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PubMed1995

Temporal thresholds of reperfusion in the middle cerebral artery occlusion model in rats.

In this study, the middle cerebral artery (MCA) of adult male Sprague-Dawley rats was occluded by the modified Koizumi method to determine the temporal thresholds of reperfusion for the treatment of cerebral embolism. Regional cerebral blood flow (rCBF) and pathological findings were measured at 1 and 2 h of ischemia and after 24 h and 7 days of reperfusion following 1 or 2 h of ischemia. rCBF was decreased the most (less than 10% of control CBF) in the parietal cortex (Pcor) and the lateral caudoputamen (Lcp) at both 1 and 2 h of ischemia. There was no significant difference in rCBF in these areas between the 2 ischemic groups. The 2 h ischemia group clearly showed infarction in the area perfused by the middle cerebral artery (including the Pcor and Lcp) after 24 h and 7 days of reperfusion, while the 1 h ischemia group showed only slight infarction. These findings suggest that temporal thresholds of reperfusion in this model exist between 1 and 2 h of ischemia, and that rCBF levels during ischemia and the duration of ischemia are the most important factors in producing brain infarction.

Animals↗

PubMed2005

Conversion of ischemic brain tissue into infarction increases with age.

BACKGROUND AND PURPOSE: Brain regions normal on diffusion-weighted imaging (DWI) but abnormal on mean transit time (MTT) maps represent tissue at risk of infarction, yet the fate of these regions is quite variable. The imperfect correlation between tissue outcome and initial imaging parameters suggests that each patient's brain may have different susceptibility to ischemic stress. We hypothesize that age is a marker for tissue susceptibility to ischemia and thus plays a role in determining tissue outcome in human stroke. METHODS: Sixty patients with acute ischemic stroke and a region of DWI/MTT mismatch that was >20% of the DWI volume were included. All patients were scanned twice, within 12 hours of symptom onset and on day 5 or later. The percentage mismatch lost (PML) was calculated as percentage of initial DWI/MTT mismatch volume that was infarcted on the follow-up MRI. The statistical analysis explored relationships among the covariates age, Trial of Org 10172 in Acute Stroke Treatment (TOAST) subtypes, time-to-MRI, and initial DWI, MTT volume, mean arterial blood pressure and blood glucose level at admission, and previous history of hypertension and diabetes mellitus. RESULTS: Univariate comparisons showed that age (P=0.003), hypertension (P=0.009), and diabetes mellitus (P=0.0002) were significantly associated with PML. Regression analyses showed age to be a significant covariate (P=0.02). The regression model predicted a change in PML of approximately 0.65% per year. The adjusted proportion of variance (R2) in PML that could be explained by age alone was 14%. CONCLUSIONS: Age-dependent increase in conversion of ischemic tissue into infarction suggests that age is a biological marker for the variability in tissue outcome in acute human stroke.

Adult↗

PubMed1987

CT in the differential diagnosis between Alzheimer's disease and vascular dementia.

A prospective series of consecutively admitted patients with Alzheimer's disease (AD) (n = 68), multi-infarct dementia (MID) (n = 79) and probable vascular dementia (PVD) (n = 46) were studied by CT of the head. In MID 88.6% and in PVD 41.3% of the patients had at least one brain infarct on CT, but only one patient (1.5%) with AD. White matter low attenuation (WMLA) also differentiated MID and PVD from AD, especially among patients aged 75 years or less, and with mild or moderate dementia. In all types, brain atrophy on CT had a positive correlation with the degree of dementia. Infarcts and WMLA on CT, but not brain atrophy seem to be of differential diagnostic value between vascular and degenerative dementia.

Aged↗

PubMed2000

[Aspirin and cerebral ischemic accidents].

At the acute phase of cerebral infarction, two recent large studies found that the use of aspirin reduces both mortality and the risk of the recurrence of stroke. In primary prevention, aspirin nearly halves the risk of myocardial infarction but does not reduce that of stroke. Concerning the secondary prevention of atherothrombotic brain infarcts, aspirin has been the most extensively studied drug, and is efficient between 50 mg and 1.3 g. In spite of the efficacy of other antiplatelets in this indication--ticlopidine (500 mg), clopidogrel (75 mg) and dipyridamole (400 mg)--aspirin remains the most cost-effective, doses between 100 and 300 mg being the most widely used. Cardiac diseases with a high embolic risk require the use of oral anticoagulation. In nonvalvular atrial fibrillation, the choice of antithrombotic drugs depends on risk stratification: oral anticoagulants are indicated in high-risk subjects, whereas aspirin is recommended in low-risk subjects and when oral anticoagulants are contraindicated. Studies with associations of aspirin and other antiplatelets are required to increase the yield of this medication in high-risk subjects, in parallel with efforts to detect and to treat the vascular risk factors.

Aged↗

PubMed2003

Design of future acute-stroke treatment trials.

Very few trials of acute stroke treatments show efficacy of a tested agent on the prespecified primary outcome. We can learn many lessons from the studies that achieve only neutral results. Preclinical studies have been flawed by use of models of transient not permanent brain ischaemia, treatments that aim to protect cerebral grey matter independently of white matter, delivery of the study drug within too short a time window after ischaemic insult, use of surrogate outcome measures in the short term instead of function in the long-term, and small sample sizes. Clinical trials have been hampered by heterogeneity in causes of stroke and inability to classify subtypes of cause; the short time available to rescue ischaemic brain tissue; the haemorrhagic transformation that can cause severe functional consequences seen frequently in infarcted brain tissue; the lack of valid, reliable, sensitive, and simple tools for assessment of functional outcome; and, above all, small treatment effects that are difficult to detect or refute. In this review, we look at the designs and results of all controlled trials of treatments for ischaemic stroke, and try to identify opportunities to improve future treatment assessment.

Clinical Trials as Topic↗

PubMedDate not supplied

Measurement and diagnostic value of cerebrospinal fluid enzymes.

The diagnostic value of cerebrospinal fluid (CSF) enzyme activities in neurological disorders has been evaluated most extensively with the enzymes aspartate aminotransferase (ASAT), lactate dehydrogenase (LDH), creatine kinase (CK) and lysozyme. Methods use for performing the assays have been similar to those employed for serum analysis. Reference intervals for these enzymes in the CSF are given from several sources and demonstrate much lower activities than in serum. Studies of these CSF enzymes in cerebral infarction, brain tumors, central nervous system (CNS) infections and acute brain injury and reviewed.

Adult↗

PubMed1993

Noninvasive measurements of regional cerebral blood flow using technetium-99m hexamethylpropylene amine oxime.

The previously reported method for quantitative measurements of whole-brain or hemispheric-brain perfusion using technetium-99m hexamethylpropylene amine oxime (HMPAO) radionuclide angiography is now further developed so that regional cerebral blood flow (rCBF) can be measured. Lassen's correction algorithm is used for the linearization of a curve-linear relationship between the radioactivity in the brain and blood flow as seen with single-photon emission tomography (SPET) images. In this algorithm, the cerebral hemisphere was chosen as the reference region and the correction factor alpha was adapted to rCBF in the reference region. This new method of measuring CBF from SPET has been validated in 33 normal subjects and 22 patients with cerebrovascular disease. Regional CBF values in 20 brain regions of the normal subjects were in good agreement with reported values measured by other methods. Regional CBF in the frontal cortex was greater than that in the temporal, parietal or occipital cortex for the entire age range. This hyperfrontal perfusion tended to be less pronounced with advancing age. Seventeen patients with unilateral brain infarction showed significantly lower rCBF than normal subjects. The infarct core showed a low rCBF value of 11.1 ml/100 g/min on average. An increase in rCBF after acetazolamide administration was observed and measured with this method in five patients with unilateral occlusive vascular pathology. These results suggest that this non-invasive method (without any blood sampling) permits the routine measurement of rCBF from HMPAO SPET tomograms of blood flow.

Acetazolamide↗

PubMed1994

Improvement of cerebrovascular reserve capacity by EC-IC arterial bypass surgery in patients with ICA occlusion and hemodynamic cerebral ischemia.

Since the negative results of the international Bypass Study, extracranial-intracranial (EC-IC) bypass surgery is infrequently employed in the treatment of patients with cerebral ischemia. Newly acquired evidence concerning the pathophysiology of cerebral ischemia, however, has facilitated the identification of a small subgroup of patients with "hemodynamic" cerebral ischemia. Characteristically, these patients demonstrate severely impaired cerebrovascular reserve capacity due to occlusive disease and insufficient collateral blood supply. Over an 8-year period, 28 patients were defined by clinical and laboratory criteria as suffering from hemodynamic cerebral ischemia. All patients had recurring episodes of focal cerebral ischemia due to unilateral internal carotid artery occlusion. Computerized tomography (CT) scans either were normal or showed evidence of border zone infarction. The cerebrovascular reserve capacity was studied using 133Xe single-photon emission CT and acetazolamide challenge and was found to be significantly impaired in all patients. Based on these criteria, superficial temporal artery-middle cerebral artery anastomosis was performed to augment collateral flow to the ischemic hemispheres. Two patients died from myocardial infarction, one 4 days and the other 2 months postoperatively. One patient died from massive brain infarction and another suffered a postoperative stroke with incomplete recovery, resulting in a major morbidity and mortality rate of 14%. Minor morbidity included one patient with a subdural hematoma who subsequently recovered completely. The postoperative course was uneventful in 23 patients (82%). Over a mean follow-up period of almost 3 years, no patient had another episode of brain ischemia. Bypass patency was confirmed by postoperative angiography in 26 patients. Follow-up studies of cerebral blood flow (CBF) and cerebrovascular reserve capacity showed significant improvement of the latter while the resting CBF was essentially unchanged. In view of these findings, the authors conclude that EC-IC bypass surgery constitutes appropriate therapy for a subgroup of patients with recurrent focal cerebral ischemia, defined using the strict selection criteria employed in this study.

Adult↗

PubMed1994

Vestibular cortex lesions affect the perception of verticality.

Seventy-one patients with unilateral supratentorial infarctions were evaluated with respect to static vestibular function in the roll plane, including determinations of the subjective visual vertical, skew deviation, and ocular torsion. Since animal studies have revealed at least four different areas of the parietal and temporal cortex involved in vestibular function, we tried to identify cortical areas in humans responsible for vestibular function in the roll plane. Infarcted areas, as demonstrated in magnetic resonance and computed tomography scans, were projected onto the appropriate sections of an atlas of the human brain. Infarctions in the territories of the posterior and anterior cerebral arteries did not affect static vestibular function in roll. Twenty-three of 52 patients with infarctions in the middle cerebral artery territory showed significant (p < 0.0005), mostly contraversive, pathological subjective visual vertical tilts. The overlapping area of these infarctions centered on the posterior insula, probably homologous to the parieto-insular vestibular cortex in the monkey. Although electrophysiological and cytoarchitectonic data in animals demonstrate several multisensory areas rather than a single primary vestibular cortex, the parieto-insular vestibular cortex seems to represent the integration center of the multisensory vestibular cortex areas within the parietal lobe.

Adolescent↗

PubMed2005

Comprehensive regional and temporal gene expression profiling of the rat brain during the first 24 h after experimental stroke identifies dynamic ischemia-induced gene expression patterns, and reveals a biphasic activation of genes in surviving tissue.

In order to identify biological processes relevant for cell death and survival in the brain following stroke, the postischemic brain transcriptome was studied by a large-scale cDNA array analysis of three peri-infarct brain regions at eight time points during the first 24 h of reperfusion following middle cerebral artery occlusion in the rat. K-means cluster analysis revealed two distinct biphasic gene expression patterns that contained 44 genes (including 18 immediate early genes), involved in cell signaling and plasticity (i.e. MAP2K7, Sprouty2, Irs-2, Homer1, GPRC5B, Grasp). The first gene induction phase occurred at 0-3 h of reperfusion, and the second at 9-15 h, and was validated by in situ hybridization. Four gene clusters displayed a progressive increase in expression over time and included 50 genes linked to cell motility, lipid synthesis and trafficking (i.e. ApoD, NPC1, G3P-dehydrogenase1, and Choline kinase) or cell death-regulating genes such as mitochondrial CLIC. We conclude that a biphasic transcriptional up-regulation of the brain-derived neurotrophic factor (BDNF)-G-protein coupled receptor (GPCR)-mitogen-activated protein (MAP) kinase signaling pathways occurs in surviving tissue, concomitant with a progressive and persistent activation of cell proliferation signifying tissue regeneration, which provide the means for cell survival and postischemic brain plasticity.

Animals↗

PubMed2001

Early prediction of irreversible brain damage after ischemic stroke at CT.

PURPOSE: To assess the capability of computed tomography (CT) in the prediction of irreversible ischemic brain damage and its association with the clinical course within 6 hours of stroke onset. MATERIALS AND METHODS: Serial CT scans obtained within 6 hours of stroke onset, at 22-96 hours (median, 1 day), and at 2-36 days (median, 7 days) after symptom onset in 786 patients with ischemic stroke were prospectively studied, and follow-up CT scans were used as the reference. Clinical variables were assessed prospectively and independently of CT evaluation. RESULTS: The specificity and positive predictive value of ischemic edema at baseline CT for brain infarcts were 85% (95% CI: 77%, 91%) and 96% (95% CI: 94%, 98%), respectively. Sensitivity and negative predictive values were 64% (95% CI: 60%, 67%) and 27% (95% CI: 23%, 32%), respectively. Patients without early CT findings were less severely affected (P<.001), developed smaller infarcts (P<.001), had fewer intracranial bleeding events (P<.001), and had a better clinical outcome at 90 days (P<.001) compared with patients with hypoattenuating brain tissue at early CT. CONCLUSION: After ischemic stroke, x-ray hypoattenuation at CT is highly specific for irreversible ischemic brain damage if detection occurs within the first 6 hours. Patients without hypoattenuating brain tissue have a more favorable clinical course.

Adolescent↗

PubMedDate not supplied

Reduction of neural damage in irreversible cerebral ischemia by calcium antagonists.

Because of the complexity and cost of clinical investigations and the virtual lack of pharmacological leads, drugs for the treatment of strokes have to be tested extensively in animal models closely mimicking the human disorder. With the recent introduction of in vivo NMR imaging (MRI) and spectroscopy (MRS), it is now possible to evaluate the consequences of strokes and to monitor the effects of therapeutic interventions in animals with the same methodology as in humans. The appearance and evolution of brain infarcts in spontaneously hypertensive rats (SHR), after occlusion of the middle cerebral artery (MCA), were detected with MRI. In coronal sections through the rat brain, regions with increased MRI signal started to become discernible after 6 h and turned out to be largely necrotic already after 24 h, as revealed by histology. The location (fronto-parietal cortex, caudate-putamen) and total infarct size, as determined from MR images or histology, were highly reproducible. Posttreatment with the dihydropyridine calcium antagonist isradipine (PN 200-110), at a daily dose of 3 X 0.3 mg/kg sc, reduced the total infarct size by 30-40%, determined by quantitative MRI and confirmed by histology. Biochemical markers of necrosis, such as the increased brain wet wt, the levels of sodium, potassium, dopamine, and noradrenaline, were changed toward normal values. The functional consequences of these morphological effects of isradipine were reflected by the parallel improvement of a neurological score. Follow-up observations made by MRI and histology indicated that the morphological differences between treated and control animals were still present to the same extent after 2 wk and, therefore, seem to be permanent. In order to elucidate the putative mechanisms involved, the influence of calcium antagonists on cerebral blood flow (CBF) and high energy phosphates (HEPs) was investigated. CBF was measured quantitatively with [14C] iodoantipyrine in MCA-occluded SHRs. Although isradipine had no effect on CBF in the contralateral hemisphere, at a dose reducing infarct size, it increased the reduced blood flow in the lesioned hemisphere toward normal values. HEPs (PCr and ATP) as well as inorganic phosphate (Pi) and intracellular pH were measured noninvasively in the rat brain by 31P MRS using a surface coil. Under normal conditions, calcium antagonists had no effect on these parameters.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1984

CAT scan and immunohistochemical findings in a case of cerebral thromboangiitis obliterans (Buerger's disease).

Immunohistochemical examinations were carried out in a case of thromboangiitis obliterans. A 26-year-old man developed 4 brain infarctions which could be demonstrated by CAT scan. He suffered from a left-sided hemiparesis, major epileptic seizures, and an ischemic optic neuritis. Immunologic studies supported a diagnosis of cerebral thromboangiitis obliterans (CTAO). The serum anti-elastin titer as well as IgE were considerably increased and a biopsy of the temporal artery showed immunohistochemical signs of an acute inflammatory vessel disease. After the diagnosis of CTAO had been made, the patient was treated with azathioprine and dexamethasone. In cases of young stroke patients, a temporal biopsy is important in confirming the diagnosis.

Adult↗

PubMed1998

Does glutamate mediate brain damage in acute encephalitis?

Cerebrospinal fluid (CSF) amino acid neurotransmitter concentrations in 23 patients with acute encephalitis were compared with those in patients with acute brain infarction, multiple sclerosis and controls. The concentration of glutamate was significantly higher in encephalitis (5.2+/-6.7 micromol/l) and stroke patients (9.6+/-14.2 micromol/l) than in MS patients (1.6+/-0.9 micromol/l) and controls (1.7+/-0.8 micromol/l; p < 0.001). The concentration of glycine was significantly higher in encephalitis (11.0+/-4.7 micromol/l) than in stroke (7.6+/-3.2 micromol/l) and MS patients (6.3+/-2.1 micromol/l) or controls (5.6+/-1.8 micromol/l; p < 0.002). Taurine levels were significantly lower in encephalitis patients than in the other groups (p = 0.04). The correlation of high glutamate levels with poor outcome was almost significant (Kendall tau 0.63, p = 0.06). Our observations suggest that exicitotoxic neurotransmission may play an important role in the series of events that lead to neuronal damage in encephalitis.

Adult↗

PubMed2004

Spreading depression induces long-lasting brain protection against infarcted lesion development via BDNF gene-dependent mechanism.

Preconditioning the rat brain with spreading depression for 48 h induces potent ischemic tolerance (infarct tolerance) after an interval of 12-15 days, consequently reducing the infarcted lesion size in the acute phase following focal cerebral ischemia. However, persistence of the morphological and functional neuroprotection has not yet been proven. We tested whether tolerance-derived neuroprotection against focal cerebral ischemia persists or merely delays the progress of cerebral infarction. Prolonged spreading depression was induced in mice by placing a depolarized focus with intracerebral microinfusion of KCl for 24 h; after intervals of 3, 6, 9 or 12 days, temporary focal ischemia was imposed. In the analysis of the infarcted lesion volume 24 h after ischemia, groups with 6 or 9 day interval demonstrated significantly smaller lesion volume compared to time-matched vehicle control group (P=0.002). Significant reduction in cerebral infarction was also observed at the chronic phase, namely 14 days after ischemia (33% reduction) (P=0.021) accompanied with less severe neurological deficits (38% reduction) (P=0.020). Using this technique, we also investigated if the mice with targeted disruption of a single BDNF allele (heterozygous BDNF-deficient mice) can gain the same potency of tolerance as the wild mice. In the result on infarcted lesion volumes following temporary focal ischemia, potent tolerance developed in the wild type (35% reduction) (P=0.007) but not in the heterozygous BDNF-deficient mice (<19% reduction) (P=0.155), indicating that BDNF expression level following spreading depression is contributing to infarct tolerance development.

Animals↗

PubMed2003

Local intra-arterial fibrinolysis of thromboemboli occurring during neuroendovascular procedures with recombinant tissue plasminogen activator.

BACKGROUND AND PURPOSE: There is a lack of systematic data regarding local intra-arterial fibrinolysis (LIF) of thromboemboli occurring during neuroendovascular procedures with the use of recombinant tissue plasminogen activator (rtPA). We report our technique for treating LIF of intracerebral thromboemboli occurring during neuroendovascular procedures. METHODS: Nine of 723 patients (1.2%) who underwent neuroendovascular procedures during the period from January 1997 to September 2002 suffered thromboembolic complications. These patients were treated by LIF with a maximum dose of 0.9 mg rtPA per kilogram body weight. Recanalization was categorized as successful (Thrombolysis in Myocardial Infarction [TIMI] grade 2 or 3) versus unsuccessful (TIMI grade 0 or 1), and clinical outcome was categorized as independent (Rankin Scale score 0 to 2) versus dependent or dead (Rankin Scale score 3 to 6). RESULTS: The minimum time between thrombus detection and beginning of LIF was 10 minutes, and the maximum time was 90 minutes. Successful recanalization was achieved in 4 of 9 patients (44%). All 9 patients suffered cerebral ischemic infarctions, and none of the patients sustained intracerebral hemorrhage. Two patients (22%) died from malignant brain infarctions. Four patients (44%) remained moderately disabled, and 3 patients (33%) were severely disabled 3 months after LIF. CONCLUSIONS: Although we used relatively high doses of rtPA, the recanalization rates and clinical outcome of LIF in our patients were not satisfactory. Strategies for the prevention of thromboemboli during neuroendovascular procedures must be improved, and novel fibrinolytic or thrombolytic techniques should be developed.

Adult↗

PubMed1997

Prenatal ischemia reduces neuronal injury caused by neonatal hypoxia-ischemia in rats.

To determine whether 'ischemic tolerance', first described in adult rodents, exists in fetal and neonatal rats, a comparison of brain injury was made between two groups of rat pups following neonatal hypoxia-ischemia (HI). One group of rat pups had previously been subjected to HI in utero (HI + HI); the other had been subjected to a sham operation (SH + HI). Brain infarct size and neuronal injury were measured 24 h after the neonatal HI insult. As indicated by 2,3,5-triphenyltetrazolium chloride staining and pathological examination, cerebral damage was significantly less in the HI+ HI group than in the SH + HI group. Induction of heat shock protein 70 (hsp70) was immunohistochemically detectable in both groups 24 h after the neonatal HI, and was proportional to the extent of tissue damage. The ischemic tolerance phenomenon observed in immature rats does not appear to be a result of induction of hsp70.

Animals↗

PubMed1991

Disturbances of speech prosody following right hemisphere infarcts.

The ability to perceive and express emotional, as well as number of linguistic prosodic qualities of speech was tested in 20 Swedish-speaking patients with right-sided cortical, as well as purely subcortical brain infarcts, and in 18 normal controls. The infarcts were assessed by clinical neurological examination, and by CT, EEG, and measurements of regional cerebral blood flow (rCBF). In the patients the identification of emotional messages was disturbed, as well as the identification and production of several linguistic prosodic qualities. The study supports the claim that prosodic impairment could be linguistic in nature, and not secondary to affective disorder. The total degree of anatomical and functional disturbance of the right hemisphere played a role for both the ability to identify emotional messages and for identification of two of the linguistic prosodic qualities tested. However, it was not possible to find support for the hypothesis that the organization of prosody in the right hemisphere mirrors that of propositional speech on the left side.

Adult↗