bluuebunny/crossref_metadata_2025 huggingface dataset:
Failure of the somatosensory evoked potential following middle cerebral artery occlusion and high-grade ischemia in the cat--effects of hemodilution.
Authors: Coyer P E , Lesnick J E , Michele J J , Simeone F A
Published: June 2011

Acute focal ischemia was created in 10 cats by unilateral retro-orbital middle cerebral artery (MCA) occlusion. Regional cerebral blood flow (CBF) was determined utilizing the hydrogen clearance technique from electrode recordings within the gray matter and white matter of the ectosylvian gyrus of both hemispheres. The somatosensory evoked potential (SSEP) was obtained during contralateral median nerve stimulation. When the MCA was clipped the white and gray matter blood flows in the ipsilateral ectosylvian gyrus were reduced to 14.8 +/- 19.6% and 19.3 +/- 23.7% of control, and the cortical component of the SSEP was abolished. In the contralateral hemisphere an average increase of 3.5% above the control latency and a 10% mean depression in the amplitude of the cortical component of the SSEP were observed following occlusion. CBF in the contralateral hemisphere was unaffected by the MCA clip. Infusion of saline or dextran to lower the hematocrit by approximately 45% did not significantly improve blood flow or restore the SSEP in the hemisphere ipsilateral to the MCA clip. However, significant increases in the contralateral hemisphere gray matter CBF occurred following hemodilution while the latency of the cortical component of the SSEP in this same hemisphere was significantly extended. Elevations in gray and white matter blood flows were achieved in the experimental hemisphere of 3 of 10 cats suggesting a wide range of variation in the collateral circulation.
Cerebral blood flow is regulated by changes in blood pressure and in blood viscosity alike.
Authors: Muizelaar J P , Wei E P , Kontos H A , Becker D P
Published: June 2011

There is still considerable controversy regarding the influence of blood viscosity upon CBF. We have measured CBF with microspheres in 23 cats. Autoregulation was disturbed in the left caudate nucleus by microsurgical occlusion of the left middle cerebral artery. Induced hypertension or hypotension was used and i.v. mannitol (1 g/kg) administered. In all cats blood viscosity decreased an average of 16% at 15 minutes and, in 16 cats, increased 10% at 75 minutes post-mannitol. CBF in the right caudate was 79 +/- 6 ml/100g/min, in the left 38 +/- 6 (p less than 0.001). Only minor changes of CBF occurred in areas with presumed normal autoregulation, including the right caudate, in conjunction with pressure or viscosity changes. In the left caudate CBF decreased 21% with hypotension and 18% with higher viscosity, more than on the right (p less than 0.01 and p less than 0.2, respectively). CBF increased in the left caudate 56% with hypertension and 47% with lower viscosity, again much more than on the right (p less than 0.001 and p less than 0.01, respectively). In the other area which is (nearly) exclusively supplied by the middle cerebral artery of the cat, i.e., the ectosylvian cortex, results were similar to those in the caudate nucleus. These results show that viscosity changes must result in compensatory readjustments of vessel diameter, but that these adjustments do not occur where autoregulation to pressure changes is known to be defective. The adjustments to viscosity changes might be called blood viscosity autoregulation of CBF. We hypothesize that pressure autoregulation and blood viscosity autoregulation share the same mechanism.
ISI values and interhemispheric differences in patients with ischemic cerebrovascular disease; correlations with clinical and angiographic findings.
Authors: Mosmans P C , Veering M M , Jonkman E J
Published: June 2011

Xenon 133 inhalation CBF studies of one hundred patients with ischemic cerebrovascular disease in the territory of the carotid artery were compared in an attempt to gain more insight into the collateral capacity, especially in those with a stenosis or occlusion of one of the major arteries. Asymmetry of the ISI values for the two hemispheres was expressed as a ratio. High ratios (greater ISI asymmetries) were found for patients with an occlusion of the internal carotid or middle cerebral artery, especially--but not exclusively--those with the more severe clinical symptoms. It also appeared that even when the patient is in a good clinical condition, an elevated ratio reflects insufficiency of the collateral supply to the affected side. The ISI values for individual patients seem to be less useful, partly due to the variable age dependency of this flow parameter.
The arterial patterns associated with internal carotid disease and cerebral infarcts.
Authors: Rodda R A
Published: June 2011

In 20 necropsies with 15 stenosed and 17 thrombotic occluded internal carotid arteries there were 46 cerebral infarcts larger than 1 cm diameter. Using portmortem arteriographic and pathological techniques the patterns of the neck and brain artery systems were correlated with the situation and extent of the brain infarcts. Massive infarcts involving two major cerebral artery territories were associated with distal internal carotid artery occlusion and grossly ineffective cervical and circle of Willis anastomoses. Isolated middle cerebral artery territory infarcts were associated with internal carotid occlusion or stenosis and impairment of the circle of Willis anastomoses, perhaps with middle cerebral artery stenosis. The pattern of adequate size arteries determined if these infarcts were total, deep central, anterior, medium or posterior partial territory infarcts. Boundary zone infarcts were associated with internal carotid artery disease and limitation of anterior or posterior circle of Willis anastomoses. These limitations determined which boundary zones were affected. Isolated anterior cerebral artery territory infarcts were associated with bilateral internal carotid disease and an anterior cerebral artery stenosis or small caliber anterior communicating artery. Isolated posterior cerebral artery territory infarcts were associated with internal carotid disease and a direct impairment of the ipsilateral posterior cerebral artery capability.
Recurrent cerebral infarctions in two brothers with antiphospholipid antibodies that block coagulation reactions.
Authors: Jacobson D M , Lewis J H , Bontempo F A , Spero J A , Ragni M V , Reinmuth O M
Published: June 2011

Inhibitors blocking coagulation reactions, often called lupus anticoagulants, are readily identifiable but rarely considered as risk factors for cerebral infarction. These inhibitors are inconsistently found in a number of diseases (often autoimmune) and after treatment with ceretain drugs and appear to be closely associated with, or identical to, antibodies to certain phospholipids. We have observed two brothers with these inhibitors who both experienced recurrent cerebral infarctions. Such familial occurrence has rarely been reported. In addition, some other family members were found to have depressed factor XII levels. Using the technique of double immunodiffusion, we found that the serum from these brothers formed precipitin lines against certain phospholipid substrates, lending further support to the antiphospholipid nature of this inhibitor.
The Italian Multicenter Study of reversible cerebral ischemic attacks: IV--Blood pressure components and atherosclerotic lesions.
Authors: Inzitari D , Bianchi F , Pracucci G , Albanese V , Argentino C , Bono G , Brambilla G L , Candelise L , De Zanche L , Mariani F
Published: June 2011

Utilizing the initial BP assessment in the 462 patients who entered the Italian Multicenter Study of reversible cerebral ischemia, an analysis of the effect of each BP component in respect of presence, extent and severity of atherosclerotic lesions, as displayed by angiography, was carried out separately for lesions located at either intra- or extracranial level. In a multivariate statistical model, among the following variables: sex, age, systolic BP, diastolic BP, cholesterol and smoking, systolic BP was found the best predictor of extent and severity of atherosclerotic lesions at extracranial level. None of the same variables was predictive of the severity of intracranial atherosclerosis. The results of this clinical study may confirm the indication, coming from physiopathologic observations, of a predominant role of systolic hypertension in the process of maintenance and acceleration of atherosclerosis in the large pre-cerebral arteries.
Quantification of cerebral infarct size by creatine kinase BB isoenzyme.
Authors: Bell R D , Alexander G M , Nguyen T , Albin M S
Published: June 2011

Creatine Kinase BB isoenzyme (CKBB) has been shown to rise in the serum and CSF following acute cerebral injury. To test the hypothesis that brain infarct size could be estimated from the appearance and disappearance of CKBB in the serum and CSF, strokes of varying size were produced in twelve mongrel dogs by silastic emboli. The rate of disappearance, Kd of CKBB (-.00732 +/- 0.001 min-1 mean +/- SE, N = 8) was determined by injecting purified CKBB (25 IU) intravenously then measuring its disappearance. Following the embolic stroke, serum samples were taken hourly for 24 hours and then at intervals for up to 160 hours for measurement of CKBB by radioimmunoassay until the animals were sacrificed. The brains were then removed, fixed in formalin, cut in 2 mm sections and photographed. The area of the infarct was measured using high pad digitizer interfaced with an Apple computer. The infarct size was then calculated from the area and thickness. Using a one-compartment mathematical model, the infarct size was estimated from the amount of CKBB appearing in the serum, the Kd of CKBB, and the amount of CKBB depleted from tissue. The computed infarct size correlated well (r = 0.94) with the measured infarct size. This model may have value in testing therapeutic modalities in the intact animal.
Community Hospital-based Stroke Programs: North Carolina, Oregon, and New York. III. Factors influencing survival after stroke: proportional hazards analysis of 4219 patients.
Authors: Howard G , Walker M D , Becker C , Coull B , Feibel J , McLeroy K , Toole J F , Yatsu F
Published: June 2011

The possible effect of age, race, sex, consciousness upon admission, geographic location, and history of selected risk factors on the survival after stroke due to infarction or hemorrhage was determined using proportional hazards analysis (Cox regression). For each diagnostic category the most significant prognostic factor was consciousness upon admission. Increasing age, cardiac disease, or previous stroke also decreased the survival time of patients with infarctions. For patients with cerebral hemorrhage, no other variable was significant after control for consciousness level.
Temporal arteritis-like presentation of carotid atherosclerosis.
Authors: Venna N , Goldman R , Tilak S , Sabin T D
Published: June 2011

A 68 year-old woman presented with a two-week history of amaurosis fugax, ipsilateral fronto-temporal headache and jaw claudication suggesting carotid giant cell arteritis. However, this syndrome proved to be due to atherosclerosis causing complete occlusion of the external carotid artery at its origin and narrowing of the internal carotid artery. Combined external and internal carotid endarterectomy relieved the symptoms. The symptom complex of temporal arteritis may be rarely mimicked by carotid atherosclerotic occlusive disease.
Focal parenchymal lesions in transient ischemic attacks: correlation of computed tomography and magnetic resonance imaging.
Authors: Awad I , Modic M , Little J R , Furlan A J , Weinstein M
Published: June 2011

Twenty-two patients with the clinical diagnosis of transient ischemic attacks were prospectively evaluated by computed tomography (CT) and proton magnetic resonance imaging (MRI). Nineteen patients also underwent cerebral angiography. The MRI studies were performed with a prototype super-conductive magnet using a 0.6 Tesla or a 1.5 Tesla magnetic field. Two pulse sequence techniques were used resulting in T1 and T2 weighted images. All studies were interpreted descriptively by a single neuroradiologist in a blinded fashion, with special attention to focal parenchymal abnormalities. Patients with previously documented clinical strokes or reversible ischemic neurologic deficits lasting more than 24 hours were excluded. The CT scans revealed focal areas of abnormalities in 7 of 22 patients (32%), while the MRI scans showed focal changes in 17 patients (77%). All the CT lesions were clearly visualized on MRI. The MRI changes were better seen on T2 weighted images as areas of increased signal intensity. There was a marked preponderance of deep hemispheric lesions on both CT and MRI studies. Focal parenchymal abnormalities were not limited to the symptomatic vascular territory. We conclude that MRI reveals focal parenchymal changes in the majority of patients with transient ischemic attacks and is more sensitive than late generation CT scans. However, specificity appears to be poor, and may limit clinical usefulness. While the significance of the MRI "lesions" remains speculative, they may represent markers of chronic cerebrovascular disease in these patients.
A dose-escalation study of large doses of naloxone for treatment of patients with acute cerebral ischemia.
Authors: Adams H P , Olinger C P , Barsan W G , Butler M J , Graff-Radford N R , Brott T G , Biller J , Damasio H , Tomsick T , Goldberg M
Published: June 2011

A dose-escalation study was performed in 27 patients to determine the highest safe and potentially optimal dose of naloxone for treatment of acute cerebral ischemia. All patients received a bolus of naloxone followed by a continuous 24 hour infusion at an hourly rate 50% of the bolus. Loading doses ranged from 2.5 to 200 mg/m2. Total patient doses ranged from 52.3 to 4978 mg. No major dose-related side effects occurred. This study was not designed to determine naloxone's efficacy in stroke, but transient or sustained improvement was observed in 13 patients. Three patients' neurological condition worsened within three hours after the naloxone was discontinued. Our experience suggests that further therapeutic trials of naloxone are worthwhile.
Regional cerebral blood flow correlates of aphasia outcome in cerebral hemorrhage and cerebral infarction.
Authors: Nagata K , Yunoki K , Kabe S , Suzuki A , Araki G
Published: June 2011

The relationship between recovery from aphasia and regional cerebral blood flow (CBF) was compared in 87 patients, 44 with cerebral hemorrhage and 43 with non-embolic cerebral infarction. CBF values correlated poorly with aphasia outcome in patients with cerebral hemorrhage whereas a tight correlation was demonstrated in patients with non-embolic cerebral infarction. A marked variability of CBF values in the acute and subacute stage might account for the poor correlation between CBF and aphasia outcome in patients with cerebral hemorrhage. On the other hand, a sharp discrimination was achieved between those with a good recovery from aphasia and those with a poor recovery by the dimensions of the hematoma on CT. In non-embolic cerebral infarction, a relative frontal ischemia was associated with motor aphasia while a relative temporal ischemia was associated with sensory aphasia. This dichotomy was not demonstrated in the regional CBF values in patients with cerebral hemorrhage.
CT enhancement after prolonged high-dose contrast infusion in the early stage of cerebral infarction.
Authors: Ito U , Tomita H , Kito K , Ueki Y , Inaba Y
Published: June 2011

To demonstrate the BBB break-down on the CT image in the acute stage of cerebral infarction, a 3 hour continuous drip infusion of 200 ml of meglumine amidotrizoate, rather than the conventional bolus injection, was used. In this study, 22 examinations were carried out in 18 patients in whom cerebral infarction due to temporary or permanent obstruction of the cerebral artery was diagnosed by CT and angiography on admission. With each examination, the first CT was obtained prior to contrast infusion, and second immediately after the end of 3 hours of continuous contrast infusion. The EMI number was calculated at 3 regions of interest in the infarction. Within 3 days after stroke episode, 4 out of 5 patients with temporary vascular obstruction demonstrated enhancement, as well as 6 out of 9 patients with permanent vascular obstruction. Between 4 and 14 days after the stroke episode, all of 8 patients showed enhancement. To further clarify the extravasation of the contrast medium during the first 3 days of a cerebral infarction, a third CT scan was performed 3-hrs after finishing the contrast infusion in 4 patients. In these latter patients, blood was sampled at the time of each of the 3 CT series. The EMI number of the blood samples was also measured. In all 4 patients, the Gado's tissue-blood ratio (the EMI number of the CT lesion divided by that of the blood sample) was higher than 17.2% in the second, and higher than 54.7% in the third CT scan. Thus break-down of the BBB which was demonstrated by prolonged contrast infusion is an earlier event in human cerebral infarction than is usually accepted.
Circulating endothelial cells fail to induce cerebral infarction in rabbits.
Authors: Iwata Y , Kuzuya F , Hayakawa M , Naito M , Shibata K , Endo H
Published: June 2011

Exfoliated cells that appear to be circulating endothelial cells were detected in human blood. Because the size of endothelial cells is larger than that of other circulating blood cells, we investigated whether the increased number of circulating endothelial cells might be responsible for cerebral embolism. We compared rabbits into which suspensions of endothelial cells were injected through the common carotid arteries with control rabbits into which blood clots or arachidonic acid were administered in the same manner. Injected endothelial cells failed to cause cerebral embolism. Because the majority of exfoliated circulating endothelial cells were degenerated and deformed, the suspensions of endothelial cells obtained from rabbit aortas were treated by ultrasonic waves. These suspensions also failed to cause cerebral embolism. We conclude that cerebral embolism cannot be induced by an increase of circulating endothelial cells alone.
Studies of the influence of biogenic amines on central nervous system ischemia.
Authors: Zivin J A , DeGirolami U
Published: June 2011

Several serotonin inhibitors have been shown to reduce neurologic deficits in experimental CNS ischemia. Using biochemical and histological methods we tested the effects of the serotonin inhibitors cyproheptadine and brom-LSD in a highly reproducible rabbit spinal cord ischemia model. Detailed mapping of regional spinal cord blood flow was used to guide sampling for the biochemical studies. We found that it is possible to study biochemical and morphological aspects of spinal cord ischemia in great detail using a combination of quite precise techniques. However, at this level of resolution there were no substantial changes in biogenic amine concentrations in severely ischemic or marginally perfused tissue after the durations of ischemia that cause the onset of irreversible tissue damage. Treatment with doses of serotonin inhibitors that produce preservation of neurological function did not cause significant alterations of tissue concentrations of biogenic amines or tissue morphology in treated versus untreated animals.
The effect of dichloroacetate on brain lactate levels following incomplete ischemia in the hyperglycemic rat.
Authors: Colohan A R , Welsh F A , Miller E D , Kassell N F
Published: June 2011

Dichloroacetate (DCA) is known to prevent the phosphorylation of the pyruvate dehydrogenase complex (PDHC) by blocking the action of PDH kinase. This action allows the active PDHC to exert its effect on the metabolism of glucose, lactate and alanine to acetyl CoA. DCA has been shown to reduce serum lactate levels in humans and animals in such conditions as diabetes, phenformin-induced hepatic failure, exercise, and endotoxin-induced shock. Lactic acidosis in the brain has often been postulated as a cause of neuronal damage following ischemia and hypoxia. Therefore, we examined the effect of intravenously administered DCA (100 mg/kg) in rats that were rendered hyperglycemic by intravenous glucose (2 g/kg), and then made to undergo 15 minutes of incomplete cerebral ischemia by bilateral carotid ligation and systemic hypotension (mean arterial pressure of 50 mm Hg). DCA significantly reduced serum lactate levels pre-ischemia, but had no effect on serum lactate levels after ischemia induction. Brain levels of lactate, ATP and PCr after 15 minutes of incomplete ischemia were unaffected by DCA. We conclude that in this in-vivo model the control of PDHC activity in the brain may be different than that in the periphery, and that DCA was not effective in reducing brain tissue lactate levels.
Vertical gaze ophthalmoplegia from infarction in the area of the posterior thalamo-subthalamic paramedian artery.
Authors: Wall M , Slamovits T L , Weisberg L A , Trufant S A
Published: June 2011

Three cases of a stroke syndrome of acute supranuclear vertical gaze ophthalmoplegia are presented. Voluntary vertical gaze and the vertical vestibulo-ocular reflex were absent or diminished initially in all three patients. The patients also had loss of convergence and alteration in their mental status. Computed tomography scans showed lesions in the region of the rostral midbrain and lower diencephalon in the area surrounding the third ventricle. The blood supply, ischemic stroke syndrome and function of this region with reference to the supranuclear control of vertical gaze are discussed.
Major cerebral infarction from tumor embolus.
Authors: Lefkovitz N W , Roessmann U , Kori S H
Published: June 2011

A major right hemispheric infarct developed in a 31-year-old man within forty-eight hours of lung resection for metastatic synovial-cell sarcoma. Post mortem exam revealed tumorous occlusion of the right internal carotid artery. Major stroke from cerebral tumor embolus should be seriously considered in patients with primary or metastatic lung cancer who have had a very recent pneumonectomy, especially when there are symptoms and signs of multi-organ or extremity ischemia.
The clinical spectrum of hemorrhagic infarction.
Authors: Ott B R , Zamani A , Kleefield J , Funkenstein H H
Published: June 2011

The hospital records and head CT scans of 44 patients with hemorrhagic infarction were retrospectively analyzed. The majority of cases (73%) were embolic or possibly embolic in etiology, and 55% were not associated with anticoagulant therapy. Adverse prognosis was most clearly related to infarct size, underlying systemic illness, and symptomatic hemorrhage. Of the nineteen patients in whom serial CT scans documented conversion from bland to hemorrhagic infarction, 12 exhibited no clinical worsening at the time that hemorrhagic infarction was observed; the remaining seven, all of whom worsened, were receiving anticoagulant therapy at the time of documented conversion. Fourteen patients in whom anticoagulant therapy was used despite the findings of hemorrhagic infarction remained stable or improved during hospitalization.
Transient cerebral ischemic attacks in the young and middle aged. A population study.
Authors: Johnson S E , Skre H
Published: June 2011

During an investigation of coronary risk factors, a population 20 to 54 years old in Tromsø, Northern Norway was screened for transient ischemic cerebral attacks. Three simple screening questions were used. Sixteen thousand six hundred and twenty-one subjects participated in the study. Among the responders, a sample of 501 were evaluated neurologically and 10 men and 16 women identified as TIA cases. Mean age for men was 41.3 years, for women 33 years. Five women (mean age 24.4) had the events during pregnancy, pointing to pregnancy as a period of risk. Five-year incidence was found to be 2.5. per 1000. Clinical expressions and ratio carotid to vertebral-basilar TIA hardly differed from that found in materials of older patients. All 26 remained stroke-free during a mean observation period of 55 months. Known risk factors like hypertension, carotid stenosis and cardiac disease were found in only a few. Five women had low blood pressure. It is suggested that TIA in younger age groups may constitute a separate entity where, among other, haemodynamic factors and pregnancy play a role.
A model of focal ischemic stroke in the rat: reproducible extensive cortical infarction.
Authors: Chen S T , Hsu C Y , Hogan E L , Maricq H , Balentine J D
Published: June 2011

In the search for a more reproducible focal ischemic stroke model in the rat, we systematically interrupted blood flow to the right middle cerebral artery territory by ligating the right middle cerebral artery, and the right and left common carotid arteries in succession. Using a laser-Doppler flowmeter, we found that the relative surface blood flow in cerebral cortex supplied by the right middle cerebral artery decreased to 62, 48, and 18% of baseline respectively after successive ligation of the right middle cerebral artery, and the right and left common carotid arteries. A focal infarct in the cerebral cortex supplied by the right middle cerebral artery was consistently noted after ligation of the right middle cerebral and the right common carotid arteries and temporary clip occlusion of the left common carotid artery for 60 min. The surface areas of infarction measured 100 +/- 6 mm2 and the maximal cross-sectional area of infarction was 10.4 +/- 1.1 mm2 (N = 10). The mortality rate was 7% (N = 70). The characteristic changes of ischemic necrosis were limited to the cortex with sparing of subcortical structures. No motor deficits occurred. Occlusion of the right middle cerebral artery alone or together with the right common carotid artery did not consistently cause gross infarction and the maximal cross-sectional area of infarction was smaller (the right middle cerebral artery, 1.7 +/- 0.8 mm2, N = 10; the right middle cerebral artery plus the right common carotid artery, 4.8 +/- 1.9 mm2, N = 10). Permanent ligation of the right middle cerebral artery and both common carotid arteries had a high mortality (60% in 3 days, N = 10).(ABSTRACT TRUNCATED AT 250 WORDS)
Physostigmine induced reversal of ischemia following acute middle cerebral artery occlusion in the rat.
Authors: Scremin O U , Scremin A M
Published: June 2011

Cerebral cortical ischemia was induced in anesthetized rats by occlusion of the middle cerebral artery (MCA). Cerebral blood flow (CBF) was measured with the H2 clearance technique in the center and periphery of the ischemic territory. A decrease of CBF to about 50% of pre-occlusion values was observed in both areas. Administration of Physostigmine, a cholinesterase inhibitor, at a dose of 0.15 mg/Kg by intravenous route, induced an increase of CBF in the ischemic cortex. This change in CBF reached 120% of pre-occlusion level in the periphery and 80% of pre-occlusion value in the center of the area of distribution of the occluded artery. Although Physostigmine induced an increase in arterial blood pressure, the cerebral hyperemia observed both in normal and ischemic cortex could still be demonstrated after blockade of the pressor effect by bleeding or Phentolamine administration.
Primary intraventricular hemorrhage in adults.
Authors: Gates P C , Barnett H J , Vinters H V , Simonsen R L , Siu K
Published: June 2011

Five adults with primary intraventricular hemorrhage are described. The presenting features included headache, confusion and drowsiness. Focal neurological signs were minimal or absent. All five had a history of hypertension, three patients had bilateral internal carotid occlusion at its origin, one had unilateral occlusion of the left internal carotid artery with severe stenosis of the contralateral siphon. Unilateral occlusion of the middle cerebral artery were present in the fifth patient. Pathological examination of the brain from one patient showed the presence of severe hemorrhagic "lacunar" infarcts adjacent to the left lateral ventricle, one showing direct continuity of blood in the lacune with the massive intraventricular hematoma. We hypothesize that such a finding illustrates one possible mechanism for this unusual type of hemorrhage. Patients with longstanding hypertension and severe occlusive disease of the internal carotid arteries may be predisposed to this unusual complication.
The sex difference in manifestations of carotid bifurcation disease.
Authors: Ford C S , Howard V J , Howard G , Frye J L , Toole J F , McKinney W M
Published: June 2011

One would think that risk factors for transient ischemic attack (TIA) and asymptomatic carotid bruit (ACB) would be similar. In our referral population and in several previously reported cohort populations, however, men outnumber women among patients with TIA. In contrast, women outnumber men among patients with ACB. We found in two independent populations that women with ACB are up to 5.7 times less likely than men to have carotid stenosis. Thus women are more prone than men to have ACB, but their bruits much less commonly reflect carotid stenosis. Women are probably predisposed to have carotid bruit even in the absence of carotid stenosis. In our referral population of ACB, this tendency among women for carotid bruit without stenosis does not seem to be related to lower hematocrit, higher prevalence of heart murmur, constitutionally smaller carotid arteries, or differences in pulse rate or body habitus.
Lipoprotein(a) as a strong indicator for cerebrovascular disease.
Authors: Zenker G , Költringer P , Boné G , Niederkorn K , Pfeiffer K , Jürgens G
Published: June 2011

To evaluate the role of lipoprotein(a) (Lp(a] in patients with cerebrovascular disease (CVD), lipid parameters were compared with a control group (CO). Additionally, the Lp(a) serum levels were investigated in a coronary artery disease (CAD) group. The CO was made up of 37 healthy persons (age: 54.5 +/- 7.7, 26 males and 11 females), the CVD group included 46 patients with sustained transient ischemic attack (TIA) prolonged reversible ischemic neurologic deficits (PRIND) and cerebral infarction (CI) (age: 53.6 +/- 9.7, 32 males and 14 females), and the CAD group was made up of 28 survivors of myocardial infarctions (age: 52.5 +/- 8.1, 18 males and 10 females). The median values of Lp(a) in CVD were significantly higher than in the CO (p less than 0.01) and did not differ significantly from the CAD. Total TC, HDL-C, TG, LDL-C and the ratio of LDL-C/HDL-C did not show any significant difference between the control and cerebrovascular disease group. For quantification of the vascular lesions of the carotid system, a Duplex Doppler score system was used. The score correlated with Lp(a) in patients between 40 to 65 years of age (r = 0.34, p less than 0.01). Thus, we conclude that Lp(a) is not only a risk factor for CAD but also for CVD.
Regional cerebral blood flow autoregulation in normotensive and spontaneously hypertensive rats--effects of sympathetic denervation.
Authors: Sadoshima S , Fujii K , Yao H , Kusuda K , Ibayashi S , Fujishima M
Published: June 2011

The present study was designed to investigate the effect of acute sympathetic denervation on the regional cerebral blood flow (CBF) autoregulation during acute elevation of blood pressure in spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY). CBF to the parietal cortex and thalamus was measured by the hydrogen clearance method and, to test autoregulation, systemic arterial blood pressure was elevated by intravenous infusion of phenylephrine. Superior cervical ganglia were removed on both sides to interrupt sympathetic innervation in the deeper structures of the brain. Acute bilateral sympathetic denervation did not alter the resting blood pressure or CBF in either SHR or WKY. In innervated SHR, resting mean arterial pressure (MAP) was 165 +/- 5 mm Hg (mean +/- SEM) and the upper limit of autoregulation in the cortex was 210 +/- 3 mm Hg, which was significantly lower than that in the thalamus (229 +/- 3 mm Hg, p less than 0.02). In bilaterally denervated SHR, the upper limits were lowered to 193 +/- 4 mm Hg in the cortex (p less than 0.02 vs. innervated SHR) and to 207 +/- 5 mm Hg in the thalamus (p less than 0.02 vs. innervated). In WKY, resting MAP was approximately 55 mm Hg lower than that in SHR. Acute denervation reduced the upper limits from 142 +/- 3 mm Hg to 130 +/- 4 in the cortex (p less than 0.05) and from 158 +/- 4 to 145 +/- 4 in the thalamus (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
Effects of long-term antihypertensive treatment on cerebral, thalamic and cerebellar blood flow in spontaneously hypertensive rats (SHR).
Authors: Fujishima M , Ibayashi S , Fujii K , Yao H , Sadoshima S
Published: June 2011

Cerebral blood flows (CBF) were measured in the parietal cortex, the thalamus and the cerebellum by the hydrogen clearance technique in anesthetized spontaneously hypertensive rats, of which hypertension was treated for 16 weeks (long-term) or 8 weeks (short-term) with antihypertensive agents of hydralazine and guanethidine. As compared to non-treated control animals, CBF in the three regions were significantly increased while the calculated cerebrovascular resistances (CVR) were decreased in hypertension-treated animals. Such CBF and CVR changes were greater in SHR with long-term than short-term therapy. Both an increase in CBF and a decrease in CVR were closely related to a fall in the blood pressure. From the present results, it was concluded that earlier and longer treatment of hypertension could lessen or even prevent the increased CVR due to the hypertensive vascular changes, and increase CBF as a result.
Glycolytic inhibition by 2-deoxyglucose reduces hyperglycemia-associated mortality and morbidity in the ischemic rat.
Authors: Combs D J , Reuland D S , Martin D B , Zelenock G B , D'Alecy L G
Published: June 2011

Numerous laboratories have shown that hyperglycemia increases cerebral ischemic damage. This presumably results from increased lactate production and accumulation during ischemia. Although increased tissue lactic acidosis is associated with increased ischemic brain damage, this damage has not been directly linked to glycolytic flux. Because 2-deoxyglucose (2-DG) is a competitive inhibitor of glycolysis we tested its ability to reduce hyperglycemia-exacerbated ischemic brain damage. Severe forebrain ischemia was produced by the four-vessel occlusion model in rats. Four rats received 3 g/kg glucose and saline while a second group (n = 5) was injected with 3 g/kg glucose plus 1.6 g/kg 2-DG. A third group (n = 5) was treated with 1 g/kg glucose plus saline and a fourth group (n = 5) received 1 g/kg glucose and 1.6 g/kg 2-DG. All rats were injected i.p. 10 minutes prior to the ischemic insult with the same volume/kg body weight. All rats receiving the high dose of glucose alone (3 g/kg) were dead within 24 hours postischemia. Rats who received 2-DG in addition to 3 g/kg glucose showed only 40% mortality (p = 0.119 Fisher's Exact). 2-DG completely eliminated convulsions during the initial two hours of recovery which was significant (p = 0.008), however, all rats in both groups showed some convulsions by 24 hours postischemia. Among rats receiving the low glucose dose (1 g/kg), none of the rats receiving 2-DG died or convulsed by 24 hours postischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
Cerebral glucose metabolism during the recovery period after ischemia--its relationship to NADH-fluorescence, blood flow, EcoG and histology.
Authors: Tanaka K , Dora E , Greenberg J H , Reivich M
Published: June 2011

Local cerebral glucose utilization (lCMRgl), NADH fluorescence, cerebral blood flow (CBF), electrocortical activity (ECoG) and histology were studied during a 4 hr recovery period following 2 hrs of left middle cerebral artery (MCA) occlusion in cats. Changes in relative reduced pyridine nucleotides and CBF were measured by fluororeflectometry, ECoG was obtained from the left middle ectosylvian gyrus (MEG), and lCMRgl was measured at the end of the recovery period autoradiographically with 14-C-2-deoxyglucose. A sham group was comprised of 4 cats. The ten animals subjected to the stroke were classified into 3 groups based on the mean amplitude of the ECoG at the end of the ischemic period. At the end of the recovery period, the relative reduced pyridine nucleotides showed a 22.5% oxidation (oxidation of NADH), a 66.2% reduction (reduction of NAD) and a 3.0% reduction compared to the sham group in the severe, moderate and mild groups, respectively. LCMRgl of the left MEG in the severe group was 64.2% of the corresponding sham value, whereas lCMRgl in the moderate and mild groups were 124.8% and 132.0% of the sham, respectively. CBF at the end of the recovery period ranged from 28.1% to 83.0% of the sham value, although there was no significant difference among these groups. Histologically, a large portion of the neurons in the left MEG in the severe group showed ischemic neuronal changes, while the damage was less severe in the moderate and mild groups. On the basis of these data, it is suggested that a relative substrate deficiency and/or a loss of mitochondrial enzymatic pool size may occur in the animals comprizing the severe group. Conversely, anaerobic glycolysis may be activated in the moderate group, while the mild group exhibits an increase in glucose metabolism that is most likely aerobic. A gradient in the magnitude of changes in lCMRgl was noted from the central MCA territory to the surrounding brain regions in the ischemic hemisphere. In addition, there was a mild, but statistically significant (p less than 0.05), depression in lCMRgl with no histological damage in the non-ischemic hemisphere of the severe group.
Early management of the patient with recent aneurysmal subarachnoid hemorrhage.
Authors: Adams H P
Published: June 2011

Despite its efficacy in preventing rebleeding, the anticipated strong trend in favor of early intracranial surgery has not been achieved. Early intracranial operation remains a useful choice in the management of recent SAH in good-risk patients, but patients must be carefully selected on an individual basis. Many patients will undoubtedly benefit from early surgery but it is not a panacea. Further investigation of surgical treatment in combination with improved preoperative and postoperative medical therapy will be required to ameliorate the outcome of SAH. In particular, the prevention and treatment of cerebral infarction deserves attention. The results of the antifibrinolytic and timing of intracranial surgery studies point to the need for an effective prevention treatment regimen for vasospasm. Further studies about the efficacy of calcium channel blocking drugs in prevention of ischemia after SAH are needed among patients given antifibrinolytic drugs or having early operation. All the advances in treatment are predicated on prompt diagnosis of SAH in good-condition patients. The medical community needs to maintain a high degree of vigilance for the diagnosis of SAH in all patients complaining of a new, unusual or severe headache. Early referral to properly equipped and staffed medical facilities remains a keystone to effective treatment of SAH.
Hypertension as a risk factor for spontaneous intracerebral hemorrhage.
Authors: Brott T , Thalinger K , Hertzberg V
Published: June 2011

To better define the etiologic importance of hypertension for spontaneous intracerebral hemorrhage, hospital records were studied for all patients sustaining intracerebral hemorrhage during 1982 in the Cincinnati metropolitan area. Hypertension pre-dating the hemorrhage was present in 45% (69 of 154), as determined by history. A more inclusive definition of hypertension, combining those with a positive history with those found to have left ventricular hypertrophy by electrocardiogram or cardiomegaly by chest radiography, applied in 56% (87 of 154). The cases were compared to controls with and without hypertension derived from the NHANES II study of blood pressure (n = 16,204) to determine relative risk. For the presence of hypertension by history, the relative risk of intracerebral hemorrhage was 3.9 (95% confidence interval, 2.7 to 5.7). For the inclusive definition of hypertension, the relative risk was 5.4 (3.7 to 7.9). Relative risk was also determined for hypertension in blacks (= 4.4), age greater than 70 (= 7), prior cerebral infarction (= 22), and diabetes (= 3). We conclude that the term "hypertensive hemorrhage" should be used very selectively, particularly in whites, and propose that hypertension be viewed as one of several important risk factors for spontaneous intracerebral hemorrhage.
Incidental subcortical lesions identified on magnetic resonance imaging in the elderly. II. Postmortem pathological correlations.
Authors: Awad I A , Johnson P C , Spetzler R F , Hodak J A
Published: June 2011

The pathological correlates of subcortical lesions noted on magnetic resonance imaging (MRI) in the elderly are not known. Postmortem in vitro proton MRI was performed on the brains of seven consecutive elderly patients dying of nonneurologic causes. Scans were done in the fresh and fixed states with the specimen immersed in saline and formaldehyde respectively. A 1.5 Tesla superconductive system was used with a multiple spin-echo protocol generating T2 weighted images. Subcortical MRI lesions were localized in three dimensions and identified at brain cutting. In addition, pathological correlations were obtained from an eighth patient who underwent MRI eleven days before death. Histological examinations were performed in a blinded fashion, including control areas from the same brains. Subcortical MRI lesions were found to be associated with arteriosclerosis, dilated perivascular spaces, and vascular ectasia (p less than 0.05). These histological changes were characteristic of "état criblé" which, like subcortical MRI lesions, is associated with age and hypertension. Shrinkage (or atrophy) of the brain parenchyma around ectatic blood vessels would result in an extensive network of tunnels filled with extracellular water. The proton MRI signal from such areas of the brain would be increased. Gliosis and small areas of infarction occasionally coexisted with "état criblé," but these were not present in all areas with MRI lesions and could not be distinguished by MRI signal alone. In conclusion, clinical and pathological correlations lend support to the uniform hypothesis that MRI provides a nonspecific index of brain parenchymal alterations caused by aging and chronic cerebrovascular disease.
Trends in mortality from cerebrovascular disease in Taiwan.
Authors: Hu H H , Chu F L , Wong W J , Lo Y K , Sheng W Y
Published: June 2011

The rate of decline in the age-adjusted death rate from cerebrovascular disease (CVD) in Taiwan is not as rapid as in the United States and Japan, and the trends of CVD mortalities have not decreased steadily during the period 1972-1983. A low record of hypertension regulation (5.0%-12.7%), a high proportion (47.1%) of stroke due to cerebral hemorrhage (by clinical assessment), and a high fatality rate (40.1%) for cerebral hemorrhage may account partially for the slower declining rate. A geographic difference in the downward trend of CVD death rate was observed in this period. Districts remote from the major cities have had the lowest decline in CVD death rate.
Cell density in the border zone around old small human brain infarcts.
Authors: Nedergaard M , Vorstrup S , Astrup J
Published: June 2011

Nine brain autopsy cases of small old cerebral infarcts were selected for neuropathological studies. Eight of the patients had cortical infarcts, in two cases with extension into the striate body. In one case the infarct involved the striate body only. The density of neurons and glial cells was measured in the coronal and the horizontal planes at various distances from the margin of the infarct. Corresponding counting points in the contralateral hemisphere served as control. On light microscopy, the infarcted cortex was irregularly shaped, but on serial sections the bulging parts appeared to be cut off from the infarcted tissue ("pseudo-infarct islands"). The zone of transition from infarcted to normal brain tissue was less than a few mm wide. In one patient, tomographic measurements of the cerebral blood flow (CBF) and a CT scan could be compared with the neuropathological findings. In this patient, CBF in the surroundings of the infarct was decreased despite a normal neuronal density. The study supports the traditional view held by pathologists that a sharp transition exists between infarcted and normal brain tissue and suggests that the hypoperfusion zone surrounding the region of complete infarction may be due to mechanisms other than selective loss of neurons.
Familial hyperlipidemia in stroke in the young.
Authors: Bansal B C , Sood A K , Bansal C B
Published: June 2011

Serum cholesterol, low density lipoproteins (LDL), very low density lipoproteins (VLDL) and chylomicron levels were studied in 25 young patients (age 40 years or less) of non-embolic ischemic stroke of unknown aetiology. Fifteen patients were males and 10 were females. The prevalence of hyperlipidemia was found to be 60%. Frederickson's type IIb hyperlipoproteinemia was the commonest (32%) abnormal pattern observed, followed by type IIa (12%), type IV (12%) and type V (4%). Family studies were carried out in all the 25 index patients (15 hyperlipidemic and 10 normolipidemic). Familial hyperlipidemia (i.e. 2 or more hyperlipidemic members in the same family) was found in 9 of the 15 hyperlipidemic index patients and in none of the normolipidemic index patients. The common pattern was found to be that of familial combined hyperlipidemia. The study indicates that screening the family members of hyperlipidemic young patients of non-embolic ischemic stroke may delineate a group of high risk individuals for possible primary prevention before they develop the disease.
Proton NMR relaxation times in ischemic brain edema.
Authors: Horikawa Y , Naruse S , Tanaka C , Hirakawa K , Nishikawa H
Published: June 2011

The state of water in cerebral ischemia was studied by using the proton nuclear magnetic resonance (1H-NMR) method. Cerebral ischemia was induced experimentally in Mongolian gerbils by unilateral ligation of the common carotid artery. Longitudinal (T1) and transverse (T2) relaxation times of the ischemic brain were measured with a pulse FT-NMR spectrometer and the water content was determined by the wet/dry method. Quantitative analysis of the relaxation times was performed sequentially during the initial 7 hours following ligation and the data were compared with those of brain edema previously reported by S. Naruse in the rat. Characteristic findings in brain ischemia include prolongation of the slow component of T2 and increase in the water content. A quantitative comparison of relaxation rate and water content demonstrates that ischemic brain edema in Mongolian gerbils is different from cytotoxic and vasogenic types of brain edema. When R2 (1/T2) was plotted against the water content, the slope value of ischemia in the gerbil was between the slope values of the TET intoxication and cold injury induced edemas reported previously. From these results, it might be said that ischemic brain edema includes both the cytotoxic and vasogenic types of brain edema. Glycerol was demonstrated to affect brain ischemia by decreasing the water content and by shortening the slow component of T2. By analysis of the relaxation times and water content, we examined the pathophysiological characteristics of water molecules in ischemic brain tissue.
Regional cerebral blood flow changes associated with ethanol intoxication.
Authors: Mathew R J , Wilson W H
Published: June 2011

Regional cerebral blood flow (CBF) was measured via the 133Xenon inhalation technique in 26 healthy volunteers before and 60 minutes after the oral administration of ethyl alcohol or placebo on a double-blind basis. The cerebral blood flow values, corrected for test-retest differences in carbon dioxide showed a significant bilateral increase after ethanol administration. Blood levels of ethanol, estimated with a breath analyser, did not correlate with the CBF changes.