Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Embolic Stroke”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 145 records · Page 8Linked to original sources
PubMed1995

Spurious hyperfixation of hexamethylpropyleneamine oxime in acute embolic stroke.

A 71-year-old man with atrial fibrillation suddenly had an embolism in the right middle cerebral artery. Single-photon emission CT was performed 4 hours after the onset of stroke and revealed markedly elevated 99mTc-hexamethylpropyleneamine oxime (HMPAO) uptake in the right frontotemporoparietal region. This area of HMPAO hyperfixation corresponded to the area of infarction, as determined by CT and MR. Our findings showed that HMPAO single-photon emission CT overestimated reflow hyperemia after reperfusion in the acute stage of embolic stroke, as it does in the subacute stage.

Acute Disease↗
PubMed1999

Recent heavy drinking of alcohol and embolic stroke.

BACKGROUND AND PURPOSE: Epidemiological evidence suggests that heavy alcohol consumption increases the risk for ischemic stroke, whereas light-to-moderate alcohol intake decreases the risk, but the role of different drinking patterns has remained unclear. We investigated recent light, moderate, and heavy alcohol drinking and former heavy drinking as risk factors for acute ischemic brain infarction by etiological subtype of stroke. METHODS: We compared 212 consecutive patients aged between 16 and 60 years, who were completely evaluated for the etiology of their ischemic stroke, with 274 control subjects admitted to the emergency unit of the same hospital. ORs, as estimates of multivariate relative risks (RRs), and 95% CIs after adjustment for possible confounding variables were calculated by logistic regression. The ORs were adjusted for age, sex, body mass index, hypertension, diabetes, hyperlipemia, current smoking, and history of migraine. RESULTS: Recent heavy drinking but not former heavy drinking was an independent risk factor for stroke (RR 1.82, 95% CI 1.08 to 3.05). Consumption of 151 to 300 g and >300 g alcohol within the week preceding the onset of stroke significantly increased the risk for cardioembolic and cryptogenic stroke. Consumption of >40 g alcohol within the preceding 24 hours increased the risk for cardiogenic embolism to the brain among those who had a high-risk source (RR 4.75, 95% CI 1.23 to 18.4), the risk for tandem embolism among those who had prominent large-artery atherosclerosis (RR 7.68, 95% CI 1.82 to 32.3), and the risk for cryptogenic stroke (RR 3.84, 95% CI 1.69 to 8.71). Light drinking did not increase the risk for stroke. CONCLUSIONS: We conclude that acute drinking of intoxicating amounts of alcohol may trigger the onset of embolic stroke among subjects who have a source of thrombus in the heart or the large arteries.

Adolescent↗
PubMed2004

Ultrasonography in embolic stroke: the complementary role of transthoracic and transesophageal echocardiography in a case of systemic embolism by tumor invasion of the pulmonary veins in a patient with unknown malignancy involving the lung.

Two-dimensional transthoracic echocardiography is commonly performed to detect a possible cardiac source of systemic embolism and it has been the mainstay of detection and diagnosis of cardiac masses. The transesophageal approach has enhanced the ability to detect cardiac sources of embolism by allowing a better visualization of posterior cardiac structures such as the left atrium with left atrial appendage, pulmonary veins and thoracic aorta and by providing higher resolution images to improve assessment of the presence and extent of cardiac masses. In this case report, echocardiography, using both transthoracic and transesophageal approach, allowed to detect a neoplastic mass arising from the upper left pulmonary vein in a patient presented with a transient ischemic attack. Further investigations showed a malignancy involving the lung. To our knowledge, this is the first reported case in which a cerebral embolic episode represents the clinical onset of a lung cancer, pointing out the importance of echocardiography in all cases of undetermined cerebral ischemic attack.

Adenocarcinoma↗
PubMed1994

Embolic stroke by compression maneuver during transcranial Doppler sonography.

BACKGROUND AND PURPOSE: Embolic complications during ultrasound examinations are a rare cause of neurological deficits. The present case documents the occurrence of embolism by a nonobstructive compression maneuver during transcranial Doppler examination, resulting in a minor stroke. CASE DESCRIPTION: A 63-year-old man suffered from recurrent transient ischemic attacks. Duplex sonography showed a small echogenic plaque at the right carotid bifurcation. During transcranial Doppler studies with a reverberating compression maneuver of the right common carotid artery low in the neck, multiple emboli signals were detected, and the patient developed a left-sided hemiparesis with slurred speech. Funduscopy revealed cholesterol emboli in the inferior temporal arteriole of the right eye. These findings suggested embolization as the cause of the stroke. CONCLUSIONS: Compression maneuvers should not be performed in patients with recent neurological symptoms, even in the case of only small lesions in the extracranial carotid territory.

Carotid Artery Diseases↗
PubMed1993

Monoclonal antibody to the ICAM-1 adhesion site reduces neurological damage in a rabbit cerebral embolism stroke model.

We evaluated the effect of antibodies directed against a leukocyte adhesion molecule (ICAM-1) in an embolic model of stroke followed by thrombolysis with tissue plasminogen activator (tPA). To test whether reperfusion injury after ischemia was related to white cell adhesion, microclots were injected into carotid circulation. The conditions examined were control, alpha-ICAM 5 min following ischemia, tPA 30 min after ischemia, and the combination of alpha-ICAM and tPA. alpha-ICAM and tPA both increased the amount of clot necessary to produce permanent neurological damage. Combined therapy was no more effective than either substance alone. A similar outcome was obtained when tPA was delayed until 90 min postischemia. When thrombolysis was delayed 3 h following embolism, neither tPA nor the tPA/alpha-ICAM combination reduced neurological damage. Thus, the alpha-ICAM antibody and tPA each effectively reduced neurological damage but the interaction was not significant.

Animals↗
PubMedDate not supplied

[Cerebral-cardiac embolism. Cerebrovascular-cardiac embolic stroke].

The diagnosis of cerebral cardioembolism requires, apart from evidence of an embolic cardiopathy, a cause-effect relation to be established between the potential cardioembolic source and the occurrence of ischemic stroke. There are several arguments in favour of this reaction, namely the neurologic aspects put forward both clinicians and neuroimaging professionals, as well as the generalization of cardiologic diagnostic techniques for the etiologic investigation of ischemic stroke. Importance should be given to primary prevention of embolic cardiopathies. Oral anticoagulation should be administered in all situations where an advantage has been established when compared to antiaggregation or placebo. Cooperation between the different health structures and the different specialties probably depends on the changes in the prevalence of cerebral cardioembolism.

Embolism↗
PubMed1990

Embolic stroke after smoking "crack" cocaine.

A 39-year-old woman had an embolic upper division middle cerebral artery branch occlusion 3 hours after smoking the free base of cocaine ("crack"). Radionuclide ventriculography demonstrated cardiomyopathy, and echocardiography documented a left atrial thrombus. This case demonstrates that embolism is one mechanism of ischemic stroke after cocaine use, and that cardiomyopathy, possibly cocaine induced, may be the source of embolus. A cardiac source of embolus should be sought in patients with cocaine-associated cerebral infarction.

Adult↗
PubMed2003

Antiactin-targeted immunoliposomes ameliorate tissue plasminogen activator-induced hemorrhage after focal embolic stroke.

Thrombolytic stroke therapy with tissue plasminogen activator (tPA) is limited by serious risks of intracerebral hemorrhage. In this study, the authors show that a novel antiactin-targeted immunoliposome significantly reduced tPA-induced hemorrhage in an established rat model of embolic focal stroke. Spontaneously hypertensive rats were subjected to focal ischemia using homologous blood clot emboli. Delayed administration of tPA (10 mg/kg, 6 hours after ischemia) induced intracerebral hemorrhage at 24 hours. In control rats treated with tPA plus vehicle, hemorrhage volumes were 9.0 +/- 2.4 uL (n = 7). In rats treated with tPA plus antiactin immunoliposomes, hemorrhage volumes were significantly reduced to 4.8 +/- 2.7 uL (n = 8, P < 0.05). No significant effects were seen when rats were treated with tPA plus a nontargeted liposome (7.8 +/- 2.1 uL, n = 9). Fluorescent immunohistochemistry showed that rhodamine-labeled targeted liposomes colocalized with vascular structures in ischemic brain that stained positive for endothelial barrier antigen, a marker of cerebral endothelial cells. These data suggest that immunoliposomes may ameliorate vascular membrane damage and reduce hemorrhagic transformation after thrombolytic therapy in cerebral ischemia.

Actins↗
PubMed2005

Identification of embolic stroke patterns by diffusion-weighted MRI in clinically defined lacunar stroke syndromes.

BACKGROUND: A number of clinical syndromes describing the presentation of deep brain infarcts are called lacunar syndromes resulting from small vessel occlusion (SVO). To verify the reliability of the clinical diagnosis "lacunar syndrome," the value was investigated with diffusion-weighted MRI (DWI). METHODS AND RESULTS: A total of 73 patients (mean age 66 years; range 35 to 83 years) with sudden onset of a classical lacunar syndrome were enrolled. On the basis of the DWI findings, patients were divided into 3 groups: group 1, single subcortical lesion (<15-mm lesion; 43 patients; 59%); group 2, large (> or =15 mm) or scattered lesions in 1 vascular territory (16 patients; 22%); and group 3, multiple lesions in multiple vascular territories (14 patients; 19%). A stroke mechanism other than SVO could be identified in 17 (23%) patients. Cardiac work-up revealed a cardiac embolic source in 8 patients (11%). Duplex sonography revealed symptomatic stenosis in 9 patients (12%). Based on the work-up information, 29 patients (40%) were found to have a potential cause of stroke other than SVO. A significant correlation with >1 single lesion on DWI-MRI and a clinical proven embolic source was observed (P=0.002). In 9 patients with MRI suspicious for a pathomechanism other than SVO, no embolic source was found. CONCLUSIONS: The use of DWI-MRI improves the accuracy of the subtype diagnosis of stroke. Inaccuracy has to be expected in approximately one third if lacunar diagnosis is based on clinical and computed tomography findings. Most of these "false-positive" cases are attributable to large artery or cardiogenic embolic stroke.

Adult↗
PubMed2005

Submassive pulmonary embolism and paradoxical embolic stroke treated with percutaneous rheolytic thrombectomy and closure of the patent foramen ovale.

The presence of patent foramen ovale (PFO) in patients with large pulmonary emboli (PE) is associated with an increased risk of stroke and mortality. Many patients are ineligible to receive thrombolytic therapy. We present a patient with bilateral PE and cryptogenic stroke who was treated effectively with rheolytic thrombectomy with AngioJet, PFO closure with CardioSeal device, and placement of an inferior vena cava filter.

Aged↗
PubMed2002

Rapid breakdown of microvascular barriers and subsequent hemorrhagic transformation after delayed recombinant tissue plasminogen activator treatment in a rat embolic stroke model.

BACKGROUND AND PURPOSE: Thrombolytic therapy with recombinant tissue plasminogen activator (rtPA) after stroke increases risk of hemorrhagic transformation, particularly in areas with blood-brain barrier leakage. Our aim was to characterize acute effects of rtPA administration on the integrity of microvascular barriers. METHODS: Stroke was induced in spontaneously hypertensive rats by unilateral embolic middle cerebral artery occlusion. Six hours after stroke, rtPA was intravenously administered (n=10). Controls received saline (n=4). Extravasation of the large-diameter contrast agent monocrystalline iron oxide nanocolloid (MION) was assessed with susceptibility contrast-enhanced MRI during rtPA injection. In addition, we performed perfusion MRI and diffusion-weighted MRI. After MRI, 2 hours after rtPA treatment, intracerebral hemorrhage was quantified with a spectrophotometric hemoglobin assay. RESULTS: Late rtPA treatment resulted in increased hemorrhage volume (8.4+/-1.7 versus 2.9+/-0.9 micro L in controls; P<0.05). In MION-injected animals, during rtPA administration, transverse relaxation rate change (DeltaR2*) increased from 12.4+/-6.0 to 31.6+/-19.2 s(-1) (P<0.05) in areas with subsequent hemorrhage. Significant DeltaR2* changes were absent in nonhemorrhagic areas, in animals without injected MION, and in saline-treated animals. Thrombolytic therapy did not improve perfusion in regions with hemorrhagic transformation (cerebral blood flow index was 22.8+/-19.7% [of contralateral] at 0.5 hours before and 22.4+/-18.0% at 1 hour after rtPA administration). CONCLUSIONS: The DeltaR2* changes during rtPA delivery in MION-injected animals indicate extravasation of MION, which reflects increased permeability of the blood-brain barrier. This implies that late rtPA treatment rapidly aggravates early ischemia-induced damage to microvascular barriers, thereby enhancing hemorrhagic transformation.

Animals↗
PubMed2002

Effects of the spin trap agent disodium- [tert-butylimino)methyl]benzene-1,3-disulfonate N-oxide (generic NXY-059) on intracerebral hemorrhage in a rabbit Large clot embolic stroke model: combination studies with tissue plasminogen activator.

BACKGROUND AND PURPOSE: It has been proposed that the novel spin trap agent disodium-[(tert-butylimino)methyl]benzene-1,3-disulfonate N-oxide (NXY-059) may be useful in the treatment of ischemia and stroke. To date, there is little information concerning the safety of NXY-059 when administered in combination with the only Food and Drug Administration-approved pharmacological agent for the treatment of stroke, the thrombolytic tissue plasminogen activator (tPA). Thus, we determined the effects of NXY-059G, a generic form of NXY-059, on hemorrhage and infarct rate and volume when administered alone or in combination with tPA. In addition, we determined whether NXY-059G affected 2 physiological variables, blood glucose levels and body temperature. METHODS: Male New Zealand White rabbits were embolized by injecting a large blood clot into the middle cerebral artery via a catheter. Five minutes after embolization, NXY-059G (100 mg/kg) was infused intravenously; control rabbits received infusions of saline, the vehicle required to solubilize NXY-059G. In tPA studies, the thrombolytic was administered intravenously starting 60 minutes after embolization (20% bolus injection/80% infusion over 30 minutes). Body temperature and blood glucose levels were measured throughout the study. Postmortem analysis included assessment of hemorrhage and infarct rate, size, and location. RESULTS: In the vehicle control group, the hemorrhage rate after a thromboembolic stroke was 52% (n=23), and this was increased by 67% if tPA was administered (n=15). The rabbits treated with NXY-059G in the absence of tPA had a 79% incidence of hemorrhage (n=19), an increase of 52% over the control group. In the combination drug-treated groups, the NXY-059G/tPA group had a 47% incidence of hemorrhage (n=15). There was a decrease of hemorrhage volume in the NXY-059G+tPA group compared with the other 3 groups included in the study. There was no significant effect of NXY-059G either alone or in combination with tPA on infarct rate or volume. NXY-059G did not significantly alter the physiological variables that were measured. CONCLUSIONS: This study suggests that NXY-059G may affect the integrity of the cerebral vasculature when administered immediately after an embolic stroke, as evidenced by an increase in hemorrhage rate. However, when NXY-059G is administered in combination with tPA, it may improve the safety of tPA by reducing the incidence of tPA-induced hemorrhage. The mechanism(s) involved in the NXY-059G-induced increase in hemorrhage rate and reduction of tPA-induced hemorrhage rate remains to be elucidated.

Animals↗
PubMed2000

Postischemic intracarotid treatment with TNK-tPA reduces infarct volume and improves neurological deficits in embolic stroke in the unanesthetized rat.

BACKGROUND AND PURPOSE: To simulate human stroke, we developed a model of focal cerebral embolic ischemia in the unanesthetized rat. Using this model, we tested the hypothesis that intra-arterial administration of TNK-tPA, a fibrin specific second generation thrombolytic agent, is effective in reducing ischemic volume without increasing intra-cerebral hemorrhage. METHODS: Under anesthesia, a catheter was inserted to the origin of the MCA of male Wistar rats. Forty-five minutes after recovery from anesthesia, the MCA was occluded in the awake rat by a single fibrin rich clot placed via the catheter. TNK-tPA (1.5 mg/kg) was administered intraarterially via the catheter at either 2 h or 4 h after stroke. All rats were sacrificed at 48 h after ischemia. Neurological deficits, gross hemorrhage and ischemic lesion volume were measured. RESULTS: A clot was detected at the origin of the MCA 4 h after MCA occlusion in the awake rats (n=4). Rats (n=12) subjected to MCA occlusion showed immediate neurological deficits which persisted for 48 h of ischemia. Ischemic rats had a lesion volume of 38.2+/-3.8% and 25% of rats exhibited gross hemorrhage. Ischemic rats (n=10) treated with TNK-tPA at 2 h showed a significant (P<0.05) reduction of neurological deficits, body weight loss and infarct volume (22.8+/-2.1%) without an increase in gross hemorrhage (10%) compared with the non treated ischemic rats (25%). Although treatment with TNK-tPA of ischemic rats (n=12) at 4 h did not significantly (P=0.06) reduce infarct volume (28.6+/-3.0%), it also did not increase gross hemorrhage (25%) compared with the control group (25%). CONCLUSIONS: This study demonstrates that intraarterial administration of TNK-tPA at 2 h of ischemia in the unanesthesthetized rat is effective in reducing neurological deficits and ischemic lesion volume without increasing hemorrhagic transformation and that administration of TNK-tPA at 4 h of ischemia does not increase the incidence of hemorrhagic transformation.

Animals↗
PubMed2006

Embolic stroke due to a left atrial thrombus two years after placement of an atrial septal defect closure device.

A 29-year-old woman who had undergone closure of a secundum-type atrial septal defect using the Amplatzer device 2 years previously developed acute and progressive altered mentation. Initial clinical and imaging data confirmed the diagnosis of multiple cerebral, cerebellar and brain stem emboli, and infarcts. She was treated urgently with an intra-arterial thrombolytic agent with only minimal improvement. Transesophageal echocardiography revealed a large thrombus attached to the left atrial disc of the atrial septal defect occluder, which was the source of the emboli. In conclusion, this is the first reported case, to our knowledge, of disseminated cerebral emboli and infarctions as a late complication of transcatheter closure of a secundum-type atrial septal defect.

Adult↗
PubMed2006

Thunderclap stroke: embolic cerebellar infarcts presenting as thunderclap headache.

Thunderclap headache is known to be a presenting feature of subarachnoid hemorrhage, unruptured intracranial aneurysm, cerebral venous thrombosis, cervical artery dissection, spontaneous intracranial hypotension, pituitary apoplexy, retroclival hematoma, and hypertensive reversible posterior leukoencephalopathy. We describe a case of thunderclap headache in the absence of focal, long-tract, or lateralizing neurological findings, as the primary clinical feature of embolic cerebellar infarcts. This case expands the differential diagnosis of thunderclap headache and reinforces the need for magnetic resonance imaging in the evaluation of such patients, even when neurologic examination, brain computed tomography, and cerebrospinal fluid analysis are normal.

Aged↗
PubMed1994

Effect of hypothermia and delayed thrombolysis in a rat embolic stroke model.

Effect of hypothermia on cerebral infarcts was studied in rats embolized in the right carotid territory. Thirty-four served as normothermic controls receiving saline infusion only. In 16 rats hypothermia of 32 degrees C was induced by cooling with a fan, followed by embolization. The rats were kept hypothermic for the following 3 h before body temperature was raised to 37 degrees C. In 26 rats, treatment with human recombinant tissue plasminogen activator (20 mg/kg i.v. during 45 min), started 2 h after embolization. Finally, 14 rats were treated similarly with hypothermia for 3 h followed by additional rt-PA treatment starting after 2 h. Thrombolytic therapy reduced median infarct volume from 19.5% of affected hemisphere among controls to 4.6% (p = 0.006) in the treated group. Three hours of hypothermia reduced infarct volume to 1.6% (p = 0.0007). Additional rt-PA could not demonstrate further improvement in this experimental setting.

Animals↗