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PubMed2003

Diagnostic performance of liquid crystal and cathode-ray-tube monitors in brain computed tomography.

The aim of this study was to evaluate feasibility of reporting brain CT examinations on liquid crystal display (LCD) flat-screen monitors vs state-of-the-art cathode-ray-tube (CRT) monitors. Ninety-five brain CT examinations of 95 patients were displayed on Picture archiving and communications system (PACS) workstations equipped either with a dedicated medical imaging LCD colour monitor or on a high-resolution CRT which is used for routine reporting of CT, MRI and digital radiography images in our institution. Fifty cases were negative and 45 cases were positive for early brain infarction (EBI), the latter being defined by a combination of one or more signs: dense artery; hypodensity of brain parenchyma; and local brain swelling verified by control scans. Ten radiologists had to rate presence or absence of EBI on a five-point scale. Ratings were evaluated by CORROC2 ROC software and areas under the ROC curve (A(z)) were computed. Significance of differences between the two viewing conditions were evaluated with Wilcoxon test. Mean A(z) of the ten observers was 0.7901 with LCD vs 0.7695 with CRT which did not show statistical significance (p=0.2030). In the setting investigated, reporting of CT studies from high-performance LCD monitors seems feasible without significant detriment to diagnostic performance.

Acute Disease↗
PubMed2001

Matrix metalloproteinase inhibitor KB-R7785 attenuates brain damage resulting from permanent focal cerebral ischemia in mice.

Matrix metalloproteinases (MMPs) are proteolytic enzymes that can degrade the extracellular matrix. MMP-9 and MMP-2 have been implicated in brain injury formation. The authors examined the effect of MMP inhibitor KB-R7785 on brain infarct formation resulting from permanent focal cerebral ischemia in mice. Ischemia was induced by intraluminal middle cerebral artery occlusion (MCAO) in mice under halothane anesthesia. Zymography was conducted to measure the MMPs activity in ischemic brain tissues. Injection of KB-R7785 (100 mg/kg) 30 min before MCAO significantly decreased both MMP-9 activity and infarct volume determined at 24 h. In addition, KB-R7785 injected twice at 1 and 4.5 h after MCAO significantly decreased infarct volume. These results indicate that KB-R7785 has a protective efficacy against focal cerebral ischemia, and our data provide further evidence that MMP-9 contributes to brain infarct formation.

Animals↗
PubMedDate not supplied

Immediate anticoagulation of embolic stroke: brain hemorrhage and management options. Cerebral Embolism Study Group.

The clinical implications of hemorrhagic transformation of embolic brain infarction were explored by studying 30 patients with cardiogenic brain embolism and either hemorrhagic infarct (HI) or intracerebral hematoma (ICH) on CT. At the time of identification of hemorrhage, 19 patients were receiving anticoagulants and 11 were not. Eight anticoagulated patients and three nonanticoagulated patients developed late HI without attendant worsening after an initial CT was nonhemorrhagic. Hemorrhagic transformation without worsening most often occurred after 12 hours but before 48 hours following stroke onset and was associated with large infarcts (82%) but not with age, blood pressure or embolic source. Seven anticoagulated patients, six with large infarcts, and one nonanticoagulated patient with a small infarct abruptly worsened from eight hours to 11 days after stroke, with CT revealing ICH or severe HI. Excessive anticoagulation or acute hypertension potentially contributed to hemorrhagic transformation in four of five patients who were receiving heparin. Brain hemorrhage in embolic strokes most often occurs with large infarcts. Early CT may not allow the identification of large embolic infarcts that are destined to later undergo spontaneous hemorrhagic transformation. For large embolic infarcts, a delay of several days before anticoagulation and special efforts to avoid excessive anticoagulation and hypertension may be prudent. The initial administration of large, bolus doses of heparin should perhaps be avoided.

Adult↗
PubMed1988

Generalized epileptic seizures as the presenting symptom of lacunar infarction in the brain.

Five elderly hypertensive patients presented with grand mal seizures and had computed tomographic (CT) findings consistent with lacunar infarction. Three of them had also a recent hemiparesis, contralateral to the side of the CT findings. Follow-up CT scans supported the diagnosis of lacunar infarction. Contrary to the accepted opinion, generalized epileptic seizures may be the presenting symptom of lacunar brain infarction.

Aged↗
PubMed2006

Neuroanatomic correlates of stroke-related myocardial injury.

BACKGROUND: Myocardial injury can occur after ischemic stroke in the absence of primary cardiac causes. The neuroanatomic basis of stroke-related myocardial injury is not well understood. OBJECTIVE: To identify regions of brain infarction associated with myocardial injury using a method free of the bias of an a priori hypothesis as to any specific location. METHODS: Of 738 consecutive patients with acute ischemic stroke, the authors identified 50 patients in whom serum cardiac troponin T (cTnT) elevation occurred in the absence of any apparent cause within 3 days of symptom onset. Fifty randomly selected, age- and sex-matched patients with ischemic stroke without cTnT elevation served as controls. Diffusion-weighted images with outlines of infarction were co-registered to a template, averaged, and then subtracted to find voxels that differed between the two groups. Voxel-wise p values were determined using a nonparametric permutation test to identify specific regions of infarction that were associated with cTnT elevation. RESULTS: The study groups were well balanced with respect to stroke risk factors, history of coronary artery disease, infarction volume, and frequency of right and left middle cerebral artery territory involvement. Brain regions that were a priori associated with cTnT elevation included the right posterior, superior, and medial insula and the right inferior parietal lobule. Among patients with right middle cerebral artery infarction, the insular cluster was involved in 88% of patients with and 33% without cTnT elevation (odds ratio: 15.00; 95% CI: 2.65 to 84.79). CONCLUSIONS: Infarctions in specific brain regions including the right insula are associated with elevated serum cardiac troponin T level indicative of myocardial injury.

Aged↗
PubMed2001

A focal embolic model of cerebral ischemia in rats: introduction and evaluation.

Cerebral thromboembolism is the most common type of acute stroke in the clinical setting. In the present study, we have described a focal embolic model of cerebral ischemia in rat. Cerebral ischemic injury in two different sizes was induced by injection of two different volumes of pre-formed clots into the middle cerebral artery (MCA). Neurological deficits were assessed at 1 and 24 h, respectively, after the MCA embolization. The brain infarction was evaluated with 2,3,5-triphenyltetrazolium chloride (TTC) staining at 72 h following embolic stroke. The incidence of gross hemorrhage was also identified on the TTC-stained brain sections. This study consisted of two groups. In the first group 10 microl of pre-formed clot was injected into MCA (n=10), and in the second group 5 microl of clot was injected (n=10). Embolizing a pre-formed clot resulted in an infarction in the territory irrigated by the MCA. Embolization with the different volume of clots resulted in different sizes of brain infarction, 32.1+/-2.9% (mean+/-S.E.) in the 10-microl group versus 23+/-4.5% (mean+/-S.E.) in the 5-microl group (P<0.05). The infarction size as well as neurological deficits correlated well with the volume of the clot injected. These results thus show that with the procedure described here a reliable and reproducible ischemic injury is produced in the brain. The model is relevant to thromboembolic ischemia in patients, and may offer a useful tool to investigate mechanisms underlying ischemic brain injury. It may also be used to test thrombolytic agents in ischemic brain injury.

Animals↗
PubMed2003

Identification of malignant brain edema after hemispheric stroke by PET-imaging and microdialysis.

Cerebral blood flow (CBF) and extent of irreversible tissue damage as well as the time course of extracellular concentration of amino acids, substrates of energy metabolism, and purine metabolites, intracranial pressure and tissue oxygen tension were assessed in 34 patients with large strokes covering more than 50% of the MCA territory. The results were compared to findings in the experimental model of transient (for 3 hours) MCA occlusion in cats. In the experimental model as well as in the clinical setting development of malignant brain infarcts (due to formation of space occupying brain edema) was predicted by the size of critically hypoperfused tissue and the volume of irreversibly damaged tissue. The course of malignant infarcts was characterized by progressive increase in concentrations of excitatory amino acids, lactate, pyruvate, glycerol, hypoxanthine and in intracranial pressure, while cerebral perfusion pressure and tissue oxygen tension decreased. These results clearly differentiate a malignant from a benign course of large hemispheric infarction. The methods can be used to identify patients at risk for formation of space occupying edema and to select patients who could benefit from invasive therapeutic strategies.

Amino Acids↗
PubMed2001

Cerebral blood flow and sources of abnormal EEG activity (VARETA) in neurocysticercosis.

OBJECTIVES: To compare two different functional procedures in the assessment of brain ischemia in patients with neurocysticercosis (NCC): (1) electroencephalography (EEG) evaluated by brain maps and EEG current sources in the frequency domain using variable resolution electromagnetic tomography and (2) blood flow analyzed by computerized tomography assessed with stable Xe (Xe-CT). METHODS: Eleven patients with NCC at different evolution stages were studied. CT and Xe-CT scans, as well as quantitative electroencephalography with source calculation in the frequency domain, were obtained. All patients showed cysts and in 6 of them there were also vascular complications: two of them presented calcifications of the middle cerebral artery, two other subjects showed calcifications of the vessels in the circle of Willis and the remaining two had brain infarctions. RESULTS: In the cyst areas important hypoperfused zones were observed, as intense as those observed in infarcted areas. Damage to the blood-brain barrier was originated by parasites in colloidal phase (final cysticerci stage) producing large areas of edema and hypoperfusion. Abnormal delta EEG activity was observed in very large lesions, probably generated by partial cortical deafferentation; and abnormal theta activity was mainly related to the presence of edema. CONCLUSIONS: Sources of abnormal EEG activity were very similar in topography to the hypoperfused areas.

Adult↗
PubMed1991

The prognostic value of blood glucose in patients with acute stroke.

We prospectively studied levels of blood glucose and glycohemoglobin, and their correlations with types, severity, and prognosis of stroke in 37 patients with brain infarction (BI) and 35 patients with brain hemorrhage (BH). We found that in the BH group, patients with an elevated glucose level due to stress, diabetes, or both, had a lower consciousness level on admission, larger hematoma size, higher incidence of rupture into the ventricles, and a worse 1-month outcome than patients with a normal glucose level (p less than 0.05). In patients with BI, however, no significant difference was found as related to levels of glucose, though a difference in 6-month mortality between stress hyperglycemic and normoglycemic patients (p less than 0.05) was found. We conclude that an elevated glucose level is associated with a worse clinical condition, larger hematoma size, higher incidence of rupture into the ventricles, and worse outcome in patients with BH. However, it seems to be the severity of the stroke, not the hyperglycemia, that causes the poor outcome. Hyperglycemia may be an epiphenomenon of stroke severity.

Aged↗
PubMed1985

Hydrogen ion buffering during complete brain ischemia.

As a first step to quantify [H+] changes in brain during ischemia we used H+-selective microelectrodes and enzyme fluorometric techniques to describe the relationship between interstitial [H+] ([H+]o) and peak tissue lactate after cardiac arrest. We found a step function relationship between [H+]o and tissue lactate rather than the linear titration expected in a homogeneous protein solution. Within a blood glucose range from 3-7 mM, brain lactate rose from 8-13 mmol/kg along with a rise in [H+]o of 99 +/- 6 nM(0.44 +/- 0.02 pH). At higher blood glucose levels (17-80 mM), brain lactate accumulated to levels of 16-31 mmol/kg; concurrently [H+]o rose by 608 +/- 16 nM (1.07 +/- 0.02 pH). The unchanging level of [H+]o between 8-13 and 16-31 mmol/kg lactate implies that [H+]o is at a steady-state, but not equilibrium with respect to [H+] in other brain compartments. We propose that ion-transport characteristics of astroglia account for the observed relationship of [H+]o to tissue lactate during complete ischemia and suggest that brain infarction develops after plasma membranes in brain cells can no longer transport ions to regulate [H+].

Animals↗
PubMed1990

Delayed decreases in specific brain mitochondrial electron transfer complex activities and cytochrome concentrations following anoxia/ischemia.

Hyperglycemic, but not normoglycemic cats exposed to anoxia develop neurologic signs following reoxygenation including fasciculations, focal and tonic-clonic seizures and coma after a symptom-free period. These symptomatic hyperglycemic cats may develop brain edema and will show diffuse neuronal injury or brain infarction depending on length of survival. Brain mitochondria isolated from symptomatic but not asymptomatic cats have decreased ADP- and uncoupler-stimulated oxygen consumption rates. Since impaired respiration could result from altered electron transport chain function, we measured cytochrome c, b, and aa3 concentrations and the activities of the five electron transfer complexes in isolated brain mitochondria. In symptomatic cats marked alterations were present in particular in complex IV, cytochrome oxidase, with a 57% reduction in activity and a 45% reduction in prosthetic group (cytochrome aa3) concentrations. Less marked reductions in other segments of the chain included 27% and 41% decreases, respectively, in cytochrome c concentrations and in electron transfer complex II, succinate:ubiquinone oxidoreductase activity. Cytochrome b concentrations and complex I, II and V activities were unchanged. Small but significant decreases in cytochrome aa3 concentrations (18%) and cytochrome oxidase activity (20%) were also present in mitochondria from postanoxic hyperglycemic cats prior to appearance of neurologic signs. These results indicate that delayed decreases in the activities of specific electron transfer complexes are correlated with impaired mitochondrial respiration and neurologic deterioration in postanoxic hyperglycemic cats. However, it is presently unclear if these postanoxic brain mitochondrial alterations are primary or secondary events in the development of brain injury.

Animals↗
PubMed1995

Pre-clinical evaluation of gadobutrol: a new, neutral, extracellular contrast agent for magnetic resonance imaging.

The Gd(3+)-complex of 10-(2,3-dihydroxy-1-hydroxymethylpropyl)-1,4,7,10-tetraazacyclo dodecane-1,4,7-triacetic acid(gadobutrol) is a new, neutral Gd-chelate for use as an extracellular contrast agent in magnetic resonance imaging (MRI). The blood level in dogs after intravenous (i.v.) injection decreased with a terminal half-life of about 45 min, the clearance was about 3.75 ml/min per kg and the distribution volume of 0.23 l/kg suggested an extracellular distribution. Biodistribution experiments in rats revealed that only a very small amount (0.16%) of the dose was left in the body 7 days after i.v. injection. Measurable amounts of Gd could be detected only in the liver, kidneys and bones. The osmolality (0.57 osmol/kg at 0.5 mol/l and 1.39 osmol/kg at 1 mol/l) is in the range of other low osmolality contrast media for MRI. Only very little interaction with biologically relevant molecules was suggested by a histamine release test and a lysozyme inhibition test. An i.v.-LD50 of 23 mmol/kg in mice combined with a comparatively high T1-relaxivity (5.6 l/mmol per s at 0.47 T and 6.1 l/mmol per s at 2 T) in plasma promises a high margin of safety. In preliminary imaging experiments, gadobutrol caused high enhancement in different lesions (cerebral infarct, brain tumor) of the rat. Tripling of the typical clinical dose of 0.1 mmol/kg was shown to provide additional diagnostic gain in lesions of this type.

Animals↗
PubMed1994

Infarcts in the anterior choroidal artery territory. Anatomical distribution, clinical syndromes, presumed pathogenesis and early outcome.

From a prospective registry of all consecutive patients with a supratentorial ischaemic stroke, those with a compatible CT lesion were selected to study topographical relationship, clinical syndrome, vascular risk factors, signs of large-vessel disease or cardiogenic embolism, and mortality in cases with an infarct in the anterior choroidal artery (AChA) territory in comparison with other infarct subtypes. First we identified the area supplied by the AChA: in accordance with the consensus in the literature the posterior two-thirds of the posterior leg of the internal capsule was considered as certain AChA territory. After reviewing CT scans, all presumed small deep AChA territory infarcts were displayed in a schematic composite picture of super-imposed areas of infarction in different shades of grey. Infarcts that were located largely outside the generally included territory were presumed to belong to a different vascular territory. Thus, 77 small deep infarcts were considered to be located within, and 83 outside the AChA territory. Twenty-nine AChA infarcts extended from the internal capsule upwards into the posterior paraventricular corona radiata region. Furthermore, the composite representation of 26 infarcts restricted to the posterior part of the paraventricular corona radiata region showed almost complete overlap with the area occupied by AChA infarcts that extended upwards. We therefore concluded that the posterior paraventricular area is most likely supplied by the AChA. The frequency of a clinical lacunar or a cortical syndrome did not differ between small deep AChA and remaining small deep infarcts. Comparison of vascular risk factors by way of multivariate regression analysis only showed that a significant carotid stenosis was more frequent (adjusted odds ratio 8.87; 95% confidence interval 1.44-54.50), and a cardioembolic source was less frequent (odds ratio 0.24; 95% confidence interval 0.07-0.92) in AChA infarcts than in the other small deep infarcts. Carotid stenosis and cardiac embolism were less frequent in AChA infarcts than in superficial infarcts (odds ratio 0.33, 0.23, respectively; 95% confidence interval 0.15-0.74, 0.09-0.52, respectively). One month and one year mortality were lower in small deep infarcts compared with superficial infarcts, but most favourable in the AChA group. However, this was probably related to younger age in the AChA patients. Larger AChA infarcts were infrequent in our series; six of such cases did not differ in any respect from superficial infarcts. We conclude that the posterior paraventricular corona radiata region is most likely supplied by the AChA, and that AChA infarcts do not constitute a separate brain infarct entity.(ABSTRACT TRUNCATED AT 400 WORDS)

Aged↗
PubMed1987

Dense middle cerebral artery sign: an indicator of poor outcome in middle cerebral artery area infarction.

Thirteen patients with a dense appearance of the horizontal part of the middle cerebral artery (MCA) "dense middle cerebral artery sign" in CT scans taken within 24 hours after onset of ischaemic stroke had considerably poorer prognosis than controls with stroke, but without the sign. A hyperdense appearance of the MCA is known to be associated with thromboembolism, but dense middle cerebral artery sign is also an early warning of a large infarction, brain oedema and poor prognosis in infarction in the MCA area.

Cerebral Arteries↗
PubMed2003

[Clinical results of LINAC-based stereotactic radiosurgery for pituitary adenoma].

PURPOSE: We retrospectively evaluated our clinical results of stereotactic radiosurgery (SRS) for pituitary adenoma. MATERIALS AND METHODS: Between 1995 and 2000, 13 patients were treated with SRS for pituitary adenoma. In all cases, the tumors had already been surgically resected. The adenomas were functional in 5 and non-functional in 8 patients. The median follow-up period was 30 months. SRS was performed with the use of a dedicated stereotactic 10-MV linear accelerator (LINAC). The median dose to the tumor margin was 15 Gy. The dose to the optic apparatus was limited to less than 8 Gy. RESULTS: MR images of 12 patients revealed tumor CR in one case and PR in 9 cases; in the remaining two patients, tumor size decreased by less than 50%. There was no recognizable regrowth of any of the tumors. In two of four GH-secreting adenomas, hormonal overproduction normalized, while the other two showed reduced hormonal production. One PRL-secreting adenoma did not respond. Reduction of visual acuity and field was seen in one patient. This patient also had a brain infarction. None of the patients developed brain radionecrosis or radiation-induced hypopituitarism. CONCLUSION: Although further studies based on greater numbers of cases and longer follow-up periods are needed, our results suggest that SRS seems to be a safe, effective treatment for pituitary adenoma.

Adenoma↗
PubMed2003

S100B and cardiac surgery: possibilities and limitations.

Serum determinations of the glial protein S100B has been found to correlate with brain damage after cardiac surgery. Forty-eight hours and later after surgery, increased S100B levels correlates with the presence of brain infarction, and the extent of infracted brain tissue. S100B at this time-point has been shown to predict long-term outcome, higher S100B levels correlated with decreased survival. Early levels (2-8 hours after surgery) of S100B have shown disparate results when trying to correlate it with postoperative cognitive decline. One reason for the lack of strong correlation could be the contamination of S100B from shed blood the first hours after surgery.

Animals↗
PubMed1986

[Effects of pentobarbital on brain lipid metabolism during global ischemia].

It is known that pentobarbital, which has been used for severe brain infarct or head injury as a brain protective drug, inhibits the increase of free fatty acids (FFAs) liberated from membrane phospholipids during ischemia. However, the mechanisms of FFA liberation from phospholipids and the mode of action of pentobarbital are still unclear. Therefore we have investigated the effects of induction of global ischemia and pentobarbital pretreatment upon lipid metabolism in rat brain. Brain ischemia was evoked by rat decapitation and pentobarbital (60 mg/kg) was administered i.p. for 15 min prior to decapitation. Removed brains were incubated for 1, 5, 15 or 30 min at 37 degrees C and then quickly frozen in liquid nitrogen. After extraction of lipids from the brains, neutral lipid and phospholipid compositions were analyzed by thin-layer and gas-liquid chromatography. The results demonstrated that FFAs, either unsaturated or saturated, were rapidly accumulated in the brain during early period of ischemia, but attenuated significantly by pentobarbital pretreatment. Pentobarbital attenuated the accumulations of stearic and arachidonic acids, with little effect on palmitic and oleic acids. Diacylglycerol (DG), which is considered to be as a plausible candidate for the source of FFA, was also produced in the ischemic brain, and its acyl chain composition was similar to that of liberated FFAs. Furthermore, the increase of DG was inhibited significantly by pentobarbital anesthesia. In particular, pentobarbital attenuated the accumulation of DG enriched in arachidonic and stearic acids. This fatty acyl composition resembled the principal composition of phosphatidylinositol (PI) in rat brain.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1999

Magnetic resonance imaging white matter hyperintensities and mechanism of ischemic stroke.

BACKGROUND AND PURPOSE: We sought to determine the relations between infarct subtype and white matter hyperintensities (WMHIs) on MRI. MATERIALS AND METHODS: We studied 395 ischemic stroke patients with 1. 0-T MRI. The number of lacunar, border-zone, and cortical infarcts was registered. WMHIs were analyzed in 6 areas. Univariate and multivariate statistical analyses were used to find the risk factors for different infarct subtypes and to study the connections between WMHIs and brain infarcts. RESULTS: Lacunar infarcts were associated with hypertension (odds ratio [OR], 1.79; 95% CI, 1.17 to 2.73), alcohol consumption (OR, 1.96; 95% CI, 1.17 to 3.28), and age (OR, 1. 03; 95% CI, 1.00 to 1.06). Border-zone infarcts were associated with carotid atherosclerosis (OR, 2.20; 95% CI, 1.15 to 4.19). Atrial fibrillation (OR, 3.02; 95% CI, 1.66 to 5.50) and carotid atherosclerosis (OR, 1.94; 95% CI, 1.12 to 3.36) were independent positive predictors, and history of hyperlipidemia (OR, 0.44; 95% CI, 0.26 to 0.75) and migraine (OR, 0.48; 95% CI, 0.25 to 0.93) were negative predictors for cortical infarcts. Patients with lacunar infarcts had more severe WMHIs than patients with nonlacunar infarcts in all WM areas (P</=0.001). Patients with border-zone infarcts showed severe periventricular lesions (P=0.002), especially around posterior horns (P=0.003). The extent of WMHIs in patients with cortical infarcts did not differ from that in those without cortical infarcts. CONCLUSIONS: Various infarct subtypes have different risk profiles. The association between lacunar infarcts and WMHIs supports the concept of small-vessel disease underlying these 2 phenomena. The connection between border-zone infarcts and periventricular WMHIs again raises the question of the disputed periventricular vascular border zone.

Aged↗