bluuebunny/crossref_metadata_2025_split huggingface dataset:
Hemorrhagic transformation in cardioembolic cerebral infarction.
Authors: Hornig C R , Bauer T , Simon C , Trittmacher S , Dorndorf W 
Published: June 2011

Because the frequency of hemorrhagic transformation of cerebral infarcts is still a matter of controversy, we performed a prospective magnetic resonance imaging study in a series of consecutive patients with cardioembolic stroke.
Among 200 consecutive patients with transient ischemic attack or ischemic stroke, 41 were identified with a computed tomographically proven supratentorial infarct due to cardiogenic embolism. Magnetic resonance imaging (T1-weighted) was performed 3 weeks after the stroke in 35 of these 41 patients. Eight patients received anticoagulants. Magnetic resonance images showed hemorrhagic transformation in 68.6% (24) of the 35 infarcts, always without clinical deterioration. In a stepwise forward logistic regression analysis only the volume of infarction edema on the initial computed tomogram was linked significantly with the risk of hemorrhagic transformation (p = 0.037). Hemorrhages were a regular finding on magnetic resonance images of infarcts exceeding a volume of 10 cm3 (94.4%, 17 of 18).
Hemorrhagic transformation is a regular finding in medium-sized and large cardioembolic infarcts. Thus, in therapeutic and preventive studies of acute stroke the severity, not the frequency, of hemorrhages into brain infarcts should be the matter of interest.
Pseudotumor syndrome associated with cerebral venous sinus occlusion and antiphospholipid antibodies.
Authors: Mokri B , Jack C R , Petty G W 
Published: June 2011

Antiphospholipid antibodies are known to be associated with increased risk of venous and arterial thrombotic events, including cerebral venous thromboses. Pseudotumor syndrome can be produced by cerebral venous thrombosis. A patient with cerebral venous thrombosis associated with antiphospholipid antibodies who exhibited pseudotumor syndrome is reported.
A 49-year-old man who noted visual blurring and persistent vertical wavy lines in his fields of vision was found to have papilledema. Cerebrospinal fluid values were normal except for an opening pressure increase to 510 mm of fluid. His visual symptoms improved with lumbar puncture and the use of acetazolamide. Imaging studies showed that the transverse sinus was occluded completely on the left and partially on the right and that there was a small left cerebellar cortical venous infarction.
Antiphospholipid syndrome should be considered in the differential diagnosis of pseudotumor syndrome related to cerebral venous thrombosis.
Prognostic factors in first-ever stroke in the carotid artery territory seen within 6 hours after onset.
Authors: Censori B , Camerlingo M , Casto L , Ferraro B , Gazzaniga G C , Cesana B , Mamoli A 
Published: June 2011

We sought to detect prognostic factors related to functional outcome during the first 6 hours after a first-ever stroke in the carotid artery territory.
All patients with these characteristics seen during a 3-year period were included. Outcome was evaluated according to a modified Rankin scale. The following variables were examined at univariate analysis: sex, age, severity of deficit at entry and at day 7, level of consciousness at entry, time after symptom onset, history of smoking, history of hypertension, diabetes, myocardial infarction, atrial fibrillation, rheumatic heart disease, dilated cardiomyopathy, all potential cardioembolic sources, presence of a consistent lesion on computed tomography at entry and at days 5-9, and the size of such lesion.
All entry criteria were met by 172 patients. Age > or = 70 years, a Canadian Neurological Scale score < 6.5 at entry and at day 7, atrial fibrillation, presence of a potential cardioembolic source, and a "large" lesion (involving more than half the cerebral lobe) on computed tomography at days 5-9 were associated with a significantly worse outcome both at 30 days and at 6 months. After multivariate analysis, a Canadian Scale score < 6.5 at entry (p < 0.0001) and atrial fibrillation (p = 0.005) were associated with a significant handicap or death at 30 days, whereas only a Canadian Scale score < 6.5 (p < 0.0001) was associated with a worse prognosis at 6 months. An association of age > or = 70 years with a worse outcome at 6 months was of borderline significance (p = 0.054).
Some prognostic indicators are available during the first few hours after onset of a carotid ischemic stroke and may be useful in the stratification of patients in clinical trials. Severity of deficit is the most important indicator, whereas the presence of atrial fibrillation worsens the prognostic outlook with respect to early handicap but not mortality.
Intracerebral hemorrhage after fibrinolytic therapy for acute myocardial infarction.
Authors: Wijdicks E F , Jack C R 
Published: June 2011

Intracerebral hematoma may complicate treatment of acute myocardial infarction in patients treated with fibrinolytic agents. We studied the clinical presentation and computed tomographic characteristics.
We studied eight patients with lobar intracerebral hematomas after fibrinolytic treatment of acute coronary occlusion. All patients had electrocardiographic and laboratory evidence of acute myocardial infarction and were treated with tissue plasminogen activator or streptokinase followed by heparin infusion to prevent reocclusion. Computed tomography scans of 17 patients with cerebral hemorrhage from other causes were used for comparison.
For most patients, outcome was fatal within hours of the ictus. Computed tomography scans showed superficially large lobar hematomas in six patients. One patient had a putaminal hemorrhage, and one had a vermis hemorrhage. Multiple sites of intracerebral hemorrhage were noted in three patients. Fluid levels inside the hematoma suggesting continuing hemorrhage into multiple compartments were common. Radiologically, fluid levels in hematomas, multiple hematomas, and blood in multiple compartments served to differentiate fibrinolysis-induced hemorrhage from hemorrhage of other causes. Severe amyloid angiopathy was found in one patient who was operated on.
Hemorrhages in multiple compartments and the presence of fluid levels inside the hematoma suggest fibrinolysis-associated cerebral hematomas. Severe amyloid angiopathy may be a crucial factor in this clinical entity. Outcome is poor, and a high proportion of patients have rapid progression to brain death. Therefore, emergency neurosurgical evacuation will probably be unsuccessful.
Transforming growth factor-beta 1 reduces infarct size after experimental cerebral ischemia in a rabbit model.
Authors: Gross C E , Bednar M M , Howard D B , Sporn M B 
Published: June 2011

The aim of this study was to examine the effect of transforming growth factor-beta 1, a cytokine shown to amelioriate cardiac ischemia, in a rabbit model of thromboembolic stroke.
An autologous clot embolus was introduced intracranially through the right internal carotid artery in 21 New Zealand White rabbits, with seven in each group receiving either vehicle control (albumin) or 10 or 50 micrograms transforming growth factor-beta 1 administered as an intracarotid bolus immediately before autologous clot embolization. Multiple physiological parameters were monitored, including regional cerebral blood flow, arterial blood gases, hematocrit, glucose, core temperature, and mean arterial pressure. The brain was harvested 4 hours after embolization, and infarct size was determined planimetrically as a percentage of the entire hemisphere.
Brain infarct size was reduced in both the 10-microgram (16.7 +/- 4.0% [mean +/- SEM], p < 0.05) and 50-microgram (21.7 +/- 4.5%) transforming growth factor-beta 1-treated groups when compared with the control group (31.9 +/- 6.6%). Regional cerebral blood flow did not show any significant intergroup or intragroup variation over time, although the 10-microgram transforming growth factor-beta 1 group experienced a greater return of cerebral blood flow in the first 2 hours after embolization.
Transforming growth factor-beta 1 reduced brain infarct size in a rabbit model of thromboembolic stroke. This effect was not related to a direct effect on blood flow. Studies are ongoing to determine the mechanism by which transforming growth factor-beta 1 salvages ischemic brain.
Cerebral blood flow and ischemia-induced neurotransmitter release in the striatum of aged spontaneously hypertensive rats.
Authors: Yao H , Ooboshi H , Ibayashi S , Uchimura H , Fujishima M 
Published: June 2011

We found age-related vulnerability to cerebral ischemia in the hippocampus and striatum in spontaneously hypertensive rats. Further study revealed that ischemia-induced release of hippocampal taurine, an inhibitory amino acid, was reduced by 40% in aged rats compared with adult rats, which suggested an impaired inhibitory function against excitotoxicity in aged rats. The purpose of this study was to examine whether ischemia-induced neurotransmitter release is altered in the striatum of aged spontaneously hypertensive rats.
Five adult (5-6 months) and five aged (18-22 months) female spontaneously hypertensive rats were subjected to 20 minutes of cerebral ischemia induced by bilateral carotid artery occlusions and 120 minutes of recirculation under amobarbital anesthesia (100 mg/kg i.p.). Cerebral blood flow was determined using the hydrogen clearance method, and extracellular concentrations of neurotransmitters were determined with the brain dialysis technique in the striatum.
During ischemia, cerebral blood flow in aged rats decreased to 8.7 +/- 1.2 (mean +/- SEM) mL/100 g per minute (11% of the resting), which was not different from 5.2 +/- 1.7 mL/100 g per minute (8% of the resting) in adult rats, and extracellular dopamine and amino acids (glutamate, aspartate, and taurine) increased by approximately 170- and 10-30-fold, respectively, and returned to baseline after 20-40 minutes of recirculation. These values of neurotransmitters, however, were not different between aged and adult rats during ischemia and reperfusion.
It is unlikely that a presynaptic mechanism is involved in age-related vulnerability in the striatum of hypertensive rats.
Recurrent ischemic events in two patients with painless vertebral artery dissection.
Authors: McCormick G F , Halbach V V 
Published: June 2011

Vertebral artery dissection causes endothelial changes and stenosis that may lead to recurrent ischemic neurological events. The diagnosis may not be obvious because the dissection may be painless and "spontaneous" (no obvious trauma). Magnetic resonance angiography has increasingly been used to screen patients for this disorder, but its accuracy has not yet been established.
Two patients were admitted with repeated transient ischemic attacks and strokes over 11 months and 1 month, respectively. Neither had a history of trauma, cervical pain, or headache. Magnetic resonance angiography failed to visualize vertebral artery dissections that were later revealed by conventional angiography. One patient's events were stopped by balloon occlusion of the vertebral artery proximal to the posterior inferior cerebellar artery branch.
Magnetic resonance angiography is not yet sensitive enough to always visualize vertebral artery dissection. Vertebral artery dissection is a life-threatening condition that requires aggressive evaluation and treatment.
Computed tomographic evidence of an extensive thrombosis and infarction of the deep venous system.
Authors: Rahman N U , al-Tahan A R 
Published: June 2011

Massive bilateral infarcts due to deep venous system thrombosis are extremely rare and poorly documented. We present a case with computed tomographic evidence of both thrombosis and infarction of the whole deep venous system.
A previously healthy 30-year-old woman who had taken oral contraceptives for 3 years complained of recurrent headaches and transient visual obscuration. Three months later, she suddenly became comatose and was found to have papilledema. She rapidly worsened, became decerebrate, and died within 48 hours. Noncontrast computed tomographic scan showed the spontaneous hyperdensity of the thrombosed deep veins and a massive bilateral centrobasilar hypodensity suggestive of a deep venous system infarction.
This case shows that cerebral venous thrombosis can masquerade during 3 months as benign intracranial hypertension and then make a dramatic extension to the deep cerebral veins. It illustrates extensive thrombosis of the deep venous system as a possible cause of rapid coma and decerebration and stresses the importance of computed tomographic scan to show both the thrombosed veins and the venous infarct, which allows delineation of the deep venous system territory.
A prospective study of stroke in young adults in Cantabria, Spain.
Authors: Leno C , Berciano J , Combarros O , Polo J M , Pascual J , Quintana F , Merino J , Sedano C , Martín-Durán R , Alvarez C 
Published: June 2011

The aim of this study was to determine the incidence, type, and prognosis of stroke in young adults in Cantabria, Spain.
We investigated prospectively all patients aged 50 years or below who were admitted with the diagnosis of a stroke to the University Hospital "Marqués de Valdecilla" from April 1, 1986, to March 31, 1988. This is the main hospital of the region to which all patients with neurological problems are referred. These patients underwent a complete clinical and laboratory assessment for stroke and had 1-year mean follow-up.
The total series included 81 patients. The annual age-specific crude incidence rates of stroke were 17.3 and 10.4 per 100,000 for males and females, respectively. Twenty-four patients (30%) were diagnosed as having nonembolic cerebral infarction, 14 (17%) embolic cerebral infarction, 20 (25%) subarachnoid hemorrhage, 22 (27%) spontaneous cerebral hemorrhage, and one case (1%) cerebral venous thrombosis. Eighteen patients (22%) died within 30 days of the cerebrovascular event, and two others died during the follow-up period. Seventy-nine percent of the survivors recovered and were completely self-sufficient.
The incidence of stroke in the young found in Cantabria is comparable with that in previous studies. The initial hospital mortality was not negligible, but the prognosis among the survivors was favorable.
Coagulation-fibrinolysis system in poststroke patients receiving antiplatelet medication.
Authors: Tohgi H , Takahashi H , Chiba K , Tamura K 
Published: June 2011

We studied the activities of the coagulation-fibrinolysis system in the chronic stage of poststroke patients and the effect of antiplatelet medication on the system.
We determined fibrinogen, antithrombin III, thrombin-antithrombin III complex, tissue plasminogen activator antigen, plasminogen activator inhibitor-1, plasmin-alpha 2 plasmin inhibitor complex, and D-dimer in plasma from 153 poststroke patients in the chronic phase (ie, 33 patients not receiving antiplatelet medication, 78 patients receiving 200 mg/d ticlopidine, and 42 patients receiving 40 mg/d aspirin), and compared the results in control subjects and among the treatment groups.
The concentrations of fibrinogen, thrombin-antithrombin III complex, antithrombin III, plasmin-alpha 2 plasmin inhibitor complex, and tissue plasminogen activator were slightly but significantly increased in all treatment groups compared with control subjects (P < .01) but did not differ among the treatment groups. The plasminogen activator inhibitor-1 levels were significantly elevated in patients not receiving antiplatelet medication compared with control subjects (P < .01), whereas they were in the normal range and significantly lower in patients receiving ticlopidine or aspirin than in patients not receiving antiplatelet medication (P < .01). The plasminogen activator inhibitor-1 levels were significantly lower in patients whose platelet aggregation was inhibited by antiplatelet medication than in patients with uninhibited platelet aggregability (P < .05).
These findings suggest that coagulation-fibrinolysis markers are mildly increased in poststroke patients in the chronic phase and that antiplatelet medication is effective in reducing the elevated plasminogen activator inhibitor-1 levels.
Amount of blood on computed tomography as an independent predictor after aneurysm rupture.
Authors: Brouwers P J , Dippel D W , Vermeulen M , Lindsay K W , Hasan D , van Gijn J 
Published: June 2011

After admission to the hospital of patients with aneurysmal subarachnoid hemorrhage, we assessed the predictive value of the extent of the hemorrhage on computed tomography in addition to that of clinical grading scales for poor outcome, infarction, and rebleeding.
We studied 471 consecutive patients with aneurysmal subarachnoid hemorrhage and used logistic regression with step-wise forward selection of variables.
On admission, poor outcome was predicted by a low Glasgow Coma Scale score (odds ratio, 0.8; 95% confidence interval, 0.7-0.9); treatment with fluid restriction (2.5; 1.6-4.0); age over 52 (2.6; 1.7-3.9); loss of consciousness at ictus (1.7; 1.1-2.6); or a large amount of subarachnoid blood (2.0; 1.3-3.1). Delayed infarction was predicted by a large amount of subarachnoid blood (1.8; 1.2-2.6) or treatment with tranexamic acid (1.6; 1.1-2.4). Rebleeding was predicted by treatment with tranexamic acid (0.4; 0.3-0.7; protective effect); age over 52 (1.9; 1.2-3.0); loss of consciousness at ictus (1.7; 1.1-2.7); or admission to a neurosurgery service (0.6; 0.3-0.9; protective effect). Comparison of the observed and predicted outcome events showed that inclusion of the amount of subarachnoid blood into a predictive model added little to the prediction of poor outcome in general, but much to the prediction of delayed cerebral ischemia.
The total amount of subarachnoid blood on the initial computed tomogram has independent predictive power for the occurrence of delayed cerebral ischemia.
Combined use of aspirin and heparin inhibits in vivo acute carotid thrombosis.
Authors: Huang Z S , Teng C M , Lee T K , Shun C T , Wang C Y 
Published: June 2011

Carotid atherosclerotic thrombosis is an important cause of ischemic stroke in Western countries. The therapeutic efficacy of either aspirin or heparin alone in this setting is still controversial. Recently we developed a simple model, the "clamp" method, to induce acute carotid mural thrombosis in vivo in guinea pigs. In this study, we used this model to evaluate the antithrombotic effects of aspirin, heparin, and their combination.
Sixty-four male guinea pigs were divided equally into control, aspirin, heparin, and combined groups. Physiological saline, aspirin (5 mg/kg body wt), heparin (200 units/kg body wt), or a combination of aspirin and heparin, respectively, was injected via the jugular vein before the use of the clamp method. Thirty minutes after the injection of saline or drug(s), Péan's forceps was used to clamp the carotid artery at a tangent angle for 3 minutes. One hour later, the carotid artery was resected and prepared for observation under a scanning electron microscope or light microscope to evaluate the degree of mural thrombosis.
The results showed that the combination of aspirin and heparin had an excellent effect in inhibiting in vivo acute carotid thrombosis (p < 0.001) and was significantly better than the effect of aspirin alone (p < 0.01) or heparin alone (p < 0.01).
Our study clearly demonstrated that the combined use of aspirin and heparin produced a much better antithrombotic effect than either agent alone at sites of carotid endothelial injury when given before the injury. This combined regimen may be useful clinically in acute carotid thrombosis secondary to carotid diseases or carotid endarterectomy.
Tissue factor contributes to microvascular defects after focal cerebral ischemia.
Authors: Thomas W S , Mori E , Copeland B R , Yu J Q , Morrissey J H , del Zoppo G J 
Published: June 2011

Microvascular perfusion defects occur after occlusion and reperfusion of the middle cerebral artery in examples of focal cerebral ischemia. In addition to cellular (eg, polymorphonuclear leukocyte) contributors to the focal "no-reflow" phenomenon, activation of coagulation may also play a role. We have tested a potential role of tissue factor-mediated coagulation in the microvascular perfusion defects seen after focal cerebral ischemia-reperfusion in a baboon model of reversible middle cerebral artery occlusion with the murine anti-tissue factor monoclonal antibody TF9-6B4. Tissue factor is the principal resident procoagulant substance in cerebral tissues and has a distinct perivascular distribution.
Microvascular patency in the basal ganglia after 3-hour middle cerebral artery occlusion and 1-hour reperfusion was quantified by computerized video imaging of carbon-tracer perfused tissues. Animals were randomized to receive intravenous TF9-6B4 (10 mg/kg) 10 minutes before middle cerebral artery occlusion (n = 6) or no treatment (n = 6) in an open study.
In the control animals, a significant decrease in patency was confirmed in microvessels less than 30 microns in diameter. Infusion of TF9-6B4 before middle cerebral artery occlusion produced a stable maximal level of circulating antibody within 10 minutes, which lasted the duration of ischemia and reperfusion. An increase in reflow in microvessels of all size classes occurred after TF9-6B4 infusion, which was significant in those 7.5 to 30 microns (P = .038) and 30 to 50 microns (P = .013) in diameter.
These results indicate that tissue factor-mediated events may also contribute to no-reflow in noncapillary microvessels after focal cerebral ischemia.
Electric injury with cerebral venous thrombosis. Case report and review of the literature.
Authors: Patel A , Lo R 
Published: June 2011

A case of accidental electrocution with previously unreported arteriographic evidence of cerebral vein thrombosis is presented. A brief description of early and late neurological complications and current theories attempting to explain the histopathological findings of electric injury are reviewed. The occurrence and persistence of late neurological complications are elucidated.
A report of an accidental electrocution with 800 V of alternating current in a young man is presented. Cerebral angiography showed a cerebral vein thrombosis. The immediate complications included loss of consciousness, confusion, memory loss, and headache. Late complications of right-sided clumsiness, sensory loss, hemianopsia, and neglect persisted for more than 1 year despite the brain being outside the current pathway.
High-voltage electric injury may cause cerebral vein thrombosis with significant early and delayed brain injury even when the brain lies outside the current pathway.