bluuebunny/crossref_metadata_2025 huggingface dataset:
The effect of intravenous lidoflazine on serotonin-induced cerebral vascular contraction--an in vivo study.
Authors: Rosenwasser R H , Tuma R F , Buchheit W A
Published: June 2011

Lidoflazine, a piperazine derivative with known selectivity for vascular smooth muscle, was evaluated as a possible agent for prophylaxis of cerebral vascular contraction induced by subarachnoid perfusion with serotonin. The animals treated with serotonin (5 X 10(-6) M), had a 60% reduction in the diameter of basilar artery but when pretreated with Lidoflazine (1 mg/kg) intravenously, only had a 20% reduction in diameter (p less than 0.01). Lidoflazine, when administered intravenously at a slow rate will not adversely lower systemic blood pressure and can prevent the contraction of cerebral vessels when the stimulus for contraction is in the subarachnoid space.
Locked-in syndrome: a review of 139 cases.
Authors: Patterson J R , Grabois M
Published: June 2011

Etiology, clinical manifestations and outcome were reviewed in 139 cases of "locked-in syndrome." Six cases were reported from our center and the remaining 133 cases were taken from a review of the literature. The results of this review emphasized the necessity for a comprehensive program of pulmonary management in this population. Furthermore, an effective system of communication for the patient is considered essential in the management of the "locked-in" state. Reported mortality in the cases reviewed was 60%. Overall, the prognosis for survival and recovery was found to be better in the group of patients whose syndrome was nonvascular in origin than those with a vascular etiology. Functional recovery was generally good in those patients with a vascular etiology who survived beyond 4 months while recovery occurred earlier and more completely in the nonvascular group. Thus, a program of intensive rehabilitation should be considered early in both groups in order to assist each patient in attaining the highest level of function possible as recovery progresses.
Forebrain ischemia in the rat. Relation between duration of ischemia, use of adjunctive ganglionic blockade and long-term recovery.
Authors: Grøgaard B , Gerdin B , Arfors K E
Published: June 2011

The relation between duration of ischemia, use of adjunctive ganglionic blockade and long-term recovery was studied in a rat model giving reversible subtotal forebrain ischemia. Ischemia was induced by bilateral carotid artery clamping and controlled hemorrhage to a mean arterial pressure of 50 mm Hg in animals artificially ventilated under 70% N2O. After variable lengths of time, the clamps were removed and the drawn blood was reinfused. In some animals, the ganglion blocker Arfonad was given (group A+) on induction of ischemia to facilitate hypotension. There was a strict dose-response relationship between duration of ischemia and mortality. Mortality was higher among animals not given Arfonad (group A-; 37% after 10 min of ischemia and 100% after 13 min) than in group A+ (about 20% after 12-13 min of ischemia, 50% after 15 min and 80% after 19 min). In group A+ more than half of the animals died later than 24 h after ischemia. All of them were hyperexcitable and 12% died during witnessed epileptic fits. Group A- animals regularly died within the first 24 h, with no indication of central nervous system involvement. Less blood had to be drawn to attain hypotension (mean arterial pressure 50 mm Hg) in group A+ (1.5 +/- 0.3 ml/100 g b.w.) than in group A- (2.5 +/- 0.2 ml/100 g b.w.). Group A+ also had less "washout" acidosis 5 min after reinfusion of the shed blood than group A- (15 min of ischemia: pH 7.24 +/- 0.07 v 6.96 +/- 0.06).(ABSTRACT TRUNCATED AT 250 WORDS)
Stroke, migraine and intracranial aneurysm: a case report.
Authors: Mas J L , Baron J C , Bousser M G , Chiras J
Published: June 2011

A man had since childhood recurrent attacks typical of ophthalmic migraine. After an otherwise unremarkable attack, he was left with a permanent quadrantanopsia due to a right occipital infarct. The remarkable pattern of progression, which characterized the visual phenomenon of subsequent attacks, favours a primary neuronal phenomenon. The first angiography revealed an occlusion of the posterior cerebral artery (PCA) but the second one, performed two years later, disclosed a PCA aneurysm. Such a finding emphasizes the need of thorough and repeated evaluations of patients with so-called "migrainous infarcts."
Progressive lacunar infarction with demonstrated patency of the middle cerebral artery.
Authors: Halsey J H
Published: June 2011

Two cases of progressive hemiplegia were closely followed by daily clinical examination. In both, the CT scan and CSF were normal on admission. In both, objective aggravation occurred in three or more steps over four days, progressing from minor finger clumsiness to total paralysis of the arm. In both cases a second CT scan a day after appearance of hemiplegia demonstrated a lacune in the corona radiata just above the internal capsule. In one case an intravenous digital subtraction angiogram demonstrated patency of the middle cerebral artery during the course of the progression. In the other case, serial study with transcranial Doppler ultrasound documented the continued patency of the middle cerebral artery. These two cases demonstrate that it is not necessary to postulate transient occlusion of the middle cerebral artery as an essential mechanism for progressive lacunar infarction.
Blood pressure course in patients with acute stroke and matched controls.
Authors: Britton M , Carlsson A , de Faire U
Published: June 2011

The natural course of blood pressure (BP) was studied after emergency hospitalization in 209 consecutive stroke patients and as many age and sex matched controls. Histories of hypertension were more common among patients than controls (46% vs 26%). On admission 69% of the stroke group and 36% of the controls had BP greater than or equal to 170/100 mm Hg. In the first four days there was a spontaneous BP decline, which was greater the higher the initial values. During the whole hospitalization though, stroke patients with previous hypertension had the highest BP levels and previously normotensive controls the lowest. Even if WHO as well as the Joint Committee for Stroke have recommended cautious antihypertensive therapy in stroke patients with extreme hypertension, such therapy is not evaluated. If this is to be done, the present findings have to be taken into consideration. Stroke controls, matched according to the initial BP level, will thus be required.
Prevention of early restenosis and thrombosis-occlusion after carotid endarterectomy by saphenous vein patch angioplasty.
Authors: Archie J P
Published: June 2011

The hypothesis that saphenous vein patch angioplasty protects against early postoperative restenosis and thrombosis-occlusion was tested by comparing the clinical outcome and carotid artery status of 100 carotid endarterectomies with and 100 without saphenous vein patch angioplasty performed by a single surgeon over a 30-month period. The patient population, selection, perioperative management, and the technical aspects of the operation, except for the vein patch, were essentially identical in both groups. Carotid artery status was assessed by direct continuous wave Doppler and Gee OPG at three to six months and again at one year postoperatively. There were two hospital deaths, both in the nonpatched group, one cardiac and the other neurologic due to internal carotid thrombosis. Two reversible neurological deficits due to thrombosis and one due to restenosis occurred in the non-patched group. Asymptomatic greater than 50% diameter restenosis occurred in four and asymptomatic occlusion in one non-patched carotids. There were no restenosis, no occlusions and no neurologic symptoms in the patched group. Morbidity, mortality, restenosis or thrombosis-occlusion occurred in 10/100 (10%) non-patched and 0/100 (0%) patched arteries (p less than 0.01 by Chi Square). Restenosis or thrombosis-occlusion occurred in 9/100 (9%) of non-patched and 0/100 (0%) patched arteries (p less than 0.01). These results support the use of saphenous vein patch angioplasty reconstruction of carotid endarterectomy to protect against early restenosis and thrombosis-occlusion.
Basilar and distal vertebral artery stenosis: long-term follow-up.
Authors: Moufarrij N A , Little J R , Furlan A J , Leatherman J R , Williams G W
Published: June 2011

Forty-four patients with greater than or equal to 50% stenosis of a distal vertebral artery (VA) and/or basilar artery (BA) were followed up for an average of 6.1 years. Angiography was performed for definite vertebrobasilar (VB) transient ischemic attacks (TIA) in 19 (43%), for VB infarcts in 13 (30%) and for non localizing symptoms in 12 (27%). Stenosis in the BA with or without VA involvement was present in 28 patients (64%), while 16 patients (36%) had occlusive disease in one or both distal VA sparing the BA. In follow up, 7 patients (16%) had definite VB TIA and 3 patients had possible VB TIA. Eight patients (18%) sustained a stroke, 5 of which were in the VB territory. The observed stroke rate was 17 times the expected rate for a matched normal population. Eight patients died during follow up, three patients due to stroke (2 brainstem infarctions, one intraventricular hemorrhage). The observed 5 year survival rate was 78% compared to 90% in a matched normal population. In comparing this data with our previous study of 93 patients with proximal VA occlusive disease, distal VB occlusive disease appears to carry a higher risk for brainstem ischemia.
An evaluation of the effect of lidocaine in experimental focal cerebral ischemia.
Authors: Shokunbi M T , Gelb A W , Peerless S J , Mervart M , Floyd P
Published: June 2011

In order to determine the effect of lidocaine in focal cerebral ischemia, the left middle cerebral artery was transorbitally occluded in twenty cats. Eleven received lidocaine hydrochloride intravenously. The infusion was begun half an hour prior to clip occlusion and the rate was adjusted to maintain an isoelectric EEG. Nine cats served as controls, receiving an equivalent volume of 5% dextrose 0.2% saline. Thirteen animals (7 lidocaine-treated and 6 control) were sacrificed after six hours of left middle cerebral artery occlusion without reperfusion. In the remaining seven cats, the vessel was occluded for four hours prior to sacrifice. Ischemic neuronal alteration was assessed by both histochemical (2'3'5' triphenyl-2H-tetrazolium hydrochloride reaction) and histological examination. With both durations of ischemia, there was no significant difference in the extent and severity of neuronal alterations between the lidocaine-treated and control groups of animals.
Monitoring CBF in clinical routine by dynamic single photon emission tomography (SPECT) of inhaled xenon-133.
Authors: Sugiyama H , Christensen J , Skyhøj Olsen T , Lassen N A
Published: June 2011

A very simple and low-cost brain dedicated, rapidly rotating Single Photon Emission Tomograph SPECT is described. Its use in following patients with ischemic stroke is illustrated by two middle cerebral artery occlusion cases, one with persistent occlusion and low CBF in MCA territory, and one with early lysis of the occlusion having high CBF (massive luxury perfusion) for some weeks. Evidence of this kind may be essential in the evaluation of therapeutic measures in ischemic stroke.
Correlation between somatosensory evoked potentials and neuronal ischemic changes following middle cerebral artery occlusion.
Authors: Steinberg G K , Gelb A W , Lam A M , Manninen P H , Peerless S J , Rassi Neto A , Floyd P
Published: June 2011

In an attempt to determine the usefulness of evoked potentials as a measure of focal cerebral ischemia, we examined somatosensory evoked potentials (SEP's) and morphological neuronal changes in cats following unilateral middle cerebral artery (MCA) occlusion. Fifteen adult cats underwent transorbital occlusion of the MCA under halothane anesthesia. In seven cats the ipsilateral SEP's were abolished after middle cerebral artery occlusion, and did not show any recovery after 6 hours. The same seven cats showed the greatest area of moderate and severe ischemic neuronal changes, ranging from 21 to 64% (mean 39 +/- 14%) of the total ipsilateral cortical area. The remaining eight cats showed a complete flattening or decreased amplitude of the SEP after occlusion, but demonstrated a considerable recovery in the amplitude of the primary cortical potential during the six hours of the study. All these cats had ischemic areas of less than 15% (mean 9 +/- 3%) of the total ipsilateral cortex. These results demonstrate that the disappearance of the SEP and their failure to recover correlate with the extent and degree of histological cerebral ischemia.
Increased cerebral blood flow during hypercapnia is not affected by lesion of the nucleus locus ceruleus.
Authors: Harik S I , Prado R , Busto R , Ginsberg M D
Published: June 2011

To test the hypothesis that the putative noradrenergic innervation of intraparenchymal cerebral blood vessels from the nucleus locus ceruleus mediates the vasodilatory response to hypercapnia, regional cerebral blood flow was measured by iodo-[14C]antipyrine autoradiography in awake and restrained rats with unilateral 6-hydroxydopamine lesion of the nucleus locus ceruleus and in unlesioned control rats. Hypercapnia, induced by the inhalation of 5% or 8% CO2 in air for 8 minutes caused a 2 to 5-fold increase in regional cerebral blood flow. However, despite a marked reduction of about 90% in cortical norepinephrine levels ipsilateral to the lesion, blood flow to the frontal and parietal cortex, hippocampus, striatum and cerebellum increased to the same extent in ipsilateral and contralateral regions. Thus, lesion of the locus ceruleus and the resultant depletion of endogenous cortical and hippocampal norepinephrine, does not influence the cerebrovascular response to hypercapnia.
Comparison of the somatosensory evoked potential and the direct cortical response following severe incomplete global ischemia: selective vulnerability of the white matter conduction pathways.
Authors: Lesnick J E , Coyer P E , Michele J J , Welsh F A , Simeone F A
Published: June 2011

Eight cats were subjected to graded hemorrhagic hypotension following bilateral carotid ligation to produce incomplete global cerebral ischemia. Three additional cats served as controls. The somatosensory evoked potential (SEP) and direct cortical response (DCR) were monitored in all animals and in each case, the cortical component of the SEP was abolished during progressive ischemia while the morphology of the DCR was well-preserved but with reduced amplitude. Determinations of adenosine triphosphate (ATP), phosphocreatine (PCr), and lactate levels in cerebral cortex and white matter were made in five experimental cats and the three controls. At the time of failure of the cortical SEP, PCr was dramatically reduced and lactate moderately elevated in the white matter while ATP remained unchanged. Cortical lactate was only mildly elevated and PCr and ATP were unchanged accounting for preservation of the DCR. In this model of global ischemia, abolition of the cortical SEP is due to a block of stimulus conduction in white matter projection pathways. A hypothesis to explain the observed metabolic changes is presented and correlation is made to clinical situations.
Appearance and disappearance of empty delta sign in superior sagittal sinus thrombosis.
Authors: Shinohara Y , Yoshitoshi M , Yoshii F
Published: June 2011

The diagnostic value of the empty delta sign on post-infusion CT films was investigated in five patients with superior sagittal sinus thrombosis subsequently verified angiographically and/or pathologically. The empty delta sign, which has been considered to be unique and reliable in the diagnosis of cerebral venous sinus occlusion, was observed only on CT films taken one to four weeks after onset, and was not seen in the extremes of the acute or the chronic stage of the illness. These observations may explain why this sign has not been apparent in some reports concerning the CT findings of superior sagittal sinus thrombosis. Recanalization within the thrombus may be the reason why this sign was no longer apparent in the chronic stage of the patients with superior sagittal sinus thrombosis.
Behavioral performance of rats following neonatal hypoxia-ischemia.
Authors: Young R S , Kolonich J , Woods C L , Yagel S K
Published: June 2011

The behavioral performance of rats subjected in the neonatal period to hypoxia-ischemia at either 37 degrees C or 21 degrees C was compared to that of sham-ligated animals. Performance on complex motor tests was significantly delayed only in the hypoxic-ischemic 37 degrees C rats. However, cognitive testing disclosed significant delay of spatial learning in animals subjected to hypoxia-ischemia at 21 degrees C and those with gross infarction at 37 degrees C. There was enhanced avoidance learning in the animals with gross infarction in the hypoxia-ischemia 37 degrees C group. Hypoxic-ischemic damage in the neonatal rat at 37 degrees C results in transient delay of complex motor skills, but longer lasting cognitive changes. Hypoxia-ischemia during hypothermia produces no motor deficits, although there may be similar alterations in learning.
Rational therapy in the neurosciences: the role of the randomized trial.
Authors: Sackett D L
Published: June 2011

How should clinicians select the specific drug, operation, splint, exercise, or conversations that will best achieve the therapeutic goal for a given patient? This essay will examine three strategies for doing so: induction from our own, individual prior experiences; abdication to the authority of our teachers and those who write review articles; and deduction from the reports of randomized clinical trials. By means of examples from the recent past, the fallibility of the first two approaches will be illustrated. Then, strategies for critically appraising the published reports of randomized trials will be described. Finally, the reasons why the results of even the proper trials may not be accepted by frontline clinicians will be introduced.
A proposed method for using a reimbursement moratorium to encourage recruitment for a randomized study of carotid endarterectomy.
Authors: Jonas S
Published: June 2011

As indicated by Barnett, Plum and Walton, a definitive clinical trial to resolve the issue of the effectiveness of carotid endarterectomy is clearly needed. A proposal to foster such a trial, through a moratorium on third-party reimbursement other than for randomized patients, has herein been presented.
Postischemic production of eicosanoids in gerbil brain.
Authors: Kempski O , Shohami E , von Lubitz D , Hallenbeck J M , Feuerstein G
Published: June 2011

The postischemic production of PGE2, PGD2, 6-keto-PGF1 alpha, and TXB2 in brain tissue was studied in Mongolian gerbils using tissue extraction as well as a new ex vivo method. This new method permits the study of prostaglandin synthesis in slices from discrete areas of the brain (cortex, hippocampus, striatum, hypothalamus). Gerbils were sacrificed at 0, 5, and 30 minutes, and 4 and 24 hours after a 15-minute occlusion of both carotid arteries. Apart from 6-keto-PGF1 alpha, tissue prostaglandins determined by the extraction method were significantly increased 3 and 30 minutes after reperfusion. The most pronounced changes found by the ex vivo method were increased productions of PGD2 immediately after reperfusion (285% in cortex, 215% in hypothalamus) and PGE2 (350% in hippocampus, 320% in striatum) 4 hours after reperfusion. At 24 hours after reperfusion PGE2 and PGD2 synthesis were significantly decreased by 23-70% of the values obtained from sham-operated controls. Thromboxane increased slightly in all areas after recirculation and subsequently decreased to values below the control level in striatum. The results obtained by ex vivo incubation of tissue slices demonstrate that ischemia and subsequent recirculation cause site-, time-, and PG-specific changes of tissue eicosanoid production.
The effect of ergotamine and dihydroergotamine on cerebral blood flow in man.
Authors: Andersen A R , Tfelt-Hansen P , Lassen N A
Published: June 2011

The effects of ergotamine and dihydroergotamine on cerebral blood flow was investigated 4 hours after i.v. injection as these drugs might be of importance for migraine treatment. Eight normal male volunteers (not suffering from migraine) received 0.5 mg ergotamine and 1 mg dihydroergotamine i.v. Cerebral blood flow was measured by the xenon-133 inhalation method and single-photon-emission computerized tomography before and after intravenous acetazolamide administration (1 g). Cerebral blood flow was measured before and 4 hours after ergotamine and dihydroergotamine administration. Strain-gauge measurements of toe-arm systolic gradients were used to monitor the effect of the drug on leg arteries. Mean hemispheric and regional cerebral blood flow was unchanged after either drug (mean +/- SEM, ml/100 g/min): for ergotamine, 57 +/- 3 before and 57 +/- 3 at 4 hours; for dihydroergotamine, 54 +/- 2 before and 55 +/- 2 at 4 hours. The acetazolamide response was unchanged as well. Only ergotamine decreased the toe-arm systolic gradient significantly (22 mm Hg at maximum after 240 minutes; p less than 0.02). Thus, our study did not support the belief that ergot alkaloids should be withheld from patients during attacks of classic migraine, but this has to be investigated further. The discrepancy in the peripheral effects of ergotamine and dihydroergotamine might also be of clinical importance.
Beta-adrenergic blockade after stroke. A preliminary closed cohort study.
Authors: Kinnander G , Viitanen M , Asplund K
Published: June 2011

To collect background data for a prospective clinical trial of beta-blocking agents in the prevention of deaths after stroke, the long-term prognosis in 60 patients discharged from a stroke unit on beta-blocker therapy was compared with the outcome in 60 matched patients with stroke but without beta-blockers. Matching included sex, age, type of stroke, and presence or absence of hypertension and cardiac failure. Thirteen patients (22%) in the beta-blocker group died during a median followup of 41 months. Of the 60 patients not on beta-blockade at discharge, 21 (35%) died during a median followup of 36 months. By life-table technique and log-rank test, the relative risk for death was 0.60:1.00 (p = 0.14). During followup, 12 recurrent strokes were observed in patients on beta-blockers and 19 in patients without beta-blockers (relative risk 0.57:1.00; p = 0.12). It appeared that the reduction in mortality could only marginally be ascribed to fewer deaths from myocardial infarction; other causes of death were also less frequent in beta-blocker-treated patients. The results emphasize that supplementary information on the effect of beta-blocking agents on mortality after stroke is needed before a larger trial of beta-blocker therapy in patients with manifest cerebrovascular disease can be initiated.
Cerebrovascular ischemia associated with lupus anticoagulant.
Authors: Levine S R , Welch K M
Published: June 2011

The lupus anticoagulant, an acquired circulating serum gamma-globulin, prolongs all phospholipid-dependent coagulation tests. Recent associations of the lupus anticoagulant and focal cerebral and/or ocular ischemia have been made. We present 5 cases of lupus anticoagulant-associated cerebrovascular ischemia and review all reported cases for the first time. Clinical spectra, cerebral angiographic findings, associated conditions, and response to therapy are presented. Typical features include a relatively young age (mean 39 years), female preponderance, transient ischemic attacks (including amaurosis fugax) or stroke, and normal or large vessel occlusions on angiography. Commonly associated conditions were systemic lupus erythematosus (34%), noncerebral venous thrombosis (31%), hypertension (28%), false-positive VDRL (28%), and spontaneous abortions (22%). Four of our 5 patients (all without systemic lupus erythematosus) and 11 of the 20 (55%) patients in the literature without systemic lupus erythematosus had other definite stroke risk factors coexisting. Response to therapy was highly variable, with no clear beneficial effect of corticosteroids.
Alcohol and stroke.
Authors: Gorelick P B
Published: June 2011

Alcohol might contribute to stroke in several ways: induction of cardiac arrhythmias and cardiac wall motion abnormalities which predispose to cerebral embolism, induction of hypertension, enhancement of platelet aggregation and activation of the clotting cascade, and reduction of cerebral blood flow by stimulation of cerebral vascular smooth muscle contraction or by altering cerebral metabolism. While these pathophysiological mechanisms have gained enthusiastic experimental and theoretical support, the findings are preliminary and will require further large-scale clinical and epidemiological analyses to substantiate their roles as causal factors or potentiators of stroke. Documentation of measurable platelet and coagulation cascade abnormalities reported in healthy volunteers who have ingested alcohol will need to be confirmed on a broader scale in stroke patients with recent ethanol consumption. The risk of stroke in those with alcohol-induced atrial fibrillation and cardiomyopathy must be ascertained for the general population. While the experimental evidence is exciting and provocative, epidemiological evidence also suggests a link between alcohol consumption and stroke. Regular alcohol ingestion is associated with hypertension, fatal and nonfatal intracranial hemorrhage, cerebral infarction, and increased risk of death from stroke. Recent, less stringently controlled studies suggest that alcohol consumption is a risk factor for cerebral infarction in young adults with occasional ethanol intoxication and middle-aged women and young men with occasional alcohol intoxication and regular heavy drinking. Alcohol may also be a risk factor for subarachnoid hemorrhage.
Stroke in the Lehigh Valley: seasonal variation in incidence rates.
Authors: Sobel E , Zhang Z X , Alter M , Lai S M , Davanipour Z , Friday G , McCoy R , Isack T , Levitt L
Published: June 2011

We investigated the seasonal pattern of stroke using the Lehigh Valley Stroke Register. This register includes all patients hospitalized with stroke or transient ischemic attack (TIA) from among the 600,000 Lehigh Valley residents. Meterological data were obtained from the National Oceanic and Atmospheric Administration. The study, which uses 18 months of data, included 1,944 cases. Using single harmonic regression analysis, the seasonal pattern of TIA and infarction, but not hemorrhage, fit a sine-cosine wavefunction with a 12-month period (R2 = 41% and 36%, respectively). For infarction, the strongest seasonal pattern was exhibited for women of all ages and for both sexes in the age groups 65-74 and 75-84, but only the sine component was significant. The peak months for TIA were June-August, while the peak months for infarcts were February-April. Correlations between ambient temperature and each type of stroke were computed. A significant positive correlation for TIA was found (r = 0.57, p = 0.01). After adjusting for a 2-month lag between the low for infarction and the peak for temperature, a significant negative correlation was found (r = -0.64, p = 0.01). No significant correlation was found for hemorrhage. Possible reasons for the opposite relations of TIA and infarct are discussed.
Studies on cerebral blood flow and oxygen metabolism in patients with established cerebral infarcts undergoing omental transposition.
Authors: Herold S , Frackowiak R S , Neil-Dwyer G
Published: June 2011

Regional cerebral blood flow, blood volume, fractional oxygen extraction, and oxygen consumption were measured by positron emission tomography in 4 stroke patients prior to and 6 months following omental transposition surgery. Preoperatively, 3 patients showed the typical picture of established infarction with a matched reduction in flow and oxygen metabolism and a normal oxygen extraction fraction in the symptomatic hemisphere. One patient showed a chronically impaired perfusion reserve with a proportionally greater reduction in flow than oxygen metabolism and a compensatory rise in oxygen extraction ratio. No change in the physiological parameters was demonstrated in the postoperative studies.
Identification of intracardiac thrombi in stroke patients with indium-111 platelet scintigraphy.
Authors: Kessler C , Henningsen H , Reuther R , Kimmig B , Rösch M
Published: June 2011

Platelet scintigraphy (PSC) with indium-111 labelled platelets has been confirmed as an adequate method for the detection of intracardiac thrombi in patients with heart disease. We performed PSC of the heart and the neck vessels in 27 stroke patients with suspected cardiac embolism and as control on 10 patients with atherosclerotic lesions of the carotid arteries without evidence of heart disease. The carotid PSC was positive in 6 of 10 patients with carotid disease, and twice in the 27 with suspected cardiac embolism. In these 27 the PSC of the heart indicated pathological conditions 13 times. Pathological platelet accumulations could be visualized in 3 cases in the atrial space, in 9 cases in the region of the left ventricle, and once at the aortic valve. Scintigraphy was negative in all 10 patients with atherosclerosis of the neck vessels. The two-dimensional echocardiography revealed pathological findings in 8 of the 13 patients with positive heart PSC (3 with intraventricular thrombi, 3 with valvular disease, 2 with decreased ventricular contractility) and was normal in the 10 control patients. Open-heart surgery was performed in 2 patients with pathological PSC and revealed an intracardiac thrombus. Three of 4 patients with positive atrial PSC showed mitral or aortic valve disease. These results suggest that PSC can provide a valuable method for detecting cardiac thrombi in stroke patients.
Evaluation of brain dysfunction in hypertensive putaminal hemorrhage with multimodality evoked potentials.
Authors: Shigemori M , Yuge T , Kawasaki K , Tokutomi T , Kawaba T , Nakashima H , Watanabe M , Kuramoto S
Published: June 2011

Changes in multimodality evoked potentials (MEP's), consisting of somatosensory evoked potentials (SEP's), visual evoked potentials (VEP's), and auditory evoked brainstem responses (AEBR's), were studied in 36 patients with hypertensive putaminal hemorrhage to ascertain the relation among areas and distribution of brain dysfunction, the size of hemorrhage on computerized tomographic scan, and the clinical outcome. Among MEP's, SEP's were most significantly involved in all patients. Abnormalities in VEP's and AEBR's remained mild or moderate when the hemorrhage did not extend to the diencephalon. If SEP's were normal or mildly abnormal, they improved early the ictus. These patients did well clinically. If SEP's were absent, the patients had poor outcome even when the hemorrhage was small and located outside the internal capsule. In contrast, deterioration or persistence of MEP's indicated secondary insult to the brain and poor patient outcome. Early and serial MEP studies are useful in evaluating primary and secondary brain dysfunction and in predicting patient outcome in hypertensive putaminal hemorrhage.
Evidence that intraluminal pressure affects high potassium- and serotonin-induced contractions differently in the bovine middle cerebral artery: an in vitro study.
Authors: Vinall P E , Simeone F A
Published: June 2011

The effects of changing intraluminal pressure on contractions induced by 70 mM potassium (K+) and 10(-7), 10(-6), and 10(-5) M serotonin (5-HT) were studied in vitro in bovine middle cerebral arteries. Changes in vessel outside diameter in whole-mounted cylindrical sections of artery were detected with a photoelectric infrared device. High K+-or 5-HT (10(-5)M)-induced contractions peaked at 25 mm Hg and were significantly correlated with increasing intraluminal pressure between 25 and 175 mm Hg. Contractions induced with lower concentrations of 5-HT (10(-6), 10(-7) M), norepinephrine, and histamine peaked at 75 mm Hg but were not significantly correlated with rising pressure. Phentolamine (2 X 10(-6) M) added to the extraluminal bath had negligible influence on pressure's ability to affect K+- and 5-HT-induced contractions differently. Reducing bath temperature to 27 degrees C reduced the K+ response at each pressure, but similar temperature changes had little affect on the 5-HT-induced contractions. The K+ response became less sensitive to increasing pressure at low temperatures. Nifedipine (10(-7) M) almost totally eliminated K+-induced contractions, while significantly reducing the responses to all concentrations of 5-HT. The 5-HT responses appeared more sensitive to increasing intraluminal pressure in the presence of nifedipine. Maximum Ca++-induced contractions in the presence of 10(-5) M 5-HT and high K+ occurred at 25 mm Hg, while Ca++-induced contractions and Ca++-induced contractions in the presence of 10(-7) 5-HT or K+ plus 5-HT were maximum at 75 mm Hg.(ABSTRACT TRUNCATED AT 250 WORDS)
Intravenous prostacyclin in acute nonhemorrhagic stroke: a placebo-controlled double-blind trial.
Authors: Hsu C Y , Faught R E , Furlan A J , Coull B M , Huang D C , Hogan E L , Linet O I , Yatsu F M
Published: June 2011

The therapeutic efficacy of prostacyclin in nonhemorrhagic cerebral infarction was assessed in a placebo-controlled double-blind trial. A total of 80 patients with stroke onset within 24 hours were randomized into placebo (37 patients) and prostacyclin (43 patients) groups. Demographic data and risk factors were comparable. Patients in the prostacyclin group received a continuous i.v. infusion of prostacyclin at an average rate of 8.5 ng/kg/min for an average of 64 hours. The placebo group received vehicle only in a similar fashion. During treatment hemodynamic changes were more prominent in the patients receiving prostacyclin and included reduction of systolic and diastolic blood pressure and increase in pulse rate. In contrast there was only a slight (but significant) reduction of diastolic blood pressure in the placebo group. Neurologic deficit scores were determined on admission, at Day 3, and at Weeks 1, 2, and 4. Mean neurologic deficit scores upon entry were comparable in the placebo and prostacyclin groups, and a significant improvement in the score for neurologic deficit was noted in both. The placebo group tended to fare better throughout the study, with a significant difference in neurologic deficit score favoring the placebo group at Week 2 (p = 0.0048). Two patients in the placebo and one in the prostacyclin group died. The only difference in adverse reactions was flushing (6 patients in prostacyclin vs. 0 in placebo group, p less than 0.05). The results of this study suggest a lack of therapeutic efficacy of prostacyclin in a defined population of patients with nonhemorrhagic cerebral infarction.
Lipid metabolism, cerebral metabolic rate, and some related enzyme activities after brain infarction in rats.
Authors: Bralet J , Beley P , Jemaa R , Bralet A M , Beley A
Published: June 2011

Multiple infarcts were produced in cerebral hemispheres of rats by injecting calibrated 50-micron microspheres into the left internal carotid artery, and alterations in lipid and energy metabolism were evaluated 24 hours later in the embolized hemisphere. Total phospholipid content was decreased by 26%, but the different classes of phospholipids were not equally affected. Phosphatidylinositol and phosphatidylserine levels were decreased by about 40% and phosphatidylcholine and phosphatidylethanolamine by 25%, while sphingomyelin level remained unchanged. There was a 3.2-fold increase in total free fatty acid content with a relatively larger rise in polyunsaturated free fatty acids 20:4 and 22:6 (20-fold increase). Determination of enzyme activities showed decreases in Na+,K+-ATPase (-21%) and hexokinase (-14%) but no changes in phosphofructokinase and pyruvate kinase. Study of energy metabolism using the closed system method of Lowry et al showed a significant depression (-36%) of the cerebral metabolic rate. Taken together, these data suggest a relation between lipid alterations and dysfunction of energy metabolism. Phospholipid degradation with subsequent free fatty acid release and alteration in membrane-bound enzymes may have a direct effect on metabolic machinery and may slow cerebral metabolic rate.
Breathing 100% oxygen after global brain ischemia in Mongolian Gerbils results in increased lipid peroxidation and increased mortality.
Authors: Mickel H S , Vaishnav Y N , Kempski O , von Lubitz D , Weiss J F , Feuerstein G
Published: June 2011

Exposure of Mongolian gerbils to a 100% oxygen atmosphere after 15 minutes of global brain ischemia resulted in a marked increase in the production of pentane, an in vivo product of lipid peroxidation. Much less pentane production occurred in animals subjected to global brain ischemia then exposed to an air atmosphere and in animals exposed to a 100% oxygen atmosphere without ischemia. Gerbils placed in 100% oxygen for 3-6 hours after 15 minutes of ischemia also had a threefold increase in 14-day mortality compared with gerbils subjected to ischemia and then placed in an air atmosphere. These findings raise a serious question about the use of oxygen-enriched atmospheres during reperfusion following ischemia.
Analysis of inhalation rCBF data.
Authors: Sullivan H G , Allison J D , Kingsbury T B , Goode J J
Published: June 2011

Relative to other approaches that have been recommended, fitting all head data, solving for a time shift, and including an air passage artifact term in the model significantly improved the estimate of gray matter blood flow by the inhalation technique. A robust algorithm, which incorporates these features, has been developed. Formulas which facilitate implementation of this algorithm are reported. An artifact from large scalp arteries was not significant and does not need to be included in the model.
Effect of 5-lipoxygenase inhibitor on experimental delayed cerebral vasospasm.
Authors: Yokota M , Tani E , Maeda Y , Kokubu K
Published: June 2011

Experimental delayed cerebral vasospasm was produced in canine basilar arteries by 2 successive injections, 2 days apart, of fresh autogenous arterial blood into the cisterna magna. When angiographic evidence of delayed vasospasm was confirmed 7 days after the initial intracisternal blood injection, a selective inhibitor of 5-lipoxygenase, 2-(12-hydroxydodeca-5,10-diynyl)-3,5,6-trimethyl-1,4-benzoqu inone (AA-861), was infused intravenously at 6.5 X 10(-4) mg/kg/min for 2 hours. However, angiographic evidence of delayed vasospasm was not reversed, and mean regional cerebral blood flow was not significantly increased. In other studies, oral doses of AA-861 at 100 mg/kg/day were given twice a day for 7 days after the initial intracisternal blood injection. In the treated group, angiographic evidence of delayed vasospasm was significantly reduced, and the contractile property of excised basilar arteries in response to vasoconstrictor agents was significantly improved. It is suggested that leukotrienes, 5-lipoxygenase products of arachidonic acid, might be important etiologic factors responsible for the development of delayed vasospasm and that AA-861 would have a therapeutic effect not on the reduction of delayed vasospasm once developed but on the prevention of the development of delayed vasospasm.
Fatty acid pattern of red blood cell membranes and risk of ischemic brain infarction: a case-control study.
Authors: Ricci S , Patoia L , Berrettini M , Binaglia L , Scarcella M G , Bucaneve G , Vecchini A , Carloni I , Agostini L , Parise P
Published: June 2011

The fatty acid composition of red blood cell membranes (which reflects dietary fat intake) was studied in 28 male patients with recent (less than 3 days) ischemic stroke and 56 matched controls. Fifteen fatty acids were measured by means of chromatographic analysis. Percentages of linoleic, 22:5, and 22:6 acids were significantly lower in red blood cell membranes of stroke patients than in those of matched controls. The results suggest that a low unsaturated fatty acid diet could be an independent risk factor for ischemic brain infarction.
Cerebral blood flow in the evolution of infarction following unilateral carotid artery occlusion in Mongolian gerbils.
Authors: Weinberger J , Nieves-Rosa J
Published: June 2011

Cerebral blood flow (CBF) was measured in gerbils 2, 4, 7, and 12 hours after unilateral irreversible carotid artery ligation to determine if the delayed ischemic damage to nerve terminals that occurs over 8 hours after stroke could be due to changes in CBF. [14C]butanol (4.5 mu Ci in 45 microliter 0.9% saline) was injected into the femoral vein, and cpm accumulating in the cerebrum and in a catheter inserted in the abdominal aorta were measured. CBF (ml/100 g/min, mean +/- SEM) in sham-operated control gerbils was 108.4 +/- 37.5 in the left hemisphere and 123.8 +/- 37.1 in the right. CBF in the ischemic left cerebrum was 41.0 +/- 7.7 at 2 hours (n = 7), 21.6 +/- 7.2 at 4 hours (n = 4), 26.2 +/- 4.6 at 7 hours (n = 7), and 9.7 +/- 3.1 at 12 hours (n = 6). CBF in the nonligated right hemisphere was 115.0 +/- 15.3 at 2 hours, 70.4 +/- 23.3 at 4 hours, 80.4 +/- 14.6 at 7 hours, and 50.9 +/- 20.1 at 12 hours. As expected, CBF was significantly reduced in the ischemic left cerebral hemisphere compared with the nonligated right cerebral hemisphere at each time, but CBF in the ischemic left cerebral hemisphere was also significantly lower at 12 hours than at 2 hours (p = 0.002) and at 7 hours (p = 0.014). CBF in the nonligated right cerebral hemisphere was also lower at 12 hours than at 2 hours (p = 0.02). No changes in PCO2 or blood pressure accounted for these differences.(ABSTRACT TRUNCATED AT 250 WORDS)
Renal blood flow in acute cerebral ischemia in spontaneously hypertensive rats: effects of alpha- and beta-adrenergic blockade.
Authors: Yao H , Sadoshima S , Shiokawa O , Fujii K , Fujishima M
Published: June 2011

The influences of acute cerebral ischemia on renal hemodynamics were examined in spontaneously hypertensive rats in which cerebral ischemia was induced by bilateral carotid artery occlusion. Renal and cerebral blood flow were measured with a hydrogen clearance technique. Either phenoxybenzamine (0.5 mg/kg body wt) or propranolol (2 mg/kg) was given i.v. immediately after ischemia was induced to examine the drugs' effects on cerebral and renal hemodynamics. One hour after ischemia, cerebral blood flow was markedly reduced to 5, 3, and almost 0% of the preischemic value in the untreated, phenoxybenzamine-treated, and propranolol-treated rats, respectively. In contrast, renal blood flow at that time was decreased to 65, 88, and 67%, respectively. The calculated renal vascular resistance was similarly increased to 151% in the untreated and 136% in the propranolol-treated rats, but decreased to 82% in the phenoxybenzamine-treated rats. The present results indicate that in acute cerebral ischemia renal blood flow was considerably decreased with concomitant increased renal vascular resistance, and that such reduction in renal blood flow was minimized by alpha-adrenergic blockade but not by beta-blockade. It is concluded that activation of the alpha-adrenergic system in acute cerebral ischemia causes renal vasoconstriction.
Extracranial carotid arterial disease in patients with familial hypercholesterolemia and coronary artery disease treated with colestipol and nicotinic acid.
Authors: Kuo P T , Toole J F , Schaaf J A , Jones A , Wilson A C , Kostis J B , Moreyra A E
Published: June 2011

Carotid bifurcation atherosclerosis was demonstrated in 34 of 108 patients with familial hypercholesterolemia and coronary artery disease by B-scan, continuous-wave Doppler sonography, and intravenous digital subtraction angiography. An intensive combined therapy of diet, colestipol, and nicotinic acid was mounted to control the hypercholesterolemia of these patients. Their serial sonographies and digital subtraction angiography were evaluated independently by technical specialists who served as coinvestigators. The data obtained suggest that extracranial arterial disease can develop concurrently with coronary artery disease in a significant proportion of patients with familial hypercholesterolemia, and amaurosis fugax, transient ischemic attack, cerebral infarction, and myocardial infarction did not recur during 58-72 months of control of familial hypercholesterolemia in this series of patients.
Frequency of cerebral infarction in patients with inherited neuromuscular diseases.
Authors: Biller J , Ionasescu V , Zellweger H , Adams H P , Schultz D T
Published: June 2011

We evaluated the frequency of cerebral infarction in 131 patients with Duchenne's muscular dystrophy, myotonic dystrophy, Becker's muscular dystrophy, or Friedreich's ataxia. Electrocardiographic abnormalities were found in 83% of patients with Duchenne's muscular dystrophy, 56% with myotonic dystrophy, 50% with Becker's muscular dystrophy, and 25% with Friedreich's ataxia. Atrial flutter occurred in 2.3% of the patients, and atrial fibrillation in only 0.9%. Evidence of cerebral infarction was found in only 2 patients (1.5%). Both patients had cardiomyopathy and either atrial fibrillation or flutter. Despite frequent cardiac involvement, cerebral infarction is an uncommon occurrence in patients with inherited neuromuscular diseases.
Platelet function and thrombin activity in patients with recent cerebral transient ischemic attacks.
Authors: Vicari A M , Giusti M C , Luoni R , Macagni A , Medaglini S , Seveso M P , Franceschi M
Published: June 2011

Platelet function and thrombin activity were investigated in 12 hospitalized patients (7 men and 5 women, mean age 53 years) who had had transient cerebral ischemic attacks in the previous 2-12 weeks. Each patient was given an extensive clinical and instrumental evaluation, including Doppler sonography of the cervical and lower limb vessels, cerebral angiography, and head computed tomography scan, after which relevant atherosclerotic disease was excluded. The controls consisted of 12 subjects hospitalized for nonvascular neurologic problems and matched for age, sex, and risk factors to the transient ischemic attack patients. Collagen-induced platelet thromboxane B2 production, plasma beta-thromboglobulin, and fibrinopeptide A were significantly higher in the patients than the controls. Platelet aggregability by collagen was the same in the 2 groups. Platelet hyperfunction and enhanced thrombin activity are present in patients some weeks after the acute episode, suggesting that the hemostatic system has a primary pathogenetic role.