injections displayed efferent connections from transplant to host. The sparse axonal outgrowth indicates major limitations for fetal rat cortical grafts to form connections with host neural circuitries after an ischemic insult.

Animals↗
PubMed1997

[Apo(a) phenotype as a risk factor for the silent brain infarction].

Silent brain infarction (SBI) in the penetrating arteries is thought to be one of risk factors for overt cerebral stroke and vascular dementia. Although both Lp(a) concentration and apo(a) phenotype have been reported as risk factors for atherothrombotic infarction in cortical arteries, the roles of Lp(a) in the pathogenesis of lacunar infarction in the penetrating arteries remains controversial. We assessed the importance of apo(a) phenotype as a risk for SBI using a case control analysis. The frequency of low molecular weight phenotype (allele a) of apo(a) was significantly higher in subjects with SBI than in those without SBI. Relative risk for SBI was significantly higher in subjects with allele a than in subjects without allele a. Apo(a) phenotype was indicated to be one of the risk factors for SBI.

Adult↗
PubMed1997

Association of extracranial carotid arterial disease, prior atherothrombotic brain infarction, systemic hypertension, and left ventricular hypertrophy with the incidence of new atherothrombotic brain infarction at 45-month follow-up in 1,482 older patients.

Comparison of 239 older patients with 40% to 100% extracranial carotid arterial disease (ECAD) with 1,243 older patients with no significant ECAD showed a higher prevalence of systemic hypertension, left ventricular (LV) hypertrophy, and prior atherothrombotic brain infarction (ABI) and a higher incidence of new ABI in patients with ECAD than in patients without ECAD. A multivariate Cox regression model showed that independent predictors of new ABI were ECAD (risk ratio = 2.5), systemic hypertension (risk ratio = 2.3), prior ABI (risk ratio = 2.3), LV hypertrophy (risk ratio = 2.3), and male sex (risk ratio = 1.3).

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PubMed1995

Association of silent myocardial ischemia with new atherothrombotic brain infarction in older patients with extracranial internal or common carotid arterial disease with and without previous atherothrombotic brain infarction.

OBJECTIVE: To correlate silent myocardial ischemia with the incidence of new atherothrombotic brain infarction (ABI) in older patients with 40 to 100% extracranial carotid arterial disease (ECAD) with and without prior ABI. DESIGN: In a prospective study of 208 older patients with 40 to 100% ECAD diagnosed by carotid duplex ultrasonography, 24-hour ambulatory electrocardiograms were obtained to detect silent myocardial ischemia. At 42-month mean follow-up, silent myocardial ischemia was correlated with the incidence of new ABI in patients with and without prior ABI. SETTING: A large long-term health care facility where 208 older patients with 40 to 100% ECAD and technically adequate 24-hour ambulatory electrocardiograms for detecting silent myocardial ischemia were studied. PATIENTS: The 208 patients included 68 men and 140 women, mean age 81 +/- 8 years (range 60 to 100). One-hundred three (50%) of the patients had prior ABI. MEASUREMENTS AND MAIN RESULTS: Sixty-nine (33%) of the 208 patients had silent myocardial ischemia. Mean follow-up was 42 +/- 25 months (range 3 to 101 months). At follow-up, the incidence of new ABI was 64% in patients with prior ABI and 32% in patients with no prior ABI (P < .0001). At follow-up, the incidence of new ABI was 65% in patients with silent ischemia and 40% in patients with no silent ischemia (P = .0005). The multivariate Cox regression model showed that patients with prior ABI have a 2.5 times higher chance of developing new ABI than those without prior ABI after controlling other prognostic variables. Patients with silent ischemia have a 2.1 times higher probability of developing new ABI than those without silent ischemia after controlling other prognostic variables. CONCLUSIONS: Prior ABI and silent ischemia are independent risk factors for the development of new ABI in patients with 40 to 100% ECAD. This probably reflects that silent ischemia is a marker for more advanced or more significant atherosclerotic disease rather than a causal factor for ABI.

Aged↗
PubMed1993

Circadian blood pressure patterns in four cases with hemodynamic brain infarction and prolonged blood-brain barrier disturbance.

We report on four patients with hemodynamic brain infarction and pathological circadian blood pressure patterns with nocturnal hypotension which gave rise to a prolonged disturbance of the blood-brain barrier. Besides at least one severe stenosis of the internal carotid artery, there was an untreated chronic arterial hypertension and a pathologically reduced vasomotor reactivity after CO2 stimulation in all patients. The 24-h blood pressure monitoring then carried out showed a distinctly pathological circadian profile with hypertensive day values and nocturnal hypotension with minimum values of 95/50 mm Hg. The range of variation between day and night values was significantly raised (systolic: 20% +/- 2.15%; diastolic: 22.9% +/- 2.58%) compared to patients with essential hypertension as well as normotensive subjects (P < 0.01), and was in excess of 40% in the individual case. There was a slow recovery of the blood-brain barrier after drug-induced normalization of the pathological circadian blood pressure profile. We conclude that the registration of circadian blood pressure patterns may be of prognostic and therapeutic relevance. It may also contribute to further clarification of the pathophysiological significance of blood pressure variability for the development of brain infarction.

Aged↗
PubMedDate not supplied

Cell density in the border zone around old small human brain infarcts.

Nine brain autopsy cases of small old cerebral infarcts were selected for neuropathological studies. Eight of the patients had cortical infarcts, in two cases with extension into the striate body. In one case the infarct involved the striate body only. The density of neurons and glial cells was measured in the coronal and the horizontal planes at various distances from the margin of the infarct. Corresponding counting points in the contralateral hemisphere served as control. On light microscopy, the infarcted cortex was irregularly shaped, but on serial sections the bulging parts appeared to be cut off from the infarcted tissue ("pseudo-infarct islands"). The zone of transition from infarcted to normal brain tissue was less than a few mm wide. In one patient, tomographic measurements of the cerebral blood flow (CBF) and a CT scan could be compared with the neuropathological findings. In this patient, CBF in the surroundings of the infarct was decreased despite a normal neuronal density. The study supports the traditional view held by pathologists that a sharp transition exists between infarcted and normal brain tissue and suggests that the hypoperfusion zone surrounding the region of complete infarction may be due to mechanisms other than selective loss of neurons.

Brain↗
PubMed1995

Silent brain infarct after carotid artery surgery: incidence and prevention.

To determine the prevalence and mechanisms of postoperative silent brain infarct, brain CT was routinely performed before and after carotid endarterectomy during the same period of hospitalization. Between June 1991 and May 1993, 69 patients who underwent 74 carotid endarterectomies (five two-staged bilateral procedures) were enrolled in the study. Ipsilateral brain infarct was observed on the preoperative CT scans in 25 cases. Of these 25 infarcts, three occurred in 20 patients (15%), without symptoms, 13 in 41 patients (32%) with transient ischemic attacks (TIAs), and 9 in 13 patients (70%) with cerebrovascular accident. After surgery, two patients (2.7% of procedures) had monoparesia of an upper limb with no corresponding abnormality seen on CT scans, and two (2.7%) had TIAs, associated with CT evidence of a new lesion in one patient. Five silent brain infarcts (6.8%) were detected, including four in the hemisphere contralateral to the restored carotid artery. These study results indicate there is no correlation between the occurrence of postoperative silent brain infarct and the presence of ulcerated stenosis of the carotid artery documented by Doppler ultrasound examination. Silent infarct was not observed in any of the 24 patients (32%) in whom a shunt had been used during the procedure. After a review of the literature, we propose wider use of intraoperative shunts to prevent postoperative silent brain infarct.

Aged↗
PubMed1993

Silent brain infarction and coronary artery disease in Japanese patients.

OBJECTIVE: Silent brain infarction is fairly common in the elderly, but predictive factors have not been definitively established. This study focuses attention on ischemic heart disease and cerebrovascular risk factors about the frequency of silent brain infarction. DESIGN: The existence of silent brain infarction, the extent of coronary artery stenosis, and cerebrovascular risk factors of consecutive 92 case series with suspected ischemic heart disease were surveyed. SETTING: A hospital for patients with ischemic heart disease. PATIENTS: Ninety-two consecutive Japanese patients with suspected ischemic heart disease were recruited. MAIN OUTCOME MEASURES: All subjects were evaluated for coronary atherosclerosis (number of coronary arteries with significant stenosis and Gensini score), the number of silent brain infarctions detected by computed tomography, the extent of carotid atherosclerosis as determined by B-mode ultrasonography, and cerebrovascular risk factors. RESULTS: Patients with silent cerebral infarctions were older (66.2 +/- 10.4 years) than those without such events (60.1 +/- 8.8 years) (P < .01). The extent of coronary atherosclerosis in patients with silent cerebral infarctions was significantly greater than in those without such events after adjustment for the effect of age (P < .001). The extent of carotid atherosclerosis and the percentages of individuals with hypertension, diabetes mellitus, a smoking habit, hypercholesterolemia, hypertriglyceridemia, and a low serum high-density lipoprotein cholesterol level did not differ between the groups with and without silent brain infarction. The frequency of silent brain infarction increased with the severity of coronary stenosis. CONCLUSION: Coronary atherosclerosis and age were important risk factors for silent brain infarction.

Adult↗
PubMed1997

[Effects of atherogenic risk factors on asymptomatic brain infarct].

This study was done to clarify the relationship between asymptomatic brain infarcts and risk factors for atherogenis. A total of 312 patients (151 men and 161 women) who had no neurologic deficits were enrolled. Their ages ranged from 41 to 83 years (mean age 63 years). The patients were divided into two groups: 158 patients without asymptomatic brain infarct and 154 patients with at least one asymptomatic brain infarct of at least 5 mm as diagnosed by magnetic resonance imaging. The patients with asymptomatic brain infarct were more likely than those without asymptomatic brain infarct to be 65 years old or older, and to have essential hypertension, diabetes mellitus, or atrial fibrillation. Among patients with hypertension the frequency of left ventricular hypertrophy or hypertensive ocular findings (Scheie's class H2) was significantly higher in those with asymptomatic brain infarct than in those without asymptomatic brain infarct. These results indicate that aging, essential hypertension (especially with left ventricular hypertrophy or hypertensive ocular findings), diabetes mellitus, and atrial fibrillation are associated with asymptomatic brain infarct.

Adult↗
PubMed1996

Fetal neocortical tissue blocks implanted in brain infarcts of adult rats interconnect with the host brain.

The purpose of the present study was to study if the connectivity of fetal neocortical tissue blocks placed in ischemic brain infarcts of adult rats would be enhanced in rats housed in an enriched environment. We also investigated whether the enriched housing conditions could enhance the postischemic and postgrafting functional outcome, in terms of motor behavior. This part of the study has been published recently. The middle cerebral artery was ligated on the right side in 37 inbred, adult male spontaneously hypertensive rats. The rats were placed at random either in an enriched environment (groups A and B) or in standard laboratory cages (group C). Three weeks after the artery occlusion, blocks of fetal sensorimotor cortex (embryonic day 17) were transplanted into the infarct cavity of rats from groups B and C. After 9 weeks all transplanted rats received an injection, into the graft, of a mixture containing the two tracers Fluoro-Gold and biotinylated Dextran amine. The transplants revealed a structured morphology with whorls and bands of cells reminiscent of normal neocortex. Tracing of efferent transplant to host fibers with biotinylated Dextran amine showed pronounced intrinsic transplant projections, as well as fibers, although significantly fewer, to the host ipsilateral sensorimotor cortex, striatum, and thalamus. Host to transplant projections were revealed by Fluoro-Gold-labeled cells found in the ipsilateral host sensorimotor cortex, the basal nucleus of Meynert, the thalamic ventrobasal, ventrolateral and posterior nuclei, and in the dorsal raphe nuclei. We conclude that fetal frontal neocortical block grafts placed in brain infarcts of adult rats develop a morphology reminiscent of normal neocortex and that both afferent and efferent neural connections, although sparse, are established with the host brain, whether the rats are reared under enriched housing conditions or not.

Animals↗
PubMed1993

Supratentorial brain infarcts in adult-onset seizures; the Maastricht Epilepsy Case Register.

We studied the frequency of supratentorial brain infarction as the cause of late-onset epilepsy in 680 patients with a first seizure after the age of 20, registered on an epilepsy register: 65 (10%) had seizures following a symptomatic supratentorial brain infarct. Brain infarction as the presumed cause of epilepsy was related to age at first seizure. A first seizure occurred within one year after brain infarction in 62%, and later than two years in 19%. Eight of 14 patients (57%) with an early seizure (< or = 2 weeks), and 28 of 41 patients (68%) with a first seizure later than two weeks post-stroke had seizure recurrences despite anti-epileptic treatment. Of 38 patients who underwent computed tomography head scan (CT), 32 (84%) had a cortical infarct, whereas six (16%) had one or more lacunar infarcts. This may indicate that lacunar infarction may be associated with post-stroke epilepsy. Using a detailed topographic brain atlas to localize the cortical infarcts, no 'specific epileptogenic' gyri could be identified. What factors predict future epilepsy in stroke patients need to be studied in prospective series of well-defined stroke subgroups.

Adult↗
PubMed1997

[MR spectroscopy in acute brain infarction: differentiation of infarcted and non-infarcted areas].

Two cases of brain infarction were studied using multivoxel proton MR spectroscopy (MRS). MRS of both cases clearly demonstrated an increased level of lactate and decreased N-acetylaspartate (NAA), resulting in a high lactate/NAA ratio (LNR). Case 1 without thrombolysis therapy revealed that the area where LNR was less than 1.0 did not develop to infarction. This was also confirmed by MRS of case 2, who received an interventional reperfusion 4 hours after onset. In acute stags of brain infarction, on LNR greater than 1.0 on H-MRS may predict the margin of the infarcted region. Elevation of lactate in the non-infarcted cerebral hemisphere has not been reported before, and farther evaluation is necessary.

Aspartic Acid↗
PubMed2003

Incidence and risk factors of silent brain infarcts in the population-based Rotterdam Scan Study.

BACKGROUND AND PURPOSE: The prevalence of silent brain infarcts in healthy elderly people is high, and these lesions are associated with an increased risk of stroke. The incidence of silent brain infarcts is unknown. We investigated the incidence and cardiovascular risk factors for silent brain infarcts. METHODS: The Rotterdam Scan Study is a prospective, population-based cohort study of 1077 participants 60 to 90 years of age. All participants underwent cranial MRI in 1995 to 1996, and 668 participants had a second MRI in 1999 to 2000 (response rate, 70%) with a mean interval of 3.4 years. We assessed cardiovascular risk factors by interview and physical examination at baseline. Associations between risk factors and incident silent infarcts were analyzed by multiple logistic regression. RESULTS: Ninety-three participants (14%) had > or =1 new infarcts on the second MRI; of these, 81 had only silent and 12 had symptomatic infarcts. The incidence of silent brain infarcts strongly increased with age and was 5 times higher than that of symptomatic stroke. A prevalent silent brain infarct strongly predicted a new silent infarct on the second MRI (age- and sex-adjusted odds ratio, 2.9; 95% confidence interval, 1.7 to 5.0). Age, blood pressure, diabetes mellitus, cholesterol and homocysteine levels, intima-media thickness, carotid plaques, and smoking were associated with new silent brain infarcts in participants without prevalent infarcts. CONCLUSIONS: The incidence of silent brain infarcts on MRI in the general elderly population strongly increases with age. The cardiovascular risk factors for silent brain infarcts are similar to those for stroke.

Age Distribution↗
PubMed2001

[Brain infarction related to hepatic arterial infusion chemotherapy].

We examined the occurrence of brain infarction with hepatic arterial infusion chemotherapy for liver cancer. One hundred and eighty-one cases of hepatic arterial infusion chemotherapy were carried out for liver cancer patients in 4 hospitals associated with Osaka University 2nd Dept. of Surgery. These included metastatic (n = 103) and primary (n = 78) liver tumors. The medication was mainly 5-FU with/without CDDP and IFN. Catheters were inserted via the left subclavian artery in 106 cases and via the femoral artery in 75 cases. Among these patients, brain infarctions occurred in seven patients. Occlusions were found in the cerebellum (n = 3), thalamus (n = 1), brain stem (n = 1) and TIA (n = 2). All these patients had catheterization from the left subclavian artery. Furthermore, 64 patients of Ikeda Municipal Hospital were examined and analyzed for brain infarction, in order to eliminate the difference between facilities (all patients in Ikeda Municipal Hospital were catheterized via the left subclavian artery). Many more brain infarctions occurred in metastatic liver cancer patients than in primary liver cancer patients. The hemostasis function deteriorated in primary liver cancer patients, and is thought to be involved in the brain infarction. Six of seven cases of brain infarction occurred in vertebral artery supply area. It may be that the occurrence of brain infarction was related to the flow of the blood vessels.

Aged↗
PubMed2002

Homocysteine, silent brain infarcts, and white matter lesions: The Rotterdam Scan Study.

Silent brain infarcts and white matter lesions are frequently seen on magnetic resonance imaging in healthy elderly people and both are associated with an increased risk of stroke and dementia. Plasma total homocysteine may be a potentially modifiable risk factor for stroke and dementia. We examined whether elevated total homocysteine levels are associated with silent brain infarcts and white matter lesions. The Rotterdam Scan Study is a population-based study of 1,077 people aged 60 to 90 years who had cerebral magnetic resonance imaging. The cross-sectional relation of total homocysteine with silent infarcts and white matter lesions was analyzed with adjustment for cardiovascular risk factors. The mean plasma total homocysteine level was 11.5 micromol/l (standard deviation 4.1). The risk of silent brain infarcts increased with increasing total homocysteine levels (odds ratio 1.24/standard deviation increase, 95% confidence interval 1.06-1.45). The severity of periventricular white matter lesions and extent of subcortical white matter lesions were also significantly associated with total homocysteine levels, even after excluding those with silent brain infarcts. The overall risk of having either a silent brain infarct or severe white matter lesions was strongly associated with total homocysteine levels (odds ratio 1.35/standard deviation increase, 95% confidence interval 1.16-1.58). We concluded that total homocysteine levels are associated with silent brain infarcts and white matter lesions independent of each other and of other cardiovascular risk factors.

Aged↗