bluuebunny/crossref_metadata_2025 huggingface dataset:
Clentiazem protects against chronic cerebral vasospasm in rabbit basilar artery.
Authors: Vorkapic P , Bevan J A , Bevan R D
Published: June 2011

Experiments were carried out in rabbits to determine whether clentiazem (8-chlorodiltiazem), a cerebrovascular-selective calcium channel blocker, administered 24 hours before subarachnoid hemorrhage influenced the subsequent cerebral vasospasm.

Subarachnoid hemorrhage was induced by multiple injections of blood into the prepontine cisterns of 35 male New Zealand White rabbits, and clentiazem (5 mg/kg) was administered 4 times daily until sacrifice. Cerebral artery diameter was assessed in vivo by angiography. Functional features of basilar arteries were measured using conventional in vitro methodology.

Clentiazem reduced the angiographic narrowing seen on days 2 and 5 from 35% and 34%, respectively (sham control, 1.42 +/- 0.31 mm [n = 22]), to 8% and 11%, respectively, and prevented the narrowing (32%) that occurred on day 9. Narrowing in the untreated rabbits was only partly reversed by papaverine; all narrowing in clentiazem-treated animals was papaverine sensitive. Clentiazem prevented or reduced many of the changes in the basilar artery caused by the subarachnoid hemorrhage. Of particular relevance to arterial narrowing were the increased wall stiffness, the transient spontaneous changes in wall force, and the reduction in relaxation to acetylcholine. Reduction of the changes in wall force induced by agonists and by stimulation of intramural sympathetic nerves was observed.

The vascular damage associated with chronic cerebral vasospasm is related to calcium entry into the smooth muscle and endothelial cells, and possibly sympathetic nerve terminals, through calcium channels sensitive to clentiazem, which suggests that clentiazem may be of value in the management of chronic cerebral vasospasm.
Racial variations in ischemic stroke-related physical and functional impairments.
Authors: Horner R D , Matchar D B , Divine G W , Feussner J R
Published: June 2011

We sought to determine whether there are racial differences in physical and functional impairments resulting from an initial ischemic stroke.

We conducted a prospective, county-wide, multisite cohort study including a university hospital, a community hospital, and a Veterans Affairs hospital. The study population was an inception cohort of 145 patients hospitalized for ischemic stroke. Physical and functional impairments were measured using a modified form of the Fugl-Meyer test and the Barthel Index, respectively. Nurses trained to use these tests made assessments at admission and 5, 30, 90, and 180 days after admission. Patient and disease-specific data along with treatment data and vital status were collected.

Forty-one patients (28%) were black. Compared with whites, black stroke patients were more likely to be widowed (51% versus 26%) and hypertensive (83% versus 63%) but less likely to be male (42% versus 69%) and alert on admission (66% versus 76%). There were no racial differences in mortality. Physical impairment was significantly more severe in black than in white patients at admission, and although physical impairment improved, it remained significantly worse in blacks. Functional impairment was also greater in black patients initially but was similar to that in white patients 90 days after the event. Multivariable analyses confirmed these findings.

These results indicate that blacks may have greater residual physical deficits from stroke than whites.
Efficacy of retrograde perfusion of the cerebral vein with verapamil after focal ischemia in rat brain.
Authors: Hosaka T , Yamamoto Y L , Diksic M
Published: June 2011

For treatment of acute stroke, drug therapy administered systemically has been unreliable due to inadequate delivery of drug into ischemic tissue. We have developed a new method to deliver drugs into the ischemic tissue by retrograde perfusion of the cerebral vein.

We examined in rats the effectiveness of administering verapamil into ischemic tissue by retrograde perfusion through the cerebral vein, starting 3 hours after occlusion of the middle cerebral artery. Twenty-four Fischer-344 rats with occlusion of the middle cerebral artery were divided into four groups of six rats each. Group A rats had no treatment, group B rats received verapamil intravenously, and groups C and D rats received verapamil by transvenous perfusion of the brain with blood and with saline, respectively. We studied local cerebral blood flow using the autoradiographic method with carbon-14-labeled iodoantipyrine and examined cerebral infarct volume with cresyl violet and Luxol fast blue staining.

As compared with group A rats, in groups C and D rats we found a significant and extensive increase of cerebral blood flow in the ischemic cortical and subcortical areas (55-119%, p less than 0.05) and a significant reduction of cerebral infarct volume (31-39%, p less than 0.05). We found no significant changes in group B rats.

This study shows that transvenous perfusion of the brain with verapamil starting 3 hours after occlusion of the middle cerebral artery produces a significantly beneficial effect in rats.
Mild hypothermia ameliorates ubiquitin synthesis and prevents delayed neuronal death in the gerbil hippocampus.
Authors: Yamashita K , Eguchi Y , Kajiwara K , Ito H
Published: June 2011

The purpose of the present study is to determine the effect of mild hypothermia on the synthesis of ubiquitin, an important protein for maintenance of cell viability, in the hippocampal neurons following transient cerebral ischemia.

Transient ischemia was induced by occluding both common carotid arteries for 5 minutes. In experiment 1, the animals were divided into four groups according to the rectal and scalp temperatures during ischemia: the normothermia group and the graded hypothermia A, B, and C groups (n = 9 per group). CA1 neuronal density was assessed at 7 days after ischemia. In experiment 2, the animals were divided into two groups designated the normothermia and the hypothermia groups (n = 6 per group). The presence of ubiquitin was examined by immunohistochemistry at 6, 24, and 48 hours after transient ischemia in various regions of the hippocampus.

In experiment 1, the mean +/- SEM neuronal density per millimeter was 12 +/- 1 in the normothermia group and 126 +/- 25, 225 +/- 10, and 214 +/- 9 in hypothermia groups A, B, and C, respectively. Mild hypothermia in groups B and C, in which the brain temperature was below 33 degrees C, ameliorated markedly the extent of ischemic neuronal damage in the CA1 sector (p less than 0.01). In experiment 2, ubiquitin immunoreactivity had disappeared in all regions of the hippocampus at 6 hours after ischemia and showed no subsequent recovery in the CA1 pyramidal neurons under normothermic conditions. Under hypothermic conditions, however, it had recovered significantly in the CA1 pyramidal neurons at 24 and 48 hours after ischemia (p less than 0.01).

We conclude that mild hypothermia, in which the brain temperature is below 33 degrees C, markedly improves the ischemic delayed neuronal damage in the CA1 sector, and that increased ubiquitin synthesis and protein ubiquitination could be one essential part of the protective mechanism afforded by mild hypothermia against delayed neuronal death.
Embolic stroke in aged rats.
Authors: Futrell N , Garcia J H , Peterson E , Millikan C
Published: June 2011

Although stroke is a disorder associated with aging, experimental studies of stroke are conducted in young adult (2-4-month-old) animals (rat life span, 27-29 months). To determine whether histopathologic changes caused by cerebral infarction would be altered in aged animals, we produced embolic cerebral infarction in 17 aged (23-24-month-old) and 16 young (2-4-month-old) rats.

The right common carotid artery was irradiated with a laser (632 nm, 200 mW/cm2, 15-20 minutes) after the intravenous injection of the photosensitizing dye Photofrin II (12.5 mg/kg). This produces a nonocclusive platelet thrombus that spontaneously embolizes to the brain. Animals were killed 4 days later.

Analysis was done on 142 infarcts, 68 in aged rats and 74 in young rats. Hypercellularity, with infiltration of macrophages, was more common within small infarcts (less than 1 mm) in young than in aged rats (p = 0.002), and hypertrophy of astroglial fibers surrounding the infarcts was more prominent in young rats. Larger infarcts (greater than or equal to 1 mm) were often hypocellular, with a trend toward more macrophages in the periphery of the infarcts in young than in old animals (p = 0.170).

The infiltration of macrophages into cerebral infarcts and the hypertrophy of astroglial fibrils surrounding these infarcts are reduced in the aged rat. These age-related differences emphasize the importance of using appropriately aged animals in experimental models of stroke.
Chronic blood hyperviscosity in subjects with acute stroke, transient ischemic attack, and risk factors for stroke.
Authors: Coull B M , Beamer N , de Garmo P , Sexton G , Nordt F , Knox R , Seaman G V
Published: June 2011

The origin and significance of blood hyperviscosity in subjects with acute stroke has been controversial. It has been argued that viscous abnormalities simply reflect either elevated hematocrit or an acute-phase response to the stroke itself. To address these issues, we measured the factors that determine blood viscosity in a cross-sectional study of 430 subjects, including 135 with acute stroke, 89 with acute transient ischemic attacks of the brain, 115 with recognized risk factors for stroke, and 91 healthy controls. The at-risk group was balanced with the acute stroke group for types of risk factors and medication usage, and all four groups were balanced for age. The viscosity of whole blood at low rates of shear and the plasma viscosity were significantly elevated in both groups with cerebrovascular symptoms and in the at-risk group compared with the healthy controls. The severity of hyperviscosity was stroke group greater than transient ischemic attack group greater than at-risk group greater than healthy controls. Increased viscosity of whole blood was associated with an elevated plasma fibrinogen concentration and with a decreased albumin/globulin ratio. This study provides evidence that blood hyperviscosity is present not only in subjects with acute brain infarction, but also in those with risk factors for stroke, and that these abnormalities are, to a considerable degree, chronic.
Treatment of acute hydrocephalus after subarachnoid hemorrhage with serial lumbar puncture.
Authors: Hasan D , Lindsay K W , Vermeulen M
Published: June 2011

Computed tomography demonstrated acute hydrocephalus less than or equal to 72 hours after subarachnoid hemorrhage in 24 (23%) of 104 patients. Of these 24 patients, six (25%) had no impairment of consciousness. In nine (11%) of the remaining 80 patients, acute hydrocephalus developed within 1 week after subarachnoid hemorrhage. With the exception of three patients, all 104 patients received antifibrinolytic treatment. Delayed clinical deterioration from acute hydrocephalus occurred in seven (29%) of the 24 patients with acute hydrocephalus on admission and in six (8%) of the remaining 80 patients. Serial lumbar puncture was performed in 17 patients. Twelve (71%) of the 17 patients treated with serial lumbar puncture, including 10 (77%) of the 13 patients with delayed deterioration from acute hydrocephalus after admission, achieved improvement in the level of consciousness. Four of these 17 patients (4% of all 104 patients) required an internal shunt. No patient deteriorated from coning following serial lumbar puncture. The rebleeding rate within 12 days after subarachnoid hemorrhage in hydrocephalic patients with serial lumbar puncture was not higher than the rate in those without hydrocephalus (two [12%] of 17 versus nine [13%] of 71). Neither meningitis nor ventriculitis was observed. We conclude that if neither a hematoma with a mass effect nor an obstructive element exists, cerebrospinal fluid drainage with serial lumbar puncture is a good alternative to ventricular drainage in patients with acute hydrocephalus after subarachnoid hemorrhage.
Hypertension, lipoprotein(a), and apolipoprotein A-I as risk factors for stroke in the Chinese.
Authors: Woo J , Lau E , Lam C W , Kay R , Teoh R , Wong H Y , Prall W Y , Kreel L , Nicholls M G
Published: June 2011

We analyzed the serum concentrations of lipids and lipoproteins and the prevalence of other risk factors in a case-control study of 304 consecutive Chinese patients with acute stroke (classified as cerebral infarction, lacunar infarction, or intracerebral hemorrhage) and 304 age- and sex-matched controls. For all strokes we identified the following risk factors: a history of ischemic heart disease, diabetes mellitus, or hypertension; the presence of atrial fibrillation or left ventricular hypertrophy; a glycosylated hemoglobin A1 concentration of greater than 9.1%; a fasting plasma glucose concentration 3 months after stroke of greater than 6.0 mmol/l; a serum triglyceride concentration 3 months after stroke of greater than 2.1 mmol/l; and a serum lipoprotein(a) concentration of greater than 29.2 mg/dl. We found the following protective factors: a serum high density lipoprotein-cholesterol concentration of greater than 1.59 mmol/l and a serum apolipoprotein A-I concentration of greater than or equal to 106 mg/dl. The patterns of risk factors differed among the three stroke subtypes. When significant risk factors were entered into a multiple logistic regression model, we found a history of hypertension, a high serum lipoprotein(a) concentration, and a low apolipoprotein A-I concentration to be independent risk factors for all strokes. The attributable risk for hypertension was estimated to be 24% in patients aged greater than or equal to 60 years. In this population, in which cerebrovascular diseases are the third commonest cause of mortality, identification of risk factors will allow further studies in risk factor modification for the prevention of stroke.
Effect of high-dose methylprednisolone and U74006F on eicosanoid synthesis after subarachnoid hemorrhage in rats.
Authors: Gaetani P , Marzatico F , Lombardi D , Adinolfi D , Rodriguez y Baena R
Published: June 2011

Free radicals and lipid peroxidation of membrane fatty acids are thought to play a role in the pathogenesis of arterial vasospasm and the physiopathologic patterns of neuronal damage after subarachnoid hemorrhage. We have evaluated the effects of treatment with either high-dose methylprednisolone every 8 hours or a single dose of U74006F on the temporal profile of ex vivo synthesis of four selected eicosanoids in brain slices after experimental induction of subarachnoid hemorrhage in rats. Prostaglandins D2 and E2, prostacyclin and leukotriene C4 levels were determined by radioimmunoassay after 1-hour incubation of the brain slices. The synthesis of prostaglandin D2 and 6-ketoprostaglandin F1 alpha at 48 hours after subarachnoid hemorrhage was significantly higher when compared to sham-operated animals (p = 0.01); prostaglandin E2 release was significantly enhanced at 6 hours after subarachnoid hemorrhage (p = 0.01). The release of the lipoxygenase metabolite was significantly enhanced at 1, 6, and 48 hours after subarachnoid hemorrhage induction. Both treatment regimens significantly reduced the ex vivo synthesis of prostaglandin D2, prostaglandin E2, and leukotriene C4 at 1, 6, and 48 hours after subarachnoid hemorrhage, whereas the effects on 6-ketoprostaglandin F1 alpha synthesis differed in the two treatment groups. U74006F enhanced the synthesis of prostacyclin metabolite in the early phase after subarachnoid hemorrhage, and high-dose methylprednisolone reduced the increasing synthesis at 48 hours. A strict comparison between the two treatments was not possible because of the different modalities of administration. However, these data suggest that the antioxidant effect of single-dose treatment with U74006F influenced the early and delayed effects on enzymatic lipid peroxidation, whereas the effects of methylprednisolone administration every 8 hours were more significant in the delayed phase.
An improved photochemical model of embolic cerebral infarction in rats.
Authors: Futrell N
Published: June 2011

To provide further evidence that the multiple cerebral infarcts found in rats following photochemical damage to the carotid artery are caused by emboli and to eliminate the systemic hypotension and heating of the blood reported with the previous photochemical embolic stroke model (rose bengal and a green laser), I have modified the photochemical technique. Brain pathology was studied in 18 Wistar rats following carotid artery irradiation with a red laser (632 nm) at powers ranging from 100 to 800 mW/cm2 for 10 or 20 minutes following the injection of the photosensitizing dye Photofrin II. Multiple cerebral arterioles were occluded by platelet aggregates containing frequent erythrocytes and leukocytes, identical to the thrombotic material in the carotid artery but different from the platelet aggregates seen in the carotid artery and the brain in the rose bengal model. Eighty infarcts were distributed randomly throughout the brain ipsilateral to the nonocclusive carotid thrombus. Significant heating (0.5 degree C or more) of the blood occurred only with laser powers higher (1,600 mW/cm2) or laser irradiations longer (25 minutes) than those used in the improved model of embolic stroke. This model mimics one mechanism of stroke in humans and provides a means to study systematically the morphological evolution of small cerebral infarcts.
Detection of arterial emboli using Doppler ultrasound in rabbits.
Authors: Russell D , Madden K P , Clark W M , Sandset P M , Zivin J A
Published: June 2011

The purpose of this study was to develop an animal model that could be used to test the ability of Doppler ultrasound to detect arterial emboli composed of materials that are often involved in cerebral emboli. Emboli introduced into the rabbit aorta via the left renal artery consisted of clotted whole blood, platelets, atheromatous material, fat, or air. The ultrasound examination was carried out continuously during the studies using a multifrequency transcranial Doppler apparatus with a 2-MHz probe, a sample volume of 15 mm, at a depth of 15 mm. The intensity of the Doppler spectrum was measured and displayed as a 15-shade color scale, each shade representing a 3-dB difference. The diameter of the aorta at the site of the ultrasound examination was similar to the diameter of the middle cerebral artery in humans. All 125 emboli introduced were clearly detected because they caused a Doppler signal at least 15 dB greater than that of the surrounding blood. These results show that the potential for emboli detection using Doppler ultrasound in the clinical situation is now considerable.
Turner's syndrome, fibromuscular dysplasia, and stroke.
Authors: Lancman M , Mesropian H , Serra P , Granillo R
Published: June 2011

We report a 43-year-old woman who presented with a right frontoparietotemporal ischemic stroke. She had been diagnosed with Turner's syndrome during childhood and had a history of chronic estrogen therapy. Cerebral angiography showed lesions characteristics of fibromuscular dysplasia involving the right internal carotid and right vertebral arteries. We are not aware of any previous reports describing an association between fibromuscular dysplasia and Turner's syndrome. Although chronic estrogen therapy cannot be ruled out as a cause of this patient's stroke, we suggest a possible etiologic relation between these two entities.
Correlation of common carotid flow volume measured by ultrasonic quantitative flowmeter with pathological findings.
Authors: Wada T , Kodaira K , Fujishiro K , Okamura T
Published: June 2011

To evaluate the possibility of quantitatively diagnosing carotid and cerebral atherosclerosis noninvasively, we measured common carotid flow volume in 60 sides (30 patients), using an ultrasonic quantitative flowmeter, and then compared these findings to the severity score of carotid and cerebral atherosclerosis as determined at autopsy. Stenosis decreased common carotid flow volume in the carotid and cerebral arteries. Increases in the severity score varied inversely with reduced flow volume, which was high in inverse correlation (r = -0.696). Patients with flow volumes of 8.5 ml/sec or greater did not have stenosis greater than or equal to 75%, whereas all patients with flow volumes of 6.4 ml/sec or less had stenosis greater than or equal to 50%, with 45% of these having stenosis greater than or equal to 75%. These pathological findings confirm that the common carotid flow volume reflects the degree of carotid and cerebral atherosclerosis present and that the lower limit of common carotid flow volume in healthy subjects is 6.5 ml/sec.
Air embolism of the brain in rabbits pretreated with mechlorethamine.
Authors: Helps S C , Gorman D F
Published: June 2011

Infusion of 400 microliters air into the left internal carotid artery of five anesthetized rabbits caused transient pial arteriole air embolism, an immediate 41.9 +/- 0.8% dilatation of the embolized vessels, suppression of the cortical somatosensory evoked response to 29.4 +/- 2.7% of baseline, and a progressive decline in ipsilateral cerebral blood flow (measured by hydrogen clearance) to 46 +/- 4.1% of baseline after 2 hours. These values were significantly different from those at baseline and from the responses of 10 control rabbits given equivalent intracarotid saline infusions. Twelve other rabbits were made leukopenic by treatment with 1.5 mg/kg i.v. mechlorethamine 72 hours prior to study. Mean +/- SEM leukocyte count decreased from 6,320 +/- 73/mm3 to 1,890 +/- 66/mm3 without any change in the leukocyte differential or erythrocyte and platelet counts. Intracarotid infusion of saline into seven of the leukopenic rabbits caused no changes. In the other five leukopenic rabbits, infusion of 400 microliters air caused air embolism but did not produce the anticipated declines in cerebral blood flow or the cortical somatosensory evoked response, both of which remained indistinguishable from baseline values and responses in the seven saline-treated leukopenic controls. Similarly, air-embolized arterioles showed nonsignificant dilatation in leukopenic rabbits. Our data suggest that the decreases in both cerebral blood flow and brain function seen after air embolism require the presence of leukocytes.
Development of a new perfusion system for pharmacological study on rabbit basilar arteries.
Authors: Ohta T , Mori M , Ogawa R , Tsuji M
Published: June 2011

We developed a constant-flow perfusion system to measure vascular responses to vasoactive agents applied intraluminally or extraluminally. The intraluminal and extraluminal sides of a cylindrical section of rabbit basilar artery were isolated completely. By loading with 0.75 g of tension, the resting condition of each preparation was made constant. The intraluminal side was perfused at a constant flow of 8 ml/min and under an intraluminal pressure of 8 mm Hg. When 30 mM KCl was administered intraluminally the preparation showed marked contraction, whereas only slight contraction was observed with extraluminal administration. When 2 x 10(-7) M 5-hydroxytryptamine was administered, no significant differences in contraction could be detected between the intraluminal and extraluminal routes. Application of 10(-6) to 10(-4) M acetylcholine after precontraction with 30 mM KCl resulted in much stronger dilatation upon intraluminal application. Thus, it was demonstrated that under certain conditions significant differences exist in the responses of rabbit basilar arteries to vasoactive agents applied intraluminally or extraluminally. This system can detect the effects of vasoactive agents administered intraluminally and extraluminally at a high level of sensitivity and shows good reproducibility as a means of analyzing vascular functions and characteristics.
Cerebral infarction verified by cranial computed tomography and prognosis for survival following transient ischemic attack.
Authors: Evans G W , Howard G , Murros K E , Rose L A , Toole J F
Published: June 2011

Of 564 consecutive patients with transient ischemic attack, 350 (62%) had cranial computed tomography performed. Except for date of admission and smoking history, there were few differences between the patients evaluated with computed tomography and the 214 who were not. Cerebral infarcts were found in 59 (17%) of the 350 tomographic evaluations. Previous clinically diagnosed stroke, older age, and male sex were all significantly associated with the occurrence of tomographically verified infarcts (p less than 0.05). After controlling for stroke history and other important covariates, patients with tomographically verified infarcts had significantly shorter survival times than did patients without evidence of infarction on computed tomography (p = 0.035). Thus, cranial computed tomography findings appear to have important prognostic value for estimating survival following transient ischemic attack.
Medullary arteries in aging and dementia.
Authors: Furuta A , Ishii N , Nishihara Y , Horie A
Published: June 2011

We examined sclerotic changes of the medullary arteries in 110 nonneuropsychiatric patients ranging in age from the second to the ninth decades, in 20 patients with subcortical arteriosclerotic encephalopathy (Binswanger's disease), and in 20 patients with dementia of the Alzheimer type. The principal sclerotic change was fibrohyaline thickening of the wall, which began to appear during the late fourth decade, increased in incidence gradually with age, and was most severe in patients with subcortical arteriosclerotic encephalopathy. Morphometry showed that the sclerotic changes of the medullary arteries were most prominent in the frontal lobe, followed by the parietal, occipital, and temporal lobes, in both the nonneuropsychiatric and demented groups. The sclerotic rate in the frontal lobe of patients with dementia of the Alzheimer type was slightly higher than that in the nonneuropsychiatric patients (p less than 0.05) but far less than that in the patients with subcortical arteriosclerotic encephalopathy (p less than 0.001). The sclerotic rate correlated well with the degree of ischemic white matter changes as well as with blood pressure.
Mechanism of enlargement of major cerebral collateral arteries in rabbits.
Authors: Lehman R M , Owens G K , Kassell N F , Hongo K
Published: June 2011

Major cerebral collateral arteries enlarge following bilateral ligation of the common and internal carotid arteries. The purpose of this investigation was to determine the relative contribution of cellular hypertrophy versus cellular hyperplasia to this vessel change in a morphometric analysis as well as the functional properties of remodeled vessels in an in vitro study. We assessed cell number and vessel dimensions by morphometric analysis of 16 perfusion-fixed rabbit basilar arteries. Results demonstrated significant increases in luminal diameter from 761 to 946 microns (p less than 0.01), medial cross-sectional area from 5.1 x 10(4) to 7.6 x 10(4) micron2 (p less than 0.005), smooth muscle cell volume from 9.19 x 10(5) to 1.44 x 10(6) micron3 (p less than 0.0005), and overall arterial length from 17.41 to 20.36 mm (p less than 0.005) in basilar arteries from the eight ligated rabbits compared with the eight sham-operated controls. Smooth muscle cell volume fraction and cell numerical density were unchanged whereas the number of cells per unit length of artery was increased significantly from 21.5 to 31.0 cells/micron (p less than 0.05). These data indicate that smooth muscle cell hyperplasia rather than hypertrophy contributes to increases in vessel mass. Functional properties of the basilar arteries from 10 ligated and 10 normal control rabbits were analyzed in vitro. Results showed increased contraction to potassium chloride (approximately 74%) (p less than 0.01) and increased sensitivity of smooth muscle to acetylcholine (p less than 0.05) while maximal relaxation was the same as control in the ligated animals.(ABSTRACT TRUNCATED AT 250 WORDS)
Prognostic parameters in spontaneous intracerebral hematomas with special reference to anticoagulant treatment.
Authors: Rådberg J A , Olsson J E , Rådberg C T
Published: June 2011

We examined a series of 200 consecutive patients with spontaneous intracerebral hematoma clinically and by computed tomography, excluding patients with trauma, aneurysm, or tumor. Hematoma volume varied from 1 to 230 (average 35) ml, and overall mortality was 30% (60 patients). Of the 200 patients, 14% (28) were receiving anticoagulants; among these 28 patients hematoma volume averaged 72 ml and mortality 57% (16 patients). The 140 survivors were followed for 2-24 months. Our findings indicate that anticoagulation therapy after previous cerebral infarction or embolism of cardiogenic origin did not predispose to intracerebral hemorrhage. Prognosis was poor when the initial level of consciousness was low and the hematoma volume exceeded 50 ml in combination with dilatation of the contralateral ventricle. An intracerebral hematoma of greater than 80 ml volume was always fatal, regardless of therapy. With volumes of 40-80 ml, early surgical evacuation of the lobar hematoma may improve outcome.
Reevaluation of transient ischemic attacks as a risk factor for early mortality.
Authors: Howard G , Evans G W , Thomas J L , Ryu J E , Kahl F R , Crouse J R
Published: June 2011

The prevailing belief that transient ischemic attack is a risk factor for cardiovascular morbidity and mortality is based primarily on comparisons of survival of patients after transient ischemic attacks to that of an age-, race-, and sex-adjusted general population. Concomitant conditions that carry a high risk of premature mortality or morbidity, such as ischemic heart disease, hypertension, and diabetes, are very prevalent among patients with transient ischemic attacks. Hence, the poor prognosis of such patients may be attributable to these factors rather than their transient ischemic attack per se, which may only serve to bring patients into the medical system. We compared the survival of 336 patients after transient ischemic attack to that of a control group with a similar risk factor profile consisting of 6,710 patients evaluated for cardiac catheterization. Survival estimates, both unadjusted and adjusted for risk factors, did not differ between the two groups. Three-year survival estimates, after adjustment to the mean value of covariates, were 94% for the patients with transient ischemic attacks and 91% for the controls. These results suggest that the transient ischemic attack may not be an independent risk factor for mortality, although it may identify patients already at increased risk from coexisting conditions.
Clinical survey of ischemic cerebrovascular disease in children in a district of Japan.
Authors: Satoh S , Shirane R , Yoshimoto T
Published: June 2011

Ischemic cerebrovascular disease in children is relatively rare. To clarify the clinical features of ischemic stroke occurring in infants and children, we evaluated 54 cases of cerebral infarction, excluding cases of moyamoya disease, in patients less than 16 years old at 24 clinics in the Tohoku (northeast) district of Japan. We observed two incidence peaks, one in little children and the other in junior high school students. Infection and minor head trauma were more frequently seen prior to ischemic strokes than was heart disease. The middle cerebral artery region, including the basal ganglia, was most commonly affected (49 patients, 91%) on computed tomograms. Angiography was performed in 48 patients (89%) and showed various types of occlusive lesions, mostly affecting the middle cerebral artery. Hemiparesis was the most common form of disability following ischemic strokes (48 patients, 89%). Surgical treatment was carried out in seven patients (13%). The clinical course of these cases showed that the recovery of children after a stroke tends to be better than that of adults, but that permanent disabilities, such as hemiparesis or mental retardation, occur commonly. Further investigation of juvenile cerebrovascular disease is important to prevent ischemic strokes in children.
Regional cerebrovascular oxygen saturation measured by optical spectroscopy in humans.
Authors: McCormick P W , Stewart M , Goetting M G , Balakrishnan G
Published: June 2011

Regional cerebrovascular oxygen saturation, a quantitative measure of hemoglobin saturation in the combined arterial, venous, and microcirculatory compartments of the brain, can be measured noninvasively with near infrared spectroscopy. We assessed the sensitivity of this aggregate saturation to cerebral hypoxia during transient cerebral hypoxic hypoxia in seven human subjects. Regional cerebrovascular oxygen saturation measured over the middle frontal gyrus and analog electroencephalogram were recorded. We compared the time to achieve two end points: the earliest paroxysmal burst of theta-delta background slowing and a cerebrovascular oxygen saturation of less than 55%. Saturation fell below 55% prior to the electroencephalographic change (p less than 0.05). In a related effort, we also compared spectroscopically measured regional cerebrovascular oxygen saturation with an estimate of this value calculated from arterial and cerebral mixed venous saturation in nine patients. A positive linear relation (n = 68, R2 = 0.55, s = 4.2) was noted.
Transesophageal echocardiography in the detection of potential cardiac source of embolism in stroke patients.
Authors: Cujec B , Polasek P , Voll C , Shuaib A
Published: June 2011

To compare the diagnostic yields of transesophageal and transthoracic echocardiography in the detection of potential cardiac sources of embolism, 63 patients (mean +/- SD age 63 +/- 15 [range 18-87] years) with transient ischemic attacks or stroke underwent both procedures. Transthoracic echocardiography revealed a potential cardiac source of embolism in 14% (nine) of the patients, all of whom had clinical evidence of heart disease. Transesophageal echocardiography revealed a potential cardiac source of embolism in 41% (26) of the patients; 27% (seven) of these patients had no clinical cardiovascular abnormalities. Abnormalities detected only by transesophageal echocardiography in the patients with unsuspected cardiac disease included atrial septal aneurysm in two, patent foramen ovale in two, left atrial appendage thrombus in one, and myxomatous mitral valve in two. The 26 patients with an identified cardiac source of embolism were older (67.5 versus 59.4 years, p = 0.04), more frequently in atrial fibrillation (62% [16] versus 8% [3], p less than 0.0001), had a larger left atrium (43 versus 37 mm, p = 0.01) and more commonly had left ventricular hypertrophy (62% [16] versus 32% [12], p less than 0.02) than the 37 patients in whom no cardiac source of embolism was identified. Thus, transesophageal echocardiography is more sensitive than transthoracic echocardiography in the detection of potential cardiac sources of embolism in patients with cerebral ischemic events.
Epidemiology of subarachnoid hemorrhage in Finland from 1983 to 1985.
Authors: Sarti C , Tuomilehto J , Salomaa V , Sivenius J , Kaarsalo E , Narva E V , Salmi K , Torppa J
Published: June 2011

The age-standardized incidence of subarachnoid hemorrhage was 33/100,000/yr among Finnish men and 25/100,000/yr among Finnish women. Subarachnoid hemorrhage represented 11% of all strokes detected during 1983-1985 in the community-based stroke register in three areas of Finland. Age-standardized mortality from subarachnoid hemorrhage was 18/100,000/yr among men and 12/100,000/yr among women aged 25-74 years, representing in men 22% and in women 23% of all deaths from stroke in the register. The case-fatality rate of subarachnoid hemorrhage was high: 35% among men and 33% among women within 2 days after the onset of the stroke attack and 48% in men and 46% in women at 1 month. Our findings suggest that the incidence and mortality of subarachnoid hemorrhage in Finland are among the highest worldwide, although differences in criteria, study methods, and classification procedures reduce the comparability of studies from different countries. The occurrence of subarachnoid hemorrhage in our present study is also higher than that previously reported in this country. We believe that this is more likely due to changes in diagnostic classification and improvements in detection of the disease than to a real increase in the morbidity and mortality of subarachnoid hemorrhage.
Clinical significance of the V-shaped space in the subluxed shoulder of hemiplegics.
Authors: Arsenault A B , Bilodeau M , Dutil E , Riley E
Published: June 2011

Recently, it has been proposed that shoulder subluxation in hemiplegia is accompanied by 1) the appearance of a V-shaped articular configuration occurring between the humeral head and glenoid fossa and 2) the presence of chronic pain. The main purpose of this study was to investigate the validity of these statements. We evaluated 40 hemiplegic subjects over 3 months. Radiographs of the affected and nonaffected shoulders were taken at both a frontal plane (0 degree) and a 45 degree incidence. From these patients, subluxed (n = 19) and nonsubluxed (n = 21) groups were formed. Pain was evaluated using the Present Pain Intensity index of the McGill Pain Questionnaire. On these x-ray films, measurements were taken of the V-shaped space, abduction of the arm, and rotation of the scapula. The statistical analysis (analysis of variance for repeated measures) contrasted the results obtained from the nonaffected side with those from the affected side over the 3 months studied. At the 45 degree angle, which better exposes the articular configuration of the shoulder, the difference in the V angle between the affected and nonaffected shoulders was significant for the subluxed group (p less than 0.01), indicating that such a V-shaped space can be identified. The measures taken also indicate that a downward subluxation of the humeral head occurs relative to the scapula without any systematic abduction of the humerus or downward rotation of the scapula. None of the results obtained from the frontal plane x-ray films was significant. Finally, no significant relation was found between subluxation and shoulder pain.
Reduction of central nervous system ischemic injury in rabbits using leukocyte adhesion antibody treatment.
Authors: Clark W M , Madden K P , Rothlein R , Zivin J A
Published: June 2011

Activated leukocytes appear to be directly involved in ischemic central nervous system injury. A surface glycoprotein (CD18) on the leukocyte is required for endothelial adherence and subsequent function and can be blocked with leukocyte adhesion antibody treatment. We used two animal models to determine the efficacy of anti-CD18 antibody treatment in preserving neurologic function after central nervous system ischemia. We gave a dose of 1 mg/kg anti-CD18 to treatment rabbits 30 minutes before inducing irreversible ischemia in the brain with intraarterial microspheres or in the spinal cord using reversible aortic occlusion. Treatment with anti-CD18 produced a significant reduction in neurologic deficits in the reversible spinal cord model, but not in the irreversible microsphere model. This protective effect supports the active role of leukocytes in central nervous system reperfusion ischemic injury and offers potential for future therapy.
Effects of U74006F on multifocal cerebral blood flow and metabolism after cardiac arrest in dogs.
Authors: Sterz F , Safar P , Johnson D W , Oku K , Tisherman S A
Published: June 2011

Lipid peroxidation reactions during reperfusion after cardiac arrest may contribute to postischemic cerebral hypoperfusion, which in turn can contribute to permanent neurological dysfunction. We designed this study to determine whether the aminosteroid U74006F, a putative inhibitor of lipid peroxidation, mitigates cerebral multifocal hypoperfusion after cardiac arrest. We used our established dog model of ventricular fibrillation cardiac arrest (no blood flow) of 12.5 minutes, reperfusion by cardiopulmonary bypass of less than or equal to 5 minutes, and control of extracerebral variables during 4 hours postarrest. Cerebral blood flow was monitored by the stable xenon computed tomography method. Changes in cerebral oxygen consumption were obtained from mean blood flow values of coronal slices and the cerebral arteriovenous (sagittal sinus) oxygen content difference. A treatment group (n = 5) received U74006F starting with reperfusion (1.5 mg/kg i.a. plus 1.5 mg/kg i.v.) and three additional (graded) doses over 4 hours (total dose 4.5, 7.5, or 14.5 mg/kg). The U74006F-treated group showed the same postarrest transient hyperemia and protracted hypoperfusion in terms of global (computed tomography slice), regional, and local (multifocal) cerebral blood flow values and the same global cerebral oxygen consumption pattern as a concurrent control group (n = 5). At 1-4 hours postarrest, in both groups there was mismatching of global cerebral oxygen consumption, which reached baseline values, in relation to global cerebral blood flow and oxygen delivery, which remained at 50% of baseline. We conclude that treatment with U74006F after prolonged cardiac arrest causes no deleterious side effects and does not seem to alter multifocal postarrest cerebral blood flow and oxygen consumption.
Captopril improves neurologic outcome from incomplete cerebral ischemia in rats.
Authors: Werner C , Hoffman W E , Kochs E , Rabito S F , Miletich D J
Published: June 2011

We investigated the effects of the angiotensin-converting enzyme inhibitor captopril on neurologic outcome in a rat model of incomplete cerebral ischemia. Twenty male Sprague-Dawley rats were anesthetized with 70% nitrous oxide in oxygen and fentanyl (10 micrograms x kg-1 i.v. bolus, 25 micrograms x kg-1 x hr-1 i.v. continuous infusion). Animals in group 1 (n = 10) received no angiotensin-converting enzyme inhibitor while animals in group 2 (n = 10) were given 10 mg x kg-1 i.v. captopril 30 minutes prior to the ischemic period. Ischemia was produced by unilateral carotid artery ligation and hemorrhagic hypotension to 35 mm Hg for 30 minutes. Body temperature, arterial blood gases, and arterial pH were maintained constant. Neurologic outcome was evaluated every 24 hours for 3 days using a graded deficit score (0, normal; 18, stroke-related death). On the third day after ischemia, captopril significantly improved neurologic outcome (median deficit score = 4) compared with controls (median deficit score = 18) (p less than 0.05). These results suggest that reduced angiotensin II levels or increased tissue kinin concentrations may decrease ischemic brain injury.
Magnesium sulfate reverses experimental delayed cerebral vasospasm after subarachnoid hemorrhage in rats.
Authors: Ram Z , Sadeh M , Shacked I , Sahar A , Hadani M
Published: June 2011

We induced experimental delayed cerebral vasospasm by the intracisternal injection of greater than 0.5 ml blood in 30 rats. Seventy-two hours later the basilar artery was exposed via the transclival approach and photographed at high-power magnification through an operating microscope. We then evaluated the effect of topical (n = 30) and intravenous (n = 20) magnesium sulfate on the spastic artery by computerized image analysis. A greater than 50% reduction in baseline diameter of the basilar artery was observed in the rats subjected to subarachnoid hemorrhage compared with the 10 controls (p less than 0.0001). Intravenous magnesium sulfate dilated the spastic artery to approximately 75% of the baseline diameter in control rats (p less than 0.0001). Topical magnesium sulfate caused dramatic dilation of the basilar artery in both the control and the subarachnoid hemorrhage groups to near 150% of the baseline diameter in the controls (p less than 0.001). All rats receiving intravenous magnesium sulfate reached therapeutic plasma levels of the ion. Hemodynamic effects were mild and immediately reversible upon cessation of magnesium sulfate administration. We suggest that magnesium has a role in the treatment of subarachnoid hemorrhage-induced vasospasm in humans.
Immunohematologic characteristics of infection-associated cerebral infarction.
Authors: Ameriso S F , Wong V L , Quismorio F P , Fisher M
Published: June 2011

We evaluated 50 consecutive patients with acute ischemic stroke to assess the prevalence of systemic infection preceding the neurological event. We analyzed the immunohematologic characteristics of patients with and without signs and/or symptoms of a preceding infectious process. Patients were examined less than or equal to 7 days after cerebral infarction and evaluated for fibrinogen, anticardiolipin antibodies, fibrin D-dimer (a fragment of cross-linked fibrin), plasminogen activator inhibitor-1, and protein S. Of the 50 patients, 17 had symptoms of infection beginning less than or equal to 1 month before the stroke (11 had upper respiratory tract infections, three urinary tract infections, two subacute bacterial endocarditis, and one pneumonia). Compared with patients without infection, patients with infection had significant increases in fibrin D-dimer concentration (5.3 +/- 1.1 versus 4.7 +/- 0.9 log-transformed ng/ml, p less than 0.05) and cardiolipin immunoreactivity, IgG isotype (1.8 +/- 1.3 versus 1.1 +/- 0.9 log-transformed phospholipid units, p less than 0.04), and, when studied less than or equal to 2 days after the stroke, increased fibrinogen levels (459 +/- 126 versus 360 +/- 94 mg/dl, p less than 0.05). In conclusion, infection-associated cerebral infarction is common and is associated with substantial immunohematologic abnormalities.
Forebrain ischemia induces selective behavioral impairments associated with hippocampal injury in rats.
Authors: Gionet T X , Thomas J D , Warner D S , Goodlett C R , Wasserman E A , West J R
Published: June 2011

Two groups of rats were tested on a variety of motor and cognitive tasks after either 10 minutes of two-vessel occlusion forebrain ischemia (n = 8) or sham operative procedures (n = 6). Histological injury was absent in the sham-operated group. In the ischemic group, hippocampal injury was restricted to field CA1, while damage in the neocortex and caudoputamen was sparse. Motor tests performed on postoperative days 18 and 28 revealed no significant differences between the ischemic and sham-operated groups. Retention performance of a radial maze discrimination task was impaired, with a significant but transient increase in both working and reference memory errors. Passive avoidance acquisition and retention were not significantly affected, although conclusions concerning the utility of this task must be reserved because of variability in the behavior of the sham-operated rats. Morris maze spatial navigation (place learning) and open-field activity were insensitive to treatment group. These functional results are consistent with the observed histological injury and what is known about hippocampal injury and behavior, and they provide further guidance for the development of neurological assays appropriate for discriminating outcome from forebrain ischemia in rats.
A review of hemoglobin and the pathogenesis of cerebral vasospasm.
Authors: Macdonald R L , Weir B K
Published: June 2011

We believe that current experimental and clinical evidence can be most satisfactorily interpreted by assuming that oxyhemoglobin is the cause of cerebral vasospasm that follows subarachnoid hemorrhage. We review the pathogenetic mechanisms by which oxyhemoglobin affects cerebral arteries. The relative importance of each of these mechanisms in the genesis of vasospasm, the biochemical pathways of oxyhemoglobin-induced smooth muscle contraction, and the intracellular actions of oxyhemoglobin on smooth muscle and on other cells in arteries are still not definitely established.