bluuebunny/crossref_metadata_2025_split huggingface dataset:
Tactile extinction and functional status after stroke. A preliminary investigation.
Authors: Rose L , Bakal D A , Fung T S , Farn P , Weaver L E 
Published: June 2011

Research has identified a number of factors associated with poststroke recovery, but the prediction of long-term functional outcome remains an uncertain endeavor. In previous work, extinction to tactile, double-simultaneous stimulation has been shown to have short-term predictive utility. The present study was designed to examine its long-term prognostic value and to determine the relative importance of tactile extinction, cognitive functioning, and visual neglect as predictors of poststroke functional status.
Successive admissions to an acute-care facility (n = 26) were assessed three times: 1 month, 3.5 months, and 6 months after stroke. Hierarchical multiple regression, a procedure that maximizes the effect of the variables first entered, was used to predict functional status. Cognitive functioning and visual neglect were forced into the equation on the first step; tactile extinction was entered on the second step. Multivariate analysis of variance was used to compare the functional status of subjects with no extinction versus those who demonstrated extinction at the first assessment and later improved and those who continued to manifest the deficit.
Tactile extinction on the left-hand side of the body was the most important predictor of functional outcome. A significant group-by-time interaction implied that the course of improvement in functional status differed between the groups.
Tactile extinction shows promise as a predictor of poststroke functional status, but further work is required to substantiate the present findings.
Effect of graded hypothermia (27 degrees to 34 degrees C) on behavioral function, histopathology, and spinal blood flow after spinal ischemia in rat.
Authors: Marsala M , Vanicky I , Yaksh T L 
Published: June 2011

We used a rat model of reversible spinal ischemia to assess the effect of spinal cord temperature on the development of neurological and histopathologic changes after 20 minutes of reversible aortic occlusion. Spinal cord blood flow and CO2 reactivity was tested by using laser Doppler before and 60 minutes after ischemia.
In halothane (1%)-anesthetized rats, the spinal cord temperature as assessed by using thermocouple in the paraspinal muscles was lowered to 34 degrees, 31 degrees, or 27 degrees C. After ischemia, spinal cord temperature was raised to 37 degrees C for the next 30 minutes. Animals were maintained in this normothermic condition for 8 hours, after which motor and sensory function were assessed. All animals were then anesthetized and perfused with 10% formalin for light microscopic analysis of spinal cords.
In normothermic animals, 20 minutes of ischemia resulted in a loss of CO2 reactivity and hind limb paraplegia with an attendant allodynia that persisted for the 8 hours of reperfusion. Even mild (34 degrees C) hypothermia resulted in significant improvement of neurological function compared with the normothermic group. In paraplegic animals, lumbosacral interneuronal pools localized primarily in laminae III through VII displayed heavy argyrophilic neurons and areas of localized necrosis. In moderate and deep hypothermic animals preservation of CO2 responsivity and complete recovery of neurological function were seen with no detectable histopathologic changes.
These results show that a slight decrease in spinal cord temperature in the peri-ischemic period provides significant protection as measured by histopathology and neurological function.
A long-half-life and fibrin-specific form of tissue plasminogen activator in rabbit models of embolic stroke and peripheral bleeding.
Authors: Thomas G R , Thibodeaux H , Errett C J , Badillo J M , Keyt B A , Refino C J , Zivin J A , Bennett W F 
Published: June 2011

We compared the activity of a new long-half-life, fibrin-specific tissue-type plasminogen activator (TPA) variant with that of wild-type TPA in rabbit models of embolic stroke and peripheral bleeding.
In the embolic stroke model. TPA-induced clot lysis is followed by continuous monitoring of a radiolabeled clot lodged in the middle cerebral artery. Twenty-four hours after embolization and treatment with either thrombolytic agent or excipient, the brains are removed, fixed, and evaluated for cerebral hemorrhage. In a parallel template bleeding time experiment, the effects of equipotent doses of the two TPA molecules were measured.
Infusion of wild-type TPA or bolus administration of the TPA variant resulted in dose-dependent clot lysis. The TPA variant was found to be an order of magnitude more potent than wild-type TPA on a milligram-per-kilogram basis. Unlike wild-type TPA, the variant caused less systemic activation of plasminogen (P < .05) and fewer hemorrhagic transformations in this model (P < .05). The TPA variant did not extend template bleeding times.
These findings show that by combining increased fibrin specificity with decreased plasma clearance, it is possible to produce a thrombolytic agent that is more convenient and more potent than wild-tpe TPA. At the same time the significant reduction in hemorrhagic conversions may be attributable to the conservation of systemic plasminogen seen with this molecule.
Modification of platelet aggregation by leukocytes in acute ischemic stroke.
Authors: Grau A J , Sigmund R , Hacke W 
Published: June 2011

Platelet aggregation plays an important role in the pathogenesis of thromboembolic cerebrovascular disease. Leukocytes can efficiently stimulate as well as inhibit platelet aggregability. We studied the influence of leukocytes on collagen-induced platelet aggregation in patients with acute ischemic stroke.
We investigated 23 patients within 2 days after stroke and 23 healthy age- and sex-matched control subjects and determined collagen-induced platelet aggregation in platelet-rich plasma with or without addition of polymorphonuclear or mononuclear leukocytes.
Platelet aggregation without leukocytes tended to be lower in patients than in control subjects (P = .06). Mononuclear leukocytes reduced (P = .018) and polymorphonuclear leukocytes tended to reduce (P = .06) platelet aggregation in patients. Leukocytes did not significantly alter platelet aggregation in control subjects. In the presence of either mononuclear or polymorphonuclear leukocytes, platelet aggregation was significantly lower in patients than in control subjects (P = .004 and P = .008). The ratio of polymorphonuclear leukocytes to platelets in venous blood was higher in patients than in control subjects (P < .001).
Mononuclear--and less clearly polymorphonuclear-leukocytes possess a platelet aggregation-inhibiting potential in the early stages after ischemic stroke, a feature with possible antithrombotic effects.
Alterations in plasma concentrations of natriuretic peptides and antidiuretic hormone after subarachnoid hemorrhage.
Authors: Isotani E , Suzuki R , Tomita K , Hokari M , Monma S , Marumo F , Hirakawa K 
Published: June 2011

Hyponatremia is a common complication after subarachnoid hemorrhage. In this study we investigated the relations among hyponatremia, plasma natriuretic peptides, and antidiuretic hormone concentrations after subarachnoid hemorrhage.
Blood samples for radioimmunoassay measurement of plasma brain natriuretic peptide-like immunoreactivity, atrial natriuretic peptide-like immunoreactivity, and antidiuretic hormone were obtained every 2 to 4 days until day 14 after subarachnoid hemorrhage.
Eleven of 20 patients with verified subarachnoid hemorrhage demonstrated mild hyponatremia (126 mEq/L < serum sodium < 135 mEq/L) during their clinical course. Atrial natriuretic peptide and antidiuretic hormone concentrations were significantly elevated on days 0 to 2 after onset of subarachnoid hemorrhage. Atrial natriuretic peptide concentrations remained high in patients who developed mild hyponatremia on days 6 to 14 after onset of subarachnoid hemorrhage. In contrast, antidiuretic hormone concentrations became significantly lower during the second week in these patients.
Mild hyponatremia after subarachnoid hemorrhage may be attributable not to the syndrome of inappropriate secretion of antidiuretic hormone but to cerebral salt-wasting syndrome. Atrial natriuretic peptide may be a causal natriuretic factor in cerebral salt-wasting syndrome.
Leukocyte-induced acute endothelial dysfunction in middle cerebral artery in rabbits. Response to aggregating platelets.
Authors: Akopov S E , Sercombe R , Seylaz J 
Published: June 2011

Recent evidence suggests a possible role for leukocytes in angiospastic reactions of large cerebral arteries. This study examined the effect of activation of endogenous circulating leukocytes on endothelium-dependent relaxation in the middle cerebral artery in rabbits.
Leukocytes were activated by rapid injection of either 40 micrograms/kg phorbol 12-myristate 13-acetate, or 0.2 mg/kg N-formyl-methionyl-leucylphenylalanine into the left carotid artery. Control rabbits received an equal volume of vehicle. Concentration-dependent isometric tension responses of the left and right middle cerebral artery to the dilators acetylcholine, ADP, sodium nitroprusside, or calcium ionophore (A23187), as well as to aggregating platelets, were compared in vitro in control animals and in animals killed 10 minutes after the injection of leukocyte activators in normal and leukocyte-depleted rabbits.
In the control animals there was no significant difference in the reactivity of the left and right middle cerebral arteries. The injection of the leukocyte activators led to enhanced contractile responses to aggregating platelets and a significant reduction in the endothelium-dependent relaxation in response to acetylcholine, ADP, and A23187 in the left middle cerebral artery (the injected side), whereas the effect of an endothelium-independent dilator sodium nitroprusside remained unchanged. In leukocyte-depleted rabbits the injection of either of the leukocyte activators used did not induce significant changes in the reactivity of the left middle cerebral artery.
Intravascular leukocyte activation appears to induce an acute disturbance of the endothelium-dependent relaxation. Under these conditions, platelet activation might result in marked angiospastic reactions of large cerebral arteries.
Calpain inhibitor AK295 protects neurons from focal brain ischemia. Effects of postocclusion intra-arterial administration.
Authors: Bartus R T , Hayward N J , Elliott P J , Sawyer S D , Baker K L , Dean R L , Akiyama A , Straub J A , Harbeson S L , Li Z 
Published: June 2011

This research was performed to determine whether a selective inhibitor of the calcium-dependent protease, calpain, could reduce ischemia-associated brain damage when peripherally administered after a vascular occlusion.
A variation of the rat middle cerebral artery occlusion model was used. A range of doses of AK295 (a novel calpain inhibitor synthesized for this purpose) was continuously infused through the internal carotid artery, beginning 1.25 hours from the initiation of the occlusion. Rats were killed at 21 hours, and the infarct volume was quantified.
Postocclusion (1.25-hour) infusion of the calpain inhibitor AK295 elicited a dose-dependent neuroprotective effect after focal ischemia. The highest dose tested (3 mg/kg per hour) afforded the maximum effect, illustrated by a 32% reduction in infarct volume 21 hours after the ischemia (vehicle, 81.7 +/- 4.7 mm3; AK295, 54.9 +/- 6.9 mm3; P < .007).
These data provide the first evidence that a peripherally administered calpain inhibitor can protect against ischemic brain damage. They offer further support for an important role of calpain proteolysis in the brain degeneration associated with cerebral ischemic events and suggest that selective calpain inhibitors provide a rational, novel, and viable means of treating such neurodegenerative problems.
Very early demonstration of secondary pyramidal tract degeneration by computed tomography.
Authors: Kazui S , Kuriyama Y , Sawada T , Imakita S 
Published: June 2011

While magnetic resonance imaging has revealed progressive changes in the pyramidal tract in accordance with histopathologic stages of wallerian degeneration secondary to a supratentorial lesion, computed tomography (CT) has only demonstrated a shrinkage of the pyramidal tract in the midbrain or pons during the chronic stage. We present a patient with frontoparietal subcortical hemorrhage in whom serial CT scans clearly demonstrated wallerian degeneration along the axis of the pyramidal tract early in the acute stage.
A 63-year-old man with a history of hypertension suddenly developed a deterioration of consciousness, transcortical mixed aphasia, and dense hemiplegia on the right side. CT scans revealed a massive intracerebral hematoma in the frontoparietal subcortices of the left hemisphere. Although initial CT did not detect any hypodense areas along the left pyramidal tract below the hematoma, ill-defined areas of decreased density appeared in the posterior limb of the internal capsule, cerebral peduncle of the midbrain, and pontine base of the left side on day 13 after the stroke. These areas became well demarcated on day 22 and persisted thereafter.
An extensive hematoma can interrupt the pyramidal tract fibers that arise not only from the motor cortex and caudal premotor cortex but also from the somatosensory and parietal cortices, allowing very early CT demonstration of wallerian degeneration of the pyramidal tract.
Cerebral emboli detected during bypass surgery are associated with clamp removal.
Authors: Barbut D , Hinton R B , Szatrowski T P , Hartman G S , Bruefach M , Williams-Russo P , Charlson M E , Gold J P 
Published: June 2011

Transcranial Doppler ultrasonography detects embolic signals during coronary artery bypass surgery. The relationship between embolization and specific events of bypass surgery is unclear.
With this technique, 20 patients undergoing bypass surgery were continuously monitored from inception to discontinuation of bypass.
Embolic signals were detected in all patients. Of all embolic signals, 34% were detected as aortic cross-clamps were removed, and another 24% as aortic partial occlusion clamps were removed. Only 5% were detected at inception of bypass. Rates for embolization were 15.15 embolic signals per minute at cross-clamp removal, 10.9 embolic signals per minute at partial occlusion clamp removal, and fewer than 3 embolic signals per minute at other times. Correlation was found between the number of emboli, severity of aortic atheromatosis, and neurocognitive deterioration.
The majority of emboli detected during coronary artery bypass grafting are associated with the release of clamps. Clamp manipulation may lead to release of aortic atheromatous debris. These emboli may be relevant to neurocognitive outcome.
Neuroprotective effects of tetrodotoxin as a Na+ channel modulator and glutamate release inhibitor in cultured rat cerebellar neurons and in gerbil global brain ischemia.
Authors: Lysko P G , Webb C L , Yue T L , Gu J L , Feuerstein G 
Published: June 2011

Studies examining the role of tetrodotoxin-sensitive ion channels in hypoxic-ischemic neuronal damage have concluded that sodium influx is an important initiating event. We examined the neuroprotectant effect of tetrodotoxin on both cultured cerebellar neurons and on CA1 hippocampal neurons of gerbils exposed to brain ischemia.
We studied neuroprotective mechanisms using cultured rat cerebellar granule cells exposed to veratridine, which induced cytotoxicity, neurotransmitter release, and calcium influx. Survival of gerbil CA1 neurons was examined by direct neuron counts 7 days after 6 minutes of global ischemia with reperfusion.
Tetrodotoxin protected cultured neurons in a dose-dependent manner from veratridine-induced toxicity (protective concentration [PC50] = 22 nmol/L). Veratridine induced [3H]aspartate efflux that was sodium dependent, only 25% calcium dependent, and was inhibited by tetrodotoxin (inhibitory concentration [IC50] = 60 nmol/L). Veratridine initiated increases in intracellular calcium that were also reversed by tetrodotoxin (IC50 = 63 nmol/L); reversal was dependent on the sodium-calcium exchanger and the sodium-potassium pump. Neuroprotection of 90% (n = 10; P = .001 versus vehicle) of gerbil CA1 hippocampal neurons was achieved by pretreatment with 2 ng of tetrodotoxin delivered three times intracerebroventricularly, without causing hypothermia.
Sodium channel blockers like tetrodotoxin may have utility in treatment of ischemic neuronal injury by preventing excessive neuronal depolarizations, limiting excitotoxic glutamate release through reversal of the sodium-dependent glutamate transporter, preventing intracellular calcium overload, preserving cellular energy stores, and allowing recovery of ionic homeostasis through operation of the sodium-calcium exchanger.
Restricted acral sensory syndrome following minor stroke. Further observation with special reference to differential severity of symptoms among individual digits.
Authors: Kim J S 
Published: June 2011

Restricted acral sensory syndrome (RASS) after minor stroke most often manifests as a cheiro-oral syndrome. However, recent studies have described more varied patterns of RASS and also have reported that the degree of sensory symptoms may vary among individual digits. Until recently, however, there have been no reports in which sufficient numbers of patients were studied with detailed information on the symptomatic severity among individual digits.
In this report, I describe 30 patients presenting with RASS secondary to minor stroke. Computed tomographic scan and/or magnetic resonance imaging identified lesions in the lateral thalamus in 11, midbrain in 2, pontine tegmentum in 8, capsulo-corona radiata in 5, and frontoparietal subcortical-cortical areas in 4 patients. The patterns of RASS were cheiro-oral in 10, cheiro-oral-pedal in 8, cheiro-pedal in 4, restricted to palm and/or fingers in 7, and periotal-pedal in 1. Dominant involvement of upper lip, thumb, and index finger was frequent, especially in patients with thalamic and thalamocortical lesions. In patients with cortical-subcortical lesions, cheiro-oral or restricted finger involvements were observed, while the foot was spared. In patients with pontine lesions, bilateral RASS was occasionally observed, and the pattern of preponderant involvement of the first two digits was not apparent.
These patterns of RASS generally agree with the previously observed sensory topography of monkeys, and they support anatomic proximity of sensory fibers from acral parts of the body. However, other mechanisms such as differential vulnerability of generation of paresthesia in different body parts or a low-threshold concept based on disproportionately large representing areas for the acral parts of the body in the human sensory system may also be required to explain some of the clinical observations.
Evaluation of risk of hemorrhagic transformation in local intra-arterial thrombolysis in acute ischemic stroke by initial SPECT.
Authors: Ueda T , Hatakeyama T , Kumon Y , Sakaki S , Uraoka T 
Published: June 2011

Thrombolytic therapy was carried out on patients with acute ischemic stroke, and the risk of hemorrhagic transformation was evaluated from the residual cerebral blood flow (CBF) by pretherapeutic single-photon emission-computed tomography (SPECT).
Local intra-arterial thrombolytic therapy was carried out using urokinase or recombinant tissue plasminogen activator (rt-PA) within 6 hours from the onset in 34 patients in whom no hypodensity areas were observed on the initial computed tomography examination. In the 20 patients with carotid territory occlusion who underwent 99mTc-labeled hexamethylpropyleneamine oxime (99mTc-HMPAO) SPECT, the residual CBF of the ischemic region was evaluated semiquantitatively by calculating two parameters: the ischemic regional activity to cerebellar activity ratio (R/CE ratio) and asymmetry index (AI).
The occluded vessels could be recanalized in 22 (92%) of the 24 patients in the urokinase group and in all 10 of the patients in the rt-PA group. Hemorrhagic transformation appeared in 4 patients in the urokinase group and 3 patients in the rt-PA group. Among the 20 patients who underwent SPECT before the treatment, the residual CBF was lower in the 5 patients who developed hemorrhagic transformation than in the 15 who did not (P < .05). Hemorrhagic transformation occurred in all patients with R/CE ratio of less than 0.35 and AI of more than 1.5.
The risk of hemorrhagic transformation after recanalization of occluded vessels by local intra-arterial thrombolytic therapy was considered to be high when the pretherapeutic residual CBF was markedly reduced.
Fish consumption and risk of stroke. The Zutphen Study.
Authors: Keli S O , Feskens E J , Kromhout D 
Published: June 2011

A low-to-moderate average daily fish consumption has been reported to convey protection against coronary heart disease incidence and mortality. Currently there is no information about its effect on stroke risk.
In 1960, 1965, and 1970 cross-check dietary histories were obtained in 552 men aged 50 to 69 years in 1970 in the town of Zutphen, The Netherlands. The association between fish consumption and stroke incidence in the period 1970 to 1985 was assessed by Cox proportional hazards models. Adjustments were made for confounding by age, systolic blood pressure, cigarette smoking, serum total cholesterol, energy intake, alcohol consumption, and prescribed diet.
The mean fish consumption in 1970 was 17.9 g/d. Men who consumed more than 20 g of fish per day in 1970 had a reduced risk of stroke compared with those who consumed less fish. The hazard ratio (HR) amounted to 0.49 (95% confidence interval [CI], 0.24 to 0.99), and did not change after adjustment for potential confounders. Fewer strokes occurred among the 301 men who always reported fish consumption between 1960 and 1970 than among the men who changed fish consumption habits between 1960 and 1970 or did not consume fish at all (HR, 0.63; 95% CI, 0.34 to 1.16).
These results suggest that consumption of at least one portion of fish per week may be associated with a reduced stroke incidence.
Changes in blood flow velocity in the middle cerebral artery during nonpulsatile hypothermic cardiopulmonary bypass.
Authors: Endoh H , Shimoji K 
Published: June 2011

We evaluated the utility of blood flow velocity measurements by transcranial Doppler ultrasonography as a tool to indirectly measure cerebral perfusion during cardiopulmonary bypass.
We simultaneously measured blood flow velocity in the middle cerebral artery and physiological variables in 18 patients undergoing cardiac surgery under hypothermic cardiopulmonary bypass in which pH and PaCO2 were managed with the alpha-stat acid-base strategy. We expressed blood flow velocity as a relative value of control obtained under normothermia and normocarbia before bypass. We also developed an original index, modified cerebral metabolic rate for oxygen, to estimate cerebral metabolic rate for oxygen.
Relative velocity was significantly (P < .01) reduced during stable aortic cross-clamp compared with before bypass and was significantly (P < .01) increased during rewarming compared with at aortic cross-clamp. Modified cerebral metabolic rate for oxygen significantly correlated with nasopharyngeal temperature during cooling, aortic cross-clamp, and rewarming (r = .756, P < .0001; r = .4, P < .01; r = .725, P < .0005, respectively). Calculated temperature coefficient for modified cerebral metabolic rate of oxygen was 2.7 +/- 1.4 (mean +/- SD, n = 10) during cooling. Only nasopharyngeal temperature and PaCO2 were significant determinants of relative velocity during aortic cross-clamp.
We can monitor cerebral perfusion and metabolism by measurements of relative velocity and modified cerebral metabolic rate for oxygen during hypothermic cardiopulmonary bypass.