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PubMed1997

Subcortical silent brain infarction as a risk factor for clinical stroke.

BACKGROUND AND PURPOSE: No prospective studies have examined the rate of symptomatic ischemic or hemorrhagic stroke in patients with subcortical silent brain infarction (SSBI) who were otherwise neurologically normal at entry into the study. This report investigates SSBI, detected by MRI, as a clinical stroke risk factor. METHODS: MRI scans were performed in 933 neurologically normal adults (30 to 81 years; mean age, 57.5 +/- 9.2 years) without history of cerebrovascular diseases who received our health screening of the brain 1 to 7 years before investigation. We obtained information of their clinical stroke onset through sending out a questionnaire for subjects. We detected SSBI (focal T2 hyperintensities larger than 3 mm with correlative T1 hypointensity), FWT2HL (focal white matter T2 hypertensity lesions similar to SSBI but without correlative T2-hypointensity), and PVH (periventricular hyperintensity) by MRI. Age, sex, family history of stroke, history of hypertension, diabetes mellitus, lipids, hematocrit, blood pressure, fasting blood sugar, smoking, alcohol habits, ischemic changes on electrocardiogram, and sclerotic changes of retinal arteries were included in the analysis. RESULTS: Incidence of SSBI was 10.6% in all subjects. No cortical infarct was detected in this series. Multiple logistic regression analysis showed that hypertension (odds ratio [OR], 4.07; 95% CI, 2.57 to 6.45), diabetes (OR, 2.41; 95% CI, 1.20 to 4.85), alcohol habits > or = 58 g/day (OR, 2.58; 95% CI, 1.50 to 4.45), retinal artery sclerosis (OR, 2.14; 95% CI, 1.32 to 2.38), and age (OR, 1.77; 95% CI, 1.32 to 2.38) were significant and independent risk factors for SSBI. For FWT2HL, hypertension (OR, 4.49; 95% CI, 2.54 to 7.96) and age (OR, 2.08; 95% CI, 1.45 to 3.00) were also independent risk factors. Risk factors for PVH were age (OR, 3.46; 95% CI, 2.23 to 5.36), hypertension (OR, 3.06; 95% CI, 1.62 to 5.78), and retinal artery sclerosis (OR, 2.25; 95% CI, 1.02 to 4.96). We found 14 brain infarctions, 4 brain hemorrhages, and 1 subarachnoid hemorrhage during observation. Annual incidence of clinical stroke was higher in the subjects with SSBI than in those without focal lesions (10.1% versus 0.77%). ORs for clinical stroke onset were 10.48 for SSBI (95% CI, 3.63 to 30.21) and 4.81 for FWT2HL (95% CI, 1.13 to 20.58). The PVH did not relate to clinical stroke onset. CONCLUSIONS: The strong association of SSBI, FWT2HL, and PVH with hypertension suggests a common underlying mechanism (presumably small-vessel vasculopathy). The SSBI showed the most significant association for clinical subcortical stroke. The FWT2HL was also a risk factor for the stroke but was less significant than SSBI. The subjects with SSBI should be considered at high risk for clinical subcortical brain infarction or brain hemorrhage.

Adult↗
PubMed2003

[Association between Bam HI RFLP p53 gene polymorphism and brain infarction volume in patients with atherothrombotic ischemic stroke].

A significant association between Bam HI RFLP p53 gene polymorphism and brain infarction volume in patients with atherothrombotic ischemic stroke (AIS) from Moscow population was found. Biallelic Bam HI polymorphism in exon 5 of p53 gene was studied in 96 AIS patients, 100 their healthy siblings, 41 patients with chronic ischemic disease and 42 their healthy siblings. Magnetic resonance tomography with morphometric program "Osiris" (the Hospital of the University, Geneva) for infarction volume measuring was used on day 1 and 7 after stroke onset. The patients with (-/-) p53 Bam HI genotype had the smaller brain infarction sizes (< 40 cm3), comparing to those with (-/+) (chi 2 = 19.7; p < 0.001) and (+/+) (chi 2 = 12.3; p < 0.001) genotypes. According to Bayes statistics, development of smaller infarction size in AIS may be predicted with over than 65% probability in the patients with (-/-) p53 Bam HI genotype. A significant association between p53 Bam HI polymorphism and infarction volume in patients with carotid atherothrombotic stroke confirms an important role of apoptosis in ischemic brain lesions formation that demands temporary antiapoptotic influence on patients with stroke.

Aged↗
PubMed1991

Patterns of brain infarctions in internal carotid artery dissections.

In 15 patients with internal carotid artery (ICA) dissections, patterns of brain infarctions visible on CT were categorized according to a pathogenetically oriented classification system. This differentiated ischemic brain damage due to low flow from thromboembolic infarctions. Simultaneously, cerebral hemodynamic reserve was evaluated by means of both CO2-dependent vasomotor reactivity and HMPAO- and 99mTc-RBC-SPECT. Six out of 11 patients with ischemic infarctions had the territorial type of brain lesion, suggesting distal embolism. Five patients revealed the pattern of hemodynamically induced low-flow infarctions. Cerebral hemodynamic reserve was significantly decreased only in these latter patients. In ICA dissections the frequencies of hemodynamically and thromboembolically induced brain infarctions is approximately equal. This finding suggests that only half of the patients with symptoms of symptomatic dissections had brain emboli, whereas in the other half the dissections lead to a low-flow effect in terminal supply areas which is so severe that non-embolic brain infarctions occur. This differentiation can help decide whether antithrombotic or hemodynamic treatment should be given.

Adult↗
PubMed2002

Alzheimer's disease and brain infarcts in the elderly. Agreement with neuropathology.

Clarifying the etiology of dementia is one of the most difficult diagnostic challenges, especially in the elderly. We examined the accuracy of clinical criteria to distinguish Alzheimer's disease (AD) and dementia associated with infarcts of the brain, either isolated (vascular dementia) or associated with degenerative lesions (mixed dementia). We carried out a prospective clinico-neuropathological study in a selected series of hospitalized patients. We evaluated the clinical aspects of 33 patients aged over 75 years by use of the criteria and scores of DSMIII, NINCDS-ADRDA, Loeb and Gandolfo, ADDTC and NINDS-AIREN and the Hachinski Ischemic Score. The neuropathological diagnosis was considered to be the gold standard. When comparing clinical criteria and neuropathology, the agreement was moderate for Hachinski's score (0.50) and Loeb's score (0.43) and substantial for the ADDTC (0.63) and the NINDS-AIREN (0.67). When mixed dementias were excluded, the agreement between all clinical criteria and scores and the pathological diagnosis rose to 0.88. Hachinski's score was the most sensitive (0.89) and the NINDS-AIREN the most specific (0.86) for the diagnosis of vascular dementia. In conclusion, all sets of clinical criteria distinguished pure AD from vascular dementia with a high accuracy whereas mixed dementia was clinically under-recognized. The NINDS-AIREN criteria were the most discriminating for the accurate identification of patients with mixed dementia.

Aged↗
PubMed2001

Association of immune responses and ischemic brain infarction in rat.

Inflammation plays an important role in the pathogenesis of neurodegenerative diseases including ischemia. Occlusion of common carotid artery and middle cerebral artery has been used to produce focal ischemic lesions in the rat. Here, we examined the associations between immune reactions and postischemic brain infarction. Ischemia/reperfusion time-dependently caused brain infarction. The kinetics of inflammatory reactions in rat brain including inflammatory cell infiltration, edema formation, cytokines/chemokines and adhesion molecules production and matrix metalloproteinase activation were relevant to the progression of ischemic infarction. Differential induction profile after ischemia suggests that this activation might contribute to secondary brain damage in ischemic tissues. On the other hand, another possibility of this response is to trigger processes that mediate the neural regeneration after ischemic injury.

Animals↗
PubMed1999

Hemodynamics and metabolism in stroke-prone spontaneously hypertensive rats before manifestation of brain infarcts.

Genomic screening of hybrids from stroke-prone (SHR-SP) and stroke-resistant spontaneously hypertensive rats (SHR) identified a STR1 locus on the rat chromosome 1, which correlates with the susceptibility to cerebral stroke but not with hypertension. The authors examined whether this genetic abnormality is associated with hemodynamic or metabolic alterations in the brain that can be detected before the manifestation of brain infarction. Starting at 6 weeks of age, SHR-SP were fed with a salt-rich diet to accelerate arterial hypertension. At the age of 12 weeks, animals developed functional symptoms and were age-matched with symptom-negative SHR-SP to differentiate between presymptomatic and postsymptomatic changes. Brains were investigated by multiparametric imaging comprising quantitative double-tracer autoradiography of CBF and cerebral protein synthesis (CPS); bioluminescence imaging of regional ATP, glucose, and lactate content; and umbelliferone fluoroscopic imaging of tissue pH. None of the animals exhibited focal hemodynamic or biochemical abnormalities. In symptom-negative SHR-SP, global CBF was 1.1+/-0.3 mL x g(-1) x min(-1), cortical CPS was 10.1+/-3.1 nmol x g(-1) x min(-1), and cortical ATP, glucose, lactate, and pH levels were in the normal range. In SHR-SP with functional symptoms, ATP, glucose, and lactate levels also were normal, but tissue pH exhibited periventricular alkalosis, CBF was significantly reduced to 0.7+/-0.2 mL x g(-1) x min(-1) (P < 0.001), and cortical CPS was significantly reduced to 6.7+/-2.1 nmol x g(-1) x min(-1) (P < 0.001). The decline in brain perfusion of SHR-SP correlated significantly with both the severity of functional deficits and the decline of protein synthesis. Our observations demonstrate that SHR-SP had already developed functional symptoms before the manifestation of overt brain infarcts and that the symptoms are initiated by a decline in global CBF and cortical CPS. Genetic abnormalities in SHR-SP are associated with a diffuse vascular process that results in global decompensation of blood flow well before the onset of focal brain infarction.

Animals↗
PubMed2000

Comparative values of erythrocyte aggregability versus other indices of hemorheological disorders in patients with ischemic brain infarcts.

The aim of the present study is comparison of changes of principal hemorheological factors responsible for blood flow disorders in the microcirculation in patients with ischemic brain infarcts. It was found that in venous blood samples the erythrocyte aggregability (examined with a direct, highly sensitive, quantitative technique) was considerably more increased (by mean of 120%) than the blood plasma fibrinogen contents, blood plasma viscosity, and hematocrit which increased only by 23.7%, 7.4% and 3.6%, respectively, as compared to the same hemorheological factors in the healthy controls. These results led us to the following conclusion: among the other tests the enhanced erythrocyte aggregability, when measured with an appropriate technique, is the best diagnostic indicator of hemorheological derangements during development of the ischemic brain infarct.

Adult↗
PubMed1999

[Cerebral hemodynamic impairment and therapeutic effect of external counterpulsation on elderly patients with brain infarction].

Hemodynamic parameters of middle cerebral artery(MCA) were measured with Transcranial Doppler (TCD) in 31 elderly patients with brain infarction during convalescence and 28 healthy elderly controls. Twenty-two elderly patients with brain infarction and cerebral hemodynamic impaired were treated by External Counterpulsation(ECP). The results showed that the Vp and Vm of MCA in patients were significantly lower than that in the healthy controls(P < 0.001), the DVp, DVm and asymmetry of MCA in patients were greater than that in the healthy elderly(P < 0.001, P < 0.005). The Vp and Vm of MCA in patients after ECP were significantly higher than before(P < 0.001). The DVp, DVm and asymmetry of MCA in patients after ECP were significantly lower than before(P < 0.001, P < 0.005). The hemodynamic therapeutic effect is 81.8%.

Aged↗
PubMed1975

An evaluation of the epidemiology of atherothrombotic brain infarction.

Review of the epidemiology of atherothrombotic brain infarction (ABI) based largely on 18 years of prospective data from the Framingham cohort reveals that stroke is a potent force in morbidity and mortality, that hypertension is its dominant precursor, that it can be predicted and suggests that only a preventive approach can substantially reduce stroke morbidity. Data from Framingham on the relative frequency of the major types of stroke found in the community reveal that 57 percent are due to ABI and only 17 percent to intracranial hemorrhage--two-thirds of which is subarachnoid. Lacunar infarcts are common accounting for 13 percent of ABI's in men and 23 percent in women. Despite the sizeable geographic, seasonal and secular trends in stroke mortality, few environmental determinants of stroke have been uncovered. However, established hallmarks of the candidate for an atherothrombotic stroke include: hypertension (systolic or diastolic), glucose intolerance, high normal hemoglobin, the cigarette habit (men only), abnormal lipids (under age 60) and cardiac impairments. Many unresolved issues remain. Nevertheless, it is possible to identify a tenth of the general population from which half the strokes will emerge. This provides a rational basis for establishing a program of prevention.

Aged↗
PubMed1994

Changes of circadian blood pressure patterns after hemodynamic and thromboembolic brain infarction.

BACKGROUND AND PURPOSE: We investigated the changes of circadian blood pressure patterns after thromboembolic and hemodynamic brain infarction and evaluated the relation between circadian blood pressure variation, infarct location, and activation of the autonomic nervous system after thromboembolic stroke. METHODS: Repeated 24-hour blood pressure measurements were performed in 45 patients with proven first-ever brain infarctions of different origins. Evaluation of serum norepinephrine concentration, prolongation of the QT interval, and degree of cardiac arrhythmias were used to determine the extent of sympathetic activation after thromboembolic stroke. RESULTS: Whereas circadian blood pressure variation was significantly increased after hemodynamic infarction compared with a control group (diastolic, -25.2 +/- 4.5% versus -13.8 +/- 6.5%; p < .005), a clearly reduced variation was observed after thromboembolic infarction (diastolic, -5.2 +/- 6.9%). Blood pressure variation was positively related to serum norepinephrine concentration (r = .79; P < .01) after thromboembolic infarction. Patients with involvement of the insular cortex showed a nocturnal rise of blood pressure significantly more frequently (66.7% versus 11.8%; P < .005) and had higher norepinephrine levels (66.7 +/- 110 pg/mL versus 290 +/- 178 pg/mL; P < .01) than patients without insular cortex infarction, indicating increased sympathetic activity. This was associated with a significantly more frequent occurrence of QT prolongation and cardiac arrhythmias. CONCLUSIONS: The observed differences in circadian blood pressure patterns may (1) help to distinguish the pathophysiological basis of the stroke, (2) help to explain worsening in some cases of hemodynamic stroke, (3) confirm the importance of the insular cortex for sympathetic activation, and (4) identify subgroups of patients with increased risk of myocardial infarction and arrhythmia.

Aged↗
PubMed1996

Abnormal heart rate variability as a manifestation of autonomic dysfunction in hemispheric brain infarction.

BACKGROUND AND PURPOSE: Abnormal heart rate variability is related to prognostically unfavorable ventricular arrhythmias and sudden arrhythmic death in coronary artery disease. Short-term electrocardiographic (ECG) recordings have shown similar abnormalities of heart rate variability in patients with acute stroke. However, there is no information regarding the clinical significance of these abnormalities and of heart rate variability in long-term ECG recordings in stroke. METHODS: In this prospective study, we analyzed the time domain and frequency domain measures of heart rate variability from 24-hour ECG recordings in 31 consecutive patients with hemispheric brain infarction in the acute phase and at 1 and 6 months after the infarction and in 31 age- and sex-matched healthy control subjects. RESULTS: All the measured components of heart rate variability, ie, standard deviation of RR intervals (P < .001), total power (P < .0001), very-low-frequency power (P < .0001), low-frequency power (P < .001), and high-frequency power (P < .05), were significantly lower than those of the control subjects in both the acute phase and 1 and 6 months later. Impaired heart rate variability correlated with the severity of neurological deficits and disability. In five patients with increased intracranial pressure due to large brain infarction, no relevant spectral components were found. CONCLUSIONS: Hemispheric brain infarction seems to cause significant long-lasting damage to the cardiovascular autonomic regulatory system manifested as abnormalities of heart rate variability. Distorted heart rate variability in the acute phase of stroke may be prognostically unfavorable.

Acute Disease↗
PubMed2001

Photothrombotic brain infarction results in seizure activity in aging Fischer 344 and Sprague Dawley rats.

This study was designed to determine whether photothrombotic brain infarction could result in epileptic seizures in adult animals. Male Fischer 344 (F344) rats at 2, 6, 12, 24, and 30 months of age and male Sprague Dawley (SD) rats at 2 and 6 months of age underwent photothrombotic brain infarction with the photosensitive dye rose bengal by focusing a wide (6 mm) or narrow (3 mm) diameter white light beam on the skull overlying left hemisphere anterior frontal, midfrontal, frontoparietal, or parietal areas. Animals were monitored with video and EEG recordings. Morphological analysis of infarct size was performed with a computer-assisted image analysis system. The primary finding of this study was that epileptic seizures were recorded in post-mature rats 2 months after lesioning the frontoparietal cortex with large photothrombotic infarcts that extended to the cortical-subcortical interface. These seizures were characterized behaviorally by motor arrest, appeared to originate in the periinfarct area, and could be distinguished from inherited spontaneous bilateral cortical discharges by the morphology, frequency, duration, and laterality of the ictal discharges. Small cortical lesions were ineffective in producing seizures except for one animal that demonstrated recurrent prolonged focal discharges unaccompanied by behavioral change. Stage 3 seizures were observed in a small number of mid-aged and aged animals lesioned with large infarcts in anterior frontal and frontoparietal areas. These results suggest that the technique of photothrombosis can be used to produce neocortical infarction as a means to study mechanisms of secondary epileptogenesis.

Aging↗
PubMed1994

Correlation between fibroblast growth factor expression and cell proliferation in experimental brain infarct: studied with proliferating cell nuclear antigen immunohistochemistry.

Astrogliosis, angiogenesis and macrophage activity are classical responses of brain to injury. The factors that induce these changes and the dynamic interaction among cells in the environs of the injured brain remain unclear. In the present rat brain infarct model, we studied the spatiotemporal relationship between basic fibroblast growth factor (bFGF) expression and cell proliferation using proliferating cell nuclear antigen (PCNA) as an S-phase marker. We demonstrated an early astrocytic and neuronal activation with enhanced expression of bFGF in areas adjacent to the infarct. This was followed by a period from 3-5 days of intense cell proliferation. Proliferating cell nuclear antigen-labeled nuclei were demonstrated in perineuronal satellite cells, endothelial cells, vascular pericytes, macrophages and glial cells. These cells appeared to respond to the same mitogen(s) and they produced bFGF during the proliferative phase. There was a simultaneous spreading of neuronal activation and glial proliferation from the infarct to the entire ipsilateral hemisphere and through the coronal radiations to the contralateral hemisphere. This spreading follows the pattern of spreading of edema fluid. Our findings suggest that cell proliferation in the brain infarct may be induced by bFGF released by neurons and sustained by bFGF and other growth factors produced by non-neural cells on an autocrine basis.

Animals↗
PubMedDate not supplied

[Recurrent brain infarctions in atherosclerosis and arterial hypertension].

In 100 cases of brain infarctions of different size and time caused by atherosclerosis and arterial hypertension, the infarctions were located in the territory of carotid arteries (44 cases), of vertebro-basilar system arteries (18 cases) and of both the systems (38 cases). The infarctions were repeated, multiple in 82 cases, single--in 18 cases. Atherothrombosis and atherostenosis, thromboembolism of the brain arteries from the heart are main pathogenetic factors. The phenomenon of "infarction in the infarction" is observed in the limits of one arterial pool.

Adult↗
PubMed1998

Silent brain infarctions in patients with coronary heart disease. A Spanish population survey.

Coronary artery disease is a recognized risk factor for symptomatic ischaemic stroke but the influence on asymptomatic stroke has not been clearly determined. The purpose of this work was to determine the relationship between coronary heart disease and silent brain infarcts and the influence of vascular risk factors and carotid atherosclerosis in a representative sample of Spanish patients with symptomatic coronary artery disease. A consecutive sample of 100 subjects with myocardial infarction, angina or both were included in the survey. Patients with a potential source of emboli from the heart were excluded. As main baseline variables, we considered vascular risk factors; complete cardiological study, including coronary angiography; brain computed tomography (CT) to detect infarcts; echo-Doppler of supra-aortic vessels to detect stenosis; and carotid angiography, when appropriate. As the outcome variable, we observed the incidence of symptomatic stroke after an 18 month mean follow-up. We found silent brain infarction in 30 patients (93% were of lacunar type). None of the vascular risk factors was related to brain infarcts either in univariate or multivariate analysis. Carotid atherosclerosis was the only significant predictor in a model of logistic regression (P < 0.0005), although the lesions were bilateral in the majority of cases. We observed a very low incidence of symptomatic stroke after a mean follow-up of 18 months. Silent brain infarcts are a frequent finding on brain CT in patients with coronary heart disease and are associated with carotid atherosclerosis; however, it does not seem to have important prognostic significance.

Adult↗
PubMedDate not supplied

Ethanol intoxication: a risk factor for ischemic brain infarction in adolescents and young adults.

Between January 1978 and December 1979 23 consecutive patients aged under 40 years with acute ischemic brain infarction were admitted to the department of neurology, Meilahti University Hospital in Helsinki. In 10 patients (43%) the onset of symptoms was preceded within 24 hours by ethanol intoxication, and all but one symptom occurred at weekends when most liquor is consumed in Finland. Ethanol intoxication preceding the stroke was 4 times as common in female and 5 times as common in male patients as ethanol intoxication in the general Finnish population of the same age and sex. The present results support those of our previous study and suggest that occasional ethanol intoxication increases the risk of ischemic brain infarction both in adolescents and young adults.

Adolescent↗
PubMed2003

Administration of nonionic iodinated contrast medium does not influence the outcome of patients with ischemic brain infarction.

Some reports indicate that exposure to iodinated contrast medium (CM) could worsen the outcome of patients with brain infarction. In this prospective study, we compared the outcome of 77 patients receiving and 128 not receiving nonionic iodinated CM. Stroke severity was assessed by the Scandinavian Prognostic Stroke Score, and outcome by the Rankin Scale. All radiological studies using intravenous or intra-arterial CM were registered. Two nonionic iodinated CM (iopamidol and iohexol) were used. Exposure to CM did not influence case fatality, ability to live at home, ability to walk, disability and stroke severity. Initial stroke severity and arterial hypertension were independent determinants of poor neurological recovery or death. Large infarct, age, male gender, and baseline stroke severity were independent determinants of major disability or death. CM enhancement on CT did not show any harmful effect on stroke severity or outcome. As a conclusion, intravascular administration of nonionic iodinated CM did not influence stroke severity or outcome of our patients.

Age Factors↗
PubMed1997

Effects of antihypertensive agents on circadian blood pressure in hypertensive patients with previous brain infarction.

To evaluate the effects of antihypertensive agents on the circadian blood pressure (BP) of patients with previous brain infarction, the ambulatory BP was measured non-invasively for 24 h before and after administration of antihypertensive agents. One hundred milligrams of acebutolol twice daily (n = 15) is effective in lowering the BP during the daytime, but has little effect during the night and the morning. Twenty milligrams of slow-release nifedipine twice daily (n = 14) produced a consistent reduction in the BP over the entire 24-h period and effectively blunted the rise in BP in the morning. Captopril (12.5 mg) twice daily (n = 15) produced a mild reduction in BP with little change in the circadian pattern. The slow-release nifedipine group had the greatest decrease in mean systolic and diastolic BP. The heart rate significantly increased after administration of slow-release nifedipine and decreased after administration of acebutolol. To reduce stroke recurrence, we should consider the effects of antihypertensive agents on circadian BP in hypertensive patients with previous brain infarction.

Acebutolol↗