bluuebunny/crossref_metadata_2025 huggingface dataset:
(S)-emopamil protects against global ischemic brain injury in rats.
Authors: Lin B W , Dietrich W D , Busto R , Ginsberg M D
Published: June 2011

(S)-Emopamil is a novel calcium channel blocker of the phenylalkylamine class, with potent serotonin S2 antagonist activity. We investigated the effect of (S)-emopamil on the histopathologic consequences of global brain ischemia in anesthetized rats. Pretreated rats (n = 15) received 20 mg/kg i.p. (S)-emopamil 30 minutes before and 2 hours following 10 minutes of bilateral common carotid artery occlusion plus arterial hypotension (50 mm Hg). Quantitative cell counts following 3 days' survival revealed a marked loss of pyramidal neurons in all subsectors of the hippocampal CA1 area of untreated ischemic rats (n = 15). In contrast, in (S)-emopamil pretreated rats numbers of normal neurons were significantly higher, by 2.4-, 1.9-, and 1.8-fold, respectively, in the medial, middle, and lateral subsectors of the CA1 area. For example, normal neuron counts in the medial CA1 subsector were 34 +/- 9 (mean +/- SEM) in untreated ischemic rats compared with 82 +/- 13 in (S)-emopamil pretreated rats (control nonischemic value [n = 5] 157 +/- 2). By semiquantitative grading, (S)-emopamil also decreased ischemic changes in the cerebral cortex. No significant effect of (S)-emopamil on ischemic injury was detected in rats treated beginning 30 minutes after the ischemic insult (n = 10). Thus, pretreatment with (S)-emopamil is beneficial in decreasing the severity of neuronal injury in global brain ischemia.
Efficiency, effectiveness, and duration of stroke rehabilitation.
Authors: Shah S , Vanclay F , Cooper B
Published: June 2011

This prospective multicenter study identifies the variables significant in the prediction of rehabilitation efficiency, achievement of rehabilitation potential and duration of rehabilitation stay in 258 persons with a first stroke admitted to comprehensive inpatient rehabilitation in Brisbane, Australia, during 1984. All three dependent variables were poorly predicted, with only 17% of the variance in rehabilitation efficiency, only 30% of the variance in achievement of rehabilitation potential, and only 22% of the variance in duration of rehabilitation stay explained. Unlike other reports, we considered most of the major medical (side of paralysis, stroke etiology, site of the lesion, arterial distribution affected, etc.), rehabilitative (initial Barthel Index score, interval from stroke onset to acute-care hospital admission, interval from hospital admission to rehabilitation commencement, neurologic measures, etc.), and demographic (age, years of education, occupation, ethnicity, etc.) variables. The high proportion of unexplained variance is likely to be due to nonmedical factors influencing the selection of patients for rehabilitation.
Intracranial hemorrhage in patients with polycystic kidney disease.
Authors: Ryu S J
Published: June 2011

To emphasize the important association of polycystic kidney disease and hypertensive cerebral hemorrhage, a registry of 900 consecutive cases of hemorrhagic stroke was reviewed. Eleven patients (1.2%) had intracranial hemorrhage (eight had hypertensive cerebral hemorrhage and the other three had aneurysmal subarachnoid hemorrhage) found to be associated with polycystic kidney disease. These 11 patients also accounted for 11% of the 98 cases of polycystic kidney disease during the 28-month study period. As verified by computed tomography, parenchymal hemorrhage occurred mainly in the putamen and the thalamus, the usual sites for hypertensive cerebral hemorrhage. One patient with cerebral hemorrhage was autopsied and one was studied angiographically, but in neither patient was an intracranial aneurysm identified. In the patients with polycystic kidney disease and intracranial hemorrhage, hypertension had been inadequately treated or even undetected; therefore, I emphasize early detection and more effective control of hypertension in patients with polycystic kidney disease for prophylaxis against hemorrhagic cerebrovascular events.
Variable angiographic findings in patients with stroke and neurosyphilis.
Authors: Landi G , Villani F , Anzalone N
Published: June 2011

We describe four patients with cerebral infarction and active neurosyphilis who had variable angiographic findings. Patients 1 and 2 had evidence of arteritis and an atheromatous ulcerated stenosis of the extracranial carotid artery, respectively. The third and fourth patients had symptoms of lacunar infarction, but cerebral angiography was normal in patient 3, whereas patient 4 had evidence of concomitant atheromatous and arteritic lesions. Neither age nor presence of cerebrovascular risk factors was of aid in predicting angiographic features. The concomitance of cerebral infarction and active neurosyphilis does not imply a cause-and-effect relation, since atherosclerotic lesions may coexist with arteritis or may even represent the only angiographic feature. Our findings underscore the importance of angiography to confirm the diagnosis in cases of suspected syphilitic arteritis.
Perfusion insufficiency in limb-shaking transient ischemic attacks.
Authors: Tatemichi T K , Young W L , Prohovnik I , Gitelman D R , Correll J W , Mohr J P
Published: June 2011

We describe a 63-year-old man with severe bilateral internal carotid artery disease who presented with repeated, brief attacks of left limb shaking precipitated by his standing up. Cerebral blood flow measured by xenon-133 inhalation showed reduced resting flows and a focal perfusion deficit in the right dorsofrontal and upper rolandic regions. Blood flow velocity and pulsatility index of the right middle cerebral artery measured by transcranial Doppler ultrasonography were also reduced. With hypercapnic challenge, both hemispheric tissue perfusion and blood flow velocity showed impaired reactivity. With induced hypotension, the focal perfusion deficit in the right dorsofrontal region was accentuated. Following right internal carotid endartectomy, resting cerebral blood flow and blood flow velocity improved, as did hypercapnic vasoreactivity. These reversible deficits in cerebral blood flow and vasoregulation, which were maximal in the dorsofrontal region, are consistent with low perfusion in the border zone territory or the distal fields and demonstrate that hemodynamic failure is the likely mechanism for limb-shaking transient ischemic attacks from severe carotid artery disease.
Reversed intracranial blood flow in patients with an intra-aortic balloon pump.
Authors: Brass L M
Published: June 2011

As a preliminary investigation into the cerebral effects of mechanical cardiac assist devices, using transcranial Doppler ultrasonography I examined the basal cerebral arteries in three patients placed on an intra-aortic balloon pump. Unassisted systoles had normal blood velocities and waveforms. When the pump was in use, diastolic blood velocity during balloon inflation increased. As the balloon was deflated and intra-aortic pressure was dramatically lowered, diastolic blood velocity within the intracranial vessels decreased sharply. In two patients there was a reversal of blood flow in the middle cerebral, anterior cerebral, basilar, and vertebral arteries during late diastole. Although the clinical effects of cessation and reversal of blood flow in the cerebral circulation while on an intra-aortic balloon pump remain to be determined, transcranial Doppler ultrasonography appears to be a useful tool for measuring these hemodynamic effects. It may also be helpful in quantifying the effects of such pumps on cerebral blood flow and devising inflation/deflation timing sequences that maximize forward blood flow.
Stroke in infective endocarditis.
Authors: Hart R G , Foster J W , Luther M F , Kanter M C
Published: June 2011

We reviewed 212 consecutive episodes of infective endocarditis in 203 patients at six hospitals between 1978 and 1986 and found that 21% were complicated by stroke. Of 133 episodes involving native mitral and/or aortic valves, brain ischemia occurred in 19%, brain hemorrhage in 7%, and non-central nervous system emboli in 11%; vegetations were identified in 56% of 113 adequate echocardiograms and did not correlate with risk of embolism. In native-valve endocarditis, most (74%) ischemic strokes had occurred by the time of presentation and an additional 13% occurred less than or equal to 48 hours after diagnosis; the incidence of brain ischemia was 13% on presentation, 3% during the first 48 hours of hospitalization, and 2%-5% during the remainder of the acute course. Stroke recurred at a rate of 0.5%/day, often heralding relapse/uncontrolled infection. Only 9% of ischemic infarcts were large (all in patients with Staphylococcus aureus infection), while 8% were small and subcortical. Brain hemorrhage occurred primarily at the time of presentation, particularly in intravenous drug abusers, and was associated with uncontrolled S. aureus infection with pyogenic arteritis. Ischemic and hemorrhagic stroke continue to be frequent and important in patients with infective endocarditis and are clustered during uncontrolled infection.(ABSTRACT TRUNCATED AT 250 WORDS)
Xenon-enhanced computed tomography compared with [14C]iodoantipyrine for normal and low cerebral blood flow states in baboons.
Authors: Wolfson S K , Clark J , Greenberg J H , Gur D , Yonas H , Brenner R P , Cook E E , Lordeon P A
Published: June 2011

The correlation between the acute, invasive diffusible [14C]iodoantipyrine technique for cerebral blood flow and the noninvasive xenon-enhanced computed tomographic method has been assessed by simultaneous measurements in the baboon. Blood flows in small tissue volumes (about 0.125 cm3) were directly compared in normal and low flow states. These studies demonstrate a statistically significant association between the two methods (p less than 0.001). Similar correlations were obtained by both the Kendall (tau) and the Spearman (r) methods (r = 0.67 to 0.92, n greater than or equal to 19 for each study). The problems and limitations of such correlations are discussed.
Carnitine treatment for stroke in rats.
Authors: Slivka A , Silbersweig D , Pulsinelli W
Published: June 2011

Changes in the concentrations of carnitine, long-chain acylcoenzyme A, and long-chain acylcarnitine in ischemic myocardium parallel those in ischemic brain. Since carnitine treatment reverses these changes and improves function in ischemic hearts, we examined whether carnitine given to rats before focal cerebral ischemia (produced by tandem right common carotid artery and middle cerebral artery occlusion) alters infarct volume in four separate experiments. Mannitol was used to control for the osmotic effect of carnitine on brain edema in one experiment. While carnitine was found to significantly decrease infarct volume compared with saline in one experiment (p less than 0.05, Student's t test), this result could not be replicated in the subsequent three experiments. Because the positive treatment effect was not reproducible despite similar experimental conditions, the result of the first experiment was attributed to a type I error. Mannitol also showed no significant effect on infarct volume. This study emphasizes the need for concurrent controls with each group of treated animals and the need for replicating the results of a single experiment when testing for drug efficacy in animal models of focal cerebral ischemia.
Predictive value of brain perfusion single-photon emission computed tomography in acute ischemic stroke.
Authors: Giubilei F , Lenzi G L , Di Piero V , Pozzilli C , Pantano P , Bastianello S , Argentino C , Fieschi C
Published: June 2011

We investigated 32 patients with completed ischemic stroke less than or equal to 6 hours after the onset of symptoms by means of computed tomography, cerebral angiography, and technetium-99m-labeled hexamethylpropyleneamine oxime single-photon emission computed tomography to study cerebral blood flow. Follow-up computed tomography and cerebral blood flow studies were performed 1 week and 1 month after admission. Poor outcome at 1 month was evident in 18 (78%) of the 23 patients with severe neurologic deficit on admission and in 11 (92%) of the 12 patients with severe hypoperfusion in the affected hemisphere on admission. All 10 patients with severe impairment of both neurologic status and cerebral blood flow had a poor outcome at 1 month. We detected severe hypoperfusion in patients with large lesions on computed tomograms or cerebral artery occlusions on angiograms. Cerebral blood flow had increased at the 1-week follow-up despite different clinical outcomes. Our data provide evidence that early evaluation of cerebral blood flow with single-photon emission computed tomography is useful to detect subgroups of patients with different clinical outcomes during the acute phase of ischemic stroke.
Placebo-controlled trial of nimodipine in the treatment of acute ischemic cerebral infarction.
Authors: Martínez-Vila E , Guillén F , Villanueva J A , Matías-Guiu J , Bigorra J , Gil P , Carbonell A , Martínez-Lage J M
Published: June 2011

Nimodipine is a 1,4-dihydropyridine derivative that shows a preferential cerebrovascular activity in experimental animals. Clinical data suggest that nimodipine has a beneficial effect on the neurologic outcome of patients suffering an acute ischemic stroke. Our double-blind placebo-controlled multicenter trial was designed to assess the effects of oral nimodipine on the mortality rate and neurologic outcome of patients with an acute ischemic stroke. One hundred sixty-four patients were randomly allocated to receive either nimodipine tablets (30 mg q.i.d.) or identical placebo tablets for 28 days. Treatment was always started less than or equal to 48 hours after the acute event. The Mathew Scale, slightly modified by Gelmers et al, was used for neurologic assessment. Mortality rate and neurologic outcome after 28 days were used as evaluation criteria. We considered 123 patients to be valid for the analysis of efficacy. Mortality rates did not differ significantly between groups. Neurologic outcome after 28 days of therapy did not differ between groups. However, when only those patients most likely to benefit from any intervention (Mathew Scale sum score of less than or equal to 65 at baseline) were analyzed separately in post hoc-defined subgroups, the nimodipine-treated subgroups showed a significantly better neurologic outcome. This result suggests that some patients with acute ischemic stroke will benefit from treatment with nimodipine tablets.
Effect of aging on endothelium-dependent vascular relaxation of isolated human basilar artery to thrombin and bradykinin.
Authors: Hatake K , Kakishita E , Wakabayashi I , Sakiyama N , Hishida S
Published: June 2011

Using strips of human basilar arteries mounted in organ chambers to record isometric tension, we investigated vascular reactivity to thrombin and bradykinin. Both agents produced endothelium-dependent relaxation of basilar artery strips precontracted with phenylephrine but had no effect on resting tension in strips with or without endothelium. The relaxations caused by thrombin were abolished by antithrombin III/heparin, hirudin, and MD805. Thrombin but not bradykinin caused complete tachyphylaxis toward a second exposure. Indomethacin did not inhibit the relaxations induced by thrombin or bradykinin, whereas bromophenacyl bromide and methylene blue did. Aging decreased the relaxation induced by thrombin but did not affect the concentration needed to reach 50% maximal relaxation, nor did it affect the maximal relaxation in response to bradykinin, calcium ionophore A23187, and sodium nitroprusside. Our results suggest that thrombin and bradykinin produce endothelium-dependent relaxations mediated by an endothelium-derived relaxing substance and that the relaxation caused by thrombin is mediated by a proteolytic action on endothelial cells. The decrease in relaxations in response to thrombin with increasing age might be due to a decrease in the number or sensitivity of thrombin receptors on endothelial cells.
Frontal white matter lesions and dementia in lacunar infarction.
Authors: Fukuda H , Kobayashi S , Okada K , Tsunematsu T
Published: June 2011

We studied the associations of mental deterioration and blood pressure with severity and location of lesions in the cerebral white matter of 35 patients (27 men and eight women) aged 52-84 (mean 70.9) years with multiple lacunar infarcts; 21 had no dementia and 14 were demented. Using magnetic resonance imaging to evaluate lesion severity, we determined that demented patients had more severe lesions than nondemented patients; this difference was especially prominent for lesions in the frontal lobe (p less than 0.001). Score on the dementia rating scale of Hasegawa et al was negatively correlated with severity of the lesions in the frontal lobe. Blood pressure was positively correlated with the severity of white matter lesions. We show that severity of lesions in the white matter, especially in the frontal lobe, is correlated with mental deterioration of patients with multiple lacunar infarcts. Because uncontrolled hypertension is related to the severity of such lesions, careful selection of antihypertensive treatment is important in preventing both the cerebral lesions and the associated mental deterioration.
Single-photon emission computed tomography and early death in acute ischemic stroke.
Authors: Limburg M , van Royen E A , Hijdra A , de Bruïne J F , Verbeeten B W
Published: June 2011

Single-photon emission computed tomography with thallium-201-labeled diethyldithiocarbamate was performed in 26 consecutive patients less than or equal to 24 hours after a supratentorial brain infarction. Computed tomography excluded other relevant pathology. Two observers assessed the initial regional cerebral blood flow deficit using a semiquantitative visual method. The size of the initial flow deficit correlated negatively with the Barthel Index score (performance of the activities of daily living) after 6 months but not with the motricity index score (a measure of severity of the hemiparesis) after 6 months. The initial flow deficit was strongly correlated with early death from tentorial herniation; all five patients with the largest initial flow deficits died less than or equal to 6 days after the stroke, but among the 21 patients with smaller initial flow deficits only one died early (p = 0.00018, Fisher's exact two-tailed test). Although depressed level of consciousness, conjugate gaze deviation, and severe hemiparesis were more prevalent in the group of six patients who died early, the differences in prevalence between this group and the 20 patients who survived were not significant. Single-photon emission computed tomography is a relatively simple method to semiquantitatively measure a blood flow disturbance immediately after its occurrence. The magnitude of this blood flow disturbance is strongly related to early death from tentorial herniation. Because of these properties, single-photon emission computed tomography to measure regional cerebral blood flow can be of great use in acute stroke research.
A simple test to assess cerebrovascular reserve capacity using transcranial Doppler sonography and acetazolamide.
Authors: Piepgras A , Schmiedek P , Leinsinger G , Haberl R L , Kirsch C M , Einhäupl K M
Published: June 2011

The goal of this study was the development of a simple bedside test to assess cerebrovascular reserve capacity using transcranial Doppler sonography. We studied 33 normal persons at rest and after stimulation of cerebral blood flow with 1 g acetazolamide. Their mean +/- SD increase in blood flow velocity in 54 middle cerebral arteries 10 minutes after stimulation was 24.4 +/- 9.2 cm/sec. We tried to validate the increase in blood flow velocity as cerebrovascular reserve capacity in 21 patients with obstructive carotid artery disease and symptoms of cerebral ischemia. The patients were studied using transcranial Doppler sonography and xenon-133 dynamic single-photon emission computed tomography after acetazolamide stimulation. Their increases in blood flow velocity (delta FV) and increases in cerebral blood flow (delta CBF) correlated significantly in both hemispheres (asymptomatic: Y = 0.32X + 10.65, r = 0.45, p = 0.04; symptomatic: Y = 0.36X + 2.28, r = 0.59, p = 0.004). There was no significant difference between the slopes of the regression lines. Blood flow velocity and cerebral blood flow at rest were not correlated. The increase in blood flow velocity after acetazolamide stimulation offers a simple and reliable method for assessing cerebrovascular reserve capacity.
Effect of hypoxia on cerebral metabolites measured by proton nuclear magnetic resonance spectroscopy in rats.
Authors: Rosenberg G A , White J , Gasparovic C , Crisostomo E A , Griffey R H
Published: June 2011

Proton nuclear magnetic resonance spectroscopy is a unique method to monitor noninvasively the concentrations of cerebral metabolites. N-Acetyl-L-aspartate, the concentration of which is assumed to be stable during hypoxia, has been used to form ratios with lactate. To determine the stability of the signal from N-acetyl-L-aspartate, we used a model of graded hypoxia in rats to monitor the percentage changes from baseline of the peak heights for lactate, lipids, and N-acetyl-L-aspartate. Anesthetized adult rats were exposed sequentially to 15% and 10% O2 while proton nuclear magnetic resonance spectra were collected with a surface coil in a 7-T 89-mm-bore spectrometer. Brain lactate concentration was either increased by feeding or infusion of glucose (n = 9) or lowered by fasting (n = 7). After death the brains were removed and frozen, and the water- and lipid-soluble compounds were extracted to identify the origin of the signals. We analyzed the data both as the percentage change from baseline for heights of the lactate (1.33 ppm), lipids (1.5 ppm), and N-acetyl-L-aspartate (2.02 ppm) peaks and as the ratios of heights of the 1.33 and 2.02 and the 1.5 and 2.02 ppm peaks. Both hypoxic episodes caused a 45% decrease from baseline in the 2.02 ppm peak. During the second hypoxic episode, the 1.33:2.02 ppm peak height ratio increased significantly in hyperglycemic rats (p less than 0.05) but was unchanged in hypoglycemic rats.(ABSTRACT TRUNCATED AT 250 WORDS)
Epidemiological characteristics of lacunar infarcts in a population.
Authors: Sacco S E , Whisnant J P , Broderick J P , Phillips S J , O'Fallon W M
Published: June 2011

This study evaluated the characteristics and natural history of patients with lacunar (small, deep) cerebral infarcts in a defined population for comparison of these characteristics to those in patients with nonlacunar infarcts.

This is a population-based study in Rochester, Minnesota, from 1960 to 1984, that used the medical record-linkage system to identify and characterize patients with cerebral infarction.

The age- and sex-adjusted average annual incidence rate of lacunar cerebral infarction was 13.4/100,000 persons, accounting for 12% of all first cerebral infarcts. Temporal trends in incidence rates, stroke recurrence rates, prevalence of diabetes mellitus, and causes of death (given survival for 30 days) for cases of lacunar infarction were not significantly different from those for cases of nonlacunar infarction. Hypertension was found in 81% of patients who had a lacunar infarct and in 70% of patients who had a nonlacunar infarct (p = 0.05). A potential cardiac source of embolism was found in 12% of patients who had a lacunar infarct and in 28% of patients who had a nonlacunar infarct (p = 0.002). Survival was significantly better after a lacunar infarct than after a nonlacunar infarct.

Small, deep cerebral infarcts had many of the epidemiological characteristics of other cerebral infarcts but there was a slightly higher frequency of hypertension, significantly lower frequency of a cardiac embolic source, and significantly better survival in patients with lacunar infarction than in those with nonlacunar infarction.
Lacunar infarcts. Pathogenesis and validity of the clinical syndromes.
Authors: Boiten J , Lodder J
Published: June 2011

In this study, we investigated the lacunar hypothesis to answer three questions: 1) Is the lacunar syndrome valid for diagnosing lacunar infarction? 2) What is the frequency of potential cardiac versus carotid sources of embolism in patients with lacunar versus cortical infarct? 3) What is the frequency of vascular risk factors in these two groups of patients?

The study was performed in a well-defined prospective series of 103 patients with a first-ever lacunar infarct and 144 other patients with a first-ever infarct involving the cortex.

Sensitivity and specificity of the lacunar syndromes in diagnosing lacunar infarction were 95% and 93%, respectively. Positive and negative predictive values of diagnosing lacunar infarction in patients with lacunar syndromes were 90% and 97%, respectively. Risk factor analysis showed no differences for either group of cerebral infarction. A cardiac source of embolism was significantly less frequent in patients with lacunar infarction (odds ratio = 0.32, 95% confidence interval = 0.17-0.61, p less than 0.001). Significant carotid stenosis (diameter reduction greater than or equal to 50%) was also less frequent in patients with lacunar infarction (odds ratio = 0.35, 95% confidence interval = 0.16-0.76, p less than 0.001).

These findings show that the lacunar syndrome is an excellent clinical test for diagnosing lacunar infarction and that cardiac and carotid embolism are unlikely causes of lacunar infarction, supporting the hypothesis that lacunar infarcts are usually caused by small vessel disease.
Clinical-computed tomographic correlations of lacunar infarction in the Stroke Data Bank.
Authors: Chamorro A , Sacco R L , Mohr J P , Foulkes M A , Kase C S , Tatemichi T K , Wolf P A , Price T R , Hier D B
Published: June 2011

Lacunar stroke was diagnosed in 337 (26%) of the 1,273 patients with cerebral infarction among the 1,805 total in the Stroke Data Bank. We analyzed the 316 patients with classic lacunar syndromes. Among these, 181 (57%) had pure motor hemiparesis, 63 (20%) sensorimotor syndrome, 33 (10%) ataxic hemiparesis, 21 (7%) pure sensory syndrome, and 18 (6%) dysarthria-clumsy hand syndrome. No striking differences were found among the risk factors for the lacunar subtypes, but differences were found between lacunar stroke as a group and other types of infarcts. Compared to 113 patients with large-vessel atherosclerotic infarction, those with lacunar stroke had fewer previous transient ischemic attacks and strokes. Compared to 246 with cardioembolic infarction, patients with lacunar stroke more frequently had hypertension and diabetes and less frequently had cardiac disease. We found a lesion in 35% of the lacunar stroke patients' computed tomograms, with most lesions located in the internal capsule and corona radiata. The mean infarct volume was greater in patients with pure motor hemiparesis or sensorimotor syndrome than in those with the other lacunar stroke subtypes. In patients with pure motor hemiparesis and infarcts in the posterior limb of the internal capsule, there was a correlation between lesion volume and hemiparesis severity except for the few whose infarct involved the lowest portion of the internal capsule; in these patients severe deficits occurred regardless of lesion volume. Taken together, the computed tomographic correlations with the syndromes of hemiparesis showed only slight support for the classical view of a homunculus in the internal capsule.
Prognostic significance of conjugate eye deviation in stroke patients.
Authors: Tijssen C C , Schulte B P , Leyten A C
Published: June 2011

We prospectively studied the prognostic significance of conjugate eye deviation in 80 patients with acute stroke and compared the 3-month mortality and disability of these patients to those of the Tilburg epidemiological study of stroke. Mortality of patients with conjugate eye deviation was higher (41%) than for the general stroke population (34%), but this difference was not statistically significant (p less than 0.179). Looking at mortality and disability together, we found the outcome of patients with conjugate eye deviation to be significantly worse (p less than 0.001). Deviation of the eyes occurred more frequently to the right (65%) than to the left (35%). In the patient group with eye deviation to the left, mortality was significantly higher (64%, p less than 0.001) than in the group with eye deviation to the right (25%); only two patients of the former group (n = 28) could return home. Compared to the Tilburg epidemiological study of stroke, the group with eye deviation to the left did significantly worse, both for mortality alone (p less than 0.001) and for mortality and disability together (p less than 0.001). The group with eye deviation to the right did significantly worse only for mortality and disability together (p less than 0.01). Our results indicate that conjugate eye deviation is a prognostic factor for poor short-term mortality and disability in stroke patients, especially when the eyes are deviated to the left.
Quantitative proton magnetic resonance imaging in focal cerebral ischemia in rat brain.
Authors: Benveniste H , Cofer G P , Piantadosi C A , Davis J N , Johnson G A
Published: June 2011

Proton magnetic resonance (MR) imaging has been recommended as a diagnostic tool for the detection of focal cerebral ischemia. We compared microscopic MR images of rat brains after focal cerebral ischemia with evidence of histological damage found on corresponding silver-impregnated or cresyl violet-stained brain sections. Ten male Wistar rats were subjected to permanent unilateral occlusions of the right middle cerebral and common carotid arteries under halothane anesthesia. Twenty-four hours later the area of injury on MR images amounted to 26% of the total slice area, whereas only 9% of the total slice area was necrotic on histological sections from the same animals. The infarcted areas on tissue sections were surrounded by regions of selective neuronal injury in the cerebral cortex and occasionally in the hippocampus. The area of injury on MR images was larger than the combined areas of infarction and selective neuronal injury on histological sections. Areas of increased T2 values on MR images extended medially into noninfarcted striatum and laterally and dorsally into noninfarcted cortex. The lateral and dorsal areas on MR images frequently coincided with cortical areas in which considerable selective neuronal injury was present in the upper cortical layers. We hypothesize that the abnormal areas on MR images above histologically normal brain tissue represent the ischemic penumbra. If true, this is the first demonstration of the ischemic penumbra by MR imaging and may reflect our use of Wistar rats, a new image analysis technique, and ultra-high resolution MR imaging.
One-year outcome after cerebral infarction in whites, blacks, and Hispanics.
Authors: Sacco R L , Hauser W A , Mohr J P , Foulkes M A
Published: June 2011

Little is known about outcome after cerebral infarction for different ethnic groups. Of 590 stroke patients hospitalized from 1983 to 1986 at the Neurological Institute, cerebral infarction over age 39 years occurred in 135 whites, 177 blacks, and 82 Hispanics. Outcome after cerebral infarction differed by ethnicity. The 1-month mortality rate was similar in whites and blacks and least in Hispanics. Whites had a slightly greater risk of recurrent stroke or death than blacks or Hispanics until 6 months after infarction, when their risk stabilized, while the risk in blacks and Hispanics continued to rise for the entire year of follow-up. By 1 year, the rate of recurrent stroke or death was 34.8 +/- 4.2% in whites, 31.1 +/- 3.6% in blacks, and 21.4 +/- 4.8% in Hispanics (p = 0.04). Differences were found in the distribution of various stroke risk factors in the three ethnic groups. A Cox proportional hazards model demonstrated that the ethnic differences in stroke risk factors and infarct subtype were responsible for the ethnic differences in outcome. An abnormal first electrocardiogram was a risk factor for stroke recurrence or death in all three ethnic groups, while a nonlacunar infarct subtype and a history of diabetes were significant only in Hispanics. Understanding the associations of stroke determinants with ethnicity may lead to more focused secondary prevention of recurrent stroke.
Angiographic vasospasm and release of platelet thromboxane after subarachnoid hemorrhage.
Authors: Juvela S , Ohman J , Servo A , Heiskanen O , Kaste M
Published: June 2011

We studied adenosine diphosphate-induced platelet aggregation and the associated release of thromboxane B2 in 49 patients with subarachnoid hemorrhage in relation to angiographic vasospasm. Postoperative cerebral angiography was performed less than or equal to 3 (median 1) days after surgery for an aneurysm 5-14 days after subarachnoid hemorrhage. Correspondingly, one sample from each patient was taken within 24 hours either before or after angiography. The occurrence of severe as well as diffuse, moderate, or severe angiographic vasospasm was associated with the presence of delayed cerebral ischemia (p less than 0.05). Patients with diffuse angiographic vasospasm had significantly higher (p less than 0.05) values for thromboxane B2 release than the others, even after adjustment by the clinical grades on admission and before surgery, the timing of surgery, the time from subarachnoid hemorrhage to angiography and blood sampling, and nimodipine therapy. Severe and diffuse angiographic vasospasm were also associated with poor outcome at 1 year (p less than 0.05). Our results suggest that augmented release of platelet thromboxane may be involved in the pathogenesis of vasospasm in large cerebral arteries.
Identification of capric acid as a potent vasorelaxant of human basilar arteries.
Authors: White R P , Ricca G F , el-Bauomy A M , Robertson J T
Published: June 2011

To determine whether naturally occurring fatty acids, especially saturated ones, might act directly as vasodilators, segments of human basilar arteries and umbilical arteries were precontracted submaximally with prostaglandin F2 alpha and then exposed to different saturated fatty acids (C4 through C16) or unsaturated fatty acids (C14:1, C18:1, C18:2, and C18:3) at concentrations from 4 microM to 4 mM. The results showed caprate (C10) to be the most potent vasorelaxant and basilar arteries to be more responsive (EC50 = 63 microM) than umbilical arteries (EC50 = 780 microM). Caprate also inhibited contractions elicited by KCl, serotonin, and the thromboxane analogue U46619. The relaxation was independent of the endothelium, and potency was not related to the weak capacity of caprate to inhibit Ca(2+)-induced contractions of K(+)-depolarized basilar arteries. The pattern of potencies for the arteries differed, but among unsaturated fatty acids the monounsaturated (C14:1, C18:1) were more potent than the polyunsaturated (C18:2, C18:3). Comparing the potencies obtained with the concentrations reported for the free fatty acid content of arteries, brain, and plasma indicates that these lipids could influence vasomotion in health and disease.
Blood-brain barrier disruption after cardiopulmonary resuscitation in immature swine.
Authors: Schleien C L , Koehler R C , Shaffner D H , Eberle B , Traystman R J
Published: June 2011

We investigated blood-brain barrier permeability in 2-3-week-old anesthetized pigs during and after cardiopulmonary resuscitation. We assessed permeability by tissue uptake of radiolabeled aminoisobutyric acid, after correcting for plasma counts in tissue with radiolabeled inulin. Among 14 regions examined, the transfer coefficient of aminoisobutyric acid in nonischemic control animals ranged from 0.0018 +/- 0.0001 ml/g/min in diencephalon to 0.0049 +/- 0.0003 ml/g/min in cervical spinal cord. After 8 minutes of cardiac arrest followed by either 10 or 40 minutes of continuous sternal compression, there was no increase in the transfer coefficient. Likewise, during the immediate period after ventricular defibrillation, there was no increase in transfer coefficient despite the brief, transient hypertension. However, after 8 minutes of arrest, 6 minutes of cardiopulmonary resuscitation, and 4 hours of spontaneous circulation, the transfer coefficient was significantly increased by 59-107% in 10 of 11 regions rostral to the pons. Plasma volume in tissue measured by inulin was not elevated, suggesting that the increased transfer coefficient was not due to increased surface area. Thus, after an 8-minute period of complete ischemia, the blood-brain barrier remains intact during and immediately after resuscitation despite large vascular pressure fluctuations. However, in contrast to previous work on adult dogs, immature pigs are prone to a delayed increase in permeability, thereby allowing circulating substances greater access to the brain.
Effects of insulin on blood, plasma, and brain glucose in hyperglycemic diabetic rats.
Authors: Hofer R E , Lanier W L
Published: June 2011

This study, in biologically bred hyperglycemic diabetic rats, examined the effect of a intravenous insulin infusion (1.5 units.hr-1) on blood, plasma, and brain glucose concentrations to determine their relationship during decreasing blood and plasma glucose levels. The data were compared to saline-treated diabetic rats and saline-treated nondiabetic littermates. The volume and duration of the treatment infusion were similar in all groups. Insulin infusion in diabetic rats produced the expected reduction in blood and plasma glucose, and normoglycemia was produced within 78 +/- 37 minutes (mean +/- SD). However, once normoglycemia was achieved, brain glucose was still significantly greater by 44% than in nondiabetic rats (p = 0.015). Moreover, the ratio of brain to plasma glucose was more than 50% greater in diabetic than nondiabetic rats, irrespective of whether or not they received insulin (p less than 0.01). We conclude that measurement of blood or plasma glucose in diabetic subjects will tend to underestimate the amount of glucose in the brain and that this relationship is not influenced by acute insulin therapy.
Thalamic atrophy following cerebral infarction in the territory of the middle cerebral artery.
Authors: Tamura A , Tahira Y , Nagashima H , Kirino T , Gotoh O , Hojo S , Sano K
Published: June 2011

We investigated shrinkage of the ipsilateral thalamus following infarction in the territory of the middle cerebral artery in 33 patients who were admitted less than or equal to 2 days after the stroke and who were followed by computed tomography for greater than 1 year with no recurrences. The thalamic area was measured on the computed tomograms, and the ratio of the ipsilateral area to the contralateral area was calculated. All values were compared with values from the initial computed tomogram taken less than or equal to 2 days after the stroke. The values of the ratio on follow-up computed tomograms decreased gradually in 15 patients. In these cases, the area of the ipsilateral thalamus was significantly reduced after 1 year (p less than 0.01) and marked atrophy was observed. These results demonstrate the significance of remote changes over a long period of time after focal cerebral infarction.
Age-related differences in recovery of blood flow and metabolism after cerebral ischemia in swine.
Authors: Ichord R N , Kirsch J R , Helfaer M A , Haun S , Traystman R J
Published: June 2011

We tested two hypotheses: 1) that cerebral blood flow, oxygen consumption, and evoked potentials recover to preischemic values at 120 minutes of reperfusion more completely in 1-2-week-old piglets than in 6-10-month-old pigs after complete ischemia; and 2) that recovery of cerebral blood flow, oxygen consumption, and electrical function in piglets and pigs at 120 minutes of reperfusion is better after incomplete than after complete ischemia. During 30 minutes of ischemia produced by intracranial pressure elevation, cerebral blood flow determined by the microspheres technique was decreased to 0-1 ml/min/100 g with complete ischemia, to 1-10 ml/min/100 g with severe incomplete ischemia, or to 10-20 ml/min/100 g with moderate incomplete ischemia. During reperfusion after complete ischemia, both piglets and pigs demonstrated hyperemia but delayed hypoperfusion occurred in more brain regions in pigs, oxygen consumption returned to preischemic values in piglets but not in pigs (70 +/- 10% of preischemic values), and evoked potentials recovered better in piglets than in pigs (24 +/- 4% and 9 +/- 4% of preischemic values, respectively). Both piglets and pigs had fewer brain areas with hyperemia and hypoperfusion and improved oxygen consumption and electrical function during recovery from incomplete than from complete ischemia. We speculate that piglets tolerate complete ischemia better than pigs because of decreased reperfusion injury and that both groups recover better from incomplete than complete ischemia because of improved substrate supply during ischemia.
Effect of elevated plasma norepinephrine on electrocardiographic changes in subarachnoid hemorrhage.
Authors: Grad A , Kiauta T , Osredkar J
Published: June 2011

We compared electrocardiographic abnormalities and plasma norepinephrine concentrations in 40 patients with subarachnoid hemorrhage within the first 24 hours, at 72 hours, and after 1 week. In 20 patients with high plasma norepinephrine concentrations within the first 24 hours, sinus tachycardia (p less than 0.02) and negative T waves (p less than 0.01) were more frequent than in the 20 patients with normal plasma norepinephrine concentrations. After 72 hours, only sinus tachycardia (p less than 0.03) was found with increased frequency in the 26 patients with high plasma norepinephrine concentrations. Although 24 patients had high plasma norepinephrine concentrations after 1 week, we found no differences in the frequency of electrocardiographic abnormalities compared to patients with normal plasma norepinephrine. However, QTc prolongation, U waves, ST depression, and arrhythmias were found with similar frequency in patients with both high and normal plasma norepinephrine concentrations. We conclude that, with the exception of sinus tachycardia and negative T waves, electrocardiographic changes in patients with subarachnoid hemorrhage do not depend on elevated plasma norepinephrine concentrations.
Effect of U74006F on forebrain ischemia in rats.
Authors: Lesiuk H , Sutherland G , Peeling J , Butler K , Saunders J
Published: June 2011

We examined the effect of a putative lipid peroxidation inhibitor, the 21-aminosteroid U74006F, on transient forebrain ischemia in rats. Acute-treatment rats received either 3 mg/kg U74006F (n = 7) or carrier vehicle (n = 5) intravenously 30 minutes before ischemia, sustained-treatment rats received the same treatment before ischemia followed by 3 mg/kg U74006F (n = 6) or carrier vehicle (n = 5) intraperitoneally every 6 hours for 48 hours, and control rats (n = 7) received no injection. Coronal magnetic resonance images were obtained daily for 3 days, followed by the histological examination of perfusion-fixed brains. Control rats demonstrated magnetic resonance image changes indicative of neuronal damage in the striatum at 24 hours postischemia, followed by changes in the hippocampus and neocortex at 48 hours. No significant effect of U74006F treatment on striatal or hippocampal injury was demonstrated. However, both the acute and sustained U74006F treatments produced a significant reduction in the severity of neuronal damage in the neocortex (p less than 0.05). Our results suggest that U74006F is of benefit in ameliorating ischemic neuronal injury, particularly in the neocortex, and raise the possibility of regional variability in lipid peroxidation following an ischemic insult.
Interaction between free radicals and excitatory amino acids in the formation of ischemic brain edema in rats.
Authors: Oh S M , Betz A L
Published: June 2011

Both oxygen free radicals and excitatory amino acids have been implicated as important cellular toxins in ischemic brain. Recent in vitro studies suggest that there may be a mutual interaction between these two mediators. We explored the relation between oxygen free radicals and excitatory amino acids in the development of ischemic brain edema in vivo. Male Sprague-Dawley rats were treated with the free radical scavenger dimethylthiourea 1 hour before ischemia or with the excitotoxin antagonist MK-801 30 minutes before ischemia produced by occlusion of the middle cerebral artery. Groups of seven or eight animals were treated with vehicle, low-dose (375 mg/kg) dimethylthiourea, high-dose (750 mg/kg) dimethylthiourea, low-dose (0.5 mg/kg) MK-801, high-dose (2.0 mg/kg) MK-801, or both high-dose dimethylthiourea and low-dose MK-801. After 4 hours of ischemia, brain water content was determined. In eight vehicle-treated controls, mean +/- SEM water content of tissue in the center of the ischemic zone was 83.29 +/- 0.18%. A significant reduction of brain edema was observed in all drug-treated groups: for example, 50.2% (p less than 0.001) in the high-dose dimethylthiourea group, 53.7% (p less than 0.001) in the low-dose MK-801 group, and 66.4% (p less than 0.001) in the combined dimethylthiourea and MK-801 group. Combined treatment with dimethylthiourea and MK-801 provided no significant additive effect over that resulting from treatment with MK-801 alone.(ABSTRACT TRUNCATED AT 250 WORDS)
Snoring and the risk of ischemic brain infarction.
Authors: Palomäki H
Published: June 2011

To determine if a history of snoring is a risk factor for brain infarction, I conducted a case-control study of risk factors for ischemic stroke using 177 consecutive male patients aged 16-60 (mean 49) years with acute brain infarction. For each patient I chose an age-matched (+/- 6 years) male control. Arterial hypertension, coronary heart disease, snoring (habitually or often), and heavy drinking (greater than 300 g/wk) were risk factors in the stepwise multiple logistic regression analysis. The odds ratio of snoring for brain infarction was 2.13. By McNemar's test this association increased strongly if a history of sleep apnea, excessive daytime sleepiness, and obesity were all present with snoring (odds ratio 8.00). My study indicates that snoring may be a risk factor for ischemic stroke, possibly because of the higher prevalence of an obstructive sleep apnea syndrome among snorers than nonsnorers.
Temporal thresholds for neocortical infarction in rats subjected to reversible focal cerebral ischemia.
Authors: Kaplan B , Brint S , Tanabe J , Jacewicz M , Wang X J , Pulsinelli W
Published: June 2011

We investigated the temporal threshold for focal cerebral infarction in the spontaneously hypertensive rat. The right middle cerebral artery and common carotid artery were occluded for 0, 1, 2, 3, 4, or 24 hours, and all the animals were sacrificed 24 hours after the onset of ischemia. Cortical infarct volumes and edema volumes were quantified in serial frozen sections of hematoxylin and eosin-stained tissue using image analysis. Upon occlusion, blood flow in the core of the ischemic zone, measured with laser-Doppler flowmetry, fell to a mean +/- standard deviation of 21 +/- 7% of the preocclusion baseline value (n = 26). During the first hour of ischemia, blood flow in the densely ischemic zone rose to 27 +/- 8% of baseline (n = 25). Release of the middle cerebral artery and common carotid artery occlusions rapidly restored cortical blood flow to 213 +/- 83% of baseline (n = 21). Focal ischemia of 1 hour's duration caused little or no infarction, while ischemic intervals of 2 and 3 hours produced successively larger volumes of infarcted cortex. Ischemic intervals of 3-4 hours' duration followed by approximately 20 hours of recirculation yielded infarct volumes that were not significantly different from those after 24 hours of permanent focal ischemia. The results indicate that 3-4 hours of focal cerebral ischemia in this rat model is sufficient to attain maximal infarction and suggest that recirculation or pharmacological interventions after this time will provide little benefit.