bluuebunny/crossref_metadata_2025_split huggingface dataset:
Lipoprotein(a) and ischemic cerebrovascular disease in young adults.
Authors: Nagayama M , Shinohara Y , Nagayama T 
Published: June 2011

Serum lipoprotein(a) level is genetically determined and remains almost constant throughout life. Based on this property, we investigated the serum lipoprotein(a) levels of ischemic stroke patients in the chronic stage (mean period after stroke, 27 months) and its relation to the types of ischemic stroke.
We measured serum lipoprotein(a) levels in 101 patients with chronic ischemic stroke and 37 normal control subjects, taking the clinical profiles into consideration.
Lipoprotein(a) levels in patients with atherothrombotic stroke were 28.0 +/- 19.6 mg/dL (mean +/- SD), which were significantly (P < .01) higher than those in patients with lacunar stroke and in normal control subjects (16.4 +/- 13.5 and 11.7 +/- 10.5 mg/dL, respectively). The lipoprotein(a) levels in patients with atherothrombotic stroke were significantly higher in the subgroup who were a younger age at onset: onset before age 50 years, 35.3 +/- 20.5; onset at age 50 to 59, 35.4 +/- 21.7; onset at age 60 to 69, 17.0 +/- 12.8; and onset at age 70 or older, 16.3 +/- 6.8 mg/dL (P < .01 for onset before age 50 versus 60 to 69 years or 70 years or older; P < .01 for onset at 50 to 59 years versus 60 to 69 years or 70 years or older). Serum lipoprotein(a) was significantly increased (40.2 +/- 20.1 mg/dL) in young adults with atherothrombotic stroke (onset at younger than age 45 years) compared with that in patients older than 45 years (P < .01).
We conclude that lipoprotein(a) is a genetic, independent, and critical risk factor for ischemic stroke, especially in young adults.
A prospective study of plasma homocyst(e)ine and risk of ischemic stroke.
Authors: Verhoef P , Hennekens C H , Malinow M R , Kok F J , Willett W C , Stampfer M J 
Published: June 2011

Several studies have reported elevated circulating homocyst(e)ine levels in subjects with cerebral atherosclerosis. We assessed prospectively whether high plasma levels of homocyst(e)ine affect risk of ischemic stroke and evaluated whether high blood pressure modifies any such effect.
The study sample was drawn from the Physicians' Health Study, a randomized, double-blind, placebo-controlled trial of aspirin and beta-carotene in 22,071 US male physicians. A total of 14,916 subjects 40 to 84 years old with no prior history of stroke, transient ischemic attack, or myocardial infarction provided blood samples at baseline and were followed for 5 years, with 99.7% morbidity and 100% mortality follow-up. Using a nested case-control design, we assayed homocyst(e)ine in samples from 109 subjects who subsequently developed ischemic stroke and 427 control subjects.
The mean plasma concentration of homocyst(e)ine was slightly higher in subjects with stroke (11.1 +/- 4.0 [+/- SD] nmol/mL) than in control subjects (10.6 +/- 3.4 nmol/mL), but the difference was not statistically significant (P = .12). The crude odds ratio of ischemic stroke for subjects in the upper 20% (> 12.7 nmol/mL) compared with those in the bottom 80% of homocyst(e)ine levels was 1.4 (95% confidence interval, 0.8 to 2.2). The odds ratio was 1.2 (95% confidence interval, 0.7 to 2.0) after controlling for several risk factors and other potential confounders. In subgroup analyses, elevated homocyst(e)ine levels appeared to be more strongly predictive of ischemic stroke in normotensive subjects and in men 60 years or younger. Although not statistically significant, in these subgroups increases in risks of 100% and 70%, respectively, were observed for men in the upper 20% of homocyst(e)ine values.
In this study, the data were compatible with a small but nonsignificant association between elevated plasma homocyst(e)ine and risk of ischemic stroke. However, since the sample size is small and the confidence intervals are wide, either no association or a moderate increase in risk cannot be excluded, particularly in subgroups otherwise at low risk, eg, younger men and those with normal blood pressure.
Crossed cerebellar hypoperfusion indicates the degree of uncoupling between blood flow and metabolism in major cerebral arterial occlusion.
Authors: Yamauchi H , Fukuyama H , Kimura J , Ishikawa M , Kikuchi H 
Published: June 2011

In patients who have major cerebral arterial occlusive disease with low perfusion, a decrease in cerebral metabolism may be reflected by a reduction in contralateral cerebellar blood flow (crossed cerebellar hypoperfusion). This study was done to investigate whether comparison of the extent of cerebral blood flow asymmetry and crossed cerebellar hypoperfusion could be used to estimate the degree of uncoupling of cerebral blood flow and metabolism on the basis of a single blood flow study.
We used positron emission tomography before and after reconstructive vascular surgery to evaluate regional blood flow and oxygen metabolism in the cerebral and cerebellar cortexes of 11 patients with major cerebral arterial occlusive disease.
Preoperatively these patients had cortical blood flow asymmetry in the middle cerebral artery territory. The degree of crossed cerebellar hypoperfusion had no relation to the extent of cerebral blood flow asymmetry but was significantly correlated with the extent of asymmetry in cerebral oxygen metabolism. The preoperative extent of asymmetry in the cerebral oxygen extraction fraction and the postoperative improvement of asymmetry in cerebral blood flow were correlated with the preoperative difference between the severity of cerebral blood flow asymmetry and crossed cerebellar hypoperfusion.
The difference between the extent of cerebral blood flow asymmetry and crossed cerebellar hypoperfusion can be used to estimate the degree of uncoupling between blood flow and metabolism, which can in turn predict the postoperative improvement of cerebral blood flow asymmetry. We suggest that this approach may be a simple means of estimating the relative uncoupling between blood flow and metabolism from a single blood flow study in patients who have major cerebral arterial occlusive disease with low perfusion.
Stroke in patients with diabetes. The Copenhagen Stroke Study.
Authors: Jørgensen H , Nakayama H , Raaschou H O , Olsen T S 
Published: June 2011

Although diabetes is a strong risk factor for stroke, it is still unsettled whether stroke is different in patients with and without diabetes. This is true for stroke type, stroke severity, the prognosis, and the relation between admission glucose levels and stroke severity/mortality.
This community-based study included 1135 acute stroke patients (233 [20%] had diabetes). All patients were evaluated until the end of rehabilitation by weekly assessment of neurological deficits (Scandinavian Stroke Scale) and functional disabilities (Barthel Index). A computed tomographic scan was performed in 83%.
The diabetic stroke patient was 3.2 years younger than the nondiabetic stroke patient (P < .001) and had hypertension more frequently (48% versus 30%, P < .0001). Intracerebral hemorrhages were six times less frequent in diabetic patients (P = .002). Initial stroke severity, lesion size, and site were comparable between the two groups. However, mortality was higher in diabetic patients (24% versus 17%, P = .03), and diabetes independently increased the relative death risk by 1.8 (95% confidence interval [CI], 1.04 to 3.19). Outcome was comparable in surviving patients with and without diabetes, but patients with diabetes recovered more slowly. Mortality increased with increasing glucose levels on admission in nondiabetic patients independent of stroke severity (odds ratio, 1.2 per 1 mmol/L; CI, 1.01 to 1.42; P = .04). This was not the case in diabetic patients.
Diabetes influences stroke in several aspects: in age, in subtype, in speed of recovery, and in mortality. Increased glucose levels on admission independently increase mortality from stroke in nondiabetic but not in diabetic patients. The effect of reducing high admission glucose levels in nondiabetic stroke patients should be examined in future trials.
Transcranial Doppler is valid for determination of the lower limit of cerebral blood flow autoregulation.
Authors: Larsen F S , Olsen K S , Hansen B A , Paulson O B , Knudsen G M 
Published: June 2011

This study validates transcranial Doppler sonography (TCD) for determination of the lower limit of cerebral blood flow (CBF) autoregulation and establishes a relation between global CBF and mean flow velocity (Vmean) in the middle cerebral artery.
Relative changes in CBF and in Vmean were compared in 12 normal volunteers (2 women and 10 men; median age, 30 years [range, 21 to 61 years]). Catheters was placed in the left radial artery and in the bulb of the right internal jugular vein, respectively. Baseline CBF was measured by single-photon emission computed tomography scanning; concomitantly, blood samples were drawn for calculation of the cerebral arteriovenous oxygen difference. Then changes in mean arterial pressure (MAP) were induced, and relative changes in global CBF were calculated according to Fick's principle assuming a constant cerebral oxygen metabolism. MAP was increased 30 mm Hg by norepinephrine infusion and was decreased by lower body negative pressure. Vmean was measured in the right middle cerebral artery by a 2-MHz probe, and blood samples were drawn at intervals of 5 mm Hg.
MAP values between 122 (range, 110 to 140) and 48 (range, 34 to 75) mm Hg were measured. The lower limit of autoregulation (the blood pressure under which autoregulation is off) as determined by Vmean did not differ significantly from that determined by relative changes in global CBF: 91 (range, 41 to 108) and 79 (range, 53 to 113) mm Hg, respectively. A significant correlation between Vmean and relative changes in global CBF was demonstrated below the lower limit of autoregulation (R2 = .73, P < .001; CBF = -6.3 + 1.0.Vmean). Above the lower limit both values were stable.
TCD is valid for determination of the lower limit of CBF autoregulation, and changes in CBF may be reliably evaluated by TCD during changes in cerebral perfusion pressure in normal subjects.
Transcranial Doppler detection of vertebrobasilar vasospasm following subarachnoid hemorrhage.
Authors: Sloan M A , Burch C M , Wozniak M A , Rothman M I , Rigamonti D , Permutt T , Numaguchi Y 
Published: June 2011

Transcranial Doppler sonography is of established value in the detection and monitoring of middle cerebral artery vasospasm. Little information exists on the utility of transcranial Doppler for detection of posterior circulation vasospasm.
Cerebral angiography and conventional hand-held transcranial Doppler sonography were compared to determine sensitivity and specificity of transcranial Doppler for detection of vertebral and basilar artery vasospasm.
Of 59 consecutive subarachnoid hemorrhage patients with transcranial Doppler angiogram correlations, 42 underwent posterior circulation angiography to evaluate 64 vertebral arteries and 42 basilar arteries during the period of risk for vasospasm and had technically adequate transcranial Doppler examinations within 24 hours of the angiogram. A mean flow velocity of 60 cm/s and above was indicative of both vertebral and basilar artery vasospasm. For the vertebral artery, there were 7 true-positive test results, 42 true-negatives, 6 false-positives (unknown cause in 3, increased collateral flow in 1, adjacent vessel vasospasm in 1, hyperperfusion in 1), and 9 false-negatives (anatomic in 7, operator error in 2). Sensitivity was 44% and specificity was 87.5%. For the basilar artery, there were 10 true-positives, 23 true-negatives, 6 false-positives (unknown cause in 4, hyperemia/hyperperfusion in 1, increased collateral flow in 1), and 3 false-negatives (operator error in 2, tortuous vessel course in 1). Sensitivity was 76.9% and specificity was 79.3%. When the diagnostic criterion was changed to > or = 80 cm/s (vertebral artery) and > or = 95 cm/s (basilar artery), all false-positive results were eliminated (specificity and positive predictive value, 100%).
Our data suggest that transcranial Doppler has good specificity for the detection of vertebral artery vasospasm and good sensitivity and specificity for the detection of basilar artery vasospasm. Transcranial Doppler is highly specific (100%) for vertebral and basilar artery vasospasm when flow velocities are > or = 80 and > or = 95 cm/s, respectively.
Prognostic value and reproducibility of measurements of carotid stenosis. A comparison of three methods on 1001 angiograms. European Carotid Surgery Trialists' Collaborative Group.
Authors: Rothwell P M , Gibson R J , Slattery J , Warlow C P 
Published: June 2011

The use of three methods of measuring carotid stenosis, which produce different values on the same angiograms, has caused confusion and reduced the generalizability of the results of research. If the results of future studies are to be properly applied to clinical practice, and if noninvasive methods of imaging are to be properly validated against angiography, a single, standard method of measurement of stenosis on angiograms must be adopted. This standard method should be selected on the bases of its ability to predict risk of ipsilateral carotid distribution ischemic stroke and its reproducibility.
The method of measurement of carotid stenosis used in the European Carotid Surgery Trial (ECST), that used in the North American Symptomatic Carotid Endarterectomy Trial (NASCET), and a method based on the measurement of the common carotid (CC) lumen diameter were studied. Their use in the prediction of ipsilateral carotid distribution ischemic stroke was assessed in 1001 consecutively selected patients randomly assigned to medical treatment in the ECST. Carotid stenosis was measured by two observers working independently, using all three methods, on the angiographic view that showed the most severe stenosis of the symptomatic carotid bifurcation. Interobserver agreement was determined, and 50 angiograms were remeasured to determine intraobserver agreement.
There was little difference in the ability of the three methods to predict ipsilateral carotid distribution ischemic stroke. The CC method was consistently the most reproducible of the three, particularly for stenosis in the clinically important range of 50% to 90%.
The CC method of measurement should be adopted as the standard method of measuring the degree of carotid stenosis on angiograms.
Further comments on the measurement of carotid stenosis from angiograms. North American Symptomatic Carotid Endarterectomy Trial (NASCET) Group.
Authors: Eliasziw M , Smith R F , Singh N , Holdsworth D W , Fox A J , Barnett H J 
Published: June 2011

Three different methods for estimating the percentage of reduction in the diameter of the internal carotid artery (ie, stenosis) have been proposed in the literature. Further comparisons of the methods were carried out with the intent of recommending a current standard for determining the percentage of stenosis from angiograms.
Angiograms from 112 patients were obtained. For each angiogram, stenosis was estimated in the manner of the European Carotid Surgery Trial (ECST method), the North American Symptomatic Carotid Endarterectomy Trial (NASCET method), and by a method using the common carotid artery lumen diameter (CC method).
Although there is much discrepancy among the estimates of stenosis arising from the three different methods for any particular patient, it is possible to predict (on average) the percentage of stenosis from one method to another. The relationship between the NASCET and CC methods is linear, with a mean ratio of distal internal carotid artery to common carotid diameter of 0.62 (SD of 0.11). The variability in the diameter of the common carotid artery lumen stabilizes only beyond 2.5 common carotid diameter units (approximately 20 to 30 mm by conventional angiography) proximal to the bifurcation. Unexpectedly, the relationships between both the ECST and NASCET methods and ECST and CC methods were parabolic (P < .001). The reasons underlying these departures from linearity are uncertain.
The comparability of our results with those reported in the literature regarding the CC and NASCET methods provides further evidence of the reproducibility of methods measuring anatomic features that can be visualized on an angiogram. Disease of the internal carotid artery is one of the important causes of ischemic symptoms. Measuring the narrowest portion of the internal artery relative to the normal portion of the same artery, well beyond the bulb, is a logical method. Moreover, benefits of carotid endarterectomy for patients with 70% to 99% stenosis as determined by the NASCET method have been well established in a clinical trial. Converting from the NASCET method to the CC method, given that the CC method is neither superior nor easier to calculate, is not recommended.
Hypothalamic dopamine release and local cerebral blood flow during onset of heatstroke in rats.
Authors: Kao T Y , Chio C C , Lin M T 
Published: June 2011

Brain dopamine has been implicated as a mediator of brain neuronal damage resulting from ischemic injury. Augmented interleukin-1 production and cerebral ischemia occurred during onset of heatstroke. This study has attempted to ascertain whether heatstroke resulting from hyperthermia causes an increase in hypothalamic dopamine release and to assess whether the administration of an interleukin-1 receptor antagonist (IL-1ra) can attenuate heat-stroke formation.
Both local cerebral blood flow and hypothalamic dopamine release during onset of heatstroke were assessed in saline-treated rats and in rats treated with an IL-1ra. Heat-stroke was induced by exposing the animals to a high ambient temperature. Hypothalamic dopamine release was determined by carbon fiber electrodes combined with in vivo differential pulse amperometry.
During onset of heatstroke, rats with heatstroke displayed higher values of colonic temperature, higher values of hypothalamic dopamine release, and lower values of blood flow in different brain regions compared with normothermic control rats. In another separate experiment in which IL-1ra (200 micrograms/kg IV) was injected 30 minutes before onset of heatstroke, both the augmented hypothalamic dopamine release and diminished cerebral blood flow during onset of heatstroke were significantly attenuated. In addition, the survival time (interval between onset of heatstroke and death) of the rats with heatstroke was prolonged by pretreatment with IL-1ra.
These results suggest that an increase in hypothalamic dopamine release and a decrease in local cerebral blood flow occur during onset of heatstroke. Pretreatment with IL-1ra attenuates the heatstroke formation resulting from cerebral ischemia by reducing hypothalamic dopamine release.
Carotid artery dissection with renal infarcts. Two cases.
Authors: Amarenco P , Seux-Levieil M L , Cohen A , Lévy C , Touboul P J , Bousser M G 
Published: June 2011

Clinical features of carotid artery dissection include ipsilateral local signs, contralateral ischemic stroke, or both. We observed two patients in whom these features were associated with renal infarcts.
A 57-year-old woman had painful Horner's syndrome caused by a right internal carotid artery dissection. On days 3 and 4 she had acute abdominal pain, first on the right side and later on the left. The computed tomographic (CT) scan showed a left renal infarct. No aortic dissection or cardiac source of embolism was found. Transesophageal echocardiography showed a mild dystrophy of the ascending aorta and of the mitral valve. Cerebral angiography showed irregularities of the V3 segment of the left vertebral artery compatible with fibromuscular dysplasia. Erythrocyte sedimentation rate was 100 mm/h, and she complained of intense fatigue. She fully recovered within 3 months. A 53-year-old man had sudden severe abdominal pain followed by headache and difficulty in swallowing. He had 9th, 10th, 11th, and 12th cranial nerve involvement on both sides due to bilateral internal carotid artery dissections and pseudoaneurysms. CT scan showed a left renal infarct. Angiography showed extensive signs of fibromuscular dysplasia involving carotid, vertebral, renal, iliac, and mesenteric arteries as well as a dissection of the left renal artery. Erythrocyte sedimentation rate was 65 mm/h, and he complained of severe fatigue. His neurological signs returned to normal in 6 months.
Renal infarct due to renal artery dissection may occur together with cerebral artery dissection. Acute abdominal pain, increased erythrocyte sedimentation rate, and intense fatigue are the warning symptoms.
Factors related to intracranial hematoma formation in patients receiving tissue-type plasminogen activator for acute ischemic stroke.
Authors: Levy D E , Brott T G , Haley E C , Marler J R , Sheppard G L , Barsan W , Broderick J P 
Published: June 2011

Several studies are currently evaluating tissue-type plasminogen activator (TPA) as a potential therapy in acute ischemic stroke. The possibility of inducing intracranial hematomas, however, introduces an important concern into ultimate evaluation of risk and benefit. This retrospective analysis sought to identify factors associated with intracranial hematoma formation in a pilot phase 1 study of TPA for stroke.
Ninety-four patients received TPA within 3 hours of the onset of an acute ischemic stroke. Five of these patients developed a symptomatic intracerebral hematoma: 3 of 74 (4%) among patients treated within 90 minutes of stroke onset and 2 of 20 (10%) among those treated at 91 to 180 minutes. Three of the 5 died within 2 weeks. The analysis investigated associations between clinical factors and intracerebral hematomas.
Factors significantly related to the development of an intracerebral hematoma were TPA dose and diastolic hypertension. Intracerebral hematomas developed in 4 (18%) of 22 patients given a TPA dose of at least 0.90 mg/kg versus only 1 hematoma in the remaining 72 patients (1%; P < .02, Fisher's exact test). Four (18%) of 22 patients who had initial diastolic blood pressures of at least 100 mm Hg suffered an intracerebral hematoma versus only 1 (1%) of 72 patients (P < .02) with lower initial diastolic pressures.
Since the study was not designed to test specific safety hypotheses, results must not be overinterpreted. Nonetheless, these data emphasize the need for caution in both patient and dose selection for further studies of thrombolytic agents in stroke.
Long-term risk of recurrent stroke after a first-ever stroke. The Oxfordshire Community Stroke Project.
Authors: Burn J , Dennis M , Bamford J , Sandercock P , Wade D , Warlow C 
Published: June 2011

There have been few community-based studies of long-term prognosis after acute stroke. This study aims to provide precise estimates of the absolute and relative risks of stroke recurrence in an unselected cohort of patients with a first-ever stroke.
Six hundred seventy-five patients were registered in a community-based stroke register (the Oxfordshire Community Stroke Project) and prospectively followed for up to 6.5 years. Their relative risk of recurrent stroke was calculated using age- and sex-specific incidence rates for first stroke in Oxfordshire.
One hundred eighty recurrent episodes of stroke were identified, of which 135 were first recurrences. Given survival, the actuarial risk of suffering a recurrence was 30% (95% confidence interval, 20% to 39%) by 5 years, about nine times the risk of stroke in the general population. The risk was highest early after the first stroke: 13% (95% confidence interval, 10% to 16%) by 1 year, 15 times the risk in the general population. After the first year the average annual risk was about 4%. The risk of stroke recurrence did not appear to be related to age or pathological type of stroke.
The absolute and relative risks of recurrent stroke are highest early after the first stroke but remain elevated for several years thereafter. Efforts at secondary prevention should be initiated as soon as possible and continued for several years to gain greatest benefit.