bluuebunny/crossref_metadata_2025 huggingface dataset:
Relationship between metabolic recovery and the EEG prolonged ischemia of cat brain.
Authors: Schmidt-Kastner R , Hossmann K A , Grosse Ophoff B
Published: June 2011

In normothermic cats, cerebral blood flow was arrested for 1 hour followed by blood recirculation for 5-6 hours. Functional recovery was evaluated by qualitative and quantitative EEG analysis, and metabolic recovery by measuring metabolite and electrolyte levels in tissue samples taken from the cerebral cortex. In 5 out of 12 animals EEG activity did not recover after ischemia (group I); in 3 animals, intermittent EEG activity (group II) and in 4 animals continuous EEG activity returned during the observation period (group III). In group I the energy state was severely disturbed and an increase of calcium was detected, in group II this disturbance was much less pronounced, and in group III changes in energy metabolism and ion concentration were absent with the only exception of lower ADP levels. During recovery, the total intensity of EEG correlated positively with ATP (p less than 0.01) and inversely with lactate (p less than 0.05), and the intensity of the delta band inversely with sodium content (p less than 0.05). The results obtained demonstrate that electrophysiological recovery after prolonged ischemia is closely correlated with the restoration of the energy state and of electrolyte homeostasis of the brain. The inverse relationship of EEG intensity with lactate and sodium are interpreted as evidence for the adverse effects of ongoing post-ischemic glycolysis, resulting in the activation of the H+/Na+ antiporter for the regulation of intracellular pH.
Autoregulation of spinal cord blood flow: is the cord a microcosm of the brain?
Authors: Hickey R , Albin M S , Bunegin L , Gelineau J
Published: June 2011

The autoregulatory capability of regional areas of the brain and spinal cord was demonstrated in 18 rats anesthetized with a continuous infusion of intravenous pentothal. Blood flow was measured by the injection of radioactive microspheres (Co57, Sn113, Ru103, Sc46). Blood flow measurements were made at varying levels of mean arterial pressure (MAP) which was altered by neosynephrine to raise MAP or trimethaphan to lower MAP. Autoregulation of the spinal cord mirrored that of the brain, with an autoregulatory range of 60 to 120 mm Hg for both tissues. Within this range, cerebral blood flow (CBF) was 59.2 +/- 3.2 ml/100 g/min (SEM) and spinal cord blood flow (SCBF) was 61.1 +/- 3.6. There was no significant difference in CBF and SCBF in the autoregulatory range. Autoregulation was also demonstrated regionally in the left cortex, right cortex, brainstem, thalamus, cerebellum, hippocampus and cervical, thoracic and lumbar cord. This data provides a coherent reference point in establishing autoregulatory curves under barbiturate anesthesia. Further investigation of the effects of other anesthetic agents on autoregulation of the spinal cord is needed. It is possible that intraspinal cord compliance, like intracranial compliance, might be adversely affected by the effects of anesthetics on autoregulation.
Evidence that vasoactive intestinal polypeptide (VIP) mediates neurogenic vasodilation of feline cerebral arteries.
Authors: Brayden J E , Bevan J A
Published: June 2011

In this study the magnitude of non-sympathetic, non-cholinergic neurogenic vasodilation of feline cerebral arteries in vitro was correlated with the extent of innervation by VIP-immunoreactive nerves. Well-innervated arteries underwent nerve-mediated relaxation whereas those that are not supplied with VIP-containing axons did not relax to transmural nerve stimulation. The relaxation of cerebral arteries that are well endowed with VIP-immunoreactive nerves was selectively and reversibly inhibited by VIP-specific antiserum. Substance P-specific antiserum did not affect the dilator responses. We conclude that VIP is a functional neurodilator transmitter in the cerebral circulation.
Transcranial Doppler and rCBF compared in carotid endarterectomy.
Authors: Halsey J H , McDowell H A , Gelman S
Published: June 2011

In eight patients undergoing carotid endarterectomy, the mean velocity and an index of pulse amplitude in the middle cerebral artery were monitored continuously by transcranial doppler ultrasound. rCBF was measured by intracarotid injection of 133 Xenon shortly before and at the time of the carotid artery occlusion, and again a few minutes after carotid flow was reestablished. Comparison of the mean velocity in the MCA and the cortical convexity rCBF revealed relatively little hysteresis in their relationship from prior to after the occlusion. There was however, considerable variability in this relationship among patients. Both the rCBF and the velocity decreased substantially at occlusion in three cases, neither changed very much in three. While in two, though the rCBF decreased significantly, the velocity did not change. The index of pulse amplitude was somewhat more sensitive to the occlusion, decreasing in the seven cases in which it was recorded, including one in which the rCBF did not change.
Calcium antagonists reduce the extent of infarction in rat middle cerebral artery occlusion model as determined by quantitative magnetic resonance imaging.
Authors: Sauter A , Rudin M
Published: June 2011

The appearance and evolution of brain infarcts over 3 days following proximal occlusion of the left middle cerebral artery (MCA) in SHR rats were measured non-invasively by magnetic resonance imaging (MRI). Infarcts were clearly visible in coronal, T2 weighted brain sections, 24, 48 and 72 h after MCA occlusion in the left hemisphere, as areas of increased NMR signals. The infarcts were quantified by pixel counting in each section, the sum of 4 sections representing an accurate estimate of the total infarct size. The location and extent of infarction, determined by MRI, were found to be highly reproducible and correlated well with post-mortem histological and biochemical data. A neurological score, made every 24 h, paralleled the evolution of the infarct size, which culminated after 48 h. Pre- or post-treatment of MCA occluded rats with the dihydropyridine calcium antagonist PN 200-110 resulted in a substantial reduction of infarct size, determined by MRI 24, 48 and 72 h after infarction, compared to vehicle treated controls. These findings were corroborated by corresponding improvements of the neurological scores as well as histological and biochemical data. Post-treatment with nimodipine showed qualitatively similar effects. These results support the notion that calcium antagonists, through vascular and/or metabolic mechanisms, are effective in treating acute stroke. Since they were obtained in a chronic, relevant model of stroke with a method directly applicable also to humans, they should encourage further clinical studies with calcium antagonists.
Carotid endarterectomy: how does it work? A clinical and angiographic evaluation.
Authors: van Alphen H A , Polman C H
Published: June 2011

In a retrospective study, the clinical and angiographic results were evaluated of 100 consecutive carotid endarterectomies, carried out in 90 patients over the period 1977 to 1983. There was no operation-associated mortality; the perioperative morbidity was 5%. Angiography, carried out, on average, 4.2 months postoperatively, revealed complete occlusion of the operated carotid artery in 16 cases (18.5%); in at least 13 cases this was completely asymptomatic. Perioperative findings suggest that microembolism is, but haemodynamic insufficiency is not, an important cause of focal cerebral ischemia. Therefore, treatment for extracranial atherosclerotic cerebrovascular disease should be focused on the elimination of the source of embolism rather than on an improvement of cerebral blood flow.
Dolichoectatic basilar artery: a review of 23 cases.
Authors: Nishizaki T , Tamaki N , Takeda N , Shirakuni T , Kondoh T , Matsumoto S
Published: June 2011

The dolichoectatic basilar artery was found in 23 cases during a 10-year period. The 19 males and 4 females ranged in age from 30 to 69 years (mean: 55 years). Hypertension was noted in 17 patients. In seventeen (74%) of the present cases this anomaly could be visualized with CT scan. Seven patients (30%) presented with pontine infarction, which was identified on CT scan in all cases. Vertebro-basilar insufficiency was found in four patients. One patient had transient ischemic attacks. There were facial spasms in four patients and impairment of the lower cranial nerves in one. One patient exhibited cerebellar hemorrhage. In two patients this anomaly was found incidentally. Associated intracranial aneurysms were identified in seven patients, including fusiform aneurysms in 4 and saccular aneurysms in 3. Three patients had an accompanying hydrocephalus. The dolichoectatic basilar artery is associated with various consequences especially in relation to the pathogenesis of brainstem infarction. When this anomaly is diagnosed by CT findings, even if it is clinically asymptomatic, it may be better to treat these patients with medical therapy used to prevent ischemic stroke.
Effect of allopurinol on ischemia and reperfusion-induced cerebral injury in spontaneously hypertensive rats.
Authors: Itoh T , Kawakami M , Yamauchi Y , Shimizu S , Nakamura M
Published: June 2011

In spontaneously hypertensive rats, we studied the participation of xanthine oxidase-linked free radical in ischemia and reperfusion-induced cerebral injury, using allopurinol, a xanthine oxidase inhibitor. The loss of righting reflex was noted in some animals after a 4 hour occlusion of bilateral common carotid arteries and 19 of 25 animals died within 72 hours after reperfusion. One hour after reperfusion, the cerebral water content increased significantly, with an increase in sodium content and a decrease in potassium content. In 7 animals treated with oral administrations of allopurinol (200 mg/kg) 24 hours and 1 hour before occlusion, no death was found either during occlusion or after reperfusion, and the loss of righting reflex was noted in only one animal 24-72 hours following reperfusion. The increase in cerebral water content and accompanied changes in electrolyte contents were clearly prevented by allopurinol. These results suggest the possibility that the production of xanthine oxidase-linked free radical participates in cerebral injury due to ischemia and reperfusion in spontaneously hypertensive rats.
Evaluation of the cerebral vasodilatory capacity by the acetazolamide test before EC-IC bypass surgery in patients with occlusion of the internal carotid artery.
Authors: Vorstrup S , Brun B , Lassen N A
Published: June 2011

Cerebral blood flow (CBF) was measured by xenon-133 inhalation tomography in 18 patients with cerebrovascular disease before and 4 months after extracranial-intracranial bypass surgery. Only patients who showed a reduced CBF in areas that were intact on the CT scan and relevant to the clinical and angiographical findings were operated. The majority of the patients had suffered a minor stroke with or without subsequent transient ischemic attacks. They were studied at least 6 weeks following the stroke. All patients had an occlusion of the relevant internal carotid artery. To identify preoperatively the patients with a compromised collateral circulation and hence reduced CBF due to reduced perfusion pressure, a cerebral vasodilatory stress test was performed using acetazolamide (Diamox). In normal subjects, Diamox has been shown to increase tomographic CBF without change of the flow distribution. In the present series 9 patients showed a significant redistribution of flow in favor of the non-occluded side ("positive" Diamox test). Two of these 9 patients showed even a paradoxical decrease in focal CBF preoperatively, i.e., a "steal" effect. These 2 patients were the only patients who improved in focal CBF after shunting. The remaining 9 patients all showed uniform flow responses ("negative" Diamox test), and none of these increased in focal CBF postoperatively. The finding of an unchanged flow map postoperatively confirmed that the low flow areas were not due to restricted flow via collateral pathways. However, an increase in the regional vasodilatory capacity was observed postoperatively in the majority of patients.
Effects of forskolin on cerebral blood flow: implications for a role of adenylate cyclase.
Authors: Wysham D G , Brotherton A F , Heistad D D
Published: June 2011

We have studied cerebral vascular effects of forskolin, a drug which stimulates adenylate cyclase and potentiates dilator effects of adenosine in other vascular beds. Our goals were to determine whether forskolin is a cerebral vasodilator and whether it potentiates cerebral vasodilator responses to adenosine. We measured cerebral blood flow with microspheres in anesthetized rabbits. Forskolin (10 micrograms/kg per min) increased blood flow (ml/min per 100 gm) from 39 +/- 5 (mean +/- S.E.) to 56 +/- 9 (p less than 0.05) in cerebrum, and increased flow to myocardium and kidney despite a decrease in mean arterial pressure. Forskolin did not alter cerebral oxygen consumption, which indicates that the increase in cerebral blood flow is a direct vasodilator effect and is not secondary to increased metabolism. We also examined effects of forskolin on the response to infusion of adenosine. Cerebral blood flow was measured during infusion of 1-5 microM/min adenosine into one internal carotid artery, under control conditions and during infusion of forskolin at 3 micrograms/kg per min i.v. Adenosine alone increased ipsilateral cerebral blood flow from 32 +/- 3 to 45 +/- 5 (p less than 0.05). Responses to adenosine were not augmented during infusion of forskolin. We conclude that forskolin is a direct cerebral vasodilator and forskolin does not potentiate cerebral vasodilator responses to adenosine.
Evaluation of 2,3,5-triphenyltetrazolium chloride as a stain for detection and quantification of experimental cerebral infarction in rats.
Authors: Bederson J B , Pitts L H , Germano S M , Nishimura M C , Davis R L , Bartkowski H M
Published: June 2011

We have evaluated the use of 2,3,5-triphenyltetrazolium chloride (TTC) as an histopathologic stain for identification of infarcted rat brain tissue. The middle cerebral artery (MCA) of 35 normal adult rats was occluded surgically. At various times after surgical occlusion, rats were sacrificed and brain slices were obtained and stained with TTC or hematoxolin and eosin (H & E); the size of the area of infarcted tissue stained by each method was quantified. In rats sacrificed 24 hr after occlusion of the MCA, the size of the area of infarction was 21 +/- 2% of the coronal section for TTC, and 21 +/- 2% for H & E (mean +/- S.D., N = 13). The size of areas of infarction determined by either staining method was not significantly different in area by the paired test, and a significant correlation between sizes determined by each method was found by linear regression analysis (r = 0.91, slope = 0.89, and the y intercept = 4.4%). Staining with TTC is a rapid, convenient, inexpensive, and reliable method for the detection and quantification of cerebral infarction in rats 24 hr after the onset of ischemia.
Cerebral and cerebellar blood flow autoregulations in acutely induced cerebral ischemia in spontaneously hypertensive rats--transtentorial remote effect.
Authors: Shiokawa O , Sadoshima S , Kusuda K , Nishimura Y , Ibayashi S , Fujishima M
Published: June 2011

Autoregulation of cerebral (CBF) and cerebellar blood flow (CeBF) was studied before, during and after acutely induced cerebral ischemia in spontaneously hypertensive rats. Cerebral ischemia of the supratentorial portion was induced for one hour by bilateral carotid artery ligation (BCL). The animals were artificially ventilated and the blood flow was measured with a hydrogen clearance technique. To test the autoregulation, the blood pressure was stepwise lowered by bleeding and maintained at a new level, i.e. 15% or 30% lower than the baseline values before, during and after cerebral ischemia. At the preischemic state, CBF and CeBF were 52.1 +/- 6.2 and 58.9 +/- 4.6 ml/100 g/min (mean +/- SEM), of which autoregulations were normally preserved. Following BCL, CBF was markedly decreased to about 10% of control value while CeBF was minimally reduced to 46.9 +/- 8.6 ml/100 g/min (80%). At the ischemic state, CBF became almost zero flow during hypotension. CeBF was also reduced to 74% and further to 58% of the resting value by 15% and 30% decrease in the blood pressure, respectively, indicating impaired CeBF autoregulation. At the 30 min post-ischemic state, CBF was recovered to 48.0 +/- 4.9 and CeBF to 53.9 +/- 5.4 ml/100 g/min. Autoregulation of CBF was still abolished, whereas CeBF was kept constant by 15% fall of blood pressure and slightly reduced to 84% by 30% hypotension, indicating almost recovery of CeBF autoregulation.(ABSTRACT TRUNCATED AT 250 WORDS)
Time-dependent effects of prolonged hypercapnia on cerebrovascular parameters in dogs: acid-base chemistry.
Authors: Warner D S , Turner D M , Kassell N F
Published: June 2011

Prolonged normoxic hypercapnia initially caused an increase in canine cerebral blood flow, as measured by the radioactive microsphere technique, accompanied by a decrease in cerebrovascular resistance. These effects persisted for 3 hours. An adaptive decrease in cerebral blood flow and increase in cerebrovascular resistance were seen when hypercapnia was maintained for an additional 3 hours. Regional variations occurred; those areas with the greatest initial hypercapnic blood flow (cortex, caudate nucleus) showed a greater rate of decay of flow over time. Cerebrospinal fluid pH, initially acidotic during hypercapnia, increased over the subsequent 5 hours from 6.99 +/- 0.02 to 7.13 +/- 0.02. This was accompanied by an increase in the cerebrospinal fluid bicarbonate ion concentration from a normocapnic baseline of 19.6 +/- 0.6 to 26.2 +/- 4 mEq/l. Total and regional cerebral blood flow were linearly related to cerebrospinal fluid pH (R2 = 0.97). Extrapolation of a full adaptive return of flow to baseline indicated a shift in the cerebrovascular sensitivity to extracellular hydrogen ion concentration during prolonged hypercapnia.
Gangliosides (GM1 and AGF2) reduce mortality due to ischemia: protection of membrane function.
Authors: Karpiak S E , Li Y S , Mahadik S P
Published: June 2011

As evidenced by their ability to reduce cerebral edema, exogenous ganglioside administration exerts acute effects on CNS injury processes. We report here that ganglioside (GM1 or AGF2) treatment results in a 52% decrease in mortality 48 hours after the induction of ischemia in gerbils by permanent unilateral ligation of the common carotid artery. By comparing the occluded vs. nonoccluded sides of the brain (cortex and hippocampus) we found a significant loss of membrane Na, K-ATPase activity due to ischemia in control animals, but no such differences were found between the hemispheres of ganglioside-treated gerbils. We hypothesize that gangliosides may be "protecting" membrane function as indicated by these ATPase analyses, reducing local CNS damage at the time of injury (i.e., reduced cell loss, fiber degeneration, membrane failure). By acutely limiting the extent of CNS tissue damage, conditions may be optimized for any subsequent CNS regrowth and functional recovery.
Plasma 3-methoxy-4-hydroxyphenylethyleneglycol and homovanillic acid concentrations in patients with subarachnoid hemorrhage.
Authors: Minegishi A , Ishizaki T , Yoshida Y , Ahagon A , Shibata N , Kobayashi H
Published: June 2011

To ask if the determination of central-nervous-system-derived catecholamine metabolites in peripheral circulation could be a useful index of brain dysfunction after subarachnoid hemorrhage, 3-methoxy-4-hydroxyphenylethyleneglycol and homovanillic acid concentrations in plasma, together with those of free catecholamines (noradrenaline, adrenaline, and dopamine), were serially measured for up to 3 weeks after the initiation of symptoms in 23 patients with aneurysmal subarachnoid hemorrhage as compared to 17 healthy and 9 patient controls. Catecholamines and their metabolites were determined by using high-performance liquid chromatography with electrochemical detection. Plasma 3-methoxy-4-hydroxyphenylethyleneglycol concentrations were markedly elevated in subarachnoid hemorrhage patients with coma compared to those without, and the maximal concentrations observed in comatose patients never occurred in normal subjects or in patients with other neurological disorders. The mean maximal plasma concentrations of free catecholamines did not differ significantly between the comatose and noncomatose groups. Combining 3-methoxy-4-hydroxyphenylethyleneglycol with homovanillic acid level data more clearly discriminated between the comatose and noncomatose subarachnoid hemorrhage groups. The results suggest that plasma concentration of 3-methoxy-4-hydroxyphenylethyleneglycol, a major metabolite of brain noradrenaline, can be a prognostic discriminator for patients with subarachnoid hemorrhage and its discriminating power can be strengthened by combining it with homovanillic acid data.
Familial occurrence of spontaneous dissection of the internal carotid artery.
Authors: Mokri B , Piepgras D G , Wiebers D O , Houser O W
Published: June 2011

Spontaneous dissections of the extracranial internal carotid artery are diagnosed more frequently as their clinical and angiographic features are more widely recognized. Familial occurrence of spontaneous dissection of the internal carotid artery has not been previously reported. We describe the occurrence of this entity in a mother and daughter and also in a father and son. The familial occurrence of spontaneous dissection of the internal carotid artery raised the possibility of an inherited disorder of the blood vessel wall that predisposes the artery to this disorder. Fibromuscular dysplasia is suspected to be the underlying arterial disease, but other unknown arteriopathies cannot be excluded.
Regional cerebral blood flow decreases during chronic and acute hyperglycemia.
Authors: Duckrow R B , Beard D C , Brennan R W
Published: June 2011

The presence of hyperglycemia prior to stroke or cardiac arrest can increase neuronal damage caused by brain ischemia. Acute hyperglycemia shows this effect in animal models of stroke. However, chronic hyperglycemia and chronic hyperglycemia with additional acute elevation of blood glucose are more common premorbid states for stroke patients. The effect of chronic hyperglycemia on regional cerebral blood flow (rCBF) is unclear but blood flow changes may play a role in this ischemic cell damage. We measured rCBF in awake restrained rats that had chronic hyperglycemia induced by treatment with streptozotocin. This was compared to that measured in rats made acutely hyperglycemic by injecting glucose into the peritoneal space. rCBF was measured in 17 brain regions using [14C]iodoantipyrine. During chronic hyperglycemia, when plasma glucose was 29 microns/ml, rCBF was decreased and a regional distribution of this effect was noted; 9 hindbrain regions showed a mean flow decrease of 14% while forebrain regions demonstrated less flow reduction. Acute elevation of plasma glucose during normoglycemia or superimposed on chronic hyperglycemia produced flow reductions of 7% for each 10 microns/ml increment in plasma glucose up to 60 microns/ml. Both chronic and acute hyperglycemia are associated with decreased rCBF and the mechanism for this effect does not appear to adapt to chronic hyperglycemia.
Additional predisposing risk factors for atherothrombotic cerebrovascular disease among treated hypertensive volunteers.
Authors: Rogers R L , Meyer J S , Mortel K F
Published: June 2011

A 7-year prospective study of a cohort of 107 neurologically normal elderly hypertensive volunteers (mean age, 65.8 +/- 8.3 years) was undertaken to investigate the predictive validities of additional risk factors for atherothrombotic cerebrovascular disease including stroke, transient ischemic attacks, reversible ischemic neurological deficits, and multi-infarct dementia. This longitudinal study has been in progress now for 7 years with a mean follow-up interval of 50.12 +/- 5.76 months. Among 107 formerly symptom-free, normal hypertensive volunteers, 25 (23%) have developed cerebrovascular disease, 7 (6.5%) sustained a stroke, 10 (9.3%) developed multi-infarct dementia, and 18 (16.8%) have transient ischemic attacks. None have suffered intracranial hemorrhage. Mean gray matter cerebral blood flow (CBF) values measured at the initial visit were sensitive predictors of cerebrovascular disease. Eight of 16 hypertensives (50%) with initial CBF values below 60.0 ml/100 g/min now exhibit signs and symptoms of cerebrovascular disease, while 11 of 43 hypertensives (25.6%) with initial CBF values between 60.1 and 69.9 ml/100 g/min and only 6 of 48 (12.5%) with initial CBF levels above 70.0 developed cerebrovascular disease. Incidence of cerebrovascular disease among cigarette smoking hypertensive volunteers (32.5%) was significantly greater than among nonsmokers (17.2%).
Is acute alcohol ingestion a risk factor for ischemic stroke? Results of a controlled study in middle-aged and elderly stroke patients at three urban medical centers.
Authors: Gorelick P B , Rodin M B , Langenberg P , Hier D B , Costigan J , Gomez I , Spontak S
Published: June 2011

To assess the role of acute alcohol ingestion as a risk factor for cerebral infarction, we administered a pretested questionnaire to 205 middle-aged and elderly acute ischemic stroke patients and 410 outpatient controls matched by age, sex, race, and method of hospital payment. Paired Mantel-Haenszel analysis revealed that alcohol ingestion within 24 (p = 0.07) and 72 (p = 0.001) hours of stroke onset and medical histories of smoking (p less than 0.0001), hypertension (p less than 0.001), and transient ischemic attacks (p = 0.051) were more common among stroke index cases than controls. Matched multiple logistic analysis revealed that both hypertension (p less than 0.05) and smoking (p less than 0.05) were independently associated with stroke, while alcohol consumption was not. In analyses to assess the possibility of mutual confounding effects of independent variables, the effect of alcohol ingestion was lost when adjusting for smoking. We conclude that acute alcohol ingestion is not an independent risk factor for cerebral infarction in middle-aged and elderly patients. The apparent association between alcohol ingestion and ischemic stroke may be the result of the confounding effects of smoking.
Glycerol and dextran combined in the therapy of acute stroke. A placebo-controlled, double-blind trial with a planned interim analysis.
Authors: Frei A , Cottier C , Wunderlich P , Lüdin E
Published: June 2011

The results of clinical trials investigating various therapies in acute ischemic stroke have been inconsistent. The effect of glycerol therapy and a combination therapy of glycerol and dextran was evaluated in a double-blind, placebo-controlled study. Repeated neurologic examinations (Day 0, Weeks 1, 6, 12, and 24) according to a modified Mathew score were performed on 62 patients. Statistical analysis showed no superiority of either treatment compared with placebo in acute ischemic stroke. A retrospective estimation of the Type II error of the study yielded approximately p = 0.25. A major side effect was hemolysis in 98% of patients treated with glycerol.
Clinico-epidemiologic study of stroke in Akita, Japan.
Authors: Suzuki K , Kutsuzawa T , Takita K , Ito M , Sakamoto T , Hirayama A , Ito T , Ishida T , Ooishi H , Kawakami K
Published: June 2011

An analysis was performed of 2,168 consecutive stroke patients who were examined by computed tomography and entered into a hospital-based stroke registry in Akita Prefecture, Japan. The occurrence of cerebral hemorrhage, cerebral infarction, and subarachnoid hemorrhage was 30, 55, and 14%, respectively. Age-specific rates of subarachnoid hemorrhage were higher in women than men; other types of stroke showed a preponderance in men. Total strokes increased in the winter; this seasonal difference was confined to cerebral hemorrhage. Putaminal hemorrhages predominated in the younger age groups; thalamic hemorrhage and cerebellar hemorrhage were predominant in the older age groups. The increased accuracy of the diagnosis of stroke subtypes by the use of computed tomography in this study is in contrast to other community-based epidemiologic studies that have relied solely on clinical diagnosis. This increased accuracy is seen to be the reason that new ratios of stroke subtype incidence have been identified.
Effects of antihypertensive treatment on the cerebral microvasculature of spontaneously hypertensive rats.
Authors: Harper S L
Published: June 2011

Experiments were performed in anesthetized 18-19-week-old spontaneously hypertensive rats (SHR) to evaluate the effects of delayed antihypertensive treatment on cerebrovascular function. Animals were treated for 25 +/- 1 days with an oral antihypertensive regimen consisting of hydralazine, reserpine, and chlorothiazide, resulting in normotension within 2 weeks. Cerebral arterioles were examined via a constantly suffused open cranial window and video microscopy. Resting cerebral blood flow was measured using radioactive microspheres and the reference organ method. While untreated SHR exhibited reductions in arteriolar diameter compared with normotensive Wistar Kyoto rats (WKY), treatment restored arteriolar dimensions to normal. Increments in microvascular wall area, associated with medial hypertrophy in untreated SHR, were completely reversed in treated SHR to a magnitude not different from control. Resting cerebral blood flow was, however, decreased in treated SHR compared with both untreated SHR and WKY; this was due to an increase in total cerebrovascular resistance compared with WKY. Additionally, microvascular pressure in the largest arterioles in treated SHR was reduced compared with both WKY and untreated SHR. There was a significant increase in the relative pressure drop accounted for by the arterial vessels upstream from the cerebral microcirculation in treated SHR. These results suggest that 1) cerebral microvascular abnormalities induced by chronic hypertension are reversed by delayed antihypertensive therapy, and 2) there is a persistent elevation in cerebrovascular resistance upstream from the microcirculation representing large vessel adaptations that may not be readily reversible with treatment.
Functional arterial changes in chronic cerebrovasospasm in monkeys: an in vitro assessment of the contribution to arterial narrowing.
Authors: Bevan J A , Bevan R D , Frazee J G
Published: June 2011

Cerebral arteries from monkeys with chronic cerebral vasospasm arising from experimental subarachnoid hemorrhage produced 5-6 days previously were examined for changes in their functional properties in an attempt to understand the basis of the narrowing. Hemorrhage was caused by puncture of the internal carotid artery just proximal to the circle of Willis. Segments taken close to the origins of the anterior and middle cerebral arteries consistently showed decreased distensibility. In addition, they exhibited large, prolonged, spontaneous increases in muscle tone. Other alterations observed include a marked reduction in the capacity of the vessel wall to contract, reduction in constrictor and dilator nerve influences on vascular tone, and some increased sensitivity to serotonin. Small pial arteries (150-200 micron o.d.) from the side of the injury showed large spontaneous irregular increases in tone. It is proposed that 5-6 days after experimental subarachnoid hemorrhage in monkeys the change most responsible for persistent narrowing in the larger arteries is an increased rigidity of the vessel wall. This is probably caused by an inflammatory response. In the smaller arteries, abnormal spontaneous contractile activity is a major factor in narrowing. This activity is not stretch-dependent. We suggest that the initial cause of the arterial narrowing after hemorrhage is the action of vasoactive substances released in the close vicinity of the arterial wall, which lead to tissue damage, abnormal tone, and an inflammatory response with fibrosis.
Assessment by fluorescein angiography of surgical treatment of occlusive carotid artery disease.
Authors: Sarkies N J , Shilling J S , Burnand K G , Browse N L , Russell R W
Published: June 2011

Fundus fluorescein angiography was performed in 10 cases of occlusive carotid artery disease at presentation and after surgery or medical treatment. An improvement in the microcirculation of the retina was observed in 4 cases after carotid endarterectomy and in 1 case after carotid endarterectomy and extracranial-intracranial bypass. Improvement was not observed in 2 cases after extracranial-intracranial bypass alone or in 3 cases in which surgical intervention was not undertaken. Our results suggest that carotid endarterectomy is a more effective procedure than extracranial-intracranial bypass in improving retinal perfusion when compromised by ipsilateral carotid obstruction.
Superior sagittal sinus thrombosis with infarction in sickle cell trait.
Authors: Feldenzer J A , Bueche M J , Venes J L , Gebarski S S
Published: June 2011

An adolescent female with sickle cell trait presented with acute neurologic deterioration during treatment for pseudotumor cerebri. Cranial computed tomography, initially normal, subsequently revealed multiple hemorrhagic infarctions. Suspected superior sagittal sinus thrombosis was confirmed by cerebral angiography. Superior sagittal sinus thrombosis associated with sickle cell trait is exceedingly rare, and the accompanying increased intracranial pressure may require aggressive management.
Apparatus for Percoll microgravimetry determinations in experimental brain edema.
Authors: Karlik S J , Noseworthy J H
Published: June 2011

A microgravimetry apparatus is described which utilizes osmotically-balanced Percoll gradients produced by a computer-driven low pressure gradient system. A plexiglass reservoir was designed to minimize parallax artifacts while allowing repeated measurements and easy retrieval of groups of 20 samples. This system provides inert and nontoxic gradients with profile flexibility, reproducibility, and longevity when used for the routine gravimetric measurement of edema in 30-mg central nervous system tissue fragments.
Graded neurologic scale for use in acute hemispheric stroke treatment protocols.
Authors: Adams R J , Meador K J , Sethi K D , Grotta J C , Thomson D S
Published: June 2011

A standardized neurologic assessment scoring instrument was developed and tested for use in a multicenter trial of hypervolemic hemodilution in acute hemispheric stroke. Components of the neurologic examination pertinent to hemispheric stroke syndromes were emphasized. The scale was evaluated using 16 acute stroke patients for concurrent validity (Pearson coefficient r = 0.89 compared with global assessments by neurologists or neurosurgeons) and interobserver reliability (r = 0.95 interobserver reliability estimate). Such a scale should prove useful in quantifying neurologic deficits in hemispheric stroke and in following changes in neurologic status during multicenter acute treatment protocols.
Regional brain calcium changes in the rat middle cerebral artery occlusion model of ischemia.
Authors: Rappaport Z H , Young W , Flamm E S
Published: June 2011

Entry of Ca ions into ischemic neurons is believed to cause cell damage. Although several investigators have demonstrated changes in extracellular Ca ionic activity consistent with Ca movement into cells, direct and quantitative evidence for Ca entry into ischemic cells is lacking. We used atomic absorption spectroscopy to measure the regional distribution of tissue Ca contents of rat brains sampled at 2, 4, and 24 hours after middle cerebral artery occlusion (MCAo). At 4 hours after MCAo, Ca concentrations increased significantly (p less than 0.005) in the ischemic middle cerebral artery territory, i.e., the pyriform and frontoparietal cortices, but not in the surrounding brain. At 24 hours, Ca concentrations in the pyriform and frontoparietal cortex were respectively 30.79 (+/- 2.90) and 29.19 (+/- 3.28) mumol/g dry tissue wt compared with 11.9 (+/- 1.7) mumol/g in sham-occluded rats. Tissue Ca concentration changes in the parasagittal cortex and basal ganglia adjacent to the infarct site were much smaller and did not differ significantly from controls until 24 hours. In the ischemic middle cerebral artery territory, greater than 1.0 mumoles of Ca entered per gram of dry tissue weight per hour during the first 4 hours after MCAo. Linear regression analysis revealed a significant correlation (r = 0.9722) between changes in tissue Ca and water, with a slope indicating that 5.88 mumoles of Ca accompanied each milliliter of water entering the lesioned hemisphere. Such massive accumulations of Ca not only confirm Ca entry into injured cells, but indicate the presence of a remarkable Ca sink which sequestered within 24 hours more than 17 times the amount of free Ca present in the tissue before MCAo.
Visually evoked dynamic blood flow response of the human cerebral circulation.
Authors: Aaslid R
Published: June 2011

The dynamics of the metabolic mechanism that regulates cerebral blood flow was studied in 10 normal human subjects using a noninvasive transcranial ultrasonic Doppler method. Flow volume in the posterior cerebral artery, supplying the visual cortex, increased 20.2% in response to light stimulation of the retina, while flow velocity in the same artery increased 16.4%. The regulation of blood flow was very rapid; only 2.3 seconds elapsed from application of the light stimulus to 50% of full response. Full regulation (90% of full response) took 4.6 seconds. The blood flow response adapted slightly after about 10 seconds. Flow velocity in the middle cerebral artery increased significantly, by 3.3%, while flow in the superior cerebellar artery showed no significant change in response to this stimulus. These findings suggest the mechanism of very fast metabolic regulation of cerebral blood flow in humans.
Regional cerebral blood flow in stroke: hemispheric effects of cognitive activity.
Authors: Gur R C , Gur R E , Silver F L , Obrist W D , Skolnick B E , Kushner M , Hurtig H I , Reivich M
Published: June 2011

Regional cerebral blood flow (rCBF) was measured with the xenon-133 inhalation technique in 15 patients with unilateral cerebral infarction and 12 matched controls. Measurements were performed during a standard resting baseline condition and during the performance of standardized verbal analogies and spatial line orientation tasks. Resting and activated CBF were lower in patients than in controls, and there were differences in the hemispheric pattern of activated CBF. Control subjects replicated earlier findings of asymmetric increase in CBF for the cognitive tasks, whereas patients showed abnormalities in lateralized CBF changes consistent with side of infarction. These findings underscore the utility of cognitive challenges in the study of rCBF in stroke. This can lead to an experimental paradigm in clinical studies of the relation between behavioral deficits and regional brain dysfunction and may also improve the utility of CBF measurements in clinical settings.
Ibuprofen improves cerebral blood flow after global cerebral ischemia in dogs.
Authors: Grice S C , Chappell E T , Prough D S , Whitley J M , Su M , Watkins W D
Published: June 2011

In a canine model of global cerebral ischemia, 6 dogs received a saline placebo prior to the event and 5 received 12.5 mg/kg ibuprofen. Cerebral venous outflow from the confluence of the sagittal and transverse sinuses, systolic and diastolic arterial pressure, cardiac output, pH, Paco2, Pao2, and arterial and sagittal sinus thromboxane B2 and 6-keto-PGF1 alpha were measured at intervals up to 120 minutes thereafter. Postischemic cerebral hypoperfusion was significantly improved in the ibuprofen pretreatment group. Control dogs showed significant increases in sagittal sinus postischemic thromboxane B2 concentrations, but pretreated dogs showed nearly complete inhibition of postischemic thromboxane B2 production. Pretreated dogs also had significantly lower levels of 6-keto-PGF1 alpha from the sagittal sinus. There were no significant differences in the other variables at any interval. We conclude that ibuprofen ameliorates postischemic cerebral hypoperfusion, and that this improvement is associated with decreased sagittal sinus levels of thromboxane B2 and 6-keto-PGF1 alpha.
S-100 protein and neuron-specific enolase in cerebrospinal fluid and serum: markers of cell damage in human central nervous system.
Authors: Persson L , Hårdemark H G , Gustafsson J , Rundström G , Mendel-Hartvig I , Esscher T , Påhlman S
Published: June 2011

The development of a radioimmunoassay for S-100 protein is described. This method was used in combination with a recently developed radioimmunoassay for neuron-specific enolase in cerebrospinal fluid and serum from 47 patients with cerebral infarction, transient ischemic attack, intracerebral hemorrhage, subarachnoid hemorrhage, and head injury. In cerebrospinal fluid, increased concentrations of both S-100 and neuron-specific enolase were found after large infarcts, whereas after small infarcts and transient ischemic attacks, only neuron-specific enolase increased. The increased concentrations of S-100 and/or neuron-specific enolase were noted 18 hours to 4 days after cerebral infarction and transient ischemic attacks. Cerebrospinal fluid concentrations of these proteins also reflected the severity of the disease in patients with intracerebral hematoma, subarachnoid hemorrhage, or head injury. Temporal changes in serum S-100 and neuron-specific enolase concentrations reflected the clinical course in 4 patients. In stroke patients, the S-100 and neuron-specific enolase concentrations may reflect the extent of brain damage and could be useful in selecting patients with major stroke for more aggressive treatment during the acute phase.
Extracranial carotid artery in patients with transient global amnesia: evaluation by real-time B-mode ultrasonography with duplex Doppler flow.
Authors: Feuer D , Weinberger J
Published: June 2011

Patients with transient global amnesia are often categorized as having cerebrovascular disease. Noninvasive carotid artery testing was performed in 56 patients with transient global amnesia to determine if they had the same incidence of extracranial atherosclerotic vascular disease as patients with focal cerebral transient ischemic attacks. Only 3 of 56 patients had hemodynamic obstruction of flow at the carotid artery bifurcation, and 41 of 56 had no evidence of any atherosclerotic disease. Other risk factors for cerebrovascular disease were present in 24 of 56 patients, but only 1 had a prior cerebrovascular event. The pathophysiology of transient global amnesia appears to differ from the pathophysiology of classical transient ischemic attacks in that there is no clear relation between transient global amnesia and the presence of extracranial atherosclerotic cerebrovascular disease.
Carotid restenosis: long-term noninvasive follow-up after carotid endarterectomy.
Authors: DeGroote R D , Lynch T G , Jamil Z , Hobson R W
Published: June 2011

Recurrent stenosis has not been a primary consideration in the selection of patients for carotid endarterectomy. We have studied the incidence of postoperative restenosis retrospectively in 265 patients following 310 carotid endarterectomies. Two hundred fourteen patients (248 endarterectomies) were examined at 6-12 month intervals using ocular pneumoplethysmography, spectral analysis, and B-mode imaging. The absolute incidence of recurrent carotid disease was 28% (69 of 248), with a 13% (33 of 248) incidence of hemodynamically significant restenosis and a 15% (36 of 248) incidence of hemodynamically insignificant disease. Life table analysis of the data projected a 32% incidence of hemodynamically significant restenosis after 7 years and a 40% incidence of hemodynamically insignificant recurrence. These data demonstrate a progressively increasing rate of restenosis. The incidence of ipsilateral neurologic events was 8% (24 of 310); 12 occurred in association with noninvasively evident recurrent disease (12 of 69, 17%), whereas 11 occurred in noninvasively determined normal arteries (11 of 179, 6%). Noninvasive follow-up was not available in 1 patient. Of the 12 events associated with recurrent disease, 5 occurred in association with hemodynamically significant restenosis (5 of 33, 15%), whereas 7 occurred in association with hemodynamically insignificant disease (7 of 36, 19%). Carotid endarterectomy is a durable operative procedure with 92% (286 of 310) of arteries remaining asymptomatic over the period of clinical follow-up. However, absolute and life table projections of the incidence of asymptomatic restenosis are high, and this factor should be considered in the selection of patients for carotid endarterectomy, particularly in the absence of lateralizing symptoms.
Aneurysmal subarachnoid hemorrhage. Complications and outcome in a hospital population.
Authors: Hijdra A , Braakman R , van Gijn J , Vermeulen M , van Crevel H
Published: June 2011

We describe total management results in a prospective series of 264 patients with aneurysmal subarachnoid hemorrhage (SAH) admitted to a neurologic unit. Referrals were actively solicited from general physicians as well as neurologists in the area. The diagnosis was based on computed tomography (CT). Secondary deteriorations were analyzed clinically and with serial CT scanning. Outcome was assessed 3 months after SAH. There were no relevant differences between the analyses of patients with and without an aneurysm confirmed by angiography or autopsy. One third of the patients either died within 1 day (12%) or remained in a poor clinical condition that precluded surgery (22%). One third were in good clinical condition, but contraindications to surgery were judged present or serious complications occurred before surgery could be performed. One third of all patients underwent surgery. Overall mortality in our series was 52%; only 26% made a good recovery. The risk of rebleeding was not related to the patients' initial clinical condition, but all other intracranial complications occurred significantly more often in patients graded poor compared with patients in good clinical condition. The most important causes of death and severe disability were hemorrhage (16%), recurrent hemorrhage (18%), and delayed cerebral ischemia (15%). The most important surgical complication was delayed deterioration caused by ischemia (20% of operated patients). We estimated that recognition of 'warning leaks,' surgery in patients over 65, and improvement of our surgical technique could decrease mortality from 52% to approximately 41%.
Cerebral vasoconstrictor responses to serotonin after dietary treatment of atherosclerosis: implications for transient ischemic attacks.
Authors: Heistad D D , Breese K , Armstrong M L
Published: June 2011

Serotonin, which is released when platelets aggregate at carotid lesions, may contribute to cerebral ischemia. Our goal was to test the hypothesis that dietary treatment of atherosclerosis reverses the augmented cerebral vasoconstrictor response to serotonin. We studied normal cynomolgus monkeys, atherosclerotic monkeys, and atherosclerotic monkeys that were fed a normal (regression) diet for 18 months. Morphometric studies indicated that the regression diet reduced intimal area in the carotid arteries by about 50-75%. Cerebral blood flow was measured with microspheres, and microvascular pressure was measured with a micropipette in pial arteries that were approximately 300 micron in diameter. Values for cerebral blood flow and arteriolar pressure were used to calculate resistance of large cerebral arteries (greater than 300 micron diameter). Infusion of serotonin produced a modest increase in the resistance of large cerebral arteries in normal monkeys. Vasoconstrictor responses to serotonin were increased more than fivefold in atherosclerotic monkeys. The major finding of the study is that dietary treatment of atherosclerosis abolishes augmented cerebral responses to serotonin.