bluuebunny/crossref_metadata_2025 huggingface dataset:
The effect of graded hypoxia on the hippocampal slice: an in vitro model of the ischemic penumbra.
Authors: Schiff S J , Somjen G G
Published: June 2011

Submerged hippocampal slices were exposed to 30 minutes of moderate or mild hypoxia at 29 degrees C and then reoxygenated. Synaptic transmission was lost at the same rate in response to either grade of hypoxia, but recovery was faster following mild hypoxia. Hyperexcitability of synaptic transmission was a lasting feature following moderate hypoxia, but it was transient following mild hypoxia; after mild hypoxia the strength of synaptic transmission eventually returned to normal. Extracellular calcium did not change during moderate hypoxia. The extracellular pH of slices was always more acid than the bath; pH decreased further in response to both moderate and mild hypoxia. Extracellular potassium increased more during moderate than during mild hypoxia, and a period of rapid potassium uptake was also more pronounced following moderate hypoxia. Extracellular DC potential demonstrated a small positive shift during hypoxia, more so during mild hypoxia. These experiments suggest that synaptic function can be reversibly suppressed in mildly hypoxic brain tissue without severe depolarization of neurons; in addition, the degree and duration of posthypoxic hyperexcitability are correlated with the degree of hypoxia and the magnitude of the release of K+ from cells into their environment.
Hemoglobin concentration and prognosis in symptomatic obstructive cerebrovascular disease.
Authors: Wade J P , Taylor D W , Barnett H J , Hachinski V C
Published: June 2011

A total of 1,377 patients with symptomatic obstructive cerebrovascular disease (most commonly, internal carotid artery occlusion) entered a trial in which they were randomized to either medical or surgical (extracranial-intracranial bypass) therapy. All but 8 had hemoglobin estimations performed at entry. The patients were followed for an average of 55.8 months. In the medical group, the 325 patients with high normal hemoglobin concentration (15 g/l or more) suffered no more ischemic strokes than the 382 patients with lower values (less than 15 g/l). Those strokes that did occur were no more severe in the high than the low hemoglobin group. Hemoglobin concentration did not emerge as a prognostic factor in those patients treated surgically (n = 662). This prospective study counters the hypothesis that high normal hemoglobin concentration is associated with poor outcome in patients with symptomatic obstructive disease of the carotid and cerebral arteries.
Cerebral blood flows and tissue oxygen levels associated with maintenance of the somatosensory evoked potential and cortical neuronal activity in focal ischemia.
Authors: Coyer P E , Michele J J , Lesnick J E , Simeone F A
Published: June 2011

The middle cerebral artery was occluded in 18 cats to evaluate the physiological consequences of cerebral blood flow reductions on the somatosensory evoked potential, spontaneous neuronal activity, and oxygen availability in the ipsilateral and contralateral hemispheres. In the ipsilateral ectosylvian gyrus high-grade ischemia was produced as blood flow in the gray matter was reduced from 52.1 +/- 8.6 (mean +/- SE) to 13.3 +/- 9.0 ml/100 g/min and in the white matter from 33.8 +/- 5.6 to 6.1 +/- 6.4 ml/100 g/min. This significant reduction (p less than 0.05) was associated with abolition of the cortical component of the somatosensory evoked potentials. In all animals occlusion resulted in a predictable extended latency change and a variable amplitude response of the cortical component of the contralaterally recorded somatosensory evoked potentials. In 5 animals, oxygen availability was measured and spontaneous neuronal activity in the contralateral hemisphere was recorded. Volume expansion and hemodilution with either dextran or saline infusions elevated cerebral blood flow in the contralateral gray matter significantly (p less than 0.05) compared with the control and clip values. Ipsilateral spontaneous activity stopped within 4-12 minutes of occlusion, while contralateral spike activity persisted at rates at least equal to those recorded immediately following occlusion.
NMR-neuropathologic correlation in stroke.
Authors: DeWitt L D , Kistler J P , Miller D C , Richardson E P , Buonanno F S
Published: June 2011

True, three-dimensional proton nuclear magnetic resonance imaging at 0.147 tesla was performed postmortem on 2 patients embodying various stroke syndromes, including chronic (4 and 15 years) infarction, subacute (within 1 week) bland infarction, acute (2 days) hemorrhagic infarction, and hematoma secondary to ruptured aneurysm. A third patient, with subcortical arteriosclerotic encephalopathy, so-called Binswanger's disease, was examined antemortem using a 0.6 tesla scanner. Nuclear magnetic resonance images were reconstructed at levels matching the pathologic specimens. Qualitative and, when available, quantitative comparisons between the results of nuclear magnetic resonance imaging and pathology were carried out. Areas of qualitatively prolonged T1 and T2 relaxation times on nuclear magnetic resonance imaging were more extensive than the corresponding areas of chronic infarction noted pathologically and were determined to be infarcts plus the adjacent areas of Wallerian degeneration. Hemorrhagic infarction, without evidence of blood on computed tomography, was found to have mildly prolonged T1 and T2 relaxation times, between those of normal brain and chronic infarction; a 10-day-old hematoma had a very short T1, slightly shorter than that of white matter, and a mildly prolonged T2, with values between those of white and gray matter. Subcortical arteriosclerotic encephalopathy was found to have areas of prolonged T1 and T2 relaxation times involving almost the entire white matter of the corona radiata.
A brief episode of severe arterial hypertension induces delayed deterioration of brain function and worsens blood flow after transient multifocal cerebral ischemia.
Authors: Dutka A J , Hallenbeck J M , Kochanek P
Published: June 2011

Transient arterial hypertension occurs sporadically following cerebral air embolism and may occur during the acute phase of stroke. This study used an animal model of multifocal cerebral ischemia induced by air embolism and reversed by recompression to assess the effect of induced hypertension on the evoked response recovery, local cerebral blood flow, intracranial pressure, and brain water in 19 anesthetized dogs (Canis familiaris). Six received 0.4 ml of air via the internal carotid artery, 8 received intracarotid air and 10 micrograms/kg norepinephrine to produce transient hypertension, and 5 received intracarotid saline and norepinephrine. The average evoked response recovery in the air-only group was 58.3 +/- 7.7% (mean +/- SEM) of control after 4 hours of recompression; the air plus hypertension group recovery was 15.4 +/- 2.7% (p less than 0.01). The final evoked response in the dogs receiving hypertension alone did not differ from control values. Seven of 8 dogs in the air plus hypertension group had very low blood flows; only 1 of 4 in the air-only group had very low flows. The amount of brain water and the intracranial pressure were not detectably different at the end of treatment among all 3 groups. These results support a role for endothelial damage produced by air and hypertension in potentiating the process of postischemic hypoperfusion.
Motor performance in rats exposed to severe forebrain ischemia: effect of fasting and 1,3-butanediol.
Authors: Combs D J , D'Alecy L G
Published: June 2011

Functional assessment of animals following experimental cerebral ischemia is often difficult due to the passive nature of many neurologic exams. We attempted to increase the objectivity of motor function evaluation by adapting quantifiable behavioral tests and actively testing rats' motor capability following a cerebral ischemic insult. It was hypothesized that active testing would reveal motor deficits which were not readily apparent upon casual observation and that such testing would provide a more sensitive means of experimental neurologic assessment. Wistar rats were exposed to reversible severe forebrain ischemia using the four-vessel occlusion technique. Motor function was evaluated using the total motor score (sum of scores for screen test, balance beam test, and prehensile-traction test) over the 48 hours which followed 20 minutes of cerebral ischemia. To manipulate neurologic outcome, rats were fed or fasted the day prior to ischemia and then pretreated with either 1,3-butanediol or saline. Fasted saline-treated animals demonstrated improved total motor performance compared with fed animals by 48 hours after ischemia. There was no improvement in motor performance by fasted vs. fed rats from among the butanediol-treated animals. Pretreatment with butanediol resulted in significantly better total motor performance among fasted rats 24 hours after ischemia; however, by 48 hours postischemia, no difference was detectable. This is the first demonstration of motor deficits produced by four-vessel occlusion in rats. The motor tests devised appear to be adequately sensitive to detect changes in motor function that are not apparent with passive observation in this model.
Acute stroke therapy trials: an introduction to recurring design issues.
Authors: Sterman A B , Furlan A J , Pessin M , Kase C , Caplan L , Williams G
Published: June 2011

We discuss selected issues concerning the design of stroke treatment trials. Key issues include the type of stroke studied, the time interval from stroke onset to patient entry, and whether to include cardioembolic strokes and allow concomitant therapy.
Primary intracerebral hemorrhage and heart weight: a clinicopathologic case-control review of 218 patients.
Authors: Bahemuka M
Published: June 2011

The mean heart weight as a measure of arterial hypertension of patients who died from spontaneous intracerebral hemorrhage (primary intracerebral hemorrhage or PIH) was compared with that of controls from the same autopsy population. All patients with valvular or congenital heart disease or disease processes associated with myocardial infiltration were excluded. In 206 cases of PIH, hypertension was diagnosed if heart weight greater than or equal to the mean heart weight of autopsy controls for either sex, plus 1.5 SD. Only 94 (46%) of all cases of PIH were hypertensive by this criterion. However, hypertension was five times more frequent in the cases than in the controls. The site of hemorrhage was clearly defined in 183 cases (88.8%) only. Of these, 80 (43.7%) had lobar hemorrhage and 69 (37.7%) bled in the basal ganglia. Only 26 cases (12.6%) had evidence of previous cerebral or myocardial infarction and there was no instance of previous intracerebral hemorrhage. These data show that arterial hypertension was present in about half the cases of PIH and suggest that other as yet unidentified risk factors for PIH may be more common than is realized. Patients who died from PIH had been healthy all their lives with no evidence of cardiovascular or cerebrovascular disease, and the PIH was their first evidence of disease.
The natural history of lacunar infarction: the Oxfordshire Community Stroke Project.
Authors: Bamford J , Sandercock P , Jones L , Warlow C
Published: June 2011

In a consecutive series of 515 first-ever strokes in a community-based study of stroke that combined prompt clinical assessment by a study neurologist with a high rate of confirmed pathologic diagnosis, 108 cases (21%) had a lacunar syndrome. A computed tomography (CT) scan was performed in 104 (96%) of these cases. Only 3 cases had primary intracerebral hemorrhage, and another 3 had "inappropriate" areas of infarcts were seen in 34 of the remaining 98 (35%) CT scans. The crude annual incidence of lacunar infarction was 0.33/1,000. There was no excess risk among men. The case fatality rates were 1% at 1 month and 9.8% at 1 year. The rate of recurrent strokes was 11.8% in the first year. Among patients surviving 1 year, 66% were capable of independent existence.
Acute stroke, hematocrit, and blood pressure.
Authors: LaRue L , Alter M , Lai S M , Friday G , Sobel E , Levitt L , McCoy R , Isack T
Published: June 2011

A population-based study of the relation between hematocrit and stroke subtype was carried out among 2,077 individuals using the Lehigh Valley Stroke Register. This register identifies all stroke patients admitted to the 8 acute care hospitals serving the Lehigh Valley area of eastern Pennsylvania-western New Jersey. The mean hematocrit was higher in patients with lacunes than with thrombotic or embolic strokes (p = 0.02). However, when blood pressure was also considered the increase in hematocrit in patients with lacunar stroke was significant only when systolic hypertension (greater than or equal to 150 mm Hg) was also present (p = 0.029); no significant difference in hematocrit was found between stroke subtypes in normotensive individuals. Therefore, we cannot exclude the possibility that hypertension interacts with hematocrit in accounting for the observed association with lacunar infarcts. There was no trend for increased in-hospital mortality for stroke patients in either the low (less than or equal to 30, 30-36%) or high (greater than or equal to 47%) hematocrit groups.
Comparison of thermal clearance measurement of regional cerebral blood flow with radiolabelled microspheres.
Authors: Hoehner P J , Dean J M , Rogers M C , Traystman R J
Published: June 2011

A thermal clearance technique for measuring cerebral blood flow is described and compared with the radiolabelled microsphere technique. The thermal technique involves measurement of the rewarming curve generated after bolus infusion of 4-5 ml of ice-cold saline into the common carotid artery with a subdural thermistor placed on the parietal cortex. Evaluation of the biexponential decay curves obtained with this technique demonstrated a close correlation with total hemispheric, parietal, and parietal gray blood flow determined by simultaneous microsphere measurement. Despite significant correlations (p less than 0.001), scatter in the data produced a broad 95% confidence interval, thus making interpretation of blood flow with the thermal clearance technique impossible. Furthermore, instrumentation with the thermal probe, which required opening of the dura, blunted the cerebral blood flow response to hypercapnia. We conclude that the major limitations of the thermal clearance technique include: nonhomogeneous clearance function, significant variability, and depression of CO2 reactivity. These limitations must be addressed before this technique can be used reliably in the laboratory.
Indomethacin, prostacyclin, and heparin improve postischemic cerebral blood flow without affecting early postischemic granulocyte accumulation.
Authors: Kochanek P M , Dutka A J , Hallenbeck J M
Published: June 2011

Six anesthetized dogs treated with indomethacin, prostacyclin (PGI2), and heparin were compared with 7 anesthetized controls (ischemia without treatment) to determine whether cyclooxygenase inhibition would lead to enhanced granulocyte accumulation because of preferential formation of lipoxygenase products. Cortical somatosensory evoked response, [14C]iodoantipyrine autoradiographic blood flow, and 111In-labelled granulocyte accumulation were compared 4 hours after a 60-minute exposure to multifocal brain ischemia. Treatment with indomethacin, PGI2, and heparin eliminated neuron-disabling brain blood flows without altering early postischemic granulocyte accumulation. Granulocyte accumulation after 4 hours of reperfusion was not significantly different in control and treated dogs. The final amplitude of the cortical somatosensory evoked response in the treated group averaged 38.0 +/- 13.6% (mean +/- SEM) of the corresponding baseline value compared with 21.0 +/- 4.6% in the control group, but this difference was not significant.
Evaluation of kinetic therapy in the prevention of complications of prolonged bed rest secondary to stroke.
Authors: Kelley R E , Vibulsresth S , Bell L , Duncan R C
Published: June 2011

We performed a prospective, controlled study of kinetic therapy in acute, severe stroke. This therapy involved continuous mobilization of a bedridden patient by means of a specially designed rotating bed. All patients with acute stroke presenting to the Neurology Service over an 18-month period were screened, and those that qualified were assigned to confinement in either a routine hospital bed or a rotating bed. We found that the most common complication of stroke with bed confinement of 4 days or longer was bacterial infection consisting of either pneumonia, sepsis, or urinary tract infection. The two variables found to be of greatest significance in affecting the rate of infection were length of bed confinement, especially for greater than 13 days (2.3-fold increased risk, p less than 0.04), and placement in a routine hospital bed (2.9-fold increased risk, p = 0.023).
Regression of carotid stenoses after corticosteroid therapy in occlusive thromboaortopathy (Takayasu's disease).
Authors: Ishikawa K , Yonekawa Y
Published: June 2011

A 34-year-old, single Japanese woman with active Takayasu's disease presented with stenosed bilateral common carotid arteries, subtotal occlusion of the left subclavian artery, and complete occlusion of the ipsilateral proximal vertebral artery, as demonstrated by angiography. A right subclavian-left vertebral bypass using an autologous saphenous vein graft was successfully performed after 36 days of corticosteroid therapy. Subsequently, warfarin was administered in addition to prednisolone. After 32 months of treatment with a gradual reduction from 50 to 3.75 mg of prednisolone daily, angiography revealed a functioning bypass graft and regression of bilateral common carotid stenoses.
Distribution of the occipital branches of the posterior cerebral artery. Correlation with occipital lobe infarcts.
Authors: Marinković S V , Milisavljević M M , Lolić-Draganić V , Kovacević M S
Published: June 2011

The occipital branches of the posterior cerebral artery were examined in 31 human brains. The authors determined the origin, course, and region of supply of each occipital branch: the parieto-occipital, calcarine, posterior temporal, and common temporal arteries, as well as the lingual gyrus artery. These vessels were found in all the brains examined except the lingual gyrus artery, which was present in only 8.3%. The occipital branches were noted to supply variable cortical regions. In addition, they sometimes took part in irrigation of deep forebrain structures. It was concluded that occlusion of a certain occipital artery may cause varying clinical signs and symptoms in different patients. The neurologic deficits that may occur following the isolated occlusion of individual occipital branches of the posterior cerebral artery are discussed.
Regional brain sodium, potassium, and water changes in the rat middle cerebral artery occlusion model of ischemia.
Authors: Young W , Rappaport Z H , Chalif D J , Flamm E S
Published: June 2011

Middle cerebral artery occlusions (MCAo) in rats produce infarcts in the pyriform and frontoparietal cortex, extending into the lateral basal ganglia and parasagittal cortex. We estimated tissue H2O concentrations from wet and dry weight measurements and determined Na and K concentrations by atomic absorption spectroscopy in these areas of rat brains. Tissue samples were analyzed at 2, 4, and 24 hours after MCAo and sham MCAo, compared with normal values measured in unoperated rats. In the pyriform and frontoparietal areas, H2O concentrations increased to 34 and 7% greater than normal by 2 hours, and 89 and 94% by 24 hours after MCAo. Na concentrations rose in these areas to 73 and 37% greater than normal by 2 hours, and 281 and 330% by 24 hours. K concentrations did not change until 4 hours, but fell to 62 and 34% of normal in these areas by 24 hours. Such large ion shifts indicate severe tissue destruction. In the parasagittal cortex and basal ganglia areas, the ion and water changes were smaller and did not become significant until 24 hours after MCAo. Rates of Na entry into the infarct site were greatest at 0-2 hours, while the rates of K loss peaked later, between 2 and 4 hours. The difference in Na influx and K efflux resulted in net ion shifts that correlated highly with water entry, yielding a correlation coefficient of 0.992 (p less than 0.001) and a slope indicating that 1 ml of water entered the tissue with each 145 mumoles of ions. These findings strongly suggest that net ion shifts cause the early edema of regional brain ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
Effect of the thromboxane A2 mimetic U 46619 on pial arterioles of rabbits and rats.
Authors: Haberl R L , Heizer M L , Ellis E F
Published: June 2011

Our previous experiments have shown that thromboxane A2 is a strong contractor of cerebral arterial smooth muscle strips. The objective of these experiments was to determine if U 46619, a stable thromboxane A2 mimetic, affects the cerebral microcirculation in vivo. Pial arteriole diameter in rabbits and rats was measured with a microscope using the closed cranial window technique. Topical application of 10(-11) to 10(-6) M U 46619 induced dose-dependent arteriole vasoconstriction in both species. In rabbits and rats the maximum vasoconstriction was 9.7 +/- 1.3% (mean +/- SEM) and 14.0 +/- 0.5%, respectively. In rats, 10(-7) and 10(-6) M U 46619 induced intravascular platelet aggregation accompanied by a further decrease in diameter and transient occlusion of the arterioles and venules. U 46619 had no significant effect on rabbit pial arterioles that were predilated by hypercapnia or hypercapnia plus hypoxia. Our data suggest that in animals with a normal vasculature, thromboxane A2 may be a moderate constrictor of cerebral arterioles and that this constrictor effect is prevented by hypercapnia and hypoxia.
Middle cerebral artery occlusion: correlation of computed tomography and angiography with clinical outcome.
Authors: Saito I , Segawa H , Shiokawa Y , Taniguchi M , Tsutsumi K
Published: June 2011

The clinical outcome of 40 cases with middle cerebral artery (MCA) occlusion was examined in relation to the site of occlusion and the findings on computed tomography (CT). Patients were treated conservatively without surgery. A few had decompressive craniotomy when necessary. Outcome in 7 (18%) was good, in 6 (15%) moderate, and in 15 (38%) severe; 12 (30%) died by the follow-up at 3 months. In cases with occlusion at the origin of the MCA, hypodensity on CT scan was usually localized to the basal ganglia, presumably because of collateral circulation through the anterior cerebral arteries; the outcome in these patients was not always favorable. Cases with occlusion of the trunk or branch vessels always showed marked CT hypodensity, and clinical outcome was poor. To assess quantitatively the extent of collateral circulation, the conduction time of contrast medium from the intracranial siphon (IC) to the insular portion of the MCA (M2) through the anterior cerebral arteries was calculated on serial carotid angiograms obtained within 24 hours after stroke onset. An IC-M2 time of 5 seconds was a critical indicator of whether extensive CT hypodensity would develop (the rule of 5 seconds). Furthermore, this method predicted the appearance and extent of infarction before CT revealed hypodensity. The significance of acute reconstructive surgery is also discussed.
Protective effects of combined superoxide dismutase and deferoxamine on recovery of cerebral blood flow and function after cardiac arrest in dogs.
Authors: Cerchiari E L , Hoel T M , Safar P , Sclabassi R J
Published: June 2011

Oxygen free radicals generated during reoxygenation after cardiac arrest may impair recovery of cerebral blood flow and function. In a randomized study in vivo, we tested the following anti-free radical combination therapy administered at the beginning of cardiopulmonary resuscitation after apnea-induced cardiac arrest of 7 minutes: 1) ventilation with 100% nitrogen for 30 seconds to allow the delivery of therapy before oxygen, 2) 10 mg/kg i.a. superoxide dismutase followed by 10 mg/kg i.v. over 1 hour to scavenge the superoxide anion radical, and 3) 20 mg/kg i.v. deferoxamine over 1 hour to prevent membrane lipid peroxidation. We evaluated the effects of this combined treatment on the recovery of cardiovascular variables, cerebral blood flow and oxygen consumption, and somatosensory evoked potentials in 20 dogs 6 hours after resuscitation. Compared with standard treatment (n = 10), the combined treatment (n = 10) did not affect cardiovascular variables, significantly mitigated cerebral blood flow changes after cardiac arrest, and enhanced recovery of somatosensory evoked potentials. We conclude that oxygen free radicals play a role in the pathogenesis of the arrest-related derangements of cerebral blood flow and function that are effectively reduced by this combined treatment; we recommend evaluation of its components in outcome studies.
Endothelium-dependent relaxation of canine basilar arteries. Part 1: Difference between acetylcholine- and A23187-induced relaxation and involvement of lipoxygenase metabolite(s).
Authors: Kanamaru K , Waga S , Kojima T , Fujimoto K , Itoh H
Published: June 2011

Vascular responses to acetylcholine (ACh) and the calcium ionophore A23187 were studied in rings of canine basilar arteries. In preparations that were precontracted to a stable plateau by 3 X 10(-6) M prostaglandin F2 alpha (PGF2 alpha), 10(-9) to 10(-7) M A23187 elicited significant relaxation of the basilar arteries if the endothelium was intact. Judging from histologic findings, the ability of a ring to relax in this manner is due to the presence of the endothelium. The same concentration of A23187 did not relax vascular tissues in which the endothelium was purposely disrupted. Although 10(-7) to 10(-3) M ACh did not sufficiently produce endothelium-dependent relaxation of canine basilar artery rings, ACh in the same concentration did produce significant relaxation in canine femoral rings. Our results suggest that the sensitivity of the muscarinic receptor of cerebral arteries appears to be appreciably different from that of peripheral (femoral) arteries. Pretreatment with 1.5 X 10(-5) M indomethacin, a cyclooxygenase inhibitor, potentiated the contractile responses produced by PGF2 alpha in intact rings. Preincubation with the lipoxygenase inhibitors nordihydroguaiaretic acid at (NDGA) at 1.5 X 10(-5) M or AA861 at 10(-5) M prevented A23187-induced relaxation. The same concentration of NDGA and AA861 did not affect endothelium-independent relaxation induced by glyceryl trinitrate. We suggest that endothelium-dependent relaxation of the canine basilar artery by A23187 may be mediated by noncyclooxygenase metabolite(s).
Lateral pontine hemorrhage: reappraisal of benign cases.
Authors: Del-Brutto O H , Noboa C A , Barinagarrementería F
Published: June 2011

We reviewed 6 computed tomography-documented cases of primary lateral pontine hemorrhage that occurred in our two institutions over a 2-year period. All patients survived the acute stroke, with excellent functional recovery in 4. The level of consciousness of the patient and the size of the hemorrhage had no consistent bearing on outcome. Both of these features have been considered important prognostic indicators in patients with pontine hemorrhage, but in our series benign outcomes were not restricted only to patients who were alert or had small hemorrhages; on the other hand, severe disability was noticed in 1 patient with a small hematoma strategically located in the pontine tegmentum. Our observations suggest that, although some patients with lateral pontine hemorrhage have a good prognosis, there is no single determinant that predicts outcome in a given patient.
Mechanisms of intracranial hemorrhage in infective endocarditis.
Authors: Hart R G , Kagan-Hallet K , Joerns S E
Published: June 2011

Analysis of 17 patients with infective endocarditis and intracranial hemorrhage yielded several different mechanisms of bleeding. Nine of 15 (60%) symptomatic intracranial hemorrhages occurred within 48 hours of admission and 3 more (20%) after hospital discharge. In 7 patients with Staphylococcus aureus endocarditis, symptomatic intracranial hemorrhage occurred within 48 hours of admission and resulted from septic arteritis in all 3 examined pathologically. Secondary hemorrhagic transformation (hemorrhagic infarction) was asymptomatic in 2 nonanticoagulated patients but was associated with clinical worsening in 2 anticoagulated patients. Anticoagulation potentially contributed to intracranial hemorrhage in 4 of the 17 patients (24%). Proven mycotic aneurysms were present in only 2 patients (12%), 1 of whom presented with massive, fatal intracranial hemorrhage. Mycotic aneurysms amenable to surgery are uncommon and underlie only a fraction of intracranial hemorrhages in infective endocarditis.
Expanding cerebellar lacunes due to dilatation of the perivascular space associated with Binswanger's subcortical arteriosclerotic encephalopathy.
Authors: Benhaïem-Sigaux N , Gray F , Gherardi R , Roucayrol A M , Poirier J
Published: June 2011

An 80-year-old hypertensive woman developed right hemiplegia and died 24 hours after admission. Neuropathologic examination revealed multiple cerebral infarcts of various ages and diffuse subcortical arteriosclerotic encephalopathy. Clusters of asymptomatic "expanding" lacunes, due to dilatation of the perivascular spaces, were found in both dentate nuclei. These cavities, which presented as space-occupying lesions, were surrounded by a single layer of flattened cells and contained 1 or more sections of normal-looking arterioles. Such a topographic grouping of lacunes in the dentate nucleus has not been described previously. The mechanism of widening of the perivascular compartment remains unclear; its occurrence in a hypertensive patient and its association with typical Binswanger's subcortical arteriosclerotic encephalopathy and severe atherosclerosis with multiple infarcts suggest a common pathophysiologic mechanism possibly including an alteration of the blood-brain barrier.
Somatosensory evoked potentials in lacunar syndromes of pure motor and ataxic hemiparesis.
Authors: Kelly M A , Perlik S J , Fisher M A
Published: June 2011

Syndromes of hemiparetic lacunar infarction include pure motor hemiparesis and ataxic hemiparesis. Twelve such patients were evaluated with somatosensory evoked potentials. Potentials were delayed or absent in all 4 patients with ataxic hemiparesis and in 1 of 8 patients with pure motor hemiparesis. Unlike pure motor hemiparesis, ataxic hemiparesis appears to be associated with abnormal somatosensory evoked potentials. These abnormalities suggest that disturbance of afferent pathways are important in ataxic hemiparesis.
Regional cerebral palmitate incorporation following transient bilateral carotid occlusion in awake gerbils.
Authors: Tone O , Miller J C , Bell J M , Rapoport S I
Published: June 2011

[14C]Palmitate was injected intravenously in awake gerbils at various times after 5 minutes of bilateral carotid artery occlusion or a sham operation. Regional rates of incorporation of plasma palmitate into the hippocampus and other regions of the anterior circulation were determined relative to the mean rate of incorporation into regions of the posterior circulation using quantitative autoradiography and a ratio method of analysis. One day after bilateral carotid occlusion, relative palmitate incorporation was elevated significantly by 16% in the CA4 pyramidal cell layer and by 20% in the dentate gyrus of the hippocampus compared with sham-operated gerbils. At 3 days, significant elevations of this magnitude were found in the CA3 and CA4 cell layers, whereas relative incorporation was reduced by 26% in the CA1 pyramidal cell layer. At 7 days, the only significant difference from control was a 15% elevated incorporation in the CA3 pyramidal cell layer. Histologic examination indicated substantial cell death in the CA1 pyramidal layer at 3 days, with extensive glial reaction and phagocytic invasion at 7 days. Our results suggest that the turnover of palmitate-containing lipids is reduced in the CA1 layer of the gerbil hippocampus but that lipid synthesis is stimulated in hippocampal regions (CA3, CA4, dentate gyrus) affected by but recovering from transient bilateral carotid occlusion.
Early component changes in corticomotor evoked potentials following experimental stroke.
Authors: Simpson R K , Baskin D S
Published: June 2011

Corticomotor evoked potentials have recently been used in experimental animals and patients as a measure of neurologic function after stroke. However, little is known about the fundamental electrophysiologic properties contributing to the formation of these potentials. To define some of these properties, corticomotor evoked potentials were recorded from the contralateral hindlimb in response to transcortical stimulation in cats anesthetized with halothane. These potentials were obtained hourly for 6 hours after middle cerebral artery occlusion. Four major identifiable components were recorded in control responses. Immediately after infarction, all component amplitudes were significantly attenuated. However, after approximately 5 hours, the early latency components exceeded control values; late latency components were also increased. Corresponding somatosensory evoked potentials were abolished and did not return throughout the recording session. Based on classic neurophysiologic studies, the amplitude increment can be explained as combined activation of low-threshold brainstem facilitatory centers and/or direct activation of subcortical axonal pathways. With further study, corticomotor evoked potentials may be a valuable adjunct to current electrophysiologic monitoring techniques, particularly with regard to defining the extent and location of an infarct, as well as to assessing functional recovery.
In vivo studies of pial vascular permeability to sodium fluorescein: absence of alterations by bradykinin, histamine, serotonin, or arachidonic acid.
Authors: Watanabe M , Rosenblum W I
Published: June 2011

We studied pial vessels in vivo in mice, examining under mercury light the permeability of these vessels to sodium fluorescein. Topical application of hypertonic solutions of NaCl caused leakage of fluorescein. However, putative chemical mediators of leakage, such as histamine, serotonin, arachidonic acid, and bradykinin, all failed to increase permeability to the dye. Apparent increases in permeability only accompanied endothelial damage caused by the dye + light combination, as indicated by production of local platelet aggregates. The technique is useful, provided inadvertent endothelial injury is recognized and avoided. The data in mice suggest that pial vessels may not participate in the permeability changes reportedly produced in parenchymal brain vessels by several of the mediators we tested. Therefore, studies of pial vascular permeability are not expected to provide reliable data concerning the actions of agents that might mediate cerebral edema.
Stroke in blacks.
Authors: Gillum R F
Published: June 2011

In an attempt to answer unresolved questions and to suggest directions for future research concerning stroke in black populations, data from the National Center for Health Statistics were examined and published studies were reviewed. Stroke was the third leading cause of death among U.S. blacks in 1982, accounting for 18,698 deaths, 8.25% of the total. Black men aged 35-74 years were 2.5 times and black women 2.4 times as likely as whites to die of stroke. A long-term decline in stroke mortality rates continued through 1982, with the declines since 1968 probably due to improved hypertension control. Data on morbidity trends are lacking. About 7% of black men and 11% of black women in the U.S. noninstitutionalized population aged 65 and over reported having had a stroke in 1977, black women having the highest prevalence of any group. In several studies, black women had higher incidence rates of stroke than white women in each age group. Black men had higher incidence rates than whites up to age 75 years. Survivorship and outcome following stroke may have been poorer in blacks than in whites. Advanced age and elevated blood pressure were the only putative risk factors for stroke for which published data were adequate to firmly establish the association in blacks. Thus, data are needed to examine trends in stroke incidence and survivorship in blacks and to assess the relation of many variables to the risk of stroke.
Stroke in thyrotoxicosis with atrial fibrillation.
Authors: Petersen P , Hansen J M
Published: June 2011

Chronic atrial fibrillation is associated with an increased risk of stroke. In elderly patients with thyrotoxicosis, atrial fibrillation is frequently encountered, and the true risk of cerebrovascular events in these patients is controversial. We retrospectively studied 610 patients with initially untreated thyrotoxicosis, 91 (14.9%) of whom had atrial fibrillation, with the highest frequency in the elderly patients. The risk of cerebrovascular events, with special attention to the first year after the diagnosis of thyrotoxicosis, was calculated using logistic regression methods with age, sex, and atrial fibrillation as independent variables. Only age was an important risk factor (p less than 0.005), whereas sex and atrial fibrillation were not significant (p = 0.09 and p = 0.17, respectively) as independent risk factors. This is contrary to other studies of patients with thyrotoxic atrial fibrillation, and the need for further clarification of this issue is clear. From our study the indication for prophylactic treatment with anticoagulants for prevention of stroke in thyrotoxic atrial fibrillation seems doubtful, especially as no controlled studies of such treatment in patients with atrial fibrillation are currently available.
Presynaptic and postsynaptic alpha 2-adrenergic receptors in human cerebral arteries and their alteration after subarachnoid hemorrhage.
Authors: Tsukahara T , Taniguchi T , Miwa S , Shimohama S , Fujiwara M , Nishikawa M , Handa H
Published: June 2011

The nature of alpha-adrenergic receptors in human cerebral arteries was characterized, and alteration of these receptors after subarachnoid hemorrhage was examined using a radioligand binding assay. Norepinephrine content of control arteries was also analyzed and compared with that of arteries after subarachnoid hemorrhage. Norepinephrine content in human cerebral arteries in cases of subarachnoid hemorrhage was about 5% of the control group. Specific binding of [3H]yohimbine, a selective alpha 2-antagonist, to cerebral arteries of the control group indicated two classes of binding sites: high-affinity sites with KD of 0.5 nM and Bmax of 18 fmol/mg protein and low-affinity sites with KD of 29 nM and Bmax of 248 fmol/mg protein. In cerebral arteries obtained from the subarachnoid hemorrhage group, [3H]yohimbine binding sites were of a single class with KD of 53 nM and Bmax of 456 fmol/mg protein. These results suggest that sympathetic denervation and subsequent alterations in alpha 2-adrenergic receptors occurred after subarachnoid hemorrhage in human cerebral arteries. These changes in sympathetic innervation to cerebral arteries were considered to be one of the antecedents of delayed vasospasm after subarachnoid hemorrhage.
Intra-arterial thrombolytic therapy improves outcome in patients with acute vertebrobasilar occlusive disease.
Authors: Hacke W , Zeumer H , Ferbert A , Brückmann H , del Zoppo G J
Published: June 2011

In this retrospective analysis we report our treatment experience in 65 consecutive patients with clinical signs of severe brainstem ischemia with angiographically demonstrated thrombotic vertebrobasilar artery occlusions who received either local intra-arterial thrombolytic therapy (urokinase or streptokinase) (43 patients) or conventional therapy (antiplatelet agents or anticoagulants) (22 patients). We analyzed the data with respect to cerebral artery occlusion patterns, posttreatment arterial recanalization, and the clinical categories of favorable/unfavorable outcome and survival/death. In subgroup analyses, recanalization in patients who received thrombolytic therapy correlated significantly with clinical outcome; in 19 of 43 patients, recanalization was demonstrated angiographically, while in 24 patients the occlusion persisted. All patients without recanalization died, but 14 of the 19 patients displaying recanalization survived (p = 0.000007), 10 with a favorable clinical outcome. Only three of the 22 patients who received conventional therapy survived, all with a moderate clinical deficit. When we compared the treatment groups, highly significant differences in both outcome quality (p = 0.017) and survival (p = 0.0005) were found to depend on establishing recanalization. Our data support the concept that technically successful thrombolysis of vertebrobasilar artery occlusions is associated with beneficial clinical outcome.
Baseline and activated platelet cytoplasmic ionized calcium in acute ischemic stroke. Effect of aspirin.
Authors: Joseph R , Welch K M , Grunfeld S , Oster S B , D'Andrea G
Published: June 2011

We measured cytoplasmic ionized calcium concentrations [( Cai2+]) in aequorin-loaded gel-filtered platelets from 38 patients with acute occlusive stroke (12 treated with aspirin, 26 untreated) and 25 healthy controls. Compared with controls, baseline [Cai2+] was higher in untreated patients (p less than 0.002), maximal 36-72 hours after the onset of neurologic dysfunction (p less than 0.0001), in those patients with as well as those without major stroke risk factors. The increase in [Cai2+] after stimulation with 0.5 and 1.0 unit/ml thrombin (p less than 0.05), 2 and 4 micrograms/ml collagen (p less than 0.02), and 0.5 and 1.0 mM platelet activating factor (p less than 0.05) were also greater in untreated patients, but the profiles of these changes were parallel to those in controls. Even though the platelets of stroke patients are more sensitive to activation, they are functionally similar to those of controls. Aspirin treatment reduced baseline [Cai2+] as well as thrombin- and collagen-induced [Cai2+] changes. Platelet activating factor-induced increase in [Cai2+] was not altered by aspirin treatment. Our results suggest that the usefulness of aspirin in stroke is limited because aspirin does not suppress platelet responsiveness to all in vivo thrombogenic stimuli. Specific platelet activating factor antagonists may prove to be useful therapeutic agents in stroke.
A new model for inducing transient cerebral ischemia and subsequent reperfusion in rabbits without craniectomy.
Authors: Molnár L , Hegedüs K , Fekete I
Published: June 2011

An artificial ball removable by an attached fiber was injected into the middle cerebral artery (MCA) of 16 rabbits, allowing the study of transient (5, 10, 15, or 30 minutes) cerebral ischemia without craniectomy. Measurements of available oxygen (aO2) in the ischemic core (the ventral part of the temporal area) followed by histologic examination verified the embolization. Electroencephalographic power spectra and steady (direct current) potentials were recorded bilaterally on the convexity remote from the actual lesion but still supplied by the MCA. Local cerebral blood flow and aO2 in the border zone between the anterior cerebral artery and the occluded MCA were measured. Embolization caused typical ischemic changes ipsilaterally and alterations characteristic of diaschisis contralaterally. Extreme border zone hyperemia developed without significant aO2 changes in the same region. Restoration of circulation via the circle of Willis induced gradual normalization. Our model for controlled embolization and recirculation proved suitable for detailed studies of the complex changes in brain function caused by transient ischemia.
Stable prostacyclin analogue preventing microcirculatory derangement in experimental cerebral ischemia in cats.
Authors: Tanaka K , Gotoh F , Fukuuchi Y , Amano T , Suzuki N , Uematsu D , Kawamura J , Yamawaki T , Itoh N , Obara K
Published: June 2011

We evaluated the effect of a stable synthetic prostacyclin analogue, TRK-100, on the microcirculatory derangement occurring in feline pial vessels with endothelial damage after middle cerebral artery occlusion. Fifteen adult cats were divided into an untreated group (Group 1, n = 8) and a treated group (Group 2, n = 7). Thirty minutes after 10 minutes of ultraviolet irradiation, which selectively damaged endothelium in the pial vessels, the middle cerebral artery was occluded in both groups and maintained for 30 minutes. In Group 2, 50 ng/kg/min TRK-100 was continuously infused intravenously following ultraviolet irradiation. In both the pial arteries and veins, platelet aggregate adhesion to the endothelium with subsequent thrombus formation was significantly (p less than 0.01 and p less than 0.05, respectively) inhibited during middle cerebral artery occlusion in Group 2 compared with Group 1. Similarly, blood flow stasis in the pial veins was effectively prevented in Group 2 during occlusion. Furthermore, the pial artery diameter returned to the control level during the late period of occlusion, whereas in Group 1 the pial artery remained constricted. Our data suggest that TRK-100 can prevent microcirculatory derangement in the acute stage of ischemic stroke.
Effect of aminophylline on postischemic edema and brain damage in cats.
Authors: Seida M , Wagner H G , Vass K , Klatzo I
Published: June 2011

We attempted to ameliorate postischemic edema and brain tissue injury in cats by administering aminophylline to reduce the reactive hyperemia that supposedly aggravates both these sequelae. Forty-one cats were subjected to 1 hour of middle cerebral artery occlusion and were killed after 3 hours, 3 days, or 14 days of recirculation; one half of the cats received 0.916 ml/kg of a 25 mg/ml solution of aminophylline by infusion at a constant rate via the femoral vein starting 10 minutes before release of the occlusion and continuing for 5 minutes after initiation of recirculation; the other half received saline. Regional cerebral blood flow was monitored by the hydrogen clearance method and water content was evaluated by specific gravity measurements after 3 hours of recirculation; the status of the blood-brain barrier was assessed with Evans blue tracer. Morphologic observations were carried out in cats killed after 3 or 14 days of recirculation. Aminophylline-treated cats killed after 3 hours of recirculation showed significantly reduced hyperemia and edema and no leakage of Evans blue, which was present in all untreated cats killed after 3 hours or 3 days of recirculation. Morphologic observations revealed conspicuously more severe ischemic brain tissue damage in the untreated than in the aminophylline-treated cats after 3 and 14 days of recirculation. Our studies indicate the beneficial effect of administration of aminophylline in the amelioration of postischemic edema and brain tissue injury, which is presumably achieved by reduction of reactive hyperemia.
Dementia due to vascular disease--a multifactorial disorder.
Authors: Scheinberg P
Published: June 2011

This review was undertaken to evaluate critically the literature pertaining to vascular dementia with the objective of determining a more useful and scientifically supported definition of vascular dementia, its relation to other causes of dementia, and the biologic mechanisms involved in its causation.