bluuebunny/crossref_metadata_2025 huggingface dataset:
Recurrent transient ischemic attacks and stroke in association with an internal carotid artery web.
Authors: Morgenlander J C , Goldstein L B
Published: June 2011

Fibromuscular dysplasia is a nonatherosclerotic vascular disease that most commonly affects cervical carotid arteries at the C1-C2 level when cephalic arteries are involved. Several histopathologic and angiographic subtypes of fibromuscular dysplasia exist; most have a benign natural history. We describe the third reported case of a pathologically proven, symptomatic proximal internal carotid artery web and suggest that patients with this lesion are at a higher risk for stroke.
Computed tomographic-angiographic findings within the first five hours of cerebral infarction.
Authors: Horowitz S H , Zito J L , Donnarumma R , Patel M , Alvir J
Published: June 2011

Modern management of acute stroke necessitates early diagnosis. To this end, we sought to delineate the radiographic features of focal hemispheric infarction within 5 hours of ictus.

Fifty patients, ages 54-79, with ischemic strokes productive of at least hemiparesis underwent computed tomographic scanning and cerebral angiography (n = 38) or carotid ultrasound (n = 12). Radiographic lesions were characterized for location, size, and pathophysiology.

Acute abnormalities, hypodensity, and mass effect were seen in 56% of scans and confirmed on a second scan 5-7 days later. Intracranial angiographic abnormalities occurred in 61% of patients: arterial occlusions in 45% and delayed arterial filling in 16%. Hemorrhagic infarctions occurred in 26% of second scans and were associated with mass effect (100%) and arterial occlusions (89%). Infarcts with hemorrhagic transformation were larger on both scans than those without (p = 0.001). Of four patients with infarctions in watershed territories on the scans, two had middle cerebral artery occlusions on angiography, thereby questioning the specificity of such scan lesions to low-flow states.

We conclude that cerebral infarctions are often visible on early scans, but their locations may not be etiologically determinative. The infarcts associated with intracranial arterial occlusions (45%) were of thromboembolic origin, but, given current controversies as to the pathophysiology of lacunar and watershed infarctions, we cannot ascertain the etiology in the remainder. These findings are relevant to the new stroke therapies that require administration in the first hours after infarction.
Determination of S-100 and glial fibrillary acidic protein concentrations in cerebrospinal fluid after brain infarction.
Authors: Aurell A , Rosengren L E , Karlsson B , Olsson J E , Zbornikova V , Haglid K G
Published: June 2011

We initiated the present study to evaluate the clinical value of consecutive concentration determinations of S-100 and glial fibrillary acidic proteins in cerebrospinal fluid from patients with brain infarction.

We took sequential samples of cerebrospinal fluid from 28 patients within 48 hours, at 7 days, and at 18-21 days after the ictus. We measured astroglial protein concentrations using an enzyme-linked immunosorbent assay and also determined size of the infarction (computed tomography), clinical state of the patient (simplified activities of daily living test), blood-brain barrier dysfunction (cerebrospinal fluid/serum albumin ratio), and a myelin marker (myelin basic protein).

We found a transient increase of both proteins in the cerebrospinal fluid during the first week after the ischemic stroke (p less than 0.05). This increment was significantly correlated with the size of the infarction and the clinical state of the patients.

Transient release of astroglial proteins into the cerebrospinal fluid possibly reflects initial focal ischemic damage and, in the later phase, ongoing destruction of astroglial cells in the penumbra zone. We suggest that determinations of cerebrospinal fluid astroglial protein concentrations can be used to estimate ischemic brain damage, which should be of particular value in clinical trials of pharmacological agents, such as calcium antagonists, on stroke patients.
MK-801 does not protect against hypoxic-ischemic brain injury in piglets.
Authors: LeBlanc M H , Vig V , Smith B , Parker C C , Evans O B , Smith E E
Published: June 2011

The excitatory amino acid inhibitor MK-801 has been shown in many animals species to protect against hypoxic-ischemic brain injury. We sought to determine whether hypoxic-ischemic injury to the newborn pig's brain could be prevented by the use of MK-801.

Hypoxic-ischemic injury to the brain was induced in forty 0-3-day-old piglets. They were randomized to receive either 3 mg/kg MK-801 (MK-801 group, n = 20) or vehicle (control group, n = 19) prior to insult. At time 0, the carotid arteries were ligated and the blood pressure was reduced by one third by hemorrhage. At 15 minutes, inspired oxygen was reduced from 50% to 6%. At 30 minutes, inspired oxygen was changed to 100%, carotid ligatures were released, and the withdrawn blood was reinfused. An additional 14 piglets received 3 mg/kg MK-801 but not hypoxic-ischemic injury (drug-only group), and a final group of 11 piglets were subjected to only a sham operation (sham group).

Neurological examination scores at 24, 48, and 72 hours showed that MK-801 and drug-only piglets were significantly worse than the controls. Pathological examination of the brains at 72 hours showed significantly greater damage in the brains of the MK-801 and control pigs relative to the sham and drug-only groups. No differences were found between the control and the MK-801 groups. No differences were found between the sham and drug-only groups.

MK-801, at a dose of 3 mg/kg, causes neurological dysfunction in piglets lasting at least 72 hours, but neither causes brain damage nor ameliorates the effects of hypoxic-ischemic injury to the brain of the newborn pig.
Evaluation of 99mTc-hexamethylpropyleneamine oxime cerebral blood flow mapping after acute focal ischemia in rats.
Authors: Bullock R , Patterson J , Park C
Published: June 2011

Although the blood flow tracer hexamethylpropyleneamine oxime is now widely used for cerebral blood flow mapping using single-photon emission computed tomography, its uptake into acutely ischemic brain has not been well studied. We performed a double-label autoradiographic study in which 99mTc-hexamethylpropyleneamine oxime uptake was compared with [14C]iodoantipyrine-derived cerebral blood flow 0.5, 24, and 72 hours after middle cerebral artery occlusion in 11 rats. We noted excellent correspondence between iodoantipyrine and hexamethylpropyleneamine oxime autoradiograms at all times with both simultaneous tracer injection and 30-minute separation of tracer injections. When the ischemic and hyperemic areas were measured from the same brain section using the two different tracers, hexamethylpropyleneamine oxime underestimated the iodoantipyrine-derived areas by less than 1% (95% confidence interval -2.9% to 2.3%). The maximum discrepancy (-19%) was seen at high flows. When the two tracers were injected separately, the uptake of hexamethylpropyleneamine oxime was not linear compared with iodoantipyrine-derived cerebral blood flow, but the relation became linear after the Lassen correction factor was applied. Hexamethylpropyleneamine oxime uptake thus accurately represents cerebral blood flow 0.5-72 hours after acute cerebral ischemia.
Central nervous system infarction related to cocaine abuse.
Authors: Daras M , Tuchman A J , Marks S
Published: June 2011

Cocaine use in the United States has reached epidemic proportions, and increased availability of "crack" since 1983 has noticeably increased the incidence of neurovascular complications. In this report, we examine the relationship between cocaine use and ischemic infarct.

This study reports 18 cases of ischemic cerebrovascular events, which occurred among 15 men and three women aged 21-47 years who were evaluated in a 2-year period. Clinical presentations include thirteen cases with hemispheric infarcts, two brain stem strokes, two anterior spinal artery infarcts, and one with both hemispheric and cerebellar infarcts. Nine patients smoked crack, four snorted cocaine, and three injected it intravenously. In two cases, the route of administration could not be determined. Two patients died, but the other survived with various degrees of neurological deficit.

Traditional risk factors for strokes were identified in only six patients, suggesting that these factors are not necessary for the occurrence of a cocaine-related infarct. Multiple overlapping mechanisms may be responsible, including vasospasm, sudden onset of hypertension, myocardial infarction with cardiac arrhythmias, increased platelet aggregation, and vasculitis.
Dietary treatment of atherosclerosis abolishes hyperresponsiveness of retinal blood vessels to serotonin in monkeys.
Authors: Faraci F M , Armstrong M L , Heistad D D
Published: June 2011

Atherosclerosis alters vascular responses of the eye to serotonin. Augmented vasoconstrictor responses in the retina to serotonin are associated with functional impairment and may contribute to amaurosis fugax. The goal of this study was to test the hypothesis that dietary treatment of atherosclerosis restores vascular responses of the eye toward normal.

We measured blood flow to the retina using microspheres in six normal monkeys, five atherosclerotic monkeys, and five atherosclerotic monkeys that were fed a normal (regression) diet for 18 months.

Infusion of 8 and 40 micrograms.min-1.kg-1 serotonin into the left atrium had little effect on blood flow to the retina in normal monkeys. In contrast, the high dose of serotonin reduced blood flow to the retina by a mean +/- SEM of 81 +/- 9% (p less than 0.05) in atherosclerotic monkeys. In monkeys that were fed the regression diet, serotonin had no effect on blood flow to the retina.

Regression of atherosclerosis abolishes augmented responses of the retinal circulation to serotonin.
Age-related vulnerability to cerebral ischemia in spontaneously hypertensive rats.
Authors: Yao H , Sadoshima S , Ooboshi H , Sato Y , Uchimura H , Fujishima M
Published: June 2011

We sought to determine the effects of aging on regional cerebral blood flow and ischemic brain damage in transient cerebral ischemia in rats.

Five adult (5-6 months) and five aged (18-22 months) female spontaneously hypertensive rats were subjected to 20 minutes of bilateral carotid occlusion and 60 minutes of recirculation under amobarbital anesthesia (100 mg/kg i.p.). Regional cerebral blood flow in the hippocampus and striatum was measured using the hydrogen clearance method. Nine adult and 14 aged rats were subjected to 20 minutes of bilateral carotid occlusion or were sham-operated under ether anesthesia. Seven days after 20 minutes of cerebral ischemia, the rats' brains were perfusion fixed. Ischemic damage in the hippocampus and striatum was graded (0 [normal] to 3 [majority of neurons damaged]).

After 20 minutes of bilateral carotid occlusion, striatal cerebral blood flow decreased to 9.1 +/- 1.5 and 3.9 +/- 2.0 ml/100 g/min in aged and adult rats, respectively, and hippocampal cerebral blood flow decreased to 8.6 +/- 2.4 and 5.7 +/- 2.4 in aged and adult rats, respectively. Although these ischemic cerebral blood flow values were not significantly different between the two age groups, scores for ischemic damage in the hippocampus CA-1 subfield and striatum were significantly higher in aged than in adult rats (p less than 0.05, Kruskal-Wallis' h test with Bonferroni correction).

We conclude that aging may be a primary factor in the development of greater ischemic neuronal damage observed in aged hypertensive rats.
Does vasospasm occur in small pial arteries and arterioles of rabbits?
Authors: Nihei H , Kassell N F , Dougherty D A , Sasaki T
Published: June 2011

Vasospasm is a serious complication associated with subarachnoid hemorrhage. Successful management of vasospasm will ultimately depend on a clear understanding of the scope of this phenomenon, including whether arterial elements of different calibers are equally affected. We therefore examined the responses to subarachnoid hemorrhage in rabbit basilar arteries, small pial arteries, and arterioles.

We compared the brain stem pial arteries of 10 perfusion-fixed male New Zealand White rabbits after experimental subarachnoid hemorrhage to those of five control rabbits using morphological analysis of cross-sections of plastic-embedded vessels. After subarachnoid hemorrhage, the internal elastic lamina was highly corrugated in all basilar arteries (mean diameter 319 +/- 51 microns). These arteries were severely constricted in comparison with the control group, in which the mean diameter was 691 +/- 17 microns, and corrugation of the internal elastic lamina was not present. In contrast, small pial arteries and arterioles very rarely demonstrated a vasoconstrictive configuration after subarachnoid hemorrhage. The contractility of the smaller vessels was confirmed by injecting 2 mg/kg BaCl2 intracisternally. Following BaCl2 injection, corrugation of the internal elastic lamina was detected in the small arteries and arterioles as well as the basilar arteries.

We conclude that experimental chronic vasospasm after subarachnoid hemorrhage in rabbits tends to occur in large conducting arteries rather than in smaller pial arteries and arterioles.
Increase in cerebrospinal fluid and plasma levels of 3-methoxy-4-hydroxyphenylglycol in acute stroke.
Authors: Kanda T , Azuma K , Sakai F , Tazaki Y
Published: June 2011

3-Methoxy-4-hydroxyphenylglycol is known to be a principal metabolite of brain norepinephrine and to be released into the blood and cerebrospinal fluid in association with activation of the central noradrenergic system. We examined changes in plasma and cerebrospinal fluid levels of 3-methoxy-4-hydroxyphenylglycol during acute stroke to see if there might be a correlation between these and the patient's clinical state.

We measured plasma levels of 3-methoxy-4-hydroxyphenylglycol in 32 control subjects and in 50 patients with brain hemorrhage and 57 patients with brain infarction who were admitted to the hospital within 72 hours after onset. In addition, we estimated 3-methoxy-4-hydroxyphenylglycol concentrations in the cerebrospinal fluid of 37 patients with brain infarction and eight control patients.

Mean +/- SEM values for plasma 3-methoxy-4-hydroxyphenylglycol in the patients with brain hemorrhage and those with brain infarction were 7.3 +/- 0.5 and 6.6 +/- 0.5 ng/ml, respectively. Both values were significantly higher than that obtained in the 32 control subjects (4.6 +/- 0.3 ng/ml, p less than 0.01). Plasma levels of 3-methoxy-4-hydroxyphenylglycol correlated well with state of consciousness and prognosis. The mean +/- SEM level of 3-methoxy-4-hydroxyphenylglycol in the cerebrospinal fluid of the 37 patients with brain infarction (10.9 +/- 0.6 ng/ml) was also significantly higher than that in the eight control patients (7.9 +/- 0.6 ng/ml, p less than 0.01).

The observed increase in plasma and cerebrospinal fluid levels of 3-methoxy-4-hydroxyphenylglycol implies that the activity of the central noradrenergic neurons may be enhanced at the onset of stroke, and these levels may be related to some extent to the clinical state and prognosis of stroke patients.
Effect of hemorrhagic hypotension on cerebrovascular reactivity and ultrastructure in the cat.
Authors: Kovách A G , Szabó C , Faragó M , Lohinai Z , Fehér E
Published: June 2011

The goal of this study was to determine the alterations in contractile and dilatory responses and ultrastructure of the feline middle cerebral artery after hemorrhagic hypotension.

In the sodium pentobarbital anesthetized cats, a steady 50 mm Hg level of hypotension was reached by bleeding into a reservoir and maintained at this level by further bleeding or autotransfusion for 2 hours. Rings of the arteries, from control animals and from animals after hypotension, were suspended for isometric tension recording in organ chambers filled with modified Krebs-Henseleit solution, aerated with 95% O2-5% CO2 at 37 degrees C, and their reactions to contractile and relaxant agents were tested. Vascular ultrastructure was studied by electron microscope.

Endothelium-dependent relaxations induced by 10(-8) M acetylcholine were enhanced, whereas there was a marked inhibition of the relaxation at 10(-6) M. Relaxations induced by adenosine triphosphate and adenosine showed an impairment. Contractions induced by norepinephrine and prostaglandin F2 alpha remained unchanged, whereas 5-hydroxytryptamine caused a more pronounced contraction after hypotension. No alterations in the morphology of endothelium or smooth muscle were found after hemorrhage. There was, however, a marked decrease in the number of transmitter vesicles in the perivascular nerve terminals.

The present results show marked alterations in cerebrovascular reactivity and ultrastructure of the adventitia after hypotension. These alterations might play an important role in the development of cerebral vasoconstriction during and after this hemorrhagic state.
Global cerebral ischemia in piglets under conditions of mild and deep hypothermia.
Authors: Sutton L N , Clark B J , Norwood C R , Woodford E J , Welsh F A
Published: June 2011

To investigate the effects of hypothermia on the rate of change and degree of recovery of brain adenosine triphosphate and phosphocreatine concentrations and intracellular pH, we have developed a model that allows phosphorus nuclear magnetic resonance spectroscopy of the intact piglet brain during circulatory arrest.

Three groups of piglets were studied. Three control animals underwent cardiopulmonary bypass at normothermia for 1 hour; five group 1 animals underwent bypass at a brain temperature of 15 degrees C, followed by a period of circulatory arrest such that adenosine triphosphate was absent for 21 minutes, followed by 1 hour of reperfusion; and five group 2 animals underwent bypass at a brain temperature of 37 degrees C, followed by a period of circulatory arrest such that adenosine triphosphate was absent for 21 minutes, followed by reperfusion for 1 hour.

Control animals showed no significant metabolic effects of bypass. Group 1 animals showed a slower decay of the adenosine triphosphate and phosphocreatine concentrations than group 2 animals, consistent with a lower metabolic rate, and had a higher pH at the onset of ischemia. Recovery of the adenosine triphosphate concentration was significantly better in group 1 animals (95%) than in group 2 animals (30%) (p less than 0.02), and recovery of the phosphocreatine concentration was also better in group 1 animals (93%) than in group 2 animals (32%) (p less than 0.02). Intracellular pH recovered in group 1 animals, but not in group 2 animals. Regional biochemical assays of metabolites performed in the group 2 piglets and in five pilot piglets exposed to deep hypothermia generally confirmed the spectroscopic findings but demonstrated considerable regional variation, specially in the group 2 piglets' brains.

We conclude that hypothermia exerts a protective effect on the piglet brain during global ischemia even after the adenosine triphosphate pool has been completely depleted.
Myoendothelial junctions in human brain arterioles.
Authors: Aydin F , Rosenblum W I , Povlishock J T
Published: June 2011

The purpose of this work was to determine whether myoendothelial junctions were present in human brains.

We examined vessels of approximately 30-70 microns i.d. from the brains of five autopsied adult patients. Myoendothelial junctions were found in vessels throughout this range, in both surface arterioles and penetrating arterioles, and were classified into three types. The number of myoendothelial junctions, expressed per unit length of vessels, was five times greater in the smallest than in the largest vessels. Thus, we found 1.62 junctions per millimeter length in arterioles less than 60 microns diameter and 0.31 junctions per millimeter length in arterioles greater than 220 microns diameter.

These findings provide an anatomic basis for communication between endothelial cells and smooth muscle of brain microvessels in humans. The function of this intercellular communication is not yet known; however, findings in animals suggest that endothelium may be required for propagated constriction in brain vessels. The existence of myoendothelial junctions in human brain provides a basis for the hypothesis that propagated constriction depends on transmission of some message or messenger between endothelial cells and muscle.
Stroke in a young adult with familial plasminogen disorder.
Authors: Furlan A J , Lucas F V , Craciun R , Wohl R C
Published: June 2011

We report a new plasminogen disorder detected in a 29-year-old man with a cerebellar infarct. To our knowledge, plasminogen disorders have not been previously linked with stroke.

Tests for well-recognized causes of stroke were negative. However, a screening hypercoagulation profile indicated low functional levels of plasminogen activity. Immunologic plasminogen (Laurell technique) was 64% of normal (normal level, 80-130%). The rate of plasmin generation induced by adding urokinase to plasma was also low. Plasminogen activator, free protease, and alpha 2-plasmin inhibitor levels were normal. Family studies detected a similar plasminogen abnormality in the patient's mother and 9-year-old son, both of whom are asymptomatic.

Our patient shows a congenital, heterozygous, functionally abnormal plasminogen. Although the exact relationship to stroke is unclear, we suggest screening young patients with unexplained stroke for plasminogen defects using commercially available assay systems.
Stroke recurrence within 2 years after ischemic infarction.
Authors: Hier D B , Foulkes M A , Swiontoniowski M , Sacco R L , Gorelick P B , Mohr J P , Price T R , Wolf P A
Published: June 2011

We prospectively studied stroke recurrence in 1,273 patients with ischemic stroke who were entered into the Stroke Data Bank. Median follow-up was 13 months. The 2-year cumulative recurrence rate among these patients was 14.1%. Age, sex, race, history of hypertension, atrial fibrillation, or transient ischemic attacks, and stroke location were not associated with a higher risk of stroke recurrence. Patients with an elevated blood pressure, an abnormal initial computed tomogram, or a history of diabetes mellitus were at a higher risk of stroke recurrence. In contrast, patients with an infarct of unknown cause were at a lower risk of stroke recurrence than patients with a defined stroke mechanism, such as lacune, embolism, or atherosclerosis. A multivariate model suggests that patients at the lowest risk for stroke recurrence have a low diastolic blood pressure, no history of stroke, no history of diabetes mellitus, and an infarct of unknown cause.
Effect of stable xenon on regional cerebral blood flow and the electroencephalogram in normal volunteers.
Authors: Hartmann A , Dettmers C , Schuier F J , Wassmann H D , Schumacher H W
Published: June 2011

We evaluated the effects of breathing 35% stable xenon in 65% oxygen on regional cerebral blood flow and the electroencephalogram in 20 normal volunteers. We measured blood flow in 32 brain regions over both hemispheres with the xenon-133 intravenous injection technique in two protocols. In the first protocol (n = 10), a baseline study was followed by a second study during 5 minutes of breathing stable xenon; in the other protocol (n = 8), the baseline study was followed by a second study after 5 minutes of breathing stable xenon. Two volunteers were excluded due to excessive movements during the inhalation of stable xenon. Some of the remaining 18 volunteers had varying alterations of consciousness accompanied by electroencephalogram changes. After stable xenon inhalation the electroencephalogram returned to normal within 2-3 minutes. During stable xenon inhalation mean +/- SD PECO2 dropped significantly from 39.4 +/- 4.4 to 33.3 +/- 5.4 mm Hg in the first protocol and from 39.4 +/- 2.6 to 34.8 +/- 4.1 mm Hg in the second protocol due to hyperventilation in 13 volunteers. Mean regional cerebral blood flow increased significantly by 13.5-25.4% without correction for PECO2. In the first protocol regional cerebral blood flow increased by greater than 12% in 11-14 (depending on the flow parameter) of the 20 hemispheres. In the second protocol regional cerebral blood flow increased by greater than 12% in 9-13 of the 16 hemispheres. We conclude that cautious interpretation is necessary in the assessment of regional cerebral blood flow with 35% xenon-enhanced computed tomography.
Atrial fibrillation after stroke in the elderly.
Authors: Friedman P J
Published: June 2011

To examine the relationship between atrial fibrillation and mortality after stroke, we studied 186 men and 167 women from the Waikato Stroke Registry whose mean age was 75.2 +/- 7.5 years. Twenty-three percent (82 of 353) had atrial fibrillation or flutter on their admission electrocardiogram. This group differed significantly from that with sinus rhythm in three respects: 1) They were older (p less than 0.01); 2) they had more severe current stroke deficit as evidenced by lower limb power (p less than 0.05) and Mini-Mental State Score (p less than 0.001), higher incidence of homonomous hemianopia (p less than 0.05), and lower incidence of lacunar syndrome stroke (p less than 0.001); and 3) they had a significantly higher incidence of cardiomegaly and congestive heart failure (p less than 0.01). Functional outcome was insignificantly better in the group with sinus rhythm. During a mean follow-up period of 18 months, mortality was significantly higher in the group with atrial fibrillation (p = 0.001). Proportional hazards modeling, however, showed that the apparently poorer survival in those patients with atrial fibrillation could be explained by factors other than cardiac rhythm, such as age, Mini-Mental State Score, level of consciousness, and interstitial edema on admission chest radiograph. Thus, atrial fibrillation was not an independent predictor of survival after stroke.
Cromakalim dilates rat cerebral arteries in vitro.
Authors: Nagao T , Sadoshima S , Kamouchi M , Fujishima M
Published: June 2011

Using an in vitro perfusion method, we examined the effects of cromakalim, a potassium channel opener, on the superior cerebellar arteries of 24 rats. Cromakalim had no effect on contractions induced by 129 mM K+ until a concentration of 10(-5) M was reached. Contractions evoked by 10(-5) M serotonin were attenuated by cromakalim in a concentration-dependent manner (p less than 0.05). The diameter of untreated superior cerebellar arteries remained almost constant with increasing perfusion pressure. However, in the presence of cromakalim vessel diameter increased with increasing perfusion pressure. At concentrations of 3 x 10(-6) M, cromakalim also inhibited basal myogenic tone and dilated unstimulated arteries (p less than 0.01). These results suggest that cromakalim is a cerebrovascular dilator acting on both receptor-mediated and myogenic contractions.
Sodium, ATP, and intracellular pH transients during reversible complete ischemia of dog cerebrum.
Authors: Eleff S M , Maruki Y , Monsein L H , Traystman R J , Bryan R N , Koehler R C
Published: June 2011

We tested the hypotheses that with the onset of cerebral ischemia, massive cellular sodium influx does not occur until adenosine triphosphate is fully depleted and that on reperfusion, neuronal sodium efflux does not occur until adenosine triphosphate is fully restored. We examined the temporal relationships among transcellular sodium, energy metabolism, and intracellular pH with sodium and phosphorus magnetic resonance spectroscopy in a new, hemodynamically stable, brain stem-sparing model of reversible, complete cerebral ischemia in eight anesthetized dogs. Inflation of a neck tourniquet after placement of glue at the tip of the basilar artery resulted in decreased blood flow to the cerebrum from 29 +/- 5 to 0.3 +/- 0.5 ml/min/100 g. Medullary blood flow was not significantly affected, and arterial blood pressure was unchanged. Sodium signal intensity decreased and did not lag behind the fall in adenosine triphosphate. After 12 minutes of ischemia, reperfusion resulted in a more rapid recovery of sodium intensity (12.4 +/- 4.8 minutes) than either adenosine triphosphate (16.5 +/- 3.7 minutes) or intracellular pH (38.9 +/- 1.8 minutes). Because intracellular sodium has a weaker signal than extracellular sodium, the decreased sodium intensity is interpreted as sodium influx and indicates that sodium influx does not require full depletion of adenosine triphosphate. Rapid recovery of sodium intensity during early reperfusion may represent sodium efflux, although increased plasma volume and sodium uptake from plasma may also contribute. If our interpretation of the sodium signal is correct, delayed recovery of adenosine triphosphate may be due to the utilization of adenosine triphosphate for the restoration of transcellular sodium gradient.
Clentiazem reduces infarct size in rabbit middle cerebral artery occlusion.
Authors: Kaminow L , Bevan J
Published: June 2011

We assessed the value of pretreatment with clentiazem (8-chlorodiltiazem), a diltiazem derivative with cerebroselective properties, on the consequences of surgical occlusion of the middle cerebral artery via a transorbital approach in 38 rabbits. Nineteen rabbits received 1.7 (n = 5), 5 (n = 8), or 15 (n = 6) mg/kg clentiazem orally four times a day for 24 hours before and 48 hours after occlusion. Upon sacrifice, a segment of the right middle cerebral artery distal to the occlusion and a corresponding segment from the nonoccluded left middle cerebral artery were mounted on myographs for in vitro study of their reactivity to histamine, acetylcholine, serotonin, norepinephrine, and electrical stimulation of intramural sympathetic nerves. Morphometric measurements of 2,3,5-triphenyltetrazolium chloride-stained brain slices permitted us to estimate infarct volume. Pretreatment with 1.7, 5, and 15 mg/kg clentiazem significantly reduced infarct volume (p less than 0.05, p less than 0.01, and p less than 0.01, respectively). Mean infarct volume of the 15 mg/kg-treated group was only 4% that of the untreated group. There were no postoperative deaths in any treated group compared with a death rate of 36% in the untreated group. Mean values for vascular smooth muscle contractility to histamine and relaxation to acetylcholine were significantly enhanced in vessels from treated rabbits. These studies indicate that pretreatment with clentiazem offers cerebral protection and significantly reduces infarct volume as well as arterial wall damage beyond the occlusion.
Probability of stroke: a risk profile from the Framingham Study.
Authors: Wolf P A , D'Agostino R B , Belanger A J , Kannel W B
Published: June 2011

A health risk appraisal function has been developed for the prediction of stroke using the Framingham Study cohort. The stroke risk factors included in the profile are age, systolic blood pressure, the use of antihypertensive therapy, diabetes mellitus, cigarette smoking, prior cardiovascular disease (coronary heart disease, cardiac failure, or intermittent claudication), atrial fibrillation, and left ventricular hypertrophy by electrocardiogram. Based on 472 stroke events occurring during 10 years' follow-up from biennial examinations 9 and 14, stroke probabilities were computed using the Cox proportional hazards model for each sex based on a point system. On the basis of the risk factors in the profile, which can be readily determined on routine physical examination in a physician's office, stroke risk can be estimated. An individual's risk can be related to the average risk of stroke for persons of the same age and sex. The information that one's risk of stroke is several times higher than average may provide the impetus for risk factor modification. It may also help to identify persons at substantially increased stroke risk resulting from borderline levels of multiple risk factors such as those with mild or borderline hypertension and facilitate multifactorial risk factor modification.
Effect of carbon dioxide and oxygen on endothelin production by cultured porcine cerebral endothelial cells.
Authors: Yoshimoto S , Ishizaki Y , Sasaki T , Murota S
Published: June 2011

We have previously reported the production of endothelin, a potent vasoconstrictor peptide, by porcine cerebral microvessel endothelia and suggested its important role in the regulation of local blood flow within the brain. In our present study, radioimmunoassay with anti-porcine endothelin antiserum revealed that endothelin, produced by cerebral microvessel endothelia grown on a filter, is released mainly to the basement membrane side, not the vascular lumen side. This finding suggests that endothelin constricts arterioles locally where it is produced by endothelia. We also found that cerebral microvessel endothelia produce less endothelin under low oxygen pressure and more endothelin under low carbon dioxide pressure. Our results suggest that endothelin has a role in the regulation of cerebral blood flow in response to oxygen and carbon dioxide pressure.
Thrombosis in a congenitally bifurcated superior sagittal sinus.
Authors: Hosley M A , Fisher M , Lingley J F
Published: June 2011

A 26-year-old woman had a peripartum venous thrombotic stroke involving the right parietal lobe. The initial thrombus was present only in the right channel of a congenitally bifurcated superior sagittal sinus. This diagnosis and subsequent thrombus extension were readily shown by magnetic resonance imaging in contrast to equivocal angiography. A subsequent, prospective review of 100 patients undergoing cranial magnetic resonance imaging showed the presence of similarly bifurcated superior sagittal sinuses in two. The patient stabilized after therapy with intravenous heparin, but switching her medication to oral warfarin sodium was followed by clinical deterioration and propagation of the thrombus, necessitating resumption of intravenous heparin. No coagulopathy was identified.
Scleroderma and central nervous system vasculitis.
Authors: Pathak R , Gabor A J
Published: June 2011

We describe a patient with scleroderma (CREST syndrome) and central nervous system vasculitis. While angiography demonstrated segmental symmetrical arterial narrowing characteristic of vasculitis, results of leptomeningeal biopsy were normal. There was no evidence of systemic vasculitis, renal failure, or malignant hypertension previously thought to be required to explain central nervous system dysfunction in patients with scleroderma. Signs and symptoms attributable to vasculitis were reversible with aggressive immunosuppressive therapy.
Leukoaraiosis and ventricular enlargement in patients with ischemic stroke.
Authors: Hijdra A , Verbeeten B
Published: June 2011

We studied the relationship between ventricular size and nonspecific periventricular lucency on computed tomograms (leukoaraiosis) in 192 patients with ischemic stroke. Leukoaraiosis did not occur in 21 patients less than 50 years of age; ventricular size could not be measured in an additional 29. Leukoaraiosis was graded from 0 to 4 on a semiquantitative scale; bicaudate, frontal horn, and posterior horn indices were used as measures of ventricular size. Patients with leukoaraiosis were older (difference between means 7 years, t = 5.3, df = 140, p less than 0.0001) and had larger bicaudate indices (difference between means 0.023, t = 3.54, df = 140, p = 0.0007) than patients without leukoaraiosis. Multiple regression analysis demonstrated that the effects of age and leukoaraiosis were independent. No effect of lesion type (cortical or lacunar infarct, or both) on bicaudate index could be demonstrated. Larger values for the bicaudate index were associated with a predominantly anterior location of leukoaraiosis. The frontal horn and occipital horn indices increased with age, but we could not find an effect of leukoaraiosis on these indices.
Time course of intracellular edema and epileptiform activity following prenatal cerebral ischemia in sheep.
Authors: Williams C E , Gunn A , Gluckman P D
Published: June 2011

The role of edema in the pathogenesis of hypoxic-ischemic injury in the immature brain is controversial. We studied 15 chronically instrumented fetal sheep following transient cerebral ischemia, to estimate changes in extracellular space using an impedance technique, to quantify the electroencephalogram with real-time spectral analysis, and to assess histologic outcome 3 days after the insult. These measurements were made in the parasagittal cortex. There was a rapid loss of extracellular space from 5 +/- 2 minutes after the onset of ischemia. Following 10 minutes of ischemia (n = 7) the intracellular edema peaked but then quickly resolved (6 +/- 4 minutes), and mild selective neuronal loss was seen. In contrast, the swelling was biphasic after 30-40 minutes of ischemia (n = 8). The early edema resolved slowly (28 +/- 12 minutes) but incompletely, and secondary swelling began at 7 +/- 2 hours and peaked at 28 +/- 6 hours. The early swelling was the more severe. Postinsult epileptiform activity began at 8 +/- 2 hours and peaked at 10 +/- 3 hours; later there was laminar necrosis of the underlying cortex. The secondary decrease of extracellular space indicates that a progressive loss of membrane function started with the onset of postischemic epileptiform activity. The increased metabolic load of the epileptiform activity may have worsened this delayed deterioration.
Allopurinol pretreatment improves evoked response recovery following global cerebral ischemia in dogs.
Authors: Mink R B , Dutka A J , Hallenbeck J M
Published: June 2011

The reperfusion of previously ischemic tissue may lead to the formation of highly reactive free radicals that promote tissue injury. Xanthine oxidase has been implicated as one source of these free radicals. We examined the role of xanthine oxidase in brain injury using a cerebrospinal fluid compression model of global cerebral ischemia with 15 minutes of ischemia and 4 hours of reperfusion. Seven dogs were pretreated with the xanthine oxidase inhibitor allopurinol (50 mg/kg for 5 days). Neurophysiological recovery was monitored with cortical somatosensory evoked potentials. As an attempt to correlate brain recovery with the mechanism of protection, free brain malondialdehyde was measured at the end of reperfusion by high-performance liquid chromatography. Brain water content was measured by wet-dry weights. Compared with seven untreated control dogs, allopurinol pretreatment significantly improved recovery of somatosensory evoked potentials after 4 hours of reperfusion. However, the amount of free malondialdehyde in the allopurinol-treated dogs was 32% greater than that in the controls. Brain water content was similar in the two groups. These results suggest that xanthine oxidase contributes to brain injury after ischemia and reperfusion. However, tissue damage caused by xanthine oxidase may be mediated through mechanisms other than free radical production.
Neurological deterioration under isovolemic hemodilution with hydroxyethyl starch in acute cerebral ischemia.
Authors: Mast H , Marx P
Published: June 2011

In a prospective study, we randomly allocated 70 patients with acute ischemic stroke to two therapy groups. Up to interim analysis, 33 patients underwent bloodletting, with simultaneous infusion of an identical volume of hydroxyethyl starch (10%, 200/0.5). The target hematocrit was 35%. A control group of 37 patients did not receive hemodilution. Apart from an unequal sex distribution, the two groups were comparable with regard to age, cardiovascular risk factors, and medical history. In the hemodilution group, the mean hematocrit fell from 44.4% to 37.7%. After 14 days, improvement on the neurological score scale was 3.3 points in the hemodilution group compared with 6.5 points in the control group (p = 0.12). Subgroups with early inclusion (less than 12 hours) or pronounced lowering of hematocrit (greater than 15% of initial hematocrit) also did not profit from hemodilution. Clinical deterioration observed in eight hemodilution group patients (p less than 0.01) led to discontinuation of the study for ethical reasons.
Effect of tissue plasminogen activator on intimal platelet accumulation in cerebral arteries after subarachnoid hemorrhage in cats.
Authors: Yamamoto Y , Clower B R , Haining J L , Smith R R
Published: June 2011

Recombinant tissue plasminogen activator may be effective in preventing cerebral vasospasm after subarachnoid hemorrhage by resolving subarachnoid clots. We previously demonstrated that blood placed on the adventitial surface of cerebral arteries enhances intimal platelet accumulation, positively correlating with endothelial damage and other pathologic changes in vessel walls. In this study, we investigated the ability of a single bolus injection of tissue plasminogen activator to prevent platelet accumulation in cerebral vessels after subarachnoid hemorrhage. Subarachnoid hemorrhage was produced in cats by the transorbital intracisternal injection of 2.5 ml autologous arterial blood around the proximal part of the right middle cerebral artery. In 10 animals, 25 micrograms tissue plasminogen activator was injected at intervals of 10 (five cats) and 60 minutes (five cats) after subarachnoid hemorrhage. Intracisternal physiological saline (0.5 ml) was injected in six cats 10 minutes after subarachnoid hemorrhage. Platelets labeled with indium-111 were injected intravenously just before subarachnoid hemorrhage, and their radioactivity was measured in cerebral arteries at death. The results indicated that, after subarachnoid hemorrhage, early injection of tissue plasminogen activator inhibited intimal platelet accumulation, but later injection did not, although the extent of subarachnoid clot was reduced at both plasminogen injection times.
Effect of atherosclerosis on cerebral vascular responses to activation of leukocytes and platelets in monkeys.
Authors: Faraci F M , Lopez A G , Breese K , Armstrong M L , Heistad D D
Published: June 2011

The goal of this study was to test the hypothesis that atherosclerosis alters responses of cerebral arteries and the ocular circulation to the activation in vivo of leukocytes and platelets. We measured blood flow to the brain and eye using microspheres and pressure in the cerebral microvessels of normal and atherosclerotic monkeys. The intracarotid injection of 10(-7) M N-formyl-L-methionyl-L-leucyl-L-phenylalanine to activate leukocytes did not alter cerebral blood flow in 11 normal or 10 atherosclerotic monkeys but increased the resistance of large cerebral arteries by 46 +/- 11% (mean +/- SEM) in the atherosclerotic animals. The injection of N-formyl-L-methionyl-L-leucyl-L-phenylalanine did not alter blood flow to the eye in 10 normal monkeys but decreased blood flow to the choroid by 38 +/- 9% in 11 atherosclerotic monkeys. The intracarotid injection of 3 x 10(-9) M prostaglandin E2, a leukocyte product, produced an increase in the resistance of large cerebral arteries in five atherosclerotic but not in six normal monkeys. Prostaglandin E2 reduced blood flow to the retina and choroid in the atherosclerotic monkeys by 62 +/- 22% and 65 +/- 17%, respectively. The intracarotid infusion of 25 micrograms/min collagen to activate platelets increased cerebral blood flow by 21 +/- 5% in 10 normal monkeys but did not alter it in 11 atherosclerotic monkeys. Collagen did not alter blood flow to the choroid in 10 normal monkeys but decreased it by 29 +/- 8% in 11 atherosclerotic monkeys.(ABSTRACT TRUNCATED AT 250 WORDS)
Stress hormone and blood glucose response following acute stroke in the elderly.
Authors: O'Neill P A , Davies I , Fullerton K J , Bennett D
Published: June 2011

We studied the relation of reactive hyperglycemia, stress hormone response, and outcome in 23 consecutive elderly patients (median age 80 [range 75-92] years) following an acute first stroke. The median delay from the onset of the stroke to the first blood sample (day 0) was 9 (range 4-22) hours. Subsequent blood samples were taken, after fasting, for the determination of blood glucose, cortisol, catecholamine, insulin, C-peptide, glucagon, and lactate concentrations on days 1, 2, 3, 7, 14, 30, and 90. For all 23 patients, a significant relation was found between the blood glucose concentration and survival (p = 0.03) and the blood glucose concentration decreased with time (p less than 0.001). There was also a significant relation between blood glucose concentration and outcome (p = 0.02). For the 15 patients with complete data, the major determinants of the blood glucose concentration were the cortisol, insulin, and glucagon concentrations (all p less than 0.001), which accounted for 42% of the variance. When all the indexes were analyzed together by logistic regression, only the cortisol concentration was related to outcome (p = 0.02). Hyperglycemia following a stroke probably reflects the intensity of the stress hormone response. We have confirmed that hyperglycemia is a predictor of outcome in persons with stroke.
Microangiopathy of the brain, retina, and ear: improvement without immunosuppressive therapy.
Authors: Gordon D L , Hayreh S S , Adams H P
Published: June 2011

We describe a pregnant young woman with branch retinal arteriolar occlusions, encephalopathy, and hearing loss in whom we demonstrated a patent foramen ovale. She improved while receiving anticoagulants and no immunosuppressive therapy. The microangiopathic syndrome of retinopathy, encephalopathy, and deafness may be due to a disturbance of coagulation and/or microembolism.
Safety and tolerance of oral dextromethorphan in patients at risk for brain ischemia.
Authors: Albers G W , Sáenz R E , Moses J A , Choi D W
Published: June 2011

Experimental ischemia models have shown the antitussive dextromethorphan to be an N-methyl-D-aspartate antagonist with neuroprotective properties. We treated 10 patients with a history of recent stroke or transient ischemic attack with oral dextromethorphan (60 mg q.i.d.) for 3 weeks in a placebo-controlled, double-blind, crossover tolerance study. We documented no clinical evidence of toxicity attributable to dextromethorphan in this preliminary study.
Risk factors for stroke as predictors of platelet membrane fluidity in Alzheimer's disease.
Authors: Zubenko G S , Brenner R P , Teply I
Published: June 2011

We have previously reported that increased platelet membrane fluidity identifies a subgroup of patients with Alzheimer's disease who have distinct clinical features including an earlier age of symptomatic onset, a more rapidly progressive cognitive decline, and a decreased prevalence of focal electroencephalographic findings. In the current study, these patients also exhibited a decreased prevalence of risk factors for stroke compared with patients who had normal platelet membrane fluidity. Our findings suggest that the platelet membrane abnormality describes a clinical subgroup of patients with Alzheimer's disease who are less likely to have coexisting cerebrovascular disease than the remaining patients who meet clinical consensus criteria for probable Alzheimer's disease.
Use of sonography to evaluate carotid atherosclerosis in the elderly. The Cardiovascular Health Study. CHS Collaborative Research Group.
Authors: O'Leary D H , Polak J F , Wolfson S K , Bond M G , Bommer W , Sheth S , Psaty B M , Sharrett A R , Manolio T A
Published: June 2011

Carotid sonography is being performed on more than 5,000 participants in the Cardiovascular Health Study, a prospective, multicenter study of cardiovascular disease in men and women aged 65 years and older. The sonographic methods used to examine and measure the extracranial carotid arteries are described. Initial validation studies were performed on 61 subjects with a mean age of 68.6 years. Analysis of within- and between-sonographer differences and between-reader differences were performed for selected variables. In general, the mean absolute differences for within- and between-sonographer comparisons were small, with even less variability between readers. Variability was less for the common carotid artery than for the internal carotid artery. These data suggest that carotid sonography is a reliable and reproducible method for use in the study of carotid atherosclerosis in population studies.