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PubMed2005

Recurrent embolic stroke originating from an internal carotid aneurysm in a young adult.

An unruptured intracranial aneurysm is an uncommon but possible embolic source to the brain. We report a young patient who developed recurrent ischemic strokes occurring mainly in the left internal carotid arterial territory within a short interval; the first stroke occurred midway through a long-distance race, and the second stroke occurred immediately following a bowel movement. The angiographical contrast deficit indicated a thrombus in the left anterior cerebral artery as a result of the embolism. A saccular aneurysm of the left distal internal carotid artery was the only detectable potential embolic source. Initially anticoagulant therapy was given, and then surgical clipping of the aneurysm was performed. The patient has been free from stroke recurrence. As a cause of ischemic stroke in young adults, a carotid saccular aneurysm should be considered. Hard exercise and a Valsalva maneuver may be important triggers of thrombus detachment from the aneurysm.

Carotid Artery Diseases↗
PubMed1985

How often can an embolic stroke be diagnosed clinically? A clinicopathological correlation.

A retrospective case note survey of 103 autopsy proven cases of cerebral infarction was carried out to assess how often a cardiac source for embolism had been correctly suspected on clinical grounds. Only 61% of 46 patients with cardiac embolic sources were so identified. Cases of rheumatic heart disease and bacterial endocarditis were more frequently identified than cases of mural thromboembolism from ischaemic heart disease. This relative failure of unaided clinical diagnostic criteria probably accounts for the discrepancy between the autopsy evidence of cardiac embolism as a cause of stroke (about 40%), and clinical studies (about 20%).

Cerebral Infarction↗
PubMed2002

Use of diffusion weighted MRI to predict the occurrence and severity of hemorrhagic transformation in a rabbit model of embolic stroke.

Severe hemorrhagic transformation (HT) is an important complication of thrombolytic therapy. A method to identify stroke victims destined to severe HT could improve the patient selection and thus the safety of such treatment. In this study, we investigated whether very early serial diffusion weighted magnetic resonance imaging (DWI) could predict the occurrence of HT in an embolic model of experimental stroke. We tested the hypothesis that the ischemic brains with very low initial apparent diffusion coefficients (ADC) are destined to severe early (<or=5.5 h) HT. We retrospectively analyzed DWI scans of 45 New Zealand white rabbits subjected to thromboembolic stroke and treated with thrombolysis. DWI was obtained 0.5, 2, 3 and 5 h after embolization. Various thrombolytics were administered 1 h post embolization. The percentage of pixels within the ischemic hemisphere with ADC values below 550 x 10(-6) mm(2)/s was calculated and then compared to the severity of HT observed on gross brain sections at 5.5 h. As early as 30 min after embolization, ischemic brains destined to severe HT exhibited a significantly greater percentage of pixels below the cut-off value compared to those without HT: severe HT: 25%, 18.75-37.25% vs. no HT: 12%, 5.00-16.00% (median, 25th-75th %, P<0.001). Petechial HT when percentages were in the intermediate range. Quantitative analysis of initial ADC value might identify individual stroke patients at risk of severe HT.

Animals↗
PubMed2006

Neuroprotective effect of hyperbaric oxygen therapy monitored by MR-imaging after embolic stroke in rats.

The potential neuroprotective effects of hyperbaric oxygen (HBO) were tested in an embolic model of focal cerebral ischemia with partially spontaneous reperfusion. Rats (n = 10) were subjected to embolic middle cerebral artery occlusion (MCAO) and diffusion weighted MRI (DWI) was performed at baseline, 1, 3, and 6 h after MCAO to determine the ADC viability threshold yielding the lesion volumes that best approximated the 2,3,5-triphenyltetrazolium chloride (TTC) infarct volumes at 24 h (experiment 1). For assessment of neuroprotective effects, rats were treated with 100% oxygen at 2.5 atmospheres absolute (ATA, n = 15) or normobaric room air (n = 15) for 60 min beginning 180 min after MCAO (experiment 2). DWI-, perfusion (PWI)- and T2-weighted MRI (T2WI) started within 0.5 h after MCAO and was continued 5 h, 24 h (PWI and T2WI only), and 168 h (T2WI only). Infarct volume was calculated based on TTC-staining at 24 h (experiment 1) or 168 h (experiment 2) post-MCAO. ADC-lesion evolution was maximal between 3 and 6 h. In experiment 2, the relative regional cerebral blood volume (rCBV) of both groups showed similar incomplete spontaneous reperfusion in the ischemic core. HBO reduced infarct volume to 145.3 +/- 39.6 mm3 vs. 202.5 +/- 58.3 mm3 (control, P = 0.029). As shown by MRI and TTC, HBO treatment demonstrated significant neuroprotection at 5 h after embolic focal cerebral ischemia that lasted for 168 h.

Animals↗
PubMed1995

Rotational vertigo in embolic stroke of the vestibular and auditory cortices.

We describe the unique case of a woman with embolic infarction within the right middle cerebral artery territory who had nonepileptic rotational vertigo, nausea, and unsteady gait that gradually resolved within a week. A well-demarcated lesion of the posterior insula (homologous to parieto-insular vestibular cortex in monkeys) was probably the cause. This is supported by a contraversive tilt of perceived vertical and by involvement of the adjacent auditory (Heschl's) cortex. Dipole source analysis of late auditory evoked potentials revealed a decreased amplitude of a dipole source in the right insular cortex, whereas two other dipoles situated in the temporal lobe showed symmetric activity.

Acoustic Stimulation↗
PubMedDate not supplied

Isolated left ventricular non-compaction as a cause of thrombo-embolic stroke: a case report and review.

Isolated left ventricular non-compaction is the result of incomplete myocardial morphogenesis, leading to persistence of the embryonic myocardium. The condition is recognised by an excessively prominent trabecular meshwork and deep intertrabecular recesses of the left ventricle. These intertrabecular recesses are prone to thrombus formation, with resultant embolic sequelae. We describe a case of cerebral thrombo-embolism in a young woman due to isolated left ventricular non-compaction.

Adult↗
PubMed1978

The sequential uptake of (14C) deoxyglucose in brain after embolic stroke.

An i.v. bolus of (14C) deoxyglucose was injected into 4 groups of rats which simultaneously were embolized through the internal carotid artery. 15 and 30 min post embolization there was a massive decrease in (14C) deoxyglucose uptake in both deep and cortical structures. At 4 h a small zone of increased (14C) deoxyglucose uptake persisted around each embolized microsphere.

Animals↗
PubMed1994

The influence of body temperature on infarct volume and thrombolytic therapy in a rat embolic stroke model.

The effect of body temperature on cerebral infarcts and thrombolytic therapy was investigated in 91 rats embolized in the right carotid territory. Hypothermia of 32 degrees C for 2 h with preembolic onset (n = 15) or hyperthermia of 39 degrees C for 2 h with postembolic onset (n = 22) was compared to normothermic controls (n = 17). After 48 h of survival, neuropathological evaluation with measurement of infarct volume was performed. Median infarct volume in percent of affected hemisphere volume was 11% (9-21, quartiles) in rats treated with hypothermia alone, compared to 46% (14-59, quartiles) in normothermic controls (P = 0.04). Hyperthermia for 2 h increased median infarct volume to 65% (37-75, quartiles). There was a positive and significant correlation between infarct volume and body temperature (R = 0.53, P = 0.0002, n = 54). Mortality rate was significantly higher among rats treated with hyperthermia compared to normothermic controls (P = 0.005). A subset of 37 rats exposed to the same temperature regimen were treated with tissue plasminogen activator (20 mg/kg i.v. during 45 min) 2 h after embolization. Judged by posttreatment carotid angiography, hyperthermic rats (n = 11) had the best degree of recanalization (P = 0.03) compared to controls (n = 17), but median infarct volume in this group was (58% (27-67, quartiles)) significantly larger (P < 0.02) than normothermic (21% (15-39, quartiles), n = 14) and hypothermic (13% (7-31, quartiles), n = 12) rats treated with thrombolytic therapy. Thrombolytic therapy following 2 h of hypothermia, could not improve the effect of hypothermia alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Embolic stroke in a woman with mitral valve prolapse who used oral contraceptives.

A case of angiographically-documented embolism is presented in a patient using oral contraceptives (OC) with marked mitral valve prolapse (MVP) and an atrial thrombus. OC use has been shown to decrease levels of antithrombin III and increase platelet coagulant activity. This increased coagulability may increase the risk of intra-atrial thrombus formation and subsequent cerebral embolism in patients with MVP. We believe that MVP, especially when redundant valve leaflets are recognized, may be a relative contraindication to OC use.

Adult↗
PubMed1990

31P spectroscopy in experimental embolic stroke: correlation with infarct size.

Serial 31P nuclear magnetic resonance spectra were acquired from the brain in 19 rats following microsphere embolization of the right internal carotid artery. The brains were sectioned and stained with 2,3,5-triphenyltetrazoline chloride 6 h post-embolization to visualize infarcted areas. There was a narrow dosage range for the effect of embolism measured by maximum decline in pH at 20 min, mortality, and infarct size. This narrow range effect may be due to occlusion of collateral channels by the 16 micron microspheres. There was a strong correlation between decline in pH at 20 min post-embolization and infarct size (r2 = 0.76); this decline was the best early marker for eventual infarct in our study. This animal model for macroscopically heterogenous brain ischemia may be useful for the evaluation of therapeutic interventions in stroke, and as an aid in the interpretation of phosphorus spectra from mixed volumes of ischemic and non-ischemic brain.

Adenosine Triphosphate↗
PubMed1992

Selective and superselective infusion of urokinase for embolic stroke.

Intraarterial administration of urokinase using Tracker microcatheter was performed in 11 patients with acute cerebral infarction caused by embolic occlusion of the internal carotid or the middle cerebral artery. Recanalization was observed in seven cases (64%) following the fibrinolytic therapy, and the time until recanalization from the start of the treatment was on the average 2.8 hours. Recanalization was seen in five out of six cases that received superselective infusion of urokinase, while it was seen in two out of five cases that received selective infusion. This study suggests that superselective infusion of urokinase is an excellent therapeutic method for embolic occlusion of the cerebral artery.

Acute Disease↗
PubMedDate not supplied

Fusiform basilar aneurysm as a cause of embolic stroke.

Giant fusiform basilar aneurysms (dolicho-ectatic basilar anomalies) are rare and have not previously been reported to cause embolic infarction in territory distal to the aneurysm. They most commonly present as posterior fossa mass lesions with brainstem compression and cranial neuropathies. Originally considered atherosclerotic in etiology, recent authors feel that they may represent a unique arteriopathy characterized by loss of elastin in the vessel wall. We report a case which presented solely as an occipital lobe infarction. To our knowledge, this is the first case in which a fusiform basilar aneurysm presented with an embolic infarction as its only manifestation.

Arterial Occlusive Diseases↗
PubMed2002

The effects of early insulin treatment combined with thrombolysis in rat embolic stroke.

The therapeutic effect of insulin alone or insulin combined with 30 min delayed thrombolytic therapy was investigated in rats embolized in the right hemisphere with a fibrin clot made from autologous blood. Animals were killed seven days after embolization and the infarct volumes were measured in % of the affected hemisphere. Mortality was calculated as the number of animals dying spontaneously before the scheduled euthanasia. The median infarct volume in control animals (n = 12) was 24%. Insulin (3 IU kg(-1)) was given subcutaneously 15 min, 3 h, and 24 h after embolization (n = 12) and reduced median infarct volume to 11%. Human recombinant tissue plasminogen activator, 8 mg kg(-1), was infused intravenously during 45 min starting 30 min after embolization (n = 14), and the median infarct volume was 18% in this group. When the two treatments were combined, the median infarct volume was reduced to 11% (n = 14). The infarct volumes in the treatment groups were not significantly different from controls (p = 0.62, Kruskal Wallis test). Mortality rates increased from 0% among controls to 47% (p = 0.01) in the insulin alone and 38% (p = 0.02) in the combination therapy group. In conclusion, insulin treatment aiming at blood glucose levels around 2-4 mmol l(-1) was detrimental to clinical outcome causing significantly increased mortality.

Animals↗
PubMed2003

[Embolic stroke with mobile thrombus in carotid artery induced by antiphospholipid antibody syndrome].

We report a 56-year-old woman suffering from an embolic brain infarction in her right frontal lobe. Carotid ultrasonogram showed a mass-shaped thrombus with little atherosclerotic change of underlying intima-media in the right common carotid artery. The thrombus was reduced with treatment and changed to mobile slender thrombus on admission. No other embolic sources were detected even using transesophageal echocardiography. Her blood test indicated existence of antiphospholipid antibody syndrome (APS) complicated with mixed connective tissue disease as an etiology of this uncommon carotid thrombus. The thrombus disappeared completely after two-week intensive antithrombotic therapy. This is a valuable report that arterial thrombi accompanied by APS could be detected by carotid ultrasound and observed until thrombus was disappeared. When we manage APS patients, it is important to rule out thrombus formation in the carotid artery using ultrasonography from the point of stroke prevention.

Antiphospholipid Syndrome↗