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PubMed1990

The silent brain infarct before and after carotid surgery.

Routine computed tomography was prospectively performed pre- and postoperatively in 114 consecutive patients undergoing a total of 131 procedures on the carotid artery. Hemispheric cerebral infarction was found preoperatively in three of the 16 hemispheres corresponding to symptomatic lesions (19%), in 18 of 109 hemispheres corresponding to transient ischemic attacks (16.5%), and in one of four hemispheres corresponding to lesions responsible for a fixed cerebral vascular accident (25%). Two surgical procedures (1.5%) were complicated by early cerebral infarctions as detected on postoperative computed tomographic scan. These complications resulted in death in one case, and left the patient with major sequelae in the other. Five procedures (3.8%) were complicated by transient ischemic attacks, three of which were associated with minimal cerebral infarctions visible on computed tomographic scan. Neurologic status was unchanged after 124 (94.6%) procedures, whereas four of these procedures were complicated by silent brain infarctions as visualized on postoperative computed tomographic scans (3.1%). This study confirms that existing pre- and postoperative neurologic classifications are far from perfect and that surgery is rarely responsible for cerebral infarction. Carotid surgery should no longer be performed without obtaining pre- and postoperative computed tomographic scans.

Aged↗
PubMedDate not supplied

Fatty acid pattern of red blood cell membranes and risk of ischemic brain infarction: a case-control study.

The fatty acid composition of red blood cell membranes (which reflects dietary fat intake) was studied in 28 male patients with recent (less than 3 days) ischemic stroke and 56 matched controls. Fifteen fatty acids were measured by means of chromatographic analysis. Percentages of linoleic, 22:5, and 22:6 acids were significantly lower in red blood cell membranes of stroke patients than in those of matched controls. The results suggest that a low unsaturated fatty acid diet could be an independent risk factor for ischemic brain infarction.

Adult↗
PubMed2002

Adenovirus-mediated Bcl-X(L) expression using a neuron-specific synapsin-1 promoter protects against disseminated neuronal injury and brain infarction following focal cerebral ischemia in mice.

The effects of an adenovirus-mediated Bcl-X(L) expression, driven by a neuron-specific human synapsin-1 promoter, on the degree of injury, were examined after transient focal ischemia in mice. Therefore, injections of vehicle, of an adenoviral E1-deleted control vector (Ad-dE1), or a Bcl-X(L) vector (Ad-Syn-Bcl-X(L)) were stereotactically made in the striatum. Seven days later, focal ischemia was induced either by 30 min or 2 h of intraluminal thread occlusion. In line with previous data, 30 min of middle cerebral artery (MCA) occlusion reproducibly resulted in disseminated neuronal injury of the striatum, as revealed by cresyl violet and TUNEL 3 days after ischemia. The degree of cell injury was significantly reduced in Ad-Syn-Bcl-X(L) treated as compared with Ad-dE1 and vehicle-treated animals. On the other hand, 2 h of MCA occlusion produced reproducible infarcts both in vehicle and Ad-dE1 treated animals 24 h after ischemia. The infarct area at the level of the striatum was significantly decreased by Ad-Syn-Bcl-X(L) treatment. The present data demonstrate that an adenoviral Bcl-X(L) expression with a neuron-specific synapsin-1 promoter provides a powerful tool, which not only diminishes disseminated neuronal injury, but also protects against tissue infarction.

Adenoviridae↗
PubMed2003

Silent brain infarcts in adult Kuwaiti sickle cell disease patients.

Although overt stroke is a common complication of sickle cell disease (SCD), its incidence is very low in Kuwaiti patients. On the other hand, the prevalence of silent brain infarcts, which is reported to be about 17-20% in American patients, has not been documented in adult Kuwaiti patients. This is a 1-year study of consecutive, asymptomatic SCD patients seen in the hematology clinic of Mubarak Al-Kabeer Hospital. Patients with a past history of seizure or any other neurological abnormality were excluded. The patients' charts were reviewed for frequency of hospitalizations, any documented complications, and steady-state CBC. MRI was done with a 1.5-Tesla unit with super-conducting magnet. T1- and T2-weighted sagittal and axial sections and proton-density axial images were obtained in 5-mm-thick sections. Thirty-five patients were studied, made up of 25 SS and 10 Sbeta(0)Thal, aged between 17 and 44 years, with a mean age of 26.9 +/- 9.3 years. MRI findings consistent with infarcts were found in 7 (20.0%) patients-6 SS and 1 Sbeta(0)thal-with a mean age of 31.8 +/- 8.2 years, which was significantly higher (P < 0.05) than the mean age of the unaffected group (25.1 - 9.0 years). There were also no differences in the mean Hb, Hb F, or any other hematological parameter in the two groups. Among the affected 6 SS, 2 had co-existent alpha-thal trait. It is interesting that, while silent infarcts are prevalent in young American patients, it is in the older age group that they occur in Kuwaiti patients. Further studies are needed to investigate the factors modulating this heterogeneity.

Adolescent↗
PubMed2003

[A case of brain infarction with nephrotic syndrome].

A 47-year-old man lost his consciousness and brought to our hospital by ambulance. On admission, he had aphasia and upper right limb paresis. Diffusion weighted MR image of the brain on admission showed multiple high intensity areas in the left middle cerebral artery (MCA) territory. Brain angiography performed on the 2nd hospital day revealed the left MCA severe stenosis. We started intravenous antithrombotic therapy on the 1st day. The left carotid angiography on 12th day demonstrated that the left MCA stenosis was improved. He had medical history of hypertension, diabetes mellitus and gout. But he had only slight atherosclerosis, and had no arrhythmia and patent foramen ovale. Blood chemistry test showed marked hypoproteinemia and hyperlipidemia, and urine examination showed proteinuria. He was diagnosed as nephrotic syndrome for the first time. Nephrotic syndrome brought hypercoagulability, so we suspected that nephrotic syndrome concerned with brain infarction.

Cerebral Infarction↗
PubMed1976

[Electroencephalographic study of brain-infarction in dogs (author's transl)].

The evaluation of EEG-findings during the acute phase of stroke-patients is somewhat difficult particularly in regard to the voltage-production, less in regard to the temporary retardation of frequency. Within comparable neurophysiological and biochemical examinations of the experimental brain-infarct under standardized conditions of silicon-rubber-embolus was introduced intracarotideally and an occlusion of the media-trunk evoked. One day prior to the embolisation and on the first, third and fifth day thereafter EEG-derivation took place which were stored on analogous-tape, digitalized and were then confronted with the FFT-Algorithm. From the statistical point of view four animal groups were the result: HO-group (control group), H1-, H3- and H5-group (each time N = 6). Visual evaluation of the curves, descriptive and inferential statistics of the spectral EEG estimators showed a significant loss of power within five days after the infarction; it always was more distinct across the focal side than across the not immediately involved hemisphere. On the fifth day the original level of voltage was almost reached again. From the clinical standpoint the neurological deficits had practically been disappeared. The biochemical finishing of the dog-brains -- the results of which are planned to be confronted with the electrophysiological results in another paper -- in accordance with the papers of other authors brings close the assumption that the decrease of tension i.e. the loss of power of the electric potential during the first days after infarction is combined with a temporary decrease of the energetic potential of the metabolically active corticocerebral cells which is tied to the phosphagene-system of the highly energetical phosphates and metabolites of the energy-metabolism in the brain.

Animals↗
PubMed1999

Multiple brain infarcts: clinical and neuroimaging patterns using diffusion-weighted magnetic resonance.

The capability of diffusion-weighted (DW) magnetic resonance imaging (MRI) to identify very early ischemic brain injury better than conventional MRI is well known. This technique, which successfully discriminates acute from old infarcts, is particularly useful in patients with multiple brain infarcts (MBI). Among 142 patients with acute stroke consecutively admitted to our primary care center, we selected 43 patients with two or more brain infarcts on conventional MRI. All patients presented with clinical deficits consistent with acute cerebral ischemia and underwent conventional spin echo for T(1) (T1-WI) and T(2)-weighted images (T2-WI), T(1)-W gadolinium-enhanced images, and echo-planar technique for DW MRI sequences. Patients underwent DW MRI examinations within 15 days of stroke onset (mean +/- SD: 3 +/- 3 days). In all but 1 case, the infarcts detected on DW MRI were also visible on T2-WI. The different signal pattern on DW MRI, compared with T2-WI, facilitated the detection of acute infarcts in all patients. T1-WI with gadolinium enhancement was only helpful in 5 (11.6%) patients. DW MRI enabled precise clinicotopographic correlations in 79% of our patients and provided additional clinically relevant findings in 72% of the patients. Based on the neuroradiological findings, patients were divided into three clinicotopographic types of MBI as follows: 13 patients (30.2%) presented with multiple acute infarcts, 24 patients (55.8%) with a single acute infarct and multiple old infarcts, and 6 patients (13.9%) with multiple acute and old infarcts. In conclusion, DW MRI can easily be added to conventional MRI in order to be able to distinguish acute from old infarcts, and to identify acute multiple lesions. Therefore, a better correlation between clinical symptoms and the site of lesions can be obtained, considerably improving patient care.

Adolescent↗
PubMed2003

Study of total homocyst(e)ine levels in type 2 diabetic patients with silent brain infarction.

Hyperhomocysteinemia is thought to have an important role in the pathogenesis of ischemic cerebral infarction. When associated with diabetes mellitus, it might worsen the neurologic course. The aim of the study was to clarify the relation between plasma homocysteine (Hcy) concentrations and silent brain infarction (SBI) in patients with type 2 diabetes mellitus. Total plasma Hcy levels were prospectively studied in 46 patients with type 2 diabetes and SBI (group I), mean age 56+/-5.4 years, as compared to 38 diabetic patients without SBI (group II) and with 31 controls (group III). Homocysteine concentrations were determined using a high-performance liquid chromatography assay. The results were compared using the Student's t test. The mean level of Hcy was 22.6+/-2.4 micromol/l in group I, 19.7+/-1.6 micromol/l in group II and 11.4+/-1.4 micromol/l in group III; between group I and group II p < or = 0.001. These data are consistent with increased Hcy levels in type 2 diabetic patients, contributing to the onset of SBI in some patients. The phenomenon should be considered in any future strategy for the therapy of hyperhomocyst(e)inemia (HHcy).

Cerebral Infarction↗
PubMed2004

Common carotid artery intima-media thickness in patients with brain infarction and intracerebral haemorrhage.

An increase in the intima-media thickness of the common carotid artery (CCA-IMT) is generally considered as an early marker of atherosclerosis and has been associated with a higher risk of stroke and myocardial infarction. There is no evidence of an association between the IMT and cerebral bleeding. We investigated cross-sectionally the diagnostic ability of vascular risk factors, including CCA-IMT, to distinguish between brain infarction (BI) and intracerebral haemorrhage (ICH). Patients suffering from BI (n = 126) had significantly (p < 0.05) higher CCA-IMT when compared to the ICH population (n = 30). The multinomial logistic regression procedure selected CCA-IMT as an independent factor able to discriminate between BI and ICH. The risk of BI versus ICH increased continuously with increasing CCA-IMT. After adjustment for cardiovascular risk factors the odds ratio for BI per 0.1 mm CCA-IMT increase was 1.29 (95% CI: 1.03-1.61). The present results demonstrate the possible predictive power of non-invasive measurement of the CCA-IMT with respect to BI versus ICH and deserve further investigation.

Aged↗
PubMed2005

Plasma homocysteine and risk of coexisting silent brain infarction in Alzheimer's disease.

BACKGROUND: Cerebrovascular disease is common in Alzheimer's disease (AD). Elevated plasma homocysteine (pHcy) levels are reported to be associated with an increased risk of poor cognition and dementia. OBJECTIVE: To determine whether high pHcy levels are associated with an increased risk of coexisting silent brain infarctions (SBIs) in AD. METHODS: Study population comprising 143 outpatients with clinical diagnosis of probable AD (73.3 +/- 7.0 years) were classified into 2 groups according to the presence or absence of SBIs on magnetic resonance imaging. RESULTS: SBIs were noted in 32.9% (47/143) of the AD patients. The pHcy levels in the AD with SBIs (14.0 +/- 4.5 micromol/l) were significant ly elevated compared with the AD without SBIs (11.7 +/- 4.7 micromol/l, p = 0.007). After adjusting for age and gender, high pHcy (>12.4 micromol/l), but not hypertension, was associated with an increased risk of developing SBIs in AD (OR = 4.61, 95% CI = 1.74-12.2, p = 0.002). However, age at onset, cognitive function, cerebrospinal tau or amyloid beta-peptide(1-42) levels were not significantly correlated with pHcy levels in AD. CONCLUSION: SBIs commonly coexist with AD, and may be a unique vascular condition in which homocysteine plays an important role. Homocysteine-lowering therapy rather than antihypertensive medication might be an appropriate strategy to prevent stroke associated with AD.

Aged↗
PubMed2005

[Autopsy findings of meningitis associated with multiple brain infarctions in two adult patients].

Cerebrovascular complications of meningitis have been extensively documented in the literature. It is little known, however, that paroxysmal, devastating, and potentially fatal complications can occur when the early signs of infection are subtle and missed. We describe the clinical course and neuropathological findings of the occurrence of brain infarctions during two atypical clinical courses of meningitis. In one patient, it was due to Serratia marcescens detected only by an autopsy specimen, and in the other, it was due to Aspergillus detected by a surgical biopsy. Death followed multiple, extensive, and progressively multiplicative infarctions in the basal ganglia, brainstem, and cerebral cortices. Autopsies revealed that the infarctions were caused by severe inflammatory change in the vascular walls, mainly of the arteries of the skull base, including the basilar and carotid arteries. Thrombus formation was also recognized in the lumen of several arteries. A number of characteristic Aspergillus hyphae were recognized in the arterial wall of one patient. Meningitis, which may be associated with severe vasculitis and lead to cerebral infarction, should be considered in the differential diagnosis of these conditions. Early diagnosis and initiation of vigorous therapy should be stressed for therapeutic success.

Aspergillosis↗
PubMed2004

[Prediction of brain infarction in hypertensive patients].

A 7-year prospective study of 379 hypertensive patients was conducted with primary comprehensive clinical and device examination of the patients in hospital followed by annual control in hospital or outpatient setting. Two groups were formed: with uncomplicated essential hypertension (EH)(n = 263, group 1); with EH complicated by brain infarction (BI) (n = 116, group 2). Overall prognostic correctness was 85.9%. BI was predicted by age, smoking, high intake of salt, absence of regular antihypertensive therapy, non-dipper pattern, low output, atherosclerotic changes of major head arteries, frequent paroxysms of cardiac fibrillation, ventricular extrasystole, abnormal blood rheology. Integral index of the patient condition calculated on the basis of the decisive prognosis rule (data of the primary examination + MI within 7-year follow-up) enables targeted prevention of cerebral complications.

Adult↗
PubMed2004

Newborn brain infarction: clinical aspects and magnetic resonance imaging.

OBJECTIVE: We describe the clinical and imaging studies of 11 full-term babies with neonatal stroke. We classify the neonatal non-hemorrhagic strokes as thrombotic, embolic, or global vascular insufficiency and determine if this classification is improved by adding magnetic resonance spectroscopy (MRS) and diffusion-weighted imaging (DWI) to conventional magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA). METHODS: Clinically, eight of the 11 babies presented with seizures, one with apnea, and two with lethargy. Conventional MRI and DWI were used to classify each infarct as being either borderzone or vascular distribution. The location of infarction revealed the presumed vascular pathophysiology. RESULTS: Infants were classified as having either embolic (bilateral middle cerebral artery,n=1), global ischemic (bilateral borderzone, n=2), or thrombotic infarction (unilateral middle cerebral artery, n=7; bilateral posterior cerebral arteries, n=1). DWI and MRS detected a small infarct better than conventional MRI in one patient. MRA showed abnormal intracranial arteries in three, all of who were in the thrombotic group. Even though MRS was more sensitive than conventional MRI in detecting ischemia/infarction in one patient, in another there was no detectable lactate in the stroke region found on conventional MRI. Clinical presentation was similar in global ischemia and focal infarctions, but newborn stroke was more likely to present with lateralizing focal motor seizures. Seizures were the most common presenting sign, with a paucity of other focal neurological deficits. CONCLUSION: MRI is the best approach to determine stroke pathophysiology. Brain infarction frequently presents with seizures. We speculate that the location and distribution of infarction might determine stroke timing, pathophysiology and outcome. Ongoing clinical studies will likely clarify this speculation.

Cerebral Infarction↗
PubMed1998

Brain infarction following 5-fluorouracil and cisplatin therapy.

Five patients with oropharyngeal cancer treated with 5-fluorouracil and cisplatin had ischemic stroke within 2 to 5 days after the drug infusion. This occurred during the second course of chemotherapy in three patients, and during the third course in two patients. There may be a relation between treatment and brain infarction because 1) there was no other cause identified despite extensive tests, including postmortem examination in one patient; 2) there was a short delay between treatment infusion and stroke; and 3) there was a similar pattern of ischemic stroke after the second or third course of chemotherapy.

Aged↗
PubMed1997

[Dissecting aneurysm of the middle cerebral artery with subarachnoid hemorrhage and brain infarction: a case report].

This report describes a surgical case of a dissecting aneurysm of the left middle cerebral artery with subarachnoid hemorrhage and ischemic insult. A 48-year-old man with pure motor aphasia was referred to our hospital. CT scans demonstrated subarachnoid hemorrhage in the left frontal region. CT scans on the next day showed a small brain infarction in the left precentral artery and central artery territories. The first left carotid angiograms showed stenosis at the M2 portion of the middle cerebral artery. On the 16th day, the second left carotid angiograms revealed a pearl and string sign. We diagnosed a dissecting aneurysm of the middle cerebral artery. The dissecting aneurysm was wrapped using the pterional approach and STA-MCA anastomosis was also performed. The postoperative course was uneventful and the motor aphasia improved.

Aortic Dissection↗
PubMed1992

Histochemical and morphometric investigation of the pathogenesis of acute brain infarction in primates.

The right medial cerebral artery of 25 primates (Macaca radiata) was occluded transorbitally with an atraumatic clip. The time courses of infarct volume and capillary morphometric changes in the ischemic lenticular nucleus, caudate nucleus and insular cortex were then determined. Volume changes of ischemic foci were studied morphometrically using an enzyme histotopochemical acid phosphatase stain. During the first 4 hours extension (or spread) of the ischemic area was small and constant. Over the next hours, the ischemic focus increased in volume, becoming maximal in the lenticular nucleus in 24 hours and in the caudate nucleus in 48 hours. In the lenticular nucleus, edema developed 4 hours after onset of ischemia and was characterized by a decrease in capillary diameter and an increase in mean intercapillary distance. In the caudate nucleus and insular cortex, in the first hours after clipping the medial cerebral artery, capillary diameter and volume increased and intercapillary distance decreased. The data demonstrate that the therapeutic window of brain infarct treatment is during the first 4-6 hours after occlusion of the medial cerebral artery.

Acid Phosphatase↗
PubMed2000

Common carotid artery intima-media thickness and brain infarction : the Etude du Profil Génétique de l'Infarctus Cérébral (GENIC) case-control study. The GENIC Investigators.

BACKGROUND-The use of intima-media thickness (IMT) as an outcome measure in observational studies and intervention trials relies on the view that it reflects early stages of atherosclerosis and cardiovascular risk. There is little knowledge concerning the relation between IMT and brain infarction (BI). METHODS AND RESULTS-We investigated the relation of IMT with BI and its subtypes in 470 cases and 463 controls. Cases with BI proven by MRI were consecutively recruited and classified into subtypes by cause of BI. Controls were recruited among individuals hospitalized at the same institutions and matched for age, sex, and center. IMT was measured at the far wall of both common carotid arteries (CCA) using an automatic detection system. Adventitia-to-adventitia diameters and CCA-IMT were measured on transverse views; lumen diameter was computed using these measures. Mean (+/-SEM) CCA-IMT was higher in cases (0.797+/-0.006 mm) than in controls (0.735+/-0.006 mm; P<0. 0001). This difference remained after adjustment for lumen diameter and when analyses were restricted to subjects free of previous cardiovascular or cerebrovascular history. The difference in CCA-IMT between cases and controls was significant in the main subtypes. The risk of BI increased continuously with increasing CCA-IMT. The odds ratio per SD increase (0.150 mm) was 1.82 (95% confidence interval, 1.54 to 2.15); adjustment for cardiovascular risk factors slightly attenuated this relation (odds ratio, 1.73; 95% confidence interval, 1.45 to 2.07). CONCLUSIONS-An increased CCA-IMT was associated with BI, both overall and in the main subtypes. An increased IMT may help select patients at high risk for BI.

Adult↗
PubMed1992

Molecular biological studies in atherothrombotic brain infarction.

Strokes due to atherosclerosis are the most prominent neurological disease affecting adults, and efforts to reduce stroke occurrence, in addition to stroke-risk reduction, will require insights into molecular mechanisms. Our studies showing abnormal metabolism of low and high density lipoproteins (LDL and HDL) in vivo and of RFLP in apoprotein AI, the major protein of HDL, in stroke-prone subjects suggest that greater exploration of fundamental mechanisms of atherothrombotic brain infarction (ABI) should yield preventative strategies, the ultimate treatment for strokes.

Apolipoprotein A-I↗