bluuebunny/crossref_metadata_2025_split huggingface dataset:
Excitotoxicity affects membrane potential and calmodulin kinase II activity in cultured rat cortical neurons.
Authors: Churn S B , Sombati S , Taft W C , DeLorenzo R J 
Published: June 2011

Glutamate-induced excitotoxicity has been implicated as a causative factor for selective neuronal loss in ischemia and hypoxia. Toxic exposure of neurons to glutamate results in an extended neuronal depolarization that precedes delayed neuronal death. Because both delayed neuronal death and extended neuronal depolarization are dependent on calcium, we examined the effect of glutamate exposure on extended neuronal depolarization and calcium/calmodulin-dependent protein kinase II (CaM kinase II) activity.
Three-week-old cortical cell cultures from embryonic rats were exposed to 500 microM glutamate and 10 microM glycine or to control medium for 10 minutes. Cells were examined for neuronal toxicity, electrophysiology, and biochemical alterations. In one set of experiments, whole-cell current clamp recording was performed throughout the experiment. In a parallel experiment, cortical cultures were allowed to recover from glutamate exposure for 1 hour, at which time the cells were homogenized and CaM kinase II activity was assayed using standard techniques.
Excitotoxic exposure to glutamate resulted in extended neuronal depolarization, which remained after removal of the glutamate. Glutamate exposure also resulted in delayed neuronal death, which was preceded by significant inhibition of CaM kinase II activity. The excitotoxic inhibition of CaM kinase II correlated with neuronal loss, was N-methyl-D-aspartate receptor-mediated, and was not due to autophosphorylation of the enzyme.
Glutamate-induced delayed neuronal toxicity correlates with extended neuronal depolarization and inhibition of CaM kinase II activity. Because inhibition of CaM kinase II activity significantly preceded the histological loss of neurons, the data suggest that modulation of CaM kinase II activity may be involved in the cascade of events resulting in loss of calcium homeostasis and delayed neuronal death.
Possible association of ischemic stroke with phentermine.
Authors: Kokkinos J , Levine S R 
Published: June 2011

Some commonly used anorexiants, including methamphetamine and phenylpropanolamine, have been associated with stroke. Because phentermine is an anorexiant with a chemical structure similar to that of amphetamines, similar side effects might be expected.
Two patients using phentermine (one was also using phendimetrazine) developed ischemic cerebrovascular disease. One suffered a cerebral infarct with angiographic evidence of vasculopathy involving multiple vascular beds. The other patient developed headache and a hemisensory disturbance of 7 days' duration.
Phentermine, and possibly phendimetrazine, should be considered an anorexiant and sympathomimetic drug that can be associated with ischemic cerebrovascular disease.
Carotid artery intraplaque hemorrhage and stenotic velocity.
Authors: Beach K W , Hatsukami T , Detmer P R , Primozich J F , Ferguson M S , Gordon D , Alpers C E , Burns D H , Thackray B D , Strandness D E 
Published: June 2011

One of the proposed mechanisms for sudden expansion of a carotid bifurcation plaque is hemorrhage within the lesion. It has been postulated that the sudden increase in plaque size will acutely reduce blood flow to the ipsilateral hemisphere and induce either a transient ischemic attack or a stroke. In this study, the relation between peak systolic velocity at the site of narrowing and its potential role in the development of intraplaque hemorrhage were investigated.
Ten patients who had carotid endarterectomy were examined by duplex Doppler sonography before surgery to determine the peak systolic velocity at the site of maximal narrowing. The excised carotid plaques were sectioned at 1-mm intervals and examined for histological evidence of intraplaque hemorrhage. The recorded peak systolic velocities in patients with intraplaque hemorrhage were compared with the velocities in cases in which no hemorrhage was identified.
Five of the ten patients had intraplaque hemorrhage. Four of the five patients with intraplaque hemorrhage had a peak systolic velocity of > 420 cm/sec and diastolic velocities of > 160 cm/sec; none of the patients without intraplaque hemorrhage had such high values.
Peak systolic velocity is significantly higher in patients with intraplaque hemorrhage. The specificity and sensitivity of a peak systolic velocity of > 420 cm/sec in predicting intraplaque hemorrhage remains to be determined.
Hemodynamic and metabolic effects of flunarizine in experimental subarachnoid hemorrhage in dogs.
Authors: De Ley G , Eechaute W , Strijckmans K , Goethals P , Lemahieu I , Van de Velde E , Weyne J 
Published: June 2011

Cerebral blood flow and oxygen metabolism were measured and a cerebral angiography was performed in dogs with experimental subarachnoid hemorrhage to assess the relation between arterial narrowing (vasospasm) and the fall of blood flow. Cerebral blood volume and the cerebrovascular CO2 reactivity were also measured to estimate the cerebrovascular reserve. Several groups of dogs were treated with flunarizine in different regimens to assess its possible therapeutic effect.
The experiments were performed in the three-hemorrhage canine model for subarachnoid hemorrhage. Cerebral blood flow and cerebral oxygen metabolism were measured in anesthetized (nitrous oxide) dogs using positron emission tomography in combination with the 15O steady-state method. Basilar artery diameter was evaluated by digital subtraction angiography.
In normal dogs, cerebral blood flow, oxygen consumption, and oxygen extraction ratio were 46.4 +/- 9.0 ml/100 ml per minute, 3.65 +/- 0.76 ml/100 ml per minute, and 39.9 +/- 3.4%, respectively; basilar artery diameter was 1.33 +/- 0.25 mm. Repeated subarachnoid blood injection (3 x 5 ml) reduced basilar artery diameter to < 20% of normal (p < 0.01). Cerebral blood flow was reduced by only 25% (p < 0.001); oxygen consumption was preserved at a low normal level by a 29% compensatory increase of the oxygen extraction (p < 0.001). Cerebral blood volume and cerebrovascular CO2 reactivity remained nearly normal. Early (after the first blood injection) peroral treatment with flunarizine (0.5 mg/kg daily) resulted in less severe basilar artery narrowing (56% of normal; p < 0.05 versus untreated). However, this treatment had no effect on cerebral blood flow, blood volume, oxygen consumption, and extraction.
The observed fall of cerebral blood flow in experimental subarachnoid hemorrhage is not related to arterial narrowing but to an increased cerebrovascular resistance at the level of the small parenchymal vessels, and the latter, in contrast to arterial narrowing, is unaffected by flunarizine.
Hydroxyl radical-dependent inactivation of guanylate cyclase in cerebral arterioles by methylene blue and by LY83583.
Authors: Kontos H A , Wei E P 
Published: June 2011

Methylene blue and 6-anilino,5,8-quinolinedione (LY83583) are used extensively to block activation of guanylate cyclase. Both agents generate oxygen radicals. Therefore, it appeared profitable to investigate whether the generation of oxygen radicals by these agents is responsible for the blockade of responses to nitrodilators that act via activation of guanylate cyclase to relax vascular smooth muscle and cause vasodilation.
We tested in anesthetized cats equipped with cranial windows responses to topical application of nitroglycerin, nitroprusside, and adenosine before and during topical application of methylene blue (5 microM). Responses to the vasoactive agents were tested during application of methylene blue after permeabilization of the cell membrane with a detergent to allow methylene blue to enter vascular smooth muscle. Responses were also tested in the presence of superoxide dismutase, catalase, deferoxamine, or dimethyl sulfoxide to scavenge reactive products of oxygen metabolism or to eliminate catalytic iron. In additional experiments we tested the effects of topical application of nitroprusside or adenosine before and after application of LY83583. The responses to the vasoactive agents were also tested in the presence of superoxide dismutase, catalase, or dimethyl sulfoxide in addition to LY83583. We also tested responses to calcitonin gene-related peptide before and in the presence of LY83583 with or without superoxide dismutase.
Methylene blue eliminated the arteriolar dilation in response to nitroprusside and nitroglycerin after permeabilization of the cell membrane with a detergent but not before. The responses to adenosine were unaffected. The blockade induced by methylene blue was reversed by superoxide dismutase, catalase, or dimethyl sulfoxide but not by deferoxamine. LY83583 blocked responses to nitroprusside but not to adenosine. The blockade was eliminated by superoxide dismutase, catalase, or dimethyl sulfoxide. LY83583 blocked the vasodilation induced by calcitonin gene-related peptide. This blockade was reversed by superoxide dismutase.
Methylene blue and LY83583 prevent the activation of soluble guanylate cyclase by nitrodilators or by calcitonin gene-related peptide by generating oxygen radicals. The mediator of this response is the hydroxyl radical. Methylene blue does not enter the vascular smooth muscle of cerebral arterioles unless the cell membrane is permeabilized.
Brain pHi, cerebral blood flow, and NADH fluorescence during severe incomplete global ischemia in rabbits.
Authors: Tomlinson F H , Anderson R E , Meyer F B 
Published: June 2011

The aim of this experiment was to study the serial changes in brain intracellular pH, cerebral blood flow, and the oxidation/reduction level of intramitochondrial nicotinamide adenine dinucleotide fluorescence across the cortical surface during severe incomplete global ischemia.
Reduced nicotinamide adenine dinucleotide fluorescence and brain intracellular pH using the pH-sensitive indicator umbelliferone were measured with in vivo panoramic fluorescence imaging of the cortical surface. Cerebral blood flow was measured with the clearance of both umbelliferone and xenon-133. Fifteen minutes of severe incomplete global ischemia was produced by temporary occlusion of the innominate, left carotid, and subclavian arteries in five fasted New Zealand White rabbits.
Baseline brain intracellular pH was homogeneous over the exposed cortex, measuring 7.00 +/- 0.02, while cerebral blood flow was 48.0 +/- 2.6 ml/100 g/min. During 15 minutes of ischemia, cerebral blood flow measured 6.3 +/- 1.8 ml/100 g/min and brain pH declined to 6.61 +/- 0.02 (p < 0.005); in addition, there were acidotic foci with pH measuring 6.40 +/- 0.10. During reperfusion, there was an initial normalization of brain intracellular pH without an alkaline shift followed by a recurrent cortical acidosis of pH 6.88 +/- 0.06. There was a heterogeneous pattern of fluorescence that increased significantly following 60 minutes of reperfusion, coinciding with a postischemic hypoperfusion. The hypoperfusion was a uniform reduction in cerebral blood flow over the brain's surface, with reductions of 42.5% and 44.2% at 30 and 45 minutes, respectively.
During incomplete global ischemia there is a heterogeneous pattern of brain intracellular pH and reduced nicotinamide adenine dinucleotide changes that do not correlate with changes in cortical blood flow. The acidotic foci that were approximately 0.2 pH units more acidotic than the surrounding cortex may be the result of continued glucose delivery under anaerobic conditions. The degree of reduced nicotinamide adenine dinucleotide fluorescence suggests that the cortex is most vulnerable to metabolic failure after 60 minutes of reperfusion following severe incomplete global ischemia. The heterogeneous pattern of brain intracellular pH and reduced nicotinamide adenine dinucleotide changes suggest that there may be a selective vulnerability of cortical tissue to an ischemic challenge.
Fulminant cerebral infarctions with membranous nephropathy.
Authors: Chaturvedi S 
Published: June 2011

Arterial thromboses, including cerebral infarction, are a rare complication of the nephrotic syndrome.
A 37-year-old woman presented with right upper extremity ischemia, left middle cerebral artery thrombosis, and right cerebellar infarction. She quickly herniated, and postmortem evaluation revealed membranous nephropathy. Increased fibrinogen and decreased free protein S levels were noted.
Membranous nephropathy can lead to rapidly progressive cerebral infarctions, with possible fatality. There is not a unifying hematologic explanation for the strokes seen with nephrotic syndrome.
Evidence for embolization from a posterior cerebral artery thrombus by transcranial Doppler monitoring.
Authors: Diehl R R , Sliwka U , Rautenberg W , Schwartz A 
Published: June 2011

Transcranial Doppler monitoring enables the detection of emboli passing through intracranial arteries. Comparison of the different intracranial vessels with respect to emboli detection can be of use in identifying the source of embolism.
We report the case of a patient with an acute posterior cerebral artery (PCA) infarct on the right side, with evidence for high-degree ipsilateral PCA narrowing on admission. During transcranial Doppler monitoring 3 days later, we found frequent emboli-like signals in the power spectrum of the right PCA distal to the stenosis but not in any other intracranial vessels. Four days later, angiography and transcranial Doppler failed to show PCA narrowing, and transcranial Doppler monitoring of the right PCA showed no further emboli-like signals. A stenosis of the right vertebral artery was regarded as the possible source of thromboembolic narrowing of the PCA.
We assume that in our patient a thrombotic clot in the PCA was resolved autolytically through detachment of small emboli into the distal part of the PCA. We speculate that in the early course of autolysis a larger fragment of the clot had occluded one of the distal branches, thus leading to the small PCA territory infarct.
Current role of electroencephalography in cerebral ischemia.
Authors: Faught E 
Published: June 2011

The electroencephalogram has been largely supplanted by neuroimaging techniques for the diagnosis and localization of ischemic stroke. However, because of its close correlation with cerebral metabolism and its ability to detect brief transient alterations in cortical function, the electroencephalogram may still be useful for certain diagnostic applications in stroke.
The relation of electroencephalographic phenomena to cerebral blood flow and metabolism is reviewed. Ten clinical questions that can be addressed by the electroencephalogram in patients with stroke are posed. The presence of seizures, confirmation of diagnosis, intraoperative monitoring, and level of consciousness are areas of proven usefulness. The electroencephalogram provides less worthwhile information about the time course, prognosis, and localization of strokes. Computerized techniques are of potential but unproven value.
The electroencephalogram retains a worthwhile place in the evaluation of patients with cerebral ischemia when it is used to answer specific questions. All patients with strokes do not need electroencephalograms, but the test can provide uniquely useful data in some.
Intracellular pH during reperfusion influences evoked potential recovery after complete cerebral ischemia.
Authors: Maruki Y , Koehler R C , Eleff S M , Traystman R J 
Published: June 2011

Increasing ischemic duration delays recovery of intracellular pH and depresses recovery of somatosensory evoked potentials. We tested whether manipulation of the rate of pH recovery influences evoked potential recovery after complete ischemia.
Four groups of eight anesthetized dogs underwent 12 minutes of complete ischemia followed by 4 hours of reperfusion with either 1) normocapnia, 2) normocapnia and acetazolamide (25 mg/kg at reperfusion plus 12.5 mg/kg per hour, 3) hypocapnia, or 4) hypercapnia. Intracellular pH was measured by phosphorus magnetic resonance spectroscopy, and intracellular bicarbonate was calculated using sagittal sinus partial pressure of CO2 during reperfusion.
In the normocapnic control group, intracellular pH decreased from 7.10 +/- 0.04 (+/- SEM) to 6.13 +/- 0.08 during ischemia and recovered to 6.90 +/- 0.08 by 30 minutes of reperfusion. Bicarbonate also largely recovered (9.9 +/- 1.6 mM). With acetazolamide pH (6.51 +/- 0.10) and estimated bicarbonate (4.8 +/- 1.3 mM) remained depressed at 30 minutes and did not fully recover until 60-75 minutes. However, percent recovery of somatosensory evoked potential amplitude at 4 hours of reperfusion was less with acetazolamide (23 +/- 4%) than in the control group (52 +/- 5%). With hypercapnic reperfusion, which delayed pH recovery but not bicarbonate recovery, evoked potential recovery was also depressed (27 +/- 5%). With hypocapnic reperfusion, which delayed bicarbonate recovery but not pH recovery, evoked potential recovery (52 +/- 6%) was not depressed compared with controls. Recovery of adenosine triphosphate and oxygen consumption was similar among groups.
Delayed recovery of intracellular pH with or without delayed recovery of bicarbonate during reperfusion further impairs somatosensory evoked potential recovery independent of recovery of high-energy phosphates. Persistence of acidosis during reperfusion can contribute to postischemic electrophysiological deficit.
Effects of dimethylthiourea on selective neuronal vulnerability in forebrain ischemia in rats.
Authors: Pahlmark K , Folbergrová J , Smith M L , Siesjö B K 
Published: June 2011

Attempts have been made to characterize conditions under which oxygen free radicals contribute to ischemic brain damage. According to one hypothesis, free radicals are likely mediators of damage only when ischemia is of such long duration that infarction develops or when either preischemic hyperglycemia or hyperthermia is present. The objective of the present study was to explore whether 15 minutes of forebrain ischemia, an insult that leads to selective neuronal vulnerability but not to infarction, is accompanied by production of pathogenetically important free radicals.
Using a histopathological end point, we studied amelioration of damage by a free radical scavenger, dimethylthiourea, administered in a dose of 750 mg/kg i.p. 60 minutes before ischemia. To study whether this insult leads to detectable protein oxidation we assessed the activity of glutamine synthetase and of carbonyl compounds in the soluble protein fraction.
In control animals, the transient ischemia resulted in the expected damage to vulnerable neurons in hippocampus, caudoputamen, and neocortex after 7 days of recovery. Glutamine synthetase activity in caudoputamen and hippocampus and carbonyl content in the soluble protein fraction after 90 minutes of recovery were not affected. However, dimethylthiourea significantly reduced damage to hippocampus and caudoputamen (p < 0.001) and neocortex (p < 0.005).
Lack of evidence of protein oxidation supports the notion that 15 minutes of forebrain ischemia results in a limited insult, confined to the neurons. Provided that unspecific effects can be excluded, the results obtained with dimethylthiourea suggest that free radicals contribute to selective neuronal necrosis.
Acute ischemic stroke from fibrocartilaginous embolism to the middle cerebral artery.
Authors: Toro-González G , Navarro-Román L , Román G C , Cantillo J , Serrano B , Herrera M , Vergara I 
Published: June 2011

Fibrocartilaginous embolism from the nucleus pulposus has been reported as a rare cause of spinal cord ischemia. We were unable to find previous reports of embolism from this source to cerebral arteries.
A previously healthy 17-year-old girl fell during a basketball game. Left hemiparesis and unresponsiveness developed followed by signs of right uncal herniation and death over a 3-day period. There was no evidence of neck, head, or spine trauma, and cardiac evaluation was normal. Neuropathological examination showed extensive ischemic infarction of the right middle cerebral artery territory, brain edema, and herniation. Complete embolic occlusion of the right middle cerebral artery by fibrocartilaginous material, consistent with nucleus pulposus, was documented. Small, terminal coronary artery branches also showed embolism by the same material and limited areas of myocardial infarction.
Acute cerebral embolism after minor trauma in a young patient may be rarely due to fibrocartilaginous embolism from the nucleus pulposus. The pathogenesis of this problem remains poorly understood, but systemic embolism appeared to have occurred in this case.
Denial of illness in stroke.
Authors: Ellis S J , Small M 
Published: June 2011

The effects of stroke on classically nondominant hemisphere functions have received less attention than those on the dominant hemisphere, but visuospatial neglect and denial of illness both produce significant morbidity.
The early literature on denial of illness is discussed and the etiological theories are examined. These are explanations based on deficits of higher mental function, impaired sensory input (especially proprioceptive), an abnormal representation of body image, psychodynamic defense mechanisms, and/or premorbid personality factors.
Denial of illness is an important consequence of stroke. No explanation thus far proposed is entirely satisfactory. The consequences on rehabilitation and strategies for therapy have not been adequately investigated.
Alteration of serum pituitary hormone levels in postmenopausal women with stroke.
Authors: Pepper G M , Koenigsberg R , Zito J L , Deutsch S 
Published: June 2011

The aim of this study was to determine if circulating levels of pituitary hormones are altered by stroke and, if so, whether these alterations offer insight into specific neurochemical pathways in the region of the central nervous system injury.
Twenty-eight consecutive postmenopausal women undergoing computed tomographic imaging of the brain for evaluation of clinical evidence of stroke underwent blood sampling for determination of serum levels of luteinizing hormone, follicle-stimulating hormone, thyroid-stimulating hormone, triiodothyronine, prolactin, estradiol, and sex hormone--binding globulin.
In stroke involving the caudate, serum levels of luteinizing hormone and follicle-stimulating hormone were reduced to 16% and 24% of concentrations found in those with stroke outside of the basal ganglia (p < 0.03 and p < 0.01, respectively). Levels of estradiol, sex hormone-binding globulin, thyroid-stimulating hormone, and prolactin were similar in all stroke groups. Nonspecific biochemical effects of stress that might influence hormone concentrations were assessed by measurement of serum triiodothyronine, the level of which is a sensitive biochemical correlate of disease severity. These levels were not different between stroke groups.
Stroke involving the caudate nucleus may interrupt neurotransmitter pathways involved in control of secretion of gonadotropins. Peripheral levels of these hormones may serve as a marker for central neurochemical disturbances associated with stroke in specific brain regions.
Spinal infarction. A follow-up study.
Authors: Pelser H , van Gijn J 
Published: June 2011

Ten patients with spinal cord infarction were followed up after 1 to 27 (median, 3) years to establish the sequelae of the disease in the long term.
Eight surviving patients were interviewed about mobility, pain, and activities of daily living. All 8 patients had residual weakness in the legs; 7 of them were able to live at home without professional help. All but 1 suffered from continuous pain, which was not dependent on the degree of weakness.
Motor function had improved to some extent in all patients, but pain is a disabling feature in the long term.