bluuebunny/crossref_metadata_2025_split huggingface dataset:
Sneddon's syndrome: diagnosis by skin biopsy and MRI in 17 patients.
Authors: Stockhammer G , Felber S R , Zelger B , Sepp N , Birbamer G G , Fritsch P O , Aichner F T 
Published: June 2011

Sneddon's syndrome, characterized by generalized livedo racemosa and cerebrovascular lesions, is an underdiagnosed disease. We evaluated clinical, laboratory, histological, and neuroradiological findings in a series of 17 patients to improve diagnostic criteria for Sneddon's syndrome.
Patients with generalized livedo racemosa and cerebrovascular events were included in the study. All underwent neurological and dermatological examination, skin biopsy, computed tomographic scan, magnetic resonance imaging as well as magnetic resonance angiography, sonography of the extracranial arteries, and a comprehensive laboratory protocol.
Completed stroke was present in eight patients, and 15 reported transient neurological deficits. Magnetic resonance imaging yielded cerebral abnormalities in 16 of 17, whereas computed tomographic scans were abnormal in only 12 of 16 patients. Magnetic resonance imaging revealed more lesions in individual patients than did computed tomography. Magnetic resonance angiography demonstrated patent intracranial vessels in 16 of 17 patients. Skin biopsy showed distinct histopathological findings in all patients. The involved vessels were small to medium-sized arteries at the border between dermis and subcutis. Early inflammatory reactions were followed by subendothelial proliferation and a late fibrotic stage. Laboratory examinations showed impaired creatinine clearance in eight patients, whereas all other laboratory tests, including antiphospholipid antibodies, were normal.
In this series, magnetic resonance imaging and skin biopsy were useful for confirmation of the diagnosis of Sneddon's syndrome. Magnetic resonance findings were not specific, but the high sensitivity for detection of asymptomatic brain lesions helped to confirm the diagnosis in patients with transient symptoms. Histological features of skin biopsies were characteristic if appropriate techniques were employed.
Risk area and infarct area relations in the hypertensive stroke-prone rat.
Authors: Coyle P , Feng X 
Published: June 2011

Our purpose was to characterize the surface area of the infarct and the surface area at risk of infarction as defined spatially by arterial anastomoses to determine whether position, size, or shape of the infarct and the area at risk were related in stroke-prone rats or hybrid rats.
Stroke-prone rats (n = 18; mean +/- SEM blood pressure, 182 +/- 8 mm Hg) and hybrid rats (n = 18; mean +/- SEM blood pressure, 147 +/- 6 mm Hg; p < 0.05) were anesthetized and the left middle cerebral artery was occluded with a ligature. The rats were killed 7 days later, arterial anastomoses were made visible with latex, the brains were fixed in formalin, and film recorded the infarct and anastomoses. Anastomoses and infarcts were digitized for measurements of risk area, luminal width, and infarct area.
Mean risk area was similar in size, length, width, and variability in stroke-prone rats (area, 85 +/- 5 mm2) and hybrid rats (area, 84 +/- 7 mm2; p > 0.05), whereas mean infarct area was larger, longer, wider, and less variable in stroke-prone rats (area, 53 +/- 6 mm2) than in hybrid rats (area, 15 +/- 11 mm2; p < 0.05). Infarct length was appreciably greater than infarct width in both groups, indicating that infarct shape was not amorphous. Spatial overlap maps indicated that the infarct area common to all stroke-prone rats was positioned centrally in the risk area and was surrounded by a variable infarct area, which indicated that the likelihood of infarction increased with distance from the anastomoses. Shape factors for both risk area and infarct area were significantly different within each rat group, which indicated that infarct shape did not uniformly parallel the anastomotic sites that determined risk area shape (p < 0.05). Risk area anastomoses and border zone width were linearly correlated in size and both were significantly wider in hybrid rats than in stroke-prone rats (p < 0.05), which suggests that the narrower border zone tissue was perfused by narrower anastomoses.
We conclude that the position of the infarct within the risk area relates to luminal widths of conterminous anastomoses that define the risk area, but not to the size or shape of the area at risk of infarction defined spatially by the anastomoses.
Stroke following injection of a melted suppository.
Authors: Bitar S , Gomez C R 
Published: June 2011

Stroke following the intravenous injection of drugs may be secondary to the direct effect of the substance itself or from embolization by the inert vehicle used in the manufacturing process of the drug.
We describe a 39-year-old man who developed a left homonymous hemianopia after intravenous injection of a melted suppository.
Paradoxical fat embolism should be added to the possible list of stroke mechanisms in intravenous drug abusers.
Long-term survival after first-ever stroke: the Oxfordshire Community Stroke Project.
Authors: Dennis M S , Burn J P , Sandercock P A , Bamford J M , Wade D T , Warlow C P 
Published: June 2011

There have been relatively few community-based studies of long-term prognosis after acute stroke. This study aimed to provide precise estimates of the absolute and relative risks of dying in an unselected cohort of patients with a first-ever stroke.
Six hundred seventy-five patients were registered by a community-based stroke register (the Oxfordshire Community Stroke Project) and prospectively followed up for up to 6.5 years. Their relative risk of death was calculated using age- and sex-specific mortality rates for Oxfordshire.
During the first 30 days, 129 (19%) patients died. Patients who survived at least 30 days after a first-ever stroke thereafter had an average annual risk of death of 9.1%, 2.3-fold the risk in people from the general population. Although the absolute (about 15%) and relative (about threefold) risks of death were highest in these 30-day survivors over the first year after the stroke, they were at increased risk of dying over the next few years (range of relative risk for individual years, 1.1-2.9). Predictably, older patients had a worse absolute survival but, relative to the general population, stroke also increased the relative risk of dying in younger patients. During the first 30 days stroke accounts for most deaths; after this time nonstroke cardiovascular disease becomes increasingly important and is the most common cause of death after the first year.
These data highlight the importance of long-term secondary prevention of vascular events in stroke patients, targeted as much at the cardiovascular as at the cerebrovascular circulation.
Failure of MK-801 to reduce infarct volume in thrombotic middle cerebral artery occlusion in rats.
Authors: Yao H , Ginsberg M D , Watson B D , Prado R , Dietrich W D , Kraydieh S , Busto R 
Published: June 2011

We examined the effects of the noncompetitive N-methyl-D-aspartate receptor antagonist MK-801 using a newly developed stroke model of thrombotic distal middle cerebral artery occlusion under conditions of carefully controlled head temperature.
Male Sprague-Dawley rats were treated with 1 mg/kg of MK-801 or saline before the induction of ischemia. An argon laser-activated dye laser (562 nm) was used to cause thrombotic distal middle cerebral artery occlusion. In experiments 1 and 2, the single laser beam (20 mW) was separated into three beams. Each beam was positioned onto the distal middle cerebral artery at three sites along the vessel. The photosensitizing dye rose bengal (20 mg/kg) was administered intravenously over 2 minutes; the three points were then irradiated for 3 minutes. In experiment 3, higher power of the laser (three separate irradiations using a single beam of 20 mW) was used. The ipsilateral common carotid artery was occluded permanently, and the contralateral carotid artery was occluded for 60 minutes. Head temperature was controlled at 36 degrees C in experiment 1 and not controlled in experiments 2 and 3. Three days after the ischemic insult, brains were perfusion-fixed and infarct volumes were determined.
Head temperature was mildly hypothermic (34-35 degrees C before ischemia, with a further decrease of 1-2 degrees C during the initial 60 minutes of ischemia) in experiment 2. However, no differences were observed in head temperature between the MK-801-treated and control groups. Cortical infarct volume in experiment 1 was 89 +/- 29 mm3 (mean +/- SD) in the treated group, which was not different from the control value of 84 +/- 40 mm3. Infarct volumes were smaller (58 +/- 35 mm3 and 54 +/- 14 mm3) in the control groups of experiments 2 and 3, respectively. However, MK-801 also failed to reduce infarct volumes in experiments 2 and 3.
MK-801 is not effective in this stroke model of focal thrombotic infarction under conditions of either controlled (normothermic) or uncontrolled (mildly hypothermic) head temperature.
Neuroprotection by corticotropin releasing factor during hypoxia in rat brain.
Authors: Fox M W , Anderson R E , Meyer F B 
Published: June 2011

Corticotropin releasing factor is an endogenous neuropeptide released by the hypothalamus that activates the pituitary-adrenocortical system in response to stressful stimuli. It has been demonstrated that corticotropin releasing factor increases the excitability of hippocampal neurons in both in vitro and in vivo studies, which may contribute to neurological injury during hypoxia. The purpose of this study was to determine the effects of corticotropin releasing factor and its synthetic competitive antagonist, alpha-CRF, on neuronal synaptic recovery after a hypoxic insult using the hippocampal slice.
Wistar rat hippocampal brain slices (n = 120) were treated with various concentrations (10(-6) to 10(-11)) of corticotropin releasing factor or its synthetic antagonist during a 10-minute hypoxic episode. Extracellular recording of population spikes was used during and after the hypoxic insult to assess neuronal recovery.
Corticotropin releasing factor provided dose-dependent neuronal protection with maximum recovery (37.95 +/- 8.71%) occurring at 10(-9) concentrations. The competitive antagonist alpha-CRF provided a similar degree of recovery at 10(-6) concentration, whereas 10(-9) molar concentration of competitive antagonist resulted in 16.84 +/- 7.68% recovery.
Corticotropin releasing factor provides moderate protection to hypoxic hippocampal neurons in the brain slice preparation. The mechanism of action is unknown but appears to be a direct neuronal effect. These results support the hypothesis that corticotropin releasing factor may act as an endogenous neuroprotective hormone during hypoxia.
Evaluation of the combination of a tissue-type plasminogen activator, SUN9216, and a thromboxane A2 receptor antagonist, vapiprost, in a rat middle cerebral artery thrombosis model.
Authors: Umemura K , Wada K , Uematsu T , Nakashima M 
Published: June 2011

We aimed to evaluate a modified tissue-type plasminogen activator, SUN9216, and the combination of SUN9216 and a thromboxane A2 receptor antagonist, vapiprost, in a rat middle cerebral artery thrombosis model.
Under anesthesia, the left middle cerebral artery was observed under an operation microscope without cutting the dura mater via a subtemporal craniotomy. Photoillumination (wave length, 540 nm) was applied to the middle cerebral artery, and then rose bengal (20 mg/kg) was administered intravenously. The reopening of the middle cerebral artery by SUN9216, injected 30 minutes after middle cerebral artery occlusion, was observed under an operation microscope for a 60-minute observation period. Twenty-four hours after the operation, sections of the cerebrum were stained with triphenyltetrazolium chloride, and the area of cerebral infarction was analyzed by a computer.
The combination of SUN9216 and vapiprost caused reopening of the middle cerebral artery in 58.8% of the rats, which was a greater percentage than that achieved with SUN9216 alone (31.6%). In contrast, saline did not cause reopening of the middle cerebral artery during the 60-minute observation period. The area of cerebral infarction in rats reperfused with SUN9216 was significantly reduced compared with that in the control group. The infarction area in rats treated with the combination of SUN9216 and vapiprost was reduced compared with that in rats treated with SUN9216 alone; this was the case whether or not the occlusion was reperfused. There was a significant correlation between the time of reopening of the middle cerebral artery and area of cerebral infarction.
A single injection of SUN9216 was effective in recanalizing the vessel and reducing the area of cerebral infarction.
Transcranial clipping of recurrent cerebral aneurysms after endovascular treatment.
Authors: Ladouceur D L 
Published: June 2011

Treatment of intracranial aneurysms by interventional neurovascular techniques may be useful as a therapeutic alternative. We describe two cases of recurrent aneurysms after endovascular treatment using detachable balloons.
Two cases are reported of recurrence 2 years after endovascular treatment of cerebral aneurysms (posterior communicating in both cases). One patient had a subarachnoid hemorrhage after rupture of a posterior communicating aneurysm. The other patient had an aneurysm diagnosed incidentally after a contrast-enhanced computed tomographic scan of the head for an unrelated problem. Endovascular balloon embolization of both aneurysms was performed without any immediate complication. Two years after treatment, a cerebral angiogram showed recurrent aneurysms. Surgical clipping excluded both aneurysms definitely.
These cases highlight the importance of control angiography at long-term follow-up and emphasize the significance of balloon migration after endovascular treatment of aneurysms.
Risk factors for cervical atherosclerosis in patients with transient ischemic attack or minor ischemic stroke.
Authors: Palomäki H , Kaste M , Raininko R , Salonen O , Juvela S , Sarna S 
Published: June 2011

Our purpose was to study potential determinants of the presence and the severity of cervical atherosclerosis in patients with transient ischemic attack or minor ischemic stroke.
Two hundred ninety-four patients up to 60 years of age were included in this cross-sectional study. The male to female ratio was 171/123. Atherosclerosis was defined as the presence of any visible atherosclerotic lesion in anteroposterior or left oblique views of cervical arteries in aortic arch angiograms. The severity of atherosclerosis was assessed using three scores, which were computed separately for the total thickness and length of all plaques as well as for the percent stenosis of the vessels.
Atherosclerosis was present in 180 patients (61.2%). In a multiple stepwise logistic regression analysis, age, serum triglycerides, smoking history for more than 20 years, arterial hypertension (defined as systolic or diastolic blood pressure values at least 150 or 100 mm Hg, respectively, or the use of antihypertensive medication), regular light alcohol consumption (inversely), and body mass index (marginal inverse association) were independent determinants of the presence of atherosclerosis; the respective odds ratios were 1.1/1 y, 1.8/1 mmol/L, 3.3, 2.4, 0.3, and 0.9/1 kg/m2. In multiple linear regression models, age was associated positively and the ratio of high density lipoprotein to total cholesterol was associated negatively with the severity of atherosclerosis regardless of the scoring method, whereas current smoking and female sex were predictors only of the percent stenosis and the length of the lesions. Arterial hypertension showed a significant association only with the length of the lesions.
Age, cigarette smoking, and arterial hypertension contribute substantially to atherosclerosis in cervical arteries, but this study also confirms the independent associations of lipid or lipoprotein variables with atherosclerotic disease. An independent inverse association of regular light consumption of alcohol with cervical atherosclerosis was also observed.
Carotid stenosis and perioperative stroke risk in symptomatic and asymptomatic patients undergoing vascular or coronary surgery.
Authors: Gerraty R P , Gates P C , Doyle J C 
Published: June 2011

The management of asymptomatic carotid stenosis found before vascular or coronary surgery is unclear from the literature. We aimed to define the relation of carotid stenosis to perioperative stroke in all patients, symptomatic and asymptomatic, and so determine a policy for the management of asymptomatic carotid stenosis in patients requiring major surgery.
We conducted a prospective clinical and Duplex ultrasound study of 358 consecutive noncarotid major vascular or coronary artery bypass operations, with a moratorium on endarterectomy for asymptomatic carotid stenosis.
There were 145 vascular and 213 coronary bypass operations. Ten of the 49 cases with prior symptoms of cerebral ischemia (38 carotid, 11 vertebrobasilar) had symptomatic stenosis of 50% or greater or occlusion, and 3 of these (30%) had ipsilateral perioperative cerebral infarction (95% confidence interval, 6.67% to 65.25%). Two of these occurred ipsilateral to symptomatic carotid occlusions, and 1 occurred ipsilateral to an 80% symptomatic stenosis. One symptomatic patient with bilateral 30% stenosis had a perioperative infarct in the asymptomatic hemisphere. Among the 309 asymptomatic patients, 1 perioperative infarct occurred ipsilateral to carotid stenosis of 30%. In all there were 5 (1.4%) perioperative (within 72 hours) and 2 late (after 18 days) strokes. All strokes were hemisphere infarcts confirmed by computed tomography. There were 53 cases with 50% or greater asymptomatic carotid stenosis or occlusion, including 28 with 80% or greater stenosis or occlusion. None had an ipsilateral perioperative stroke (95% confidence interval, 0% to 6.72%).
We conclude that the risk of perioperative stroke related to symptomatic carotid stenosis may be high, but for asymptomatic carotid stenosis the risk is low and does not justify preoperative prophylactic carotid endarterectomy.
A comparison of five stroke scales with measures of disability, handicap, and quality of life.
Authors: De Haan R , Horn J , Limburg M , Van Der Meulen J , Bossuyt P 
Published: June 2011

Recently much debate has arisen on the appropriateness of assessing stroke outcomes with stroke impairment scales. Our purpose was to study the relationship between long-term impairments and functional outcomes in terms of disability, handicap, and quality of life.
We studied 87 patients who had a stroke 6 months earlier. Impairments were scored on five stroke scales: the Orgogozo Scale, the National Institutes of Health scale, the Canadian Neurological Scale, the Mathew scale, and the Scandinavian Stroke Scale. Disability was assessed with the Barthel Index, handicap with the Rankin scale, and quality of life with the Sickness Impact Profile. The linear relationship between stroke scales and functional scales was assessed with correlation coefficients. We used regression analyses to explain functional health.
The stroke scales were highly related to one another (range, r = -.85 to .92). The correlation between stroke scales and functional scales was < .70 and decreased from Barthel (mean r2 = 47.5%) to Rankin (mean r2 = 36.5%) to Sickness Impact Profile (mean r2 = 33%). Stroke scales were rather poorly correlated with patients' psychosocial conditions (mean r2 = 11.5%). Functional health status was mainly related to leg power and orientation. The standardized stroke scale weights of the explanatory items were lower than their standardized regression weights.
Stroke scales only partly explain functional health. The impact of impairments on functional outcomes seems to be underestimated by the stroke scale weights. The correlation patterns give empirical support to the hierarchical structure of the International Classification of Impairments, Disabilities and Handicaps.
Rate of successful recording of blood flow signals in the middle cerebral artery using transcranial Doppler sonography.
Authors: Itoh T , Matsumoto M , Handa N , Maeda H , Hougaku H , Hashimoto H , Etani H , Tsukamoto Y , Kamada T 
Published: June 2011

To assess the usefulness of transcranial Doppler sonography, we investigated the rate of blood flow signal recording failure in the middle cerebral artery in Japanese subjects. Furthermore, we studied the effect of increased emitted power on the rate of successful recording in some of the patients in whom recording failure had been detected at the standard transducer power of 100 mW/cm2.
To evaluate the rate of successful recording, we measured blood flow signals in 597 patients (age range, 16 to 89 years) for screening of cerebrovascular disease by using a 2-MHz range-gated, pulsed-wave Doppler instrument at the standard transducer power. In 18 elderly patients with recording failure at the standard power, we assessed the effect of increased emitted power of 400 mW/cm2 on flow signal recording.
Blood flow signals were recorded in 920 (77.1%) of the 1194 middle cerebral arteries of the 597 patients studied. The rate of successful recording of bilateral middle cerebral artery flow signals (70.9%; 423 of 597 patients) decreased with age, especially in females (17.0% in women aged 70 years or older). In 12 of 18 elderly patients with recording failure at the standard power, blood flow signals could be detected at the increased emitted power of 400 mW/cm2.
The rate of successful recording of blood flow signals in Japanese subjects decreases with advancing age, especially in females. Increasing the emitted power markedly improves the successful recording rate.
Measuring carotid stenosis. Time for a reappraisal.
Authors: Alexandrov A V , Bladin C F , Maggisano R , Norris J W 
Published: June 2011

Data from recent multicenter carotid endarterectomy trials have questioned the validity and reliability of Doppler ultrasound in the assessment of carotid stenosis.
We prospectively analyzed 45 patients undergoing carotid angiography to compare the North American Symptomatic Carotid Endarterectomy Trial (NASCET) and European Carotid Surgery Trial (ECST) methods of measuring carotid stenosis with those of direct visualization ("eyeballing") and duplex ultrasound. Linear NASCET and ECST measurements were also converted into area using the pi r2 function and termed "squared NASCET" (N2) and "squared ECST" (E2). In 15 of 45 patients undergoing carotid endarterectomy, the carotid plaque was removed intact, sectioned, and photographed for computer measurement of cross-sectional area. Comparison of this "gold standard" was then made to each method of measurement.
Comparison between duplex and the various angiographic measurement techniques revealed significant differences between NASCET and duplex (P < .0001), ECST and duplex (P < .01), and E2 and duplex (P < .01) but not between N2, eyeballing, and carotid duplex methods. Even the NASCET and ECST methods themselves differed significantly (P < .006). When comparison was made with computerized planimetric measurements of the carotid plaque, there were significant differences for both NASCET (P < .0007) and ECST (P < .007). Correlation was demonstrated only between planimetry and N2, E2, and duplex.
NASCET and ECST angiographic methods of measurement consistently underestimate the "true" anatomic stenosis. As such, they represent only "indexes" of carotid stenosis severity. Duplex provides a more accurate measurement of carotid stenosis.