bluuebunny/crossref_metadata_2025_split huggingface dataset:
Assessment of scales of disability and handicap for stroke patients.
Authors: Wolfe C D , Taub N A , Woodrow E J , Burney P G 
Published: June 2011

The purpose of the study is to compare the reliability of the Barthel activities of daily living score, which assesses disability, with the Rankin scale, which assesses handicap, and to determine their mutual agreement.
Fifty patients with stroke of varying severity were identified by a community-based stroke register and interviewed by two of three research nurses on two occasions that were 2-3 weeks apart.
There was no evidence of a systematic difference between the first and second measurements. Repeatability was assessed using a kappa statistic with quadratic disagreement weights (kappa w) to take account of extreme differences. This measure was very good for both Barthel (kappa w = 0.98) and Rankin (kappa w = 0.95) scales. There was also excellent agreement between raters for the Barthel scale (kappa w greater than or equal to 0.88), but some indication of disagreement (kappa w = 0.75) between raters for the Rankin scale. Analysis of variance confirmed these findings. A conversion from the Barthel to the Rankin scale can be derived by assigning the most common Rankin score for the subjects with a given Barthel score, producing a kappa w of 0.91 for agreement.
The Barthel scale is a more reliable and less subjective scale for assessing disability, from which a Rankin handicap score can then be derived to enable those managing stroke patients to assess aspects of handicap as well as disability.
Polymorphonuclear leukocytes occlude capillaries following middle cerebral artery occlusion and reperfusion in baboons.
Authors: del Zoppo G J , Schmid-Schönbein G W , Mori E , Copeland B R , Chang C M 
Published: June 2011

Microvascular perfusion defects may accompany sustained occlusion and subsequent reperfusion of the middle cerebral artery; however, the nature of such "no-reflow" defects remains unclear.
In the absence of antithrombotic pretreatment, we documented lenticulostriatal microvascular flow integrity following 3-hour middle cerebral artery occlusion and 1-hour reperfusion in a baboon occlusion/reperfusion model by two methods identifying 1) microvascular occlusion and 2) microvascular patency.
Microvascular "no-reflow" involved capillaries (vessels of 4.0-7.5 microns diameter) of the lenticulostriatal territory. Capillary reflow included 27-39% of all capaillaries in two subjects, indicating a significant reduction of perfusion from normal (2p = 0.045). In identical experimental preparations, single polymorphonuclear leukocytes completely occluded 4.7% of microvessels of capillary diameter in randomly selected fields, partially occluded 3.5% of postcapillary venules, and occluded 40% (four of 10) of capillaries in linear reconstruction along a 110 microns length. Circumferential contact between polymorphonuclear leukocytes and the luminal endothelial cell membranes was documented, with an intrecellular gap of, at most, 160 nm. Fibrin was found with degranulated platelets when the latter were associated with granulocytes, but not with polymorphonuclear leukocytes alone.
The finding of capillary-obstructing polymorphonuclear leukocytes in the microvascular bed following middle cerebral artery reperfusion in focal ischemia in this model satisfies an essential requirement for postulating their role in early microvascular injury and the "no-reflow" phenomenon.
Autosomal dominant syndrome with strokelike episodes and leukoencephalopathy.
Authors: Tournier-Lasserve E , Iba-Zizen M T , Romero N , Bousser M G 
Published: June 2011

We conducted a prospective survey of a family presenting a new syndrome characterized mainly by recurrent strokelike episodes and neuroimaging evidence of leukoencephalopathy.
Forty-five members of a single family were studied clinically and with magnetic resonance imaging. Nine had strokelike episodes, including transient ischemic attacks, and minor or major strokes starting between the fourth and sixth decades, with neuroimaging evidence of small, deep infarcts and a widespread white matter disorder. Other symptoms included migraine (three), dementia (two), epilepsy (one), and hearing loss (one). In some patients, we found various immunologic anomalies and muscular lipidosis without ragged-red fibers. Eight other family members were clinically normal, but had identical neuroimaging signs of leukoencephalopathy. No abnormality was detected in the 28 other members of the family examined. Extensive investigations failed to reveal any known cause of cerebral ischemia.
There appears to be a new syndrome in this family that is characterized by recurrent subcortical strokelike episodes, leukoencephalopathy, immunologic anomalies, muscular lipidosis, and an autosomal dominant pattern of transmission.
A critical appraisal of stroke evaluation and rating scales.
Authors: Lyden P D , Lau G T 
Published: June 2011

To judge the efficacy of new, putative stroke therapies, we need a method to measure neurological deficit accurately in groups of patients before and after treatment. No single measurement technique has yet proven to be universally acceptable, but one approach is the use of rating instruments that summarize the neurological deficit found on clinical examination. Currently, stroke assessment scales may be based on the examination of physical deficits, an inventory of activities of daily living, or a global evaluation of functional outcome.
Scientific methods for authenticating stroke scales are available in the psychometric and statistical literature. We review currently available stroke scales for their validity and reliability and propose investigations needed to refine further the standardized measurement of neurological deficit following stroke.
We suggest that clinical stroke trials include a physical deficit scale and a global rating during the acute phase and that an activities of daily living scale be added at later points in recovery.
Cerebral blood flow and neuropsychological asymmetries in unilateral stroke.
Authors: Brown G G , Ewing J R , Robertson W M , Welch K M 
Published: June 2011

This study sought to determine the degree of agreement between asymmetries of neuropsychological functioning and nine methods of quantifying asymmetries of regional cerebral blood flow.
The regional cerebral blood flow methods combined three markers of cerebral blood flow asymmetry (percent hemispheric difference, maximum percent probe-pair asymmetry, and number of probe-pair asymmetries) with three indexes of regional cerebral blood flow (fast compartment flow, initial slope index, and initial slope). Eleven patients with left hemispheric ischemic strokes and 13 with right hemispheric ischemic strokes were studied with the xenon-133 inhalation technique and neuropsychological tests.
Blind clinical judgments of neuropsychological asymmetry significantly correlated with all nine methods of cerebral blood flow asymmetry determination; correlations ranged from -0.42 to -0.77. Clinical judgment of asymmetry of neuropsychological functioning accurately predicted the hemisphere of lower flow in 71-92% of cases, depending on the method of cerebral blood flow asymmetry determination. Agreement between cerebral blood flow and neurobehavioral signs of asymmetry was greater for initial slope and initial slope index than for the fast flow index. The initial slope and initial slope index showed equally good agreement. The use of the number of asymmetrical probe pairs to detect cerebral blood flow asymmetries agreed less well with neurobehavioral asymmetry than did the other two markers studied.
Both the initial slope index and the initial slope measures of cerebral blood flow are useful in predicting neuropsychological asymmetries, especially when the magnitude of the asymmetry is taken into account.
Deriving clinical prediction rules from stroke outcome research.
Authors: Hier D B , Edelstein G 
Published: June 2011

Our purpose was to determine whether clinical prediction rules could be derived from current stroke outcome research.
We reviewed 92 articles on stroke outcome research to determine their suitability for implementation as a clinical prediction rule. Methodological problems in many of these studies made implementation of their results as a clinical prediction rule difficult.
Implementation of stroke outcome research as clinical prediction rules would be facilitated by description of patient population demographics; precise definitions of predictor and outcome measures; stratification of patients by stroke mechanism; use of adequate patient sample sizes; and description of the mathematical methods used, including coding schemes, cutpoints, beta coefficients, constant terms, and a priori probabilities.
Lacunar infarctions due to cholesterol emboli.
Authors: Laloux P , Brucher J M 
Published: June 2011

Hypertension is commonly considered the major cause of lacunar infarctions. However, in some cases, it has been suggested that lacunes could be caused by cerebral emboli from cardiac or carotid sources. Cholesterol cerebral emboli have been rarely reported as a cause of lacunes.
We describe a 79-year-old patient with a progressive multi-infarct dementia who developed transient motor aphasia and paresis of the right arm. Computed tomography showed lacunar infarcts in the right caudate nucleus, left thalamus, and left putamen, as well as an old right frontal infarction. Neuropathological examination demonstrated no prominent vascular hyalinosis, but did show multiple cholesterol emboli occluding small arteries around lacunar infarcts and leptomeningeal arteries near cortical infarcts. The cholesterol material presumably originated in the extended atheromatous changes along the aortic arch.
Our report confirms that lacunes can be caused by cholesterol emboli in some patients. Small cerebral emboli should not be overlooked as a cause of lacunes.
Vertebrobasilar ischemia after neck motion.
Authors: Frisoni G B , Anzola G P 
Published: June 2011

Vertebrobasilar ischemic strokes may occur after chiropractic manipulation of the cervical spine or, less often, after spontaneous and abrupt head movement.
We describe three such cases of vertebrobasilar ischemic strokes and review 36 other reported cases.
We give evidence that 1) the population at risk cannot be identified a priori in the vast majority of cases; 2) symptoms may develop after many uneventful manipulations; 3) clinical syndromes consist of occipital lobe (5%), cerebellar (8%), locked-in (8%), Wallenberg's (28%), other brain stem (49%), and unclassifiable (2%); 4) mortality or very severe long-term impairment occurs in 28% of cases; 5) the development of transient neurological symptoms during previous manipulations, the presence of known or suspected ligament laxity, and, if known, the presence of a vertebral artery terminating in posterior inferior cerebellar artery should always contraindicate any chiropractic neck maneuver; and 6) the pathogenetic mechanism involves vertebral artery dissection at the atlantoaxial joint with intimal tear, intramural bleeding, or pseudoaneurysm that can lead to thrombosis or embolism.
Vascular risks of asymptomatic carotid stenosis.
Authors: Norris J W , Zhu C Z , Bornstein N M , Chambers B R 
Published: June 2011

We sought to determine the risks of stroke, myocardial ischemia, and vascular death in patients with asymptomatic carotid stenosis.
Six hundred ninety-six patients with asymptomatic carotid stenosis referred to the Doppler laboratory were followed prospectively for a mean time of 41 months. These patients were studied both clinically and by carotid Doppler ultrasound, including evaluation of the effect of stroke risk factors.
Transient ischemic attacks occurred in 75 patients and stroke in 29, while 132 had ischemic cardiac events. Five patients died from stroke and 59 from cardiac causes. Annual stroke rate was 1.3% in patients with carotid stenosis less than or equal to 75% and 3.3% in those with stenosis greater than 75%. Ipsilateral stroke rate was 2.5% in patients with greater than 75% carotid stenosis. Annual cardiac event rate was 8.3% and death rate 6.5% in patients with severe carotid stenosis.
With carotid stenosis less than or equal to 75%, the stroke rate is negligible (1.3% annually) whereas the combined risk of cardiac ischemia and vascular death is as high as 9.9%. With stenosis greater than 75%, combined transient ischemic attack and stroke rate is 10.5% per year, with 75% of events ipsilateral to the stenosed artery.
Atrial natriuretic factor and salt wasting after aneurysmal subarachnoid hemorrhage.
Authors: Wijdicks E F , Ropper A H , Hunnicutt E J , Richardson G S , Nathanson J A 
Published: June 2011

The causes of volume depletion and hyponatremia after subarachnoid hemorrhage are not fully understood but may be in part due to natriuresis or "cerebral salt wasting." Because previous studies using infrequent hormone sampling have given inconsistent results, we determined if elevations in atrial natriuretic factor concentrations preceded negative sodium and fluid balances.
We measured diurnal atrial natriuretic factor and vasopressin concentrations and sodium balance for 5 days in 14 consecutive patients after aneurysmal subarachnoid hemorrhage.
Plasma concentrations of atrial natriuretic factor on admission were elevated in subarachnoid hemorrhage patients (mean +/- SD 106 +/- 59 pg/ml) compared with acutely ill controls (39 +/- 30 pg/ml). In eight patients, high peak concentrations of atrial natriuretic factor, greater than 300 pg/ml or a twofold increase above baseline, were followed by natriuresis and a negative sodium balance. Three patients, two of whom became hyponatremic, developed cerebral infarcts after natriuresis. Vasopressin concentrations were slightly elevated just after hemorrhage but subsequently declined to normal values.
A markedly increased atrial natriuretic factor concentration precedes natriuresis in some patients and, with other abnormalities of water handling possibly including a relatively diminished vasopressin concentration, may cause volume depletion. Patients with natriuresis appear to be at increased risk for delayed cerebral infarction after subarachnoid hemorrhage.
Residual lesions on computed tomography after intracerebral hemorrhage.
Authors: Franke C L , van Swieten J C , van Gijn J 
Published: June 2011

We investigated the residual abnormalities on computed tomography in a series of patients with proven intracerebral hemorrhage to determine whether the type of lesion is related to the site and size of the initial hematoma.
In a partially prospective follow-up study, we studied computed tomographic scans of 42 patients with spontaneous intracerebral hemorrhage after 2-24 (median 9) months.
Lobar hemorrhages had occurred in 20 patients; the other 22 hemorrhages were in the basal ganglia or thalamus. No residual lesions were found on seven scans (17%), despite residual handicap in three of these seven patients (slight, moderate, and moderately severe). In five cases, the scan showed only focal atrophy, and in two there were only focal calcifications. There were six patients with slit-like lesions (only after deep hemorrhages), 12 with rounded and isolated hypodense areas, and 10 with rounded hypodense areas connected to the ventricular system. The connection between the residual lesion and the ventricular system depended to a large extent on the size of the initial hematoma, but very little on whether it had initially ruptured into the ventricular system.
A retrospective diagnosis of cerebral hemorrhage on radiological grounds can be made with confidence only in a small group of patients with slit-like lesions in the basal ganglia. This diagnosis is impossible in approximately one third of cerebral hemorrhages because the abnormalities are aspecific or have completely disappeared.
Platelets augment rabbit cerebral artery constriction by activating protein kinase C.
Authors: Germann P , Laher I , Bevan J A 
Published: June 2011

We tested the hypothesis that activated platelets augment cerebral artery responsiveness to thrombin by activating protein kinase C, a possible intracellular modulator of Ca2+ sensitivity.
Ring segments of rabbit basilar artery were prepared for in vitro measurements of isometric force. Cumulative concentration-response curves to thrombin were made in the absence or presence of activated platelets.
Arteries contracted to thrombin in a concentration-dependent manner; freshly obtained human platelets (8.5 x 10(8) cells/ml) activated with 10 micrograms/ml collagen increased the arteries' sensitivity to thrombin by threefold while augmenting the maximal response from 40 +/- 11% to 66 +/- 12% of the maximal response to 0.3 mM histamine. At 10 nM, staurosporine, an inhibitor of protein kinase C activity, blunted the platelet-induced augmentation of the response to thrombin but did not alter the sensitivity or the maximal contraction to 8-64 mM K+. Removal of the endothelium did not alter the characteristics of the thrombin concentration-response curve. The addition of activated platelets increased the tissue sensitivity of endothelium-denuded arteries to thrombin by a factor of 30, and the maximal response to thrombin was 101 +/- 27% of the histamine response.
Our findings suggest that amplification of the arterial contractile response to thrombin caused by platelet-derived mediators may be due to activation of protein kinase C. There may also be a protective role for the cerebrovascular endothelium since endothelium reduced the extent of augmentation of protein kinase C-mediated tone by vasoactive agents released by activated platelets. Thus, increased vascular responsiveness caused by activated platelets may in part be due to protein kinase C-mediated changes in the intracellular sensitivity to Ca2+.
Neurochemical analysis of focal ischemia in rats.
Authors: Uemura Y , Miller J M , Matson W R , Beal M F 
Published: June 2011

Increases in uric acid follow experimental stroke, which may be related to free radical formation by xanthine oxidase. The present study examined the time course of changes in xanthine and uric acid and their relationship to changes in the free radical scavengers glutathione, cysteine, and ascorbic acid.
Focal ischemia was induced by occluding the middle cerebral artery, followed by transient occlusion of the common carotid arteries for 60 minutes. At varying time points, animals were sacrificed, and ischemic cortex was dissected. Neurochemical measurements were made by high-performance liquid chromatography with 16-sensor electrochemical detection.
Marked increases in uric acid were seen at all time points, with a maximal increase at 1 day and a persistent increase lasting up to 21 days. There were smaller reciprocal decreases in xanthine. Glutathione, cysteine, and ascorbic acid showed significant decreases, consistent with the generation of free radicals. Reductions in levels of cysteine and glutathione were significantly correlated with increases in uric acid levels.
These findings confirm marked alterations in purine metabolism following focal ischemia and suggest that xanthine oxidase contributes to the generation of free radicals.
Hypertension with hemodilution prevents multifocal cerebral hypoperfusion after cardiac arrest in dogs.
Authors: Leonov Y , Sterz F , Safar P , Johnson D W , Tisherman S A , Oku K 
Published: June 2011

Improved neurological outcome with postarrest hypertensive hemodilution in an earlier study could be the result of more homogeneous cerebral perfusion and improved O2 delivery. We explored global, regional, and local cerebral blood flow by stable xenon-enhanced computed tomography and global cerebral metabolism in our dog cardiac arrest model.
Ventricular fibrillation cardiac arrest of 12.5 minutes was reversed by brief cardiopulmonary bypass, followed by life support to 4 hours postarrest. We compared control group I (n = 5; mean arterial blood pressure, 100 mm Hg; hematocrit, greater than or equal to 35%) with immediately postarrest reflow-promoted group II (n = 5; mean arterial blood pressure, 140-110 mm Hg; hypervolemic hemodilution with plasma substitute to hematocrit, 20-25%).
After initial hyperemia in both groups, during the "delayed hypoperfusion phase" at 1-4 hours postarrest, global cerebral blood flow was 51-60% of baseline in group I versus 85-100% of baseline in group II (p less than 0.01). Percentages of brain tissue voxels with no flow, trickle flow, or low flow were lower (p less than 0.01) and mean regional cerebral blood flow values were higher in group II (p less than 0.01). Global cerebral oxygen uptake recovered to near baseline values at 3-4 hours postarrest in both groups. Postarrest arterial O2 content, however, in hemodiluted group II was 40-50% of that in group I. Thus, the O2 uptake/delivery ratio was increased (worsened) in both groups at 2-4 hours postarrest.
After prolonged cardiac arrest, immediately induced moderate hypertensive hemodilution to hematocrit 20-25% can normalize cerebral blood flow patterns (improve homogeneity of cerebral perfusion), but does not improve cerebral O2 delivery, since the flow benefit is offset by decreased arterial O2 content. Individualized titration of hematocrit or hemodilution with acellular O2 carrying blood substitute (stroma-free hemoglobin or fluorocarbon solution) would be required to improve O2 uptake/delivery ratio.
Uptake and release of serotonin in rat cerebrovascular nerves after subarachnoid hemorrhage.
Authors: Szabò C , Emilsson K , Hardebo J E , Nystedt S , Owman C 
Published: June 2011

Serotonin released from platelets has been suggested as one substance causing the vasospasm following subarachnoid hemorrhage. We studied whether such serotonin is able to constrict pial vessels.
We studied the uptake of serotonin in pial perivascular nerves by immunohistochemistry. We measured the contractile response in rat basilar artery after in vitro incubation with serotonin and during electrical field stimulation of perivascular nerves following experimental subarachnoid hemorrhage.
After incubation with serotonin, electrical field stimulation caused a tetrodotoxin- and ketanserin-blockable contractile response. We observed no such response in vessels from rats treated with 6-hydroxydopamine or after blockade of serotonin uptake. After subarachnoid hemorrhage, a pronounced network of serotonin-immunoreactive nerve fibers was demonstrated in the vessel wall. In vessels from control rats, no serotonin fibers were seen, and in vessels from 6-hydroxydopamine-treated animals with subarachnoid hemorrhage only a few such fibers were seen. Electrical field stimulation of the basilar artery from rats tested 2 or 16 hours (but not 10 minutes or 24 hours) after subarachnoid hemorrhage showed contractile responses that were prevented by tetrodotoxin, ketanserin, and prior 6-hydroxydopamine treatment.
Our study demonstrates a capacity of the perivascular sympathetic nerves to take up serotonin both in vitro and during the early phase of subarachnoid hemorrhage. Such uptake may help to remove excess serotonin from the subarachnoid space. Only if serotonin is subsequently released upon nerve activation may minor smooth muscle contraction develop.