bluuebunny/crossref_metadata_2025 huggingface dataset:
A model for management of patients with stroke during the acute phase. Outcome and economic implications.
Authors: Odderson I R , McKenna B S
Published: June 2011

The purpose of the study was to develop a clinical pathway for patients with nonhemorrhagic stroke during the acute hospital phase to improve the quality of care and reduce costs.

The pathway included standard admission orders and a swallow screen on day 1 of hospitalization. Physical therapy, occupational therapy, speech therapy, and social worker assessments were done on day 2. A physiatry consult was performed on day 3 if indicated, and by day 4 a discharge target date and disposition were addressed.

Outcomes for 121 patients during the first year of pathway implementation are reported. The average length of stay on the acute service decreased from 10.9 days to 7.3 days (P < .05), reducing the charges per patient by 14.6%. Complications in the form of urinary tract infections and aspiration pneumonia rates decreased by 63.2% (P < .05) and 38.7%, respectively.

We conclude that the implementation of a clinical pathway for patients with acute, nonhemorrhagic stroke resulted in a significant reduction in length of stay, charges, and complications while improving the quality of care.
Relationship of transcranial Doppler flow velocities and arteriovenous malformation feeding artery pressures.
Authors: Fleischer L H , Young W L , Pile-Spellman J , terPenning B , Kader A , Stein B M , Mohr J P
Published: June 2011

Feeding mean arterial pressure immediately proximal to the nidus of arteriovenous malformations may influence the frequency of spontaneous intracerebral hemorrhage. This study assessed the usefulness of transcranial Doppler ultrasound velocities as a noninvasive estimate of feeding mean arterial pressure.

We studied 41 patients undergoing 73 staged treatments of arteriovenous malformations with endovascular embolization, surgery, or both. Before treatment during the awake state, transcranial Doppler mean and peak velocities were recorded in proximal Willisian vessels. During superselective angiography with the patient under conscious sedation or during surgery with the patient under general anesthesia, feeding mean arterial pressure was measured through a 1.5F transfemoral intracranial microcatheter or a 26-g needle by direct puncture. Measurement of insonated artery diameter was possible in 41 embolizations, and a flow velocity index (mL/min) and Reynolds' number were estimated.

Mean +/- SEM feeding mean arterial pressure was 38 +/- 2 mm Hg at a systemic mean arterial pressure of 77 +/- 2 mm Hg; mean velocity was 102 +/- 4 cm/s. There was an inverse correlation between feeding mean arterial pressure and parent artery mean velocity (y = -0.74x + 130, r = .35, P = .0025). The best correlation was for the first treatment in each patient (n = 27) using the highest peak velocity obtainable in a Willisian vessel ipsilateral to the arteriovenous malformation (y = -1.61x + 221, r = .62, P = .0005). Flow velocity index (775 +/- 106 mL/min) did not correlate with feeding mean arterial pressure, but there was a weak correlation with Reynolds' number (y = -12x + 1616, r = .27, P = .1283). Mean Reynolds' number was 1257 +/- 119.

Transcranial Doppler mean velocity is correlated with feeding mean arterial pressure but only weakly predictive. Considerations influencing the relation of distal feeding mean arterial pressure to proximal mean velocity might include the influence of other fistulae in the circuit between major inflow and outflow channels as well as turbulent flow at vascular branch points between point of insonation and the nidus, as suggested by Reynolds' number values of more than 400.
Clinical features, pathogenesis, and computed tomographic characteristics of internal watershed infarction.
Authors: Bladin C F , Chambers B R
Published: June 2011

Infarction in the internal border-zone region has been described radiologically and pathologically. The aim of this study was to define the clinical and pathophysiological correlates of internal watershed infarction.

Eighteen consecutive stroke patients with evidence of internal watershed infarction on computed tomography (CT) were studied.

Two CT patterns were identified: 6 patients had confluent internal watershed infarction (CIWI), and 12 patients had partial internal watershed infarction (PIWI). Syncopal symptoms and/or documented hypotension were prominent in both groups. Patients with CIWI usually presented with stepwise onset of contralateral hemiplegia and recovered poorly; patients with PIWI usually had discrete episodes of brachiofacial sensorimotor deficit and good recovery. Both groups had evidence of cortical involvement as part of their clinical deficit. Severe carotid occlusive disease was seen in 10 patients, and 12 patients had evidence of transiently impaired cardiac output. Carotid disease (P < .001), cardiac disease (P < .01), and diabetes mellitus (P < .01) were more prevalent in patients with internal watershed infarction compared with our stroke population as a whole.

Distinguishing internal watershed infarction from lacunar and other subcortical infarctions is important because the different pathological mechanisms demand different therapeutic strategies.
A quantitative investigation of the variability of the major cerebral arterial territories.
Authors: van der Zwan A , Hillen B , Tulleken C A , Dujovny M
Published: June 2011

We have previously reported that the topographic variability of the territories of the anterior, middle, and posterior cerebral arteries is much larger than is generally considered in the literature. In the current study, we quantitatively investigated the variability of the territorial distribution of the major cerebral arteries and analyzed its relation to the variability of the circle of Willis.

In 23 human brains, the volumes of the major cerebral territories were calculated and the diameters of the contributing arteries were measured and standardized for size.

The variability of the standardized territorial volumes proved to be considerably large and strongly correlated with the variability of the diameters of the arteries emanating from the circle of Willis. Furthermore, the relative vascular densities in the gray and white matter were determined. Taking these densities into account, an estimation of the relative peripheral resistance of the contributing arteries was made.

We hypothesize that the morphological variability of the cerebral vascular system is related to the peripheral resistance of the major cerebral arteries and, consequently, to flow patterns, both of which are hemodynamic factors. We suggest that hemodynamic factors predominantly determine the form and size of the cerebral vascular system.
The ultrastructure of photochemically induced thrombi with embolization in a rat model.
Authors: Futrell N , Riddle J M
Published: June 2011

Photochemical techniques, currently used in stroke and cancer research, produce endothelial damage and thrombosis. To further characterize these thrombi and to determine whether they embolize, we studied the ultrastructure of photochemically damaged carotid arteries and small vessels distal to the irradiated carotid.

The right carotid artery of 9 Wistar rats was irradiated with a laser (632 nm, 200 mW/cm2, 15 minutes) after the injection of the photosensitizing dye Photofrin II, 12.5 mg/kg. There were 6 additional control rats: laser only, 2 rats; dye only, 2; carrier only (5% dextrose), 1; and normal, 1. The carotid artery and cerebral arterioles were studied using scanning and transmission electron microscopy.

Endothelial damage was present in all irradiated carotid arteries, and consisted of exposure of the subendothelium and the formation of a nonocclusive thrombus. Although most cerebral arterioles were normal, 32 of these vessels contained peripheral blood elements, with platelet or red blood cell aggregates present in 15. The endothelium adjacent to the aggregates was intact. A few scattered endothelial cells had been lost in the carotid artery of control animals (compatible with normal cell turnover), with a few platelets adhering to the exposed subendothelium.

Aggregates of blood cells and platelets in cerebral vessels in the absence of endothelial denudation verifies embolism as the mechanism for cerebral vascular occlusion in this experimental model. The possibility of embolization distal to the site of photochemical irradiation has implications for potential applications of photochemistry for cancer treatment and the ablation of vascular malformations and/or aneurysms.
The kinetics of lymphocyte subsets and macrophages in subarachnoid space after subarachnoid hemorrhage in rats.
Authors: Kubota T , Handa Y , Tsuchida A , Kaneko M , Kobayashi H , Kubota T
Published: June 2011

Although it has been suggested that humoral immunity plays a role in the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage, there has been no quantitative assay for cellular immunity. We studied the kinetics of immune cells in the subarachnoid space after subarachnoid hemorrhage in the rat.

One hundred fourteen Sprague-Dawley rats were used in this study. The animals were divided into two groups and injected with either autologous blood (0.3 mL) or saline into the major cistern. They were killed at the specified time: 10 minutes or 1, 2, 3, 5, or 7 days after subarachnoid hemorrhage. For immunohistochemical analysis, the rats' whole brains were frozen, and cryostat sections were prepared. For flow cytometric analysis of immune cell presence, their whole brains underwent enzymatic digestion.

Histopathologic study revealed pathological change of the arterial wall, and immunohistochemical study revealed the existence of macrophages and T cells in the subarachnoid space in animals with a survival time of 2 to 5 days after subarachnoid hemorrhage. A flow cytometric study revealed the peak of appearance of T cells and macrophages 2 days after subarachnoid hemorrhage. The helper-suppressor T cell ratio also reached a peak 2 days after subarachnoid hemorrhage.

A serial response of immunoreactive cells, which resembles that of the chronic allergic reaction observed in autoimmune diseases or delayed-type hypersensitivity, exists in the subarachnoid space after subarachnoid hemorrhage. The present results suggest that the initial response in cellular immunity, which is followed by humoral immunity and eicosanoid reactions, plays a role in eliciting the development of cerebral vasospasm.
The effect of nitric oxide synthase inhibition on infarct volume after reversible focal cerebral ischemia in conscious rats.
Authors: Kuluz J W , Prado R J , Dietrich W D , Schleien C L , Watson B D
Published: June 2011

Previous in vitro and in vivo studies of the effects of nitric oxide synthase inhibition in the central nervous system have yielded conflicting results concerning the role of nitric oxide in the events that lead to ischemic injury. In this study, we tested the hypothesis that preischemic inhibition of nitric oxide synthase increases infarct volume after reversible focal cerebral ischemia in rats.

NG-nitro-L-arginine methyl ester hydrochloride 15 mg/kg IV or an equivalent volume of saline was administered to adult Wistar rats 15 minutes before middle cerebral artery occlusion by the intraluminal suture method. After 2 hours of ischemia, the suture was withdrawn, and rats were allowed to survive for 3 days. Areas of infarction in 10 hematoxylin-eosin-stained sections were measured and used to determine infarct volume.

Administration of NG-nitro-L-arginine methyl ester hydrochloride increased hemispheric infarct volume by 137% over control (60.9 +/- 30.5 to 144.3 +/- 19.6 mm3, P < .05; mean +/- SEM). Cortical and subcortical infarct volumes were increased by 176% (33.8 +/- 21.9 to 93.3 +/- 15.2 mm3, P < .05) and 103% (25.1 +/- 9.4 to 51.0 +/- 5.5 mm3, P < .03), respectively.

Nitric oxide synthase inhibition increases infarct volume and decreases the variability of the response to middle cerebral artery occlusion in Wistar rats, a strain that is normally resistant to focal cerebral ischemic injury owing to extensive collateralization. The mechanism of the deleterious effect of nitric oxide synthase inhibition likely involves a more severe degree of blood flow reduction during and after middle cerebral artery occlusion, primarily by preventing the vasodilatory response of collateral vessels to proximal middle cerebral artery occlusion. Maintenance of nitric oxide synthase activity during and after focal cerebral ischemia appears to minimize ischemic injury.
In vivo mapping of brain benzodiazepine receptor changes by positron emission tomography after focal ischemia in the anesthetized baboon.
Authors: Sette G , Baron J C , Young A R , Miyazawa H , Tillet I , Barré L , Travère J M , Derlon J M , MacKenzie E T
Published: June 2011

Recent reports have shown an increase in specific binding (in vitro) of [3H]PK 11195 to peripheral-type benzodiazepine receptors in both experimental animals and humans, reflecting a glial/macrophagic reaction within and around focal ischemic insults. We have evaluated by positron emission tomography the time course of changes in brain uptake in vivo of 11C-labeled PK 11195 and flumazenil (an antagonist of central benzodiazepine receptors) as indirect and direct markers of neuronal loss, respectively, after focal cerebral ischemia.

Ten anesthetized baboons were submitted to sequential positron emission tomography studies between day 1 and day 91 after unilateral middle cerebral artery occlusion. The studies consisted of successive assessments, in the same positron emission tomography session, of [11C]PK 11195, [11C]flumazenil, cerebral blood flow, and oxygen consumption; late computed tomographic scans were obtained to map the approximate contours of infarction and to define a concentric peri-infarct area.

We found a significant time-dependent increase in [11C]PK 11195 uptake in the peri-infarcted area, maximum at 20 to 40 days after occlusion. In contrast, there was a time- and perfusion-independent significant decrease in [11C]flumazenil uptake in the infarcted area, stable from day 2 onward, and already present in one baboon at day 1. Challenge studies with saturating doses of cold ligands confirmed that these changes represented alterations in specific binding. [11C]Flumazenil uptake was not affected in hypometabolic (but apparently noninfarcted, ie, deafferented) cortical areas.

The delayed and apparently transient increases in [11C]PK 11195 specific uptake in vivo presumably represent glial/macrophage reaction; the marked depression in [11C]flumazenil specific binding, which appears selective for synaptic damage, is both precocious and sustained and thus may be better suited for the early assessment of ischemic damage in humans.
The Stroke Prevention Patient Outcomes Research Team. Goals and methods.
Authors: Matchar D B , Duncan P W , Samsa G P , Whisnant J P , DeFriese G H , Ballard D J , Paul J E , Witter D M , Mitchell J P
Published: June 2011

The aim of the present study, based at Duke University and involving 14 other institutions, is to identify the most appropriate and cost-effective clinical strategies for prevention of ischemic (thrombotic or embolic) stroke in high-risk individuals and to design and test an intervention to disseminate this information to providers and the public.

The study uses (1) secondary data from literature review, Medicare claims, and population-based data from three epidemiological studies and (2) primary data generated in national physician and patient surveys and in demonstration trials. Phases I through III involve data collection and analysis using a decision/cost-effectiveness model and consensus development methods. Phase IV includes intervention in physicians' practice patterns. Data is collected by literature survey and abstraction, review of medical records, claims analysis, and patient and physician surveys.

A structured decision model and a well-defined clinical focus provide a successful organization for a PORT on stroke prevention.
Free protein S deficiency in acute ischemic stroke. A case-control study.
Authors: Mayer S A , Sacco R L , Hurlet-Jensen A , Shi T , Mohr J P
Published: June 2011

Deficiency of free protein S, a naturally occurring anticoagulant, may be acquired in the setting of acute illness and increasingly has become recognized as a possible stroke risk factor. We sought to determine whether free protein S deficiency is associated with acute cerebral infarction among older individuals at risk for stroke.

Free protein S was measured by Laurell rocket immunoelectrophoresis in 94 adults admitted for acute cerebral infarction and in 94 hospitalized control subjects of similar age, sex, and race. Patients with a history of cerebrovascular disease, acute thrombotic or hematologic diseases, or medical conditions known to cause free protein S deficiency were excluded from the control group.

The percentage of patients with free protein S deficiency (< 20% normal total protein S) was similar in the case and control groups (21% versus 20%, respectively). Among all subjects, free protein S deficiency was more common in blacks than nonblacks (34% versus 13%, p = 0.001). A very low free protein S (< 15% normal total protein S) was more frequent among case patients than control subjects (11% versus 5%), but this trend failed to reach statistical significance.

Free protein S deficiency is common among hospitalized patients, even in the absence of a recognized predisposing condition. Our findings indicate that acquired deficiency of free protein S is not a major risk factor for ischemic stroke.
Interaction of endothelium with dilation produced by inhibitors of cyclic nucleotide diesterases in mouse brain arterioles in vivo.
Authors: Rosenblum W I , Shimizu T , Nelson G H
Published: June 2011

In vitro evidence gathered from extracerebral conductance vessels suggests interaction between the endothelium-derived relaxing factor for acetylcholine (EDRFACh) and cyclic nucleotide action in vascular smooth muscle. The purpose of this study was to examine this interaction in vivo in pial arterioles. As had been done in vitro, we used phosphodiesterase inhibitors that elevate cyclic nucleotide levels in vascular smooth muscle.

Pial vessels of mice were observed with television microscopy. Diameter of the arterioles was monitored with an image-splitting technique. The responses to topically applied phosphodiesterase inhibitors were tested before and after focal endothelial injury or before and during application of N-guanidino-L-monomethyl arginine (L-NMMA). Both treatments are known to eliminate the endothelium-dependent response to acetylcholine in this preparation.

Phosphodiesterase inhibitors dilated pial arterioles. This was true for phosphodiesterase inhibitors elevating levels of both adenosine 3',5'-cyclic monophosphate (cAMP) and guanosine 3',5'-cyclic monophosphate (cGMP) as well as for inhibitors thought to selectively affect either nucleotide. The dilation was inhibited by endothelial injury and by L-NMMA.

The data suggest that brain arterioles are dilated by both cAMP and cGMP but that this action is impaired if EDRFACh levels are reduced. Since EDRFACh elevates cGMP levels, these data support the hypothesis that the relaxing actions of cGMP and cAMP depend upon adequate basal levels of cGMP in vascular smooth muscle. This hypothesis, originally introduced in studies of extracerebral conductance arteries in vitro, can now be applied to brain resistance vessels in vivo.
Middle cerebral artery occlusion without craniectomy in rats. Which method works best?
Authors: Laing R J , Jakubowski J , Laing R W
Published: June 2011

Our purpose was to assess the effectiveness of middle cerebral artery occlusion in producing acute focal ischemia in the rat by the use of Koizumi's and Longa's methods, in which occlusion is achieved by passing a nylon thread into the internal carotid artery.

Cerebral blood flow was measured by using the hydrogen clearance method, and the brains were examined histologically to assess ischemic damage.

By Koizumi's method profound reduction in cerebral blood flow was achieved in 28 of 30 rats (93%). The mean cerebral blood flow in the middle cerebral artery territory was 10.7 (95% confidence interval, 9.9-11.5) ml/100 g per minute. By Longa's method reduction in cerebral blood flow was achieved in only 29 of 52 rats (56%), and in these animals mean cerebral blood flow was 33 (95% confidence interval, 28.3-33.7) ml/100 g per minute (p < 0.001 compared with Koizumi's method). Cerebral blood flow was reduced to < 16 ml/100 g per minute in only seven animals (24%).

By Koizumi's method the depth of ischemia is more profound, occlusion is achieved in a much higher proportion of cases, and the incidence of perforation of the intracranial internal carotid is much less frequent than by Longa's method.
A prospective study of cerebral ischemia in the young. Analysis of pathogenic determinants. The National Research Council Study Group.
Authors: Carolei A , Marini C , Ferranti E , Frontoni M , Prencipe M , Fieschi C
Published: June 2011

The etiology of stroke in the young is different from that in older patients and remains unknown in almost one third of the cases. To gain further insight into both pathogenic and etiologic determinants, we prospectively studied a large number of consecutive young adults with focal cerebral ischemia.

Three hundred thirty-three patients aged 15-44 years with transient ischemic attack or ischemic stroke within the 8 weeks before hospital admission were recruited and investigated by using a standardized protocol of clinical evaluation, blood tests, electrocardiography, echocardiography, chest roentgenography, and brain computed tomography. Presumed etiology was diagnosed by prospectively applied criteria.

Women predominated (61%) among patients under 35 years of age, mainly due to the frequency of cerebral ischemia related to oral contraceptive use, while men outnumbered women (60%) among patients over that age because of a higher prevalence of atherothrombotic disease. Potential cerebral embolism of cardiac origin was the presumed cause of stroke in 23.7%, but conventional sources of emboli were found only in 7.5% of cases. There was a low prevalence of atrial fibrillation among young patients with cerebral ischemia. Mitral valve prolapse was found in 8.4%, as expected, predominantly (71.4%) among the younger patients. The prevalence of stroke over transient ischemic attack was proportional to the likelihood of cardiac embolism. Acute alcohol intoxication was considered a precipitating factor in only three patients. The percentages of cerebral ischemia attributed to arterial dissection (0.3%), oral contraceptive use in women (8.1%), migraine (1.2%), and other associated medical diseases (1.5%) were lower than reported in recent clinical series.

Two different groups of pathogenic determinants predominate in younger women and in older men, supporting public health measures aimed at strict medical control of the recognized cerebrovascular risk factors.
Causes of urinary incontinence after acute hemispheric stroke.
Authors: Gelber D A , Good D C , Laven L J , Verhulst S J
Published: June 2011

We prospectively studied bladder function in stroke patients to determine the mechanisms responsible for poststroke urinary incontinence.

Fifty-one patients with recent unilateral ischemic hemispheric stroke admitted to a neurorehabilitation unit were enrolled. The presence of urinary incontinence was correlated with infarct location, neurological deficits, and functional status. Urodynamic studies were performed on all incontinent patients.

Nineteen patients (37%) were incontinent. Incontinence was associated with large infarcts, aphasia, cognitive impairment, and functional disability (p < 0.05) but not with age, sex, side of stroke, or time from stroke to entry in the study. Urodynamic studies, performed on all 19 incontinent patients, revealed bladder hyperreflexia in 37%, normal studies in 37%, bladder hyporeflexia in 21%, and detrusor-sphincter dyssynergia in 5%. All of the patients with normal urodynamic studies were aphasic, demented, or severely functionally impaired. All of the patients with hyporeflexic bladders had underlying diabetes or were taking anticholinergic medications. Forty-six percent of incontinent patients treated with scheduled voiding alone were continent at discharge compared with 17% of patients treated pharmacologically.

There are three major mechanisms responsible for poststroke urinary incontinence: 1) disruption of the neuromicturition pathways, resulting in bladder hyperreflexia and urgency incontinence; 2) incontinence due to stroke-related cognitive and language deficits, with normal bladder function; and 3) concurrent neuropathy or medication use, resulting in bladder hyporeflexia and overflow incontinence. Urodynamic studies are of benefit in establishing the cause of incontinence. Scheduled voiding is a useful first-line treatment in many cases of incontinence.
Absence of elevation of big endothelin in subarachnoid hemorrhage.
Authors: Hamann G , Isenberg E , Strittmatter M , Schimrigk K
Published: June 2011

Endothelin peptides are potent vasoconstrictors and thus are seen as potential cause of cerebral vasospasm after subarachnoid hemorrhage (SAH). Earlier reports showed elevated or normal endothelin levels in plasma and cerebrospinal fluid in patients suffering from SAH. The present study was designed to determine whether endothelin is a causal factor in SAH.

We studied 11 patients with acute SAH. Seven of these 11 patients had a proven aneurysm and six had experienced vasospasm. Big endothelin levels were determined by a radioimmunoassay recognizing the C-terminal peptide (normal range, 1-11 fmol/ml).

There were no elevations of big endothelin in the 59 plasma samples and the 17 simultaneously estimated cerebrospinal fluid samples. Differences between plasma and cerebrospinal fluid did not reach significant levels. Big endothelin values between patients with and without vasospasm showed no significant differences.

Our findings suggest that plasma elevation of the endothelins is not reproducible in SAH and that big endothelin is unlikely to be a causal plasma factor in the complex multifactorial development of vasospasm after SAH.
Subarachnoid hemorrhage and endothelial L-arginine pathway in small brain stem arteries in dogs.
Authors: Katusić Z S , Milde J H , Cosentino F , Mitrović B S
Published: June 2011

Experiments were designed to determine the effect of subarachnoid hemorrhage on endothelium-dependent relaxations in small arteries of the brain stem. A "double-hemorrhage" canine model of the disease was used, and the presence of vasospasm in the basilar artery was confirmed by angiography.

Secondary branches of both untreated basilar arteries (inner diameter, 324 +/- 11 microns; n = 12) and arteries exposed to subarachnoid hemorrhage for 7 days (inner diameter, 328 +/- 12 microns; n = 12) were dissected and mounted on glass microcannulas in organ chambers. Changes in the intraluminal diameter of pressurized arteries were measured using a video dimension analyzer.

In untreated arteries, 10(-11) to 10(-7) M vasopressin, 10(-10) to 10(-6) M bradykinin, and 10(-9) to 10(-6) M calcium ionophore A23187 caused endothelium-dependent relaxations. At 10(-6) and 3 x 10(-4) M the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME) abolished relaxations to vasopressin and produced small but significant rightward shifts of the concentration-response curves to bradykinin and A23187. At 10(-3) M L-arginine prevented the inhibitory effect of L-NAME. Subarachnoid hemorrhage abolished relaxations to vasopressin but did not affect relaxations to bradykinin or A23187.

These studies suggest that in small arteries of the brain stem vasopressin causes relaxations by activation of the endothelial L-arginine pathway. This mechanism of relaxation is selectively inhibited by subarachnoid hemorrhage. Preservation of endothelium-dependent relaxations to bradykinin and A23187 is consistent with the concept that small arteries are resistant to vasospasm after subarachnoid hemorrhage.
Cerebral autoregulation during moderate hypothermia in rats.
Authors: Verhaegen M J , Todd M M , Hindman B J , Warner D S
Published: June 2011

Little is known about the effects of hypothermia on cerebral autoregulation. The present study was designed to examine cerebral blood flow responses to controlled hemorrhagic hypotension in normothermic and hypothermic rats.

Cortical blood flow was measured with a laser-Doppler flowmeter in halothane-anesthetized rats assigned to one of three groups: normothermic group 1 (n = 8) with a pericranial temperature of approximately 36.5 degrees C or hypothermic group 2 (n = 8) or group 3 (n = 8) with a pericranial temperature of approximately 30.5 degrees C. In group 2, a PaCO2 of approximately 40 mm Hg was maintained without correction for body temperature. To evaluate the role of PaCO2, in group 3 animals PaCO2 was kept at approximately 40 mm Hg as corrected for body temperature. In all animals, the mean arterial blood pressure was reduced by hemorrhage in increments of 10 mm Hg every 2 minutes.

In group 1 animals, a typical autoregulatory curve was observed with cerebral blood flow first falling at or below 75% of baseline at a mean arterial pressure of 57 +/- 15 mm Hg (mean +/- SD). Absolute normotensive cerebral blood flow in group 2 fell to < or = 75% of baseline at a mean arterial pressure of 73 +/- 21 mm Hg. In group 3, no evidence of autoregulation was seen. Cerebral blood flow reached values < or = 75% of baseline at a mean arterial pressure of 82 +/- 14 mm Hg, whereas calculated cerebrovascular resistance failed to show any compensatory vasodilation as the mean arterial pressure decreased.

Different PaCO2 management schemes used during hypothermia may have profound effects on cerebral blood flow and on autoregulation. If PaCO2 is maintained at 40 mm Hg after correction for temperature, autoregulation is abolished. If uncorrected PaCO2 is maintained at approximately 40 mm Hg, some degree of autoregulation is preserved, albeit with a right-shifted "knee."
Potentiation by hypoxia of contractions caused by angiotensin II in dog and monkey cerebral arteries.
Authors: Yoshida K , Okamura T , Toda N
Published: June 2011

Hypoxia alters the responsiveness to endogenous substances of cerebral arteries, possibly resulting in the modulation of blood supply to ischemic brain regions. The present study was undertaken to analyze the mechanism of potentiation by hypoxia of angiotensin II-induced cerebroarterial contractions.

Monkey and dog cerebral arterial strips with endothelium were suspended for isometric tension recording in Ringer-Locke solution aerated with 95% O2-5% CO2 (partial pressure, 570-600 mm Hg) or 95% N2-5% CO2 (approximately 10 mm Hg).

Contractions induced by angiotensin II and substance P were potentiated by exposure to hypoxia, whereas contractile responses to prostaglandin F2 alpha were not influenced. Treatment with cyclooxygenase inhibitors abolished the peptide-induced contraction but did not alter the prostaglandin F2 alpha-induced contraction. Relaxations induced by arachidonic acid were suppressed by indomethacin and hypoxia, whereas those caused by a prostaglandin I2 analogue were unaffected.

The potentiation by hypoxia of cerebroarterial contractions caused by angiotensin II and substance P appears to be due to an interference with the synthesis of prostaglandin I2 from arachidonic acid and a resultant increase in the production of vasoconstrictor prostaglandins.
Angiographic evaluation of brain infarction limited to the anterior cerebral artery territory.
Authors: Kazui S , Sawada T , Naritomi H , Kuriyama Y , Yamaguchi T
Published: June 2011

Brain infarction localized in the anterior cerebral artery territory is rather uncommon, and its etiology has not yet been fully elucidated.

Based on computed tomographic findings, 17 patients with solitary anterior cerebral artery territory infarction were selected from among 3,619 patients admitted consecutively to our institute. Patients without angiographic examinations were excluded. The angiographic findings and clinical category of stroke were analyzed in each patient.

Angiographic abnormalities were revealed in all patients. These consisted of occlusive changes (n = 10) or reversible segmental dilatation (n = 3) of the anterior cerebral artery, A1 hypoplasia (n = 5), and occlusive changes of the carotid artery (n = 3). In one patient with anterior cerebral artery occlusion, the occluded artery was reopened and subsequently became reoccluded. The clinical category of stroke was classified as atherothrombotic in 10 patients, cardioembolic in three, and undetermined in the remaining four. In eight of the 10 patients with atherothrombotic infarction, the anterior cerebral artery was narrowed or occluded. In all patients with cardioembolic infarction, the A1 segment contralateral to the infarction was hypoplastic.

In our series, solitary anterior cerebral artery territory infarction was attributable most commonly to local atherothrombosis and occasionally to cardiogenic embolism. A hypoplastic A1 segment may facilitate the occurrence of embolism in the anterior cerebral artery. Reversible dilatatory and occlusive changes of this artery may be another important cause of infarction.
Cerebral blood flow alterations in a rat model of cerebral sinus thrombosis.
Authors: Ungersböck K , Heimann A , Kempski O
Published: June 2011

Outcome from sinus vein thrombosis is very variable, with symptoms from headache to coma. Experimental findings suggest that an involvement of cortical veins is necessary to affect the cerebral microcirculation. Laser Doppler flowmetry was used to investigate the regional and temporal changes in local cortical blood flow after experimental occlusion and thrombosis of the superior sagittal sinus and tributary cortical veins in rats.

Thrombosis was induced by slow injection of kaolin-cephalin suspension after frontal and caudal ligation of the sagittal sinus in rats. Local cerebral blood flow was measured by laser Doppler flowmetry and correlated with parenchymal damage found 24 hours after induction of thrombosis.

Local cerebral blood flow 1 hour after sinus occlusion and induction of thrombosis had decreased to 60.92 +/- 29.05% (p < 0.01); however, there was a large variability among individual animals. Only five of 12 rats showed histological damage and intracerebral hemorrhages 24 hours after induction of thrombosis. A subgroup analysis revealed that parenchymal damage occurred in concurrence with reduced blood flow values after sinus ligation and injection of the thrombogenic material. Sinus thrombosis alone, without alteration of blood flow, did not cause tissue necrosis.

The data support the contention that sinus vein thrombosis evolves gradually, with major symptoms occurring only if the thrombus expands from the sinus into bridging and cortical veins. Collateral venous outflow pathways are thereby occluded, and local blood flow may become reduced to and below the ischemic threshold.
The role of bradykinin in mediating ischemic brain edema in rats.
Authors: Kamiya T , Katayama Y , Kashiwagi F , Terashi A
Published: June 2011

We investigated the hypothesis that bradykinin generation may induce ischemic brain edema in spontaneously hypertensive rats.

Cerebral ischemia lasting 3 hours was produced by bilateral common carotid artery occlusion in 67 rats. After the ischemic period, the rats were reperfused. Cerebral water content and energy metabolites (adenosine triphosphate, lactate, and pyruvate), as well as plasma and tissue bradykinin, were measured. Additionally, using the same experimental paradigm, bradykinin synthesis inhibitors (aprotinin [n = 7] and soybean trypsin inhibitor [n = 7]) were administered immediately after ischemia induction to determine the relation of bradykinin generation to the progression of ischemic brain edema.

Cerebral water content increased during the 3-hour ischemic period, peaked at 30 minutes of reperfusion, and declined thereafter. Bradykinin levels in plasma and tissue rose markedly 30 minutes after reperfusion and fell thereafter. The progressive loss of adenosine triphosphate was mirrored by the rise in lactate. In the treated groups, aprotinin and soybean trypsin inhibitor administration significantly attenuated cerebral edema (p < 0.01 and p < 0.05, respectively). The treated groups also showed less lactate accumulation and more adenosine triphosphate preservation than did the controls.

These results demonstrate that bradykinin levels in plasma and tissue corresponded to cerebral edema progression and that bradykinin suppression decreased edema formation. These novel findings indicate that bradykinin activation augments the progression of ischemic brain edema.
Isolated or predominant ocular motor nerve palsy as a manifestation of brain stem stroke.
Authors: Kim J S , Kang J K , Lee S A , Lee M C
Published: June 2011

There have been few reports of strokes producing isolated or predominant ocular motor nerve palsies as a clinical manifestation.

We studied seven patients with brain stem stroke who had ocular motor palsies as the only or the predominant neurological manifestation, and we correlated their clinical features with radiological findings.

Five patients had small strokes in the area of oculomotor nuclei or fascicles and showed various combinations of oculomotor disturbances. Three of these patients showed vertical gaze paresis of the opposite eye. One patient with a small hemorrhage near the aqueduct of Sylvius showed fourth nerve palsy on the contralateral side, and a patient with a small infarct in the pontine tegmentum showed isolated sixth nerve palsy. Nonocular minor neurological signs included trigeminal sensory changes in four patients and clumsy arm in two. Ocular and nonocular dysfunctions generally improved within several months. Radiological findings of the brain stem correlated well with the ocular signs.

We conclude that acute brain stem stroke should be included in the differential diagnosis of isolated ocular motor nerve palsies and that appropriate diagnostic investigations should be performed in these cases.
Cigarette smoking and alcohol consumption as risk factors for aneurysmal subarachnoid hemorrhage.
Authors: Juvela S , Hillbom M , Numminen H , Koskinen P
Published: June 2011

Aneurysmal subarachnoid hemorrhage is a serious disease despite recent improvements in medical and surgical treatment. Hence, identification of modifiable risk factors for subarachnoid hemorrhage is important.

We compared the smoking and drinking habits of 278 consecutive patients with aneurysmal subarachnoid hemorrhage, aged 15-60 years (145 men and 133 women) with those of 314 hospitalized control patients (164 men and 150 women) who did not differ in regard to age, day of onset of symptoms, and acuteness of disease onset.

Multiple logistic regression analysis showed that recent alcohol intake and smoking, but not hypertension, were significant independent risk factors for hemorrhage. After adjustment for age, hypertension, and smoking status, men who had consumed 1-40, 41-120, or > 120 g of alcohol within the 24 hours preceding the onset of illness had a relative risk of hemorrhage of 0.3 (95% confidence interval [CI], 0.1-0.8), 2.5 (95% CI, 1.1-5.5), and 4.5 (95% CI, 1.5-12.9), respectively, compared with men who had consumed 0 g. Women who had consumed 1-40 or > 40 g of alcohol had a risk of hemorrhage of 0.4 (95% CI, 0.2-0.8) and 6.4 (95% CI, 2.3-17.9), respectively, compared with women without use of alcohol. Heavily smoking (> 20 cigarettes per day) men and currently smoking women had adjusted relative risks of hemorrhage of 7.3 (95% CI, 3.8-14.3) and 2.1 (95% CI, 1.2-3.6), respectively, compared with men who had never smoked and with women who were not current smokers. Higher levels of erythrocyte mean corpuscular volume in patients with subarachnoid hemorrhage than in control subjects supported the notion of different smoking and drinking habits.

Recent heavy alcohol intake and current smoking seem to be independent risk factors for aneurysmal subarachnoid hemorrhage.
Sneddon's syndrome: diagnosis by skin biopsy and MRI in 17 patients.
Authors: Stockhammer G , Felber S R , Zelger B , Sepp N , Birbamer G G , Fritsch P O , Aichner F T
Published: June 2011

Sneddon's syndrome, characterized by generalized livedo racemosa and cerebrovascular lesions, is an underdiagnosed disease. We evaluated clinical, laboratory, histological, and neuroradiological findings in a series of 17 patients to improve diagnostic criteria for Sneddon's syndrome.

Patients with generalized livedo racemosa and cerebrovascular events were included in the study. All underwent neurological and dermatological examination, skin biopsy, computed tomographic scan, magnetic resonance imaging as well as magnetic resonance angiography, sonography of the extracranial arteries, and a comprehensive laboratory protocol.

Completed stroke was present in eight patients, and 15 reported transient neurological deficits. Magnetic resonance imaging yielded cerebral abnormalities in 16 of 17, whereas computed tomographic scans were abnormal in only 12 of 16 patients. Magnetic resonance imaging revealed more lesions in individual patients than did computed tomography. Magnetic resonance angiography demonstrated patent intracranial vessels in 16 of 17 patients. Skin biopsy showed distinct histopathological findings in all patients. The involved vessels were small to medium-sized arteries at the border between dermis and subcutis. Early inflammatory reactions were followed by subendothelial proliferation and a late fibrotic stage. Laboratory examinations showed impaired creatinine clearance in eight patients, whereas all other laboratory tests, including antiphospholipid antibodies, were normal.

In this series, magnetic resonance imaging and skin biopsy were useful for confirmation of the diagnosis of Sneddon's syndrome. Magnetic resonance findings were not specific, but the high sensitivity for detection of asymptomatic brain lesions helped to confirm the diagnosis in patients with transient symptoms. Histological features of skin biopsies were characteristic if appropriate techniques were employed.
Risk area and infarct area relations in the hypertensive stroke-prone rat.
Authors: Coyle P , Feng X
Published: June 2011

Our purpose was to characterize the surface area of the infarct and the surface area at risk of infarction as defined spatially by arterial anastomoses to determine whether position, size, or shape of the infarct and the area at risk were related in stroke-prone rats or hybrid rats.

Stroke-prone rats (n = 18; mean +/- SEM blood pressure, 182 +/- 8 mm Hg) and hybrid rats (n = 18; mean +/- SEM blood pressure, 147 +/- 6 mm Hg; p < 0.05) were anesthetized and the left middle cerebral artery was occluded with a ligature. The rats were killed 7 days later, arterial anastomoses were made visible with latex, the brains were fixed in formalin, and film recorded the infarct and anastomoses. Anastomoses and infarcts were digitized for measurements of risk area, luminal width, and infarct area.

Mean risk area was similar in size, length, width, and variability in stroke-prone rats (area, 85 +/- 5 mm2) and hybrid rats (area, 84 +/- 7 mm2; p > 0.05), whereas mean infarct area was larger, longer, wider, and less variable in stroke-prone rats (area, 53 +/- 6 mm2) than in hybrid rats (area, 15 +/- 11 mm2; p < 0.05). Infarct length was appreciably greater than infarct width in both groups, indicating that infarct shape was not amorphous. Spatial overlap maps indicated that the infarct area common to all stroke-prone rats was positioned centrally in the risk area and was surrounded by a variable infarct area, which indicated that the likelihood of infarction increased with distance from the anastomoses. Shape factors for both risk area and infarct area were significantly different within each rat group, which indicated that infarct shape did not uniformly parallel the anastomotic sites that determined risk area shape (p < 0.05). Risk area anastomoses and border zone width were linearly correlated in size and both were significantly wider in hybrid rats than in stroke-prone rats (p < 0.05), which suggests that the narrower border zone tissue was perfused by narrower anastomoses.

We conclude that the position of the infarct within the risk area relates to luminal widths of conterminous anastomoses that define the risk area, but not to the size or shape of the area at risk of infarction defined spatially by the anastomoses.
Stroke following injection of a melted suppository.
Authors: Bitar S , Gomez C R
Published: June 2011

Stroke following the intravenous injection of drugs may be secondary to the direct effect of the substance itself or from embolization by the inert vehicle used in the manufacturing process of the drug.

We describe a 39-year-old man who developed a left homonymous hemianopia after intravenous injection of a melted suppository.

Paradoxical fat embolism should be added to the possible list of stroke mechanisms in intravenous drug abusers.
Long-term survival after first-ever stroke: the Oxfordshire Community Stroke Project.
Authors: Dennis M S , Burn J P , Sandercock P A , Bamford J M , Wade D T , Warlow C P
Published: June 2011

There have been relatively few community-based studies of long-term prognosis after acute stroke. This study aimed to provide precise estimates of the absolute and relative risks of dying in an unselected cohort of patients with a first-ever stroke.

Six hundred seventy-five patients were registered by a community-based stroke register (the Oxfordshire Community Stroke Project) and prospectively followed up for up to 6.5 years. Their relative risk of death was calculated using age- and sex-specific mortality rates for Oxfordshire.

During the first 30 days, 129 (19%) patients died. Patients who survived at least 30 days after a first-ever stroke thereafter had an average annual risk of death of 9.1%, 2.3-fold the risk in people from the general population. Although the absolute (about 15%) and relative (about threefold) risks of death were highest in these 30-day survivors over the first year after the stroke, they were at increased risk of dying over the next few years (range of relative risk for individual years, 1.1-2.9). Predictably, older patients had a worse absolute survival but, relative to the general population, stroke also increased the relative risk of dying in younger patients. During the first 30 days stroke accounts for most deaths; after this time nonstroke cardiovascular disease becomes increasingly important and is the most common cause of death after the first year.

These data highlight the importance of long-term secondary prevention of vascular events in stroke patients, targeted as much at the cardiovascular as at the cerebrovascular circulation.