bluuebunny/crossref_metadata_2025_split huggingface dataset:
Middle cerebral artery velocity changes during transfusion in sickle cell anemia.
Authors: Venketasubramanian N , Prohovnik I , Hurlet A , Mohr J P , Piomelli S 
Published: June 2011

Sickle cell disease is associated with cerebral hyperemia, which is therapeutically reduced by transfusion; however, the process of transfusion-induced cerebral perfusion changes has heretofore not been observed.
We document the acute changes of intracranial arterial velocity in 10 patients (7 with strokes, 3 without) undergoing transfusion therapy using transcranial Doppler ultrasonography. Middle cerebral artery velocities were bilaterally measured every 30 minutes for the duration of transfusion (4 to 5 hours). Regional cerebral blood flow was quantified in 5 of these patients before the transfusion and 24 hours later by the 133Xe technique.
Velocities in stroke-associated vessels (64.33 +/- 18.65 cm/s; n = 6) were significantly lower than in uninfarcted territories (99.54 +/- 27.39 cm/s; n = 13), and both types of vessels showed a robust reduction of blood flow velocities during transfusion. The rates of reduction were not significantly different as a function of prior stroke but did correlate with pretransfusion velocities and with the rise in hematocrit (multiple r = .887, P < .001). These reductions occurred rapidly within the first 3 hours of transfusion. Velocities attained at the end of transfusion were maintained in the hour after transfusion and the next day.
We conclude that transfusion induces rapid changes in cerebral hemodynamics that are related to pretransfusion velocities and a rise in hematocrit. Transcranial Doppler provides a safe, simple, and noninvasive technique of monitoring these changes and may provide a means of making therapeutic decisions regarding transfusion therapy in patients with sickle cell anemia.
Sensory symptoms and signs and results of quantitative sensory thermal testing in patients with lacunar infarct syndromes.
Authors: Samuelsson M , Samuelsson L , Lindell D 
Published: June 2011

Quantitative data on sensory impairment in stroke patients are limited. We measured the perception thresholds for temperature and thermal pain in patients with different lacunar syndromes, correlated the results with clinical and magnetic resonance imaging (MRI) findings, and studied the long-term prognosis of sensory dysfunction.
Quantitative thermal testing was performed by means of the Marstock method in 39 patients with lacunar syndromes (pure motor, sensorimotor, or pure sensory stroke) and MRI findings compatible with occlusion of a single perforating artery. Thresholds for cold, warmth, and heat pain were obtained bilaterally from the cheek, hand, and leg. The unaffected side was used as control. Follow-up included clinical assessments and repeated quantitative thermal testing (in 17 patients) up to 1 year after stroke onset.
Patients with pure sensory stroke and sensorimotor stroke (n = 22) had a significant thermal hypoesthesia on the affected side for all modalities and test locations. Patients with pure motor stroke (n = 17) exhibited thermal hypoesthesia for cold and heat pain in the hand and for cold perception in the leg. On MRI, infarcts causing pure motor and sensorimotor stroke were predominantly lenticulocapsular, while a thalamic site of infarction was found in pure sensory stroke. The prognosis of sensory impairment was favorable, except for poststroke pain syndromes in three patients.
Quantitative thermal testing confirmed an involvement of spinothalamic pathways in lacunar infarcts causing pure sensory and sensorimotor stroke and revealed a subclinical sensory impairment in patients with pure motor stroke. Infarction sites were similar in patients with pure motor and sensorimotor stroke.
Frequency and pathogenesis of hemodynamic stroke.
Authors: Bladin C F , Chambers B R 
Published: June 2011

Hemodynamic stroke is a recognized but poorly described entity. The aim of this study was to define the frequency and pathogenic mechanisms of hemodynamic stroke.
We prospectively studied 300 consecutive patients with acute ischemic stroke for evidence of a hemodynamic mechanism. All patients with a probable or possible thromboembolic source were excluded.
Twenty-nine patients (9.6%) had documented or presumed hypotension at stroke onset, with 27 of 29 (93%) having watershed infarction on computed tomography (CT). Most (21/29) patients had a slow (hours to days) progressive onset to stroke. Myocardial infarction, cardiac arrhythmias, and orthostatic changes in blood pressure related to diabetic dysautonomia and antihypertensive therapy were the predominant causes of hypotension. Ten patients had moderate or severe carotid stenosis (frequently bilateral); 9 had carotid occlusion (19/29 [66%]). Patients with normal carotid arteries (10/29 [34%]) had hypotension with a stuttering onset to stroke and watershed infarction on CT. Many patients continued to have progressive neurological deterioration, often with ongoing hemodynamic instability. Three of 7 patients who underwent carotid endarterectomy had further perioperative ischemic events. Five patients had myocardial infarction, and overall 4 died during 18.4 months of follow-up (mortality, 9%/y).
Recognition of the clinical and CT features of hemodynamic stroke allows early identification and management of cardiac and carotid disease and correction of iatrogenic causes of hypotension, which may reduce the risk of further events.
Value of immunologic testing in stroke patients. A prospective multicenter study.
Authors: Montalbán J , Rio J , Khamastha M , Davalos A , Codina M , Swana G T , Calcagnotto M E , Sumalla J , Mederer S , Gil A 
Published: June 2011

The aims of this prospective and multicenter study were to determine the frequency of anticardiolipin and antinuclear antibodies in an unselected ischemic and hemorrhagic stroke population and to evaluate the clinical significance of these autoantibodies.
Over a 1-year period, we collected plasma from 481 consecutive patients with ischemic or hemorrhagic stroke attending four different hospitals. Blood (10 mL) was drawn from each subject into a citrated glass tube. Plasma was obtained immediately by centrifugation and was stored at -70 degrees C until use. Concentrations of IgM and IgG anticardiolipin antibodies were measured at room temperature in normal (not heat-treated) plasma by standardized enzyme-linked immunosorbent assay. All sera were treated by indirect immunofluorescence on mouse liver and kidney sections for antinuclear antibodies.
A total of 481 patients (325 men, 156 women) 16 to 90 years in age (mean age, 61 years) were studied. Anticardiolipin antibodies were present in 5 of 481 (1.04%) patients. One patient was IgG positive and four patients were IgM positive. Of 481 patients, 35 (7.2%) were positive for antinuclear antibodies. Anti-DNA antibodies were not demonstrable in any patient.
The frequency of anticardiolipin antibodies in a heterogeneous stroke population is possibly lower than reported. The routine screening of anticardiolipin and antinuclear antibodies in a stroke population is of questionable value.
Nitric oxide promotes arteriolar dilation during cortical spreading depression in rabbits.
Authors: Colonna D M , Meng W , Deal D D , Busija D W 
Published: June 2011

Pial arterioles transiently dilate during cortical spreading depression (CSD), although the mechanisms are unclear. We tested the hypothesis that increased production of nitric oxide (NO) promotes arteriolar dilation.
Urethane-anesthetized rabbits were equipped with cranial windows, and the diameter (reported in micrometers) of a pial arteriole was determined via intravital microscopy. In each rabbit, a baseline CSD was elicited by microapplication of KCl onto the cortex, and resultant pial arteriolar dilation was measured. Either 100 mumol/L N omega-nitro-L-arginine methyl ester (L-NAME) or 50 mumol/L NG-nitro-L-arginine (L-NA), both competitive NO synthase inhibitors, was then applied to the brain surface. A CSD was elicited as before. The L-NAME and L-NA were then removed by artificial cerebrospinal fluid washes. An additional CSD was induced with KCl as before.
Control CSD in the L-NAME group dilated pial arterioles; baseline diameter, 66 +/- 7 mm, with CSD = 106 +/- 8 mm (59% increase). After topically applied L-NAME, CSD dilated pial arterioles less: baseline diameter, 61 +/- 7 mm, with CSD = 77 +/- 6 mm (26% increase), P < .05 compared with control CSD diameter. Topical L-NA had similar effects on CSD: control CSD dilated pial arterioles 51%; after topical L-NA, only 14% (P < .05). After removal of L-NAME or L-NA, CSD-induced pial arteriolar dilation was similar to original control values.
The reversible inhibition of CSD-induced pial arteriolar dilation by either L-NAME or L-NA suggests that NO contributes to arteriolar dilation observed with CSD.
Evidence for episodic platelet activation in acute ischemic stroke.
Authors: van Kooten F , Ciabattoni G , Patrono C , Schmitz P I , van Gijn J , Koudstaal P J 
Published: June 2011

Enhanced thromboxane biosynthesis has previously been reported in patients with acute ischemic stroke. In this study we examined the time course of thromboxane biosynthesis after the onset of symptoms in 13 patients with acute cerebral infarction.
We obtained five to eight consecutive 6-hour urine samples from each of these 13 patients within the first 48 hours after onset of symptoms to study the dynamics of platelet activation in this setting. The urinary excretion of the major enzymatic metabolite of thromboxane B2, 11-dehydro-thromboxane B2, was measured by a previously validated radioimmunoassay. The excretion rate was compared with that of 20 control patients with nonvascular neurological diseases.
Eleven patients (85%) had at least one value exceeding 2 SD of the control mean (251 pmol/mmol creatinine). The proportion of samples with an elevated 11-dehydro-thromboxane B2 level was markedly similar in each of the eight 6-hour collection periods (mean, 52 +/- 8%; range, 40% to 67%). In 4 patients (31%) the excretion rate was elevated in all measurements obtained. In the 11 patients with enhanced thromboxane biosynthesis, no uniform pattern of changes over time in metabolite excretion emerged, with 3 patients having peak values at 0 to 12 hours, 3 at 12 to 24 hours, 3 at 24 to 36 hours, and 2 at 36 to 48 hours. The level and dynamics of 11-dehydro-thromboxane B2 excretion were related neither to the neurological symptoms nor to the type or site of the cerebral ischemia.
We conclude that episodes of platelet activation occur repeatedly during the first 48 hours after the onset of symptoms of an acute ischemic stroke. Given its apparent dynamic nature, this ongoing process may be amenable to pharmacologic modulation.
Magnetic resonance abnormalities and cardiovascular disease in older adults. The Cardiovascular Health Study.
Authors: Manolio T A , Kronmal R A , Burke G L , Poirier V , O'Leary D H , Gardin J M , Fried L P , Steinberg E P , Bryan R N 
Published: June 2011

Cerebral magnetic resonance imaging often detects abnormalities whose significance is unknown. The prevalence and correlates of findings such as ventricular enlargement, sulcal widening, and increased white matter signal intensity were examined in 303 men and women aged 65 to 95 years participating in a multicenter study of cardiovascular disease.
Cerebral magnetic resonance imaging was performed and interpreted according to a standard protocol, and findings were correlated with measures of cardiovascular disease and its risk factors.
Measures of cerebral atrophy increased with age and were greater in men than in women (each P < .01). Ventricular enlargement and sulcal widening were associated with prior stroke, hypertension, diabetes, and white race (each P < .03). Extent of white matter hyperintensity was associated with age, prior stroke, hypertension, and use of diuretics (each P < .004). On multivariate analysis, age, male gender, white race, and prior stroke retained strong associations with increased ventricular and sulcal scores. After adjustment for age, prior stroke, and other risk factors, white matter hyperintensity was associated with atherosclerosis as measured by increased internal carotid artery thickness on ultrasound.
Cerebral atrophy and white matter hyperintensity are common in the elderly and are associated with age, prior stroke, and known cardiovascular risk factors. Though these findings have been suggested to represent normal aging, their wide variability and associations with cardiovascular disease argue against their inevitability with advancing age and support the need to identify modifiable risk factors for these abnormalities.
Predicting the disability of first-time stroke sufferers at 1 year. 12-month follow-up of a population-based cohort in southeast England.
Authors: Taub N A , Wolfe C D , Richardson E , Burney P G 
Published: June 2011

The purpose of this study was to predict the functional outcome at 1 year of first-time stroke patients aged younger than 75 years in relation to the severity of stroke and demographic characteristics.
Population registers in three districts of southeast England were established in August 1989, with notification by stroke registry field-workers, general practitioners, and rehabilitation practitioners. Assessments were made using the Barthel index for activities of daily living at the time of maximum impairment and at 3 and 12 months after the stroke.
Of 639 registered stroke patients, 392 without previous disability survived and were assessed for disability at 3 months, of whom 34 (9%) were severely disabled and 60 (15%) moderately disabled. Initial incontinence was the best single predictor of disability with a sensitivity of 60% and a specificity of 78%. Two hundred twenty-five patients (35%) were eligible for 12-month follow-up; 11% had moderate or severe disability, for which initial incontinence was the best predictor.
There is no evidence from this study of an association between demographic characteristics and the disability status of stroke survivors in the medium term. Multivariable predictors of disability had little advantage over incontinence within 24 hours of the stroke. The estimates of the prevalence of disability from this large population-based study are relevant when assessing the medium-term needs of stroke patients.
Noninvasive detection of intracranial vascular lesions by recording blood flow sounds.
Authors: Kurokawa Y , Abiko S , Watanabe K 
Published: June 2011

Transorbital blood flow sound recordings have the potential to be used for noninvasive detection of cerebral aneurysms and arteriovenous malformations. We describe our system and experience in detecting intracranial cerebrovascular disease.
We investigated the noninvasive detection of intracranial vascular lesions by recording and analyzing the intracranial blood flow sounds. A new small transducer was placed on the unilateral eyelid to record the intracranial blood flow sounds, which were amplified and converted to digital data at a sampling frequency of 2000 Hz to provide a spectral analysis.
No spectral peaks were recorded in 30 healthy adults. Sharp peaks were recorded in 12 of 15 patients with unclipped aneurysms, and broad peaks were recorded in two patients with vasospasm after aneurysmal clipping and in all patients with severe intracranial internal carotid artery stenosis.
This noninvasive technique has the potential to be very useful in the detection of intracranial cerebrovascular disease, including aneurysm and arterial stenosis, and could be used in mass screening examinations.
Nitric oxide synthase inhibition alters cerebral blood flow and oxygen balance in focal cerebral ischemia in rats.
Authors: Wei H M , Chi O Z , Liu X , Sinha A K , Weiss H R 
Published: June 2011

This study investigated whether the nitric oxide synthase inhibitor NG-nitro-L-arginine-methyl ester (L-NAME) would alter blood flow and oxygen balance in the ischemic cerebrocortex of isoflurane-anesthetized Long-Evans rats.
Fifteen minutes after middle cerebral artery occlusion, L-NAME (1.5 mg/min per kilogram) was infused intravenously to the L-NAME group (n = 14), and normal saline was given to the control group (n = 14) for 45 minutes. In each group, regional cerebral blood flow was determined with [14C]iodoantipyrine, and arterial and venous oxygen saturations were determined by microspectrophotometry.
In both groups regional cerebral blood flow of the ischemic cortex was significantly lower than that of the contralateral cortex ([mean +/- SD] 55 +/- 13 versus 110 +/- 29 mL/min per 100 g in the control group and 35 +/- 13 versus 90 +/- 24 mL/min per 100 g in the L-NAME group). Compared with the blood flow in the ischemic cortex of the control group, L-NAME significantly reduced ischemic blood flow by 36%. Venous oxygen saturation was significantly increased in the ischemic cortex (41 +/- 1% versus 44 +/- 3%) but decreased in the contralateral cortex (65 +/- 3% versus 61 +/- 4%) by L-NAME. Calculated ischemic cortical oxygen consumption in the L-NAME group was 39% lower than that in the corresponding control group, whereas the difference was only 11% in the contralateral sides between groups. In both groups, the ratio of oxygen supply to consumption was lower in the ischemic than in the nonischemic regions. In the ischemic cortex, this ratio was significantly lower in the control group than in the L-NAME group (1.7 +/- 0.1 versus 1.9 +/- 0.1). In contrast, the ratio tended to be decreased by L-NAME in nonischemic regions.
These observations suggest that despite a decrease in cerebral blood flow, inhibition of nitric oxide synthesis mildly improves the oxygen supply and consumption balance in the ischemic cortex.
Neuron-specific enolase concentrations in blood as a prognostic parameter in cerebrovascular diseases.
Authors: Schaarschmidt H , Prange H W , Reiber H 
Published: June 2011

To investigate the clinical relevance of plasma concentrations of neuron-specific enolase (NSE) in patients with severe cerebrovascular diseases, serial analyses were performed during the first 10 days after the acute event.
Plasma samples taken from 61 patients (30 with brain infarction, 13 with intracerebral hemorrhage, 11 with cardiogenic hypoxia-ischemia, and 7 with myocardial infarction [as control group]) were analyzed for NSE concentration using an enzyme immunoassay. The time course of plasma NSE was correlated with clinical findings, clinical outcome, cranial computed tomography, intracranial pressure, and other laboratory data.
In cases of hypoxia-ischemia there was close correlation between plasma NSE values during the first 72 hours and the clinical outcome. In brain infarction and intracerebral hemorrhage, high plasma NSE mostly indicated an unfavorable outcome, but low values did not permit a reliable prognostic estimation. In cases of cerebral infarction and intracerebral hemorrhage with secondary neuronal destruction (for example, due to malignant edema), increasing NSE concentrations in plasma preceded the change of clinical or other diagnostic parameters.
The course of plasma NSE levels is seen as a relevant parameter for assessing the prognosis of cerebral hypoxia-ischemia. Additionally, it may prove to be a useful tool for monitoring space-occupying brain infarctions and intracerebral hemorrhages and therefore may contribute to improved therapeutic management of severe cerebrovascular diseases.
Characteristics of patent foramen ovale associated with cryptogenic stroke. A biplane transesophageal echocardiographic study.
Authors: Homma S , Di Tullio M R , Sacco R L , Mihalatos D , Li Mandri G , Mohr J P 
Published: June 2011

Patent foramen ovale is associated with ischemic stroke in patients without a clearly identifiable etiology for stroke (cryptogenic stroke). Paradoxical embolization is thought to be a potential mechanism. However, patent foramen ovale is also found in patients with known cause of stroke. Therefore, using contrast transesophageal echocardiography, we characterized the patent foramen ovale in cryptogenic stroke patients to assess morphological factors that may contribute to paradoxical embolization.
Contrast transesophageal echocardiographic studies of 74 consecutive patients referred for ischemic stroke were reviewed. Twenty-three patients with patent foramen ovale were identified. These patients were classified as having strokes of determined origin or cryptogenic strokes according to criteria developed for the Stroke Data Bank of the National Institute of Neurological Disorders and Stroke. Separation of septum primum from secundum and the number of microbubbles appearing in left atrium were then quantitated. These parameters were compared between patients with cryptogenic stroke and those with known cause of stroke.
The patent foramen ovale dimension was significantly larger in patients with cryptogenic stroke compared with patients with an identifiable cause of stroke (2.1 +/- 1.7 mm versus 0.57 +/- 0.78 mm [mean +/- SD]; P < .01). The number of microbubbles was also greater in patients with cryptogenic stroke compared with patients with an identifiable cause of stroke (13.9 +/- 10.7 versus 1.6 +/- 0.8 [mean +/- SD]; P < .0005).
Patients with cryptogenic stroke have larger patent foramen ovale with more extensive right-to-left interatrial shunting than patients with stroke of determined cause. Transesophageal echocardiographically identifiable characteristics of patent foramen ovale may be important in defining the clinical significance of individual patent foramina.
Changes in locomotor activity and passive avoidance task performance induced by cerebral ischemia in Mongolian gerbils.
Authors: Karasawa Y , Araki H , Otomo S 
Published: June 2011

We investigated changes in locomotor activity, passive avoidance task performance, and hippocampal CA1 neurons induced by cerebral ischemia in Mongolian gerbils to examine the relation between these behavioral changes and CA1 neuronal damage.
Spontaneous locomotor activity was measured using the open field method before and 1, 3, 7, 14, or 28 days after 1- to 5-minute occlusion of the bilateral common carotid arteries. Locomotor activity after the second episode of 5-minute ischemia was also measured at 1-month intervals. The passive avoidance task was performed 7 or 28 days after induced ischemia. Histopathological changes in CA1 neurons after ischemia were assessed.
Locomotor activity was increased 1 and 3 days after induced ischemia but not 14 and 28 days later. When the gerbils were again subjected to 5-minute ischemia 1 month after the initial 5-minute induced ischemia, locomotor activity even 1 day later was significantly increased. In contrast, passive avoidance impairment depended on the duration of ischemia, as determined 7 and 28 days after induced ischemia. Hippocampal CA1 neuronal damage was progressive, that is, changes in CA1 neurons were apparent even 1 day after 5 minutes of induced ischemia, and the CA1 neurons disappeared 7 days after 5 minutes of ischemia.
Passive avoidance impairment after ischemia is related to damage of CA1 neurons. Changes in locomotor activity after induced ischemia do not seem to be linked to CA1 neuronal damage.