bluuebunny/crossref_metadata_2025_split huggingface dataset:
Perimesencephalic subarachnoid hemorrhage. Additional perspectives from four cases.
Authors: Schievink W I , Wijdicks E F , Piepgras D G , Nichols D A , Ebersold M J 
Published: June 2011

Nonaneurysmal perimesencephalic hemorrhage, a distinct form of subarachnoid hemorrhage, is a recently described variant of intracranial hemorrhage. We describe two patients who presented with unusual features of this type of subarachnoid hemorrhage and also two patients who had a perimesencephalic pattern of hemorrhage due to a ruptured posterior circulation aneurysm.
The first patient, a 41-year-old woman with perimesencephalic hemorrhage, underwent an exploratory craniotomy because angiography had suggested an anomaly of the basilar tip. No source of hemorrhage could be identified at the time of surgery. The second patient was a 3-year-old boy who presented with opisthotonos and who was found to have a perimesencephalic hemorrhage. Angiography revealed no source for the hemorrhage. The third patient, a 54-year-old man, had a perimesencephalic pattern of subarachnoid hemorrhage from a vertebrobasilar junction aneurysm associated with a fenestration that was missed on the initial angiographic study. The fourth patient, a 43-year-old man, suffered a perimesencephalic pattern of subarachnoid hemorrhage from a small posterior cerebral artery aneurysm, which had not been recognized on two angiograms.
These patients elaborate on the clinical spectrum of subarachnoid hemorrhage with a perimesencephalic pattern. First, a negative exploratory craniotomy suggests that the source of nonaneurysmal perimesencephalic hemorrhage may not be arterial. Second, nonaneurysmal perimesencephalic hemorrhage may also occur in children. Finally, the index of suspicion for a posterior circulation aneurysm should remain high in patients who present with a perimesencephalic pattern of subarachnoid hemorrhage, and these aneurysms may rise from unusual locations.
Iron-related damage in acute ischemic stroke.
Authors: Dávalos A , Fernandez-Real J M , Ricart W , Soler S , Molins A , Planas E , Genís D 
Published: June 2011

Although iron-mediated mechanisms are important in experimental brain injury after carotid occlusion, their clinical role in acute ischemic stroke has not been determined. We evaluated the influence of iron stores, measured as serum ferritin, on the outcome of acute cerebral infarct.
Admission and fasting glycemia, glycosylated hemoglobin, serum cortisol, serum ferritin, and 24-hour urinary free cortisol levels were measured on the first day of hospitalization in 67 patients admitted with an acute ischemic stroke of less than 24 hours' duration. Patients were classified into two groups according to their Canadian Stroke Scale (CSS) score on day 30: good outcome group (alive and CSS score > 7 points) and poor outcome group (dead or CSS score < or = 7 points).
Thirty-three patients (49%) had good outcome and 34 (51%) poor outcome. Fasting glycemia (P = .001), serum cortisol (P < .001), and urinary free cortisol (P = .001) but not admission glycemia and glycosylated hemoglobin had higher levels in patients with poor outcome. Serum ferritin values were greater in the poor outcome group (218 +/- 156 micrograms/L versus 133 +/- 125 micrograms/L; P = .004), and a correlation between ferritin values and degree of worsening or improvement of the CSS score on day 30 was found (P = .002). Serum cortisol (odds ratio [OR], 6.7; 95% confidence interval [CI], 1.7 to 26), fasting glycemia (OR, 5.4; 95% CI, 1.2 to 24), and serum ferritin (OR, 4.6; 95% CI, 1.1 to 19) were independently related to poor outcome in a logistic regression analysis.
High serum ferritin levels within the first 24 hours of hospitalization for an acute ischemic stroke are related to a poor prognosis, independent of the stress response. More research is needed to determine the origin of increased serum ferritin levels and the therapeutic implications.
Relations of intimal-medial thickness among sites within the carotid artery as evaluated by B-mode ultrasound. ARIC Investigators. Atherosclerosis Risk in Communities.
Authors: Howard G , Burke G L , Evans G W , Crouse J R , Riley W , Arnett D , de Lacy R , Heiss G 
Published: June 2011

B-mode ultrasound is a widely used technique for the clinical and epidemiological assessment of carotid atherosclerosis. This article describes the relation between arterial intimal-medial thickness (IMT) at different sites within the extracranial carotid artery.
IMT was measured by B-mode real-time ultrasound as an index of atherosclerotic involvement in the extracranial carotid arteries as part of the population-based Atherosclerosis Risk in Communities (ARIC) study. The relation between IMT at different sites was described by correlation coefficients and percentile regression techniques based on between 4034 and 9386 pairs of measurements (variation in sample size depending on the paired sites).
Increased IMT at one site was associated with increased IMT at other sites. The correlation between right and left IMT at the same anatomic location in the carotid artery ranged from .34 to .49; the correlation at different anatomic locations in the carotid artery on the same side ranged from .25 to .43. The distribution of IMT, described by the percentiles of IMT at the inference site as a function of IMT at the index site, showed constricted percentiles of IMT at the inference site for small IMT at the index site and an increase in the spread of percentiles with increasing IMT.
Although increased carotid IMT at one site is positively associated with thickened walls at other carotid sites, the ability to accurately predict wall thickness at a site given the wall thickness at other sites is modest. The general association between sites supports the systemic nature of atherosclerosis, while the lack of tight agreement between sites supports the focal nature of the atherosclerotic process.
The importance of family history in cerebrovascular disease.
Authors: Graffagnino C , Gasecki A P , Doig G S , Hachinski V C 
Published: June 2011

The role of genetics in cerebrovascular disease remains controversial. The purpose of this study was to assess the influence of family history on atherothrombotic infarction or transient ischemic attack.
Ninety patients with stroke or transient ischemic attack and 90 age- and sex-matched community control subjects were studied prospectively. Medical and family histories were obtained from all subjects, and a complete physical examination was performed.
Eighty-five patients and 86 control subjects knew their family history for ischemic heart disease and stroke. A positive history for ischemic heart disease was present in 62 (73%) of the patients and 46 (53%) of the control subjects (P = .019), and a positive family history for stroke was present in 38 (47%) of the patients and 21 (24%) of the control subjects (P = .014).
Although a positive vascular family history was not an independent risk factor in a multivariate analysis, it was an excellent marker of the presence of other established vascular risk factors. Personal histories of ischemic heart disease, hypertension, and hyperlipidemia were found to be significant independent risk factors for stroke.
Cost of acute stroke care in Toronto, Canada.
Authors: Smurawska L T , Alexandrov A V , Bladin C F , Norris J W 
Published: June 2011

Stroke cost consumes a large proportion of the gross domestic product in all developed countries, and while health care costs are rising, the ability to contain them is diminishing.
We calculated the cost of acute stroke care for all first admissions to a teaching hospital in Toronto, Canada, in 1991 through 1992 for 285 consecutive patients.
The average cost per patient was $27,500 Canadian, and strokes in men cost less than in women ($23,000 versus $32,000 Canadian), for a total cost of $8 million Canadian over 2 years. More women died than men (34% versus 17%, P < .02), mainly from systemic complications of stroke, but because women stayed hospitalized longer, they cost more in the long term. The major factor determining cost was social support, and more men than women went home or to rehabilitation units (P < .02). Family support was greater for men (82%) than women (39%, P < .0002).
Significant cost reductions are more likely to be achieved by altering discharge policies and improving social conditions for early return to the home than by reducing laboratory or medical personnel costs.
Spinal cord infarcts during long-term inhibition of nitric oxide synthase in rats.
Authors: Blot S , Arnal J F , Xu Y , Gray F , Michel J B 
Published: June 2011

Chronic hypertension is a major predisposing factor for stroke in humans. It has recently been shown that long-term inhibition of nitric oxide synthase activity causes a gradual time-dependent increase in arterial blood pressure in rats. We used this new animal model of chronic hypertension to study the occurrence and spatial features of infarcts in the central nervous system.
Rats were treated with a nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester, dissolved in the drinking water at 50 mg/kg per day for 11 weeks. The brains and spinal cords of hypertensive rats with and without motion disturbances were processed for standard microscopic examination.
Seventy-nine percent of the hypertensive rats showed motion dysfunctions, especially front leg paralysis, and/or died suddenly when their systolic blood pressure reached approximately 215 mm Hg after approximately 7 weeks of treatment. All of the hypertensive rats with stroke had spinal cord infarcts (90% at the cervical or cervicothoracic level) either alone or combined with brain lesions (30%). These structural alterations ranged from focal areas of pale, spongy tissue to large necrotic sites with vascular alterations, including thickened or fibrinoid degenerated vessel wall, macrophage invasion, and reactive astrocytes.
Infarcts occurred in the central nervous system with a high incidence in the spinal cord of hypertensive rats in which nitric oxide synthase was chronically blocked. This location of the hypertensive neuropathologic sequelae contrasts with the model of stroke-prone spontaneously hypertensive rats. The results suggest that nitric oxide is a key factor in spinal cord arteriolar vasomotion and structure in rats.
Brain nitric oxide synthase activity in normal, hypertensive, and stroke-prone rats.
Authors: Clavier N , Tobin J R , Kirsch J R , Izuta M , Traystman R J 
Published: June 2011

Nitric oxide-mediated cerebral vasodilation is altered in spontaneously hypertensive stroke-prone rats. Stroke predisposition in this strain could be related to a genetic defect of brain nitric oxide synthase, the enzyme responsible for nitric oxide production. We tested the hypothesis that brain nitric oxide synthase activity is altered in spontaneously hypertensive stroke-prone rats compared with spontaneously hypertensive or Wistar-Kyoto rats.
A colony of spontaneously hypertensive stroke-prone rats was bred, in which the rate of neurological events under salt load was assessed. In a separate cohort of animals brain nitric oxide synthase activity was measured in spontaneously hypertensive stroke-prone rats (n = 6) and in spontaneously hypertensive (n = 6) and genetically related Wistar-Kyoto rats (n = 6). Calcium dependency of nitric oxide synthase was also assessed in cortical brain samples from the three rat strains to determine if altered calcium-dependent activation of nitric oxide synthase was present.
Brain nitric oxide synthase activity was highest in the cerebellum (eg, spontaneously hypertensive stroke-prone rats: cerebral cortex, 10.6 +/- 0.9; cerebellum, 50.1 +/- 12.0; brain stem, 14.7 +/- 10.3 pmol/mg protein per minute); however, there was no difference among the three rat strains in any region (eg, cerebral cortex: spontaneously hypertensive stroke-prone, 10.6 +/- 0.9; spontaneously hypertensive, 10.8 +/- 0.5; Wistar-Kyoto, 10.9 +/- 0.7 pmol/mg protein per minute) or at any calcium concentration tested.
A genetic defect of brain nitric oxide synthase is unlikely to be the cause of stroke predisposition in spontaneously hypertensive stroke-prone rats.
Changes of circadian blood pressure patterns after hemodynamic and thromboembolic brain infarction.
Authors: Sander D , Klingelhöfer J 
Published: June 2011

We investigated the changes of circadian blood pressure patterns after thromboembolic and hemodynamic brain infarction and evaluated the relation between circadian blood pressure variation, infarct location, and activation of the autonomic nervous system after thromboembolic stroke.
Repeated 24-hour blood pressure measurements were performed in 45 patients with proven first-ever brain infarctions of different origins. Evaluation of serum norepinephrine concentration, prolongation of the QT interval, and degree of cardiac arrhythmias were used to determine the extent of sympathetic activation after thromboembolic stroke.
Whereas circadian blood pressure variation was significantly increased after hemodynamic infarction compared with a control group (diastolic, -25.2 +/- 4.5% versus -13.8 +/- 6.5%; p < .005), a clearly reduced variation was observed after thromboembolic infarction (diastolic, -5.2 +/- 6.9%). Blood pressure variation was positively related to serum norepinephrine concentration (r = .79; P < .01) after thromboembolic infarction. Patients with involvement of the insular cortex showed a nocturnal rise of blood pressure significantly more frequently (66.7% versus 11.8%; P < .005) and had higher norepinephrine levels (66.7 +/- 110 pg/mL versus 290 +/- 178 pg/mL; P < .01) than patients without insular cortex infarction, indicating increased sympathetic activity. This was associated with a significantly more frequent occurrence of QT prolongation and cardiac arrhythmias.
The observed differences in circadian blood pressure patterns may (1) help to distinguish the pathophysiological basis of the stroke, (2) help to explain worsening in some cases of hemodynamic stroke, (3) confirm the importance of the insular cortex for sympathetic activation, and (4) identify subgroups of patients with increased risk of myocardial infarction and arrhythmia.
Trends in incidence, case-fatality rate, and severity of stroke in northern Sweden, 1985-1991.
Authors: Stegmayr B , Asplund K , Wester P O 
Published: June 2011

BACKGROUND AND PURPOSE--Incidence, case-fatality rate at 28 days, and severity of acute stroke were recorded for 7 years in a large population-based stroke register to understand the reasons for the decline in stroke mortality in northern Sweden.
Within the framework of the World Health Organization MONICA Project, acute stroke was monitored in people aged 35 to 74 years in northern Sweden from 1985 through 1991 (target population in 1985, 238,948).
The annual incidence of stroke decreased by an average of 2.3%/y in men aged 35 to 64 years (P = .074) and increased significantly by 1.1%/y in men aged 65 to 74 years (P = .041). No significant changes in incidence occurred in either age group in women. The 28-day case-fatality rate in first-ever strokes (both sexes together) declined from 21.9% to 15.4% in patients aged 65 to 74 years (P = .02). Among survivors, the proportion with extensive motor deficits (at any time during the first 28 days) declined in patients younger than 65 years as well as in those older than 65 years (P = .007 and P = .019, respectively). In patients aged 35 to 64 years, the proportion with aphasia/dysphasia also decreased significantly (P = .032), but no such trend was seen in those aged 65 to 74 years.
A shift toward higher ages has been noted in the occurrence of first-ever strokes in men, while incidence has remained unchanged in women. During the 7 years of observation, stroke has become a less severe disease.
Dynamic transcranial Doppler assessment of positional vertebrobasilar ischemia.
Authors: Sturzenegger M , Newell D W , Douville C , Byrd S , Schoonover K 
Published: June 2011

A hemodynamic as opposed to an embolic origin of vertebrobasilar ischemia may be suspected when symptoms are brief and triggered by changes in the position of the head or neck. It may be difficult, and not without risk, to reproduce the symptoms and to prove the short-lived hemodynamic changes during angiography. If transcranial Doppler sonography (TCD) could detect these changes, it would be useful as a noninvasive screening method to select patients for further diagnostic evaluation.
TCD monitoring of the P1 segments of both posterior cerebral arteries was performed during different head movements in 14 patients referred for evaluation of suspected hemodynamic vertebrobasilar ischemia and in 10 healthy control subjects with a two-channel, 2-MHz, computerized Doppler system. Patients' symptoms were correlated with the Doppler findings.
Four patients with stereotypical symptoms had a severe drop in posterior cerebral artery blood flow velocities (BFVs) to 20% of baseline (mean; SD, 14.3; range, 0% to 48%) and subsequent reactive hyperemia with an increase in BFV to 149% (mean; SD, 20.6; range, 110% to 186%) dependent on head rotation to one side (group 1). Compared with the values found in group 2 patients and in control subjects, these drops were significant (P = .0001 for both). Symptoms together with BFV changes could be reproduced several times. Angiography confirmed severe vertebral artery obstruction during head rotation and the presence of anomalies in the posterior circulation. In 10 patients (group 2), symptoms were not short-lived, stereotyped, or clearly dependent on head movements and could not be reproduced during TCD testing. Their BFVs dropped to 88% (mean; SD, 9.0; range, 64% to 102%) of baseline values during maximal head rotation, to 86% (mean; SD, 10.3; range, 64% to 100%) during flexion, and to 88% (mean; SD, 6.7; range, 75% to 103%) during extension. In the 10 control subjects, BFVs dropped to 86% (mean; SD, 8.8; range, 61% to 98%) of baseline values during rotation, to 90% (mean; SD, 10.3; range, 74% to 107%) during flexion, and to 76% (mean; SD, 17.1; range, 54% to 104%) during extension.
Monitoring posterior cerebral artery BFV during head movements is a simple, noninvasive method to document a hemodynamic etiology of symptoms in patients with suspected positional vertebrobasilar ischemia. The correlation of symptoms to the hemodynamic findings proved a useful screening method to identify those patients with true position-evoked hemodynamic insufficiency in the posterior circulation. These patients should be selected for angiographic evaluation to identify the source and site of arterial compression.
Callosal atrophy in patients with lacunar infarction and extensive leukoaraiosis. An indicator of cognitive impairment.
Authors: Yamauchi H , Fukuyama H , Ogawa M , Ouchi Y , Kimura J 
Published: June 2011

It is unclear why only some patients with lacunar infarction and radiological evidence of diffuse white matter abnormalities have dementia. The purpose of this study is to investigate the value of callosal atrophy as an indicator of cognitive impairment.
We used magnetic resonance imaging to evaluate 11 right-handed male patients with lacunar infarction and extensive white matter hypodensities on computed tomography (8 with dementia and 3 without dementia). The midsagittal corpus callosum area on T1-weighted images was compared with the IQ determined by the Wechsler Adult Intelligence Scale. The relation between these parameters and cerebral oxygen metabolism measured with positron emission tomography was also evaluated in the 8 patients with dementia.
All patients showed diffuse high-intensity areas in the bilateral hemispheric white matter on T2-weighted images. Compared with 19 age- and sex-matched right-handed normal control subjects, the patients had a significantly smaller callosal area. The severity of callosal atrophy, which varied from mild to severe, was significantly related to the total IQ. In the 8 demented patients, the total callosal area was significantly correlated with the mean level of oxygen metabolism in the cerebral white matter.
In patients with lacunar infarction and diffuse white matter abnormalities, the presence of callosal atrophy may indicate cognitive impairment. Callosal atrophy may reflect the severity and extent of white matter damage associated with a decrease in oxygen metabolism, which may determine the severity of intellectual decline.
ST segment depression detected by continuous electrocardiography in patients with acute ischemic stroke or transient ischemic attack.
Authors: McDermott M M , Lefevre F , Arron M , Martin G J , Biller J 
Published: June 2011

Forty percent of patients with a history of ischemic stroke or transient ischemic attack (TIA) have concomitant coronary artery disease. ST segment depression, detected by continuous electrocardiography, is associated with increased cardiac morbidity and mortality in patients with known coronary artery disease. While electrocardiographic changes have been associated with acute stroke, the etiology and significance of these changes remain unclear. In this pilot study we report the prevalence of ST segment depression and ventricular arrhythmias in patients with acute ischemic stroke or TIA monitored by continuous electrocardiography. Clinical predictors of ST segment depression and ventricular arrhythmia are also identified.
Consecutive patients presenting with acute ischemic stroke or TIA were enrolled within 72 hours of hospital admission and monitored by continuous electrocardiography for 48 hours. The electrocardiographic results were analyzed for periods of ST segment depression and ventricular arrhythmias.
Of 51 patients with ischemic stroke or TIA, 15 (29%) had episodes of ST segment depression (95% confidence interval, 15% to 43%), and 18 (35%) had ventricular arrhythmias (95% confidence interval, 21% to 49%). In logistic regression analysis, increasing age (P < .02) and a left-sided neurological event (P < .01) were significant predictors of ST segment depression. Increasing numbers of atherosclerotic risk factors, a history of cardiac disease, and increasing or decreasing mean arterial pressure were not predictive of ST segment depression.
Patients with acute ischemic stroke or TIA have a 29% prevalence of ST segment depression within the first 5 days after their event. In comparison, the prevalence of ST depression is 2.5% to 8% in asymptomatic adults and 43% to 60% in patients with symptomatic coronary artery disease. The association of ST segment depression with left-sided neurological events suggests that the electrocardiographic changes are in part neurologically mediated. Further study is necessary to better define the brain-heart interaction and to determine whether ST segment depression in patients with ischemic stroke or TIA reflects underlying coronary artery disease.