bluuebunny/crossref_metadata_2025_split huggingface dataset:
Subarachnoid blood causes pial arteriolar constriction in newborn pigs.
Authors: Parfenova H , Shibata M , Leffler C W 
Published: June 2011

The present study was designed to determine in newborn animals the delayed effect of subarachnoid blood on pial arteriolar diameter and eicosanoid concentrations in cortical periarachnoid fluid.
Forty-eight to 96 hours after subarachnoid blood installation, closed cranial windows were implanted over the cerebral area exposed to blood in anesthetized, artificially ventilated newborn piglets. All pial arterioles greater than 60 microns in diameter were measured, and cortical periarachnoid fluid was collected for the determination of eicosanoids.
Subarachnoid blood resulted in a 20% to 30% decrease in the average diameter of pial arterioles exposed to blood for 48 to 96 hours, a decreased number of large pial arterioles (greater than 200 microns), and an increased number of small arterioles (60 to 100 microns). No changes in dilator prostanoids (prostacyclin [as 6-keto-prostaglandin F1 alpha] and prostaglandin E2) were detected. Concentrations of vasoconstrictor prostanoids in cortical cerebrospinal fluid increased. Thromboxane B2 increased to 430 +/- 70 pg/mL, and prostaglandin F2 alpha increased to 1370 +/- 180 pg/mL compared with 250 +/- 20 and 860 +/- 70 pg/mL, respectively, in the control group. The concentration of peptidoleukotrienes increased to 400 to 600 pg/mL 72 to 96 hours after blood installation, while the level in the control group was less than 80 pg/mL.
The altered balance between vasodilator and vasoconstrictor eicosanoids could contribute to cerebral vasoconstriction after subarachnoid blood installation in newborn pigs.
Interleukin-1 beta mRNA expression in ischemic rat cortex.
Authors: Liu T , McDonnell P C , Young P R , White R F , Siren A L , Hallenbeck J M , Barone F C , Feurestein G Z 
Published: June 2011

Interleukin-1 beta is a proinflammatory cytokine produced by blood-borne and resident brain inflammatory cells. The present study was conducted to determine if interleukin-1 beta mRNA was produced in the brain of rats subjected to permanent focal ischemia.
Rat interleukin-1 beta cDNA, synthesized from stimulated rat peritoneal macrophage RNA by reverse transcription and polymerase chain reaction and cloned in plasmid Bluescript KS+, was used to evaluate the expression of interleukin-1 beta mRNA in cerebral cortex from spontaneously hypertensive rats and normotensive rats subjected to permanent middle cerebral artery occlusion. Interleukin-1 beta mRNA was quantified by Northern blot analysis and compared with rat macrophage RNA standard. To correct for gel loading, blots were also analyzed with cyclophilin cDNA, which encodes an abundant, conserved protein that was unchanged by the experimental conditions.
Interleukin-1 beta mRNA produced in the ischemic zone was significantly increased from 6 hours to 120 hours, with a maximum of 211 +/- 24% of interleukin-1 beta reference standard, ie, 0.2 ng stimulated rat macrophage RNA, mRNA compared with the level in nonischemic cortices (4 +/- 2%) at 12 hours after ischemia (P < .01; n = 6). Interleukin-1 beta mRNA at 12 hours after ischemia was markedly elevated in hypertensive rats over levels found in two normotensive rat strains. Neurological deficits were also apparent only in the hypertensive rats.
Brain interleukin-1 beta mRNA is elevated acutely after permanent focal ischemia and especially in hypertensive rats. These data suggest that this potent proinflammatory and procoagulant cytokine might have a role in brain damage following ischemia.
Interobserver reliability of a clinical classification of acute cerebral infarction.
Authors: Lindley R I , Warlow C P , Wardlaw J M , Dennis M S , Slattery J , Sandercock P A 
Published: June 2011

The Oxfordshire Community Stroke Project (OCSP) clinical classification of subtypes of cerebral infarction (total and partial anterior circulation infarction, lacunar infarction, and posterior circulation infarction) can be used to predict early mortality, functional outcome, and whether the infarct was likely due to large- or small-vessel occlusion. The OCSP classification was originally developed and tested by neurologists as part of a community-based study of first-ever stroke, in which some cases were seen after the acute phase. We examined the interobserver reliability of the classification when used in everyday clinical practice in patients seen during the acute phase of stroke shortly after admission to the hospital.
Two clinicians independently assessed consecutive patients admitted to the hospital with an acute stroke and recorded both the neurological features and their opinion of the subtype of infarct.
Eighty-five patients were assessed. Interobserver agreement for the classification was moderate to good (kappa = 0.54; 95% confidence interval, 0.39 to 0.68). Differences in the assessment of the commonly elicited neurological signs explained many of the disagreements: interobserver agreement was good for some signs (hemiparesis [kappa = 0.77], dysphasia [kappa = 0.70]), moderate for some (hemianopia [kappa = 0.39]), and poor for others (sensory loss [kappa = 0.15]).
The classification was simple and practicable (and could be widely used in routine clinical practice, randomized controlled trials, and audit), and interobserver reliability was satisfactory.
Factors associated with early presentation of acute stroke.
Authors: Feldmann E , Gordon N , Brooks J M , Brass L M , Fayad P B , Sawaya K L , Nazareno F , Levine S R 
Published: June 2011

Patients with stroke symptoms commonly delay many hours before seeking medical attention. We sought to explore the factors associated with early presentation of stroke patients to physicians.
We prospectively studied 100 consecutive acute stroke patients presenting to three large, urban medical centers. Using a standardized, structured interview and chart review, we assessed patient education about stroke, risk factors, clinical features of the stroke, source of stroke recognition, and timing of presentation. We did not study the distance from the site of stroke onset to the site of physician contact.
Stroke onset time was known in 96 of the patients. Mean patient age was 71.3 years, 79% had at least one stroke risk factor, 26% had prior transient ischemic attack, 19% had prior stroke, 74% had some high school education, and 86% had regular physicians. Only 8% had been previously educated about stroke symptoms. Eighty one percent of strokes were ischemic. The mean time to physician contact was 13.4 +/- 2.3 hours (median, 4.0 hours) and to neurologist contact was 21.2 +/- 2.9 hours. A skewed distribution of presentation times accounts for the mean-median differences. A small number of patients presenting very late could have an effect on the correlations between presentation time and the variables studied. Early presentation time was associated with increased age, the sudden onset of a stable deficit, and recognition that the symptoms signified stroke. Only the sudden onset of a stable deficit correlated independently with early presentation time (P = .0048). There was no correlation between presentation time and prior transient ischemic attack or stroke, headache, vomiting, loss of consciousness or seizures at onset, or stroke subtype, but a type II error could not be excluded.
Despite their education level, regular health care, and risk factors, especially prior stroke and transient ischemic attack, these patients were not knowledgeable about stroke and delayed many hours before contacting physicians. The course of symptoms and recognition that they signified stroke were associated with earlier presentation. Patient education focused on groups at risk may hasten the presentation and treatment of acute stroke.
Lacunar infarcts and white matter attenuation. Ophthalmologic and microcirculatory aspects of the pathophysiology.
Authors: Schneider R , Rademacher M , Wolf S 
Published: June 2011

By means of neurological and ophthalmologic examinations we considered whether there is a microcirculatory disorder not related to hypertension and diabetes in patients with lacunar infarcts and whether there are microcirculatory differences in patients with lacunar infarcts compared with those with white matter attenuation.
Eighty neurological patients with a lacunar infarct underwent computed tomography and, based on the results, were prospectively assigned to subgroups as follows: (1) patients without changes; (2) patients with white matter attenuation but without lacunar infarcts; (3) patients with lacunar infarcts alone; and (4) patients with both lacunar infarcts and white matter attenuation. Clinical and ophthalmologic parameters were monitored. The retinal microcirculation was studied by videofluorescence angiography. These neurological patients were compared with control ophthalmologic patients matched for age, sex, hypertensive and diabetic ocular fundus changes, and smoking habits.
On average, the 80 patients with lacunar infarcts had a significantly (P = .0001) slower arteriovenous passage time (2.6 +/- 0.7 seconds) than the ophthalmologic control subjects (1.6 +/- 0.6 seconds). Arteriovenous dye passage time through the retinal microcirculation was nearly normal (2.2 +/- 0.8 seconds) in patients with white matter attenuation alone, but was significantly prolonged in patients with lacunar infarcts (2.9 +/- 0.8 seconds, P = .00085) or both white matter attenuation and lacunar infarcts (2.8 +/- 0.4 seconds, P = .008).
Patients with lacunar infarcts are characterized by an additional disorder of retinal microcirculation independent of arterial hypertension and diabetes. Our data suggested that white matter attenuation and lacunar infarcts may be phenomena with only weak interdependence.
Ultrasound findings in spontaneous extracranial vertebral artery dissection.
Authors: Sturzenegger M , Mattle H P , Rivoir A , Rihs F , Schmid C 
Published: June 2011

In this study we analyzed the value of ultrasound examination for diagnosis of vertebral artery dissection.
The vertebrobasilar arterial system was assessed in 14 patients using transcranial and extracranial pulsed-wave Doppler and duplex sonography.
The dissections were verified by angiography (in 1 patient), magnetic resonance imaging (in 5), or both (in 8). The dissected segments were atlantoaxial (V-3) in 6, V-3 and intertransverse (V-2) in 3, V-3 and intracranial (V-4) in 3, and V-2 in 2 patients. Extracranial and transcranial Doppler examination of the atlas loop, involved in 12 patients, showed absent flow signal in 5, low bidirectional flow signal in 1, and poststenotic low blood flow velocities in 3 patients. Seven of these patients had high-grade stenosis or occlusion. The stenotic segment with increased flow signal could be identified directly in 2 patients. Duplex examination of the intertransverse segment confirmed absent flow in 4 patients, making technically insufficient examination unlikely. In the 2 patients with directly detected stenosis, duplex examination showed low flow velocities before the stenosis. The combined use of extracranial and transcranial Doppler and duplex sonography increases the diagnostic yield to detect vertebral artery pathology. If any abnormal sonographic finding was considered, the yield was 86%; relying only on definitively abnormal findings (absent flow signal, severely reduced vertebral artery blood flow velocities, no diastolic flow, bidirectional flow, and a stenosis signal), the yield was 64%.
In most cases, there is no pathognomonic ultrasound finding for vertebral artery dissection. However, if a patient presents with suggestive symptoms, ultrasound may corroborate the clinical suspicion and aid in the decision regarding early anticoagulant treatment. A definite diagnosis can be made noninvasively when magnetic resonance imaging demonstrates hematoma in the vessel wall. Angiography yields additional information such as nature of underlying vascular disease, site and extent of dissection, intracranial extension, and presence of pseudoaneurysm.
Nitric oxide and S-nitroso-L-cysteine as endothelium-derived relaxing factors from acetylcholine in cerebral vessels in cats.
Authors: Kukreja R C , Wei E P , Kontos H A , Bates J N 
Published: June 2011

The predominant view is that the endothelium-derived relaxing factor generated by acetylcholine from blood vessels is nitric oxide. However, there is evidence suggesting that certain nitric oxide-containing compounds such as nitrosothiols resemble the endothelium-derived relaxing factor generated by acetylcholine more closely than does nitric oxide itself. Accordingly, we compared the effects of nitric oxide and S-nitroso-L-cysteine on cerebral arteriolar caliber in relation to the associated increments in nitrite concentration in the effluent.
Acetylcholine, nitric oxide, and S-nitroso-L-cysteine were administered by continuous superfusion in oxygen-free solution through the space under a cranial window in anesthetized cats. Nitrite concentration was measured in the effluent. The degree of vasodilation induced was evaluated in relation to the increment in nitrite concentration.
All agents induced dose-dependent vasodilation and dose-dependent increments in nitrite concentration in the effluent. For any given degree of vasodilation, the increments in nitrite concentration were equivalent during acetylcholine or S-nitroso-L-cysteine infusion, whereas the nitrite concentrations were 10 times higher during nitric oxide infusion. After administration of nitroarginine, a competitive inhibitor of nitric oxide synthesis from arginine, there was depression in the vasodilation as well as the increment in nitrite concentration induced by acetylcholine.
S-Nitroso-L-cysteine resembles endothelium-derived relaxing factor from acetylcholine more closely than does nitric oxide.
Effect of a novel thromboxane A2 receptor antagonist, S-1452, on postischemic brain injury in rats.
Authors: Matsuo Y , Izumiyama M , Onodera H , Kurosawa A , Kogure K 
Published: June 2011

Arachidonate metabolites have been implicated in the development of cerebral injury after ischemia. Particular importance has been placed on the balance of thromboxane A2 and prostaglandin I2 because of its regulative activity on platelet functions and arterial tone. The purpose of the present study was to shed light on the role of thromboxane A2 in postischemic brain injury.
We evaluated the effects of S-1452, a novel thromboxane A2 receptor antagonist, on brain edema, infarct areas, and survival rate in rats with middle cerebral artery occlusion. A transient middle cerebral artery occlusion model was produced by inserting a piece of silicon-coated nylon thread into the internal carotid artery.
The ratio of plasma thromboxane B2 to 6-keto-prostaglandin F1 alpha significantly rose at 0 hour (P < .05), 1 hour (P < .01), 3 hours (P < .05), and 12 hours (P < .05) and then nearly returned to the normal level at 24 hours after reperfusion following 1-hour occlusion. Pretreatment with S-1452 (5, 10, or 50 mg/kg PO) significantly attenuated the increase in postischemic water content in the cerebral cortex perfused by the anterior cerebral artery and the cerebral cortex perfused by the middle cerebral artery in a dose-dependent manner but slightly attenuated it in the caudate putamen 24 hours after reperfusion following 1-hour occlusion. Pretreatment with S-1452 (10 mg/kg PO) also significantly decreased the areas of infarction in the front parts of the cerebrum. The survival rate of animals after 2 hours of occlusion tended to be improved by treatment with S-1452 (10 mg.kg-1.d-1 PO), although there was no statistical significance.
Our results suggest that thromboxane A2 is closely related to postischemic brain injury in the early phase of recirculation and that S-1452 may have a protective effect on postischemic brain injury.
Hemibody tremor related to stroke.
Authors: Dethy S , Luxen A , Bidaut L M , Goldman S 
Published: June 2011

Hemibody tremor is an uncommon manifestation of stroke. We describe a case investigated by both brain magnetic resonance imaging and positron emission tomography using [18F]fluorodeoxyglucose.
Three months after a pure motor stroke, a 65-year-old man developed a right arm and leg tremor. The tremor was of large amplitude, intermittent at rest; its frequency was 5 to 6 Hz. Neither rigidity nor akinesia was detected, and administration of L-dopa was ineffective. Brain magnetic resonance imaging revealed an ischemic lesion in the left centrum semiovale and a left caudate lacunar infarction. We suspected that the resting unilateral tremor was related to this lacunar lesion. Positron emission tomography demonstrated glucose hypermetabolism in the left sensorimotor cortex.
This case suggests that unilateral tremor may be related to a lacunar stroke in the caudate nucleus and may be accompanied by an increased glucose metabolism in the contralateral sensorimotor cortex.
Recovery of functional status after stroke. A postrehabilitation follow-up study.
Authors: Ferrucci L , Bandinelli S , Guralnik J M , Lamponi M , Bertini C , Falchini M , Baroni A 
Published: June 2011

Information on predictors of long-term change in functional capacity after a rehabilitation program in stroke patients is scant. This study describes the long-term evolution of self-reported functional ability after discharge from rehabilitation and its relation with age, level of neural impairment at discharge, and changes in neural impairment during follow-up.
Fifty patients (31 men and 19 women; mean +/- SD age, 66.0 +/- 9.9 years; range, 47-86 years) with a first unilateral stroke and no severe cognitive impairment were consecutively enrolled. Self-reported disability in activities of daily living and neural impairment measured by the Fugl-Meyer Scale were evaluated after discharge from a rehabilitation program and 3 and 6 months later.
Functional disability was significantly reduced after 3 and 6 months. Attenuation of disability occurred mainly among those patients with more severe baseline neural impairment. In this group, patients aged > or = 65 years were more disabled at baseline than younger individuals, but they had the same rate of improvement. In patients aged < 65 years, changes in disability over time could be attributed to changes in neural function, whereas older patients' functional recovery was greater than that expected from their improvement in neural impairment alone.
These results suggest that in stroke patients with severe neural damage further functional improvement occurs even after completion of a rehabilitation program. There is evidence that older patients may be more likely to employ compensatory strategies to overcome some of the neural impairment that remains after stroke.
Secular trend of mortality from cerebral infarction and cerebral hemorrhage in Taiwan, 1974-1988.
Authors: Chang C C , Chen C J 
Published: June 2011

Pathological patterns of stroke are different in various races, with the predominant stroke type in the Chinese being intracerebral hemorrhage. A total of 31,078 deaths from cerebral infarction and 77,773 deaths from cerebral hemorrhage in Taiwan were reported for groups of subjects aged 40-79 years during the period 1974-1988 to elucidate their secular trends.
Vital statistics and demographic data were collected for analyzing the truncated age-adjusted mortality rates. Poisson regression analysis was used to estimate the relative risk and 95% confidence interval.
The mortality rates for cerebral hemorrhage were greater than those for cerebral infarction. The mortality rates increased exponentially with age for both subtypes. The decline in age-specific mortality for the period 1974-1983 was much more striking for cerebral hemorrhage than for cerebral infarction. Mortality from cerebral infarction and hemorrhage increased with age for all birth cohorts except the cerebral hemorrhage mortality of the oldest cohort. Male/female ratios for both cerebral infarction and hemorrhage were greater in the younger age groups. The cerebral hemorrhage/infarction ratio during the period 1984-1988 was highest for the younger age groups and lowest for the oldest age groups.
The different secular trends of mortality from cerebral infarction and hemorrhage imply that these two patterns of stroke may be associated with some different risk factors.
Increased thromboxane biosynthesis in patients with acute cerebral ischemia.
Authors: Koudstaal P J , Ciabattoni G , van Gijn J , Nieuwenhuis H K , de Groot P G , Sixma J J , Patrono C 
Published: June 2011

Clinical and experimental studies suggest that platelets have a major role in the pathogenesis of cerebral ischemia. However, ex vivo both platelet aggregation studies and measurements of platelet-derived products in patients with cerebral ischemia have shown inconsistent results. The present study was designed to resolve this inconsistency.
We have measured the urinary excretion of a thromboxane metabolite, 11-dehydro-thromboxane B2, by a previously validated radioimmunoassay technique in 51 patients with acute cerebral ischemia who had experienced either a transient ischemic attack (14 patients) or an ischemic stroke (37 patients) and in 20 control patients with nonvascular neurological disorders. The median time between the onset of symptoms and urine sampling was 24 hours (range, from 2 hours to 8 days).
The excretion rate of immunoreactive 11-dehydro-thromboxane B2 ranged between 39 and 478 pmol/mmol creatinine in patients with a transient ischemic attack and between 23 and 5,916 pmol/mmol creatinine in stroke patients, with 29% (p = 0.18) and 51% (p = 0.004) of the urine samples, respectively, exceeding the upper limit of the control samples (251 pmol/mmol creatinine [mean +/- 2 SD]) (p = 0.01). In stroke patients, metabolite excretion was not related to the type (cortical or "lacunar") or site of cerebral infarction. Low-dose aspirin (50 mg per day for 7 days) reduced the urinary excretion by approximately 85% in 11 consecutive stroke patients.
We conclude that 1) episodes of enhanced thromboxane biosynthesis are detected infrequently in patients with a transient ischemic attack, 2) aspirin-suppressible episodes of increased thromboxane formation can be detected during the early phase of acute ischemic stroke, and 3) this finding may provide a rationale for testing the efficacy and safety of this drug in this setting.