bluuebunny/crossref_metadata_2025 huggingface dataset:
A Study of Blood Coagulation Following an Acute Stroke
Authors: GASTON LAMONT W. , BROOKS JOHN E. , BLUMENTHAL HARVEY J. , MILLER CRAIG E.
Published: June 2011

A battery of blood coagulation tests were performed on 14 acute stroke patients. Various abnormalities were found, notably elevation of blood fibrinogen, factor VIII, prothrombin, platelet factor 3, and a shortened P.T.T. The significance of these findings is discussed and they are considered to be of no importance since similar changes were noted in the blood of healthy subjects of the same age range.
Long-Term Prognosis of Transient Cerebral Ischemic Attacks
Authors: GOLDNER JOHN C. , WHISNANT JACK P. , TAYLOR WILLIAM F.
Published: June 2011

A 15-year follow-up of 140 patients who had transient cerebral ischemic attacks and were first seen at the Mayo Clinic for this complaint in 1950 through 1954 is reported. There was no significant difference in mortality related to sex or location of residence. Patients hypertensive at onset of symptoms had no significant increase in mortality compared to normotensive patients but the survival trend favored normotensive patients. Probability of surviving 15 years was significantly less than expected for patients less than 65 years old. Patients who were 65 or older at their first attack had a survival similar to that of the standard population. The difference between the expected and observed 15-year survivals for patients with primarily motor symptoms was about the same as that difference for patients with primarily sensory symptoms. Information concerning stroke occurrence was incomplete but 37% of local residents are known to have had a stroke, a higher rate than expected. Among patients who died during this study, 50% died of a cardiac cause and 36% died of a stroke.
Cerebral Apoplexy (Stroke): Pathogenesis, Pathophysiology and Therapy as Illustrated by Regional Blood Flow Measurements in the Brain
Authors: PAULSON OLAF B.
Published: June 2011

Pathophysiological and pathogenetic concepts, particularly in occlusive cerebrovascular disease, are reviewed and discussed with emphasis on the results of current research. Therapy is discussed in the context of these concepts.

When focal ischemia, with or without cerebral infarction, is not associated with definable arterial occlusion, studies of regional cerebral blood flow strongly support the thromboembolic theory; the arterial defect is relatively transient and is caused by an embolus or thrombus which rapidly disappears (fragments or is lysed). The treatment of transient ischemic attacks by the administration of anticoagulant or surgical reconstruction of the appropriate artery is discussed.

When cerebral infarction is caused by arterial occlusion there is vasomotor paralysis (loss of autoregulation and of reactivity to carbon dioxide). In some instances hypercapnia apparently causes only the vessels in nonaffected brain to dilate so that an increased amount of blood streams to these parts while blood pressure falls in collaterals leading to the focus and blood flow to the infarct is decreased (steal syndrome). If blood flow is decreased to nonaffected brain, by vasoconstriction caused by hyperventilation, increased amounts of blood may be shunted into the infarct (reverse steal) where autoregulation is lost. Vasoconstriction, as a treatment, might be beneficial. However, in patients with severe cerebral infarction no convincing favorable affect has been noted. The potential therapeutic action of hyperventilation in patients with mild cerebral infarction has not been studied.

Extensive (global) changes in the cerebral blood flow in cerebral infarction, certain aspects of intracerebral hemorrhage, and the role of hypertension in cerebrovascular disease are also dealt with.
Effects of Freezing on Major Arteries
Authors: COOPER IRVING S. , SAMRA KHAIRY , WISNIEWSKA KRYSTYNA
Published: June 2011

Thirty experiments were performed in dogs to assess the effects of freezing on carotid and femoral arteries. These vessels withstood freezing and thawing without rupture. Blood within the vessels did not clot and was lysed during thawing.

Histological changes of vessel walls consisted of early degeneration followed by a reparative process. Occasional secondary thrombosis occurred close to bifurcation of ligated branches and was related to extent and frequency of freezing and thawing.
Indium-111-labeled platelet scintigraphy in carotid atherosclerosis.
Authors: Minar E , Ehringer H , Dudczak R , Schöfl R , Jung M , Koppensteiner R , Ahmadi R , Kretschmer G
Published: June 2011

We evaluated platelet accumulation in carotid arteries by means of a dual-radiotracer method, using indium-111-labeled platelets and technetium-99m-labeled human serum albumin, in 123 patients (92 men, 31 women; median age 60 years). Sixty patients had symptoms of transient ischemic carotid artery disease, and 63 patients with peripheral arterial occlusive disease served as controls. Antiplatelet treatment with acetylsalicylic acid was taken by 53 of the 123 patients. In 36 of the 60 symptomatic patients, platelet scintigraphy was repeated 3-4 days after carotid endarterectomy. Comparison of different scintigraphic parameters (platelet accumulation index and percent of the injected dose of labeled platelets at the carotid bifurcation) showed no significant differences between symptomatic and asymptomatic patients, and the severity of stenosis and the presence of plaque ulceration also had no influence on the parameters. There was no difference between patients with a short (less than 4 weeks) or long (greater than 4 weeks) interval from the last transient ischemic attack to scintigraphy and no difference between patients with or without antiplatelet treatment. Classifying the patients according to plaque morphology judged by high-resolution real-time ultrasonography also demonstrated no differences. No significant correlation was found between any scintigraphic parameter and other platelet function parameters such as platelet survival time, platelet turnover rate, and concentration of platelet-specific proteins. Quantification of platelet deposition after carotid endarterectomy in 36 patients demonstrated a significant increase of the median platelet accumulation index and the percent injected dose index. There were no significant differences between patients receiving high-dose (1.0 g/day) or low-dose (1.0 g/day) acetylsalicylic acid in scintigraphic results.(ABSTRACT TRUNCATED AT 250 WORDS)
Morbidity and mortality in the Systolic Hypertension in the Elderly Program (SHEP) pilot study.
Authors: Perry H M , Smith W M , McDonald R H , Black D , Cutler J A , Furberg C D , Greenlick M R , Kuller L H , Schnaper H W , Schoenberger J A
Published: June 2011

The pilot study of the Systolic Hypertension in the Elderly Program was a randomized, double-blind, placebo-controlled trial of drug therapy for isolated systolic hypertension. It followed 551 elderly participants with untreated blood pressures of greater than 160/less than 90 mm Hg for an average of 34 months. Mean age of the participants was 72 years; 63% were women, and 82% were white. Pretreatment blood pressures averaged 172/75 mm Hg. Participants were randomly assigned to treatment with chlorthalidone or placebo as Step I medication. Blood pressures at annual visits averaged 141/68 and 157/73 mm Hg for the drug-treated and placebo-treated groups, respectively, with 60% and 33% of the survivors on blinded medication having systolic blood pressures of less than 160 mm Hg at their last annual visit. All-cause mortality rates for the drug-treated and placebo-treated groups were 25.4 and 22.7 deaths per 1,000 participant-years of risk, and rates for definite "first stroke" were 8.3 and 12.8 per 1,000 years of risk. Differences between groups were significant for systolic and diastolic blood pressure but not for death or stroke rates. A full-scale study has begun to determine the effects of drug therapy for isolated systolic hypertension on stroke and mortality rates.
Reversible middle cerebral artery occlusion without craniectomy in rats.
Authors: Longa E Z , Weinstein P R , Carlson S , Cummins R
Published: June 2011

To develop a simple, relatively noninvasive small-animal model of reversible regional cerebral ischemia, we tested various methods of inducing infarction in the territory of the right middle cerebral artery (MCA) by extracranial vascular occlusion in rats. In preliminary studies, 60 rats were anesthetized with ketamine and different combinations of vessels were occluded; blood pressure and arterial blood gases were monitored. Neurologic deficit, mortality rate, gross pathology, and in some instances, electroencephalogram and histochemical staining results were evaluated in all surviving rats. The principal procedure consisted of introducing a 4-0 nylon intraluminal suture into the cervical internal carotid artery (ICA) and advancing it intracranially to block blood flow into the MCA; collateral blood flow was reduced by interrupting all branches of the external carotid artery (ECA) and all extracranial branches of the ICA. In some groups of rats, bilateral vertebral or contralateral carotid artery occlusion was also performed. India ink perfusion studies in 20 rats documented blockage of MCA blood flow in 14 rats subjected to permanent occlusion and the restoration of blood flow to the MCA territory in six rats after withdrawal of the suture from the ICA. The best method of MCA occlusion was then selected for further confirmatory studies, including histologic examination, in five additional groups of rats anesthetized with halothane. Seven of eight rats that underwent permanent occlusion of the MCA had resolving moderately severe neurologic deficits (Grade 2 of 4) and unilateral infarcts averaging 37.6 +/- 5.5% of the coronal sectional area at 72 hours after the onset of occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)
Survival after stroke and transient ischemic attacks during the 1970s and 1980s.
Authors: Terént A
Published: June 2011

Survival after stroke and transient ischemic attack was studied in Söderhamn, Sweden, during the periods 1975-1979 and 1983-1987; 640 patients with first-ever stroke and 97 with first-ever transient ischemic attack were registered and followed for 1-3 years. Approximately 90% of the patients were treated in the Department of Internal Medicine of Söderhamn Hospital. The protocols for physical rehabilitation and antithrombotic treatment changed between study periods. Between periods, 3-year survival after stroke increased by 16% (p less than 0.003). The 95% confidence intervals of the relative survival rates were 0.524-0.648, 0.435-0.567, and 0.337-0.475 at 1, 2, and 3 years, respectively, during the first period and 0.616-0.728, 0.600-0.732, and 0.576-0.748 during the second period. Fewer patients suffered fatal complications of stroke during the second period. The rate of stroke recurrence was approximately 10%/year during both study periods. Four patients suffered fatal hemorrhage during the first period, but no patient did so during the second period. Observed survival after transient ischemic attack did not differ from that expected in the first 2 years of follow-up during either study period. The risk for stroke after transient ischemic attack was approximately 5%/year during both periods. The higher survival rates after stroke during the second period seems to be the result of fewer fatal complications rather than of a reduced risk for recurrent stroke.
Computed tomographic study of cervical carotid calcification.
Authors: Culebras A , Otero C , Toledo J R , Rubin B S
Published: June 2011

Contrast-enhanced computed tomography of the neck permits low-risk evaluation of morphologic complications of carotid plaque, including (and foremost) calcification. To investigate the patterns and clinical significance of calcified deposits in the cervical carotid arteries using computed tomography we studied 40 patients with unilateral symptoms of hemispheric ischemia. Calcium deposits observed in the external, internal, and common carotid arteries were oriented in space and individually scored. We found calcified deposits in 39 patients. Stepwise multiple regression of the data provided evidence strongly suggesting a correlation between advancing age and calcium scores. Calcium was more heavily concentrated in the posterior half of arteries (p less than 0.01), in particular of the internal and common carotid arteries, and always in relation to an atheromatous plaque, suggesting a causative link to hemodynamic forces within the arteries. There was no difference in calcification scores between symptomatic and asymptomatic sides, indicating that calcium deposits do not contribute to the development of symptoms.
Stroke in the People's Republic of China.
Authors: Shi F L , Hart R G , Sherman D G , Tegeler C H
Published: June 2011

Recent epidemiologic studies confirm that stroke is the most frequent cause of death in the People's Republic of China, with an incidence (219/100,000 people) more than fivefold that of myocardial infarction. Intracerebral hemorrhage causes about one third of all strokes, nearly three times the frequency in North American stroke registries. A marked regional variation in stroke incidence exists, with a threefold higher stroke incidence in northern than in southern Chinese cities, suggesting important environmental or dietary influences. Stroke treatment often involves a combination of modern and traditional herbal medicine; the latter may modify platelet aggregation and blood viscosity. Stroke, particularly intracerebral hemorrhage, is the most frequent and important vascular disorder in the People's Republic of China.
Hypercortisolism revealed by the dexamethasone suppression test in patients [corrected] with acute ischemic stroke.
Authors: Olsson T , Aström M , Eriksson S , Forssell A
Published: June 2011

Using the dexamethasone suppression test, we studied the activity of the hypothalamic-pituitary-adrenal axis within the first week after onset in 62 patients with acute ischemic stroke. Compared with two control groups (one comprising 25 elderly patients with various acute medical disorders and the other comprising 33 80-year-old volunteers), stroke patients had higher postdexamethasone cortisol levels (p = 0.08 and p = 0.001, respectively). By multiple regression analysis, high postdexamethasone cortisol levels in the stroke patients were significantly associated with proximity of the lesion to the frontal pole of the brain (p = 0.008) and with disorientation (p = 0.03), whereas no association with major depression was seen. Many stroke patients are exposed to hypercortisolism, which may have negative consequences upon organ functions. The extent to which dexamethasone administration suppresses cortisol levels seems to be determined mainly by the site of brain lesion and cannot be used as an indicator of major depression early after stroke.
Anterior cerebral artery velocity changes in disease of the middle cerebral artery stem.
Authors: Brass L M , Duterte D L , Mohr J P
Published: June 2011

Transcranial Doppler ultrasonography can map the changes in blood velocity that result from stenosis or occlusion of the middle cerebral artery. To evaluate patterns of collateral blood flow in disease of the middle cerebral artery stem, we used both cerebral angiography and transcranial Doppler ultrasonography to study the systolic blood velocities in both anterior cerebral arteries in 10 consecutive patients with middle cerebral artery stenosis or occlusion. Five patients had no evidence of hemodynamically significant carotid disease and good-quality measurements of systolic velocity in each anterior cerebral artery. Two of the five patients had middle cerebral artery stem stenosis and the other three had occlusion. The ratios of mean blood velocity in the normal compared with the abnormal side for the five patients (mean 1.34 +/- 0.23, range 1.15-1.74) were significantly higher than ratios for 10 controls (mean 1.04 +/- 0.12, range 0.76 +/- 1.19) using an unpaired t test (t = 3.492, 0.0005 less than p less than 0.005). Our results suggest that transcranial Doppler ultrasound measurements of anterior cerebral artery blood velocity may be a useful index of collateral blood flow from the anterior cerebral artery territory into the middle cerebral artery territory. Changes in mean velocity ratio may document the evolution and adequacy of collateral blood flow over the cerebral convexity in middle cerebral artery stem disease. In addition, the changes in anterior cerebral artery blood velocity appear to be an important corroborative finding for middle cerebral artery stem occlusion.
Site and pathogenesis of infarcts associated with carotid endarterectomy.
Authors: Krul J M , van Gijn J , Ackerstaff R G , Eikelboom B C , Theodorides T , Vermeulen F E
Published: June 2011

We analyzed perioperative strokes in 658 carotid endarterectomies with the purpose of explaining the pathogenesis from the morphologic aspect of the infarct on cerebral computed tomograms. All endarterectomies were performed with continuous electroencephalographic monitoring. Of the 42 ischemic strokes (6.4% of all endarterectomies), 34 could be studied. Seven infarcts were hemodynamically induced (five watershed infarcts, two patients with bilateral ischemia); all seven occurred during surgery. Twenty-three of the remaining 27 infarcts were within the territory of the middle cerebral artery (20) or anterior cerebral artery (three) and were probably of thromboembolic origin; 13 of these 23 occurred during surgery (57%). If intraoperative stroke was heralded by permanent electroencephalographic changes, these were not related to the moment of cross-clamping. In four patients the computed tomogram was normal. We believe these facts favor the hypothesis that thromboembolism is the most important factor in the pathogenesis of perioperative stroke associated with carotid endarterectomy under conditions of optimal cerebral monitoring.
Incidence of transient ischemic attacks in Oxfordshire, England.
Authors: Dennis M S , Bamford J M , Sandercock P A , Warlow C P
Published: June 2011

The Oxfordshire Community Stroke Project is a prospective register of all new cases of stroke and transient ischemic attack (TIA) in a population of 105,000 residents of Oxfordshire, England. Between November 1, 1981, and October 31, 1986, 184 patients presented for the first time to a general practitioner or hospital with a TIA. The crude annual incidence rate was 0.35/1000, 0.42/1000 standardized to the 1981 population of England and Wales. We estimate that each year approximately 21,000 patients in England and Wales (about half of whom are greater than 70 years old) consult a doctor for the first time with a TIA. Approximately 80% of our 184 patients had TIAs in the carotid distribution; the remainder had TIAs in the vertebrobasilar distribution or TIAs of uncertain vascular distribution. The incidence of TIA increased sharply with increasing age, and the overall incidence in men was very similar to that in women (incidence ratio 1.3). However, in middle age, men were much more likely to suffer a TIA than women (odds ratio 2.6), which probably explains the marked male predominance in most hospital-based studies and treatment trials in which the elderly, and thus women, are underrepresented. This has important implications for the design and interpretation of clinical trials of treatment for TIAs.
Changes in survival following stroke in five North Carolina counties observed during two different periods.
Authors: Howard G , Toole J F , Becker C , Lefkowitz D S , Truscott B L , Rose L , Evans G W
Published: June 2011

We evaluated survival following stroke for patients from a five-county area of rural North Carolina enrolled in either of two community hospital-based stroke survey programs. In this area, the first program enrolled 843 stroke patients between 1970 and 1973 and the second program enrolled 786 stroke patients between 1979 and 1980. One-year survival increased from 49% in the first program to 62% in the second for all stroke patients, from 54% to 68% for patients with cerebral infarction, and from 18% to 55% for patients with cerebral hemorrhage. While other reports have attributed declining stroke mortality to a decline in the incidence of stroke, our study suggests that increased survival after stroke may account for a large portion of the decrease in stroke mortality.
Protective effect of a 21-aminosteroid on the blood-brain barrier following subarachnoid hemorrhage in rats.
Authors: Zuccarello M , Anderson D K
Published: June 2011

The effects of subarachnoid injection of blood on blood-brain barrier permeability to albumin was assessed in a rat model. Subarachnoid injection of blood caused a significant sixfold increase in Evans blue extravasation, whereas sham operation or NaCl injection had no effect. In addition, subarachnoid injections of arachidonic acid or FeCl2 increased blood-brain barrier permeability to Evans blue 16- and 10-fold, respectively. The capillary permeability after subarachnoid injection of blood was normalized by pretreatment with a novel 21-aminosteroid, U-74006F, that has antioxidant and antilipolytic activity. Pretreatment with U-74006F also reduced the vascular leakage induced by subarachnoid injection of arachidonic acid or FeCl2 by 50% and 45%, respectively. We conclude that damage to membrane lipids by peroxidative and/or lipolytic processes is involved in the subarachnoid hemorrhage-induced blood-brain barrier opening and that U-74006F protects the blood-brain barrier against the effects of subarachnoid hemorrhage by preventing or limiting these pathologic membrane lipid changes.
Blunt traumatic carotid dissection with delayed symptoms.
Authors: Pozzati E , Giuliani G , Poppi M , Faenza A
Published: June 2011

We describe five patients with blunt traumatic carotid dissection with delayed clinical presentation that varied from 2 weeks to 6 months. Four patients had severe head injury, and one patient had direct blunt trauma to the neck. Cerebrovascular symptoms developed in four patients. The fifth patient suffered loss of vision as a result of a concurrent giant intracranial dissecting aneurysm. Arteriography demonstrated a "string sign" in two cases and a cervical carotid aneurysm in three; two of the latter also had siphon occlusion, and one of these had a superimposed supraclinoid dissecting aneurysm. One patient was treated by thromboendarterectomy, one by aneurysmorraphy, another by carotid ligation, and the other two patients were treated medically. Mechanisms of injury, forensic problems, and therapeutic options are discussed.
Plasma lipoproteins in cortical versus lacunar infarction.
Authors: Adams R J , Carroll R M , Nichols F T , McNair N , Feldman D S , Feldman E B , Thompson W O
Published: June 2011

We investigated the relation of plasma lipids to the risk for ischemic stroke by comparing clinical and biochemical characteristics of survivors of cortical (n = 48) and lacunar (n = 36) brain infarction. By analysis of variance, no differences were observed in the concentrations of total cholesterol, triglycerides, low density lipoprotein cholesterol, very low density lipoprotein cholesterol, or apoproteins A1 and B. Patients with lacunar infarction, however, had higher concentrations of high density lipoprotein (HDL)-cholesterol than patients with cortical stroke. This HDL-cholesterol difference was due primarily to a strikingly low HDL-cholesterol content in white patients with cortical stroke. These data suggest that previously demonstrated differences in HDL-cholesterol concentrations between patients with ischemic stroke and control subjects without stroke may apply to patients with cortical but not lacunar infarction. Separation of cerebral infarction into subtypes based on mechanism may help clarify lipid-related risk factors in cerebrovascular disease.
Transvenous perfusion of the brain with verapamil during focal cerebral ischemia in rats.
Authors: Ueda T , Yamamoto Y L , Diksic M
Published: June 2011

We report on the effect of calcium channel blocker verapamil administered into the inferior cerebral vein in rats 1 hour after occlusion of the middle cerebral artery. Twenty-four rats were divided into four groups of six rats each. Group A rats received no medication. The other three groups received 0.1 mg verapamil/kg/2 hr. Group B rats received verapamil intravenously. Group C and D rats received verapamil and autologous arterial blood by transvenous perfusion of the brain, Group C rats at 100 mm Hg perfusion pressure and Group D rats at 150 mm Hg perfusion pressure. The administration of verapamil started 1 hour after middle cerebral artery occlusion and lasted for 2 hours. Three hours after occlusion, we used double- or single-tracer autoradiography with 4-[18F]fluoroantipyrine or [14C]iodoantipyrine and [14C]alpha-aminoisobutyric acid as tracers to study the brains for local cerebral blood flow and blood-brain barrier permeability changes. Group C showed a significant increase of local cerebral blood flow in the parietal cortex (89%, p less than 0.01) and sensorimotor cortex (64%, p less than 0.05) compared with Group A. Group D showed an extensive and striking increase in local cerebral blood flow of the ischemic cortical and subcortical areas (57-100%, p less than 0.05). Group B showed no significant changes but exhibited further reduction of local cerebral blood flow in the ischemic cerebral hemisphere associated with slightly increased local cerebral blood flow in the nonischemic cerebral hemisphere compared with Group A. There was no change of blood-brain barrier permeability in any group.(ABSTRACT TRUNCATED AT 250 WORDS)
Effects of elevated plasma magnesium versus calcium on cerebral ischemic injury in rats.
Authors: Blair J L , Warner D S , Todd M M
Published: June 2011

Both Mg2+ and Ca2+ have been implicated as having roles in the pathomechanisms of cerebral ischemia. To further study the effects of these ions on postischemic histologic outcome, fasted rats were given one of three intravenous infusions: 5.0 mmol/kg MgCl2, 5.0 mmol/kg MgCl2 + 0.035 units/kg regular insulin, or 1.0 mmol/kg CaCl2. This resulted in elevated plasma Mg2+ or Ca2+ concentrations in the corresponding groups. A fourth group received 0.9% NaCl (saline). Preinfusion plasma glucose concentration was similar for all groups and was unchanged after infusion in rats receiving either saline or MgCl2 + insulin. In contrast, postinfusion glucose concentration was increased in the MgCl2 group (p less than 0.001) and decreased in the CaCl2 group (p less than 0.001) relative to saline-treated rats. Following respective infusions, all rats underwent 10 minutes of reversible forebrain ischemia (bilateral carotid artery occlusion and systemic hypotension) followed by 7 days' recovery. Six of 12 CaCl2-treated rats died 2-3 days after ischemia; all other rats remained neurologically indistinguishable, without gross neurologic deficits. Histologic injury in the neocortex and caudate was moderate in all groups. In the hippocampus, MgCl2 + insulin resulted in 66 +/- 6% (mean +/- SD) dead CA1 pyramidal cells, which was similar to the amount in saline-treated rats (68 +/- 10%). Injury was increased in the MgCl2 group (79 +/- 4% dead cells), while in surviving CaCl2-treated rats, injury was decreased (54 +/- 13%). We conclude that the increased injury in MgCl2-treated rats and the decreased injury noted in surviving rats receiving CaCl2 are due to the plasma glucose concentrations present prior to ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
Neurologic and neuropathologic outcome after middle cerebral artery occlusion in rats.
Authors: Persson L , Hårdemark H G , Bolander H G , Hillered L , Olsson Y
Published: June 2011

Focal cerebral ischemia was produced in 45 rats by occlusion of the left middle cerebral artery. Groups of rats were investigated over a long period after occlusion, that is, from a few hours to 42 days after the production of focal ischemia. Light microscopy showed infarcts in the frontoparietal cortex and the lateral caudoputamen. The ischemic changes closely resembled those found in ischemic infarcts in humans and followed a similar pattern over time. Measurements of the sizes of the infarct, the ipsilateral (operated) hemisphere, and the contralateral hemisphere from camera lucida drawings revealed that the infarct size changed with time after occlusion. Rats killed during the first 7 days (acute phase) had the largest infarcts; in rats killed thereafter, the infarct size diminished. The size of the ipsilateral hemisphere also changed with time; during the first 7 days after occlusion this hemisphere was swollen and larger than the contralateral hemisphere. We suggest that these acute changes are caused by cerebral edema. After the first 7 days, enlargement of the ipsilateral hemisphere gave way to a significant reduction in the size of both the ipsilateral hemisphere and the infarct. We believe that the major reasons for this shift in size are resorption of fluid together with diminished production of edema and elimination of dead cells by macrophages. We suggest that the amount of tissue loss (i.e., the degree of atrophy and the remaining infarct "scar") found 21-42 days after occlusion (during the late phase) is a measure of the total amount of tissue that succumbed as a consequence of ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
Cerebral blood flow in humans following resuscitation from cardiac arrest.
Authors: Cohan S L , Mun S K , Petite J , Correia J , Tavelra Da Silva A T , Waldhorn R E
Published: June 2011

Cerebral blood flow was measured by xenon-133 washout in 13 patients 6-46 hours after being resuscitated from cardiac arrest. Patients regaining consciousness had relatively normal cerebral blood flow before regaining consciousness, but all patients who died without regaining consciousness had increased cerebral blood flow that appeared within 24 hours after resuscitation (except in one patient in whom the first measurement was delayed until 28 hours after resuscitation, by which time cerebral blood flow was increased). The cause of the delayed-onset increase in cerebral blood flow is not known, but the increase may have adverse effects on brain function and may indicate the onset of irreversible brain damage.
Prevalence of stroke in Taiwan.
Authors: Hu H H , Chu F L , Chiang B N , Lan C F , Sheng W Y , Lo Y K , Wong W J , Luk Y O
Published: June 2011

We investigated the prevalence of stroke in Taiwan in an epidemiologic study of stroke, diabetes, and cardiovascular disease that used a two-phase survey design. The study population was drawn by cluster sampling and consisted of both urban and rural communities from four regions of Taiwan. There were 8,705 people 36 years of age or older interviewed during the period of October 1 to December 31, 1986, and 143 cases of completed stroke were later identified by a neurologist. The point prevalence rate for people aged 36 or older in our study was 1,642/100,000 population (95% confidence interval 1,389-1,942/100,000). Prevalence rates differed significantly among the four study regions and between urban and rural communities; prevalence was greater in northern Taiwan and in urban communities. Percentages of the major types of stroke in 143 stroke survivors were as follows: cerebral infarction 67.1% (96 cases), cerebral hemorrhage 14.0% (20 cases), subarachnoid hemorrhage 4.2% (six cases), and unclassified 14.7% (21 cases). Of the stroke survivors, 67.1% were independent in activities of daily living, and 75.5% were independent in ambulation. Hypertension, heart disease, diabetes mellitus, and a family history of stroke were significantly more common in stroke survivors than in strokefree individuals.
Long-term culture of microvascular endothelial cells derived from Mongolian gerbil brain.
Authors: Minakawa T
Published: June 2011

A method for long-term culture of microvascular endothelial cells from Mongolian gerbil brain and their biologic properties in vitro are described. Microvessels were isolated from Mongolian gerbil brain by a combination of enzymatic treatment, filtration, and centrifugation and were seeded onto a gelatin-coated dish. A morphologically homogeneous cell plaque showing a cobblestone appearance was removed 2 to 3 weeks after the seeding, and the cells were subcultured. The cultured cells grew as monolayers of flat polygonal cells and were carried for more than 20 passages without morphologic change. These cells synthesized prostacyclin and retained an endothelial specific marker, factor VIII-related antigen. When the cells were cultured in a collagen gel, they rapidly formed capillarylike tubular structures without endothelial cell growth factor or special substrata. Long-term culture of purified microvascular endothelial cells derived from Mongolian gerbil brain will facilitate the study of the function of microvascular endothelial cells in human brain under normal and pathologic conditions.
Moyamoya disease associated with polycystic kidney disease and eosinophilic granuloma.
Authors: Pracyk J B , Massey J M
Published: June 2011

Moyamoya disease has been associated with renal artery stenosis, cerebral hemorrhage, and multiple cranial traumas. We report a unique case of moyamoya disease associated with polycystic kidney disease and eosinophilic granuloma. Although the etiology of moyamoya disease is unknown, a familial pattern of occurrence has been documented. Of particular importance is its presentation with polycystic kidney disease, an autosomal dominant disease, suggesting a hereditary component to the etiology of this unusual vasculitic disease.
Immediate and long-term results of carotid endarterectomy.
Authors: Healy D A , Clowes A W , Zierler R E , Nicholls S C , Bergelin R O , Primozich J F , Strandness D E
Published: June 2011

We review the long-term results of carotid endarterectomy in 200 consecutive patients operated on from 1980 to 1987. The patients were part of an ongoing study using duplex scanning to assess the status of the carotid bifurcation before and after endarterectomy. The average follow-up for the patients was 31 months. The indications for surgery were transient ischemic attacks in 87 (43.5%) and stroke in 36 (18%) patients; 77 patients (38.5%) were asymptomatic. In 176 sides (88%), the degree of stenosis exceeded 50% in terms of diameter reduction. The perioperative stroke rate was 2.3% in patients with transient ischemic attacks, 2.8% in patients with strokes, and 1.3% in asymptomatic patients. There was one perioperative death (0.5%). There were five occlusions of the internal carotid artery, one during the perioperative period and four after discharge; in three patients the occlusion was associated with the development of a stroke. There was a restenosis rate of 19.7% secondary to myointimal hyperplasia; such lesions did not appear to contribute to new ischemic events during or after their development. The mean stroke incidence after the decision was made for carotid endarterectomy was 2.8%/yr in the patients with transient ischemic attacks, 6.2%/yr in the patients with stroke, and 0.65%/yr in the asymptomatic patients. The annual death rate was 6% for the entire group, 5.5%/yr in the patients with transient ischemic attacks, 9.2%/yr in the patients with stroke, and 4.6%/yr in the asymptomatic patients.
Baclofen does not protect against cerebral ischemia in rats.
Authors: Rosenbaum D M , Grotta J C , Pettigrew L C , Ostrow P , Strong R , Rhoades H , Picone C M , Grotta A T
Published: June 2011

Presynaptic release of glutamate into the extracellular compartment and activation of receptor-operated calcium channels may contribute to ischemic neuronal damage. We evaluated the effect of baclofen, a selective inhibitor of presynaptic glutamate release, on mortality, working memory, and light microscopic hippocampal and cortical damage in the four-vessel occlusion model of cerebral ischemia using 64 male Wistar rats. Baclofen (10 mg/kg i.p.) given 1 hour before and 30-60 minutes after 20 minutes of global ischemia did not lessen mortality, prevent ischemic cellular damage, or significantly improve working memory compared with no treatment. We conclude that preischemic and postischemic administration of baclofen does not protect neurons from ischemic injury.
Transient monocular visual loss patterns and associated vascular abnormalities.
Authors: Bruno A , Corbett J J , Biller J , Adams H P , Qualls C
Published: June 2011

To determine if certain transient monocular visual loss patterns predict the associated vascular abnormalities, we prospectively evaluated 100 consecutive patients. Each patient had hematologic tests, a carotid artery study (arteriography in 74, duplex ultrasonography in the remaining 26), and an ophthalmologic examination. Patients with altitudinal or lateralized transient monocular visual loss were more likely to have carotid artery stenosis, carotid artery ulceration, cardiac sources of emboli, or visible retinal emboli than patients with other visual loss patterns. Our findings suggest that altitudinal or lateralized transient monocular visual loss is primarily caused by embolism but that other visual loss patterns are usually caused by nonembolic mechanisms.
Acetazolamide effect on cerebellar blood flow in crossed cerebral-cerebellar diaschisis.
Authors: Bogsrud T V , Rootwelt K , Russell D , Nyberg-Hansen R
Published: June 2011

We studied the effect of acetazolamide on cerebellar blood flow in 11 stroke patients with large, unilateral cerebral hemispheric infarcts and no evidence of cerebellar infarction, but with cerebrocerebellar diaschisis of cerebral blood flow. Blood flow was determined with xenon-133 inhalation and dynamic single-photon emission computed tomography at rest and 20 minutes after the intravenous injection of 1.0 g acetazolamide. After acetazolamide, the mean +/- SD increases in blood flow in the affected and contralateral cerebellar hemispheres were 11.1 +/- 3.7 and 12.0 +/- 5.3 ml/100 g/min, respectively; the difference between hemispheres was not significant. The absolute increase in cerebellar flow in these 11 patients was of the same magnitude as that in 12 healthy controls. We conclude that cerebellar vasoreactivity is intact in stroke patients with crossed cerebrocerebellar diaschisis of cerebral blood flow. Our results lend further support to the concept that reduced cerebellar blood flow is secondary to functional deactivation. Our patients were studied 2 weeks to 5 years after their stroke, indicating that this phenomenon may be persistent.
Prognosis and disability of stroke patients after 5 years in Akita, Japan.
Authors: Kojima S , Omura T , Wakamatsu W , Kishi M , Yamazaki T , Iida M , Komachi Y
Published: June 2011

The system of registering stroke patients was begun in 1963 in Ikawa Town, Akita Prefecture, Japan. The town is located in the northeastern part of the country and in 1975 had a population of 6,427. From 1975 to 1981, 109 patients who suffered their first stroke were registered and were monitored for 5 years. The average annual incidence rates of stroke were 2.8 and 2.0 per 1,000 population in males and females, respectively. Mean age at stroke onset was 63.3 and 71.4 years in males and females, respectively (p less than 0.01). According to the clinical classification of stroke, 76 patients suffered cerebral infarction, 21 cerebral bleeding, and six subarachnoid hemorrhage; six strokes were unclassified. The survival rates were compared by sex, age, and clinical stroke type using Cox's proportional hazards model. The survival rate of female stroke patients was lower than that of males, but not significantly so. The survival rate of stroke patients greater than or equal to 65 years old was significantly lower (p less than 0.01) than that of younger patients. Moreover, the survival rate of patients with cerebral bleeding was significantly lower (p less than 0.01) than that of patients with cerebral infarction. In the analysis of self-care among the survivors, performance of the activities of daily living in older patients indicated significantly less independence (p less than 0.01) in younger patients. Follow-up of new stroke cases showed that age and clinical stroke type were significantly associated with survival and that age was also related to disability of the survivors.
A 21-aminosteroid reduces hydrogen peroxide generation by and chemiluminescence of stimulated human leukocytes.
Authors: Fisher M , Levine P H , Cohen R A
Published: June 2011

Leukocytes recruited to regions of focal cerebral ischemia may contribute to tissue injury by their ability to promote inflammation. A novel group of drugs, the 21-aminosteroids, have been observed to reduce neurologic damage and vasogenic cerebral edema in animal models of stroke by inhibiting lipid peroxidation. Production of hydrogen peroxide and free radicals by leukocytes during the inflammatory response may contribute to lipid peroxidation and other consequences of free radical-mediated tissue injury. We assessed the effect of U74500A, a 21-aminosteroid, on the generation of hydrogen peroxide by and on the chemiluminescence of stimulated polymorphonuclear leukocytes and monocytes from normal humans. U74500A significantly reduced the generation of hydrogen peroxide by polymorphonuclear leukocytes (p less than 0.001) and monocytes (p less than 0.01) in a dose-dependent manner. Monocyte chemiluminescence was also significantly inhibited (p less than 0.05), but polymorphonuclear leukocyte-associated chemiluminescence was unchanged. Our results indicate that U74500A can reduce the concentration of oxygen metabolites associated with stimulated human leukocytes, and this effect may explain in part how 21-aminosteroids reduce lipid peroxidation, ischemic injury, and vasogenic edema.
Retinal infarction during sleep and wakefulness.
Authors: Bruno A , Biller J , Adams H P , Corbett J J
Published: June 2011

Brain and retinal infarctions during sleep have been attributed to focal hypoperfusion caused by systemic hypotension combined with underlying arterial stenosis, rather than to embolism. Because some retinal emboli may be visualized on ophthalmoscopy, we studied 24 consecutive patients (18 men and six women) aged 26-78 (mean 58) years with recent retinal infarction and determined whether the infarction had occurred during sleep or wakefulness. All patients underwent dilated ophthalmoscopy and a carotid artery study (arteriography in 20, duplex ultrasound in the remaining four), and 12 had echocardiography. Retinal infarction occurred during sleep at an unexpectedly rate (14 of 24 observed compared with eight of 24 expected, p = 0.02). Retinal cholesterol emboli were seen in one half of the patients regardless of whether the retinal infarction had occurred during sleep or wakefulness. Carotid artery disease was found in seven of the 14 patients in whom infarction had occurred during sleep and in eight of the 10 patients in whom infarction had occurred during wakefulness (p = 0.21). Cerebrovascular occlusive disease was not found in the five patients aged less than 50 years. Our findings suggest that embolism is a common mechanism of retinal infarction during sleep or wakefulness, that in patients aged greater than 50 years extracranial carotid artery disease is a common source of retinal emboli, and that the retina may be especially susceptible to infarction during sleep.
Cerebrospinal fluid atrial natriuretic factor in intracranial disease.
Authors: Diringer M N , Kirsch J R , Ladenson P W , Borel C , Hanley D F
Published: June 2011

We tested the hypothesis that the concentration of atrial natriuretic factor in the cerebrospinal fluid is an indicator of brain injury in patients with intracranial disease. Atrial natriuretic factor concentration was measured in 72 samples of cerebrospinal fluid from 28 patients with intraventricular drains and in nine samples from outpatient controls undergoing diagnostic lumbar puncture. Levels were correlated with diagnosis; systemic fluid administration; concentration of atrial natriuretic factor in the plasma; intracranial pressure; sodium, glucose, and protein concentrations, osmolality, and cell count in the cerebrospinal fluid; sodium concentration in the serum; and hemodynamics. Atrial natriuretic factor concentration was highest in cerebrospinal fluid from patients with intracerebral hematoma, followed by those with obstructive hydrocephalus and subarachnoid hemorrhage (19 +/- 2, 13 +/- 3, and 8 +/- 2 pg/ml, respectively); atrial natriuretic factor concentration was less than 4 pg/ml in the controls. Patients treated with fluid restriction had significantly higher atrial natriuretic factor levels than those receiving maintenance or high-volume fluids (16 +/- 3, 8 +/- 2, 10 +/- 1 pg/ml, respectively). The concentration of atrial natriuretic factor in the plasma was significantly elevated in patients with intracerebral hematoma and subarachnoid hemorrhage (155 +/- 38 and 92 +/- 20 pg/ml, respectively) and did not correlate with fluid administration or the concentration of atrial natriuretic factor in the cerebrospinal fluid. Neither cerebrospinal fluid nor plasma concentrations of atrial natriuretic factor correlated with intracranial pressure; cerebrospinal fluid sodium, glucose, or protein concentrations, osmolality, or cell count; serum sodium concentration; or hemodynamics. We conclude that the concentration of atrial natriuretic factor in the cerebrospinal fluid is a nonspecific indicator of brain injury.(ABSTRACT TRUNCATED AT 250 WORDS)
Natural history of progressive ischemic stroke in a population treated with heparin.
Authors: Slivka A , Levy D
Published: June 2011

Data on the acute natural history of progressive stroke with or without heparin treatment are limited. To define the acute course of patients treated with heparin for progressive stroke, we examined the charts of 69 such patients identified through the Cornell Neurology Database from October 1979 to June 1985. Analysis included determining whether further clinical deterioration or hemorrhagic complications were associated with readily identifiable clinical or laboratory variables. Twenty-five patients (36%) continued to deteriorate while receiving heparin, another two (3%) worsened due to intracerebral hemorrhage, and a total of 10 patients (14%) had bleeding complications. No clinical features or heparin dosing regimens distinguished the patients likely to benefit from heparin. Clinical progression or hemorrhage did not correlate with the level of anticoagulation as measured by the average heparin dose per day or the mean partial thromboplastin time. Without unequivocal evidence demonstrating heparin's ineffectiveness for progressive stroke, many clinicians managing such patients will continue to use heparin. Our results suggest that this decision should not be governed by such clinical features as a patient's age or sex or by the vascular distribution of the stroke. Furthermore, frequent measurement of and overzealous efforts to adjust the partial thromboplastin time may be unnecessary since it does not correlate with outcome.