bluuebunny/crossref_metadata_2025_split huggingface dataset:
Pure sensory stroke. Clinical-radiological correlates of 21 cases.
Authors: Kim J S 
Published: June 2011

Although pure sensory stroke is a relatively common lacunar syndrome, the responsible lesions are often unidentified because of their small size. I reported 21 cases of pure sensory stroke in which the lesions could be identified by head computed tomography and/or magnetic resonance imaging and correlated the clinical findings with the radiological lesions.
Eleven patients had thalamic strokes. Lacunes confined to the posterolateral part of the thalamus were found in nine cases, and hemorrhages of relatively large size were found in two. Five patients showed a loss of all sensory modalities, but six with very small lacunes showed minor or restricted sensory changes. Seven patients with lacunes or hemorrhages in the lenticulocapsular region or corona radiata showed abnormalities of spinothalamic tract sensation. Two patients with a small lacune and a hemorrhage in the pontine tegmentum showed a selective sensory deficit of the medial lemniscal type. One patient with a small cortical infarct showed a cortical sensory loss that was preceded by cortical sensory transient ischemic attacks.
Pure sensory stroke can occur with lesions in various areas of the somatosensory system. Hemisensory deficits of all modalities usually are associated with a relatively large lacune or hemorrhage in the lateral thalamus, whereas tract-specific or restricted sensory changes suggest very small strokes in the sensory pathway from the pons to the parietal cortex.
Short-term prognosis of stroke due to occlusion of internal carotid artery based on transcranial Doppler ultrasonography.
Authors: Hedera P , Traubner P , Bujdáková J 
Published: June 2011

The clinical course of stroke due to occlusion of the internal carotid artery is influenced by amount of collateral flow. We measured mean frequency shifts in the middle cerebral artery by transcranial Doppler ultrasonography to determine its prognostic value.
Patients with proven extracranial occlusion of the internal carotid artery and ipsilateral hemispheral stroke were enrolled in our study. We performed transcranial Doppler ultrasonography on 31 patients within 48 hours after the stroke onset and followed up 25 patients in 28 days. At the same time, neurological examination with quantification of neurological deficit was done. We correlated values of flow frequency shifts on the side of stroke with degree of neurological deficit at the onset and at 28 days as well as the degree of clinical improvement and the value of frequency shifts.
We found a negative correlation between blood flow frequency shifts in the middle cerebral artery and degree of neurological deficit at the onset (Spearman rank correlation coefficient, -0.567; p less than 0.001). We also found a positive correlation between the change of the neurological deficit during follow-up and frequency shifts at the onset (Spearman rank coefficient, 0.548; p less than 0.05).
Diminished blood flow velocity (mean frequency shift) in the area of stroke is a negative prognostic factor for the degree of neurological deficit at the onset and a negative prognostic factor for possible improvement. Knowledge of hemodynamic conditions in the stroke area may help to improve therapeutic decisions.
Changes in extracellular glutamate concentration produced in the rat striatum by repeated ischemia.
Authors: Ueda Y , Obrenovitch T P , Lok S Y , Sarna G S , Symon L 
Published: June 2011

Evidence suggesting that ischemia-induced neuronal damage may be linked to an extracellular overflow of glutamate has accumulated, and previous studies have shown that repetitive ischemic insults may have a cumulative effect. The purpose of this study was to investigate changes in the extracellular glutamate concentration produced by repeated brief ischemic episodes of varied severity.
Four consecutive 3- or 5-minute periods of bilateral hemispheric ischemia were produced in rats, each ischemic period followed by 27 minutes of reperfusion. Extracellular glutamate in the striatum was monitored using microdialysis, and the electroencephalogram and extracellular direct current potential were recorded in the same tissue site to assess the severity of ischemia.
The results suggest that the kinetics of the increase in the extracellular glutamate concentration produced by a brief ischemic episode are similar, irrespective of whether it is a single insult or part of a repeated sequence. In all cases, the extracellular glutamate concentration increased throughout ischemia and returned to its preischemic level early during reperfusion. The pattern of changes in the ischemia-induced glutamate overflow during repetitive insults varied with the severity of ischemia, in common with the pattern of changes in the direct current potential, supporting the concept that ionic changes associated with anoxic depolarization are a major determinant of ischemia-induced glutamate overflow.
There may be no cumulative effect of brief repeated episodes of ischemia on the extracellular glutamate concentration, even though repeated 5-minute ischemic episodes apparently caused progressive deterioration of ionic homeostasis in some cases.
Time course of cerebral blood flow and histological outcome after focal cerebral ischemia in rats.
Authors: Hakim A M , Hogan M J , Carpenter S 
Published: June 2011

The relation between time-dependent changes in cerebral blood flow and the appearance of infarction after focal cerebral ischemia is still a matter for debate. The aim of this study was to measure perfusion after simultaneous occlusions of the left middle cerebral artery and ipsilateral common carotid artery in rats and correlate it with the timing and distribution of histological changes.
We studied histological and cerebral blood flow changes 5 minutes and 4, 24, and 48 hours after the onset of focal ischemia. Blood flow was determined autoradiographically using [14C]iodoantipyrine. A coronal template subdivided into regions of interest was applied to the autoradiographs and the histological data.
In some regions of the nonoccluded hemisphere, cerebral blood flow 5 minutes after occlusion fell below 50% of normal. Many ischemic structures showed stable blood flow for 48 hours after occlusion, confirming that in this model reperfusion is minimal. Infarction occurred eventually in all areas in which blood flow at 5 minutes fell below 10% of that in control rats, but infarction appeared earlier in regions in which blood flow at 5 minutes was below 5% of that in control rats. When blood flow at 5 minutes rose above 12% of that in control rats, the occurrence of infarction became unpredictable.
Despite the general dependence of infarction on perfusion levels, blood flow was not a reliable indicator of those regions committed to infarction.
Prevention of postischemic canine neurological injury through potentiation of brain energy metabolism by acetyl-L-carnitine.
Authors: Rosenthal R E , Williams R , Bogaert Y E , Getson P R , Fiskum G 
Published: June 2011

Mechanisms of ischemia/reperfusion brain injury include altered patterns of energy metabolism that may be amenable to pharmacological manipulation. The purpose of this study was to test the effectiveness of postischemic acetyl-L-carnitine administration on potentiation of metabolic recovery and prevention of neurological morbidity in a clinically relevant model of complete, global cerebral ischemia and reperfusion.
Neurological deficit scoring as well as spectrophotometric and fluorescent assays of frontal cortex lactate and pyruvate levels were used in a canine model employing 10 minutes of cardiac arrest followed by restoration of spontaneous circulation for 2 or 24 hours.
Dogs treated with acetyl-L-carnitine exhibited significantly lower neurological deficit scores (p = 0.0037) and more normal cerebral cortex lactate/pyruvate ratios than did vehicle-treated control animals.
Postischemic administration of acetyl-L-carnitine potentiates normalization of brain energy metabolites and substantially improves neurological outcome in a clinically relevant model of global cerebral ischemia and reperfusion.
Increases in cerebral blood flow in rat hippocampus after medial septal injection of naloxone.
Authors: Nishimura J , Endo Y , Kimura F 
Published: June 2011

In a previous study, we occasionally found that the rat given naloxone in the preoptic region develops behavioral seizures. In view of knowledge that the forebrain including the medial septal nucleus provides cholinergic projections to the hippocampal formation, the present study examined the effects of naloxone injected into the medial septal nucleus on the local blood flow in the hippocampus.
A polyurethane-coated platinum electrode with a 1-mm bare tip for measurement of blood flow and a guide cannula made of stainless steel tube for naloxone injection were implanted chronically into the brain. The cerebral blood flow was measured by the hydrogen clearance method in freely moving rats.
The injection of 50 micrograms naloxone caused a significant increase in hippocampal blood flow, with its peak at 20 minutes. Twenty micrograms naloxone caused a similar increase, but 10 micrograms caused only a slight increase that peaked at 30 minutes, suggesting a dose-response of naloxone effect. Hippocampal blood flow was not changed after the injection of saline into the medial septal nucleus and after the injection of naloxone into the caudate nucleus.
Taken together with previous findings, the results suggest that endogenous opioids exert a decreasing effect on the local blood flow in the hippocampus, probably mediated by the magnocellular cholinergic neurons projecting to the hippocampus.
Effect of oral nimodipine on platelet function.
Authors: Feinberg W M , Bruck D C 
Published: June 2011

Nimodipine, a calcium antagonist, has been reported to have beneficial effects in acute ischemic infarction. Some calcium channel antagonists have antiplatelet effects. We investigated the effect of oral nimodipine on platelet function in healthy volunteers.
Twelve healthy volunteers (6 men and 6 women, mean age 32.9 +/- 5.6 years) took 30 mg nimodipine every 6 hours for 24 hours, followed by a week with no medication, followed by 60 mg every 6 hours for 24 hours. Ex vivo platelet function was measured at baseline, 1 hour after the first dose at each dosage strength, and 1 hour after the last dose at each dosage. Platelet studies included aggregation and adenosine triphosphate release in response to collagen, epinephrine, and adenosine diphosphate; maximal rate of primary aggregation; threshold adenosine diphosphate concentration for second-phase aggregation; and thromboxane B2 release at threshold aggregation. The bleeding time was measured at baseline and after the last 60-mg dose of nimodipine.
No change in any platelet function study was seen with 30 mg nimodipine every 6 hours. Platelet function studies were also unchanged after 60 mg every 6 hours, except for a slight decrease in aggregation and adenosine triphosphate release in response to suprathreshold (10 microM) adenosine diphosphate (p = 0.001, Student's paired t test). There was no significant change in bleeding times.
Oral nimodipine has minimal antiplatelet activity in young, healthy subjects.
Flow-induced relaxation of the rabbit middle cerebral artery is composed of both endothelium-dependent and -independent components.
Authors: Gaw A J , Bevan J A 
Published: June 2011

The flow-induced relaxation of a branch of the rabbit middle cerebral artery was examined to determine if an endothelial-independent as well as -dependent component occurs in pial as well as systemic small arteries and the possible role of products of the cyclooxygenase and the L-arginine nitric oxide synthase pathways.
Intraluminal flow was achieved by the infusion of a tissue bath solution into isometrically mounted rabbit pial arteries in a resistance artery myograph through a small pipette.
Intraluminal flow caused relaxation of the artery segment precontracted with 10 microM histamine. Treatment of endothelium-intact vessels with the nitric oxide synthase inhibitors NG-nitro-L-arginine (L-NNA) (100 microM) or NG-nitro-L-arginine methyl ester (L-NAME) (0.3 mM) significantly reduced the relaxation at flow rates of 5-30 microliters/min. This effect was partially reversed by 1 mM L-arginine. These inhibitors had no effect on the flow-induced relaxation of endothelium-denuded vessels. L-NNA did not influence the relaxation to 1 and 3 microM papaverine. Exposure to 10 microM aspirin, 10 microM indomethacin, or 300 nM tetrodotoxin had no effect on the flow-induced relaxation of either endothelium-intact or -denuded vessels (n = 6). Flow-induced relaxation was attenuated, but not abolished, by removal of the cerebrovascular endothelium. This reduction was not statistically significant.
These results show that intraluminal flow caused relaxation of a branch of the rabbit middle cerebral artery, in part through a mechanism sensitive to inhibitors of nitric oxide synthase, most likely the generation of nitric oxide from the vascular endothelium. The major component of the relaxant response is independent of the endothelium and of nitric oxide synthesis through an L-NNA- or L-NAME-sensitive mechanism. The relaxation does not involve cyclooxygenase products nor neurogenic mediators. These results suggest that pial arteries, like those of the rabbit ear, exhibit a novel mechanism for the flow-induced relaxation of agonist-induced tone that is intrinsic to the tissues of the vascular wall subjacent to the endothelium.
Ischemic stroke due to deficiency of coagulation inhibitors. Report of 10 young adults.
Authors: Martinez H R , Rangel-Guerra R A , Marfil L J 
Published: June 2011

Deficiencies in coagulant inhibitors protein C, protein S, and antithrombin III increase the risk of venous thrombosis. We describe 10 young adults with cerebral arterial thrombosis due to deficiencies in these factors.
Sixty patients younger than 45 years were hospitalized because of acute ischemic stroke diagnosed through computed tomography or magnetic resonance imaging. Cerebral angiography was performed in 54 cases. Hematologic and coagulation profiles, autoantibody screen, syphilis serology, and lupus anticoagulant were analyzed in all patients. Among the total cases, Holter monitoring was performed in 13 patients, echocardiography in 20, and cerebrospinal fluid studies for cysticercosis and tuberculosis in two. The quantitative analysis of protein C, protein S (by Laurell rocket immunoelectrophoresis), and antithrombin III (by radial immunodiffusion) was performed on admission and 3 months after stroke in all patients and in relatives of six patients.
In 10 cases (17%) the stroke was attributed to deficiency of coagulation inhibitors: three men had protein C deficiency, two women had protein S deficiency, and five had antithrombin III deficiency (three men and two women). The cerebral infarction involved the carotid territory in these 10 patients. None had previous thromboembolic disease. Eight patients showed a complete recovery. An acquired disorder was presumed in one protein S-deficient and in two antithrombin III-deficient patients; the remainder were considered heterozygous.
The cerebral vasculature may be primarily involved in the deficiency of these natural anticoagulants. Young adults seem to be the most often affected. A knowledge of these new clotting defects will enable the clinician to improve the prevention and treatment of this devastating neurological disease.
Decline in autopsies for deaths attributed to cerebrovascular disease.
Authors: Lanska D J 
Published: June 2011

United States national autopsy rates have declined in recent years. In the present study, changes in autopsy rates for deaths due to stroke are examined and compared with changes in autopsy rates for all deaths.
National Center for Health Statistics data on United States national autopsy rates were examined for the years 1955, 1958, and 1972-1988.
Since at least 1955, nonstroke deaths were more than twice as likely to be autopsied as deaths due to cerebrovascular disease. The annual autopsy frequency for all deaths, for deaths due to stroke, and for deaths due to each stroke subtype declined precipitously after 1972. Since 1982, less than 5 percent of deaths attributed to stroke have been documented by autopsy. Information obtained at autopsy was frequently ignored in the determination of cause of death on the death certificate.
Careful consideration of the value of autopsy for education, research, and quality assurance is urgently needed. Unless the present problems in obtaining, processing, disseminating, and using autopsy data are adequately addressed, the autopsy rate will continue to decline.
Regional cerebral blood flow in chronic stroke patients.
Authors: Rodriguez G , Nobili F , De Carli F , Francione S , Marenco S , Celestino M A , Hassan K , Rosadini G 
Published: June 2011

The aim of this study was to investigate regional cerebral blood flow parameters during the postacute phase of unilateral ischemic stroke and to correlate them with clinical data.
Regional cerebral blood flow was measured in 187 patients in the stabilized phase of stroke by the xenon-133 inhalation method with 32 extracranial detectors. Thirty-eight patients were reexamined after a mean +/- SD time of 32 +/- 21.4 months.
The overall detection of hypoperfusion was 92.0%, with asymmetries as the most sensitive index, especially for patients with a lesser degree of neurological disability. Neurological disability score was strongly associated with regional cerebral blood flow in the affected hemisphere (p < 0.0001) and with asymmetries (p < 0.0001). The presence of carotid obstruction further decreased the regional cerebral blood flow in the affected hemisphere and significantly increased asymmetry (p < 0.0001). Subjects who had no hypoperfusion at absolute values analysis were more frequently free of carotid disease and had less severe disability than those who had bilateral or unilateral regional absolute cerebral blood flow reduction. In 38 patients without new cerebrovascular events, a significant (p = 0.005) reduction of hemispheric regional cerebral blood flow asymmetries was found on a follow-up examination.
These data confirm the value of regional cerebral blood flow asymmetries in stroke detection and point out that important clinical information is also contained in absolute values analysis.
Thrombolytic therapy in acute ischemic stroke. A Danish pilot study.
Authors: Overgaard K , Sperling B , Boysen G , Pedersen H , Gam J , Ellemann K , Karle A , Arlien-Søborg P , Olsen T S , Videbaek C 
Published: June 2011

In a feasibility and safety study of thrombolytic therapy in acute ischemic stroke, we explored the usefulness of measurements of regional cerebral blood flow.
Twenty-three patients with acute ischemic stroke were treated with 100 mg recombinant tissue plasminogen activator infused intravenously over 1 hour. Thrombolytic therapy was initiated 78 to 355 minutes after onset of symptoms.
Angiography 16 to 24 hours after treatment in 17 patients showed patient intracranial arteries in 12, partial occlusion of the middle cerebral artery in 3, and total occlusion of the middle cerebral artery in 2. rCBF with 99mTc-hexamethylpropyleneamine oxime intravenously was measured 5 minutes before and within 24 hours after thrombolytic therapy in 12 patients. 10 of the 12 patients showed brain tissue reperfusion and 2, with angiographically documented middle cerebral artery occlusion, showed no reperfusion, thus documenting a relationship between reperfusion measured by regional cerebral blood flow and angiographic patency (P = .015). Three patients died. Patients who were reperfused within 24 hours (documented by repeated regional cerebral blood flow measurements) showed greater clinical improvement on the Scandinavian Stroke Scale the sooner their thrombolytic therapy was started and the more severe their neurological deficits.
Acute cerebral ischemia can be documented by rCBF measurements without delay of thrombolytic therapy, and repeated rCBF measurements can reveal whether cerebral reperfusion has occurred. In our study, early reperfusion was associated with clinical improvement.
Evidence from comparative investigations that impaired platelet activation is not specific for stroke-prone spontaneously hypertensive rats.
Authors: Klee A , Vater S , Schmid-Schönbein G W , Seiffge D 
Published: June 2011

Platelet behavior of Sprague Dawley (SD), Wistar (WI), Wistar-Kyoto (WKY), spontaneously hypertensive (SHR), and stroke-prone spontaneously hypertensive rats (SHRSP) was studied in vivo to evaluate the importance of hypertension-related hemostatic disorders.
The study was based on the model of stimulus-induced pulmonary microembolization of labeled platelets. After injection of 51Cr-labeled homologous platelets into urethane-anesthetized rats, the organ distribution of the platelets was continuously monitored by gamma detectors. Count rates of two detectors--one placed above the animals' thoraxes (C1), the other above their abdomens (C2)-and the ratio of C1:C2 were calculated. The following platelet activators were applied intravenously: adenosine diphosphate (ADP; 50 micrograms/kg), collagen (100 micrograms/kg), and thrombin (50 IU/kg).
All three substances caused a reversible pulmonary accumulation of the labeled platelets and hence an increase in C1/C2 (delta C1/C2%). ADP induced a shift of 75% in SD, 52% in WI, 32% in WKY, 30% in SHR, and 31% in SHRSP. Thrombin-mediated shift was 79% in SD, 64% in WI, 58% in WKY, 48% in SHR, and 54% in SHRSP. Collagen induced a shift of 85% in SD, 96% in WI, 84% in WKY, 56% in SHR, and 62% in SHRSP.
Because indistinguishable results were observed in both hypertensive strains, we conclude that impaired platelet aggregation is not specific for SHRSP. Hence, it may not primarily be responsible for the increased occurrence of stroke in these animals.
Improved posthypoxic recovery of synaptic transmission in gerbil neocortical slices treated with a calpain inhibitor.
Authors: Hiramatsu K , Kassell N F , Lee K S 
Published: June 2011

Among the various calcium-induced biologic events occurring in hypoxic neurons, activation of the calcium-activated neutral proteinase (calpain) is a likely mediator of neuronal degeneration. In this study, we assessed the protective effects of a calpain inhibitor (Cbz-Val-Phe-H) against hypoxic damage to the neocortex.
An in vitro neocortical slice model from gerbils was used to study the delay to hypoxic depolarization during hypoxia and the recovery of synaptic responses after hypoxia. These responses were examined in control slices and slices treated with Cbz-Val-Phe-H.
The delay to hypoxic depolarization did not differ between treated and control groups. In contrast, synaptic recovery after a fixed period of hypoxia (15 minutes) was significantly improved in the Cbz-Val-Phe-H-treated slices (P < .01). Concentrations of Cbz-Val-Phe-H of 50 mumol/L or greater were significantly more protective than a concentration of 20 mumol/L (P < .01).
The data indicate that calcium-activated proteolysis plays a critical role in hypoxic damage to the neocortex and that calpain inhibitors may be useful therapeutic agents.