bluuebunny/crossref_metadata_2025 huggingface dataset:
Implications of the angiographic string sign in carotid atherosclerosis.
Authors: Fredericks R K , Thomas T D , Lefkowitz D S , Troost B T
Published: June 2011

We identified 60 patients (42 men and 18 women with an average age of 62.6 years) with angiographically documented carotid stenoses of greater than or equal to 95%; a string sign was demonstrated in 28. Twenty of the 60 patients (33%) were asymptomatic on presentation, 26 (43%) had hemispheric transient ischemic attacks, 21 (35%) had amaurosis fugax, and nine (15%) had previous ipsilateral infarctions. Demographics, mode of presentation, and prevalence of atherosclerotic risk factors were not significantly different between patients with and without a string sign. Doppler frequencies recorded in patients with a string sign were less than 6 or greater than 16 KHz. Real-time ultrasonography imaged a patent lumen in all but three cases with a string sign. Surgery was performed in 26 patients with a string sign and in 21 patients without a string sign. The rate of major perioperative complications was not influenced by the presence of a string sign, contralateral extracranial stenosis, or ipsilateral siphon stenosis. Average lumen size of the endarterectomy specimens was 0.94 mm in those with and 1.7 mm in those without a string sign. We conclude that combined noninvasive testing has a sensitivity of 83% for demonstrating a residual lumen in patients with greater than or equal to 95% carotid stenosis and that the angiographic string sign does not affect the mode of presentation or surgical outcome of these patients.
Hemorrhagic infarct induced by arterial hypertension in cat brain following middle cerebral artery occlusion.
Authors: Saku Y , Choki J , Waki R , Masuda J , Tamaki K , Fujishima M , Ogata J
Published: June 2011

The purpose of this experiment was to determine whether an acute rise in brain perfusion pressure causes hemorrhagic transformation of an infarct without a reopening of the occluded artery. We raised the blood pressure of 22 cats by aortic obstruction 5-24 hours after transorbital middle cerebral artery clipping; hemorrhagic infarcts were induced in 11. Mean arterial blood pressure increased by 57.2 +/- 16.9 mm Hg (mean +/- SD) in the 11 cats with hemorrhagic infarcts and by 40.4 +/- 16.9 mm Hg in the 11 remaining cats with pale brain infarcts (p less than 0.05). Induction of hypertension increased regional cerebral blood flow in the ischemic cortical gray matter more in three cats with hemorrhagic infarcts than in seven with pale infarcts. Our results demonstrate that hemorrhagic transformation of an infarct can be induced by a rapid increase in perfusion pressure to brain tissue already exposed to focal ischemia. We also suggest that the restoration of blood flow through leptomeningeal collaterals plays an important role in the pathogenesis of hemorrhagic infarction in cases without reopening of occluded arteries.
Cerebrovascular disease in Ehlers-Danlos syndrome type IV.
Authors: Schievink W I , Limburg M , Oorthuys J W , Fleury P , Pope F M
Published: June 2011

We describe two patients with cerebrovascular complications of Ehlers-Danlos syndrome type IV. A 16-year-old girl with spontaneous internal carotid artery dissection and a 46-year-old woman with aneurysmal subarachnoid hemorrhage and multiple aortic dissections were both deficient in collagen type III, analyzed in cultured skin fibroblasts. To our knowledge, spontaneous carotid artery dissection associated with collagen type III deficiency has not been reported previously. Early clinical recognition of this syndrome is of great importance in view of the hazards of angiography and surgery. Collagen type III deficiency plays a role in the pathogenesis of intracranial saccular aneurysms and may also be involved in the pathogenesis of carotid cavernous fistulas and dissections of the cervical arteries.
Prostanoids determine the range of cerebral blood flow autoregulation of newborn piglets.
Authors: Chemtob S , Beharry K , Rex J , Varma D R , Aranda J V
Published: June 2011

To assess whether prostanoids have a role in setting the blood pressure limits of cerebral blood flow autoregulation in newborn animals, we measured cerebral blood flow and prostanoid concentrations in blood from the sagittal sinus over a wide range of mean systemic blood pressures (17-117 mm Hg) in eight newborn piglets treated with 30 mg/kg i.v. ibuprofen and in eight vehicle-treated piglets. Blood pressure was adjusted by inflating balloon-tipped catheters placed at the aortic isthmus and root to induce hypertension and hypotension, respectively, 80 minutes apart in each piglet. Cerebral blood flow and concentrations of prostaglandins E and F2 alpha, 6-keto-prostaglandin F1 alpha, and thromboxane B2 in blood from the sagittal sinus and left subclavian artery were measured 20 minutes before (baseline) and during each blood pressure adjustment. In vehicle-treated piglets, cerebral blood flow was constant at blood pressures between 50 and 90 mm Hg (r = 0.06, p = 0.85). When blood pressure was reduced to less than 50 mm Hg, thromboxane B2 concentration in the sagittal sinus increased by 597 +/- 42% and concentrations of the prostaglandins increased by an average of 308 +/- 45% (p less than 0.05). When blood pressure was raised to greater than 90 mm Hg, concentrations of the prostaglandins increased by an average of 46 +/- 11%, with no change in the concentration of thromboxane B2. Treatment with ibuprofen reduced the baseline concentrations of all prostanoids and prevented their changing during hypotension and hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
Collagenase-induced intracerebral hemorrhage in rats.
Authors: Rosenberg G A , Mun-Bryce S , Wesley M , Kornfeld M
Published: June 2011

Intracranial bleeding is an important cause of brain masses and edema. To study the pathophysiology of intracerebral hemorrhage, we produced experimental hemorrhages in 53 rats and characterized the lesion by histology, brain water content, and behavior. Adult rats had 2 microliters saline containing 0.5 unit bacterial collagenase infused into the left caudate nucleus. Histologically, erythrocytes were seen around blood vessels at the needle puncture site within the first hour. By 4 hours there were hematomas, the size of which depended on the amount of collagenase injected. Necrotic masses containing fluid, blood cells, and fibrin were seen at 24 hours. Lipid-filled macrophages were observed at 7 days and cysts at 3 weeks. Water content was significantly increased 4, 24, and 48 hours after infusion at the needle puncture site and for 24 hours in posterior brain sections. Behavioral abnormalities were present for 48 hours, with recovery of function occurring during the first week. Brain tissue contains Type IV collagen in the basal lamina. Collagenase, which occurs in an inactive form in cells, is released and activated during injury, leading to disruption of the extracellular matrix. Collagenase-induced intracerebral hemorrhage is a reproducible animal model for the study of the effects of the hematoma and brain edema.
Clinical study of 227 patients with lacunar infarcts.
Authors: Arboix A , Martí-Vilalta J L , García J H
Published: June 2011

We describe an analysis of 227 patients with lacunar infarcts; 177 were inpatients and the remaining 50 were outpatients. The group comprised 11% of all inpatients with cerebrovascular pathology and 16% of all consecutive inpatients with brain infarcts studied at the Department of Neurology of the Hospital de la Santa Creu i Sant Pau. The main risk factors identified in these patients were arterial hypertension in 164 (72%), diabetes mellitus in 64 (28%), and heart disease in 58 (26%). The most common clinical syndromes were pure motor hemiparesis in 125 (55%), pure hemisensory stroke in 42 (18%), the sensorimotor deficit syndrome in 34 (15%), ataxic hemiparesis in seven (3%), and the dysarthria-clumsy hand syndrome in four (2%); atypical syndromes were observed in 15 patients (7%). Lacunes were demonstrated by computed tomography in 100 patients (44%) and by magnetic resonance imaging in 35 (78%) of the 45 patients in which it was applied. Magnetic resonance imaging was significantly better (p less than 0.001) than computed tomography for imaging lacunes, especially those located in either the pons (p less than 0.005) or the internal capsule (p less than 0.001). After the acute phase, mild or no neurologic disability was detected in 178 patients (78.4%), moderate disability persisted in 48 patients (21.1%), and severe disability was recorded in one case (0.4%). Lacunar infarcts are a clearly defined entity with characteristic clinical features and an excellent short-term prognosis. Magnetic resonance imaging is the current method of choice for demonstrating these small brain lesions.
Changes in the concentrations of cerebral proteins following occlusion of the middle cerebral artery in rats.
Authors: Inuzuka T , Tamura A , Sato S , Kirino T , Yanagisawa K , Toyoshima I , Miyatake T
Published: June 2011

Using an immunoblotting technique, we investigated changes in the concentrations of microtubule-associated protein 2, 200-kDa neurofilament, tubulin, myelin-associated glycoprotein, and 2':3'-cyclic nucleotide 3'-phosphodiesterase in the brains of 40 rats following occlusion of the left middle cerebral artery or sham operation. Compared with those 4 hours after surgery, concentrations of all proteins decreased significantly in the left hemisphere 3 days after surgery (p less than 0.01). Microtubule-associated protein 2 was the most susceptible to ischemia, and its mean +/- SEM concentration decreased to 23 +/- 9.4% of that in concurrent sham-operated controls. Degradation products of microtubule-associated protein 2 and myelin-associated glycoprotein were detected on the blots. Furthermore, in the contralateral hemisphere (where calpain might be activated), concentrations of these two proteins decreased to 57 +/- 12.0% and 83 +/- 4.3% of those in concurrent sham-operated controls, respectively, 3 days after surgery. Changes in the concentrations of cerebral proteins in the contralateral hemisphere are important for understanding clinical symptoms not attributable solely to the ipsilateral lesion following a focal cerebral stroke.
Kappa-opioid receptor changes and neurophysiological alterations during cerebral ischemia in rabbits.
Authors: Scavini C , Rozza A , Bo P , Lanza E , Favalli L , Savoldi F , Racagni G
Published: June 2011

Endogenous opioids have been shown to produce beneficial effects in experimental stroke. To evaluate both neurophysiological and biochemical parameters, we induced massive cerebral ischemia in 11 rabbits according to the method standardized in our laboratory, using microspheres injected through the internal carotid artery. Binding studies were performed in the 11 embolized, in nine control, and in five sham-operated rabbits using the appropriate concentration of [3H]dynorphin A (1-8). Neurophysiological parameters were evaluated under baseline conditions and 1 hour after embolization, surgical preparation, or sham operation in 17 rabbits. Comparison of visual readings of the electroencephalograms and analyses of the quantified electroencephalograms under baseline conditions and after embolization indicated a marked and statistically significant (p less than 0.01) increase in bilateral delta activity; histologic examination confirmed bilateral brain edema. Binding studies on kappa-opioid receptors indicate that 1 hour after embolization there were significantly more (28%) kappa-opioid receptors (Bmax) in six embolized rabbits than in five sham-operated animals. No significant changes were observed in the affinity parameters, particularly in the dissociation constant (Kd). Our results indicate a role for endogenous dynorphin peptides in the pathogenesis of stroke.
Multiple intracerebral hemorrhages after smoking "crack" cocaine.
Authors: Green R M , Kelly K M , Gabrielsen T , Levine S R , Vanderzant C
Published: June 2011

After smoking "crack" cocaine and consuming large quantities of ethanol, a 36-year-old man developed multiple, bilateral, deep, and superficial cerebral hematomas. He was hypertensive for several days, but angiography revealed no evidence of vascular malformation or vasculitis. The multifocality of the hematomas and lack of underlying disease suggest that the hemorrhages resulted from cocaine-induced acute hypertension or arterial spasm, possibly potentiated by heavy ethanol consumption.
Blood-brain barrier disturbance following subarachnoid hemorrhage in rabbits.
Authors: Johshita H , Kassell N F , Sasaki T
Published: June 2011

We studied disruption of the blood-brain barrier after experimental subarachnoid hemorrhage induced by an injection of 4 ml autologous arterial blood into the cisterna magna of rabbits. The animals were killed at 40 minutes, 6 hours, 1 day, 2 days, 4 days, or 6 days after subarachnoid hemorrhage. We assessed the integrity of the barrier function of intraparenchymal vessels in the ventral brain stem and cerebral hemispheres morphologically with transmission electron microscopy, using horseradish peroxidase as a tracer. In the ventral brain stem, which was in direct contact with the cisternal clots, markedly increased peroxidase staining toward the core of the brain stem was observed on the first day after subarachnoid hemorrhage. In an area of the cerebral hemispheres distant from the clots, barrier disturbance was prominent in the 6-hour specimens, and permeation of the tracer was spotty. From the distribution and morphological findings of these lesions, permeability changes in the ventral brain stem may have been caused by a direct effect of the cisternal clots; in the cerebral hemispheres, hemodynamic factors and changes in intracranial pressure associated with the elderly stages of subarachnoid hemorrhage seemed to be responsible. These results suggest that barrier disturbance associated with subarachnoid hemorrhage may be multifactorial in time course and location.
Ultrastructural changes in cerebral pericytes and astrocytes of stroke-prone spontaneously hypertensive rats.
Authors: Tagami M , Nara Y , Kubota A , Fujino H , Yamori Y
Published: June 2011

We examined the ultrastructure of cerebral pericytes and astrocytes in 20 normotensive Wistar-Kyoto rats and 60 asymptomatic stroke-prone spontaneously hypertensive rats killed at 4-52 weeks of age. Another 30 stroke-prone spontaneously hypertensive rats were killed soon after they showed symptoms of stroke. We found two kinds of pericytes around the capillaries: granular pericytes and filamentous pericytes. Granular pericytes possibly serve as scavenger cells in the central nervous system and became active and grew in size with time. In contrast, filamentous pericytes degenerated during the development of hypertension. Degeneration of the filamentous pericytes was involved in an increase of endothelial permeability. Increased permeability caused focal and then circumferential swelling of the astrocytes around the capillaries. Swelling of the astrocytes seemed to accelerate the production of attachment plaques. Following this increase in the number of attachment plaques, numerous astrocytic filaments were produced within the cytoplasm. As a result, fibrous astrocytes were fully developed. Adjacent to the fibrous astrocytes we detected opening of the interendothelial junctions as well as dead neurons. From these observations we propose that astrocytes perform the main function in trophic interactions among cerebral endothelial cells, astrocytes, and neurons and that dysfunction of astrocytes disturbs the neural environment, resulting in neuronal death.
Ischemic stroke due to protein C deficiency.
Authors: Kohler J , Kasper J , Witt I , von Reutern G M
Published: June 2011

Plasma protein C exerts anticoagulatory effects by inactivating factors V and VIII. Hereditary protein C deficiency is transmitted as an autosomal dominant disorder. Homozygous individuals usually develop purpura fulminans as newborns; heterozygous protein C-deficient individuals are at increased risk for venous thrombosis and pulmonary embolism. However, arterial thrombosis has been only rarely observed. We describe a young patient with heterozygous protein C deficiency who experienced a severe stroke due to thrombotic occlusion of the left middle cerebral artery.
International trends in stroke mortality: 1970-1985.
Authors: Bonita R , Stewart A , Beaglehole R
Published: June 2011

We compared the pattern of cerebrovascular disease (stroke) mortality in men and women aged 40-69 years in 27 countries during 1970-1985 with the decline in coronary heart disease mortality during the same period. Stroke mortality rates declined in 21 and 25 countries for men and women, respectively. In 23 countries the decline in stroke mortality in women was greater than that in men. Countries with the highest rates of stroke mortality are also those with the least favorable secular trend. The rate of decline for stroke mortality is greater than that for coronary heart disease mortality in those countries that experienced a decline in both categories. International comparisons of risk factor levels over time are required to explain the striking differences between countries.
Hypertension with or without hemodilution after cardiac arrest in dogs.
Authors: Sterz F , Leonov Y , Safar P , Radovsky A , Tisherman S A , Oku K
Published: June 2011

We studied blood flow-promoting therapies after cardiac arrest in 18 dogs. Our model consisted of ventricular fibrillation (no blood flow) lasting 12.5 minutes, controlled reperfusion with cardiopulmonary bypass and defibrillation within 5 minutes, controlled intermittent positive-pressure ventilation to 20 hours, and intensive care to 96 hours. Group I (control, n = 6) dogs were reperfused under conditions of normotension (mean arterial blood pressure 100 mm Hg) and normal hematocrit (greater than or equal to 35%). Group II (n = 6) and III (n = 6) dogs were treated with norepinephrine at the beginning of reperfusion to induce hypertension for 4 hours. In addition, group III dogs received hypervolemic hemodilution to a hematocrit of 20% using dextran 40. There were no differences in the time to recovery of electroencephalographic activity among groups. All six group I dogs remained severely disabled; in groups II and III combined, six of the 12 dogs achieved good outcome (p less than 0.01). Some regional histopathologic damage scores at 96 hours were better in groups II and/or III than in group I (neocortex: p less than 0.05 group II different from group I; hippocampus: p less than 0.01 both groups II and III different from group I). Total histopathologic damage scores were similar among the groups. A hypertensive bout with a peak mean arterial blood pressure of greater than or equal to 200 mm Hg beginning 1-5 minutes after the start of reperfusion was correlated with good outcome (p less than 0.01). Our results support the use of an initial bout of severe hypertension, but not the use of delayed hemodilution.
Effect of steroids on edema and sodium uptake of the brain during focal ischemia in rats.
Authors: Betz A L , Coester H C
Published: June 2011

Steroids reduce permeability of the blood-brain barrier and inhibit active sodium transport by brain capillaries in vitro. Since the rate of edema formation during the early stages of ischemia is related to the rate of sodium transport from blood to brain, this study was designed to determine whether steroids reduce ischemic edema formation by inhibiting blood-brain barrier sodium transport. Dexamethasone was compared with progesterone since the latter is a more potent inhibitor of sodium transport in isolated capillaries. Sprague-Dawley rats were treated with vehicle (n = 22) or 2 mg/kg of either dexamethasone (n = 22) or progesterone (n = 17) 1 hour before occlusion of the middle cerebral artery. After 4 hours of ischemia, brain water content and blood-brain barrier permeability to [3H] alpha-aminoisobutyric acid and sodium-22 were determined. In controls, mean +/- SEM water content of tissue in the center of the ischemic zone was 82.4 +/- 0.2%. Brain edema was significantly reduced following pretreatment with either dexamethasone (80.6 +/- 0.1%, p less than 0.001) or progesterone (81.5 +/- 0.3%, p less than 0.05). There was also a significant reduction in blood-brain barrier permeability to alpha-aminoisobutyric acid in normal brain following either treatment (e.g., 2.21 +/- 0.19 and 1.37 +/- 0.10 microliters/g/min, p less than 0.001, for control and dexamethasone treatments, respectively), but no effect on the permeability to sodium (e.g., 1.19 +/- 0.05 and 1.12 +/- 0.11 microliters/g/min for control and dexamethasone treatments, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
Learning impairment and microtubule-associated protein 2 decrease in gerbils under chronic cerebral hypoperfusion.
Authors: Kudo T , Tada K , Takeda M , Nishimura T
Published: June 2011

A coiled stainless steel wire clip was made that allowed us to chronically reduce cerebral blood flow in Mongolian gerbils. After 6 weeks of reduced cerebral blood flow in 15 experimental gerbils, we evaluated their learning ability and found it to be impaired relative to that in 15 control gerbils. Eight weeks after surgery, regional cerebral blood flow in the parietal cortex measured by the hydrogen clearance method in the experimental gerbils was 73-76% of that in the control gerbils. Light microscopy showed minimal histologic changes in the brains of the experimental gerbils. Concentrations of brain proteins analyzed using sodium dodecyl sulfate polyacrylamide gel electrophoresis showed that among water-soluble brain proteins, the concentrations of cytoskeletal proteins (microtubule-associated protein 2, calspectin, and clathrin) declined in the experimental gerbils. In particular, the concentration of microtubule-associated protein 2 declined significantly. Our findings show that the reduction of cerebral blood flow via carotid stenosis impairs the learning behavior in gerbils, with an associated decrease in the concentration of microtubule-associated protein 2. We believe that Mongolian gerbils with chronically reduced cerebral blood flow are a useful animal model of chronic brain hypoperfusion.
Acoustic recordings from experimental saccular aneurysms in dogs.
Authors: Sekhar L N , Sun M , Bonaddio D , Sclabassi R J
Published: June 2011

In an effort to isolate and characterize the emission of acoustic signals from saccular aneurysms, we made a series of invasive microphone recordings from experimental aneurysms created on the common carotid arteries of dogs using the vein pouch technique. Using a modified probe microphone, we compared recordings from the common carotid artery before creation of the aneurysm to recordings from the aneurysmal surface, both before and after clip occlusion. We then performed spectral analysis, band-pass filtering, and spectrographic analysis to compare the dominant frequency and width of the frequency range of both the aneurysmal and carotid recorded signals. The aneurysmal signals had a significantly higher dominant frequency (p less than or equal to 0.05) and a significantly wider frequency range (p less than or equal to 0.05) than the carotid signals. Aneurysmal signals recorded under conditions of systemic hypotension had a significantly lower frequency (p less than or equal to 0.05) than aneurysmal signals recorded under conditions of hypertension. Our results support the assumptions that acoustic signals from experimental saccular aneurysms are distinct from those of the parent vessel and that the aneurysmal signal can be characterized using passive microphone recordings.
Stroke in neuroborreliosis.
Authors: May E F , Jabbari B
Published: June 2011

A 20-year-old man suffered two thalamic infarctions during the course of neuroborreliosis and was successfully treated with intravenous ceftriaxone. Review of 11 additional cases of stroke and cerebral vasculitis in neuroborreliosis suggests that there is a meningovascular form of the infection with predilection for the posterior circulation and an association with the European strains of Borrelia burgdorferi.
The fallacy of the lacune hypothesis.
Authors: Millikan C , Futrell N
Published: June 2011

We review the definition, pathogenesis, natural history, and prognosis and describe the first experimental model of lacunes. Defined pathologically or radiologically, lacunes are small cerebral infarcts which become cystic and are caused by occlusion of small arteries. The clinical definition of lacune is confused. The word "lacune" means a small stroke. While the immediate mortality rate from a small stroke is low, many patients are unable to return to work and the long-term prognosis is guarded. Photochemical damage to the carotid artery of rats produces microemboli to the brain, resulting in cavitary lesions resembling lacunes in humans. The "lacune hypothesis" is a fallacy because small cerebral infarcts are not caused solely by a combination of hypertension and small vessel disease, and the various "lacunar syndromes" are simply small strokes which should be investigated as such.
Phenytoin affects metabolism of free fatty acids and nucleotides in rat cerebral ischemia.
Authors: Kinouchi H , Imaizumi S , Yoshimoto T , Motomiya M
Published: June 2011

We investigated the effects of phenytoin on the rate of enzymatic release of free fatty acids and on the levels of energy metabolites and nucleoside phosphates in ischemic brain. Phenytoin (10 mg/kg i.v.) was administered 30 minutes before the onset of ischemia induced in 30 male Wistar rats by occluding the basilar and both common carotid arteries. The rats' brains were frozen in situ after 0, 5, or 30 minutes of ischemia or 10, 30, or 60 minutes of recirculation following 30 minutes of ischemia (n = 5 at each time). Nucleoside triphosphate levels were higher in the phenytoin-treated rats than in corresponding untreated rats at each time during and after ischemia. Phenytoin significantly attenuated the accumulation of lactate and free fatty acids (arachidonic acid and stearic acid) during ischemia and accelerated their recovery during recirculation. These results suggest that phenytoin has favorable protective effects on ischemic brain and that phenytoin may inhibit calcium-mediated phenomena, especially the inositol cycle, in cerebral ischemia.
Functional outcome measures in stroke rehabilitation.
Authors: Vanclay F
Published: June 2011

I examine statistical considerations in the analysis of functional outcome following stroke and discuss the mathematical relation between improvement in function and discharge functional score. I demonstrate mathematically that the predictor variables of improvement and discharge functional score are the same and that the regression coefficients for improvement and discharge functional score will be equal, except for the admission functional score, for which a mathematically defined relation exists. I argue that the relation between admission functional score and discharge functional score must be positive and strong and that the relation between admission functional score and improvement must be negative for the stroke population. I believe that an ignorance of statistical concepts, especially confounding, and of the differences between raw correlations, partial correlations, and predictors have led to much confusion in functional outcome research.
Monosialoganglioside in subarachnoid hemorrhage.
Authors: Papo I , Benedetti A , Carteri A , Merli G A , Mingrino S , Bruno R
Published: June 2011

We studied 119 patients with disturbance of consciousness following subarachnoid hemorrhage, due mostly to verified aneurysm rupture, admitted to five Italian neurosurgical departments over 18 months. Level of consciousness as assessed by score on the Glasgow coma Scale ranged from 8 to 14 before the beginning of treatment; level of consciousness was assessed again 7, 14, and 21 days later. Patients were randomly allocated to treatment with monosialoganglioside or placebo according to a double-blind experimental design. The two treatment groups were homogeneous at entry with regard to the main clinical parameters. Both groups improved, but the rate and degree of improvement were greater in the monosialoganglioside-treated group. The difference was significant on days 14 (p = 0.04) and 21 (p = 0.02). Our results seem to confirm the hypothesis that monosialoganglioside reduces brain edema and provides nonspecific neuronal membrane protection.
Middle cerebral artery blood velocity and cerebral blood flow in sickle cell disease.
Authors: Brass L M , Prohovnik I , Pavlakis S G , DeVivo D C , Piomelli S , Mohr J P
Published: June 2011

To understand better the relationship between blood velocity measured by transcranial Doppler and cerebral blood flow measured by the 133Xe inhalation method, we examined 23 patients undergoing evaluation in the Comprehensive Sickle Cell Center at Columbia University. Blood velocity in the middle cerebral artery was directly related to cerebral flow (r = 0.77; p less than 0.05). A multivariate analysis in this sample made it possible to improve this correlation to account for more than 90% of the variability in cerebral blood flow by the use of transcranial Doppler measures of velocity and pulsatility along with the patient's age and hematocrit (r = 0.95; p less than 0.001). It is likely that the combination of Doppler and clinical or demographic variables in other diseases will similarly improve the quantitative estimation of cerebral blood flow.
Mild hypothermic intervention after graded ischemic stress in rats.
Authors: Chopp M , Chen H , Dereski M O , Garcia J H
Published: June 2011

We investigated the effect of mild (34 degrees C) postischemic hypothermia on hippocampal neuronal damage in 43 rats as a function of the duration of forebrain ischemia. Two temperatures and two durations were investigated. In two normothermic groups ischemia lasted 8 (n = 15) and 12 (n = 10) minutes, respectively. In two hypothermic groups ischemia lasted 8 (n = 9) and 12 (n = 9) minutes, respectively, and was followed immediately by the lowering and maintenance of rectal temperature to 34 degrees C for 2 hours. Seven days after the ischemic insult, the rats were sacrificed and the brains were prepared for histologic analysis; the percentage of necrotic neurons among the total neuronal population in selected CA1/2 sectors of the hippocampus was determined. There was a significant decrease in the percentage of necrotic neurons in the central (77.5% versus 55.5%, p = 0.006) and lateral (62.5% versus 38.9%, p=0.005) areas and in the overall CA1/2 sector of the hippocampus (71.8% versus 52.2%, p = 0.008) for the 8-minute hypothermic group compared with the 8-minute normothermic group. In contrast, no differences were detected in any area of the hippocampus between the 12-minute normothermic and the 12-minute hypothermic groups (p = 0.29-0.49). Our data indicate that mild postischemic whole-body hypothermia ameliorates neuronal survival when ischemia lasts 8 minutes but not 12 minutes.
Effects of atrial natriuretic peptide on ischemic brain edema in rats evaluated by proton magnetic resonance method.
Authors: Naruse S , Aoki Y , Takei R , Horikawa Y , Ueda S
Published: June 2011

We examined the effect of atrial natriuretic peptide on cerebral edema in 96 rats. Forty-four rats were given 30 (n = 11), 120 (n = 26), or 150 (n = 7) micrograms/kg of the peptide intravenously over 24 hours after occlusion of the left middle cerebral artery to induce cerebral ischemia. We then measured the brain water content, the brain sodium and potassium contents, the in vitro proton nuclear magnetic resonance longitudinal (T1) and transverse (T2) relaxation times, and the area of the edematous regions. Compared with saline treatment (n = 39), peptide treatment decreased the brain water content in a dose-dependent manner and decreased the brain sodium content significantly (p less than 0.05). Peptide treatment also suppressed the lengthening of both T1 and T2 in edematous tissue (p less than 0.05 and p less than 0.01, respectively) and reduced the area of the edematous regions observed by magnetic resonance imaging (p less than 0.01). Atrial natriuretic peptide appears to have a pharmacological effect on ischemic brain edema, possibly by suppressing the elevation of water content through regulation of electrolyte transport in the brain.
Assessment of scales of disability and handicap for stroke patients.
Authors: Wolfe C D , Taub N A , Woodrow E J , Burney P G
Published: June 2011

The purpose of the study is to compare the reliability of the Barthel activities of daily living score, which assesses disability, with the Rankin scale, which assesses handicap, and to determine their mutual agreement.

Fifty patients with stroke of varying severity were identified by a community-based stroke register and interviewed by two of three research nurses on two occasions that were 2-3 weeks apart.

There was no evidence of a systematic difference between the first and second measurements. Repeatability was assessed using a kappa statistic with quadratic disagreement weights (kappa w) to take account of extreme differences. This measure was very good for both Barthel (kappa w = 0.98) and Rankin (kappa w = 0.95) scales. There was also excellent agreement between raters for the Barthel scale (kappa w greater than or equal to 0.88), but some indication of disagreement (kappa w = 0.75) between raters for the Rankin scale. Analysis of variance confirmed these findings. A conversion from the Barthel to the Rankin scale can be derived by assigning the most common Rankin score for the subjects with a given Barthel score, producing a kappa w of 0.91 for agreement.

The Barthel scale is a more reliable and less subjective scale for assessing disability, from which a Rankin handicap score can then be derived to enable those managing stroke patients to assess aspects of handicap as well as disability.
Polymorphonuclear leukocytes occlude capillaries following middle cerebral artery occlusion and reperfusion in baboons.
Authors: del Zoppo G J , Schmid-Schönbein G W , Mori E , Copeland B R , Chang C M
Published: June 2011

Microvascular perfusion defects may accompany sustained occlusion and subsequent reperfusion of the middle cerebral artery; however, the nature of such "no-reflow" defects remains unclear.

In the absence of antithrombotic pretreatment, we documented lenticulostriatal microvascular flow integrity following 3-hour middle cerebral artery occlusion and 1-hour reperfusion in a baboon occlusion/reperfusion model by two methods identifying 1) microvascular occlusion and 2) microvascular patency.

Microvascular "no-reflow" involved capillaries (vessels of 4.0-7.5 microns diameter) of the lenticulostriatal territory. Capillary reflow included 27-39% of all capaillaries in two subjects, indicating a significant reduction of perfusion from normal (2p = 0.045). In identical experimental preparations, single polymorphonuclear leukocytes completely occluded 4.7% of microvessels of capillary diameter in randomly selected fields, partially occluded 3.5% of postcapillary venules, and occluded 40% (four of 10) of capillaries in linear reconstruction along a 110 microns length. Circumferential contact between polymorphonuclear leukocytes and the luminal endothelial cell membranes was documented, with an intrecellular gap of, at most, 160 nm. Fibrin was found with degranulated platelets when the latter were associated with granulocytes, but not with polymorphonuclear leukocytes alone.

The finding of capillary-obstructing polymorphonuclear leukocytes in the microvascular bed following middle cerebral artery reperfusion in focal ischemia in this model satisfies an essential requirement for postulating their role in early microvascular injury and the "no-reflow" phenomenon.
Autosomal dominant syndrome with strokelike episodes and leukoencephalopathy.
Authors: Tournier-Lasserve E , Iba-Zizen M T , Romero N , Bousser M G
Published: June 2011

We conducted a prospective survey of a family presenting a new syndrome characterized mainly by recurrent strokelike episodes and neuroimaging evidence of leukoencephalopathy.

Forty-five members of a single family were studied clinically and with magnetic resonance imaging. Nine had strokelike episodes, including transient ischemic attacks, and minor or major strokes starting between the fourth and sixth decades, with neuroimaging evidence of small, deep infarcts and a widespread white matter disorder. Other symptoms included migraine (three), dementia (two), epilepsy (one), and hearing loss (one). In some patients, we found various immunologic anomalies and muscular lipidosis without ragged-red fibers. Eight other family members were clinically normal, but had identical neuroimaging signs of leukoencephalopathy. No abnormality was detected in the 28 other members of the family examined. Extensive investigations failed to reveal any known cause of cerebral ischemia.

There appears to be a new syndrome in this family that is characterized by recurrent subcortical strokelike episodes, leukoencephalopathy, immunologic anomalies, muscular lipidosis, and an autosomal dominant pattern of transmission.
A critical appraisal of stroke evaluation and rating scales.
Authors: Lyden P D , Lau G T
Published: June 2011

To judge the efficacy of new, putative stroke therapies, we need a method to measure neurological deficit accurately in groups of patients before and after treatment. No single measurement technique has yet proven to be universally acceptable, but one approach is the use of rating instruments that summarize the neurological deficit found on clinical examination. Currently, stroke assessment scales may be based on the examination of physical deficits, an inventory of activities of daily living, or a global evaluation of functional outcome.

Scientific methods for authenticating stroke scales are available in the psychometric and statistical literature. We review currently available stroke scales for their validity and reliability and propose investigations needed to refine further the standardized measurement of neurological deficit following stroke.

We suggest that clinical stroke trials include a physical deficit scale and a global rating during the acute phase and that an activities of daily living scale be added at later points in recovery.
Cerebral blood flow and neuropsychological asymmetries in unilateral stroke.
Authors: Brown G G , Ewing J R , Robertson W M , Welch K M
Published: June 2011

This study sought to determine the degree of agreement between asymmetries of neuropsychological functioning and nine methods of quantifying asymmetries of regional cerebral blood flow.

The regional cerebral blood flow methods combined three markers of cerebral blood flow asymmetry (percent hemispheric difference, maximum percent probe-pair asymmetry, and number of probe-pair asymmetries) with three indexes of regional cerebral blood flow (fast compartment flow, initial slope index, and initial slope). Eleven patients with left hemispheric ischemic strokes and 13 with right hemispheric ischemic strokes were studied with the xenon-133 inhalation technique and neuropsychological tests.

Blind clinical judgments of neuropsychological asymmetry significantly correlated with all nine methods of cerebral blood flow asymmetry determination; correlations ranged from -0.42 to -0.77. Clinical judgment of asymmetry of neuropsychological functioning accurately predicted the hemisphere of lower flow in 71-92% of cases, depending on the method of cerebral blood flow asymmetry determination. Agreement between cerebral blood flow and neurobehavioral signs of asymmetry was greater for initial slope and initial slope index than for the fast flow index. The initial slope and initial slope index showed equally good agreement. The use of the number of asymmetrical probe pairs to detect cerebral blood flow asymmetries agreed less well with neurobehavioral asymmetry than did the other two markers studied.

Both the initial slope index and the initial slope measures of cerebral blood flow are useful in predicting neuropsychological asymmetries, especially when the magnitude of the asymmetry is taken into account.
Familial association of intracranial aneurysms and cervical artery dissections.
Authors: Schievink W I , Mokri B , Michels V V , Piepgras D G
Published: June 2011

BACKGROUND AND PURPOSE: The familial occurrence of intracranial aneurysms and cervical artery dissections has been described in different families and supports the hypothesis that a primary arteriopathy may play a role in the pathogenesis of these disorders. Although the basis for this arteriopathy is generally not believed to be similar among cases of intracranial aneurysms and cervical artery dissections, several similarities exist in the epidemiology of these disorders and a common underlying arterial abnormality may be suspected. SUMMARY OF REPORTS: The medical records of all 175 patients with spontaneous dissections of the cervical arteries who were seen at the Mayo Clinic between 1970 and 1989 were reviewed to identify families in which intracranial aneurysms and cervical dissections coexisted. Three families were identified in which intracranial aneurysms and cervical artery dissections were observed among siblings. These families are described in detail. CONCLUSIONS: The familial occurrence of intracranial aneurysms and cervical artery dissections within the same families provides support to the importance of a common underlying arteriopathy in the pathogenesis of both these disorders. The underlying vascular defect may, at least in some cases, be inherited.
Deriving clinical prediction rules from stroke outcome research.
Authors: Hier D B , Edelstein G
Published: June 2011

Our purpose was to determine whether clinical prediction rules could be derived from current stroke outcome research.

We reviewed 92 articles on stroke outcome research to determine their suitability for implementation as a clinical prediction rule. Methodological problems in many of these studies made implementation of their results as a clinical prediction rule difficult.

Implementation of stroke outcome research as clinical prediction rules would be facilitated by description of patient population demographics; precise definitions of predictor and outcome measures; stratification of patients by stroke mechanism; use of adequate patient sample sizes; and description of the mathematical methods used, including coding schemes, cutpoints, beta coefficients, constant terms, and a priori probabilities.
Lacunar infarctions due to cholesterol emboli.
Authors: Laloux P , Brucher J M
Published: June 2011

Hypertension is commonly considered the major cause of lacunar infarctions. However, in some cases, it has been suggested that lacunes could be caused by cerebral emboli from cardiac or carotid sources. Cholesterol cerebral emboli have been rarely reported as a cause of lacunes.

We describe a 79-year-old patient with a progressive multi-infarct dementia who developed transient motor aphasia and paresis of the right arm. Computed tomography showed lacunar infarcts in the right caudate nucleus, left thalamus, and left putamen, as well as an old right frontal infarction. Neuropathological examination demonstrated no prominent vascular hyalinosis, but did show multiple cholesterol emboli occluding small arteries around lacunar infarcts and leptomeningeal arteries near cortical infarcts. The cholesterol material presumably originated in the extended atheromatous changes along the aortic arch.

Our report confirms that lacunes can be caused by cholesterol emboli in some patients. Small cerebral emboli should not be overlooked as a cause of lacunes.
Vertebrobasilar ischemia after neck motion.
Authors: Frisoni G B , Anzola G P
Published: June 2011

Vertebrobasilar ischemic strokes may occur after chiropractic manipulation of the cervical spine or, less often, after spontaneous and abrupt head movement.

We describe three such cases of vertebrobasilar ischemic strokes and review 36 other reported cases.

We give evidence that 1) the population at risk cannot be identified a priori in the vast majority of cases; 2) symptoms may develop after many uneventful manipulations; 3) clinical syndromes consist of occipital lobe (5%), cerebellar (8%), locked-in (8%), Wallenberg's (28%), other brain stem (49%), and unclassifiable (2%); 4) mortality or very severe long-term impairment occurs in 28% of cases; 5) the development of transient neurological symptoms during previous manipulations, the presence of known or suspected ligament laxity, and, if known, the presence of a vertebral artery terminating in posterior inferior cerebellar artery should always contraindicate any chiropractic neck maneuver; and 6) the pathogenetic mechanism involves vertebral artery dissection at the atlantoaxial joint with intimal tear, intramural bleeding, or pseudoaneurysm that can lead to thrombosis or embolism.
Vascular risks of asymptomatic carotid stenosis.
Authors: Norris J W , Zhu C Z , Bornstein N M , Chambers B R
Published: June 2011

We sought to determine the risks of stroke, myocardial ischemia, and vascular death in patients with asymptomatic carotid stenosis.

Six hundred ninety-six patients with asymptomatic carotid stenosis referred to the Doppler laboratory were followed prospectively for a mean time of 41 months. These patients were studied both clinically and by carotid Doppler ultrasound, including evaluation of the effect of stroke risk factors.

Transient ischemic attacks occurred in 75 patients and stroke in 29, while 132 had ischemic cardiac events. Five patients died from stroke and 59 from cardiac causes. Annual stroke rate was 1.3% in patients with carotid stenosis less than or equal to 75% and 3.3% in those with stenosis greater than 75%. Ipsilateral stroke rate was 2.5% in patients with greater than 75% carotid stenosis. Annual cardiac event rate was 8.3% and death rate 6.5% in patients with severe carotid stenosis.

With carotid stenosis less than or equal to 75%, the stroke rate is negligible (1.3% annually) whereas the combined risk of cardiac ischemia and vascular death is as high as 9.9%. With stenosis greater than 75%, combined transient ischemic attack and stroke rate is 10.5% per year, with 75% of events ipsilateral to the stenosed artery.
Atrial natriuretic factor and salt wasting after aneurysmal subarachnoid hemorrhage.
Authors: Wijdicks E F , Ropper A H , Hunnicutt E J , Richardson G S , Nathanson J A
Published: June 2011

The causes of volume depletion and hyponatremia after subarachnoid hemorrhage are not fully understood but may be in part due to natriuresis or "cerebral salt wasting." Because previous studies using infrequent hormone sampling have given inconsistent results, we determined if elevations in atrial natriuretic factor concentrations preceded negative sodium and fluid balances.

We measured diurnal atrial natriuretic factor and vasopressin concentrations and sodium balance for 5 days in 14 consecutive patients after aneurysmal subarachnoid hemorrhage.

Plasma concentrations of atrial natriuretic factor on admission were elevated in subarachnoid hemorrhage patients (mean +/- SD 106 +/- 59 pg/ml) compared with acutely ill controls (39 +/- 30 pg/ml). In eight patients, high peak concentrations of atrial natriuretic factor, greater than 300 pg/ml or a twofold increase above baseline, were followed by natriuresis and a negative sodium balance. Three patients, two of whom became hyponatremic, developed cerebral infarcts after natriuresis. Vasopressin concentrations were slightly elevated just after hemorrhage but subsequently declined to normal values.

A markedly increased atrial natriuretic factor concentration precedes natriuresis in some patients and, with other abnormalities of water handling possibly including a relatively diminished vasopressin concentration, may cause volume depletion. Patients with natriuresis appear to be at increased risk for delayed cerebral infarction after subarachnoid hemorrhage.