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PubMed2002

Association between influenza vaccination and reduced risk of brain infarction.

BACKGROUND AND PURPOSE: Because infections subsequent to influenza may play a role in promoting the complications of atherosclerotic disease and may also induce hypercoagulation, we hypothesized that influenza vaccination may protect against brain infarction. METHODS: During the influenza epidemic period we studied 270 subjects, including 90 consecutive patients older than 60 years admitted to the hospital for brain infarction and 180 population-based controls, matched for age, sex, and district of residency in Paris. We conducted a structured interview on whether they had been vaccinated during the last influenza vaccination campaign or every year during the 5 last years. RESULTS: We found significantly fewer vaccinated subjects during the last vaccination campaign among patients with brain infarction than among controls (46.7% versus 59.4%; P=0.036) and fewer patients vaccinated every year during the last 5 years (41.1% versus 56.1%; P=0.017). After adjustment for age, traditional risk factors, and recent use of antibiotics, the risk of stroke was reduced in the subjects vaccinated during the year of the study and in those vaccinated during the last 5 years, with an odds ratio of 0.50 (95% CI, 0.26 to 0.94; P=0.033) and 0.42 (95% CI, 0.21 to 0.81; P=0.009), respectively. Similar associations were observed in cases and controls free of previous cardiovascular history. Subjects younger than 75 years and subjects free of risk factors or in high social class were significantly less often vaccinated than controls. CONCLUSIONS: Influenza vaccination may protect against brain infarction by reducing infections or may identify a subgroup of patients at low risk for stroke because of a better lifestyle. These results give rise to a new hypothesis for research into stroke prevention.

Aged↗
PubMed1993

Histologic assessment of the age of recent brain infarcts in man.

In order to design a dating system based on the microscopic picture of brain infarcts of recent onset, we performed the histological examination of 31 infarcts covering the first 4 weeks of evolution in 30 autopsy cases. The date of the cerebral vascular accident was clinically established in every case. There were 13 men and 17 women with a mean age of 65 years. Hemorrhagic infarcts were found in 15 cases and anemic infarcts in 16 cases. Based on the histological features four periods were identified: the first period, from day 1 through day 4, was characterized by the predominance of eosinophilic neurons and necrotic oligodendrocytes; the second period, from day 5 through day 7, differed from the first by the appearance of macrophages and of newly formed blood vessels; the third period, from day 8 through day 14, showed neuronal ghosts, macrophages, astrocytic proliferation, gemistocytes, and absence of neutrophils; and in the fourth period, from day 15 through day 27, there were no eosinophilic neurons, and neither necrotic oligodendrocytes nor myelin in the central portion of the infarct were identified. By assessing the histological features and accurately correlating the findings with the corresponding clinical data, we have been able to describe four distinct microscopic patterns of the first month of evolution of brain infarcts. The present findings may be considered useful morphological clues to better characterize the early evolutional phase of brain infarcts in humans.

Aged↗
PubMed1996

Precipitants of brain infarction. Roles of preceding infection/inflammation and recent psychological stress.

BACKGROUND AND PURPOSE: Antecedent febrile infection and psychological stress are described as predisposing risk factors for brain infarction. We examined the temporal relationship between preceding infection/inflammation and stroke onset as well as the role of recent psychological stress as a potential precipitant for brain infarction. METHODS: In this case-control study, a standardized evaluation including a signs/symptoms-based questionnaire was used to characterize the prevalence and timing of recent prior (< 1 month) infectious and inflammatory syndromes in 37 adults with acute brain infarction, 47 community control subjects, and 34 hospitalized nonstroke neurological patient controls. Recent psychological stress was measured with scales of stressful life events and negative affect. RESULTS: The prevalence of infection/inflammation was significantly higher in the stroke group only within the preceding 1 week compared with either community control subjects (13/37 versus 6/47, P < .02) or hospitalized neurological patient controls (3/34, P < .02). Upper respiratory tract infections constituted the most common type of infection. A substantial proportion of stroke patients with preceding (< 1 week) infection/inflammation (5/13) had no accompanying fever or chills. There were no significant differences between the stroke and control groups in the levels of stressful life events within the prior 1 month or in negative-affect scale scores within the prior 1 week. CONCLUSIONS: Our data suggest that both febrile and nonfebrile infectious/inflammatory syndromes may be a common predisposing risk factor for brain infarction and that the period of increased risk is confined within a brief temporal window of less than 1 week. Results of this study argue against a role for recent psychological stress as a precipitant for cerebral infarction.

Acute Disease↗
PubMed1992

Human brain infarction: proton MR spectroscopy.

Two-dimensional proton magnetic resonance (MR) spectroscopic imaging studies were performed of the distributions of the major hydrogen-1 metabolites of choline, creatine, N-acetyl aspartate (NAA) and lactate in normal (n = 6) and subacutely to chronically infarcted (n = 10) human brain. The two dimensions of phase encoding were applied over a 20-mm-thick section of brain tissue that had been selected with a double spin-echo localization method. Normal brain showed bilaterally symmetric metabolite distributions and no detectable lactate. Nine of 10 studies of brain infarction showed substantial decreases in NAA, creatine, and choline in the infarcted area compared with control areas; averaged for all studies, the decreases were 77% +/- 8, 63% +/- 11, and 54% +/- 12, respectively (mean +/- standard error). The decreased metabolite concentrations are probably due primarily to diminished cell density in the infarct. The decrease in NAA was larger than the decreases in choline and creatine. Findings in all of the studies showed lactate in the infarcted tissue and/or ventricles. The continued presence of lactate in the infarct indicates increased anaerobic glycolysis due to ischemia or other factors.

Adult↗
PubMed2000

Neuronal death in brain infarcts in man.

The mechanism of neuronal death in brain ischaemia remains unclear. Morphology, terminal transferase-mediated dUTP-digoxigenin nick end-labelling (TUNEL) and immunohistochemistry for the pro-apoptotic enzyme caspase-3 (CASP3), for its substrates poly(ADP-ribose) polymerase (PARP) and the DNA-dependent protein kinase catalytic subunit (DNA-PKCS) and for poly(ADP-ribose) (PAR), an end-product of PARP activity, were used to investigate neuronal death in brain infarcts from 15 men and 20 women, aged 46-95 years. The infarcts varied in age from 18 h to several months. Neuronal death was characterized morphologically by cell shrinkage, cytoplasmic hypereosinophilia and moderate nuclear pyknosis with later chromatin dispersal and disintegration, but not features of apoptosis. Occasional apoptotic bodies were seen but these appeared to be related to inflammatory cells, endothelial cells and occasional glia, including satellite cells. Neurones within infarcts showed strong nuclear and cytoplasmic labelling for CASP3 during the first 2 days after infarction. Neuronal DNA-PKCS, PARP and poly(ADP-ribose) immunoreactivity was demonstrable in scattered neurones in and adjacent to infarcts for 18-24 h but thereafter declined to below detectable levels in most cases. TUNEL labelled cells towards the edge of the infarcts, particularly at 2-4 days, but most of the labelling could be prevented by preincubation of the sections in diethyl pyrocarbonate to inactivate endogenous nucleases. Between 3 days and 3 weeks, CASP3 and DNA-PKCS were detected in proliferating capillaries and CASP3, PARP and poly(ADP-ribose) in infiltrating macrophages. Our findings indicate that neuronal death in human brain infarcts has some of the early biochemical features of programmed cell death, with upregulation of CASP3 and rapid disappearance of DNA-PKCS and PARP. However, the morphological changes are not those of apoptosis, the DNA cleavage occurs relatively late, and some of the TUNEL is probably mediated by the release of endogenous endonucleases during protease or microwave pretreatment of the damaged tissue.

Adult↗
PubMed1988

Neovasculature and blood-brain barrier in ischemic brain infarct.

The cellular events occurring in ischemic brain infarcts of 1 day to 8 weeks duration were investigated. The material consisted of 17 human postmortem brains with anemic infarcts caused by occlusive vascular diseases. Using antiserum against human plasma albumin as a marker for the breakdown of blood-brain barrier and ammoniacal silver nitrate stain to demonstrate the vasculature, the onset and distribution of the extravasated plasma protein was compared with histological changes in the blood vessels. It was observed that extravasation occurred in several separate regions of the infarct during different time periods. During the first few days, plasma proteins exudated from the vessels located at the marginal zone surrounding the infarct. This was followed by a prolonged phase of intense extravasation that coincided with the production of new capillaries originating from the blood vessels at the margin of the infarct and from pial vessels. It is postulated that the actively proliferative and migratory activities of the endothelial cells and pericytes in the neovasculature may be responsible for the extravasation which is reflected in the contrast enhancement of the infarct observed clinically during the recovery phase.

Blood-Brain Barrier↗
PubMed1988

Three-year follow-up of risk factors correlated with new atherothrombotic brain infarction in 708 elderly patients.

A prospective study correlated cigarette smoking, systolic or diastolic hypertension, diabetes mellitus, hypercholesterolemia, low serum high-density lipoprotein cholesterol, hypertriglyceridemia, and obesity with development of new atherothrombotic brain infarction in 192 elderly men and 516 elderly women. Mean follow-up was 36 +/- 6 months (range 19-39). New atherothrombotic brain infarction occurred in 24 of 192 men (13%) and in 63 of 516 women (12%), difference not significant. Risk factors for atherothrombotic brain infarction in elderly men were cigarette smoking (p less than 0.001), systolic or diastolic hypertension (p less than 0.001), and diabetes mellitus (p less than 0.005). Risk factors for atherothrombotic brain infarction in elderly women were systolic or diastolic hypertension (p less than 0.001), diabetes mellitus (p less than 0.001), and obesity (p less than 0.005).

Aged↗
PubMedDate not supplied

Clozapine for blepharospasm, obsessive-compulsive symptoms, and psychotic symptoms in a patient of old brain infarction.

Blepharospasm, psychotic symptoms, and obsessive-compulsive symptoms can result from brain infarction. However, a presentation of these 3 symptoms simultaneously is rare. This report describes a 65-year-old woman who had old brain infarction and presented with these 3 symptoms for 2 years. The patient recovered after receiving a regimen of clozapine 125 mg/d for 3 months. No recurrences of symptoms were noted during a 6-month follow-up. This is the first case report demonstrating that clozapine is effective for a patient with blepharospasm, obsessive-compulsive symptoms, and psychotic symptoms presenting simultaneously. This report also reminds physicians of the possible organic causes of unusual presentations in elderly patients.

Aged↗
PubMed2004

Peak plasma interleukin-6 and other peripheral markers of inflammation in the first week of ischaemic stroke correlate with brain infarct volume, stroke severity and long-term outcome.

BACKGROUND: Cerebral ischaemia initiates an inflammatory response in the brain and periphery. We assessed the relationship between peak values of plasma interleukin-6 (IL-6) in the first week after ischaemic stroke, with measures of stroke severity and outcome. METHODS: Thirty-seven patients with ischaemic stroke were prospectively recruited. Plasma IL-6, and other markers of peripheral inflammation, were measured at pre-determined timepoints in the first week after stroke onset. Primary analyses were the association between peak plasma IL-6 concentration with both modified Rankin score (mRS) at 3 months and computed tomography (CT) brain infarct volume. RESULTS: Peak plasma IL-6 concentration correlated significantly (p < 0.001) with CT brain infarct volume (r = 0.75) and mRS at 3 months (r = 0.72). It correlated similarly with clinical outcome at 12 months or stroke severity. Strong associations were also noted between either peak plasma C-reactive protein (CRP) concentration or white blood cell (WBC) count, and all outcome measures. CONCLUSIONS: These data provide evidence that the magnitude of the peripheral inflammatory response is related to the severity of acute ischaemic stroke, and clinical outcome.

Aged↗
PubMed2000

Deep white matter lesions on MRI, and not silent brain infarcts are related to headache and dizziness of non-specific cause in non-stroke Japanese subjects.

OBJECTIVE: Silent or asymptomatic cerebrovascular disease is believed to be an important risk factor for symptomatic stroke and vascular dementia. Although non-specific complaints such as mild to moderate headache and/or dizziness may also be caused by silent stroke, which remains a topic of controversy. METHODS: To investigate the relationship between silent brain infarcts and non-specific complaints, we assessed findings on magnetic resonance images using a common protocol in the following three groups of subjects; Group 1:78 subjects with non-specific complaints, Group 2:47 subjects with vascular risk factors, and Group 3:75 normal subjects without any subjective complaints or vascular risk factors. In addition to silent stroke, deep white matter lesions on MRI were also evaluated. All subjects were recruited from 12 institutes of the study group located at various parts of Japan. RESULTS: Silent brain infarcts were demonstrated in 44%, 43%, and 20% of subjects in Groups 1, 2, and 3, respectively. In Group 1, the average number of infarcts per individual who had silent brain infarction was 1.8, which was significantly fewer than 3.8 in Group 2 or 3.5 in Group 3 (p<0.0167). White matter lesions were found in 68%, 49%, and 11% in Groups 1, 2, and 3, respectively, indicating that non-specific complaints are more closely related to deep white matter lesions than to silent infarct lesions. Such white matter lesions were found more frequently in subjects with depressive state than in non-depressed subjects (67% vs. 39%, p=0.0155). CONCLUSION: The present results suggest that deep white matter lesions, rather than silent brain infarcts, appear to be important in producing headache and/or dizziness of non-specific cause and also to be related to the depressive state.

Aged↗
PubMed1994

Isolated hemiataxia after supratentorial brain infarction.

Acute isolated hemiataxia is in most cases due to infratentorial (cerebellar) stroke. It has only twice been described in supratentorial stroke--namely, after thalamic infarction and a capsular haemorrhage. Three patients with isolated hemiataxia after a supratentorial brain infarct are described. These patients were seen in a period of five years during which 899 patients with a first supratentorial brain infarct were registered. Clinically the hemiataxia was of the cerebellar type. In two patients, CT and MRI showed a small, deep (lacunar) infarct restricted to the posterior limb of the internal capsule, a site not previously reported in isolated hemiataxia. The third patient had a small, deep (lacunar) infarct in the thalamus extending into the adjacent posterior limb of the internal capsule. Isolated hemiataxia after a supratentorial brain infarct is a very rare clinical stroke syndrome. The cerebellar type hemiataxia was most likely caused by interruption of the cerebellar pathways at the level of the internal capsule. Our cases confirm prior observations that the cerebellar pathways run through the posterior part of the posterior limb of the internal capsule separately from the motor and sensory pathways.

Acute Disease↗
PubMed1978

Does ethanol intoxication promote brain infarction in young adults?

76 consecutive patients aged under 40 with ischaemic brain infarction verified by carotid angiography and/or serial brain scanning were studied. In at least 15 cases (20%) the onset of symptoms was preceded within 24 hours by a bout of alcohol drinking. Ethanol-related cases comprised 40%, 25%, and 13% of the patients in the age-groups 16-19, 20-29, and 30-39 years, respectively. Ethanol intoxication preceding the stroke was 2-3 times as common in male and 3-4 times as common in female patients as ethanol intoxication in the general Finnish population of the same ages and sex. Occasional ethanol intoxication seems to carry an increased risk of ischaemic brain infarction in young adults.

Adolescent↗
PubMed1997

Early CCT signs of supratentorial brain infarction: clinico-radiological correlations.

Early signs of brain infarction can be detected by modern CCT technology even within the first 6 h after stroke. Little is known about the prognostic significance of early infarction signs in CCT. We prospectively evaluated clinical and CCT findings of 95 consecutive patients with an acute ischemia in the territory of the middle cerebral artery. All patients were admitted to our stroke unit within 6 h after stroke. In 55 patients CCT was performed within 3 h, and in 40 cases between 3 and 6 h. In all patients the clinical findings were assessed by the Scandinavian Stroke Scale (SSS). The disability due to stroke was evaluated after 4 weeks by use of the modified Rankin Scale. We could demonstrate the following early signs of cerebral infarction: focal hypodensity (23.2%), obscuration of basal ganglia (12.6%), focal brain swelling (22.1%), hyperdense middle cerebral artery sign (HMCA; 11.5%). In 3 patients early edema led to ventricular compression, in 1 patient to midline shift. The occurrence of early infarction signs did not depend on the etiology of ischemia but was significantly associated with a severe neurological deficit at admission and an unfavourable disability status 4 weeks after stroke. Focal brain swelling and HMCA were often followed by extensive infarction lesions on the follow-up CCT. In conclusion, early signs of hemispheric brain infarction visible on CCT scans performed within 6 h after stroke are correlated with severe stroke and an unfavourable functional outcome. However, a substantial part of our patients had a benign course of the disease in spite of early CCT pathology. Decisions on therapy in individual patients therefore should not depend on early CCT findings exclusively.

Acute Disease↗
PubMed2006

[High b-value diffusion-weighted imaging of acute brain infarction].

High b-value diffusion-weighted (DW) imaging obtained with a b-value of 2,000 s/mm2 offers theoretical advantages over DW imaging obtained with a b-value of 1,000 s/mm2 for detection of acute brain infarction. The purpose of this study was to determine whether high b-value DW images (b=2,000) are better than b=1,000 images for detection of diffusion change in patients with acute brain infarction. We compared diffusion-weighted (DW) images obtained with a b-value of 1,000 s/mm2 with those obtained with a b-value of 2,000 s/mm2 in 84 patients with small lesions (brain stem infarction, lacuna infarction) examined within 24 hours of clinical onset. Qualitative analysis was performed concerning lesion conspicuity. In quantitative analysis, contrast ratios (CR) were measured and findings of b=1,000 and b=2,000 images were compared. False-negative rate of b=1,000 and b=2,000 images were 23.8% and 3.6%, respectively, relative to the presense or absense of infarction on the follow-up MR or CT images. On qualitative analysis, lesions were more conspicuous on b=2,000 images. On quantitative analysis, as the b-value increased, mean CR increased. DW images aquired with a b-value of 2,000 s/mm2 were better than DW images aquired with a b-value of 1,000 s/mm2 for detection of diffusion change in patients with acute brain infarction.

Acute Disease↗
PubMed1998

Cerebral blood flow and metabolism in patients with silent brain infarction: occult misery perfusion in the cerebral cortex.

OBJECTIVES: Silent brain infarction (SBI) is of growing interest as a possible risk factor for symptomatic stroke. Although morphological characteristics of SBI have been well defined, their characteristic patterns of cerebral blood flow (CBF) and metabolism are in dispute. The purpose of this study was to elucidate CBF and metabolism in patients with SBI in relation to symptomatic stroke. METHODS: The patients underwent PET and were separated into three groups; control group (C group), with no lesions on CT (n=9, mean age 57), SBI group, with no neurological signs or history of stroke, but with ischaemic lesions on CT (n=9, mean age 63), and brain infarction group (BI group), with neurological deficits and compatible CT lesions in the area supplied by perforating arteries (n=19, mean age 56). Regional CBF, oxygen extraction fraction (OEF), cerebral metabolic rate for oxygen (CMRO2), and cerebral blood volume (CBV) were measured by PET. RESULTS: Mean values for CBF to the cerebral cortex and deep grey matter were lower in the SBI group (31.6 (SD 5.8) and 34.3 (SD 6.9) ml/100 g/min, respectively) and in the BI group (30.8 (SD 5.2), 33.9 (SD 5.9), respectively) than in the C group (36.0 (SD 6.6) and 43.5 (SD 9.5), respectively). Although mean CMRO2 of deep grey matter (2.36 (SD 0.52) ml/100 g/min) was significantly decreased in the SBI group compared with the C group (2.76 (SD 0.480), p<0.01), CMRO2 of the cortical area was as well preserved in the SBI patients (2.36 (SD 0.39)) as in the controls (2.48 (SD 0.32)) with a compensatory increase of mean OEF (0.45 (SD 0.06) and 0.41 (SD 0.05), respectively). CONCLUSIONS: Patients with SBI showed decreased CBF and CMRO2 in deep grey matter. On the other hand, decreased CBF with milder increased OEF, resulting in preserved CMRO2 in the cerebral cortex indicates the presence of occult misery perfusion, suggesting that patients with SBI have reduced cerebral perfusional reserves.

Adult↗
PubMed2002

The 2-oxopyrrolidinacetamide piracetam reduces infarct brain volume induced by permanent middle cerebral artery occlusion in male rats.

In this study, the temporal development of focal cerebral infarction induced by permanent middle cerebral artery occlusion (pMCAO) and the effects of piracetam, a derivative of gamma-aminobutyric acid widely used in clinical practice as a nootropic agent, on infarct area and volume were investigated. pMCAO caused a cerebral infarct whose size progressively increased after 3, 6, 9, and 24 h. Piracetam (125 mg/kg i.p.), administered 6, 9, and 22 h after pMCAO, did not reduce pMCAO-induced brain infarct area size detected at the 24th hour. By contrast, when this agent was administered at the doses of 250 and 500 mg/kg, it caused a marked reduction of the infarct area size. This reduction was observed in almost every brain slice affected by pMCAO, although statistical differences (p <0.05) were detected in slices located at 3-5.5 mm posterior to the anterior pole in animals treated with 250 mg/kg piracetam and in slices located at 3.5-5 mm in those receiving 500 mg/kg. When the mean total volumes of brain infarct resulting from pMCAO were calculated, it was observed that in animals which had received piracetam (250 or 500 mg/kg) infarction volume was markedly ( approximately 50%) and significantly (p <0.05) reduced in comparison with saline injected rats. Finally, piracetam (250 mg/kg administered i.p. 6, 9, and 22 h after the ischemic insult) significantly reduced brain infarct area evaluated 48 h and 7 days after pMCAO.

Animals↗
PubMed2002

Brain infarction after percutaneous implantation of port-catheter system via the left subclavian artery.

The aim of this study was to evaluate the incidence of brain infarction after percutaneous implantation of a port-catheter system via the left subclavian artery for hepatic arterial infusion chemotherapy. In 90 patients with inoperable liver cancer, a port-catheter system was implanted via the left subclavian artery. In 5 patients (5.6%) brain infarction occurred after port-catheter implantation. In one patient (1.1%) thrombi formed around the catheter, as confirmed by autopsy. The risk of brain infarction should be taken into consideration when a trans-left subclavian arterial access route is used for the percutaneous implantation of a port-catheter system for hepatic arterial infusion chemotherapy.

Adult↗
PubMed1992

T1 in subacute and chronic brain infarctions. Time-dependent development.

RATIONALE AND OBJECTIVES: Time-dependent behavior of T1 in brain infarcts and in brain tissue of the contralateral hemisphere was studied in the subacute and early chronic stages of stroke. METHODS: T1 was measured from magnetic resonance images (MRIs) of 29 patients as a function of infarct location and age. Another group of 11 patients was studied with consecutive MRI studies during the first 5 weeks after the onset of infarct, and the distribution of T1 in the infarctions was analyzed from T1 maps using a histographic method. RESULTS: During the first 2 months after a stroke, T1 was longer in the infarcted gray matter than in the infarcted white matter (P = .002), and prolonged linearly in both. The histographic analysis showed a component arising from tissue breakdown products that could be identified for up to 5 weeks. A transient lengthening in T1 of the contralateral hemisphere, reaching a maximum at 3 weeks, also was observed. CONCLUSIONS: These characteristics of recent infarctions differentiate them from older, gliotic lesions. The lengthening of T1 in the contralateral hemisphere may reflect remote flow and metabolic effects of brain infarctions.

Acute Disease↗