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PubMed2006

Comparison of erythrocyte aggregability changes during ischemic and hemorrhagic stroke.

The aim of this work was to perform a comparative investigation of erythrocyte aggregability changes in the peripheral and cerebral circulation during ischemic and hemorrhagic stroke. Subjects of the present study were patients with ischemic brain infarcts (14 patients) and with hemorrhagic stroke (21 patients) from the Intensive Care Unit of the Institute of Neurology and Neurosurgery. The blood samples were obtained from the following blood vessels: the common carotid artery carrying blood to the primarily damaged brain hemisphere, both jugular veins carrying blood from the primarily damaged and the contralateral hemispheres, as well as from the cubital vein to obtain specimens of the systemically circulating blood. Erythrocyte aggregation was evaluated by using the "Georgian technique". We found that the RBC aggregation indices increased in both the regional as well as the systemic circulation of the hemorrhagic stroke patients as compared to ischemic stroke patients. The results of the present study demonstrate different changes of erythrocyte aggregation in ischemic and hemorrhagic stroke patients. Therefore, the role of blood rheological properties in their pathogenesis seems also to be different.

Brain Ischemia↗
PubMed1983

Serial nuclear magnetic resonance (NMR) imaging in patients with cerebral infarction.

Seven patients with supratentorial infarction were studied by means of serial nuclear magnetic resonance imaging using saturation recovery (SR) and proton density (PD) sequences. The earliest changes were visible in the more sensitive T1 dependent images (SR) and may reflect the cytotoxic component of ischemic brain edema. Further progress was also clearly discernible in the PD images and may mainly reflect the slower vasogenic component of ischemic brain edema. Nuclear magnetic resonance imaging seems to provide a new approach to early diagnosis of ischemic brain infarction. Furthermore, it may elucidate some aspects of the pathophysiology of ischemic stroke in man.

Adult↗
PubMed2001

Angiographic evaluation of middle cerebral artery reperfusion caused by platelet glycoprotein IIb/IIIa receptor complex antagonist murine 7E3 F(ab')2 in a model of focal cerebral ischemia in rats.

OBJECT: Antagonists of the glycoprotein IIb/IIIa (GPIIb/IIIa) receptor complex are currently used for the treatment of acute coronary syndromes. The platelet GPIIb/IIIa mediates platelet aggregation, and blocking this receptor complex can reduce or prevent arterial thrombosis. To study the recanalization efficacy of a GPIIb/IIIa antagonist in treating cerebral ischemia, we investigated the therapeutic effects of murine 7E3 F(ab'), in a focal embolic cerebral ischemia model in rats. METHODS: Focal cerebral ischemia was produced by introducing an autologous thrombus into the right side of the middle cerebral artery (MCA). Thirty male Wistar rats were randomly divided into three groups of 10 rats each: control, 7E3 F(ab')2 administered 1 hour postischemia, and 7E3 F(ab')2 administered 3 hours postischemia. Animals in the therapeutic groups received intravenous infusion of 6 mg/kg 7E3 F(ab')2 at 1 or 3 hours following cerebral embolization. Brain infarct volume, neurobehavioral scores, duration of bleeding, and findings on angiograms of the MCA (before and after infusion) were assessed in all animals. Angiographic evaluation revealed full MCA recanalization in three of 10 animals in each 7E3 F(ab')2 treatment group. Animals in these groups exhibited a significant reduction in infarct volume when compared with animals in the control group: 1) infarct volume 1 hour postischemia, 22 +/- 13.9% (p = 0.005); 2) infarct volume 3 hours postischemia, 22.1 +/- 14.8% (p = 0.008); and 3) infarct volume in control animals, 42.4 +/- 16%. Postischemia treatment with 7E3 F(ab')2 also improved the animal's neurobehavioral performance. The duration of bleeding significantly increased by more than two times, but there was no associated increase in intracerebral hemorrhage in any group. CONCLUSIONS: On the basis of their findings, the authors conclude that murine 7E3 F(ab'), is a potent and safe antiplatelet agent in this experimental focal embolic cerebral ischemia model. Neuronal lesions were significantly reduced when the treatment was delayed up to 3 hours.

Animals↗
PubMed2004

Transcriptional response to circumscribed cortical brain ischemia: spatiotemporal patterns in ischemic vs. remote non-ischemic cortex.

Focal brain infarcts are surrounded by extended perilesional zones that comprise the partially ischemic penumbra but also completely non-ischemic cortex of the remote ipsilateral hemisphere. To delineate the impact of lesion-associated vs. remote processes on transcriptional programming after focal ischemia, we used cDNA array analysis, quantitative real-time polymerase chain reaction and immunohistochemistry in the photothrombosis model of circumscribed cortical ischemia in rats. At an early stage of 4 h after ischemia, gene induction occurred to a similar extent in the ischemic infarct and remote non-ischemic cortex of the ipsilateral hemisphere. Among the genes induced in non-ischemic cortex we found the NGF-inducible genes PC3, VGF and Arc, the transcriptional regulators I kappa B-alpha and Stat3, and the beta-chemokine MIP-1 alpha (CCL3). At 3 days, the spatial pattern of gene expression had changed dramatically with brain fatty acid-binding protein as the only gene significantly induced in non-ischemic ipsilateral cortex. In contrast, numerous genes were exclusively regulated at the lesion site, comprising genes involved in cell cycle regulation, proteolysis, apoptosis, lipid homeostasis and anti-inflammatory counter-regulation. Cortical spreading depression was identified as the main mechanism underlying gene induction in remote non-ischemic cortex. Our data demonstrate a dynamic spatiotemporal pattern of gene induction, which may contribute to delayed progression of damage or, alternatively, mediate neuroprotection, tissue remodeling and functional compensation.

AIDS-Related Complex↗
PubMed2000

Disseminated zygomycosis simulating cerebrovascular disease and pulmonary alveolar haemorrhage in a patient with systemic lupus erythematosus.

Patients with systemic lupus erythematosus (SLE) may be complicated with serious cerebrovascular accidents and pulmonary alveolar haemorrhage. The authors report an autopsy-proven angioinvasive zygomycosis in a patient with SLE. The clinical features of systemic zygomycosis in this patient masqueraded as SLE-related stroke and pulmonary haemorrhage. The case demonstrates that the simultaneous occurrence of complications that clinically suggest pulmonary haemorrhage and multiple brain infarcts in SLE patients should include the rare disseminated zygomycosis in the differential diagnosis.

Adolescent↗
PubMed1998

Cerebral infarcts in patients with autopsy-proven Alzheimer's disease: CERAD, part XVIII. Consortium to Establish a Registry for Alzheimer's Disease.

OBJECTIVE: To study the relation between cerebral infarction and clinical and neuropsychologic manifestations in patients with autopsy-proven Alzheimer's disease (AD) enrolled in the Consortium to Establish a Registry for Alzheimer's Disease (CERAD). BACKGROUND: Prior studies report that subjects with neuropathologic evidence of AD and concomitant brain infarcts had poorer cognitive function and higher frequency of dementia than those with AD alone. METHODS: Clinical and neuropsychologic manifestations of dementia were studied in 74 subjects with neuropathologic findings of AD alone and 32 with AD and concomitant cerebral infarcts or lacunar lesions. RESULTS: The 32 patients with both AD and vascular lesions were significantly older at time of death (median age, 81 years) than the 74 patients with AD alone (76 years; p = 0.02). At the final follow-up visit, the severity of the dementia was greater in AD patients with vascular lesions (median Clinical Dementia Rating [CDR] = 3) than in those with AD alone (CDR = 2; p = 0.03). Patients with AD and vascular lesions performed significantly worse on verbal fluency, Boston Naming, and Mini-Mental State Examination (MMSE) tests. No differences between the groups were observed, however, in the semiquantitative measures of frequency of neuritic plaques or neurofibrillary tangles. CONCLUSIONS: The clinical-neuropathologic correlations in CERAD patients generally confirm those in prior studies, indicating that the presence of cerebral infarction in patients with AD is associated with greater overall severity of clinical dementia and poorer performance on specific tests of language and cognitive function.

Aged↗
PubMed1989

A method of analysis of SPECT blood flow image data for comparison with computed tomography.

A consistent method for the qualitative analysis of regional cerebral blood flow on single-photon emission computed tomography (SPECT) imaging has not yet been realized. Regional analysis usually refers an area of abnormal tracer uptake to another region of brain (e.g., the contralateral hemisphere), but region of interest size and analysis differ between investigators. In patients who have had a stroke, the flow deficit size on the SPECT image often appears much larger than the abnormality visualized on computed tomography (CT), and confounds attempts to differentiate between "purely" infarcted brain tissue, ischemic brain tissue, edema, or brain tissue having diminution of flow resulting from deafferentation. The author presents a method to determine a flow deficit volume that can be easily calculated from the SPECT image, which yields a volume size that is equivalent to a hypothetical volume having zero blood flow. The method of calculation is objective, independent of region of interest size, and provides a SPECT volume deficit that may be correlated with the CT volume deficit, thus helping to differentiate "purely" infarcted tissue from tissue having infarction, edema, ischemia, and deafferentation.

Aged↗
PubMed1994

A young case with multi-infarct dementia associated with lupus anticoagulant.

A 39-year-old man was admitted because of an abrupt onset of right-side weakness and dysarthria. During the 2 years before admission, he had suffered from insomnia, depressed mood and progressive memory disturbance. Neurological and psychiatric examination revealed severe intellectual impairment in addition to the neurological deficits. Neuroradiological examinations revealed multiple brain infarcts. He had no risk factor for stroke except for lupus anticoagulant. He was diagnosed as having multi-infarct dementia associated with antiphospholipid antibodies. This case suggests that it is necessary to investigate antiphospholipid antibodies in addition to neuroradiological examination when relatively young patients present with unexplained cognitive or behavioral symptoms.

Adult↗
PubMed1998

A glycine site antagonist, ZD9379, reduces number of spreading depressions and infarct size in rats with permanent middle cerebral artery occlusion.

BACKGROUND AND PURPOSE: Spreading depressions (SDs) occur in experimental focal ischemia and contribute to lesion evolution. N-Methyl-D-aspartate (NMDA) antagonists inhibit SDs and reduce infarct size. The glycine site on the NMDA receptor complex offers a therapeutic target for acute focal ischemia, potentially devoid of many side effects associated with competitive and noncompetitive NMDA antagonists. We evaluated the effect of the glycine antagonist ZD9379 on SDs and brain infarction. METHODS: Male Sprague-Dawley rats (n = 18) weighing 290 to 340 g undergoing permanent middle cerebral artery occlusion (MCAO) were randomly and blindly assigned to receive drug or placebo: group 1 (pre-MCAO treatment group; n=5), a 5-mg/kg bolus of ZD9379 over 5 minutes followed by 5 mg/kg per hour drug infusion for 4 hours beginning 30 minutes before MCAO; group 2 (post-MCAO treatment group; n=7), a 5-mg/kg bolus of ZD9379 30 minutes after MCAO followed by 5 mg/kg per hour drug infusion for 4 hours; and group 3 (control group; n=6), vehicle for 5 hours beginning 30 minutes before MCAO. SDs were monitored electrophysiologically for 4.5 hours after MCAO by continuous recording of cortical DC potentials and electrocorticogram. Infarct volume was measured 24 hours after MCAO by 2,3,5-triphenyltetrazolium chloride staining. RESULTS: Corrected infarct volume was 90+/-72 mm3 (mean+/-standard deviation) in group 1, 105+/-46 mm3 in group 2, and 226+/-40 mm3 in group 3 (P<.001). The corresponding numbers of SDs in the three groups were 8.2+/-5.8, 8.1+/-2.5, and 16.0+/-5.1, respectively (P<.01). When all animals (n=18) were analyzed, infarct volumes and the number of SDs were significantly correlated (r=.68, P=.002). CONCLUSIONS: This study demonstrated that ZD9379 initiated before or after MCAO significantly reduced the number of SDs and infarct volume in a permanent focal ischemia model, implying that ZD9379 is neuroprotective and its neuroprotective effect may be related to inhibiting ischemia-related SDs.

Analysis of Variance↗
PubMedDate not supplied

[Urinary uropepsin activity in patients with different forms of stroke].

The investigations were carried out in 30 control cases, in 20 patients with acute transient cerebral circulatory failure, 20 patients with intracerebral haemorrhage, and 22 patients with thrombotic encephalomalacia. The determinations of uropepsin activity were done on the 1st, 3rd, 7th and 14th days of the disease. Uropepsin activity in 24-hour urine was determined by the method of West, Ellis and Scott. In the group of patients with acute transient cerebral circulatory failure abnormalities in urinary uropepsin activity were not significant. The mean activity of uropepsin in 24-hour urine in patients with intracerebral haemorrhage and brain infarction on the 1st day of the disease was significantly higher than in controls. The rise in the activity of this enzyme in patients with encephalomalacia was lower in relation to patients with intracerebral haemorrhages. During improvement of the condition of patients with brain stroke the uropepsin activity in 24-hour urine decreased.

Acute Disease↗
PubMedDate not supplied

[Obstacles for recruiting organ donors in intensive care units can be overcomed. Identified obstacles are attitudes, ethics, resources and competence, as shown by an inquiry].

The aim of this study was to identify obstacles for recruiting organ donors in the ICU. All specialists in neurosurgery and half of the specialists in anaesthesiology in Sweden were surveyed. Response rate was 67%. The following obstacles were identified: A neutral approach of the physicians when requesting organ donation of the families instead of a pro-donation approach; ethical problems concerning non-therapeutic ventilation and requesting donation of grieving families; varying competence in diagnosing brain infarction; lack of resources at the ICU. Suggestions for organizational and educational improvements are given.

Adult↗
PubMed1994

Atherosclerotic disease of the aortic arch and the risk of ischemic stroke.

BACKGROUND: Atherosclerotic disease of the aortic arch has been suspected to be a potential source of cerebral emboli. We conducted a study to quantify the risk of ischemic stroke associated with atherosclerotic disease of the aortic arch. METHODS: Using transesophageal echocardiography, we performed a prospective case-control study of the frequency and thickness of atherosclerotic plaques in the ascending aorta and proximal arch in 250 consecutive patients admitted to the hospital with ischemic stroke and 250 consecutive controls, all over the age of 60 years. RESULTS: Atherosclerotic plaques > or = mm in thickness were found in 14.4 percent of the patients but in only 2 percent of the controls. After adjustment for atherosclerotic risk factors, the odds ratio for ischemic stroke among patients with such plaques was 9.1 (95 percent confidence interval, 3.3 to 25.2; P < 0.001). Among the 78 patients who had brain infarcts with no obvious cause, 28.2 percent had plaques > or = 4 mm in thickness, as compared with 8.1 percent of the 172 patients who had infarcts whose possible or likely causes were known (odds ratio, 4.7; 95 percent confidence interval, 2.2 to 10.1; P < 0.001). Plaques of > or = 4 mm in the aortic arch were not associated with the presence of atrial fibrillation or stenosis of the extracranial internal carotid artery. In contrast, plaques that were 1 to 3.9 mm thick were frequently associated with carotid stenosis of > or = 70 percent. CONCLUSIONS: These results indicate a strong, independent association between atherosclerotic disease of the aortic arch and the risk of ischemic stroke. The association was particularly strong with thick plaques. Atherosclerotic disease of the aortic arch should be regarded as a risk factor for ischemic stroke and as a possible source of cerebral emboli.

Aged↗
PubMed1982

Effects of agents used in the pharmacotherapy of cerebrovascular disease on the oxygen consumption of isolated cerebral mitochondria.

A number of drugs used in the pharmacotherapy of cerebral metabolic and vascular disease have been studied for their effects on the respiration of mitochondria isolated from the rat brain. Some of these agents increased the respiratory control ratio by more than 5% from base-line values (at p less than 0.05), namely, aminophylline, dihydroergotoxine, ifenprodil, nicergoline, raubasine, and vincamine. The ability of these agents to increase the efficiency of mitochondrial respiration could be correlated with two other attributes peculiar to these five drugs: their ability to contract cerebrovascular smooth muscle when studied in vitro and their ability to decrease the volume of infarcted brain tissue following experimental occlusion of the middle cerebral artery in the cat. Papaverine and its derivatives (naftidrofuryl, viquidil, YC-93) decreased respiratory control, an effect that might correlate with their capacity to effect a vasodilatation of the cerebral vessels and their inefficacy in models of acute cerebral infarction. There is a considerable body of evidence suggesting that one of the earliest and most fundamental perturbations of cerebral ischaemia is a loss of respiratory control. Ifenprodil, vincamine, and some related "anti-ischaemic" compounds are capable of increasing respiratory control in normal cerebral mitochondria, and this capacity might well help to explain their therapeutic potential in cerebrovascular disorders in which energy supply to the brain is limited.

Animals↗
PubMed1992

Vimentin immunoreactivity in normal and pathological human brain tissue.

Vimentin immunoreactivity was examined in brain tissues from non-neurological and various human central nervous system disease cases. In all brain tissues examined, vimentin immunoreactivity was intensely positive in ependymal cells and subpial tissues, and weakly positive in some capillaries and some white matter astrocytes. In affected areas of Alzheimer's disease (AD), Pick's disease, amyotrophic lateral sclerosis (ALS), multiple sclerosis (MS) and cerebral infarction cases, numerous intensely vimentin-immunopositive astrocytes of both protoplasmic and fibrous morphology were demonstrated. A few such astrocytes were also observed in Parkinson's disease and progressive supranuclear palsy. ALS, MS and infarction brains also had numerous, strongly vimentin-positive, round and fat-laden microglia/macrophages. In AD and ALS, a few reactive microglia with irregularly enlarged shapes were vimentin positive. In AD, they were almost exclusively related to senile plaques.

Aged↗
PubMed2002

Aging, the brain and human prion disease.

Human prion diseases (PrD) preferentially manifest in the elderly. Their neuropathology may coexist with tau immunoreactive neuropil threads, neurofibrillary tangles, and beta-amyloid senile plaques, most likely representing an age-related change rather than a pathogenic link with Alzheimer's disease. Cerebrovascular disease with brain infarction, another malady preferring the elderly, is useful to prove the origin of PrD-associated prion protein deposition exclusively from neurons.

Aging↗
PubMed1976

Spontaneous calcific emboli from calcific mitral annulus fibrosus.

Clinically important complications resulting from calcific mitral annulus fibrosus (CMAF) are unusual. They include mitral regurgitation, mitral stenosis, and complete heart block. In one patient with massive CMAF associated with multiple systemic calcific emboli originating from the mitral valve, the emboli were the cause of multiple brain infarcts and a clinical course of unexplained neurological deterioration. We believe that this is the first report of such a complication occurring with CMAF.

Brain↗
PubMed1998

[Treatment of embolic cerebral infarct via thrombolysis and cytoprotection with U-74389-G in rats].

INTRODUCTION: The best treatment for cerebral ischemic will probably comprise the association of inhibition of ischemia-reperfusion injury mediators and early reperfusion. OBJECTIVE: We tried to demonstrate if reperfusion by thrombolysis (rt-PA) and free radical scavenging (U-74389-G) reduces ischemic-reperfusion cerebral injury in a rat model of embolic brain infarction. MATERIAL AND METHODS: 39 female Long Evans rats were embolized in right hemisphere with an autologous clot. Three groups are considered; A: control (n = 15), B: rt-PA i.v., 20 mg/kg starting 90-120 minutes after embolization (n = 15), C: rt-PA, same dose, and U-74389-G i.v., 3 mg/kg before and after embolization (n = 9). Arterial blood pressure, gasometry, glycemia and temperature were controlled. Volume of cerebral lesion in surviving animals 24 hours was measured. Autopsy was performed to verify the cause of death in rats which died. RESULTS: Mortality: group A: 8/15; group B: 9/15; group C: 8/9. Early death was related to cerebral injury except for five rats which developed peritoneal bleeding. We found severe acidosis in rats from group C. Differences in mean volume of ischemic lesion in group A and B are nosignificant despite a tendency to a reduction after thrombolysis. CONCLUSIONS: In this model thrombolysis alone and in association with U-74389-G failed to reduce cerebral lesion and mortality.

Animals↗
PubMed1993

Relation of laboratory and clinical variables to the grade of carotid atherosclerosis.

BACKGROUND AND PURPOSE: To clarify diagnostic entities in ischemic stroke we analyzed the relation between the severity of carotid atherosclerosis, coagulation parameters, lipoproteins, neurological status, and risk factors in 232 patients. METHODS: Duplex ultrasonography, computed tomography scan, and laboratory investigations were performed between the third and tenth days after stroke. Based on carotid ultrasound scores, we categorized the patients into four groups (A, B, C, and D) according to severity of atherosclerosis. Corresponding laboratory variables and clinical data were statistically analyzed. RESULTS: Ultrasound scores were significantly (P < .05) higher in the male (n = 126) versus female (n = 106) patients. The hematocrit was significantly higher and thrombin time was significantly shorter in the male group compared with the female group. Severe atherosclerosis (group C) and occlusion (group D) of the internal carotid artery was associated with smoking (C = 56%; D = 78%), hypertension (C = 43%; D = 35%), claudication (C = 13%; D = 5%), and antecedent myocardial infarction (C = 9%; D = 13%). There was no statistical correlation between ultrasound scores and the patients' neurological condition. Cholesterol and plasma fibrinogen levels were significantly higher and high-density lipoprotein cholesterol was significantly lower in groups with severe atherosclerosis compared with patients with slight intimal damage. The presence of multiple plaques or thrombosis of the internal carotid artery was concordant with the prevalence of single cerebral infarcts. CONCLUSIONS: Severity of carotid atherosclerosis corresponded well with the following factors: age, smoking, and low concentration of high-density lipoprotein cholesterol. Elevation of plasma fibrinogen combined with a loss of high-density lipoprotein cholesterol is strongly associated with severe atherosclerosis and results in brain infarction.

Alcoholism↗