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At least 865 records · Page 48Linked to original sources
PubMed2003

[An autopsy case of pseudomesotheliomatous adenocarcinoma of the lung complicated with brain stem infarction due to nonbacterial thrombotic endocarditis].

A 53-year-old man was admitted to our hospital for back, left shoulder and upper limb pain. Chest radiography and CT on admission revealed right pleural effusion and a focal plate-like thickening of the major fissure. Pleural effusion cytology revealed adenocarcinoma, which was diagnosed as non-small-cell lung cancer with bone metastasis. The patient suffered from DIC, melena and multiple cerebral infarctions during chemotherapy and died on the eighth day of the second course of chemotherapy. Autopsy revealed a pseudomesotheliomatous adenocarcinoma covering the pleura of the right middle lobe, systemic thromboembolism and vegetations on the aortic valves due to nonbacterial endocarditis. Pseudomesotheliomatous adenocarcinoma of the lung, a rare form of lung cancer, complicated with DIC and nonbacterial endocarditis, is reported.

Adenocarcinoma↗
PubMed1989

Detection of lacunar infarction in brain CT-scans: no evidence of bias from accompanying patient information.

Interobserver agreement in assessing brain CT-scans is, in general, high. The extent, however, to which such agreement is caused by bias through knowledge of other clinical details remains uncertain. The hypothesis that observers are somehow prejudiced before assessing ambiguous CT-scans in this particular situation was tested. Sixteen neurologists and 16 radiologists volunteered to interpret two ambiguous brain CT-scans, with regard to the presence or absence of a lacunar infarct in the region of the internal capsule. The scans were accompanied by "patient" information that was or was not suggestive of a stroke. These scans were camouflaged by a variety of other scans, to be assessed in the same way, to mask the purpose of the study. It was assumed that the observers, in their assessments of the scans, would somehow let their ratings of the likelihood of a lacunar infarction in or near the internal capsule be subject to the accompanying information. Results showed lower ratings produced by neurologists (i.e., less likelihood of an infarction) than by radiologists in the majority of all assessments, but no bias by the accompanying information.

Cerebral Infarction↗
PubMed2004

Temporal changes in cerebral antioxidant enzyme activities after ischemia and reperfusion in a rat focal brain ischemia model: effect of dietary fish oil.

This study investigated the neuroprotective effects of dietary supplementation of fish oil on both brain infarction and the activities of antioxidant enzymes. Male Sprague-Dawley rats (4-weeks old) were divided into two groups and received either a regular diet (RD) or a fish-oil-supplemented diet (FOD) for 6 weeks prior to middle cerebral artery (MCA) occlusion. The infarction volume of the brain was calculated using image analysis after staining. Antioxidant enzymes were measured before ischemia (BI), after 2 h of ischemia (AI) and after 24 h (24hR), 48 h (48hR) and after 7 days (7dR) of reperfusion. The infarction volume of the brain was significantly smaller in the FOD group than in the RD group after 24 h of reperfusion (p<0.05). Before ischemia, the levels of lipid peroxide and the glutathione peroxidase (GPx) activity were higher in the FOD group than in the RD group. During reperfusion, the catalase (CAT) activity in the FOD group remained at the preischemia level until after 48 h of reperfusion, while those in the RD group did not. The Mn-superoxide dismutase (SOD) activity and GPx activity were higher in the FOD group than in the RD group only after 2 h of ischemia. In the fatty acid analysis, the ratio of docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) were higher in the FOD group than in the RD group (p<0.05). Our results demonstrate that supplementing the diet with fish oil could decrease the cerebral infarction volume following ischemia and reperfusion (I/R) partly by working directly as an antioxidant and partly by modulating antioxidant enzyme activities.

Animals↗
PubMed1994

A rapid, reliable, and valid method for measuring infarct and brain compartment volumes from computed tomographic scans.

BACKGROUND AND PURPOSE: Clinical stroke trials require objective and reproducible end point variables. Morphometry of cerebral structures, including infarct volume, provides numerical measures that represent the amount of tissue damaged and potentially salvaged by therapy. However, morphometry may be time-consuming and labor-intensive, and it requires standardization across multiple centers, which may be difficult to achieve in large multicenter trials. We developed a brain morphometry method that is unbiased, rapid, reliable, and based on well-accepted stereological techniques. We now extend this method to analysis of routine computed tomographic (CT) scans such as might be obtained during a clinical stroke trial. METHODS: We studied CT scans from 18 stroke patients and 14 asymptomatic control patients obtained over 5 years at the San Diego Veterans Administration Medical Center. Three observers independently measured the volume of the cranial vault, cerebrum, cortex, white matter, deep gray structures, ventricle, sulcal cerebrospinal fluid space, visible infarction, and cerebellum/brain stem. RESULTS: The two patient groups were well matched demographically. The intracranial volume of 1400 +/- 40 mL in control subjects was not different from the 1311 +/- 41 mL in patients. Cerebral volume was 1250 +/- 36 mL compared with 1070 +/- 36 mL (control subjects versus patients, P < .001), and infarction volume was 55 +/- 16 mL in patients. For all structures, intraclass correlation coefficients among the observers ranged from 0.87 to 0.03; the best agreement was found for lesion, ventricle, and intracranial volume. White matter and cortex volume predicted the National Institutes of Health Stroke Scale score but not the late outcome scores on the Barthel Index or Rankin Scale. Each scan required 70 to 90 minutes for analysis. CONCLUSIONS: We developed a stereological method for cerebral morphometry from CT scans that is reliable, rapid, and simple. The measurements are unbiased, can be made on slices of any known thickness, and are independent of machine variables. Our results are remarkably similar to values obtained with more labor-intensive methods. This method should be of use in large-scale, multicenter trials of stroke therapy.

Aged↗
PubMed1996

[Etiology and mechanism in cerebral infarction].

Cerebrovascular disease is the 3rd leading cause of death and an important cause of hospital admission and long-term disability in most industrialized populations. Many studies have shown that brain infarct is the most frequent form of cerebrovascular disease (83%). Brain infarct is a heterogeneous entity with several etiologies (mainly large-artery disease, small-artery disease, cardiac embolic disease). Different mechanisms are involved including arterial occlusion, thrombosis (atherosclerosis), embolism (from a cardiac or intraarterial source), and hemodynamic mechanisms (systemic hypoperfusion). Careful neurological assessment (cerebral computed tomogram, magnetic resonance imaging, Doppler ultrasound and angiography in selected cases) provides greater precision regarding these mechanisms and the choice of treatment.

Aortic Dissection↗
PubMed1977

[Radioisotope scanning in the diagnosis of cerebral infarction].

Cerebral scanning was performed in 52 cases of brain infarctions (in 43 cases in the system of middle brain arteries and in 9 cases in the vertebro-basillar basin). For this purpose in 46 of the studied cases human albumin serum, labeled readioactive I131 was used and in 6 cases-Tc 99m. Positive scannograms were received only in 16 patients with infarctions in the system of the middle brain arteries. The clinical picture in both groups of patients with positive and negative scannograms did not differ significantly from each other. This may indicate the fact that the process of accumulating radioactive isotopes in brain infarctions depends upon manifold reasons: the state of collateral circulations, the traits of angioarchitectonics in the affected area, the level of metabolism in the focus of lesions, disturbed permeability of the menatoencephalic barrier, etc. In doubtful cases for the differential diagnosis between brain infactions and tumors the most valid criteria in scanning is the dynamics of the focus of accuumulation of radioactive isotopes.

Adult↗
PubMed2003

Ischemic lacunar stroke in patients with and without potential mechanism other than small-artery disease.

BACKGROUND AND PURPOSE: Autopsy studies found that lacunar strokes differ in the size of the underlying brain infarct and that small lacunes are usually caused by hypertensive small-artery disease (SAD) and larger ones by atheromatous or embolic perforator occlusion. These findings suggest that larger lacunar infarcts might cause more severe neurological deficits and a higher detection rate on brain imaging compared with lacunar strokes caused by SAD. This prospective observational study was performed to investigate whether (1) neurological outcome, (2) prevalence of stroke risk factors, (3) prevalence of clinically asymptomatic occlusive cerebral artery disease, and (4) detection rate of underlying lacunar infarcts at brain imaging differ in ischemic lacunar strokes with (non-SAD) and without potential etiologies other than SAD. METHODS: Consecutive patients with lacunar stroke (n=244), defined by both clinical findings and brain imaging, were studied. Neurological deficit was quantified at presentation with the use of the National Institutes of Health Stroke Scale (NIHSS) and after 3 months with the NIHSS and the modified Rankin Scale (mRS). Cerebral arteries were investigated by ultrasound. RESULTS: Compared with patients with SAD lacunar strokes (n=155; 64%), patients with non-SAD lacunar strokes (n=89; 36%) had (1) higher NIHSS scores at presentation and higher NIHSS and mRS scores after 3 months (P<0.05); a higher prevalence of (2) hypertension (P<0.05), (3) coronary artery disease (P<0.0001), (4) previous transient ischemic attacks (P<0.01), and (5) asymptomatic stenoses of intracranial cerebral (P<0.01 to P<0.0001) and extracranial carotid (30% to 50% narrowing; P<0.01) arteries; and (6) a higher detection rate of the underlying lesion at brain imaging (P<0.01). CONCLUSIONS: Our data suggest that patients with non-SAD lacunar strokes have a worse clinical outcome and a higher prevalence of large cerebral and coronary artery disease than patients with SAD lacunar strokes.

Adolescent↗
PubMedDate not supplied

Neuron-specific enolase in cerebrospinal fluid and plasma of patients with acute ischemic brain disease.

The objective of this research was to determine the dynamics of change of neuron-specific enolase concentration in patients with acute ischemic brain disease in cerebrospinal fluid and plasma. The study included 103 patients, their mean age 58-66 years. The control group consisted of 16 patients, of matching age and sex, with radicular lesions of discal origin, subjected to diagnostic radiculography. Concentration of neuron-specific enolase was measured by a flouroimmunometric method. The results showed that the concentration of neuron-specific enolase in cerebrospinal fluid and plasma of patients with brain ischemic disease within first seven days significantly increased compared to the control. The highest increase of concentration was established in brain infarction, somewhat lower in reversible ischemic attack, and the lowest in transient ischemic attack. Maximal concentration was established on the 3rd-4th day upon the brain infarction. Neuron-specific enolase concentration in cerebrospinal fluid and plasma may be an indicator of pathophysiological processes in the acute phase of brain ischemia and is significant in early diagnostics and therapy of the disease.

Acute Disease↗
PubMed1997

Protective effect of zonisamide, an antiepileptic drug, against transient focal cerebral ischemia with middle cerebral artery occlusion-reperfusion in rats.

PURPOSE: The antiepileptic effects of zonisamide (ZNS) have been well documented experimentally and clinically. The purpose of this study was to examine whether ZNS reduces cerebral damage after transient focal ischemia in rats. METHODS: Ischemia was induced by a transient occlusion of the left middle cerebral artery (MCA) with a 3-0 nylon monofilament for 90 min. Neurological evaluation was performed by measuring the event of neurological deficit of the contralateral forepaw and hindpaw at 10 min and 1 day after MCA occlusion (MCAo). Brain infarct size was determined by measuring triphenyltetrazonium chloride-negative stained area of the serial brain sections 1 day after MCAo. RESULTS: The pre- or postischemic treatment with ZNS [(10-100 mg/kg p.o.), 30 min before and 4 h after or 15 min and 4 h after the occlusion] markedly reduced cerebral damage in the ipsilateral hemisphere and the neurological deficit induced by transient ischemia. The reducing effect on the damage was observed in the cortical and subcortical regions. Preischemic treatment with carbamazepine (CBZ 60 mg/kg p.o. twice 30 min before and 4 h after MCAo) tended to reduce the cerebral damage and neurological deficit, but the lower dose (20 mg/kg p.o. twice) did not. Valproate (VPA 1,000 mg/kg p.o. twice) also had no effect. CONCLUSIONS: ZNS at the anticonvulsant dose, unlike CBZ and VPA, ameliorated the brain infarction and the event of neurological deficit after transient focal cerebral ischemia. These data suggest that ZNS has therapeutic potential in protecting against ischemic cerebral damage, such as stroke.

Animals↗
PubMed1980

[Management and relapse prophylaxis of cerebral transitory ischemic attack (TIA) (author's transl)].

The paper gives a definition of the clinical concept of TIA, pointing out that the difference between TIA and ischemic brain infarction is not a qualitative but a quantitative one. Anatomy, physiology and metabolism of the brain will be discussed and clinical symptoms of TIA in the supply areas of the carotid and the vertebro-basilar arteries will be presented. Pathogenetic factors of TIA mentioned are: cardiac embolism, intravascular microembolism within the framework of cerebrovascular arteriosclerosis and alterations of blood composition, intracerebral steal mechanism, especially in cases of decreased systemic blood pressure and collateral circulation in stenotic or thrombotic vascular diseases. The paper stresses the importance of early diagnosis of TIA in view of the fact that approx. 30% of TIAs are not only followed by recurrent episodes but also develop into brain infarction. Clarification of the pathogenesis by appropriate examinations and causal therapy are therefore of particular importance. The significance of anticoagulant therapy, platelet aggregation inhibitors and cardiac therapy will be stressed and possible surgical management, especially the surgical bypass, will be presented. The curative and preventive effect of these forms of treatment will be evaluated.

Humans↗
PubMed1997

Post-treatment of transient focal cerebral ischemia in rats with the novel cerebrovascular-selective Ca2+ channel antagonist (+/-)-(E)-1-(3-fluoro-6,11-dihydrodibenz[b,e]-oxepine-11-yl)-4-(3-pheny l-2-propenyl)-piperazine dimaleate.

The efficacy of post-ischemic treatment with AJ-3941 ((+/-)-(E)-1-(3-fluoro-6,11-dihydrodibenz[b,e]-oxepine-11-yl )-4-(3-phenyl-2- propenyl)-piperazine dimaleate, CAS 143110-70-7), a cerebrovascular selective Ca2+ channel antagonist, on brain infarction induced by focal ischemia-reperfusion in rats was evaluated. Focal ischemia was induced by transient occlusion of middle cerebral artery (MCA) with a 3-0 nylon monofilament for 90 min. One day after MCA occlusion (MCAo), brain infarct size was determined by measuring 2,3,5-triphenyltetrazonium chloride-negative stained area of the serial brain sections. The development of cerebral infarction was observed in both regions of cortex and subcortex, such as striatum, caudatum, putamen, hippocampus and corpus callosum. Post-ischemic treatment with AJ-3941 (1 or 3 mg/kg p.o., 10 min and 3 h after the occlusion) significantly reduced the infarct size and volume in the ipsilateral hemisphere in a dose-dependent manner, compared to the solvent control. The reducing effect was observed mainly in the cortical region, and a significant reduction of the subcortical infarct volume was found at the higher dose (3 mg/kg). Post-ischemic treatment with the thromboxane A2 synthetase inhibitor, sodium ozagrel (150 micrograms/kg/min i.v. infusion, between 1 h and 24 h after the MCAo) did not reduce the infarct volume in the hemisphere after ischemia-reperfusion. AJ-3941 had only minimum effect on the elevation of body temperature during ischemia-reperfusion. These results indicate that post-ischemic treatment with AJ-3941 may ameliorate the brain injury after the transient focal cerebral ischemia, and they suggest that AJ-3941 has beneficial effects for treatment of ischemic cerebral damage, such as stroke.

Animals↗
PubMed1997

Multiple brain gas embolism after ingestion of concentrated hydrogen peroxide.

We present a 63-year-old man who developed multiple brain infarction after ingesting a 35% hydrogen peroxide solution. Neurologic examination revealed left hemiparesis, primarily affecting the lower limb, and mild weakness of the right lower limb. Gadolinium-enhanced MRI revealed patchy bilateral brain lesions. Oxygen gas embolization is the likely cause of the brain infarctions.

Accidents↗
PubMed1999

Use of diffusion-weighted MRI and neurological deficit scores to demonstrate beneficial effects of isradipine in a rat model of focal ischemia.

The neuroprotective effects of isradipine, a 2,4-dihydropyridine calcium channel blocker, has been well studied in the rat model of focal ischemia (induced by middle cerebral artery occlusion, MCAO). The present study was designed to evaluate whether isradipine pretreatment caused early (0-3 h after stroke) ischemic changes in diffusion- weighted magnetic resonance imaging (DWI) and if such changes were predictive of previously documented protection in brain infarction. An initial dose-response study using neurological deficit scores and estimates of protection from brain infarction (by histology) showed that isradipine reduced cortical infarctions compared to vehicle-treated animals at most doses (between 1.25 and 5 mg/kg/day s.c. for 6 days) with the best results obtained at 5 mg/kg/day, where a 78.5% reduction was observed. This dose was utilized to perform the DWI study. Early quantitative estimates of infarct size, as measured by DWI at 1, 2 and 3 h after MCAO, were similar to those obtained with late histology at 24 h. These data indicate that in pretreatment protocols, DWI can be used to quantitatively predict areas at risk of permanent damage. This work also demonstrates that neurological deficits, developing from the damaged forebrain following focal stroke, may provide an index of isradipine's neuroprotective activity.

Animals↗
PubMedDate not supplied

[Pathogenesis and clinical aspects of stroke].

The pathogenesis of brain infarctions, intracerebral hematomas and subarachnoidal hemorrhages is described. It is believed that defects in microcirculation are important factors in the development of brain infarctions, whereas hypertension and microaneurysms or vascular malformations are sources of intracerebral hematomas and subarachnoidal hemorrhages. Detection and differential diagnosis are presented from clinical aspects. Possibilities and limits of laboratory methods, especially CCT, are emphasized.

Aged↗
PubMed1996

[FLAIR images of cerebral and brain stem infarction].

FLAIR (fluid-attenuated inversion recovery) images are MR images obtained with an inversion recovery sequence having a long inversion time (TI) and a long echo time (TE). We examined 47 cases (56 graphics) of lacunar infarction (LI), 28 cases (32 graphics) of cortical infarction (CI) and 16 cases (23 graphics) of stem infarction (SI) with a FLAIR sequence having a repetitive time (TR) of 6500 msec, a TI of 1700 msec and a TE of 110 msec, and compared these graphics with T2-weighted images by spin-echo sequence (TR 2500 msec, TE 90 msec). LI and CI were better demonstrated with FLAIR images than with conventional T2-weighted images. FLAIR images were very useful in detecting lesions adjacent to the lateral ventricles and the cerebral sulci in particular, because the cerebrospinal fluid signals in the lateral ventricles and the cerebral sulci were low-intensity, with brain tissue appearing as high-intensity areas. In a number of old infarctions, FLAIR images revealed cystic structures, constructed out of internal low-intensity areas and peripheral high-intensity areas. These structural changes suggested that FLAIR images can provide information on pathological changes.

Aged↗