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PubMed1996

Complement activation in the central nervous system following blood-brain barrier damage in man.

The central nervous system (CNS) is virtually isolated from circulating immunological factors such as complement (C), an important mediator of humoral immunity and inflammation. In circulation, C is constantly inhibited to prevent attack on host cells. Since a host of diseases produce an abnormal blood-brain/cerebrospinal fluid (blood-brain/CSF) permeability allowing C protein extravasation, we investigated if C activation occurs in CSF in vitro and in CNS in vivo during subarachnoid hemorrhage (SAH) or brain infarction. After SAH (n = 15), the terminal complement complex (TCC) concentration on days 0 to 2 was higher in the CSF, 210 +/- 61 ng/ml, than in the plasma, 63 +/- 17 ng/ml, but null in the CSF of controls (n = 8) or patients with an ischemic stroke (n = 7). TCC was eliminated from the CSF after SAH (24 +/- 10 ng/ml on days 7 to 10). Incubation of normal human CSF with serum in vitro also activated the terminal C pathway. In 10 fatal ischemic brain infarctions, immunohistochemical techniques demonstrated neuronal fragment-associated deposition of C9 accompanied by neutrophil infiltration. We conclude that the C system becomes activated intrathecally in SAH and focally in the brain parenchyma in ischemic stroke. By promoting chemotaxis and vascular perturbation, C activation may instigate nonimmune inflammation and aggravate CNS damage in diseases associated with plasma extravasation.

Adult↗
PubMedDate not supplied

Cerebral thromboembolism among young women and men in Denmark 1977-1982.

In the period 1977-1982, the Danish National Patient Register recorded 1000 cases of cerebral thromboembolic attacks among women 15-44 years of age, and 971 cases among men of the same age. Cerebral infarction accounted for 70% of cases and transient ischemic attacks (TIA) for the remaining 30%. By analysing this material we found an average age-adjusted incidence rate of cerebral thromboembolism of 14.4/100.000 among men and 15.5/100.000 among women. The incidence rates rose rapidly with increasing age. Women aged 15-34 had significantly higher incidence rates of brain infarction and TIA compared to those of men of the same age. This was reversed in the age group 35-44. The magnitude of the ratio between the female and the male mean incidence rates by increasing age corresponded exactly to the age distribution of the use of oral contraceptives in Denmark. The relative risk for developing cerebral thromboembolism among users of oral contraceptives was estimated to be 3.2-6.5. The mortality in male patients with brain infarction was 3.3% and in females 1.7%. The mean duration of stay in hospital was 8.8 days for TIA and about 26 days for cerebral infarction. Sixteen percent of men and 13.6% of women had hypertension during their stay.

Adolescent↗
PubMed1997

[Modification of the surgical strategy based on intraoperative echographic findings of atherosclerotic ascending aorta].

To prevent the atheroembolic complications such as brain infarction due to the manipulation of atherosclerotic ascending aorta during cardiac surgery, the ascending aorta of 55 patients including 6 emergencies (mean age: 67.7 +/- 6.9 years, valvular disease: n = 12, ischemic heart disease only or combined with valvular disease: n = 43) were evaluated with intraoperative echography as a routine, to enable a proper placement of the cannulae, clamp etc. Irregular elevated lesions into the aortic lumen from the intima were identified in 7 patients (13%, mean age: 71.0 +/- 6.9 years) of ischemic heart disease, which included 2 emergent cases. Arch cannulation was employed in 3 patients with wide-spread lesions on the posterior wall and femoral cannulation was done in 1 patient with wide-spread lesions on the anterior wall. Two of these patients received CABG with in situ arterial conduits under ventricular fibrillation, and the other 2 patients received CABG with aortic cross clamping at the lesion-free site during proximal anastomosis of vein grafts (single clamp technique). Two patients with localized lesion were done CABG with partial aortic clamping and one of them had cerebral infarction during the operation. We recognized that manipulation of the ascending aorta has to be done with a meticulous care and well away from the diseased site. In another patient with localized lesion, the arch cannulation and the single clamp technique were used 2 cm away from that lesion. The brain infarcted patient completely recovered without any sequelae and the others also had no atheroembolic complications. Although calcified lesions on CT were correlated with atheromatous lesions on echogram (p = 0.004), these atheromatous plaques were not detected by enhanced CT, except in only one patient. For screening of the atherosclerosis of ascending aorta, the CT examination was not so effective and the intraoperative echography was the most sensitive and could be easily accomplished. In conclusion, in order to prevent the atheroembolism that might occur due to the improper manipulation of the diseased ascending aorta during usual procedures, surgical strategies have to be modified according to the position, extent and quality of the atherosclerotic lesions, diagnosed by intraoperative echoscanning of the aorta.

Aged↗
PubMed2001

S100B as a predictor of size and outcome of stroke after cardiac surgery.

BACKGROUND: Stroke after cardiac surgery is a clinical problem with often fatal or disabling outcome. To assess severity and probable outcome in affected patients only from clinical and radiological examinations is difficult. The glial-derived protein S100B has been suggested to be a marker of cerebral ischemia, and increased blood concentrations of S100B have been shown to correlate with size of lesion and prognosis after stroke. We studied the validity of S100B as a predictor of size of brain lesion and median term outcome in a consecutive group of patients suffering from stroke after cardiac surgery. METHODS: During a period of 17 months, 20 patients with clinical signs of postoperative stroke were investigated with S100B measurement, sampled at 5, 15 and 48 hours after surgery. All patients were examined with computed tomography or magnetic resonance imaging to confirm the diagnosis, and the size of cerebral infarction was estimated from the radiological examinations. The patients were followed up for survival 24 to 39 months after surgery. RESULTS: S100B concentration in blood 48 hours after surgery correlated with the size of infarcted brain tissue (r = 0.68, p < 0.001). Nine patients had S100B levels exceeding 0.5 microg/L and a 2-year mortality of 78%, whereas the 11 patients with S100B below 0.5 microg/L had a mortality of 18%. CONCLUSIONS: Increased S100B in patients with a stroke following cardiac surgery correlate with the size of infarcted brain tissue. High S100B levels 48 hours after surgery have a negative predictive value for median term survival.

Aged↗
PubMed2004

Antiepileptic drug treatment of nonconvulsive seizures induced by experimental focal brain ischemia.

Nonconvulsive seizures (NCSs) after traumatic and ischemic brain injury are often refractory to antiepileptic drug therapy and are associated with a decline in patient outcome. We recently characterized an in vivo rat model of focal brain ischemia-induced NCS and here sought to evaluate potential pharmacological treatments. Electroencephalographic activity was recorded continuously for 24 h in freely behaving rats subjected to permanent middle cerebral artery occlusion (MCAo). Rats were treated with an antiepileptic drug from one of seven different drug classes at ED(50) and 2x ED(50) doses (as reported in other rat seizure models), delivered as a single i.v. injection 20 min post-MCAo. Vehicle-treated rats (n = 9) had an 89% incidence of NCS with an average number of NCS of 8.6 +/- 1.9. The latency to onset of NCS was 32.5 +/- 3.4 min post-MCAo with an average duration of 49.1 +/- 8.2 s/event. The high doses of ethosuximide, gabapentin, fos-phenytoin, and valproate significantly reduced the incidence of NCS (11, 14, 14, and 38%, respectively), whereas midazolam, phenobarbital, and dextromethorphan had no significant effect at either dose. Across treatment groups, there was a low but significant correlation between the number of NCS events per animal and volume of brain infarction (r = 0.352). Antiepileptic drug therapy that prevented the occurrence of NCS also reduced mortality from 26 to 7%. Based on combined effects on NCS, infarction, neurological recovery, and mortality, ethosuximide and gabapentin were identified as having the best therapeutic profile.

Amines↗
PubMed2005

The effects of venous ischaemia on the subependymal and choroid plexus morphology in rat.

Morphological changes of ependyma, subependyma and choroids plexus regions were evaluated after experimental anastomotic venous occlusion in twenty male Sprague-Dawley rats. In this model, small burr holes were made over the anterior and posterior anastomotic veins and after precisely locating these vessels, bipolar coagulation and microscissors were used to perform permanent occlusion. Three days later, rats were sacrificed by perfusion and fixation and specimens were evaluated by histopathological techniques. Morphological changes of ependymal, subependymal and choroids plexus cells were evaluated in operated and intact hemispheres and revealed cell proliferation in the subventricular zone adjacent to the territory of venous occlusion in the operated hemisphere as well as midline shift, brain oedema, subcortical petechial haemorrhage, brain infarction and hemispheric swelling. In conclusion, following anterior (the vein of Throlard) and posterior (the vein of Labbé) anastomotic vein occlusion, cell proliferation can be seen in the choroids plexus, ependymal and subependymal regions in rats. We conclude that these morphological changes might be part of a self-repairing mechanism in the brain.

Animals↗
PubMed1987

Increased monoamine metabolite concentrations and cholinesterase activities in cerebrospinal fluid of patients with acute stroke.

Twenty-one patients with acute brain infarction, 8 with transient ischemic attack and 20 controls were investigated for lumbar cerebrospinal fluid (CSF) monoamine metabolites and cholinesterases. The diseased patients were lumbar punctured on 2 occasions, mean Days 1 (0-3) and 5 (3-9) after debut of symptoms. Monoamine concentrations were determined by reverse phase liquid chromatography with electrochemical detection and the cholinergic enzymes were measured photometrically. Increased concentrations of 3-methoxytyramine (3-MT), homovanillic acid (HVA), 5-hydroxyindoleacetic acid (5-HI-AA) and increased activity of acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE) in lumbar cerebrospinal fluid was found in patients with acute brain infarction when compared to control values, while the levels of 3-methoxy-4-hydroxyphenylglycol (MHPG) were not altered. No change of any neurotransmitter metabolite concentration/enzyme activity were found between Day 1 and Day 5 in the diseased patients. These data suggest an increased release of these neurotransmitter markers from necrotic brain areas into the cerebrospinal fluid and/or altered barriers between blood, brain and CSF and/or a dysfunction of the arachnoid villi to clear substances from the CSF. We therefore concluded that CSF neurotransmitters may be useful as specific brain markers in acute stroke.

Acute Disease↗
PubMed2006

Diagnostic accuracy of MRI for middle cerebral artery stenosis: a postmortem study.

BACKGROUND AND PURPOSE: Magnetic resonance imaging (MRI) has been widely applied in detecting intracranial large artery stenosis, but there have been few validation studies to compare with histopathology. The aim of the postmortem study is to assess the accuracy of MRI in identifying middle cerebral artery (MCA) stenosis. METHODS: We recruited, consecutively, Chinese postmortem autopsies in our hospital during 19 months. MRI was performed in the postmortem brains to scan the cross-sections of MCAs with barium expanding the artery lumen. The MCAs were then removed for histopathologic studies. With histopathology as a reference standard, the accuracy of MRI was evaluated, and the correlation between MCA stenosis identified by MRI and radiologically or histopathologically evident brain infarcts was investigated. RESULTS: Seventy-six consecutive autopsies were recruited. The sensitivity and specificity of MRI in detecting more than 30% MCA stenosis were 38.6% and 92.2%, with a positive predictive value of 87.2% and negative predictive value of 52.2%, and the corresponding values of MRI in identifying more than 50% MCA stenosis were 57.1%, 90.8%, 50%, and 83.0%, respectively. Both more than 30% and more than 50% MCA stenosis identified by MRI were found to be associated with infarctions in the corresponding MCA territory (P= 0.001, odds ratio = 4.365, 95% CI: 1.684-11.313; and P= 0.039, odds ratio = 2.694, 95% CI: 1.139-6.377). CONCLUSIONS: Our study demonstrates the agreement between ex vivo MRI and histopathology in identifying MCA stenosis, and the correlation between the MCA stenosis identified by MRI and radiologically or histopathologically evident brain infarcts.

Aged↗
PubMed1997

Mitral annulus calcification is not an independent risk factor for stroke: a cohort study of 657 patients.

All studies but one in the past have shown a strong relative risk of mitral annulus calcification for stroke, but the contribution of associated cardiac and vascular risk factors, especially carotid atheroma has not been appreciated. We studied the risk of stroke in selected patients with mitral annular calcification, adjusting for clinical, echocardiographic and therapeutic factors influencing stroke risk. Of 8,160 consecutive patients with echocardiograms, 657 with and 562 without mitral annulus calcification were followed for a mean of 2.4 years (range 1-6.6) to determine stroke risk by means of proportional hazards models with clinical, echocardiographic, and therapeutic variables that influence the risk of stroke. We also determined the association of mitral annulus calcification with subtypes of ischaemic brain lesions generally considered to be specific for an underlying cardioembolic cause. We therefore distinguished between territorial, small deep, and asymptomatic (silent) brain infarcts. Fifty-one patients with mitral annulus calcification and 27 controls had a stroke in the follow-up period. Mitral annulus calcification was not significantly associated with stroke in proportional hazards models (hazard ratio 0.76, 95% confidence interval 0.42-1.36, P = 0.3), or with any of the stroke subtypes, or with the presence of silent brain infarcts after adjustments for risk factors for generalized vascular disease Hypertension and carotid atheroma, with or without stenosis, ipsilateral or contralateral to the side of the stroke, were significantly associated with stroke in our patients. This study does not support the view that mitral annulus calcification is a risk factor for stroke. As others have found strong associations between mitral annulus calcification and cardiac and vascular risk factors for stroke, the increased risk of stroke in patients with mitral annulus calcification reported may be explained by these confounding risk factors. Therefore, in our opinion, mitral annulus calcification requires treatment of cardiovascular risk factors, but generally no specific measures such as surgery or oral anticoagulants are required to lower the risk of stroke.

Aged↗
PubMed1976

A general cardiovascular risk profile: the Framingham Study.

Persons at high risk of cardiovascular disease can be effectively identified from a measurement of their serum cholesterol and blood pressure, a smoking history, an electrocardiogram and a determination of glucose intolerance. One general function for identifying persons at high risk of cardiovascular disease is also effective in identifying persons at risk for each of the specific diseases, coronary heart disease, atherothrombotic brain infarction, hypertensive heart disease and intermittent claudication, even though the variables used have a different impact on each particular disease. The 10 percent of persons identified with use of this function as at highest risk accounted for about one fifth of the 8 year incidence of coronary heart disease and about one third of the 8 year incidence of atherothrombotic brain infarction, hypertensive heart disease and intermittent claudication. Hence the function provides an economic and efficient method of identifying persons at high cardiovascular risk who need preventive treatment and persons at low risk who need not be alarmed about one moderately elevated risk characteristic.

Adult↗
PubMed2004

Timing the valve replacement in infective endocarditis involving the brain.

Neurological complications are very frequent in patients with infective endocarditis (20-40 %). In these patients it is unclear at what time a valve replacement should be performed. In order to develop a data based recommendation we studied 12 patients of our own and analyzed 228 patients from the literature. We included patients with valve replacement after a neurological complication of endocarditis and documented the time between manifestation and operation and the outcome. Based on these 240 patients we calculated the risk of neurological deterioration after the valve replacement. After brain infarction this risk is 20% within three days, 20-50% between day 4 and 14, but declines to < 10% after 14 days and < 1% after 4 weeks. Valve replacement within the first four weeks after intracranial hemorrhage has been reported to be successful only in individual cases. The risk of deteriorating declines later to 15%. Based on these limited data we suggest that valve replacement in patients with brain infarction should be considered within the first 72 hours if they have severe heart failure, otherwise after four weeks. Only a few selected patients with intracranial hemorrhage and progressive heart failure might benefit from valve replacement within the first four weeks. For all other neurological complications there are no reliable data. We propose a structured approach depending on cardiac and neurological complications and the time course of the disease.

Adult↗
PubMedDate not supplied

[Infection and tissue ischemia: role of cellular rheology].

It is not clear how acute infection is associated with a subsequent ischaemic brain infarction. Infection may, indeed, cause changes in blood fluidity. Abnormalities in blood flow, particularly in white blood cell rheology, are known to be precipitating factors for ischaemic events. Therefore, the rheological behaviour of the erythrocytes and of the main leucocyte subpopulations (granulocytes = G; mononuclear cells = MNL) were studied in 29 patients 30 days after the onset of acute bacterial infections. A group of 49 controls (matched for sex, body mass index and cardiovascular risk factors) was also evaluated. A significant impairment in the flow properties of the mononuclear leucocyte subpopulation was found in the patients as compared to control. These results indicate that disturbances in leucocyte rheology might be considered an additional risk factor for ischaemic brain infarction when this occurs shortly after febrile infection.

Aged↗
PubMed1996

[The prognostic value of analytical hemorheological factors in stroke].

Plasmatic hyperviscosity is a known vascular risk factor which depends, among other parameters, upon total proteins, haematocrit value and fibrinogen. The aim of this study was to determine the relationship between these analytical haemorrological parameters and mortality and acute stroke sickness rate. We studied 216 patients with brain infarct and spontaneous intracerebral haemorrhage out of a sample of 256 acute stroke patients. We evaluated neurological affectation using the Canadian scale upon admission, on the seventh day and after three months. We determined plasmatic haemorrological factors (haematocrit, fibrinogen and total proteins) upon admission and again after one week and then at three months High fibrinogen levels in plasma were related to brain infarct mortality regardless of the cause of death.

Adult↗
PubMed1997

Predisposing factors to enlargement of spontaneous intracerebral hematoma.

BACKGROUND AND PURPOSE: Enlargement of intracerebral hemorrhage is a major cause of clinical deterioration. Identification of factors that predispose to hematoma enlargement is important in managing patients. METHODS: We selected 186 patients (71 women and 115 men; mean age, 64.8 +/- 12.5 years) with spontaneous intracerebral hemorrhage who had undergone an initial CT within 24 hours and a second scan within 120 hours of symptom onset. We compared patients with (n = 41) and without (n = 145) hematoma enlargement according to clinical characteristics and laboratory data. RESULTS: By multiple logistic regression analysis (n = 139), interaction of long interval (> 6 hours) from onset to first CT and small hematoma (< 25 cm3) strongly reduced risk of enlargement. The analysis also demonstrated that the following factors independently predisposed to enlargement: history of brain infarction; liver disease; interaction of fasting plasma glucose > or = 141 mg/dL and systolic blood pressure on admission > or = 200 mm Hg; and interaction of glycosylated hemoglobin A1c > or = 5.1% and systolic blood pressure on admission > or = 200 mm Hg. CONCLUSIONS: A patient examined > 6 hours after ictus who has a hematoma volume < 25 cm3 is unlikely to experience further hematoma growth. Prevention of brain infarction and premorbid management of liver disease may serve to lower the risk of hematoma enlargement. Although it remains controversial whether antihypertensive drugs should be used in the acute phase of intracerebral hemorrhage, poorly controlled diabetics with high systolic blood pressure (> or = 200 mm Hg) on admission also were at high risk of hematoma enlargement.

Aged↗
PubMed2004

Microembolic signals detected by transcranial Doppler sonography during carotid endarterectomy and correlation with serial diffusion-weighted imaging.

BACKGROUND AND PURPOSE: Embolic events are a major cause for procedure-related strokes after carotid endarterectomy (CEA). Transcranial Doppler sonography can reveal embolic events as microembolic signals (MES) during CEA. MES during declamping and shunting are frequently detected. MES during shunting are rare and known to be correlated with the neurological outcome of the patient. In the present study, we analyzed the occurrence of MES within different stages of CEA and whether MES within those stages were correlated with cerebral ischemia, as detected by diffusion-weighted imaging (DWI), and brain infarction, as detected by contrast-enhanced MRI. METHODS: Thirty-three patients were monitored intraoperatively for MES using transcranial Doppler sonography. DWI was performed within 24 hours before and after surgery. Positive postoperative DWI led to reexamination with contrast-enhanced T1-MRI 7 to 10 days after CEA for detection of cerebral infarction. RESULTS: MES were detected in 32 of 33 patients. The highest number of MES was found during shunting and declamping. A significant correlation was found between MES and DWI-lesions during dissection. A significant correlation was found between MES during dissection and shunting, and nonsignificant correlation was found between MES and the occurrence of cerebral infarction. CONCLUSIONS: MES could be regularly detected during CEA. Dissection and shunting seem to be the most vulnerable stages of the procedure.

Aged↗
PubMed2006

Obstacles to organ donation in Swedish intensive care units.

OBJECTIVE: To identify obstacles to organ donation in Swedish intensive care units. DESIGN: A survey exploring attitudes and experiences of organ donation activities was sent to half of all anaesthetists and all neurosurgeons in Sweden (n=644). Total response rate was 67%; 69% from the anaesthetists and 54% from the neurosurgeons. RESULTS: Neurosurgeons had more experiences of caring for potential donors and requesting donation than anaesthetists. Twenty-seven percent of the anaesthetists were not confident with clinical neurological criteria for brain incarceration. Nine per cent found donation activities solely burdensome, and 14% wanted an external team to take over the donation request. A quarter regarded the request definitely as an extra load on the family, and more than half of the respondents had refrained from asking in emotionally strained situations. Forty-nine per cent had a neutral approach to relatives when requesting donation while 38% had a pro-donation approach. Thirty-six per cent terminated ventilator treatment for a potential donor without waiting for total brain infarction. Lack of resources in the ICUs resulted in not identifying a possible donor according to 29% of respondents. Knowing the prior wish of the deceased was regarded as the single most important factor that facilitated the work with organ donation for the intensivists. CONCLUSIONS: The identified obstacles (neutral approach of donation request, ethical problems concerning the potential donor and the relatives, varying competence in diagnosing total brain infarction, and lack of intensive care bed resources) require tailored efforts in order to increase organ donation. Checking these factors can be used as a quality control when analysing donation activities at hospitals.

Adult↗
PubMed1996

Computerised tomography findings as a risk factor in carotid endarterectomy: early and late results.

OBJECTIVES: To evaluate whether preoperative CT evidence of brain infarction is associated with an increased risk of early and late stroke and death in patients undergoing CEA. DESIGN: Retrospective clinical study. MATERIALS AND METHODS: We evaluated 844 CT scanning records from 893 patients undergoing CEA from 1986-1994: 43% (367) CT positive for cerebral infarction and 57% (477) negative. Univariate and multivariate analysis was performed for risk factors and preoperative symptoms in patients with positive and negative CT scans, and Kaplan Meier survival curves for late events. RESULTS: A positive CT was significantly more frequent in males vs. females (p < 0.0001; O.R. 2.52; C.I. 1.73-3.73), diabetics vs. non-diabetics (p = 0.03; O.R. 1.52; C.I. 1.03-2.26), symptomatics vs. asymptomatics (p < 0.001; O.R. 2; C.I. 1.93-3.53) and contralateral occlusion vs. patency (p < 0.001; O.R. 2; C.I. 1.30-3.10). The perioperative disabling stroke/ death rate was higher in patients with a positive CT (p = 0.002; O.R. 6.27; C.I. 1.73-34.20); in asymptomatic patients this difference was striking (5 patients vs. O, p = 0.0002). Multiple logistic regression analysis for risk factors, CT findings, symptoms preceding surgery, and congruity of brain infarction confirmed a significantly higher incidence of perioperative stroke/death rate (p = 0.003; O.R. 6.37; C.I. 5.12-7.63) and early and late stroke (p = 0.02; O.R. 1.95; C.I. 1.38-2.53) and death (p = 0.0005; O.R. 2.38; C.I. 1.89-2.88) in patients with brain lesions. After 7 years, the survival rate (p = 0.0009) and stroke-free interval (p = 0.003) were lower in patients with a positive CT. After 5 years, in asymptomatic patients the survival rate (p = 0.003) and stroke-free interval (p = 0.01) were lower in the positive CT group. CONCLUSIONS: A positive CT finding, regardless of congruity of the lesion, should be regarded as an indicator of an increased risk of stroke and death in patients scheduled for carotid surgery, especially in those with asymptomatic stenosis.

Adult↗
PubMed1999

[Usefulness of current and retrospective markers of glycemia for early prognostication of ischemic stroke in diabetics and non-diabetics].

Diabetes mellitus is associated with an increased incidence of ischaemic stroke but it is not established whether it may exacerbate its clinical course and prognosis. In the study we have assessed relations of fasting (1st-2nd day of illness) and pre-stroke glycaemia (measured as HbA1 and FA) with recent clinical manifestation and outcome within one month in 22 diabetics and 37 non-diabetics with ischaemic brain infarction in the internal carotid territory. Merely enhanced HbA1 in the majority of non-diabetic stroke patients confirmed impaired pre-stroke glucose tolerance but did not influence severity of hemiparesis and further prognosis. Abnormally high both HbA1 and dFA in diabetics, reflecting non-sufficient metabolic control of illness did not exacerbate acute manifestation of stroke and outcome. Fasting post-stroke glycaemia that expresses a stress response of brain origin was determinative for clinical state but not for one-month prognosis in diabetics and non-diabetics with brain infarction.

Aged↗