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PubMed1994

Intracranial MR angiography: its role in the integrated approach to brain infarction.

PURPOSE: To determine the contribution of cranial MR angiography (MRA) for the evaluation of patients with acute and subacute brain infarction. METHODS: MR and MRA studies performed on 78 adult patients with acute and subacute stroke were retrospectively reviewed and correlated with the clinical records. RESULTS: There were 50 acute and 28 subacute infarctions in our series. Five of 78 MRA exams (6%) were nondiagnostic. Sixty examinations (80%) were positive for stenosis or occlusion. The distribution of stenotic or occlusive vascular lesions correlated with the location of infarction in 56 of the 60 positive cases (93%). MRA provided information not obtained from the MR images in 40 cases (55%). One hundred four individual vessels in 8 patients who underwent conventional cerebral angiography were compared with the MRA appearance. The MRA interpretations correlated with the conventional angiographic evaluations for 90 vessels (87%). CONCLUSIONS: Vascular lesions demonstrated on intracranial MRA show a high correlation with infarct distribution. MRA provides information adjunctive to conventional MR in a majority of cases. We conclude that MRA is an important component of the complete evaluation of brain infarction.

Acute Disease↗
PubMed1992

Low and high density lipoprotein metabolism in atherothrombotic brain infarction.

BACKGROUND AND PURPOSE: Elevated low density lipoprotein and reduced high density lipoprotein cholesterol may increase the risk of atherothrombotic brain infarction, but the metabolic mechanisms accounting for this relation are poorly understood. METHODS: The kinetic parameters of low density and high density lipoprotein were studied in nine subjects with atherothrombotic brain infarction or identifiable (by noninvasive testing) extracranial occlusive disease and in 12 control subjects. Autologous iodine-125-labeled lipoproteins were injected intravenously. Blood samples were drawn 10 minutes after injection and periodically thereafter for 10 days. Kinetic parameters were calculated from the decay curves. RESULTS: The stroke-risk group showed significantly higher triglyceride (p less than 0.05), total cholesterol (p less than 0.02), and low density lipoprotein cholesterol (p less than 0.01). The fractional catabolic rate of low density lipoprotein was significantly lower (p less than 0.001) and the high density lipoprotein rate higher (p less than 0.02) in the stroke-risk group than in the control group. Regression analysis (using all subjects) of serum lipoproteins and their respective fractional catabolic rates correlated significantly (for low density lipoprotein, r = 0.684, p less than 0.001; for high density lipoprotein, r = 0.595, p less than 0.002). Mean percent stenosis showed a significant relation with triglyceride level (r = 0.678, p less than 0.01) and low density lipoprotein cholesterol (r = 0.535, p less than 0.02) but not with high density lipoprotein cholesterol. Mean percent stenosis also showed correlation with both fractional catabolic rate of low density lipoprotein (r = 0.667, p less than 0.002) and with serum high density lipoprotein levels (r = 0.504, p less than 0.02). CONCLUSIONS: Our study provides insights into the role of altered low and high density lipoprotein metabolism in the pathogenesis of carotid stenosis. The statistically significant association of serum lipoprotein metabolic rates with carotid stenosis, rather than their respective serum concentrations, implies that metabolic parameters may be more important in predicting stroke risk.

Carotid Stenosis↗
PubMed1981

Quantitative 99mTechnetium cerebral circulation time in brain infarction. Its relation to clinical findings, electroencephalograms and conventional radionuclide studies.

Four circulation time parameters were measured by intravenously injected 99mTechnetium and a gamma camera in 183 patients displaying a unilateral supratentorial brain infarction. The mean values of all the calculated circulation time parameters in the infarcted hemisphere were significantly slower than those of the contralateral hemispheres. The difference between the hemispheres proved a more sensitive parameter than absolute values. Both the quantitative circulation time differences between the hemispheres and the absolute circulation time values showed significant correlations with several clinical findings, e.g. severity of infarction, recovery from infarction, and patient's age. However, quantification gave only a minor addition to the number of the patients with abnormalities detected by routine static and dynamic brain scintigrams. Though the value of the quantitative intravenous 99mTechnetium method in routine clinical work is limited, it provides valuable information on the haemodynamics in brain infarction, e.g. the persistence of measurable asymmetry suggesting decreased function even of non-infarcted parts of the affected hemisphere ("deafferentiation").

Adult↗
PubMed1996

Risk factors for brain infarction in patients with Cushing's disease. Case reports.

Two women aged 51 and 52 years old, respectively, developed a brain infarction before and after undergoing treatment for Cushing's disease. A biochemical remission was obtained more than ten years after the onset of signs or symptoms of Cushing's disease. The arteriosclerotic changes of the cerebral vessels progressed even during replacement therapy for posttreatment hypopituitarism after they underwent either ablative surgery or radiotherapy. One patient, who showed the signs of Nelson's syndrome, demonstrated severe progressive cerebrovascular sclerotic changes, especially around the irradiated site. It is thus suggested that hypercortisolemia, external pituitary irradiation, and posttreatment hypopituitarism may be risk factors for brain infarction. The early diagnosis and adequate treatment are therefore important to prevent cerebrovascular complications in patients with Cushing's disease.

Cerebral Infarction↗
PubMed1991

[Long-term changes in cerebral blood flow in patients with atherothrombotic and embolic brain infarction].

Cerebral blood flow (CBF) was measured twice at years interval using xenon-133 inhalation technique in patients with atherothrombotic and embolic supratentorial brain infarction. The purpose of the study was to elucidate factors influencing long-term change in CBF in two subtypes of brain infarction of different mechanisms. Those patients were excluded from the study, who had bilateral hemispheric lesions, significant arterial lesion in the contralateral carotid axis and recurrent stroke before the second measurement of CBF. Of 46 patients studied, 23 (17 men and 6 women) were classified as atherothrombotic and 23 (15 men and 8 women) as embolic infarction based on the diagnostic criteria reported earlier. Their age at onset was 60.6 +/- 8.9 years old (mean +/- S.D.) for atherothrombotic patients, and 60.2 +/- 11.0 years old for embolic patients. The first measurement of CBF was performed between 31 and 87 days and the second measurement between 13 and 99 months after onset. In atherothrombotic group, mean hemispheric CBF (mCBF) of the affected side tended to be higher in patients examined at intervals shorter than 30 months, but tended to decrease in those at longer interval. The multivariate stepwise regression analysis indicated only "the interval between 2 measurements" to have a significant effect on reduction of mCBF, although in addition to the interval (p less than 0.05), infarct-size (p less than 0.01) and change in PaCO2 (p less than 0.05) were suggested to be possible factors by single regression analysis. In embolic group, an increase in hematocrit had a significant effect on reduction of mCBF, even when being evaluated with multivariate stepwise regression analysis.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1992

Blood glucose, glycosylated haemoglobin, and outcome of ischemic brain infarction.

From August 1987 through December 1989 all consecutive conscious patients younger than 70 years with a recent (less than 48 h) brain infarction of the carotid territory were prospectively included in the study. Blood samples for fasting blood glucose and glycosylated haemoglobin (HbA1c) were taken after a median delay of 23 h of the onset of symptoms. The severity of hemiparesis was assessed on admission, at 1 week, 3 weeks, and 3 months. The functional outcome was assessed at 3 months. Computed cerebral tomography was performed on admission, and later on at 3 weeks or 3 months. The brain infarct volume was measured from the CTs. The patients were diagnosed to have prestroke normoglycemia (n = 76) and prestroke hyperglycemia (n = 23) on basis of the HbA1c level. The case fatality rate, severity of hemiparesis, functional outcome, and infarct size did not differ between these 2 groups. On the other hand, fasting blood glucose level of the non-diabetics correlated strongly with the severity of hemiparesis and predicted stroke outcome. A statistically significant correlation was observed between blood glucose values and the volumes of cortical infarcts in non-diabetics. Because prestroke blood glucose level, in contrast to post-stroke blood glucose level, did not have any predictive value concerning stroke outcome it is concluded that high fasting blood glucose values after stroke reflect a stress response to a more severe ischemic brain lesion.

Adult↗
PubMed2002

[A case of Turner syndrome complicated with brain infarction].

A 21 year-old female college student with a history of Turner syndrome at age 9, and 6-year growth hormone replacement therapy noticed weakness of right extremities when she got up on March 26, 2001. On admission, she showed right hemiparesis (4+/5) and hypesthesia on the right of body. The hemiparesis progressed (3-/5) in spite of antithrombotic therapy. Brain MRI revealed a high intensity lesion with a diameter of 1.5 cm in the posterior limb of the left internal capsule and putamen on DWI and T2WI. MR angiography and TC-CFI revealed no stenosis in her left middle cerebral artery, but > 50% stenosis in the horizontal portion (M1) of her right middle cerebral artery. Branch lesions were presumed to exist in the left M1. Non-atherosclerotic angiopathy, coagulopathy, and other conventional risk factors of brain infarction were not found. Pathogenesis of Turner syndrome might have played a role in the development of brain infarction in this patient.

Adult↗
PubMed2001

Elevated plasma homocysteine levels and risk of silent brain infarction in elderly people.

BACKGROUND AND PURPOSE: Silent brain infarction (SBI) on MRI is common in elderly people, and recent studies have demonstrated that SBI increases the risk of progression to clinically apparent stroke and cognitive decline. Therefore, an early and accurate detection of SBI and a search for potential treatable risk factors may have a significant impact on public health. METHODS: Community-dwelling elderly people aged >/=66 years who participated in the present study (n=153) underwent brain MRI and standardized physical and neuropsychological examinations as well as blood biochemistry determinations, including total plasma homocysteine (pHcy), renal function, vitamin status, and polymorphisms of the methylenetetrahydrofolate reductase gene. RESULTS: SBI was found in 24.8% of the participants. In the univariate analysis, the pHcy levels in subjects with SBI (13.6+/-4.1 micromol/L) were significantly higher (P=0.0004) than those in subjects without SBI (11.0+/-3.3 micromol/L). When pHcy levels were stratified into high (>/=15.1 mmol/L), moderate (11.6 to 15.0 mmol/L), and low (</=11.5 mmol/L) groups, age (P<0.0001), male sex (P<0.0001), the habits of cigarette smoking (P<0.0001) and of alcohol consumption (P=0.0002), and folate levels (P=0.01) were significantly associated with an elevation of pHcy levels. The elevated pHcy levels were significantly associated with SBI after individual adjustment for age, sex, hypertension, renal function, and the habits of smoking and alcohol consumption. CONCLUSIONS: pHcy level is associated with age and nutritional and other lifestyle factors, and it contributes to a risk for SBI.

Age Distribution↗
PubMed2004

The role of brain infarcts and hippocampal atrophy in subcortical ischaemic vascular dementia.

We investigated if, in patients with vascular lesions, the variable that best discriminated demented from non-demented patients was the severity of the vascular pathology or the degree of hippocampal atrophy. A total of 39 patients multiple subcortical infarcts, who could be considered as possible vascular dementia with small vessel pathology, with underwent a neuropsychological study and brain magnetic resonance imaging (MRI) DSM IV criteria supported by neuropsychological data were used to distinguish demented from non-demented patients. The MRI study took into account the degree of hippocampal atrophy (hippocampal height and interuncal distance) and the severity of vascular pathology (number of brain infarcts). The distribution of lesions and a factor analysis showed that hippocampal atrophy is a better predictor of dementia than the number of brain infarcts. Multiple subcortical infarcts alone are probably not able to cause clinical dementia but the presence of vascular lesions increases the expression of concomitant Alzheimer's disease.

Aged↗
PubMed1993

Brain infarction is not reduced in SOD-1 transgenic mice after a permanent focal cerebral ischemia.

Using a mouse model with intraluminal blockade of the middle cerebral artery (MCA) which produced both cortical and striatal infarction, the effect that superoxide radicals have on cerebral infarction, local cerebral blood flow, and neurological deficits after 24 h of permanent focal cerebral ischemia in transgenic mice (Tg) overexpressing human CuZn-superoxide dismutase (SOD-1) was examined. There were no difference between SOD-1 Tg mice and non-Tg littermates observed in the infarct areas of brain slices, the infarct volume, the local cerebral blood flow, or the neurological deficits. These data suggest that pre-existing high levels of antioxidant enzyme failed to provide neuronal protection against permanent focal cerebral ischemia.

Animals↗
PubMed1997

A chronological evaluation of experimental brain infarct by diffusion-mapping and magnetization transfer contrast imaging.

BACKGROUND AND PURPOSE: There is a complex system of evolving physiochemical processes in the ischemic brain. The evaluation of this chain of processes is a major challenge of recent stroke studies. Two magnetic resonance imaging techniques: diffusion-weighted (DW) and magnetization transfer contrast (MTC) imaging were introduced in experimental studies and were shown to have sensitivity for different stages of brain infarct. MATERIALS AND METHODS: We used a reproducible middle cerebral artery (MCA) occlusion model in rat to examine infarcts of different time courses. Magnetic resonance T2-weighted (T2). DW, and MTC imaging were performed 3 h, 1 d, 3 d, 5 d, 2 w, 3 w, and 4 w after MCA occlusion. Haematoxylin/eosin (HE) stained sections, which revealed sub regions within infarct lesions, were compared to T2, DW, diffusion-mapping and MTC-mapping images. RESULTS: On DW images 3 hours post occlusion lesions were detected as an area with high signal intensity, while T2 imaging does not raise significant contrast of the lesion at this early stage. Three sub regions of the lesion having different ADCs, are discernible on diffusion-mapping images from 1 day to 7 days. The decrease of MTC effect was measured within the infarct lesion from core to marginal zone, from 7 days to 4 weeks. CONCLUSIONS: Diffusion-mapping imaging may help to examine brain infarction from 3 hours to 5 days. MTC imaging recognizes infarcts 7 days after the onset. Following this stage, MTC-mapping images may provide a quantitative method to assess infarct size.

Animals↗
PubMed1994

Patent foramen ovale and brain infarct. Echocardiographic predictors, recurrence, and prevention.

BACKGROUND AND PURPOSE: Paradoxical embolism through a patent foramen ovale is a recognized cause of stroke, but clinical predictors, recurrence rate, and prevention of brain infarcts in patients with patent foramen ovale have not been determined. We reviewed transesophageal echocardiographic records to ascertain echocardiographic predictors and optimal prophylaxis for patent foramen ovale-related infarcts. METHODS: A patent foramen ovale was identified in 74 patients during 615 transesophageal echocardiograms by color Doppler or saline contrast during a 60-month period. On the basis of final clinical situation, the patients were divided into the following groups: group 1, infarct with patent foramen ovale a likely cause (n = 16); group 2, infarct with patent foramen ovale an unlikely cause (n = 23); and group 3, no infarct (n = 35). Transesophageal echocardiograms were reviewed to assess patent foramen ovale characteristics and associated cardio-embolic sources without knowledge of clinical details or group assignment. Follow-up after a patent foramen ovale-related infarct was obtained by telephone or written correspondence in 15 of 16 group 1 patients. RESULTS: Atrial septal aneurysms were more common in group 1 (38%) compared with group 2 (10%) and group 3 (8%) (P = .02). Contrast right-to-left shunting occurred in 88% of group 1 (P = .06) and 86% of group 2 (P = .07) compared with 60% of group 3. Prevention of recurrence in subjects with presumed patent foramen ovale-related brain infarcts varied. Aspirin was usually chosen after initial brain ischemia. Warfarin and patent foramen ovale closure were usually reserved for subjects with symptoms of brain ischemia while taking aspirin or those who required warfarin or cardiac surgery for other indications. No recurrent infarcts occurred in 15 patients during a mean follow-up period of 28 months. CONCLUSIONS: Atrial septal aneurysm and right-to-left shunt may be predictive of a patent foramen ovale that predisposes a patient to stroke. Aspirin may provide sufficient infarct prophylaxis after initial ischemia. Warfarin and surgical correction should likely be reserved for those in whom aspirin is not effective or those who require warfarin or cardiac surgery for other reasons until prospective studies are available.

Adult↗
PubMed1996

Bilateral suppression of the sympathetic nervous system in hemispheric brain infarction.

To assess sympathetic system function after hemispheric brain infarction rostral to the hypothalamus we investigated 24 patients with infarction in the territory of the middle cerebral artery. Anisocoria and basal lacrimal gland secretion were determined. The ninhydrin test was performed and the sympathetic skin response recorded in both hands and feet. The functions assessed by these tests were found to be reduced bilaterally. No significant lateralisation of the sympathetic nervous system could be demonstrated.

Adult↗
PubMed1998

Magnetic resonance angiography in patients with brain infarction.

This study evaluated the role of magnetic resonance angiography (MRA) in detecting extra- or intracranial vascular disease in 118 patients with brain infarction and the accuracy of MRA diagnosis when compared with conventional angiography in patients who had both investigations. Magnetic resonance angiography ruled out extra- and intracranial large vessel disease in 36% of the patients. MRA also demonstrated extra- or intracranial disease in 56% (probably symptomatic in 31, possibly symptomatic in 18, and asymptomatic in 17 patients), and provided no information in 8% of the 118 patients. Among the 176 major vessels visualized by both MRA and conventional angiography, conventional angiography confirmed the presence of 9/10 extracranial and 32/40 intracranial large vessel abnormalities detected on MRA. There were two false-negative findings on MRA: occlusion of a distal branch of middle cerebral artery, and an asymptomatic posterior cerebral artery stenosis. Magnetic resonance angiography is a clinically useful method for screening extra- and intracranial disease in patients with brain infarction and selecting high-yield patients for conventional angiography.

Cerebral Angiography↗
PubMed2005

Formalin fixation alters water diffusion coefficient magnitude but not anisotropy in infarcted brain.

This study was designed to determine whether formalin fixation alters diffusion parameters in the infarcted brain. Diffusion tensor images were obtained from anesthetized mice 1 hr after middle cerebral artery occlusion and repeated after formalin fixation of brains. In live animals, there was a significant decrease in the trace of the diffusion tensor (Tr(D)) in infarcted cortex and external capsule compared with contralateral brain areas, with no change in relative anisotropy (RA). After formalin fixation, Tr(D) was reduced 30-80%. However, the Tr(D) differential present in vivo between injured and healthy tissues was lost, with Tr(D) reduced to similar values in all tissues except for the edge of the cortical infarction, where it was lower than in surrounding tissues. RA values were unchanged after fixation. This study supports the preservation of diffusion anisotropy for both healthy and injured white matter in fixed mouse brain. However, the sensitivity of water diffusion in detecting tissue injury in vivo is not preserved in fixed tissues.

Animals↗
PubMed1993

Brain infarct causes under the age of fifty: a comparison between an east-Asian (Thai) and a western (Dutch) hospital series.

Proportion and causes of brain infarction among young persons may differ between Western world and developing countries, which may require different diagnostic and treatment strategies. We compared a Thai series of 56 hospitalized brain infarct patients younger than 50 years (16% of 357 similar patients from all ages) with a series of 55 Dutch patients (8% of 694 patients). The Thai patients had 12% (95% confidence interval: 3-21) more often a cardioembolic stroke cause, due to a higher frequency of rheumatic heart disease in the Thai series. The percentage of patients with atherothrombotic stroke cause was higher in the Dutch series, whereas the percentage of those with hematologic abnormalities, or those with vasculopathies did not differ. Patients in the Thai series had 17% (95% confidence interval: 7-27) more often an unidentified stroke cause, which was probably related to less extensive ancillary investigations compared with the Dutch series. We conclude that especially centers in developing countries that treat young stroke patients should be supplied with ancillary testing facilities, such as cardiac echo, carotid ultrasound, and some laboratory facilities. Early treatment of infections, especially acute rheumatic fever, could lower the incidence of stroke in the young.

Adolescent↗
PubMed2003

Myeloperoxidase polymorphisms in brain infarction. Association with infarct size and functional outcome.

Myeloperoxidase (MPO) has been shown to contribute to several diseases and more particularly to atherosclerosis through excessive ROS production via the MPO/H(2)O(2)/Cl(-) oxidation system. The aim of this study was to determine whether there is an association between MPO polymorphisms and brain infarction (BI), one of the main consequences of atherosclerosis. We investigated MPO G-463A and G-129A polymorphisms in 450 patients with BI confirmed by magnetic resonance imaging (MRI) and 450 controls of the GENIC (Génétique de l'Infarctus Cérébral) Study. Genotype determination of MPO was performed by polymerase chain reaction and allele-specific oligonucleotide hybridization (ASO). Genotype distributions for each of both MPO polymorphisms were found to be similar between cases and controls overall, and according to etiologic subtypes or gender. The frequency of the A allele of the G-463A polymorphism was 22% (95% confidence interval, 19.4 to 24.9) and the frequency of the A allele of the G-129A polymorphism was 6.8% (95% confidence interval, 5.3 to 8.6). The odds ratio (OR) for BI in carriers of the A allele of the G-129A polymorphism was 0.92 (95% confidence interval, 0.61 to 1.39), and the OR for BI in carriers of the A allele of the G-463A polymorphism was 1.15 (95% confidence interval, 0.88 to 1.52). No association between the main risk factors for BI such as hypertension, cholesterol, diabetes and MPO polymorphisms was found. In analyses restricted to cases, we identified an association between the A allele of the G-129A polymorphism and the size of the brain infarct (P=0.01). Furthermore, the A allele of the G-463A polymorphism was associated with a poorer functional short-term outcome as evaluated by the Rankin score (P=0.02). In conclusion, MPO polymorphisms were associated with the extent of brain damage and the functional outcome rather than with the risk of developing a BI.

Adolescent↗
PubMed1996

Hemorrhagic transformation of brain infarct: predictability in the first 5 hours from stroke onset and influence on clinical outcome.

OBJECTIVE: To identify, in the first 5 hours of acute brain infarct, clinical and radiologic predictors of subsequent hemorrhagic transformation (HT), and to evaluate its influence on the clinical course. BACKGROUND: The identification of early predictors of HT might be important to plan antithrombotic or thrombolytic treatments. PATIENTS: One hundred fifty consecutive patients with cerebral anterior circulation infarct systematically underwent a first CT within 5 hours of onset. During the first week after stroke, we performed a repeat CT or autopsy to look for HT. Outcome measures were early neurologic deterioration within the first week of onset and 30-day case fatality rate and disability. RESULTS: HT was observed in 65 patients (43%): 58 (89%) had a petechial HT and seven (11%) a hematoma. Among initial clinical an CT findings, the only independent predictor of HT was early focal hypodensity. Its presence was associated with subsequent HT in 77% of cases (95% CI, 68 to 86%), whereas its absence predicted the absence of subsequent HT in 94% of cases (95% CI, 89 to 99%). No baseline clinical or CT characteristic differentiated patients with petechial HT from those with hematoma. Antithrombotic and antiplatelet agents did not influence the occurrence of either type of HT. The frequency of early neurologic deterioration and of 30-day death or disability in HT patients was twice as high as in those without HT. However, a large-sized infarct and the presence of mass effect at the repeat CT or autopsy were the only factors independently linked to both the outcome events, irrespective of the development of HT. Clinical evolution of HT patients given antithrombotics was comparable with that of HT patients not receiving these drugs. CONCLUSIONS: HT of a brain infarct is a common event that occurs independently of anticoagulation and can be reliably predicted as early as 5 hours from stroke onset by the presence of focal hypodensity at CT. Apart from the infrequent cases of massive hematoma, HT does not influence prognosis, whereas a poor outcome in HT patients is correlated with a higher frequency of large edematous infarcts in this subgroup. The clinical course and final outcome of HT in anticoagulated patients does not differ from that of non-anticoagulated HT patients.

Aged↗