bluuebunny/crossref_metadata_2025 huggingface dataset:
Cerebral venous blood gas tensions in elevated intracranial pressure.
Authors: Grady P A , Blaumanis O R
Published: June 2011

Cerebral venous blood gas tensions were correlated with elevated intracranial pressure in spontaneously breathing dogs lightly anesthetized with nitrous oxide/halothane. Intracranial pressure was elevated by infusion of artificial cerebrospinal fluid into a lateral ventricle. Respiration and blood pressure were monitored. The results of these experiments indicate that cerebral venous carbon dioxide tension is increased in association with elevation in intracranial pressure. Moreover, it appears that cerebral venous pCO2 is effectively regulated at a mean of about 52 mm Hg over a wide range of intracranial pressure.
Effects of oxygen and glucose deprivation on vasoactivity in isolated bovine middle cerebral arteries.
Authors: Vinall P E , Simeone F A
Published: June 2011

The effects of oxygen and glucose deprivation on vasoactivity were investigated using helical strips of bovine middle cerebral artery. Hypoxia, created by reducing the PO2 of the bath, or oxidative inhibition with 2,4 dinitrophenol (DNP) or sodium azide, significantly reduced contractions induced by serotonin. Normal tonic contractions induced with fresh and aged whole blood, or 5-HT became phasic and quickly relaxed to baseline in a hypoxic environment. Glucose elimination from the Krebs medium, or the inhibition of the glycolytic pathway with iodoacetic acid (IAA), did not significantly reduce serotonin-induced contractions. However, contractions were inhibited more with the combination of oxygen and glucose deprivation, or DNP + IAA, than with oxygen deprivation alone. Efforts to produce rigor in this preparation by oxygen/substrate reduction or metabolic inhibition were unsuccessful. Tonic contractions induced by 70 mM potassium became phasic as the Ca++ concentration was reduced. Contractions resulting from the readdition of Ca++ to arteries exposed to calcium-free high potassium solution were significantly reduced in the presence of oxidative and/or glycolytic inhibitors. The uptake of 45Ca++, as measured by the lanthanum technique, decreased as the bath PO2 was reduced in both serotonin stimulated and unstimulated arteries. Glucose deprivation alone did not affect 45Ca++ uptake. This study suggests that hypoxia has a direct inhibitory affect on cerebral vasoactivity mediated by reductions in sarcoplasmic Ca++ uptake.
Effect of Fluosol on oxygen availability, regional cerebral blood flow, and infarct size in a model of temporary focal cerebral ischemia.
Authors: Kolluri S , Heros R C , Hedley-Whyte E T , Vonsattel J P , Miller D , Zervas N T
Published: June 2011

Twenty-four cats had an intravenous infusion of either Fluosol or saline and then were subjected to 2 hours of middle cerebral artery occlusion. All the animals infused with Fluosol and one-half the animals infused with saline were ventilated with 100% O2. Tissue oxygen availability and regional cerebral blood flow were measured by platinum electrodes using direct voltage recordings for oxygen measurements and hydrogen clearance curves for measurements of cerebral blood flow. With 100% oxygenation tissue oxygen availability increased significantly in the Fluosol treated animals, however, during the time of ischemia oxygen availability decreased below baseline values to about an equal level whether the animals were treated with Fluosol or saline. Regional cerebral blood flow fell to a similar value in all groups during the time of occlusion. One hour after reperfusion blood flow increased considerably above baseline values in all groups and oxygen availability also increased in all groups but particularly in the Fluosol treated animals. Overall mortality and the size of infarction 1 week after the ischemic insult were not significantly different in the three groups. Mortality was directly related to the size of the infarct which, in turn, was related to the degree of ischemia during the time of occlusion.
Cerebral ischemia and asymptomatic coronary artery disease: a prospective study of 83 patients.
Authors: Di Pasquale G , Andreoli A , Pinelli G , Grazi P , Manini G , Tognetti F , Testa C
Published: June 2011

A prospective cardiologic evaluation was performed in 83 consecutive patients with transient cerebral ischemia or mild stroke and without symptoms or electrocardiographic signs of ischemic heart disease. Patients were studied with an electrocardiographic exercise test; a positive test was followed by exercise Thallium-201 myocardial scintigraphy. Results were compared to those obtained in a group of 83 age and sex-matched healthy subjects submitted to the same study protocol. Asymptomatic coronary artery disease was detected in 28% of cerebrovascular patients with adequate electrocardiographic exercise test. A scintigraphic perfusion defect of variable extension was found in 19 of them. In the control group the electrocardiographic exercise test was positive in only 6% (p less than 0.01). Our results support the concept that: asymptomatic ischemic heart disease is often associated with cerebrovascular disease; therefore cerebral ischemic attacks may be a marker of coronary artery disease, an active investigation of the heart should be considered in cerebrovascular patients in order to plan optimal, comprehensive management.
Atherosclerotic disease of the middle cerebral artery.
Authors: Bogousslavsky J , Barnett H J , Fox A J , Hachinski V C , Taylor W
Published: June 2011

Three hundred and fifty-two patients with atherosclerotic middle cerebral artery stenosis (MCAS, 53%) or occlusion (MCAO, 47%) have been systematically studied. The study involved all patients entered into the EC/IC Bypass Study with isolated MCA disease or a tandem lesion predominating in the MCA ipsilateral to the ischemic events (18 patients with a tandem lesion of greater magnitude in the internal carotid artery were not included). The Asian patients represented 58% of all Asians entered into the EC/IC Bypass Study, whereas the white patients represented 18% of all whites and the black patients 34% of all blacks. Isolated TIAs were less frequent in MCAO (12%) than in MCAS (34%). Warning TIAs before a stroke occurred in one third of the cases. Presentation with stroke or isolated TIA was not influenced by sex, age, level of MCA obstruction, collateral circulation nor associated carotid disease. In MCAS, no major difference in presentation was found between severe and moderate stenosis. Pure motor hemiparesis occurred in 15% and pure sensory stroke in 2% of the patients with stroke and 30% of the MCA territory infarcts were small and limited to the lenticulocapsular area, confirming that so-called lacunar infarcts may be due to large vessel disease. During follow-up (42 months) of 164 medically-treated patients, further cerebrovascular events (TIA and stroke) occurred in 11.7% of the patients per year. In MCAO the stroke rate was 10.1% per patient-year and the ipsilateral infarct rate was 7.1% per patient-year. In MCAS, the stroke rate was 9.5% per patient-year and the ipsilateral stroke rate was 7.8% per patient-year.(ABSTRACT TRUNCATED AT 250 WORDS)
No effect of acetylsalicylic acid on B-thromboglobulin and platelet factor 4 plasma levels in patients with transient ischaemic attacks.
Authors: Carrieri P , Orefice G , Indaco A
Published: June 2011

We studied the effect of acetylsalicylic acid (ASA) versus placebo on B-thromboglobulin (B-TG) and platelet factor 4 (PF4) plasma levels and ADP-induced platelet aggregation in 25 male patients with transient ischaemic attacks (TIA). The patients were allocated randomly to two groups: 14 patients received oral treatment with ASA 500 mg b.i.d. for 14 days, 11 patients placebo b.i.d. for the same period. B-TG and PF4 plasma levels and ADP-induced platelet aggregation were determined in basal conditions, and two hours, and seven and fourteen days after starting with ASA or placebo. In addition, the same parameters were studied in a group of 20 healthy males of matched age. Basal levels of plasma B-TG and PF4 and the maximal amplitude of ADP-induced platelet aggregation were abnormally high in TIA patients. ASA caused a significant reduction of B-TG plasma levels in TIA patients 2 hours after the first administration, but no effect was observed at the 7th and 14th day of treatment. PF4 plasma levels were unaffected by ASA treatment. It is concluded that ASA, at the dose conventionally used in clinical trials, does not affect the release of two alpha-granule proteins.
Angiotensin delays platelet aggregation after injury of cerebral arterioles.
Authors: Rosenblum W I , el-Sabban F , Hirsh P D
Published: June 2011

Endothelium of cerebral surface vessels (pial arterioles and venules) was injured with a light/dye technique in anesthetized mice. This induced platelet aggregation at the site of injury. The onset of aggregation was monitored through a microscope in mice given angiotensin II acetate, 4 micrograms i.v. 30 minutes earlier. Aggregation latency was compared with that in vehicle treated (saline) mice. Angiotensin II caused a highly significant delay in aggregation within the arterioles which was not related to a change in shear rate of blood. Angiotensin II added to platelet rich plasma, failed to influence the aggregation produced by subsequent addition of 0.5 microM ADP or 0.5 mM sodium arachidonate. Angiotensin is a well known stimulator of prostacyclin synthesis or release, and angiotensin has been reported to inhibit platelet aggregation ex vivo by increasing prostacyclin in the effluent superfusing the mass of aggregating platelets. Our data represent the first report of an antiaggregating effect of angiotensin II in vivo in an intact microvascular bed. The data is consonant with the literature describing increased prostacyclin levels following angiotensin II infusion. The antiaggregating effect of angiotensin in cerebral microvessels may help explain a recent observation describing increased survival of gerbils treated with angiotensin following carotid ligation.
The effects of hyperosmolar solutions on cerebral arterial smooth muscle.
Authors: Sasaki T , Kassell N F , Fujiwara S , Torner J C , Spallone A
Published: June 2011

The present study was conducted to clarify the effect of hyperosmolar solutions on the constrictor responses of cerebral arteries to vasoactive agents, in vitro. The canine basilar arteries under resting tension were slightly relaxed with both mannitol (0.5, 1 and 2%) and sucrose (1, 2, and 4%). Constrictor responses of canine basilar arteries to 40 mM K+, 10(-7) M serotonin or 10(-6) M prostaglandin F2 alpha (PGF2 alpha) were markedly suppressed by pretreatment with either mannitol or sucrose. The rate of suppression correlated well to osmolarity changes in the Kreb's solution. When the specimens were incubated in Ca++-free medium, 10(-6) M PGF2 alpha elicited small contractions. Addition of 1 mM Ca++ to the bath promptly elicited larger contractions. The large contractions in response to the influx of extracellular Ca++ were markedly suppressed by pretreatment with mannitol or sucrose, while the small contractions induced by intracellular Ca++ were not inhibited. In addition, the contractions induced by the addition of Ca++ to the specimens depolarized with 80 mM K+ in Ca++-free medium were dose-dependently inhibited with either mannitol or sucrose, while the caffeine-induced contractions in Ca++-free medium were not altered by mannitol. These results suggest that hyperosmolar solutions produce non-specific vasodilation of cerebral arteries by inhibiting the influx of external Ca++ rather than the release of intracellularly stored Ca++. This direct vasodilatory effect may account in part for the transient increase of cerebral blood flow following administration of hyperosmolar mannitol.
MR imaging of a false carotid aneurysm.
Authors: Hanigan W C , Wright R M , Berkman W A , Szymke T E
Published: June 2011

Two months after a gunshot wound to the head of a 12-year-old boy, MR imaging outlined an asymptomatic false aneurysm of the carotid artery. The scan's ability to image in multiple planes with noninvasive visualization of pulsatile vessel flow suggests its use for follow-up examinations of traumatic injuries to the head or neck.
Painful tonic spasms caused by putaminal infarction.
Authors: Merchut M P , Brumlik J
Published: June 2011

Lacunar infarcts in the basal ganglia are known to cause various movement disorders, such as chorea, focal dystonia, and hemichorea-hemiballismus. We report here a case of putaminal lacunar infarction which presented with "painful tonic spasms" of the contralateral limbs. This consisted of paroxysmal brief, painful, flexor contractures of the upper, and occasionally the lower limb. These were not focal seizures but were controlled with carbamazepine, which has been used for the "painful tonic spasms" well-associated with multiple sclerosis. The putaminal infarct we describe is probably related to a lupus anticoagulant and systemic lupus erythematosus.
Direct evidence of acute, massive striatal dopamine release in gerbils with unilateral strokes.
Authors: Brannan T , Weinberger J , Knott P , Taff I , Kaufmann H , Togasaki D , Nieves-Rosa J , Maker H
Published: June 2011

Dopamine release into the extracellular space was measured with in vivo electrochemical detection in the ipsilateral and contralateral striata in Mongolian gerbils that suffered a stroke after acute unilateral carotid artery ligations. A sevenfold increase in the dopamine signal occurred within 15 minutes of carotid ligation in the ischemic side, while the unlesioned side had no significant change. Increased extracellular levels of dopamine persisted throughout the 3-hour recording period. Pretreatment with alpha-methyl-p-tyrosine 6 hours prior to recording significantly attenuated the signal increase. This study is the first direct demonstration of the marked, continuous dopamine release that occurs during acute cerebral ischemia.
Evidence that in vivo constriction of cerebral arterioles by local application of tert-butyl hydroperoxide is mediated by release of endogenous thromboxane.
Authors: Rosenblum W I , Bryan D
Published: June 2011

Pial arterioles of mice were suffused in situ with tert-butyl hydroperoxide (TBHP). This agent has been reported to stimulate synthesis or release of the constrictor, thromboxane. In the present study we observed pial arterioles by in vivo microscopy. Locally applied TBHP produced dose-dependent constriction, significantly inhibited by each of three drugs: acetylsalicylic acid, OKY-046, and SQ-29548. These drugs are respectively a cyclooxygenase inhibitor, a thromboxane synthetase inhibitor, and a thromboxane receptor blocker. Since each acts by a different mechanism to interfere with thromboxane-mediated responses and each inhibited the contractile response to TBHP, thromboxane appears to be a mediator of this response. Platelet aggregation was not seen after local application of TBHP, and the dwell time of platelets at the site of TBHP application is less than 1 second. Thus, platelets are an unlikely source of the thromboxane mediating the local constriction. It is much more likely that the source of thromboxane is either the wall of the pial vessels or the underlying brain and/or its vessels. These data do not distinguish between the latter two possibilities, but if this suggestion is correct, then the data show for the first time that thromboxane can be released from normal brain and/or brain vessels in amounts sufficient to cause arteriolar constriction.
Ataxic hemiparesis with contralateral trigeminal nerve impairment due to pontine hemorrhage.
Authors: Ambrosetto P
Published: June 2011

A most unusual case of right-sided ataxic hemiparesis with left trigeminal involvement is reported. Computerized tomographic scan revealed a small hemorrhage in the basis pontis.
Influence of age on carotid atheroma in patients with reversible ischemic attacks.
Authors: Landi G , Guidotti M , Valsecchi F
Published: June 2011

To evaluate the influence of age on carotid atheroma we reviewed the angiographic findings in 120 patients with reversible ischemic attacks. The prevalence and severity of atherosclerotic lesions increased significantly with age, and this difference persisted after adjusting for hypertension. These results may at least partly explain the poor long term prognosis for elderly subjects with reversible ischemic attacks, and underscore the importance of taking age into account when relating clinical and angiographic findings in patients with cerebrovascular ischemia.
Leukocyte rheology in recent stroke.
Authors: Ernst E , Matrai A , Paulsen F
Published: June 2011

Eighteen patients with recent ischemic stroke were compared with an equal number of matched controls. Standardized suspensions of red cells as well as of red and white cells were filtered in a new filtration apparatus capable of discriminating between cell deformability and filter occlusion. Results show that red cell deformability, although slightly lower than in controls, is not significantly altered in stroke patients. Filter occlusion, however, was significantly higher in patients when red and white cell suspensions were filtered, but not when red cell suspensions were used, suggesting that white cell filterability is impaired after stroke, which could be due to decreased deformability and/or increased adhesiveness of leukocytes. Slowed white cell passage may also occur in the living microcirculation and may present an obstacle to nutritive flow in exchange vessels, possibly contributing to local ischemia and tissue necrosis after stroke.
Clinical vasospasm after subarachnoid hemorrhage: response to hypervolemic hemodilution and arterial hypertension.
Authors: Awad I A , Carter L P , Spetzler R F , Medina M , Williams F C
Published: June 2011

Delayed neurologic deterioration from vasospasm remains the greatest cause of morbidity and mortality following subarachnoid hemorrhage. The authors assess the incidence and clinical course of symptomatic vasospasm following subarachnoid hemorrhage using a uniform management protocol over a 24-month period. One hundred eighteen consecutive patients were admitted to the neurovascular surgery service within 2 weeks of subarachnoid hemorrhage not attributed to trauma, tumor, or vascular malformation (113 patients had aneurysms). Early surgery was performed whenever possible, and hypertensive hypervolemic hemodilution therapy was instituted at the first sign of clinical vasospasm. Forty-two patients (35.6%) developed characteristic signs and symptoms of clinical vasospasm with angiographic verification of spasm in 39 cases. All patients with clinical vasospasm received hypervolemic hemodilution therapy aiming for a hematocrit of 33-38%, a central venous pressure of 10-12 mm Hg (or a pulmonary wedge pressure of 15-18 mm Hg), and a systolic arterial pressure of 160-200 mm Hg (120-150 mm Hg for unclipped aneurysms) for the duration of clinical vasospasm. Over the course of treatment, 60% of patients with clinical vasospasm had sustained improvement by at least 1 neurologic grade, 24% maintained a stable neurologic status, and 16% continued to worsen. At the end of hypervolemic hemodilution therapy, 47.6% had become neurologically normal, 33.3% had a minor neurologic deficit, and 19% had a major neurologic deficit or were dead. There were 3 instances of cardiopulmonary deterioration (7%), all of which were in patients without Swan-Ganz catheters, and all resolved with appropriate diuresis. One patient rebled and died while on hypervolemic hemodilution therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
An epidemiologic study of cerebrovascular disease in western Japan: with special reference to transient ischemic attacks.
Authors: Urakami K , Igo M , Takahashi K
Published: June 2011

The prevalence and incidence ratios of cerebrovascular disease, with special reference to transient ischemic attack (TIA), were studied in the towns of Daisen and Ama in western Japan. There have been no previous reports on this subject in Japan. The prevalence ratios of TIA were estimated to be 4.4 in Daisen and 2.0 in Ama per 1,000 people over 40 years old. The ratio of carotid arterial system TIA to vertebrobasilar arterial system TIA was about 1 to 1. The incidence ratios of stroke were 319.6 in Daisen and 314.5 in Ama per 100,000 people of all ages. The prevalence ratios of stroke were estimated to be 14.8 in Daisen and 13.5 in Ama per 1,000 people of all ages. The prevalence ratio of TIA in Japan is about one-third to one-half of that in Western countries. However, the prevalence of complete stroke is much higher in Japan compared with that in Western countries. Therefore, the ratio of TIA to stroke is much lower in Japan than in Western countries. The obstruction of small intracranial arteries, in addition to heart disease, might play an important role in TIA in Japan, whereas in Western countries TIA might be mostly caused by heart disease or the atherosclerosis of extracranial arteries.
Impairment of endothelium-dependent vasodilation induced by acetylcholine and adenosine triphosphate following experimental subarachnoid hemorrhage.
Authors: Nakagomi T , Kassell N F , Sasaki T , Fujiwara S , Lehman R M , Torner J C
Published: June 2011

The effect of subarachnoid hemorrhage (SAH) on endothelium-dependent vasodilation of isolated rabbit basilar artery was examined using an isometric tension recording method. Thirty-five rabbits that had 2 successive blood injections were divided into 3 groups: normal animals (control), 4 days, and 3 weeks after the first SAH. Acetylcholine (ACh) (10(-6)-10(-4) M) and adenosine triphosphate (ATP) (10(-6)-10(-4) M) were used to evoke dose-dependent vasodilation of isolated arterial rings previously contracted by 10(-6) M serotonin. In the animals killed 4 days after the first SAH, both ACh- and ATP-induced relaxation were suppressed, and the degree of relaxation of this group was 38 +/- 4.5% (mean +/- SEM) and 22 +/- 3.9% of the initial contractile tone in response to 10(-4) M ACh and 10(-4) M ATP, respectively. Suppression of the relaxation induced by ATP was seen even in the animals killed 3 weeks after the first SAH. Moreover, pretreatment with hemoglobin (10(-6) and 10(-5) M) inhibited endothelium-dependent vasodilation induced by ACh in the arterial rings from the animals killed 4 days after the first SAH. The present experiments suggest that impairment of the endothelium-dependent vasodilation following SAH may be involved in the pathogenesis of cerebral vasospasm.
Factors influencing the survival of 451 transient ischemic attack patients.
Authors: Howard G , Toole J F , Frye-Pierson J , Hinshelwood L C
Published: June 2011

Four hundred fifty-one patients with transient ischemic attacks (TIA) occurring within 1 month of hospitalization, admitted during 1977-1983, were analyzed to establish the effect on survival of age, race, sex, distribution of TIA, cigarette smoking, previous cerebral infarction or hemorrhage, previous TIA, or history of ischemic heart disease, valvular heart disease, cardiac dysrhythmia, hypertension, and diabetes mellitus. Proportional hazards analysis revealed that decreased survival was associated with increasing age, carotid artery distribution TIAs (compared with vertebrobasilar distribution TIAs), cigarette smoking, previous contralateral stroke, ischemic heart disease, and diabetes mellitus. We found great variation in the estimated survival of TIA patients, ranging from 5-year survivals of greater than 95% for 60-year-old patients with none of these risk factors to less than 25% for patients with all of these risk factors. Although the survival of the strata differed, the average mortality rates for this series of patients was about one-half of that observed for 225 patients accessed and followed by our center during 1961-1973.
Hyperglycemia reduces the extent of cerebral infarction in rats.
Authors: Ginsberg M D , Prado R , Dietrich W D , Busto R , Watson B D
Published: June 2011

Although hyperglycemia is known to exacerbate neuronal injury in the setting of reversible brain ischemia, its effect on irreversible thrombotic infarction is less well understood. In this study, unilateral thrombotic infarction was induced photochemically in the parietal cortex of Wistar rats. Seven days later, brains were perfusion-fixed for light microscopy. Infarct areas were measured by computer-assisted planimetry on multiple coronal sections at 250-micron intervals; these data were integrated to yield infarct volumes. Fasted, normoglycemic rats were compared with hyperglycemic rats that had received 1.2-1.5 ml of 50% dextrose i.p. 15 minutes prior to the induction of infarction. Infarct volume averaged 12.5 +/- 4.0 mm3 (mean +/- SD) in rats (n = 14) with plasma glucose levels of 72-184 mg/dl; this differed statistically from the average volume of 9.3 +/- 3.3 mm3 observed in rats (n = 13) with elevated plasma glucose (range 264-607 mg/dl). Spearman rank correlation analysis confirmed a significant correlation of larger infarct volumes with lower plasma glucose levels. In contrast, rats receiving mannitol i.p. to produce an osmotic load comparable with that of the dextrose-pretreated animals showed larger infarct volumes than saline-treated controls. The small but definite beneficial effect of hyperglycemia in this end-arteriolar thrombotic infarction model is possibly attributable to improved local energy metabolism at the periphery of the lesion during the early period of lesion expansion.
Effects of calcium antagonists on isolated bovine cerebral arteries: inhibition of constriction and calcium-45 uptake induced by potassium or serotonin.
Authors: Wendling W W , Harakal C
Published: June 2011

The purpose of this study was to determine the mechanisms by which organic calcium channel blockers inhibit cerebral vasoconstriction. Isolated bovine middle cerebral arteries were cut into rings to measure contractility or into strips to measure radioactive calcium (45Ca) influx and efflux. Calcium channel blockers (10(-5) M verapamil or 3.3 X 10(-7) M nifedipine) and calcium-deficient solutions all produced near-maximal inhibition of both potassium- and serotonin-induced constriction. In calcium-deficient solutions containing potassium or serotonin, verapamil and nifedipine each blocked subsequent calcium-induced constriction in a competitive manner. Potassium and serotonin significantly increased 45Ca uptake into cerebral artery strips during 5 minutes of 45Ca loading; for potassium 45Ca uptake increased from 62 to 188 nmol/g, and for serotonin from 65 to 102 nmol/g. Verapamil or nifedipine had no effect on basal 45Ca uptake but significantly blocked the increase in 45Ca uptake induced by potassium or serotonin. Potassium, and to a lesser extent serotonin, each induced a brief increase in the rate of 45Ca efflux into calcium-deficient solutions. Verapamil or nifedipine had no effect on basal or potassium-stimulated 45Ca efflux. The results demonstrate that verapamil and nifedipine block 45Ca uptake through both potential-operated (potassium) and receptor-operated (serotonin) channels in bovine middle cerebral arteries.
Comparisons of oxygen metabolism and tissue PO2 in cortex and hippocampus of gerbil brain.
Authors: Nair P K , Buerk D G , Halsey J H
Published: June 2011

Recessed oxygen microelectrodes (tip diameter less than 2 microns) were positioned stereotactically into either the cerebral cortex or the hippocampus of sodium pentobarbital anesthetized gerbils (n = 21). The mean tissue PO2 levels (+/- SEM) were not significantly different between cortex (35.4 +/- 1.7 torr) and hippocampus (33.6 +/- 1.4 torr) although differences in the tissue PO2 distributions were seen. The disappearance rate for oxygen (-dPO2/dt) was measured after brief (less than 15 seconds) bilateral carotid artery (total brain blood flow) occlusion. The mean (+/- SEM) disappearance rate was significantly higher (p less than 0.05) in the cortex (23.8 +/- 1.5 torr/sec, 160 locations in 21 gerbils) than in the hippocampus (17.0 +/- 0.7 torr/sec, 119 locations in 16 gerbils). The maximum oxygen consumption rates (VO2max) for Michaelis-Menten kinetics were calculated from the disappearance rates, correcting for gerbil oxyhemoglobin. The mean VO2max was 8.28 +/- 0.51 and 6.13 +/- 0.25 ml O2/100 g/min for the cortex and hippocampus, respectively. The apparent Michaelis-Menten kinetic constants (Km) for the 2 regions were not significantly different (overall mean 3.3 +/- 0.4 torr). Differences in the recovery of tissue PO2 after releasing the occlusion were seen, with more hyperemic responses in the hippocampus.
Control of glial cell volume in anoxia. In vitro studies on ischemic cell swelling.
Authors: Kempski O , Zimmer M , Neu A , von Rosen F , Jansen M , Baethmann A
Published: June 2011

Volume regulation of C6 glial cells was studied in anoxia in vitro to improve the understanding of ischemic cell swelling in the brain. Contrary to in vivo conditions, anoxia or anoxia plus iodoacetate for additional inhibition of anaerobic energy metabolism did not induce glial swelling. However, intracellular K+ was markedly decreased while intracellular Na+ increased. Induction of energy failure by anoxia plus iodoacetate was found to prevent the regulatory volume decrease on hyposmotic exposure of the cells, which is regularly observed in normoxic control conditions. Hyposmotic exposure in anoxia plus iodoacetate led only to an initial tendency of cell volume normalization followed by secondary cell swelling. This was associated with a net increase of intracellular Na+ that may explain the failure of volume regulation under these circumstances. Maintenance of a normal glial cell size during complete energy deprivation by anoxia plus iodoacetate in isotonic medium strongly indicates that energy failure per se does not suffice to induce cell swelling. Cell swelling in cerebral ischemia in vivo thus is likely to require additional mechanisms, most likely an increase of membrane permeability to Na+, which may be caused by release and accumulation of excitotoxins such as glutamate or by an extracellular release of K+. Such a mechanism would hardly influence the extracellular homeostasis in vitro due to the large medium-to-cell volume ratio. The findings demonstrate, nonetheless, the significance of a competent energy metabolism to support cell volume regulation. This is concluded from the failure of regulatory volume decrease of hypotonically suspended glial cells in anoxia plus iodoacetate.(ABSTRACT TRUNCATED AT 250 WORDS)
Effect of stable xenon in room air on regional cerebral blood flow and electroencephalogram in normal baboons.
Authors: Hartmann A , Wassman H , Czernicki Z , Dettmers C , Schumacher H W , Tsuda Y
Published: June 2011

Measurement of regional cerebral blood flow (rCBF) was performed in 6 healthy baboons during ventilation with 35% stable xenon in artificial air. rCBF was measured with the intraarterial xenon-133 method. EEG was recorded continuously. All CBF areas of interest over one hemisphere reacted in the same way. Mean flow increased during short-term exposure to stable xenon and decreased if stable xenon inhalation was continued for at least 24 minutes. EEG showed a decrease of alpha- and beta-wave patterns a short time after the start of stable xenon inhalation without further changes over the period when rCBF finally decreased. CO2 reactivity increased in most animals, and autoregulation to mild arterial hypotension was significantly impaired with increased flow. It is concluded that 35% stable xenon in artificial air increases rCBF after short-term exposure and decreases rCBF after longer exposure. EEG changes were noted after short-term exposure. rCBF and EEG recovered rapidly after the end of stable xenon inhalation.
Artery-to-artery embolism from a thrombus formed in stenotic middle cerebral artery. Report of an autopsy case.
Authors: Masuda J , Ogata J , Yutani C , Miyashita T , Yamaguchi T
Published: June 2011

The authors report an autopsy case with repeated transient ischemic attacks and subsequent strokes demonstrating evidence of artery-to-artery embolism from thrombi generated in the stenotic middle cerebral artery to the distal cortical branches. This case substantiates the existence of intracranial artery-to-artery embolism as a cause of transient ischemic attacks and subsequent strokes, and has potential relevance for therapy.
Neurologic and neuropsychological morbidity following major surgery: comparison of coronary artery bypass and peripheral vascular surgery.
Authors: Shaw P J , Bates D , Cartlidge N E , French J M , Heaviside D , Julian D G , Shaw D A
Published: June 2011

As part of a prospective study of the neurologic and neuropsychological complications of coronary artery bypass graft surgery, 312 patients were compared with a control group of 50 patients undergoing major surgery for peripheral vascular disease. The purpose of comparing the 2 groups was to determine to what extent neurologic complications after heart surgery can be attributed to cardiopulmonary bypass. The 2 groups were similar with respect to age, preoperative neurologic and intellectual status, anesthetic methods, duration of operation, perioperative complications, and time spent in the intensive therapy unit. Certain potential risk factors for cerebrovascular disease were more common in the control than the coronary bypass patients. The important difference between the 2 groups was that only the latter group underwent cardiopulmonary bypass. In this group 191 of 312 (61%) and 235 of 298 (79%), respectively, developed early neurologic and neuropsychological complications. By the time of hospital discharge 17% had neurologic disability and 38% had significant neuropsychological symptoms. In the control group 9 of 50 (18%) developed neurologic complications resulting largely from trauma to lower limb sensory nerves. Two patients developed primitive reflexes. Fifteen of 48 (31%) showed neuropsychological impairment on 1 or 2 subtest scores. Moderate or severe intellectual dysfunction was not seen in the control patients in contrast to the 24% thus affected in the coronary bypass group. The difference in frequency and severity of central nervous system complications between the 2 groups is likely to reflect cerebral injury resulting from cardiopulmonary bypass.
Angiography of nonhemorrhagic cerebral infarction in young adults.
Authors: Smoker W R , Biller J , Hingtgen W L , Adams H P , Toffol G J
Published: June 2011

The radiographic examinations and hospital records of 93 young adult patients (15-45 years of age) with nonhemorrhagic cerebral infarction evaluated at our institution during the past 9 years were reviewed. The angiographic examinations were abnormal in 76% of patients. The most common abnormalities were embolic disease and atherothrombotic disease. Forty-seven patients underwent angiography within 7 days of their event. There were no major neurologic or systemic complications related to early angiography. We believe that angiography performed early in the course of the illness is a high-yield, safe procedure that may significantly alter the management of acute stroke in young adults.
Platelet deposition at carotid endarterectomy sites in humans.
Authors: Stratton J R , Zierler R E , Kazmers A
Published: June 2011

Following carotid endarterectomy, early postoperative thrombosis or late restenosis occurs in up to 20% of vessels. Both complications may be related to platelet mechanisms. To assess platelet deposition at endarterectomy sites, we injected indium-111 labelled platelets in 24 men less than 30 minutes after carotid endarterectomy, with subsequent imaging 24-96 hours later. To determine if deposition decreased over time, 12 patients had follow-up studies 0.5-24 months later. For comparison, 2 control groups were studied: 1) patients with noncarotid surgery (n = 6) and 2) normal young subjects without endarterectomy and without evidence of carotid disease (n = 12). Quantitative analysis was performed performed using a deposition index that compared activity in operated with unoperated sites in surgical patients or activity in the right with left carotid arteries in normal subjects. Patients with recent endarterectomy had a mean deposition index of 1.7 +/- 0.5 (range 1.2-3.5) compared with a similarly determined ratio of 1.1 +/- 0.1 in normal subjects and 1.2 +/- 0.1 in the surgical controls (both p less than or equal to 0.05 vs. acute endarterectomy). At follow-up after endarterectomy, the mean deposition index decreased to 1.0 +/- 0.1, documenting reduced platelet deposition over time. We conclude that the arterial injury of carotid endarterectomy results in early platelet deposition, which is no longer present in most patients who are studied late. These findings suggest a reduction in platelet thrombus formation with time and are compatible with reendothelialization of the endarterectomized surface. This model may be useful for the in vivo assessment of therapies designed to reduce platelet accumulation following endothelial injury in humans.
Deteriorating stroke model: histopathology, edema, and eicosanoid changes following spinal cord ischemia in rabbits.
Authors: Jacobs T P , Shohami E , Baze W , Burgard E , Gunderson C , Hallenbeck J M , Feuerstein G
Published: June 2011

Secondary motor dysfunction is often observed following ischemic episodes in the central nervous system. To study potential mechanisms of postischemic motor deterioration, we developed a rabbit spinal cord ischemia model that has characteristics similar to the clinical condition termed deteriorating stroke. In this model, 70% of the rabbits regained substantial motor function by 4 hours after complete hindlimb paralysis during lumbar spinal cord ischemia; however, over the next 20 hours motor function steadily declined to the point where only 30% of the rabbits had minimal hopping function. The role of eicosanoids in spinal cord ischemia was studied by radioimmunoassay of several prostaglandins (6-keto-PGF1 alpha, PGE2, and TxB2) in the spinal cord. After 5 minutes of reperfusion, TxB2 levels were markedly elevated (p less than 0.05) while 6-keto-PGF1 alpha levels did not change. The TxB2:6-keto-PGF1 alpha ratio was also significantly increased. After 30 minutes of reperfusion, PGE2 levels were also elevated (p less than 0.05). Tissue edema measured by microgravimetry was also increased after 30 minutes of reperfusion in both gray and white matter. By 4 hours of reperfusion, rabbits regained near-normal hindlimb motor function while PGE2, 6-keto-PGF1 alpha, TxB2, and tissue water content were back to normal. However, by 18 hours of reperfusion, when hindlimb function was deteriorating, TxB2 levels were elevated again, and edema in gray and white matter was increased as was the number of necrotic neurons observed by light microscopy. These results suggest that the secondary deterioration of motor neurologic function was due to the excess formation of TxA2 primarily in the late reperfusion phase. However, further studies are necessary to elucidate the relation of TxA2 with ischemic neural injury.
Opioid peptide levels in gerbil brain after transient ischemia: lasting depletion of hippocampal dynorphin.
Authors: Fried R L , Nowak T S
Published: June 2011

Peptides derived from each of the 3 endogenous opioid precursors were measured in gerbil brain regions at various times after transient bilateral carotid artery occlusion using radioimmunoassays specific for beta-endorphin-, met-enkephalin-, and dynorphin A-related peptides. Lasting changes were observed only in the hippocampus. The most striking effect was on dynorphin A immunoreactivity, which was reduced by 30-40% as early as 1 hour after recirculation and remained at 50% of the control level for at least 1 week. In some experiments dynorphin levels showed a transient recovery at 24 hours. These results demonstrate a unique sensitivity of the dynorphin-containing dentate granule cell-mossy fiber pathway to transient ischemia. Although these cells remain histologically intact, the decrease in dynorphin level precedes and continues during the delayed loss of hippocampal CA1 neurons characteristic of this model and further defines the selective vulnerability of hippocampal circuitry following ischemia. These observations clearly identify the hippocampus as a well-defined brain region in which further studies of the postischemic pathophysiology of endogenous opioid peptides may provide a rational basis for evaluating the place of opiate pharmacology in stroke treatment.
Cerebral venous thrombosis with lupus anticoagulants. Report of two cases.
Authors: Levine S R , Kieran S , Puzio K , Feit H , Patel S C , Welch K M
Published: June 2011

Lupus anticoagulants are circulating autoantibodies, primarily directed against phospholipids, that prolong the partial thromboplastin time. They have been previously associated with systemic arterial and venous thrombosis and arterial stroke, but not with cerebral venous thrombosis. We describe 2 young patients with cerebral venous thrombosis documented by intravenous digital subtraction angiography in whom a lupus anticoagulant was demonstrated. Both patients improved with corticosteroid and anticoagulant therapy.
Disability and use of rehabilitation services following stroke in Rochester, Minnesota, 1975-1979.
Authors: Dombovy M L , Basford J R , Whisnant J P , Bergstralh E J
Published: June 2011

Medical records of all residents of Rochester, Minnesota, who had a first stroke in 1975-1979 were reviewed to determine level of disability, disposition, and use of rehabilitation services. Of the 292 persons with a first stroke, 251 (86%) (mean age 70 years) survived greater than 1 week. The mean Rankin disability score (Grade 1, no disability, through Grade 5, severe disability) changed from 1.7 before stroke to 2.8 in survivors at hospital discharge; 29% of those discharged required further institutional care. The level of disability in survivors remained relatively constant from 6 months after stroke through 5 years of observation. Of the 112 patients with an admission score of 5, 40 (36%) were alive at 1 year and only 5 of those (13%) improved to relative independence (Rankin scores of 1 or 2). The most common comorbidity contributing to disability was cardiovascular disease (31%). After the first 18 months, the mortality in patients with stroke was similar to that in a normal population having the same age and sex distribution. Of the 251 1-week survivors, 132 (53%) had rehabilitation (physiatrist) evaluations, 127 (51%) received physical therapy, 103 (41%) received occupational therapy, and 33 (13%) received speech therapy. Thirty-four of the 132 patients (26%) referred for rehabilitation evaluations were transferred to the rehabilitation unit.
Two-year longitudinal study of poststroke mood disorders: diagnosis and outcome at one and two years.
Authors: Robinson R G , Bolduc P L , Price T R
Published: June 2011

As part of a prospective study of mood disorders in stroke patients, interviews were obtained from 37 patients at 1 year and 48 patients at 2 years follow-up. In-hospital evaluations for these 65 follow-up patients found that 9 patients (14%) had symptom clusters of major depression, 12 patients (18%) had symptom clusters of dysthymic or minor depression, and 44 patients (68%) did not meet the DSM III diagnostic criteria for depression. Although overall prevalence of depression did not change significantly over time, the prognosis for individual patients, depending on diagnostic group, was different. All of the follow-up patients with major depression in-hospital were improved by 2 years, with a significant reduction in their mean depression scores and improvement in their activities of daily living, whereas only 30% of follow-up patients with dysthymic depression improved by this time. There was no significant improvement in their mean depression scores or mean activities of daily living score. Of the patients followed up who were not depressed in-hospital, 34% had developed major or minor depression by 2 years, and their mean depression scores were significantly increased. These data suggest that the prevalence of depression among the follow-up patients remains high (between 30 and 40%) for the first 2 years after stroke, but that untreated poststroke major depression has a natural course of about 1-2 years, with associated improvement in activity of daily living scores, whereas the prognosis for poststroke dysthymic depression is frequently unfavorable and often persists for greater than 2 years.
Atrial septal aneurysm: association with cerebrovascular and peripheral embolic events.
Authors: Belkin R N , Hurwitz B J , Kisslo J
Published: June 2011

Patient records in 36 consecutively identified patients with typical echocardiographic findings of atrial septal aneurysm were reviewed. Ten of the 36 (28%) had cerebrovascular events. Of these 10, 5 had completed strokes of definite embolic origin on the basis of clinical, angiographic, and computed tomographic findings; 2 had transient ischemic attacks of probable embolic origin. One of the 36 patients had a definite peripheral vascular embolus. Thus, 6 of 36 consecutively identified patients with atrial septal aneurysm (17%) had definite embolic events and 8 of 36 (22%) had definite or possible embolic events. The cause of the association between atrial septal aneurysm and emboli is unknown. While aneurysm-associated thrombus has been suggested, the high proportion (90%) of patients with interatrial shunting demonstrated by contrast echocardiography in this study suggests paradoxical embolization as a potential cause. Whatever its mechanism, the high prevalence of embolic events in this series strongly supports the premise that atrial septal aneurysm is a cardiac abnormality with embolic potential.
Lack of association between carotid plaque hematoma and ischemic cerebral symptoms.
Authors: Lennihan L , Kupsky W J , Mohr J P , Hauser W A , Correll J W , Quest D O
Published: June 2011

To investigate the association between carotid plaque hematoma and symptoms of cerebral ischemia a retrospective review of 200 consecutive carotid endarterectomies at the Neurological Institute of New York was carried out. Data analyzed included cerebral ischemic symptoms, angiographic findings, preoperative use of antithrombotic agents, and microscopic pathology of endarterectomy specimens. No association was found between ischemic symptoms ipsilateral to the endarterectomy and presence, size, or age of plaque hematomas. Plaque hematomas were less common among patients who took antithrombotic agents preoperatively than among those who did not. The presence of plaque hematoma was associated with angiographic carotid cross-sectional area stenosis of greater than 75%. Patients with stenosis of less than 75% were more likely than those with stenosis of greater than 75% to have ischemic symptoms ipsilateral to the endarterectomy, suggesting that criteria for surgical treatment of carotid atherosclerosis differ for those who are symptomatic vs. those who are asymptomatic. These results demonstrate the limitation of using a surgical series to extend causal inferences about the relation between plaque hematoma and cerebral ischemic symptoms to the general population of people with carotid atherosclerosis.
Effect of acetazolamide on cerebral blood flow in subacute and chronic cerebrovascular disease.
Authors: Højer-Pedersen E
Published: June 2011

Acetazolamide increases cerebral blood flow. The generalized and regional changes in blood flow after administration of acetazolamide were evaluated by the xenon-133 inhalation technique in a series of patients with subacute or chronic focal cerebral ischemia. Acetazolamide augmented interhemispheric asymmetry of cerebral blood flow in patients with unilateral occlusion of major cerebral arteries, whereas no significant side-to-side asymmetry was evident in patients with minor arterial lesions. Low flow areas in relation to computed tomography-verified infarcts tended to be larger after administration of acetazolamide. Hyperfrontality was present at rest and during stimulation with acetazolamide. A decline of cerebral blood flow with advancing age was greater in patients than in normal controls. The vasodilator response to acetazolamide did not change with age.