bluuebunny/crossref_metadata_2025_split huggingface dataset:
Coexistence of fibromuscular dysplasia and cystic medial necrosis in a patient with Marfan's syndrome and bilateral carotid artery dissections.
Authors: Schievink W I , Björnsson J , Piepgras D G 
Published: June 2011

A primary arteriopathy is suspected in most patients with spontaneous dissections of the carotid artery, although the nature of this arteriopathy usually remains elusive. Angiographic changes of fibromuscular dysplasia (FMD), however, are found in 10% to 20% of patients with carotid dissections.
A 26-year-old woman with Marfan's syndrome presented with bilateral amaurosis fugax after surgical repair of an aortic dissection. Angiography revealed a dissection extending from the ascending aorta into the right internal carotid artery and, separate from the aortic dissection, a dissection of the left internal carotid artery. After surgery, microscopic examination of the right carotid artery revealed a medial dissection but no evidence of an underlying arteriopathy, while the left internal carotid artery displayed the typical features of FMD. Eighteen months later the patient died after resection of a large thoracoabdominal aortic dissecting aneurysm. Microscopic examination of the aorta revealed moderately extensive cystic medial necrosis.
Carotid dissections associated with Marfan's syndrome may be the result of an extension of an aortic dissection or occur isolated from the aorta, even in the same patient. The occurrence of FMD in a patient with Marfan's syndrome in conjunction with previous reports of FMD in a variety of connective tissue disorders suggests that FMD, like cystic medial necrosis, may be a nonspecific disease entity.
Failure of aspirin treatment after stroke.
Authors: Bornstein N M , Karepov V G , Aronovich B D , Gorbulev A Y , Treves T A , Korczyn A D 
Published: June 2011

Despite its low efficacy, aspirin is the most widely used drug for secondary stroke prevention. The reasons why stroke recurs while patients are on aspirin are unknown. We have analyzed a series of patients who had recurrent strokes while on aspirin.
Out of 2231 consecutive patients who were admitted to the Tel Aviv Medical Center from May 1988 through December 1992 with the diagnosis of ischemic stroke, 129 admissions were due to recurrent ischemic strokes while the patients were already on aspirin, and these were defined as aspirin failures. The clinical characteristics of those patients in whom aspirin treatment failed were compared with three control groups, each comprising 129 patients who had had only a single ischemic stroke and were then taking aspirin. One control group was matched for aspirin dose and date of first stroke; another control group was matched for age, sex, and date of first stroke; and a third control group was matched for age, sex, date of first stroke, and aspirin dose. Statistical analysis was carried out by two-tailed Student's t test and chi 2 test.
The average period until stroke was longer for patients on higher aspirin doses. Patients matched for aspirin dose and date of first stroke did not differ significantly in age (72.4 years in aspirin failures versus 74.2 years in the first control group) and sex (89 versus 94 men, respectively). Matching for age, sex, and date of first stroke but not for aspirin dose demonstrated a trend toward high frequency of aspirin failure in patients taking lower doses of aspirin (chi 2 test for trend = 3.5; P = .06). Comparison of aspirin-failure patients with a control group matched for age, sex, date of first ischemic stroke, and aspirin dose demonstrated that these patients more commonly had statistically significant hyperlipidemia (odds ratio, 2.6; 95% confidence interval, 1.0 to 6.8; P = .04) and ischemic heart disease (odds ratio, 2.3; 95% confidence interval, 1.3 to 3.9; P = .002).
We conclude that age and sex do not influence the efficacy of aspirin. Lower aspirin dose in patients with stroke recurrence suggests that aspirin doses of 500 mg daily or more should be used in secondary stroke prevention. Hyperlipidemia and ischemic heart disease are risk factors for stroke recurrence despite aspirin treatment, which requires further clinical and laboratory evaluation.
Hemostatic markers in acute transient ischemic attacks.
Authors: Fon E A , Mackey A , Côté R , Wolfson C , McIlraith D M , Leclerc J , Bourque F 
Published: June 2011

Hemostatic abnormalities have been shown previously in stroke patients. The purpose of this study was to assess the activity of selected parameters of the coagulation system in acute reversible cerebral ischemia.
We measured fibrinopeptide A, thrombin-antithrombin III, and D-dimer in 36 patients in both the acute (< 7 days) and postacute stage (1 and 3 months) after a transient ischemic attack (TIA). The results were compared with those of 20 asymptomatic patients with a history of remote TIA and 65 age- and sex-matched controls.
Mean fibrinopeptide A and thrombin-antithrombin III values were elevated in the acute stage after a TIA (P < .02) compared with levels at 1 month. In contrast, D-dimer was significantly increased at all three times points after the event when compared with remote TIA (P < .05) or control subjects (P < .001). No association could be found between marker levels and clinical outcome or the degree of cervical atherosclerosis as assessed by duplex ultrasonography.
These findings suggest that after acute reversible cerebral ischemia, there is early transient activation of thrombogenesis and ongoing fibrinolysis.
Space-occupying cerebellar infarction. Clinical course and prognosis.
Authors: Hornig C R , Rust D S , Busse O , Jauss M , Laun A 
Published: June 2011

Because the timing and strategy of surgical intervention in massive cerebellar infarction remains controversial, we report our experience with the management of 52 such patients.
Case records, computed tomographic scans, surgical reports, and angiograms of 52 patients with space-occupying cerebellar infarction defined by computed tomographic criteria were reevaluated with regard to clinical course, etiology, therapeutic management, mortality, and functional outcome.
In most cases clinical deterioration started on the third day after stroke, and a comatose state was reached within 24 hours. Sixteen patients were treated medically, and 30 by suboccipital craniectomy (22 plus ventriculostomy, 12 plus tonsillectomy). Ten patients primarily had ventriculostomy, which in 4 patients was supplemented by craniotomy because of continuing deterioration. Twenty-nine patients made a good recovery, 15 remained disabled, and 8 died. Even comatose patients had a 38% chance of a good recovery with decompressive surgery. Age older than 60 years (P = .0043) and probably initial brain stem signs (P = .0816) and a late clinical stage (P = .0893) were linked with a fatal or disabling outcome.
Decompressive surgery should be the treatment of choice for massive cerebellar infarction causing progressive brain stem signs or impairment of consciousness.
Decreased cerebrovascular dilatory capacity in subjects with asymptomatic periventricular hyperintensities.
Authors: Isaka Y , Okamoto M , Ashida K , Imaizumi M 
Published: June 2011

The clinical significance of the periventricular hyperintensity incidentally found on magnetic resonance images of the brain is questionable. We evaluated resting cerebral blood flow and cerebrovascular dilatory capacity of subjects with asymptomatic periventricular hyperintensities to study their cerebral hemodynamics.
Magnetic resonance imaging of the brain was performed in 28 asymptomatic subjects with cerebrovascular risk factors to determine the severity of periventricular hyperintensity. Mean gray matter flow was computed by a 133Xe-clearance technique in subjects at rest and after the administration of 1 g acetazolamide. Flow values were correlated with the scores for periventricular hyperintensity.
Resting gray matter flow was not significantly correlated with the severity of periventricular hyperintensity for the whole brain (rs = -.364), whereas flow after acetazolamide loading (rs = -.783, P < .001) and the absolute value of increased flow (rs = -.567, P < .01) were significantly and negatively correlated with the severity of periventricular hyperintensity.
A decrease in vasodilatory capacity and compensatory vasodilation occur in the cerebral cortex of subjects with asymptomatic periventricular lesions and maintain cerebral blood flow.
Draining vein pressure increases and hemorrhage in patients with arteriovenous malformation.
Authors: Miyasaka Y , Kurata A , Tokiwa K , Tanaka R , Yada K , Ohwada T 
Published: June 2011

Recent radiological studies have shown that arteriovenous malformations with impaired venous drainage may be susceptible to hemorrhage. To evaluate this hypothesis using a hemodynamic approach, we measured intravascular pressure during surgery in three patients with arteriovenous malformation.
In three patients we measured intravascular pressures in the draining venous system and the feeding arteries simultaneously before removal of arteriovenous malformations with marked segmental stenotic or occlusive draining veins and evidence of hemorrhage. The draining vein pressures at prestenotic (or preocclusive) sites in the three patients were 38, 25, and 40 mm Hg, respectively, all significantly above the normal cortical venous pressure, whereas pressure measurements in poststenotic sites and the sagittal sinus pressure in the venous drainage system approached normal values. The feeding artery pressures in the patients were lower than normal cortical artery pressure because of the arteriovenous shunt.
Intraoperative vascular pressure measurements support the hypothesis that arteriovenous malformations with impaired venous drainage may be associated with a local increase in venous pressure and thus may be susceptible to hemorrhage.
A prospective community-based study of stroke in Warsaw, Poland.
Authors: Czlonkowska A , Ryglewicz D , Weissbein T , Baranska-Gieruszczak M , Hier D B 
Published: June 2011

Poland is a country with high morbidity and mortality rates from cardiovascular diseases. No recent studies have evaluated the contribution of cerebrovascular diseases to this morbidity and mortality. Our aim was to accurately determine stroke incidence rates in Warsaw, Poland.
A 2-year prospective and population-based stroke registry was maintained for health care units 2 and 3 in Warsaw, Poland (population, 182,285). Case subjects were ascertained by surveying hospital admissions, outpatient visits, and death certificates.
During the 2 years of the study (1991 to 1992), 633 cases of first-event strokes were registered, 462 of which were first ever in a lifetime. Computed tomography or necropsy was performed in 72% of first-ever stroke cases. The crude annual incidence rate for first-ever stroke was 127/100,000 (95% confidence intervals, 111 to 145); the rate standardized to the European population was 111 (95% confidence intervals, 96 to 128). Our incidence rates for first-event strokes were found to be in the middle of the range among other first-event studies. When comparing our first-ever stroke incidence rates with those of comparable studies performed throughout Europe, they were found to be similar for groups aged younger than 65 years but lower in the older age groups. The distribution of ischemic and hemorrhagic stroke subtypes was similar to that of other countries.
This first population-based prospective stroke registry in Poland showed that incidence rates were not high compared with other studies throughout Europe and the world. These stroke incidence rates are not a large contributing factor to high cardiovascular morbidity rates in Poland.
Stroke incidence and case fatality in Australasia. A comparison of the Auckland and Perth population-based stroke registers.
Authors: Bonita R , Anderson C S , Broad J B , Jamrozik K D , Stewart-Wynne E G , Anderson N E 
Published: June 2011

Population-based studies are crucial for identifying explanations for the decline in mortality from stroke and for generating strategies for public health policy. However, the present particular methodological difficulties, and comparability between them is generally poor. In this article we compare the incidence and case fatality of stroke as assessed by two independent well-designed incidence studies.
Two registers of acute cerebrovascular events were compiled in the geographically defined metropolitan areas of Auckland, New Zealand (population 945,369), during 1991-1992 for 12 months and Perth, Australia (population 138,708), during 1989-1990 for 18 months. The protocols for each register included prospective ascertainment of cases using multiple overlapping sources and the application of standardized definitions and criteria for stroke and case fatality.
In Auckland, 1803 events occurred in 1761 residents, 73% of which were first-ever strokes. The corresponding figures for Perth were 536 events in 492 residents, 69% of which were first-ever strokes. Both studies identified a substantial proportion of nonfatal strokes managed solely outside the hospital system: 28% in Auckland and 22% in Perth of all patients registered. The age-standardized annual incidence of stroke (all events) was 27% higher among men in Perth compared with Auckland (odds ratio, 1.27; P = .016); women tended to have higher rates in Auckland, although these differences were not statistically significant. In both centers approximately a quarter of all patients died within the first month after a stroke. There were significant differences in the prevalence of hypertension among first-ever strokes.
These two studies emphasize the importance of identifying all patients with stroke, both hospitalized and nonhospitalized, in order to measure the incidence of stroke accurately. The incidence and case fatality of stroke were remarkably similar in Auckland and Perth in the early 1990s. However, there are differences in the sex-specific rates that correspond to differences in the pattern of risk factors.
Magnetic resonance imaging and dynamic CT scan in cervical artery dissections.
Authors: Zuber M , Meary E , Meder J F , Mas J L 
Published: June 2011

The typical magnetic resonance imaging picture of arterial dissection, namely, a narrowed eccentric signal void surrounded by a semilunar signal hyper-intensity (corresponding to the mural hematoma) on T1- and T2-weighted images, has been repeatedly reported, but the sensitivity of magnetic resonance imaging for the diagnosis of cervical dissection is poorly known. Another technique, dynamic computed tomography, may provide evidence of mural hematoma, but there has been no systematic evaluation of this technique. The aims of this study were to assess both the sensitivity of routine 0.5-T magnetic resonance imaging for the detection of a typical picture of cervical artery dissection and the value of dynamic computed tomographic scans to provide evidence of dissecting hematoma.
Fifteen consecutive patients with angiographically confirmed extracranial internal carotid (n = 9) or vertebral (n = 10) dissections were studied using a standardized 0.5-T spin-echo magnetic resonance imaging protocol with axial slices. Twelve of these patients had dynamic computed tomographic scans at the site of the dissection suggested by angiography.
A typical magnetic resonance imaging picture of cervical artery dissection was observed in 12 of 15 (80%) patients and in 13 of 19 (68%) dissected vessels. The sensitivity of magnetic resonance imaging was higher in internal carotid (78%) than in vertebral (60%) dissections and in stenotic-type dissections (85%) than in occlusive or aneurysmal-type dissections. The dynamic computed tomographic scan showed the mural hematoma in 11 of the 12 (92%) patients and in 12 of 15 (80%) dissected vessels.
Routine 0.5-T magnetic resonance imaging with axial slices is a sensitive technique for the diagnosis of dissection, but in about 20% of patients with cervical artery dissection magnetic resonance imaging will demonstrate no typical abnormality. Dynamic computed tomographic scans are a sensitive neuroimaging procedure to confirm the presence of the mural hematoma, but it needs to be directed by prior angiography.
The role of superoxide anions in the pathogenesis of cerebral vasospasm.
Authors: Shishido T , Suzuki R , Qian L , Hirakawa K 
Published: June 2011

To determine the role of superoxide anions in the pathogenesis of cerebral vasospasm after aneurysmal subarachnoid hemorrhage, we studied the preventive effect of human recombinant copper-zinc superoxide dismutase (h-r SOD) in a rabbit subarachnoid hemorrhage (SAH) model.
Forty-five rabbits receiving intracisternal injection of 3 mL autologous nonheparinized blood or 3 mL saline were divided into four groups as follows: (1) saline injected and no treatment (control group, n = 6); (2) blood injected and no treatment (SAH group, n = 20); (3) blood injected and treated by multiple intracisternal injections of 30,000 U of h-r SOD in 0.5 mL saline (SOD group, n = 9); and (4) blood injected and treated by multiple intracisternal injections of 0.5 mL saline (saline group, n = 10). Serial angiograms were performed after the blood injection, and the diameter of the basilar artery was measured. Three animals from the control group and five animals from the SAH and SOD groups each were killed 2 days after SAH, and their basilar arteries were processed for transmission electron microscopic observations.
In the SAH and saline groups, the diameter of the basilar arteries was significantly reduced (28 +/- 14% and 27 +/- 9%, respectively) at 2 days after the blood injection, then recovered to pre-SAH levels until 11 days. In the SOD group, the diameter of the basilar artery was only minimally changed during the follow-up period. Transmission electron microscopy revealed endothelial injury in all basilar arteries in the SAH group, whereas endothelial injury was minimal in the SOD group.
We determined that h-r SOD prevents the occurrence of vasospasm, possibly as a result of preventing endothelial injury initiated by superoxide anions.
Deferoxamine posttreatment reduces ischemic brain injury in neonatal rats.
Authors: Palmer C , Roberts R L , Bero C 
Published: June 2011

Iron catalyzes the formation of damaging reactive species during cerebral reperfusion. Brain iron concentration is highest at birth, so the brain of the asphyxiated newborn may be at increased risk of iron-dependent injury. We investigated whether the ferric iron chelator deferoxamine could reduce hypoxic-ischemic brain injury in neonatal rats. Because deferoxamine has concentration-dependent activities other than iron chelation, we measured brain deferoxamine levels and calculated deferoxamine pharmacokinetic parameters.
We produced hypoxic-ischemic injury to the right cerebral hemisphere of 7-day-old rats by right common carotid artery ligation followed by 2.25 hours of hypoxia in 8% oxygen. At 5 minutes of recovery from hypoxia the rats received 100 mg/kg deferoxamine mesylate or saline subcutaneously. Rats (saline, n = 33; deferoxamine, n = 38) were killed at 42 hours of recovery to assess early acute edema by measurement of hemispheric water content. Other rats (saline, n = 31; deferoxamine, n = 32) were killed at 30 days of age for morphometric determination of right hemisphere atrophy. In still other rats, we measured deferoxamine levels in blood and brain after hypoxia-ischemia.
Deferoxamine significantly reduced right hemisphere injury as measured by early water content (P < .01) and later atrophy (P = .019). Deferoxamine brain levels peaked between 100 and 200 mumol/L at 40 to 60 minutes after injection and exceeded serum levels by +/- 70%.
Deferoxamine administered after induction of cerebral hypoxia-ischemia reduces injury in 7-day-old rats. Deferoxamine concentrates in the brain at levels between 100 and 200 mumol/L. At the concentrations achieved, deferoxamine might protect the brain through mechanisms unrelated to its ability to chelate iron.
Prophylactic neuroprotection for cerebral ischemia.
Authors: Fisher M , Jonas S , Sacco R L , Jones S [corrected to Jonas S ] 
Published: June 2011

Treatments for acute ischemic stroke have evolved as knowledge about the pathophysiology of ischemic brain injury has advanced. Treatment strategies under development are aimed at offering neuroprotection acutely after focal cerebral ischemic injury, but delayed initiation of therapy may reduce efficacy. Pretreatment before ischemia begins could offer distinct advantages in patient groups at high risk for ischemic stroke.
If a neuroprotective drug were available orally, safe, and relatively inexpensive, it could be considered for prophylactic use in high-risk populations. Prophylactic neuroprotection would include (1) short-term neuroprotection before and after high-stroke risk procedures, (2) long-term neuroprotection for primary and secondary intervention in populations at high risk for stroke, and (3) concomitant neuroprotection with agents that have multiple treatment effects. Patients undergoing procedures such as cardiac surgery, endarterectomy, or endovascular therapy, which have a risk of cerebral ischemic events during a defined period, might be considered for short-term, periprocedure prophylactic neuroprotection. Several populations at high long-term risk for initial ischemic stroke have been identified and include those with combinations of vascular risk factors, transient ischemic attacks, atrial fibrillation, and asymptomatic carotid stenosis. Such people, as well as those at risk for stroke recurrence after minor strokes, are readily identifiable and perhaps appropriate for long-term prophylactic neuroprotection. Patients with hypertension and cerebrovascular atherosclerosis have a high stroke risk, and therapies directed at these underlying disorders are available that also have concomitant neuroprotective effects. An ideal drug for trials in these patient groups has not yet been developed, and establishing its efficacy may prove to be an arduous and lengthy task.
The possibility of ameliorating the consequences of an acute ischemic stroke by pretreating high-risk patients with appropriate neuroprotective agents needs to be explored. Several types of high-risk population for prophylactic neuroprotection can be envisioned and then studied in clinical trials.