bluuebunny/crossref_metadata_2025 huggingface dataset:
Ultrastructural morphometry of hypertensive medial damage in lenticulostriate and other arteries.
Authors: Takebayashi S
Published: June 2011

Characteristic medial damage occurs in the distal lenticulostriate arteries in patients with hypertensive cerebral hemorrhage. Medical changes were studied in the proximal and distal lenticulostriate arteries and cortical circumflex arterioles. Additionally, intramyocardial coronary, gastric submucosal and renal interlobular arterioles were examined in hypertensive patients. Hypertensive medial damage consisted of irregular atrophy and paucity of smooth muscle with accumulation of nonfatty debris and basement membranes. These changes were diffuse, extensive and not uniform, and were unrelated to atherosclerosis or bifurcation. By electron microscopic morphometry smooth muscle occupied 28% of the media in the distal lenticulostriate arteries of hypertensive patients as compared with 80% in controls. The proximal lenticulostriate and cortical branches in hypertensive patients showed values higher than 50%, as did the coronary, gastric and renal arterioles. Massive primary hemorrhages are prevalent in the area supplied by the distal lenticulostriate artery, 150-660 microns in diameter. Fibrinoid necrosis and microaneurysm occur in more peripheral arterioles, 70-200 microns. Thus, hypertensive medial damage with significant reduction of the smooth muscle area to less than 50% of the total media is viewed as an additional important factor which predisposes to sudden arterial rupture and massive cerebral hemorrhage.
Transient neurological deficits due to embolic occlusion and immediate reopening of the cerebral arteries.
Authors: Taneda M , Shimada N , Tsuchiya T
Published: June 2011

The authors present two cases of transient occlusion of the major cerebral arteries which occurred during transfemoral catheterization of the carotid artery. Right hemiplegia and aphasia developed suddenly in both cases, and disappeared completely within 14 hours in one case and 25 minutes in the other. On the angiograms performed at the moment of onset of the symptoms, the site of the occlusion was the left internal carotid artery in one case and the left middle cerebral artery in the other. Angiograms which were repeated soon after clinical improvement revealed complete dissolution of the occluding emboli. These cases present direct radiographic evidence that embolic occlusion of a major cerebral artery and its disappearance is the mechanism of the transient manifestation of the neurological deficits associated with cerebrovascular catheterization.
The relevance of in vitro smooth muscle experiments to cerebral vasospasm.
Authors: Wellum G R , Peterson J W , Zervas N T
Published: June 2011

An overview of the possible factors that might contribute to the development of cerebral vasospasm is presented, with particular emphasis on the possibility that spasm arises from a malfunction of the regulatory or contractile processes in smooth muscle cells. This possibility is emphasized because the evidence for cellular damage and the delayed occurrence of vasospasm are suggestive of pathological alteration. Data regarding the development of spasm in vivo has been reviewed and, to the extent possible, correlated with in vitro studies of cerebrovascular smooth muscle contractility. Short-term in vitro studies of normal cerebral arteries may be of little relevance to the prolonged and severe cerebral vasoconstriction that occurs only after a delay of several days from the initial insult.
Delay in referral of patients with ruptured aneurysms to neurosurgical attention.
Authors: Kassell N F , Kongable G L , Torner J C , Adams H P , Mazuz H
Published: June 2011

Aneurysmal subarachnoid hemorrhage is a neurosurgical emergency. Early medical intervention is axiomatic for minimizing rebleeding and ischemia from vasospasm and achieving optimum results. The purpose of this study was to document the length and causes of the delay in referral which occur in patients following aneurysmal subarachnoid hemorrhage. The case histories of 150 consecutive patients admitted to The University of Iowa with proven ruptured aneurysms were studied. Medical records from The University of Iowa and referring hospitals were reviewed, and patients, families, and referring physicians interviewed. Overall, only 36% were referred within 48 hours of their first clear cut, recognizable sign or symptom of subarachnoid hemorrhage. Median time to referral was 3.6 days. Delay was due to physician diagnostic problems in 37%, delayed referral policy in 23%, unstable patient condition in 7%, failure of patients to recognize severity of illness in 8%, and logistical reasons in 12%. These data suggest that a large proportion of patients have a delay in achieving definitive neurosurgical care following aneurysm rupture, and that for the most part this delay is avoidable. More emphasis must be placed on public health and primary physician education regarding subarachnoid hemorrhage.
Effects of extra-intracranial arterial bypass on cerebral blood flow and oxygen metabolism in humans.
Authors: Samson Y , Baron J C , Bousser M G , Rey A , Derlon J M , David P , Comoy J
Published: June 2011

Twelve patients, eleven with a carotid obstruction and one with an occlusion of the middle cerebral artery, were studied before and after a successful unilateral extra-intracranial arterial by-pass, (EIAB) using PET and the 15-0 steady-state technique to measure regional cerebral blood flow (CBF), oxygen extraction fraction and oxygen metabolic rate (CMRO2). In the whole group of patients, both CBF and CMRO2 increased significantly on both cerebral hemispheres after EIAB, returning toward control levels defined in age-matched subjects. Mean oxygen extraction fraction, on the other hand, was not affected. Individually, three different effects of EIAB emerged: 1) Alleviation of a state of long standing unilateral "misery-perfusion", as reported earlier; 2) parallel increase of CBF and CMRO2 bilaterally, which appeared due to improvement of a hemodynamic depression of metabolism, the precise mechanism of which remains obscure; 3) Complex, unexpected changes in the CBF-CMRO2 couple again resulting in increases in CMRO2. This metabolic improvement afforded by EIAB in our patients has not been reported before; it suggests that long-standing hemodynamic failure may induce a metabolic depression that is still potentially reversible by surgical revascularization.
Epidemiologic features of isolated syncope: the Framingham Study.
Authors: Savage D D , Corwin L , McGee D L , Kannel W B , Wolf P A
Published: June 2011

To obtain epidemiologic information regarding syncope, 2336 men and 2873 women aged 30 to 62 years at entry to the study were evaluated for syncope. During 26 years of surveillance, evidence of cardiac or neurologic morbidity and mortality was also recorded. At least one syncopal episode was reported by 71 (3.0%) of the men and 101 (3.5%) of the women during the course of the study. Criteria for isolated syncope (i.e., transient loss of consciousness in the absence of prior or concurrent neurologic, coronary, or other cardiovascular disease stigmata) were met by 56 (79%) of the 71 men and by 89 (88%) of the 101 women with syncope. During 26 years of follow-up isolated syncope was not associated with any excess of stroke (including transient ischemic attack) or myocardial infarction. Similarly, isolated syncope was not associated with any excess of all-cause or cardiovascular mortality (including sudden death).
Enhanced in vivo platelet activation in subtypes of ischemic stroke.
Authors: Shah A B , Beamer N , Coull B M
Published: June 2011

It remains uncertain whether platelet activation in ischemic stroke is contributory or secondary to brain ischemia. The efficacy of aspirin (ASA) in stroke prevention suggests that platelet activation contributes to the occurrence of stroke. On the other hand, platelet activation may be simply a generalized consequence of cerebral ischemic damage. To examine this issue, plasma levels of the platelet specific proteins beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4) were measured in fifty-eight patients with various defined types of acute ischemic strokes. beta-TG was a broader indicator of platelet activation than PF4. Compared with an age-matched control group, thromboembolic and cardioembolic stroke patients had significantly elevated beta-TG levels (p less than 0.001). Also, beta-TG levels in these stroke categories were significantly higher in samples drawn within the first week after the event than in those drawn later (p less than 0.001). In contrast, beta-TG levels in lacunar stroke patients and in most TIA patients were normal. beta-TG levels did not correlate with the volume of cerebral infarction as measured by planimetry from CT scans. Moreover, beta-TG levels in patients on chronic ASA therapy at the time of stroke did not differ from those in patients of the same diagnostic categories not taking aspirin. These data indicate that platelet activation may be important in some, but not all, subtypes of ischemic stroke and that platelet activation can occur in stroke even though the platelet cyclooxygenase pathway is suppressed.
Chronological changes in spontaneous intracerebral hematoma--an experimental and clinical study.
Authors: Takasugi S , Ueda S , Matsumoto K
Published: June 2011

A model of intracerebral hematoma that closely resembles the state in humans after spontaneous intracerebral hematoma was developed. Sequential changes in experimental intracerebral hematomas were compared with the in vivo findings in spontaneous intracerebral hemorrhage. The clinical series consisted of 28 patients with spontaneous intracerebral hemorrhage observed by CT during their natural course from 1976 through 1978. The experimental series consisted of 26 adult mongrel dogs with intracerebral hematoma near the basal ganglia studied by CT and histological examinations. In neither the clinical nor the experimental series was the time of decrease in density beginning in the periphery of the hematoma or the first appearance of ring enhancement and its concentric concentration toward the center of the hematoma affected by the size of the hematoma. In the experimental series, the tissue reaction near the periphery of the intracerebral hematoma showed constant processes: First, a necrotic layer appeared; this was then replaced by immature connective tissue with newly formed vessels and argentophilic fibers, and finally the immature layer was gradually transformed into mature connective tissue with collagenous fibers. Ring enhancement was accompanied by the appearance of immature connective tissue and capillaries. This process of change was also unrelated to the size of the hematoma. The following correlations were suggested from the chronological observation of CT images and the histological appearance: 1) acute stage - homogeneous high density extending to the periphery, appearance of the necrotic layer; 2) subacute stage - decreased density spreading from the periphery and formation of ring enhancement, appearance of immature connective tissue with argentophilic fibers; 3) chronic stage - concentric concentration of ring enhancement and development of mature connective tissue with collagenous fibers.
Simultaneous therapy with antiplatelet and anticoagulant drugs in symptomatic cardiovascular disease.
Authors: Miller A , Lees R S
Published: June 2011

Twenty of approximately 1000 patients attending the arteriosclerosis clinic at MIT during a 13 year period were treated simultaneously with aspirin and warfarin for symptomatic atherosclerotic (19) or rheumatic (1) heart or vascular disease. The average duration of therapy was 5.8 years. Thirteen patients suffered from familial hyperlipoproteinemia; only one patient had none of the major risk factors for arteriosclerosis. Refractory symptoms were related to the central nervous system in 13, peripheral vascular system in 5 and the heart in 2. All twenty patients became asymptomatic or showed marked clinical improvement on aspirin plus warfarin therapy. While on this therapy, complications, both thrombotic and hemorrhagic, occurred in 7 of the 20 patients (graft embolus in 1, and bleeding in 6; with one death as a result of intracranial bleeding) and sudden death, probably from acute myocardial ischemia, in a further 2 patients. We conclude that when alternative therapies are impossible or have proven to be of no avail in patients suffering from the complications of advanced atherosclerosis, the simultaneous administration of aspirin and warfarin may be a therapeutic alternative, although very close and careful followup of the patients' prothrombin times and clinical status is essential.
The effects of extreme hemodilutions on the autoregulation of cerebral blood flow, electroencephalogram and cerebral metabolic rate of oxygen in the dog.
Authors: Maruyama M , Shimoji K , Ichikawa T , Hashiba M , Naito E
Published: June 2011

The effects of profound (hematocrit value, Ht 20%) and extreme (Ht 5%) hemodilutions on the relationship between the mean arterial pressure (MAP) and the cerebral blood flow (CBF) were studied in pentobarbital-anesthetized dogs. A regression line was found between the CBF and Ht values during normotensive hemodilution (MAP 100 torr): CBF (ml/100g X min) = -98.9 log Ht (%) + 195.5 (p less than 0.001). The CBF was increased by hemodilution, but the range of its autoregulation was narrowed, suggesting a progressive susceptibility of CBF to blood pressure with hemodilution. The electroencephalogram (EEG) was not significantly changed by hemodilution within the range of the CBF autoregulation, below which it became slowed. In contrast, the cerebral metabolic rate of oxygen (CMRo2) was decreased by hemodilution even within the range of the CBF autoregulation, while there were no significant differences in CMRo2 values between MAPs of 100 and 40 torr. Thus, the brain function in terms of the EEG seemed to correlate more with the autoregulatory mechanism of the CBF than with the CMRo2 value in the hemodiluted states.
Cellular actions of halothane on cat cerebral arterial muscle.
Authors: Harder D R , Gradall K , Madden J A , Kampine J P
Published: June 2011

The effects of halothane on intracellular membrane potential (Em) and force development in cat MCA were studied. Halothane (0.07-0.14 mM/1) relaxed isolated MCA which had developed myogenic tone. Measurement of Em showed that halothane depolarized this preparation in a dose-dependent fashion in the face of vessel relaxation, demonstrating uncoupling of electrical and mechanical activity. Halothane markedly inhibited the contractile effects of histamine and serotonin suggesting that, apart from its direct action on cerebral arterial tone, it also blunts the action of vasoactive agents. When this preparation is partially depolarized from -62 to -50 mV with excess K+, halothane, while having only a small (1.2 mV) additional depolarizing effect, consistently elicits contraction rather than relaxation. Thus, the action of this particular volatile anesthetic on cerebral arteries can depend upon the resting level of Em. These studies indicate that halothane relaxes myogenic tone in cat MCA by an intracellular mechanism, but that the direction of its effect (i.e., relaxation vs. contraction) may depend upon the prior level of Em and muscle cell activation.
Distribution of acidic glycosaminoglycans, lipids and water in normal human cerebral arteries at various ages.
Authors: Murata K
Published: June 2011

Functional alterations in arterial acidic glycosaminoglycans (AGAG) may be related to the pathogenesis of some forms of cerebrovascular disease. We measured the AGAG, lipid and water content of human cerebral artery of 275 normal males at various ages. These measures were separately carried out in the main trunk and distal branches. The AGAG components were analyzed by an enzymatic assay method employing specific enzymes which digest AGAG to assess topographic change and aging variations. The total AGAG content was higher in the main cerebral artery than in the distal branches. The main AGAG component of the normal main cerebral artery was heparan sulfates (HS), constituting half the total AGAG, followed by moderate amounts of dermatan sulfate (DS), chondroitin-6-sulfate (C-6S) and chondroitin-4-sulfate (C-4S). Hyaluronic acid (HA) was a minor component and it was more prominent in young arteries. Heparin could be occasionally detected. With advancing age, the relative amounts of HS, HA, chondroitin and C-4S both in the main trunk and distal branches decreased but those of DS and C-6S increased. The total lipid, cholesterol ester and triglyceride content was greater in the main trunk than in the distal branches; the total lipid content increased with age. A possible function of the cerebral arterial AGAG is discussed with respect to change in lipid and water content according to topographic sites and aging.
Intracerebral haemorrhage and angiographic beading following ingestion of catecholaminergics.
Authors: Stoessl A J , Young G B , Feasby T E
Published: June 2011

We report two cases of serious intracerebral haemorrhage occurring in young women following their first use of oral medications containing catecholaminergic agents (phenylpropanolamine in combination with ephedrine or pseudoephedrine). Both women were previously well, and there was no evidence for systemic vasculitis, coagulopathy, aneurysm or arteriovenous malformation. Angiography in both cases, performed approximately forty hours following drug ingestion, revealed the beading pattern typical of that seen in previously reported cases of presumed amphetamine-induced "vasculitis." We believe that this arteriographic abnormality is non-specific and should not be construed as necessarily indicative of arteritis.
Measurement of cerebral blood flow during xenon inhalation as measured by the microspheres method.
Authors: Gur D , Yonas H , Jackson D L , Wolfson S K , Rockette H , Good W F , Maitz G S , Cook E E , Arena V C
Published: June 2011

Measurements of cerebral blood flow (CBF) were performed using the microsphere technique in non-human primates (baboons) to assess the effect of non-radioactive xenon gas inhalation on CBF. Blood flows in small tissue volumes (approximately 1 cm3) were directly measured before and during the inhalation of xenon/oxygen gas mixtures. The results of these studies demonstrated that when inhaled in relatively high concentrations, xenon gas does increase CBF, but the changes are more global than tissue-specific. The problems and limitations of such evaluations are discussed.
Perforating branches of the middle cerebral artery. Microanatomy and clinical significance of their intracerebral segments.
Authors: Marinkovic S V , Milisavljevic M M , Kovacevic M S , Stevic Z D
Published: June 2011

Perforating branches of the middle cerebral arteries (MCA) were examined on the forebrain hemispheres of fourteen human brains. It was noticed that their intracerebral segments arose from the MCA main trunk, and its terminal and collateral (cortical) branches. They terminated in certain parts of the basal ganglia and internal capsule. The course, direction, shape, diameters and branches of these segments were examined in detail. Classification of all the vessels was made according to caliber. It was concluded that the size of lacunar infarcts depends on the caliber and ramification zone extent of the occluded perforating vessels. Diameters of the intracerebral segments of vessels ranged from 80 to 840 microns, of their terminal branches from 80 to 780 microns, and of the collateral branches from 50 to 400 microns. The average size of the ramification zone was: 41.6 X 15.5 mm for the entire perforating artery; 37.9 X 15.5 mm for the intracerebral segment; 23 X 13 mm for the terminal branches; 8.9 X 5.5 mm for larger collateral branches; and 2.6 X 1.4 mm for the smallest branches.
Effects of estradiol on platelet aggregation in cerebral microvessels of mice.
Authors: Rosenblum W I , el-Sabban F , Allen A D , Nelson G H , Bhatnagar A S , Choi S C
Published: June 2011

Mice were implanted subcutaneously with a pellet containing 0.5 mg estradiol or with a placebo. Eight to 12 days later platelet aggregation was produced in pial arterioles by injuring their endothelium in vivo with a noxious light/dye stimulus. The time between the onset of the noxious stimulus and the appearance of platelet aggregates was significantly shortened (p less than .02) by estradiol treatment in young (2 month old) mice. The same treatment had the opposite effect in 4-6 month old mice and significantly delayed the onset of aggregation (p = .01). When platelet rich plasma (PRP) was prepared, aggregation by sodium arachidonate was always inhibited in PRP from estradiol treated mice, irrespective of age. Estradiol treatment had no effect on aggregation induced ex vivo by ADP. Thus the enhanced aggregation observed in pial arterioles of young estradiol treated mice may not reflect direct effects of estradiol on the platelet itself. The data are discussed in light of the literature suggesting enhancement of ischemic vascular disease, including strokes, in patients receiving estrogens, and especially high doses of estrogens.
Prospective analysis of long term control of mild hypertension on cerebral blood flow.
Authors: Meyer J S , Rogers R L , Mortel K F
Published: June 2011

A group of 12 otherwise normal elderly volunteers (mean age = 69.8 years), were detected to have mild hypertension. Cerebral blood flow (CBF) values were measured using 133Xe inhalation method prior to initiating medical treatment and repeated at 6, 12, 24 and 36 months after BP was adequately controlled and restored to normal (below 150/90). Results indicate that CBF values increased markedly during follow-up intervals at 6, 12 and 24 months but not at 36 months. Hypertension is known to be a risk factor for stroke and 4 of the 12 subjects subsequently developed symptoms of cerebrovascular disease (stroke, multi-infarct dementia or transient ischemic attacks) despite control of hypertension. Analyses separating asymptomatic and symptomatic groups indicated that the eight asymptomatic patients continued to maintain increased CBF levels throughout the entire three year interval, whereas the 4 symptomatic patients developed declines in CBF which began, and progressively decreased below the initial pretreatment values, during the second and third years.
A pathologic correlate of the 'steal' phenomenon in a patient with cerebral arteriovenous malformation.
Authors: Costantino A , Vinters H V
Published: June 2011

A patient died after therapeutic bucrylate embolization and resection of a right occipital arteriovenous malformation, which received significant blood supply from the right posterior cerebral artery. At autopsy, there was marked diffuse neuron loss and gliosis in all cell layers of the right hippocampus--pathology which we hypothesize was secondary to a 'steal' of blood from this structure into the malformation. This report represents pathologic evidence for a phenomenon believed to be of major clinical importance in the symptomatology of many AVMs.
Major cerebral arterial and venous disease in osteopetrosis.
Authors: Makin G J , Coates R K , Pelz D , Drake C G , Barnett H J
Published: June 2011

Two patients with osteopetrosis were studied in whom severe stenosis of one or both internal carotid arteries was demonstrated. One patient had autosomal dominant osteopetrosis and the other patient had the autosomal recessive form of the disease. In one patient, probable occlusion of one internal jugular vein and retrograde thrombosis of the contributing dural venous sinuses was present. Venous drainage of parts of the brain occurred through dilated emissary and scalp veins. It appears that major extracranial vessels may be impinged upon by dysplastic bone in osteopetrosis, although this is the first report of such an occurrence. A posterior fossa aneurysm was present in one case, and may have been related to abnormal intracranial hemodynamics.
The specificity of the collaterals to the brain through the study and surgical treatment of moyamoya disease.
Authors: Matsushima Y , Inaba Y
Published: June 2011

Moyamoya disease presents clinically as chronic progressive ischemia in the young brain. The brain is surrounded by concentric collateral networks but all of these networks are not available as collaterals in the early stage of cerebral ischemia. The anatomical characteristics precluding their early use include the presence of the watery layer of subarachnoid fluid between the cortical and dural vessels and of a closed bony box intervening between the dural and scalp arterial networks. These barriers isolate the brain from the abundant blood flow of the external carotid system as if they were the moat (the subarachnoid fluid layer) and the walls (the skull) of a castle. Based on these concepts, we have developed a surgical procedure, the encephalo-duro-arterio-synangiosis to treat moyamoya disease in children. This operation surmounts the above mentioned two obstacles to collateral formation to the brain by perforating the castle wall and bridging the moat by granulation tissue, without injuring the collaterals which are already formed. This procedure was performed on 70 sides in 38 pediatric moyamoya patients. Revascularisation of the brain was obtained in 100 percent of the cases with varying improvement in the symptoms.
Selective functional vulnerability of cortical neurons following transient MCA-occlusion in the cat.
Authors: Rosner G , Graf R , Kataoka K , Heiss W D
Published: June 2011

Simultaneous recordings of several cortical neurons were obtained before, during and after transient 15 min occlusion of the middle cerebral artery in cats. With the use of a multiple electrode array consisting of 4-7 platinum/iridium microelectrodes, the cortical pericellular blood flow was concurrently measured by means of the hydrogen clearance technique. Hydrogen clearance measurements revealed a homogeneous blood flow distribution throughout all phases of the experiment in the area covered by the different microelectrodes. Considering only the results of experiments with low residual blood flow during ischemia (less than 0.1 ml/g/min), single unit activity ceased immediately after occlusion and remained so during the ischemic period. The recovery time of action potentials after reperfusion ranged from 10 min to 3 hours depending on the examined neuron. Lower values for discharge rates of the individual cells were generally observed after reoccurrence, although some units exhibited temporarily an even higher spike frequency. Furthermore, the spike form usually changed in that the hyperpolarizing afterpotentials were enlarged after recirculation. However, some cells with a nearly unchanged spike form were found as well. The results indicate that the recovery of cell function largely depends on the individual neuron which supports the idea of a selective functional vulnerability of cortical neurons in response to ischemia.
Characterization of beta adrenergic receptors in human cerebral arteries and alteration of the receptors after subarachnoid hemorrhage.
Authors: Tsukahara T , Taniguchi T , Shimohama S , Fujiwara M , Handa H
Published: June 2011

The nature of beta adrenergic receptors in human cerebral arteries was characterized and alteration of these receptors after subarachnoid hemorrhage was examined using a radioligand binding assay. The specific 3H-dihydroalprenolol, a beta adrenergic antagonist, binding to human cerebral arteries was saturable and of high affinity (KD = 12.3 nM) with a Bmax of 790 fmol/mg protein. Ki values and Hill coefficients of adrenergic agents for 3H-dihydroalprenolol were as follows; propranolol, 4.1 X 10(-8)M, 1.01; isoproterenol, 1.7 X 10(-6)M, 0.80; epinephrine, 8.3 X 10(-6)M, 0.48; norepinephrine, 2.3 X 10(-5)M, 0.45; metoprolol, 6.8 X 10(-8)M and 7.9 X 10(-6)M, 0.62; butoxamine, 2.2 X 10(-8)M and 2.1 X 10(-6)M, 0.43. The analysis of inhibition of specific 3H-dihydroalprenolol binding by these adrenergic agents suggests that human cerebral arteries contain a high density of beta adrenergic receptors and that the receptors are classified into two types, namely beta 1 and beta 2 adrenergic receptors. The calculated beta 1/beta 2 ratio from Hofstee plots was approximately 4/6. KD and Bmax of 3H-dihydroalprenolol binding to the cerebral arteries after subarachnoid hemorrhage were compared with those of control group. KD and Bmax of 3H-dihydroalprenolol binding of subarachnoid hemorrhage group were 13.9 nM and 1140 fmol/mg protein, respectively. The calculated beta 1/beta 2 ratio was approximately 6/4. These data suggest that the density of total beta adrenergic receptors increased without any significant change in the affinity after subarachnoid hemorrhage and that the increase of beta 1 adrenergic receptors was dominant.
Vasodilator proteins: role in delayed cerebral vasospasm.
Authors: White R P
Published: June 2011

Blood proteins could play a critical role in the pathogenesis of cerebral vasospasm in subarachnoid hemorrhage (SAH) as agonists and as antagonists of vasoconstriction. The present study was designed primarily to quantify the inhibition produced by antithrombin III of the phasic responses elicited by cumulative doses of KCl, serotonin (5-HT), uridine triphosphate (UTP), and thrombin in isolated canine basilar arteries, and to ascertain whether other proteins might act similarly. Antithrombin III (1 unit/ml and 3 units/ml) given 2 min beforehand inhibited all agonists. The inhibition was not dependent on a functional endothelium nor due to stimulation of the electrogenic sodium pump. Alpha2-macroglobulin (0.1 mg/ml and 0.4 mg/ml) inhibited the contractile responses to high K+, 5-HT and thrombin. Kallikrein (1 and 4 units/ml) did not inhibit UTP but inhibited high K+ and 5-HT through an effect on the endothelium. Kallikrein (1 unit/ml) irreversibly blocked the responses to thrombin. Globulins (3 mg/ml) and fibrinogen (0.3 mg/ml) were not inhibitory. The results demonstrate that anticoagulant proteins are very effective nonspecific inhibitors of the vasoconstriction, whereas the serine protease kallikrein selectively blocks thrombin. The remarkable potency of antithrombin III suggests that it may protect cerebral arteries from exhibiting vasospasm in SAH.
Polymorphonuclear leukocyte accumulation in brain regions with low blood flow during the early postischemic period.
Authors: Hallenbeck J M , Dutka A J , Tanishima T , Kochanek P M , Kumaroo K K , Thompson C B , Obrenovitch T P , Contreras T J
Published: June 2011

In an anesthetized canine model in which ischemia was induced by incremental air embolism, 16 animals were exposed to 1 hr of ischemia and monitored for 10 min (n = 4), 60 min (n = 6), or 240 min (n = 6). Fourteen animals were observed for corresponding periods without being subjected to ischemia 70 min (n = 4), 120 min (n = 4), or 300 min (n = 6). Autologous granulocytes were labeled with 111In and reinfused just before ischemia. At the conclusion of each experiment, a 14C-iodoantipyrine autoradiographic blood flow study was performed. Granulocyte accumulation measured by gamma scintigraphy (cpm/gm) occurred in the injured hemisphere of ischemic animals at 60 min in anterior brain segments and at 240 min in anterior, middle, and posterior segments. By means of a double-label autoradiography technique, clustering of punctate granulocyte images was detected in regions of low flow or heterogeneous flow in half of the animals at both 60 min and 240 min postischemia. Granulocyte clustering did not occur in the autoradiograms of nonischemic animals. The results implicate granulocyte participation in the acute phase of ischemic brain injury and signal a convergence of hemostatic and inflammatory processes during the immediate postischemic period.
Community Hospital-based Stroke Programs: North Carolina, Oregon, and New York. I: Goals, objectives, and data collection procedures.
Authors: Yatsu F M , Becker C , McLeroy K R , Coull B , Feibel J , Howard G , Toole J F , Walker M D
Published: June 2011

In order to assess the impact of variations in stroke care on outcomes, and to make geographic comparisons, the three Community Hospital-Based Stroke Programs in North Carolina, Oregon, and New York, aggregated their data on 4,132 hospitalized stroke patients. Complete demographic data or "Major Profile" were obtained on 2,390 (57.8%) of the 4,132 stroke patients. This includes those patients on whom informed patient and physician consents were obtained during the hospitalization. Of the major profile patients, 1,490 (62.3%) were followed for periods up to one year, 502 (21.0%) were lost to followup and 398 (16.6%) died within the one year followup period. Incomplete demographic data or "Minor Profile" were observed on 1,742 (42.1%) of the 4,132 patients. Minor profile includes those who died before comprehensive interviews were completed or those for whom informed consent for an interview could not be obtained. Of the minor profile group, 813 (46.7%) died in hospital, and 929 (53.3%) were alive when discharged from the hospital. This paper, which describes the programs, data collection procedures, and study cases, also highlights specific issues on stroke diagnosis, risk factors associated with stroke, and the influence of interventions on stroke outcomes. We conclude that: 1) the merging of data on hospitalized stroke cases from rural and urban hospitals in geographically distinct regions can be used in the study of stroke diagnosis, the use of diagnostic tests, and the effect of interventions on stroke outcomes; and 2) these data are consistent with the hypothesis that part of the national decline in mortality from stroke is due to a decline in stroke severity.
Characterization of muscarinic cholinergic receptors in human and dog cerebral arteries.
Authors: Tsukahara T , Usui H , Taniguchi T , Shimohama S , Fujiwara M , Handa H
Published: June 2011

Various concentrations of acetylcholine (ACh) produced dose dependent relaxations of isolated, helical preparations of human cerebral arteries and these responses were blocked by atropine. The median effective concentration (EC50) of ACh was 6.1 +/- 0.2 X 10(-6)M. ACh produced dual responses in isolated dog cerebral arteries. ACh in low concentrations produced relaxation, and contraction occurred when the concentration was raised to 1 X 10(-5)M. The EC50 of ACh which produced relaxation, in dog cerebral arteries was 7.2 +/- 0.2 X 10(-7)M. Muscarinic cholinergic receptors in these arteries were analyzed directly using 3H-QNB as the ligand. The specific 3H-QNB binding to the arteries was saturable and of KD = 1.5 nM and Bmax = 93 fmol/mg protein in human cerebral arteries and KD = 0.59 nM, Bmax = 340 fmol/mg protein in dog cerebral arteries. Specific binding of 3H-QNB was displaced by muscarinic cholinergic agents. Ki values and Hill coefficients were as follows: QNB, 1.0 X 10(-9)M, 0.89; atropine, 1.1 X 10(-8)M, 0.95; ACh, 0.8 X 10(-8)M and 2.1 X 10(-6)M, 0.54; carbachol, 1.2 X 10(-7)M and 4.3 X 10(-5)M, 0.33 in human cerebral arteries and QNB, 0.55 X 10(-9)M, 0.85; atropine 0.9 X 10(-9)M, 1.00; ACh, 0.9 X 10(-9)M and 1.1 X 10(-6)M, 0.43; carbachol 6.3 X 10(-8)M and 1.1 X 10(-5)M, 0.36 in dog cerebral arteries. Endogenous choline acetyltransferase (ChAT) activity was 1.6 +/- 0.4 nmol/mg protein/hr in human cerebral arteries and 3.7 +/- 0.1 nmol/mg protein/hr in dog cerebral arteries.(ABSTRACT TRUNCATED AT 250 WORDS)
Rehabilitation for stroke: a review.
Authors: Dombovy M L , Sandok B A , Basford J R
Published: June 2011

Survivors of stroke are often left with severe mental and physical disabilities, which create a major social and economic burden. Many investigators have attempted to assess the role of rehabilitation in reducing such disability. Few controlled studies provide accurate assessment and documentation of benefit. Because of the presence of multiple variables and inadequate measures of outcome, it is difficult to design studies evaluating the effectiveness of rehabilitation for stroke. It is unclear how early rehabilitation should begin and what aspects of rehabilitation are important. Intensive rehabilitation is an expensive and limited resource; thus, the ability to identify the subgroup of patients with stroke who are likely to benefit is a critical issue. Although preliminary guidelines for the selection of patients who are appropriate for rehabilitation are given, no uniform criteria reliably differentiate patients who need rehabilitation from those who will recover spontaneously or do poorly. Controlled studies in the practice of rehabilitation for stroke will provide much useful information for patient management.
Visual disturbance and carotid artery disease. 500 symptomatic patients studied by non-invasive carotid artery testing including B-mode ultrasonography.
Authors: Gaul J J , Marks S J , Weinberger J
Published: June 2011

Non-invasive carotid artery testing was performed on 500 consecutive patients with visual disturbances not related to local ophthalmic pathology to determine the extent of carotid artery disease, particularly in patients with symptoms not typical of amaurosis fugax. Three hundred eighty six patients (77.2%) had an abnormal study. However, the incidence of hemodynamically significant lesions was only 16%. The patients could be divided into three groups: Patients with symptoms that could be explained on an ocular basis, including amaurosis fugax, had a 79% incidence of ipsilateral carotid plaques. Patients with symptoms which could not be easily explained on an ocular basis, such as bilateral blurred vision, bilateral visual loss (both transient and permanent), and homonymous hemianopsia had an incidence of carotid artery plaques similar to patients with amaurosis fugax. Patients with unilateral blurred vision and bilateral scintillations had a lower incidence (57%) of carotid plaques than the other groups. Younger symptomatic patients had less carotid plaques than the overall series. Twenty-one percent of patients under age 50 had the Doppler finding of early systolic flutter turbulence, which is usually of mitral valve origin. Women predominated in the under 50 age group by about 2:1. In view of the prevalence of carotid plaques in the population of patients with visual symptoms other than amaurosis fugax, evaluation of these patients with non-invasive testing is indicated to determine which of these patients has hemodynamically significant obstruction to flow at the carotid artery bifurcation.
Long-term cerebral outcome after open-heart surgery. A five-year neuropsychological follow-up study.
Authors: Sotaniemi K A , Mononen H , Hokkanen T E
Published: June 2011

A prospective 5 years' neuropsychological, neurological, cardiological and electroencephalographical follow-up study was carried out in 44 patients who had undergone open-heart surgery for valve replacement. A distinct interrelationship was found between the clinical outcome immediately after operation and the neuropsychological long-term course despite the rapid recovery of occasional clinical disorders related to operative procedures. In fact, the psychometric performance scores of those who did not develop clinical signs of cerebral dysfunction induced in operation showed a significant difference only years after operation. Similarly, the harmful effects of long perfusion time (extracorporeal circulation) in operation were reflected in the long-term neuropsychological performance. Some evidence seemed to suggest that the correction of the prolonged circulatory disorder might possibly afford real enhancement of higher cerebral functions. The long-term results not only emphasize the importance of a careful clinical evaluation but also emphasize the necessity of considering the subclinical level of events both before and after operation when assessing the overall outcome and cerebral safety of cardiac surgery patients.
The syndrome of unilateral tuberothalamic artery territory infarction.
Authors: Bogousslavsky J , Regli F , Assal G
Published: June 2011

The study of 3 personal cases and 5 published cases of unilateral infarct limited to the territory of the tuberothalamic artery suggests that this syndrome should be differentiated from the other thalamic syndromes. The onset is usually sudden, with moderate contralateral weakness. Sensory changes may be present but remain mild. The patients are apathetic, show perseveration and may be disoriented. In left-sided infarcts, transcortical aphasia, verbal and visual memory impairment and sometimes acalculia are found. In right-sided infarcts, hemispatial neglect, visual memory impairment and disturbed visuospatial processing are common. A decreased level of consciousness, disturbed ocular movements, severe motor weakness and delayed abnormal movements do not occur. Involvement of the ventral lateral and dorsomedial nucleus with sparing of the intralaminar nuclei, posterolateral formation and upper midbrain may explain this picture. The fact that the tuberothalamic artery arises from the posterior communicating artery, which often receives its supply from the carotid system, further justifies considering unilateral tuberothalamic infarcts as a syndrome.
Hypotension as a complication of hypoglycemia leads to enhanced energy failure but no increase in neuronal necrosis.
Authors: Auer R N , Hall P , Ingvar M , Siesjo B K
Published: June 2011

The hypothesis that arterial hypotension aggravates hypoglycemic brain damage was tested. Thirty minutes of insulin induced hypoglycemia with a flat EEG ("isoelectricity") was compared in seven series of rats. In three series of animals, the energy state of the cerebral cortex was determined at blood pressures of 140, 100 and 80 mm Hg respectively. Hypotension during hypoglycemia exacerbated cortical energy failure. In the fourth to sixth series, blood pressure was adjusted during isoelectricity to 160, 100 and 60 mm Hg, respectively. A seventh series had induced hypotension to 60 mm Hg only in the recovery period. Quantitation of neuronal death was performed in the fourth to seventh series of rats by direct visual counting of acidophilic neurons in sub-serially sectioned brains after one week survival. Although the first three series demonstrated enhanced deterioration of the cerebral energy state with lower blood pressures during hypoglycemia, the fourth to seventh series showed no augmentation of quantitated hypoglycemic neuronal necrosis. The distinct distribution of hypoglycemic brain damage, suggesting a fluid-borne toxin, was present at normal and reduced blood pressures, with no tendency toward an ischemic pattern of pathology. In spite of previously demonstrated reductions of cerebral blood flow to ischemic levels in regions with pronounced loss of autoregulation, no regional exacerbation of neuronal necrosis was seen in these brain areas. It is concluded that hypoglycemic brain damage is distinct from ischemic brain damage, and that the two insults are not additive. Furthermore, moderate hypotension to 60 mm Hg does not aggravate the damage in spite of an enhanced energy failure.
Reperfusion after cerebral ischemia: influence of duration of ischemia.
Authors: Todd N V , Picozzi P , Crockard H A , Russell R R
Published: June 2011

The influence of the duration of ischemia on the pattern of cerebral blood flow in recirculation was studied in anesthetised rats. Severe incomplete cerebral ischemia (mean ischemic flow = 5.8 +/- 0.4 ml/100 g/min) was produced by four-vessel occlusion and recirculation permitted after 15, 30 or 60 minutes ischemia. All three groups showed an immediate hyperemia followed by hypoperfusion. Hyperemia was maximal following 15 minutes ischemia and least pronounced following 60 minutes ischemia (p = 0.0249). Hypoperfusion started most quickly following 15 minutes ischemia and was delayed following 60 minutes ischemia (p less than 0.001). In established hypoperfusion there was no difference in flow between the three groups. The possible mechanisms of these changes in flow are discussed.
Flunarizine limits hypoxia-ischemia induced morphologic injury in immature rat brain.
Authors: Silverstein F S , Buchanan K , Hudson C , Johnston M V
Published: June 2011

We examined the impact of pre-treatment with the calcium antagonist flunarizine on the development of hypoxic-ischemic brain injury in the immature rat. Unilateral carotid artery ligation and subsequent exposure to 2 hours of 8% oxygen in 7-day-old rats was used as a model for perinatal hypoxic-ischemic encephalopathy. This procedure leads to atrophy in the cerebral hemisphere ipsilateral to carotid occlusion, with prominent foci of neuronal infarction in the caudate-putamen (striatum). The morphologic injury develops after 1 1/2 hours of hypoxia; and there is an equivalent time threshold for duration of hypoxic exposure needed to acutely stimulate dopamine release in the ipsilateral striatum. Parenteral administration of 30 mg/kg of flunarizine before hypoxic exposure limited both the release of dopamine acutely and the extent of morphologic damage observed two weeks after the insult. Oral administration of 30 mg/kg of flunarizine in a different vehicle prevented morphologic damage but had no effect on stimulated dopamine release. The drug vehicle for the parenteral preparation also prevented tissue injury, but to a lesser degree than flunarizine. However the parenteral vehicle was equipotent with parenteral flunarizine in limiting acute stimulation of dopamine release. The results demonstrate that flunarizine has potent neuroprotective properties against morphologic brain injury from hypoxia-ischemia, acting by a mechanism which is independent of effects on dopamine release.
Cerebrovascular projections from the sphenopalatine and otic ganglia to the middle cerebral artery of the cat.
Authors: Walters B B , Gillespie S A , Moskowitz M A
Published: June 2011

The location of the postganglionic parasympathetic cell bodies projecting to cerebral arteries is unknown. Using axonal tracing techniques, we examined whether the sphenopalatine ganglia (associated with the seventh cranial nerve) and otic ganglia (associated with ninth cranial nerve) contain perikarya which send axons to the feline middle cerebral artery (MCA). The tracers horseradish peroxidase (HRP: 3 cats) or wheat germ agglutinin (WGA: 6 cats) were applied to the MCA in a slow release polymeric system. Three days later the SPG, otic ganglia, and rete mirabile were harvested bilaterally and processed for tracer by the TMB method (HRP) or immunohistochemistry (WGA). In a given animal, approximately equal numbers of cells containing axonal tracer were found in both SPG. Labeled fibers occasionally could be seen extending into the vidian nerve. Positive cells were also found in the otic ganglia and in the walls of the internal rete mirabile. These results provide the first identification of parasympathetic cell bodies projecting to cerebral blood vessels.
Endothelial dependent relaxation demonstrated in vivo in cerebral arterioles.
Authors: Rosenblum W I
Published: June 2011

The endothelium of mouse pial arterioles was injured in situ with a light/dye technique. The response of the arterioles to acetylcholine or to bradykinin was compared before and after the injury. All vessels failed to dilate after injury. In fact the predominant response now became constriction. The injured vessels were still capable of dilating to papaverine. Uninjured vessels continued to dilate to acetylcholine or bradykinin. The data show that relaxation of pial arterioles to acetylcholine or bradykinin is dependent on a normal endothelium. This is in keeping with demonstrations by others that an endothelial dependent relaxing factor or factors is(are) the mediator of the dilation to either acetylcholine or bradykinin. The present demonstration of such endothelial dependence is important because in contrast with the bulk of the literature it deals with in vivo, rather than in vitro data, and with microcirculation rather than large vessels. It is also important because it concerns brain circulation. The data suggests that endothelial injury, known to occur in a wide variety of pathologic states, could enhance vasospastic potential by eliminating dilating influences and/or converting them to constricting forces.