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PubMed2003

Brain microembolism.

PURPOSE: To alert clinicians about the occurrence of a subtype of brain infarction, its suspected etiology, and its detection by specific neuroimaging techniques. METHODS: The article presents 5 nonconsecutive patients admitted to the stroke services of 2 tertiary care hospitals, who presented with acute or subacute symptoms suspicious, but at times atypical, of brain ischemia. FINDINGS: Each patient had evidence of 3 to > 20 small areas of recent brain infarction detected by diffusion-weighted imaging (DWI). When available, brain computerized tomography images were not helpful for the diagnosis of these recent infarcts. Most lesions were present on magnetic resonance imaging fluid-attenuated inversion recovery sequences, but the diffusion-weighted images allowed the determination of their acuity. Further evaluation revealed a potential source of embolism in each patient. Brain microembolism was suspected in all cases. CONCLUSION: Small and multiple areas of acute or subacute brain infarction occasionally present with clinical features atypical for brain embolism. They can be detected by magnetic resonance DWI studies.

Aged↗
PubMed1996

[Memory performance of Parkinson patients with and without sleep apnea syndrome].

We investigated the effect of SAS on the long term memory in PD patients and compared them with patients with brain infarction or cataract (control group), respectively. PD patients develop SAS and cognitive impairments more often then healthy people. Since SAS leads to a fragmentation of the sleep structure it interferes with memory. Therefore SAS may be a pathogenic factor of cognitive impairment in PD. We studied 14 patients (7 with and 7 without SAS) with PD, brain infarction or cataract using the LGT-3, which measures the verbal, numeric and figural long term memory. All patients answered subtest 7 of the Wechsler-Memory-Scale at night and in the morning. The saving between the evening and morning measure was calculated. An analysis of variance was performed using the SAS-condition and the different groups as independent variable. A significant difference (p < or = 0.005) of all memory measurements between patients with and without SAS but not between the different groups has been proved with a superiority of the patients without SAS. A significant difference of the influence of the SAS for verbal memory score on patients with PD (pp < or = 0.05) and brain infarction (pp < or = 0.005) respectively and the control group could be demonstrated. Therefore we found a quantitative difference of memory consolidation in PD patients with SAS. The influence of SAS on memory in patients with neurological disease is more pronounced compared to the control group.

Cataract↗
PubMed2005

Hyperhomocysteinemia is associated with volumetric white matter change in patients with small vessel disease.

BACKGROUND: Hyperhomocysteinemia is associated with cerebral small vessel disease (SVD). We examined the relationship between homocysteine and 1) volumetric measure of white matter change (WMC), 2) silent brain infarcts, 3) cerebral atrophy on MRI and 4) cognition on a consecutive cohort of patients with stroke associated with SVD. SUBJECTS AND METHODS: Fifty-seven patients consecutively admitted to the Acute Stroke Unit in a university hospital due to stroke associated with SVD were recruited and assessed three months after the stroke. Non-fasting homocysteine was obtained. Using MRI, the number of infarcts, volume of WMC and cerebral atrophy were measured. General cognitive functions were assessed using the Mini Mental State Examination and Alzheimer's disease Assessment Scale. Mattis Dementia Rating Scale - Initiation/Perseveration subset was used to assess executive cognitive functions. RESULTS: Hyperhomocysteinemia (> or = 14.88 micromol/L) significantly accounted for the volume of WMC on MRI in a multivariate stepwise regression model (adjusted R(2)=0.058, p <0.05) after adjustment for age and folate level. Patients in the highest quartile of WMC volume had significantly higher levels of homocysteine than those in lowest quartile (p <0.001). No significant relationship was found between homocysteine and silent brain infarcts, cerebral atrophy and performance on psychometric tests. CONCLUSION: Hyperhomocysteinemia is associated with volumetric measure of WMC among patients with SVD. The role of homocysteine in the development of silent brain infarcts and cerebral atrophy as previously reported cannot be ascertained in this study. No direct relationship was found between homocysteine and cognitive functions.

Aged↗
PubMed1990

Influence of amphetamine treatment on somatosensory function of the normal and infarcted rat brain.

The consequences of acute amphetamine administration on the metabolic responsiveness of the cerebral cortex to physiologic activation were studied in normal and infarcted rats. Treated rats received a 4 mg/kg intravenous injection of d-amphetamine 1 hour before unilateral vibrissae stimulation and 2-deoxyglucose study. In nontreated normal rats, metabolic activation was restricted to the major relay stations of the vibrissae-barrel circuit. In amphetamine-treated rats, stimulation-induced increased glucose utilization was widespread, including ipsilateral and contralateral cortical regions outside the barrel field circuit. For example, an 84% increase in glucose utilization above control was seen in cortical areas anterior to the barrel field region. Increased glucose utilization induced by stimulation was severely depressed in nontreated rats that had undergone infarction of the left cortical barrel field 2 weeks previously. Vibrissae stimulation failed to increase glucose utilization significantly in cortical areas remote from the infarct. In contrast, bilateral increases in glucose utilization were observed within cortical regions of treated infarcted rats. For example, a 50% increase in glucose utilization was detected in cortical areas bordering the infarct. Thus, in the normal and infarcted rat, amphetamine appears to promote alternate circuit activation--a pharmacologic property that may be advantageous for recovery after injury.

Amphetamines↗
PubMed2000

Reproducibility of computer-quantified carotid plaque echogenicity: can we overcome the subjectivity?

BACKGROUND AND PURPOSE: We sought to assess the reproducibility, interobserver variability, and application to clinical studies of a new method for the quantitative assessment of carotid plaque echogenicity. METHODS: Carotid plaques were scanned with the use of ultrasound, and their images were stored in a computer. They were normalized by assigning certain gray values to blood and adventitia, and the gray scale median (GSM) was used to quantify their echogenicity. The variability between storage media, between degrees of magnification, and between probes was assessed. The method was applied to 232 asymptomatic carotid plaques causing 60% to 99% stenosis in relation to the presence of ipsilateral CT-demonstrated brain infarcts. In all parts of the study the plaque GSM was measured before and after normalization to evaluate its effect. Interobserver agreement for the scanning process was assessed. RESULTS: The GSM mean difference before and after normalization for variability studies of storage media, degrees of magnification, and probes was -14.5 and -0.12, 2.24 and 1.68, and -8.3 and -0.7, respectively. The median GSM of plaques associated with ipsilateral nonlacunar silent CT-demonstrated brain infarcts was 14, and that of plaques that were not so associated was 30 (P:=0.003). The interobserver GSM difference was -0.05 (95% CI, -1.7 to 1.6). CONCLUSIONS: Our method decreases the variability between storage media and between probes but not the variability between degrees of magnification. It separates echomorphologically the carotid plaques associated with silent nonlacunar CT-demonstrated brain infarcts from plaques that are not so associated.

Carotid Stenosis↗
PubMed1993

Coronary artery disease, myocardial infarction, and brain embolism.

The incidence of in-hospital stroke complicating acute myocardial infarction is approximately 1%. This rate is largely unaffected by thrombolytic therapy. Large myocardial infarctions, anterior wall involvement, prior stroke, and increasing age are risk factors for ischemic stroke. Left ventricular thrombi commonly occur with anterior wall infarctions. There is some evidence that anticoagulation reduces their incidence and uncontrolled studies suggest that anticoagulation may reduce the risk of embolization. Left ventricular aneurysms have a low rate of embolization and do not require systemic anticoagulation. Treatment of acute myocardial infarction with t-PA and anisoylated plasminogen streptokinase activator complex are associated with a higher risk of stroke than treatment with streptokinase; this excess risk is attributable to an increased rate of cerebral hemorrhages.

Brain↗
PubMed2004

[Neuro-protective effect of naomaitong to brain damage after focal cerebral ischemia reperfusion (I/R) in the aged rats].

OBJECTIVE: To study neuro-protective effect of naomaitong on brain damage after focal cerebral ischemia reperfusion (I/R) in the aged rats. METHOD: 11 groups of 20-22-month old SD rats were subjected to 3 hours of middle cerebral artery occlusion with the intraluminal filament technique, followed by 12 hours of reperfusion. Nervous symptom, oedema of brain, infarct size, morphology and superfine structure of brain, etc were monitored thoughout cerebral ischemia and reperfusion. RESULT: Infarct size of brain in ischemia and reperfusion groups were significantly greater. Oedema of it was higher, nervous symptom of it was more serious, and morphology and superfine structure brain were more obvious than those of sham-operated group. Nervous symptom, oedema of brain, infarct size, morphology and superfine structure of brain in treated groups were ligher than those of untreated groups (P < 0.001). CONCLUSION: Naomaitong can protect brain damage after focal cerebral I/R in the aged rats.

Age Factors↗
PubMed1994

Immunohistochemistry with an antibody to human liver carboxylesterase in human brain tissues.

Human liver carboxylesterase (CE) is an enzyme capable of metabolizing drugs, and may also function as a regulator of lipid metabolism. We examined one isoform of CE by immunohistochemistry in the brains of neurologically normal, Alzheimer disease (AD), amyotrophic lateral sclerosis (ALS) and cerebral infarction cases. In all but the infarcted brains, the anti-CE antibody stained only capillary endothelial cells in the brain and spinal cord tissues. In infarct brain areas, intense immunoreactivity of the macrophages was seen. In contrast, the macrophages in the ALS lateral columns and the reactive microglia located in the center of classical senile plaques in AD, as well as other reactive microglial cells in the grey matter, showed no immunoreactivity. In the central nervous system, CE may function as a protective factor against foreign chemicals in capillary endothelial cells, and the antibody to CE may serve as a marker for invading macrophages from the systemic circulation.

Adult↗
PubMed1991

Idiopathic ischemic infarction of the brain stem in children.

Three cases of idiopathic brain-stem infarction are added to the literature on 12 children. There is no age predilection, and the youngest case is 3 years old. However, there is a striking male preponderance of 13:2. The residual neurological deficit covers the range of normal to quadriparesis. Laboratory studies investigating hypercoagulopathy, platelet dysfunction and atrial septal defect may provide an etiology for some cases in the future.

Adolescent↗
PubMed2007

Procoagulant and fibrinolytic activity in cerebrospinal fluid from adults with bacterial meningitis.

OBJECTIVES: This study investigated levels of coagulation and fibrinolysis factors in cerebrospinal fluid (CSF) from adults with bacterial meningitis in relation to development of brain infarction. METHODS: CSF was collected from 92 adults with community-acquired bacterial meningitis, who participated in the prospective Dutch Meningitis Cohort Study; 8 patients with viral meningitis and 9 healthy control subjects. Levels of proteins involved in the coagulation cascade were determined by means of immunoassays. RESULTS: Bacterial meningitis was accompanied by local activation of coagulation, as shown by significantly higher CSF soluble tissue factor (P<0.001) and prothrombin fragment F1+2 concentrations (P<0.001) as compared to viral meningitis patients and controls. This was accompanied by a significantly higher D-dimer formation (P<0.001). In addition, in bacterial meningitis fibrinolysis was attenuated, since CSF plasminogen activator inhibitor (PAI)-1 levels were significantly higher as compared to the controls (P=0.02). In patients with bacterial meningitis who developed brain infarction, CSF PAI-1 levels were higher than in those without infarction (P=0.04). CONCLUSIONS: Activation of coagulation and attenuation of fibrinolysis in the CSF are important features of bacterial meningitis; the net effect on fibrin turnover may contribute to the development of brain infarction.

Adolescent↗
PubMed1998

Cobalt-57 and technetium-99m-HMPAO-labeled leukocytes for visualization of ischemic infarcts.

UNLABELLED: Previous studies have shown the usefulness of divalent cobalt isotopes to visualize cerebral damage after stroke. The site of accumulation of cobalt ion is unknown but may be explained by neuronal influx, analogous to that of calcium ion. Additionally, uptake may be due to infiltrating leukocytes or protein-bound cobalt. The aims of this study were to compare 57Co-SPECT with leukocyte SPECT and to compare the SPECT findings with clinical outcome as scored by the Orgogozo scale. MATERIALS: Ten patients with a CT scan positive for middle cerebral artery infarcts were included in the study (7 men, 3 women; mean age 70 yr). Technetium-99m leukocyte and cobalt-SPECT (interval 2-4 days) were made with a double-headed gamma camera, after the injection of 10-15 mCi 99mTc-HMPAO-labeled leukocytes and 0.4 mCi 57Co, respectively. Scans were performed within 5-30 days after onset of the first symptoms. Regions of interest (ROI) containing the area of infarction in the slices displaying enhanced radioactivity or the middle cerebral artery (MCA) region in four successive slices were defined for calculating enhancement ratios. The 99mTc leukocyte enhancement ratio (LER) and cobalt enhancement ratio (CER) were defined as the quotient of radioactivity in the ROI and an identical contralateral ROI. The MCA stroke-scale according to Orgogozo was used to assess neurological deficits at the time of scanning and discharge. RESULTS: Cobalt-57 and 99mTc-HMPAO showed uptake in the infarcted brain area in five patients; the quantitative uptake in the infarcted brain area of the two tracers correlated significantly (p < 0.05). Both the LER and the CER correlated significantly (p < 0.05) with the Orgogozo score at the time of scanning. Only the LER correlated significantly (p < 0.05) with the Orgogozo score at discharge. CONCLUSION: Uptake of cobalt and leukocytes in the peri-infarct tissue suggests that 57Co may visualize a component of the inflammatory response. Divalent 57Co may be convenient to predict clinical prognosis after stroke.

Aged↗
PubMed1989

Serum creatine kinase isoenzyme BB is a poor index to the size of various brain lesions.

We divided patients with brain lesions into three groups: (a) patients with primary or metastatic brain cancer, (b) brain infarctions, and (c) brain contusion(s). We analyzed each patient's sera for creatine kinase isoenzyme BB (CK-BB), using a monoclonal antibody kit (Impres-BB; International Immunoassay Laboratories). Computerized axial tomography (CAT) scans were performed on each patient. The size of the various lesions was measured from the CAT scan and recorded in milliliters. Total CK, CK-BB, and their ratios were compared with the volume of damaged brain tissue. We found no correlation between any of the variables and the various brain lesions. We attribute this lack of correlation to an intact blood-brain barrier, the rapid elimination or inactivation of CK-BB, or some combination of these factors.

Brain Concussion↗
PubMed2001

Clinically unidentified dissection of vertebral artery as a cause of cerebellar infarction.

BACKGROUND AND PURPOSE: Dissection of vertebral arteries has been reported in association with minor neck movements without signs of trauma on the surface of the neck. In addition, injury of a vertebral artery can cause brain infarctions. However, few cases have been reported in which fatal brain infarction was due to nonocclusive, clinically undetected, traumatic thrombus formation in a vertebral artery. CASE DESCRIPTION: A 62-year-old man was hit by a car, and a right cerebellar infarction was found the day after the accident. The cause of the infarction could not be detected by angiography. Although the patient recovered favorably after surgical removal of the right lateral hemisphere of the cerebellum, he died suddenly 2 weeks after the accident. An autopsy and a microscopic study revealed pulmonary thromboembolism and organizing traumatic lesions of the right vertebral artery without occlusion or noteworthy stenosis of the artery. CONCLUSIONS: We concluded that the patient sustained traumatic lesions of the right vertebral artery during the traffic accident 2 weeks before death and that his cerebellar infarction was due to a thrombus resulting from these traumatic lesions.

Accidents, Traffic↗
PubMed2004

Plasma amyloid beta, apolipoprotein E, lacunar infarcts, and white matter lesions.

Lacunar brain infarcts and cerebral white matter lesions are frequently observed on magnetic resonance imaging scans in elderly subjects. These lesions are also frequent in patient with cerebral amyloid angiopathy. We examined whether plasma amyloid beta peptide (Abeta) levels are associated with lacunar infarcts and white matter lesions in the general population, and whether the apolipoprotein E (APOE) genotype modifies these associations. We studied 1,077 participants within the population-based Rotterdam Scan Study, who were 60 to 90 years of age and free of dementia. Cross-sectional associations were analyzed by regression models with adjustments for age, sex, creatinine levels, and hypertension. In APOE epsilon4 carriers, plasma Abeta levels were positively associated with lacunar infarcts and white matter lesions, whereas in noncarriers no associations were observed. Per standard deviation increase in Abeta(1-40) and Abeta(1-42) levels the odds ratios for lacunar infarcts were 1.72 (95% confidence interval [CI] = 1.22-2.43) and 1.93 (95% CI = 1.31-2.85), the periventricular white matter lesion grade increased by 0.32 (95% CI = 0.08-0.57) and 0.29 (95% CI = 0.00-0.57), and the subcortical white matter lesion volume increased by 0.48 ml (95% CI = 0.04-0.91) and 0.24 ml (95% CI = -0.27-0.75). Higher Abeta levels are associated with more lacunar infarcts and white matter lesions in elderly subjects who carry an APOE epsilon4 allele.

Aged↗
PubMed2006

[Ischemic cerebral stroke in the young].

The authors of the review discuss etiological factors, pathogenesis, and diagnostic peculiarities of ischemic stroke in young patients (less than 45). Special attention is paid to the role of arterial hypertension, heart diseases, and blood pathology in ischemic stroke pathogenesis. The frequency of brain infarction grows due to meningovascular syphilis and drug abuse. Genetic aspects of ischemic stroke are discussed in detail. Brain infarction diagnostics is shown to require interdisciplinary approach, which provides early diagnosis, timely and appropriate therapy, favorable outcome, and prevention of recurrent ischemic strokes in young patients.

Adult↗
PubMed1988

[Experimental study of brain stem infarction in dogs--effect on BAEP, SSEP, blink reflex and EEG of perforator occlusion].

Assessment of the lesion in the brain stem by evoked potentials has not been well established. We have already developed a model of brain stem ischemia by occluding the perforators of the posterior cerebral arteries of the dog. The ischemic lesions locates mainly in the ventral side of the midbrain. Using this model, we assessed brain stem function by brain stem auditory evoked potential (BAEP), surface- and depth-recorded (in medial lemniscus) short latency somatosensory evoked potential (SSEP), blink reflex (BR) and electroencephalography (EEG), and investigated the correlation between the electrophysiological abnormalities and the lesion in the brain stem. The studies were performed for 6 hours after perforator occlusion. Furthermore, depth-recorded SSEP and regional cerebral blood flow (rCBF) were measured under induced hypotension by withdrawal of arterial blood. BAEP did not change in 13 of 16 animals. Surface-recorded SSEP remained unchanged in all 6 animals. The results are probably due to the fact that the lesion does not involve the auditory and somatosensory pathways and the accompanying events such as edema does not affect the both pathways. Depth-recorded SSEP remained unchanged after occlusion and did not disappear even when rCBF fell below 10 ml/100 g/min. It may be suggested that the threshold for electrical failure in the brain stem is much lower than that in the cortex. In BR, R1 did not change but ipsilateral R2 became nearly invisible immediately after perforator occlusion in all animals. The fact that the ischemic lesion did not involve the pons and disturbed reticular formation in the midbrain may probably account for the remaining of R1 and the disappearance of ipsilateral R2.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗