bluuebunny/crossref_metadata_2025 huggingface dataset:
Atherosclerotic Changes in the Carotid Artery Bulb as Measured by B-Mode Ultrasound Are Associated With the Extent of Coronary Atherosclerosis
Authors: Hulthe Johannes , Wikstrand John , Emanuelsson Håkan , Wiklund Olov , de Feyter Pim J. , Wendelhag Inger
Published: June 2011

Background and Purpose
Ultrasound is increasingly used to measure atherosclerotic development in carotid and femoral arteries. The aim of this study was to investigate the relationship between coronary atherosclerosis as measured by quantitative angiography and peripheral atherosclerosis as measured by ultrasound in three different arterial regions.

Methods
Patients (n=32) with at least two coronary segments with visible signs of atherosclerosis as defined in a computer-assisted analysis of coronary angiograms were also examined with B-mode ultrasound. The extent of coronary atherosclerosis was expressed as the average diameter stenosis of coronary segments, and peripheral atherosclerosis was defined as intima-media thickness (IMT) and plaque occurrence in the common carotid artery, the carotid bulb, and the common femoral artery.

Results
The results showed a significant correlation between the ultrasound measurement of IMT of the carotid bulb and diameter stenosis of the included coronary segments (
r
=.68,
P
=.01) and of carotid plaques and diameter stenosis (
P
<.001). The correlation between common carotid IMT and diameter stenosis of included coronary segments was not statistically significant (
r
=.31, NS). There were no significant relationships between common femoral IMT or femoral plaques and diameter stenosis of included coronary segments.

Conclusions
Although this study is small, it points to a very important aspect of ultrasound measurements of atherosclerosis: measurements performed in the common carotid artery or the femoral artery may not relate to coronary atherosclerosis in the same way as measurements performed in the carotid bulb. The findings underline the importance of measuring IMT not only in the common carotid artery but also in the carotid bulb and present data separately. These results have to be confirmed in a larger-scale study.
Microembolic Signals With Serial Transcranial Doppler Monitoring in Acute Focal Ischemic Deficit
Authors: Del Sette Massimo , Angeli Silvia , Stara Isabella , Finocchi Cinzia , Gandolfo Carlo
Published: June 2011

Background and Purpose
The occurrence of microembolic signals (MES) in patients with transient ischemic attack (TIA) or stroke has already been described, but the diagnostic and prognostic value of this finding is still debated.

Methods
We evaluated 90 consecutive patients admitted for their first hemispheric TIA or ischemic stroke within 72 hours of onset. All of them underwent 30-minute bilateral transcranial Doppler monitoring of middle cerebral arteries, within 72 hours of onset. The monitoring was repeated after an additional 24 hours and after 7 days. We then classified the episodes in the following etiologic categories: cardioembolic, atherothrombotic, small-vessel disease, mixed cases, unknown origin, and other causes.

Results
We included 75 patients, with a mean interval of registration of 32.04±19.39 hours. There were 9 patients with MES (12%). All MES were recorded only on the symptomatic middle cerebral artery, and the majority were recorded during the first or the second registration. No statistically significant difference was found in risk factors and hematologic parameters. Five patients (56%) had atherothrombotic episodes, 3 patients (33%) had cardioembolic episodes, and 1 patient (11%) had a protein S deficit. No patient with MES had small-vessel disease (
P
=.01).

Conclusions
MES are an infrequent finding in patients with TIA or ischemic stroke within 72 hours of onset, but they can be recorded more easily with serial registration. In our patients, MES were found only on the symptomatic middle cerebral artery and were present in atherothrombotic and cardioembolic episodes but not in small-vessel disease.
Cerebral Microembolism and Early Recurrent Cerebral or Retinal Ischemic Events
Authors: Babikian Viken L. , Wijman Christine A. C. , Hyde Charles , Cantelmo Nancy L. , Winter Michael R. , Baker Errol , Pochay Val
Published: June 2011

Background and Purpose
We investigated whether cerebral microembolism as detected by transcranial Doppler ultrasonography (TCD) identifies patients at an increased risk for early, recurrent cerebral or retinal ischemic events.

Methods
Records of consecutive patients examined during a 40-month period in the Neurovascular Laboratory were reviewed for the presence of cerebral microembolism. Of the original 302 patients, 229 with 310 arteries met inclusionary criteria. Follow-up information was obtained from the laboratory’s database as well as the hospital records. Microembolus detection studies were performed on TC-2000 or TC-2020 instruments equipped with special software, and criteria established a priori were used for microembolus selection. TCD testing was performed a median interval of 9 days after the initial symptoms of cerebral ischemia. Severity of arterial stenosis was determined by cerebral angiography or noninvasive methods.

Results
Microembolic signals were detected more frequently in symptomatic (40/140; 28.6%) than asymptomatic (21/170; 12.4%) arteries (
P
<.001). Ten recurrent ischemic events occurred during a median follow-up of 8 days after TCD examination, all in the territories of symptomatic arteries. Nine events occurred in the territories of microembolic signal–positive arteries (9/61; 14.8%) and one in the territory of a microembolic signal–negative artery (1/249; 0.4%) (
P
<.001). No association was detected in the subgroup with known cardiac lesions. Microembolic signals were more frequent in arteries with lesions causing 70% or more stenosis or occlusion (26/99; 26.3%) than in those with a degree of stenosis less than 70% (17/126; 13.5%) (
P
=.016).

Conclusions
In this retrospective study, microembolic signals were more common in the territories of symptomatic arteries and particularly those with severely stenotic lesions. During a short follow-up, recurrent ischemic events were more common along the territories of arteries with TCD-detected microembolism and previous symptoms of cerebral or retinal ischemia.
Transoccipital Power-Based Color-Coded Duplex Sonography of Cerebral Sinuses and Veins
Authors: Baumgartner Ralf W. , Nirkko Arto C. , Müri René M. , Gönner Friedrich
Published: June 2011

Background and Purpose
Power-based transcranial color-coded duplex sonography is a new development for cerebrovascular imaging that is suited for detection of slow velocities. The purpose of this study was to evaluate the ability of this technique to detect cerebral sinuses and veins by means of the occipital window and to provide reference data.

Methods
The straight and inferior sagittal sinuses, great and internal cerebral veins, and basal veins were insonated in 120 normal subjects. The number of identified vessels, peak systolic (PSV) and end-diastolic (PDV) velocities, and resistance indices were determined.

Results
In subjects aged 20 to 59 years, straight sinuses were identified in 81% and great and internal cerebral veins in 34%. In subjects aged 60 to 79 years, straight sinuses were detected in 50%, great cerebral veins in 20%, and internal cerebral veins in 13%. All insonated inferior sagittal sinuses and basal veins were missed. Velocities were highest in straight sinuses (PSV, 35 [7 to 64] cm/s; PDV, 23 [2 to 43] cm/s), slower in great cerebral veins (PSV, 23 [12 to 34] cm/s; PDV, 16 [7 to 26] cm/s), and slowest in internal cerebral veins (PSV, 14 [10 to 18] cm/s; PDV, 10 [5 to 15] cm/s) (mean with 95% confidence intervals [CIs]). Straight sinus velocities decreased with age for PSV (20 to 39 years, 40 [7 to 73] cm/s; 60 to 79 years, 28 [9 to 46] cm/s;
P
<.01) and PDV values (20 to 39 years, 28 [4 to 52] cm/s; 60 to 79 years, 16 [5 to 26] cm/s;
P
<.001) (mean with 95% CIs) and were higher in women than men in the group aged 20 to 39 years. (
P
<.05). Resistance indices increased with age in the straight sinus (20 to 39 years, 0.30 [0.18 to 0.42]; 60 to 79 years, 0.42 [0.31 to 0.53];
P
<.001) (mean with 95% CIs).

Conclusions
Transoccipital power-based color-coded duplex sonography enabled imaging and velocity measurements in the straight sinus of subjects aged 20 to 59 years. In elder subjects detection rate of the straight sinus decreased, and it was low for deep cerebral veins in all age groups.
The Influence of Visual Neglect on Stroke Rehabilitation
Authors: Kalra L. , Perez I. , Gupta S. , Wittink M.
Published: June 2011

Background and Purpose
The poor outcome observed in stroke patients with visual neglect may be due to greater stroke severity or nonspecialist management.

Methods
The effects of visual neglect were studied prospectively in 150 consecutive stroke patients with comparable stroke pathology and motor severity managed on a stroke unit. A randomized study was subsequently undertaken in 50 stroke patients with visual neglect to evaluate the effectiveness of spatial cueing during motor activity on functional outcome and resource use in these patients.

Results
Visual neglect was present in 47 (32%) of a selected group of 146 patients (mean age, 77.0±8.2 years; 42% men) with moderate stroke severity. There were no differences in demography, prestroke function, or motor power in the arm (2.6±1.7 versus 2.3±2.1) or the leg (3.2±1.4 versus 3.0±1.6) on the affected side compared with 99 patients with no visual neglect. Although patients with visual neglect had lower median initial (4 versus 5,
P
<.01) and discharge (14 versus 16,
P
<.01) Barthel Index scores, equal proportions of patients were discharged home (60% versus 65%) or to institutions (34% versus 33%) in both groups. The durations of hospitalization (64 versus 36 days,
P
<.001) and therapy input (47.7 versus 27.8 hours,
P
<.01), however, were significantly greater in patients with visual neglect. The randomized controlled study showed a trend toward higher Barthel scores at 12 weeks (14 versus 12.5,
P
=NS) and significant reduction in median length of hospital stay (42 versus 66 days) in patients receiving spatiomotor cueing and early emphasis on functional rehabilitation.

Conclusions
Patients with visual neglect managed on a stroke unit have similar destination of discharge despite lower Barthel Index scores compared with patients of equal stroke severity who do not have this deficit. Spatiomotor cueing and early emphasis on function can improve outcome and reduce resource use in these patients.
Polymorphisms of the Human Platelet Antigens HPA-1, HPA-2, HPA-3, and HPA-5 on the Platelet Receptors for Fibrinogen (GPIIb/IIIa), von Willebrand Factor (GPIb/IX), and Collagen (GPIa/IIa) Are Not Correlated With an Increased Risk for Stroke
Authors: Carlsson Lena E. , Greinacher Andreas , Spitzer Carsten , Walther Reinhard , Kessler Christof
Published: June 2011

Background and Purpose
A recent study has described a high incidence of the human platelet antigen (HPA)-1b alloantigen in patients with myocardial infarction. We investigated the distribution of gene polymorphisms of platelet glycoproteins (GPs) in patients with cerebrovascular disease (CVD) and stroke. The polymorphic systems we have studied are HPA-1 and HPA-3 on the fibrinogen receptor (GPIIb/IIIa), HPA-2 on the von Willebrand factor receptor (GPIb/IX), and HPA-5 on one of the platelet collagen receptors (GPIa/IIa).

Methods
DNA was isolated from peripheral blood collected from 218 consecutive stroke patients, 165 neurological inpatients without signs of CVD, and 321 healthy blood donors. The genotypes of HPA-1, HPA-2, HPA-3, and HPA-5 were determined by sequence specific primer polymerase chain reactions.

Results
The calculated allele frequencies were as follows: for CVD patients, HPA-1a/b 0.81/0.19, HPA-2a/b 0.91/0.09, HPA-3a/b 0.61/0.39, and HPA-5a/b 0.92/0.08; for inpatients, HPA-1a/b 0.83/0.17, HPA-2a/b 0.91/0.09, HPA-3a/b 0.62/0.38, and HPA-5a/b 0.93/0.07; and for blood donors, HPA-1a/b 0.85/0.15, HPA-2a/b 0.94/0.06, HPA-3a/b 0.60/0.40, and HPA-5a/b 0.92/0.08. There were no statistically significant differences for the analyzed HPA polymorphism frequencies either between the CVD patients and the non-CVD inpatients or the CVD patients and blood donors. However, the HPA-1b genotype was slightly more frequent in patients (CVD and non-CVD) than in the healthy blood donors.

Conclusions
Our results indicate that the HPA-1, HPA-2, HPA-3, and HPA-5 polymorphisms are not associated with an increased risk for stroke.
Diagnosis of Cerebral Amyloid Angiopathy
Authors: Greenberg Steven M. , Vonsattel Jean-Paul G.
Published: June 2011

Background and Purpose
Examination of cortical tissue obtained surgically is an important tool for diagnosis of cerebral amyloid angiopathy (CAA) during life. Analysis of a single sample of cortical tissue, however, might lead to conclusions that are either falsely positive (because of the high frequency of CAA in the healthy elderly) or falsely negative (because of the patchy distribution of CAA pathology). We therefore attempted to estimate the sensitivity and specificity of cortical biopsy for diagnosis of CAA as the cause of intracerebral hemorrhage.

Methods
To simulate biopsy in CAA, we took biopsy-sized cortical samples from postmortem brains with known extents of CAA: either CAA-related hemorrhage or mild to severe CAA without hemorrhage. Samples were stained with the use of methods routinely available in surgical pathology laboratories and blindly examined for vascular amyloid and amyloid-related vasculopathic changes.

Results
The presence of vascular amyloid was a sensitive marker for CAA-related hemorrhage, occurring in all 28 specimens from brains with hemorrhage. Conversely, the appearance of fibrinoid necrosis in amyloid-laden vessels was relatively specific for CAA-related hemorrhage. This finding occurred in 13 of the 28 specimens (46%) from brains with hemorrhage but in none of 27 sections from brains with mild CAA and in only 4 of 42 specimens with moderate to severe CAA without hemorrhage.

Conclusions
These data help to define criteria for the diagnosis of CAA-related hemorrhage from surgical specimens.
Multiple-Dose Mannitol Reduces Brain Water Content in a Rat Model of Cortical Infarction
Authors: Paczynski R. P. , He Y. Y. , Diringer M. N. , Hsu C. Y.
Published: June 2011

Background and Purpose
Repeated use of mannitol in the setting of ischemic infarction is a controversial and poorly defined therapeutic intervention. The purpose of this study was to examine the effects of repeated mannitol infusions on brain water content and tissue pressure in a well-defined rat model of focal ischemic stroke.

Methods
Mannitol infusions (0.5, 1.5, or 2.5 g/kg) were given by intravenous bolus 4 or 24 hours after 90-minute transient cortical ischemia in the territory of the right middle cerebral artery in rats and every 4 hours thereafter for a total of 24 hours. Fluid replacement was limited to 0.5 mL IV isotonic saline administered immediately after each mannitol dose. Control rats received 0.5 mL IV saline at the same intervals and were otherwise under ad libitum conditions. Water contents (percent H
2
O) of whole hemispheres and of cortical biopsies were measured with the wet-dry method, and blood samples were analyzed for plasma osmolality and chemistries. In a subgroup of rats, tissue pressure was also measured within the hemisphere ipsilateral to the infarct.

Results
Repeated mannitol infusions resulted in a dose-dependent increase in plasma osmolality and a dose-dependent decrease in the percent H
2
O of the ischemic middle cerebral artery cortex and ipsilateral hemisphere. In contrast, percent H
2
O of the contralateral cortex and hemisphere was significantly decreased only in the groups given the highest dose of mannitol (2.5 g/kg). Mannitol infusions at a dose of 1.5 g/kg begun 24 hours after reperfusion were also associated with a significant reduction of tissue pressure.

Conclusions
In a rat model of ischemic cortical infarction, repeated mannitol infusions resulted primarily in a decrease in the percent H
2
O of the infarct and ipsilateral hemisphere, as well as decreased tissue pressure.
Cerebrovascular and Cardiovascular Measurements During Neurally Mediated Syncope Induced by Head-Up Tilt
Authors: Schondorf Ronald , Benoit Julie , Wein Theodore
Published: June 2011

Background and Purpose
This study examines changes in systemic hemodynamics and in cerebral blood velocity that occur during neurally mediated syncope (NMS) to determine whether cerebral autoregulation is intact or impaired in patients with recurrent NMS.

Methods
Beat-to-beat recordings of heart rate, blood pressure (volume clamp photoplethysmography), stroke volume (impedance cardiography), and right middle cerebral artery blood velocity (transcranial Doppler sonography) were performed at rest and during 80° head-up tilt. Twelve patients with NMS and 10 healthy control subjects were studied.

Results
Baseline values and the initial response to head-up tilt of control subjects and patients with NMS were similar. The mean latency to onset of syncope was 11.8±11.1 minutes. At syncope, heart rate, systolic and diastolic blood pressure, and diastolic cerebral blood velocity decreased significantly, whereas systolic cerebral blood velocity did not change. Calculated cerebrovascular resistance was significantly reduced from 1.85±0.60 to 1.32±0.27 mm Hg/cm per second, whereas the pulsatility index increased from 0.92±0.16 to 1.52±0.21. We never observed a change in cerebral blood velocity before the rapid decline in blood pressure, nor did we observe any significant change in respiratory pattern.

Conclusions
The decrease in cerebrovascular resistance during NMS indicates that the integrity of cerebrovascular autoregulation is maintained even when syncope is imminent. The selective loss of diastolic flow during syncope and the increase in pulsatility index are likely caused by collapse of downstream vessels as diastolic blood pressure decreases below the critical closing pressure of cerebral vessels.
Comparison of Transcranial Color-Coded Sonography and Magnetic Resonance Angiography in Acute Stroke
Authors: Kenton A. R. , Martin P. J. , Abbott R. J. , Moody A. R.
Published: June 2011

Background and Purpose
We sought to compare the ability of transcranial color-coded Doppler sonography (TCCS) and magnetic resonance angiography (MRA) to identify circulatory changes that occur after acute stroke.

Methods
Forty-four patients with a clinical diagnosis of acute stroke were studied with both TCCS and MRA within 24 hours of stroke onset. The appearances of all vessels identified on MRA were divided into three categories: normal, attenuated, and absent vessels. The basal cerebral arteries were identified with the use of TCCS, and their velocities were measured with pulsed-wave Doppler. The side-to-side asymmetry was calculated and expressed as an asymmetry index.

Results
Five patients could not be studied with TCCS because of lack of a suitable acoustic window. An additional 4 patients were too restless to tolerate MRA scanning. Three patients had intracerebral hemorrhages, 2 patients had intracerebral gliomas, and the remaining 30 patients had cerebral infarctions. In the group of patients with acute cerebral infarction, TCCS identified 10 patients with normal asymmetry indices, 1 patient with an increased asymmetry index, 9 patients with decreased asymmetry indices, and 10 patients with occlusion of the symptomatic middle cerebral artery (MCA). MRA identified 8 normal angiograms, 6 patients had attenuated MCA branch vessels, 4 patients had MCA branch occlusions, 2 angiograms demonstrated MCA main stem attenuation, and 10 angiograms showed MCA occlusion.

Conclusions
TCCS and MRA are both noninvasive techniques that can be used to study the acute stroke patient. They both yield information regarding the pathophysiology of acute stroke and may be useful techniques in deciding on therapeutic interventions. The findings agree closely with each other, and these techniques may be useful in the long-term follow-up of stroke patients.
Does the Association of Risk Factors and Atherosclerosis Change With Age?
Authors: Howard George , Manolio Teri A. , Burke Gregory L. , Wolfson Sidney K. , O’Leary Daniel H.
Published: June 2011

Introduction
A decrease in the estimated relative risk of cerebrovascular and cardiovascular diseases associated with known disease risk factors has been observed among elderly cohorts, perhaps suggesting that continued risk factor management in the elderly may not be as efficacious as with younger age groups. In this paper, the differential magnitude of the association of risk factors with atherosclerosis across the age spectrum from 45 years to older than 75 years is presented.

Methods
Subclinical atherosclerosis as measured by carotid ultrasonography and risk factor prevalence were assessed using similar methods among participants aged 45 to 64 years in the Atherosclerosis Risk in Communities (ARIC) study and among participants 65 years and older in the Cardiovascular Health Study (CHS). Pooling these two cohorts provided data on the relationship of risk factors and atherosclerosis on nearly 19 000 participants over a broad age range. Regression analyses were used to assess the consistency of the magnitude of the association of risk factors with atherosclerosis across the age spectrum separately for black and white participants in cross-sectional analyses.

Results
As expected, each of the risk factors was globally (across all ages) associated with increased atherosclerosis. However, the magnitude of the association did not differ across the age spectrum for hypertension, low density lipoprotein cholesterol (LDL-c), fibrinogen, or body mass index (BMI). For whites, there was a significantly greater impact of smoking and HDL-C among older age strata but a smaller impact of diabetes. For black women, the impact of HDL-C decreased among the older age strata.

Conclusions
These data suggest that most risk factors continue to be associated with increased atherosclerosis at older ages, possibly suggesting a continued value in investigation of strategies to reduce atherosclerosis by controlling risk factors at older ages.
Association Between Acute Cerebrovascular Ischemia and Chronic and Recurrent Infection
Authors: Grau Armin J. , Buggle Florian , Ziegler Christoph , Schwarz Wolfgang , Meuser Jutta , Tasman Abel-Jan , Bühler Alexandra , Med Cand , Benesch Christoph , Becher Heiko , Hacke Werner
Published: June 2011

Background and Purpose
We performed a case-control study to investigate whether chronic or recurrent respiratory, ear-nose-throat (ENT), and dental infections are risk factors for cerebrovascular ischemia.

Methods
Using a standardized questionnaire we investigated past infectious diseases in 166 consecutive patients with acute cerebrovascular ischemia and in 166 age- and sex-matched nonstroke neurological patient controls. In subgroups, we performed standardized ENT (69 patients, 66 control subjects) and dental examinations including orthopantomography (66 patients, 60 control subjects). Dental status was determined by a total dental index (TDI) that reflects caries, periapical lesions, periodontitis, and other dental lesions and by an orthopantomography index (OPGI) that was assessed blinded.

Results
Frequent (≥2 episodes in each of the 2 preceding years) or chronic bronchitis was associated with cerebrovascular ischemia in age-adjusted multiple logistic regression analysis (odds ratio, OR, 2.2; 95% confidence interval, CI, 1.04 to 4.6). Groups were not different in ENT examination. Patients tended to have a worse dental status (TDI:
P
=.070; OPGI:
P
=.062) and had more severe periodontitis (
P
=.047) and periapical lesions (
P
=.027) than control subjects. In age-adjusted multiple logistic regression analysis with social status and established vascular risk factors, poor dental status (TDI) was independently associated with cerebrovascular ischemia (OR, 2.6; 95% CI, 1.18 to 5.7).

Conclusion
Recurrent or chronic bronchial infection and poor dental status, mainly resulting from chronic dental infection, may be associated with an increased risk for cerebrovascular ischemia.
Increase in Elastin Gene Expression and Protein Synthesis in Arterial Smooth Muscle Cells Derived From Patients with Moyamoya Disease
Authors: Yamamoto Mari , Aoyagi Masaru , Tajima Shingo , Wachi Hiroshi , Fukai Naomi , Matsushima Yoshiharu , Yamamoto Kiyotaka
Published: June 2011

Background and Purpose
Moyamoya disease is a progressive cerebrovascular occlusive disease that is rare in all ages but frequently presents in children. The etiology of the disease is unknown. We examined elastin gene transcripts and elastin synthesis in cultured arterial smooth muscle cells (SMCs) derived from moyamoya patients and compared them with those in SMCs from age-matched control subjects.

Methods
We used six cell strains from moyamoya patients and four from controls. The expression of elastin protein was observed by Western blot analysis and metabolic labeling with
3
H-valine. Elastin gene transcripts were identified by Northern blot analysis.

Results
Elastin mRNA and protein levels were elevated in all SMCs from moyamoya patients compared with control SMCs. Although transforming growth factor-β1 (TGF-β1), a potent enhancer of the expression of elastin in arterial SMCs, upregulated elastin mRNA and protein levels in SMCs from both moyamoya patients and control subjects, the maximum levels of elastin synthesis and elastin gene transcripts in response to exogenous TGF-β1 were significantly greater in moyamoya SMCs than control SMCs. In addition, quiescent moyamoya SMCs secreted significantly more TGF-β1 into the culture medium than quiescent control SMCs (
P
<.01).

Conclusions
Our findings suggest that moyamoya disease may result, at least in part, from an abnormal regulation of extracellular matrix metabolism that leads to increased steady state levels of elastin mRNA and elastin accumulation in the intimal thickening and that increased elastin accumulation is a stable marker of SMCs from patients with moyamoya disease.
Pure or Predominant Sensory Stroke Due to Brain Stem Lesion
Authors: Kim Jong S. , Bae Yeong H.
Published: June 2011

Background and Purpose
Pure or predominant hemisensory symptoms can be seen in patients with brain stem stroke. However, there have been no reports in which sufficient numbers of patients were studied with detailed descriptions on the sensory patterns and imaging findings.

Methods
We describe 17 patients presenting with pure or predominant hemisensory symptoms due to brain stem stroke in whom CT scan and/or MRI identified appropriate lesions.

Results
Eleven patients had an infarct and 6 had a hemorrhage. Aside from sensory deficit, the majority had dizziness and gait ataxia. Fifteen patients had paramedian dorsal pontine lesions associated with pure or predominant lemniscal sensory involvement, often in the cheiro-oral (n=4) or leg dominance (n=4) patterns. The lesions of the former group tended to be located more medially compared with those of other patients, which is in agreement with the sensory topography of the pontine lemniscal sensory tract. Bilateral facial or perioral sensory symptoms were noted in 6 patients. One patient with a dorsolateral pontine lesion had selective spinothalamic modality impairment, while one with a lateral midbrain infarct had sensory deficit of all modalities.

Conclusions
Pure or predominant brain stem sensory stroke is most often produced by small infarcts or hemorrhages in the paramedian dorsal pontine area and may be differentiated from thalamic pure sensory stroke by the following characteristics: frequent association of dizziness/gait ataxia, predominant lemniscal sensory symptoms, occasional leg dominance or cheiro-oral pattern, and frequent bilateral perioral involvement.
Sleep-Disordered Breathing in Patients With Acute Supra- and Infratentorial Strokes
Authors: Bassetti Claudio , Aldrich Michael S. , Quint Douglas
Published: June 2011

Background and Purpose
Although recent studies suggest a high prevalence of obstructive sleep apnea (OSA) in patients with acute stroke, a systematic characterization of sleep-disordered breathing based on the severity and topography of stroke has not been performed.

Methods
We prospectively studied 39 noncomatose adult subjects (15 women, 24 men; mean age, 57 years) with a first acute stroke. Sleep history, cardiovascular risk factors, stroke severity as estimated by the Scandinavian Stroke Scale, and extent of stroke demonstrated on a computed tomographic or magnetic resonance imaging scan of the brain were assessed. Polysomnography was performed a mean of 10 days (range, 1 to 49 days) after stroke onset. Monitoring of breathing during wakefulness, non–rapid eye movement sleep, and rapid eye movement sleep included measurements of nasal/oral airflow, respiratory effort, and oxygen saturation.

Results
Breathing was abnormal during wakefulness in 7 (18%) subjects and during sleep in 26 (67%). Obstructive sleep apnea (apnea-hypopnea index >10) was found in 14 subjects, Cheyne-Stokes–like breathing was observed in 4, and a combination of obstructive sleep apnea and Cheyne-Stokes–like breathing was observed in 7. Sustained tachypnea and ataxic breathing were rare. No significant differences were found in age, body mass index, history of snoring or hypersomnia, or stroke topography or severity between subjects with and without sleep-disordered breathing. Prevalence and severity of breathing disturbances were also similar between patients with supratentorial stroke (n=28) and those with infratentorial (n=11) stroke.

Conclusions
Sleep-disordered breathing is frequent in patients with acute stroke, rarely has localizing value, and can also be found in patients with mild neurological deficits. Respiratory disturbances in stroke victims can be explained only in part by topography and extension of acute brain damage.
Assessment of Benzodiazepine Receptors Using Iodine-123–Labeled Iomazenil Single-Photon Emission Computed Tomography in Patients With Ischemic Cerebrovascular Disease
Authors: Dong Yun , Fukuyama Hidenao , Nabatame Hidehiko , Yamauchi Hiroshi , Shibasaki Hiroshi , Yonekura Yoshiharu
Published: June 2011

Background and Purpose
[
123
I]Iomazenil (IMZ) is a tracer used for single-photon emission computed tomography (SPECT) that has the characteristics of selectively binding to central benzodiazepine receptors (BZR) in the neuron membrane. To determine whether IMZ SPECT provides new information on assessing neuronal damage after ischemic insult to the brain, we compared IMZ SPECT images with the cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO
2
), and cerebral metabolic rate of glucose (CMRGlc) studied by positron emission tomography in the chronic stage of ischemic stroke.

Methods
Five patients (male; mean age, 63.2±6.0 years) with ischemic cerebrovascular disease and 6 age- and sex-matched normal control subjects were studied. IMZ images obtained 180 minutes after injection were analyzed for BZR binding, and these images were compared with the CBF, CMRO
2
, and CMRGlc obtained by positron emission tomography in the same perfusion areas both visually and quantitatively.

Results
In the visual analysis of data obtained from 4 patients with subcortical infarction, decreased IMZ accumulation was observed locally in the overlying normal-appearing cortices of the affected hemisphere, where extensive hypoperfusion and hypometabolism were seen on the images of CBF, CMRO
2
, and CMRGlc. The regional relative IMZ uptake (regional to cerebellar ratio) for all 5 patients was significantly correlated with the corresponding regional CMRO
2
values (
r
=.45,
P
<.05). However, no significant correlation was found of the IMZ uptake with either the regional CBF or the regional CMRGlc.

Conclusions
The use of IMZ SPECT provides new information on the neuronal alteration induced by chronic ischemic cerebrovascular disease.
Impairment of Vasodilator Function in Basilar Arteries From Aged Rats
Authors: Arribas Silvia M. , Vila Elisabet , McGrath John C.
Published: June 2011

Background and Purpose
Aging is associated with a reduction in cerebral perfusion. Impaired vasodilatation in large brain arteries could be implicated. This study sought age-related changes in vasodilator responses to norepinephrine in rat basilar artery and investigated which aspects of norepinephrine’s action are responsible. To study the effect of aging per se, we used the rat, an animal with resistance to development of age-related pathologies.

Methods
Vascular responses were studied in basilar arteries from young (3 to 4 months old) and old (20 to 22 months old) normotensive Sprague-Dawley rats with wire myography. Endothelial structure was assessed with confocal microscopy.

Results
There was no age-related difference in blood pressure and in KCl or 5-hydroxytryptamine (5-HT) contractions. Relaxation to bradykinin or its absence predicted an intact or denuded endothelium, confirmed by confocal microscopy. Norepinephrine produced concentration-dependent relaxation that was significantly smaller in old rats, with or without endothelium. This response was significantly smaller in endothelium-denuded vessels, or after preincubation with
N
G
-nitro-
l
-arginine methyl ester or propranolol, but not with rauwolscine.

Conclusions
In old and young rats the vasodilator action of norepinephrine in basilar artery is dependent on β-adrenoceptors and nitric oxide. The impaired vasodilatation to norepinephrine found in the basilar artery from old rats might be caused by (1) a reduction in nitric oxide production and/or release or (2) β-adrenoceptor alteration at the endothelium and/or the vascular smooth muscle. This impairment of vasodilator function can be ascribed to the aging process per se and not to other age-related alterations, such as hypertension.
The Role of Blood Pressure and Aldosterone in the Production of Hemorrhagic Stroke in Captopril-Treated Hypertensive Rats
Authors: MacLeod Andrew B. , Vasdev Sudesh , Smeda John S.
Published: June 2011

Background and Purpose
We tested the hypothesis that the lowering of plasma aldosterone levels contributed to the antistroke effects of captopril treatment in Wistar Kyoto stroke-prone spontaneously hypertensive rats (SHRSP).

Methods
The suppression of plasma aldosterone by captopril treatment (50 mg · kg
–1
· d
–1
) was prevented by the subcutaneous infusion of aldosterone into captopril-treated SHRSP. We studied the effect this had on blood pressure (BP) and stroke development.

Results
SHRSP fed a Japanese-style diet containing 4% NaCl developed hypertension and a 100% mortality associated with intracerebral hemorrhage by 14 weeks of age. Captopril treatment from 6 weeks of age did not lower the BP but increased survival past 35 weeks of age. Hydralazine treatment (40 to 80 mg/L of drinking water) lowered BP in SHRSP but was less effective than captopril in retarding stroke. Plasma aldosterone levels were elevated with age in SHRSP after 10 weeks and were higher in poststroke versus prestroke SHRSP. Captopril treatment suppressed plasma aldosterone. When we elevated plasma aldosterone in captopril-treated SHRSP to levels between those present in untreated pre- and poststroke SHRSP, the ability of captopril to retard stroke development was negated. The effects of aldosterone were mimicked by deoxycorticosterone (40 mg/kg, SC2 times/wk) but not by dexamethasone (0.1 mg · kg
–1
· d
–1
, SC). Spironolactone treatment (20 mg · kg
–1
· d
–1
, SC) of SHRSP reduced BP but had little effect on stroke development.

Conclusions
Elevations in plasma aldosterone enhance stroke development within captopril-treated SHRSP through mechanisms that do not involve stimulation of mineralocorticoid receptors or the enhancement of hypertension. The antistroke effects of captopril treatment may be partially mediated through the suppression of plasma aldosterone.
Autoregulation of Cerebral Blood Flow in Orthostatic Hypotension
Authors: Novak Vera , Novak Peter , Spies Judith M. , Low Phillip A.
Published: June 2011

Background and Purpose
—We sought to evaluate cerebral autoregulation in patients with orthostatic hypotension (OH).

Methods
—We studied 21 patients (aged 52 to 78 years) with neurogenic OH during 80° head-up tilt. Blood flow velocities (BFV) from the middle cerebral artery were continuously monitored with transcranial Doppler sonography, as were heart rate, blood pressure (BP), cardiac output, stroke volume, CO
2
, total peripheral resistance, and cerebrovascular resistance.

Results
—All OH patients had lower BP (
P
<.0001), BFV_diastolic (
P
<.05), CVR (
P
<.007), and TPR (
P
<.02) during head-up tilt than control subjects. In control subjects, no correlations between BFV and BP were found during head-up tilt, suggesting normal autoregulation. OH patients could be separated into those with normal or expanded autoregulation (OH_NA; n=16) and those with autoregulatory failure (OH_AF; n=5). The OH_NA group showed either no correlation between BFV and BP (n=8) or had a positive BFV/BP correlation (
R
2
>.75) but with a flat slope. An expansion of the “autoregulated” range was seen in some patients. The OH_AF group was characterized by a profound fall in BFV in response to a small reduction in BP (mean ΔBP <40 mm Hg;
R
2
>.75).

Conclusions
—The most common patterns of cerebral response to OH are autoregulatory failure with a flat flow-pressure relationship or intact autoregulation with an expanded autoregulated range. The least common pattern is autoregulatory failure with a steep flow-pressure relationship. Patients with patterns 1 and 2 have an enhanced capacity to cope with OH, while those with pattern 3 have reduced capacity.
Clinical Correlations of Doppler Microembolic Signals in Patients With Prosthetic Cardiac Valves
Authors: Sliwka Ulrich , Georgiadis Dimitrios
Published: June 2011

Background
—The clinical relevance of Doppler microembolic signals (MES) in patients with prosthetic cardiac valves was evaluated by merging and statistically reanalyzing patient data from four research institutions (Departments of Neurology, Universities of Aachen, Halle, and Münster, Germany; Department of Medicine and Therapeutics, University of Glasgow, Scotland, and Department of Cardiothoracic Surgery, Western Infirmary, Glasgow, Scotland).

Methods
—Transcranial Doppler monitoring for MES was performed over the middle cerebral arteries for 30 to 60 minutes per patient. Prevalence of neurological complications was evaluated with a standard neurological questionnaire in patients carrying the valve implant longer than 3 months (n=369).

Results
—Significant differences in MES prevalence and counts were noted among the 580 patients depending on valve type (presented with medians and [95% confidence intervals]): St Jude Medical, n=200, 72%, 4 [3 to 6]; Björk Shiley Monostrut, n=99, 92%, 133 [93 to 181]; Medtronic Hall, n=80, 47%, 1 [2 to 5]; ATS, n=61, 52%, 3 [2 to 5]; Tecna, n=38, 71%, 2 [1 to 4]; Carbomedics, n=37, 81%, 8 [5 to 13]; Carpentier-Edwards supraannular, n=54, 39%, 1 [0 to 3]; Sorin biological, n=11, 9%, 0 [0 to 0]. No relation between MES counts and valve size, international normalized ratio, patients’ age, cardiac rhythm, or implant duration was noted. No significant differences in MES counts or prevalence (22 [3 to 68] versus 5 [3 to 6] and 63% versus 69%, both
P
>.05), in valve duration, valve position, valve type, patients’ age, sex, cardiac rhythm, or international normalized ratio were evident between neurologically symptomatic (n=42) and asymptomatic patients.

Conclusions
—MES in patients with prosthetic cardiac valves depend on the type and, in certain valve types, the position of the valve implant and possess no direct clinical significance.
Control of Vascular Tone by Endogenous Endothelin-1 in Human Pial Arteries
Authors: Thorin Eric , Nguyen Thanh-Dung , Bouthillier Alain
Published: June 2011

Background and Purpose
—Endothelin-1 (ET) has been shown to be involved in human pathological conditions, but its physiological function remains to be elucidated. The aim of this work was to assess whether endothelium-derived ET was involved in the overall responsiveness of freshly isolated human pial arteries.

Methods
—Samples of cerebral cortex, otherwise discarded, were obtained during tumor or epileptic lesion resections (n=10 donors). Arterial segments were isolated and mounted on a microvessel myograph.

Results
—Inhibition of nitric oxide (NO) formation with
N
ω
-nitro-
l-
arginine (L-NA, 100 μmol/L) increased basal tone by 7±1%E
max
(n=5). This increase in tone was fully abolished in the presence of BQ123 (1 μmol/L; ET
A
receptor antagonist,
P
<.05) but potentiated by a subthreshold concentration of exogenous ET (1 nmol/L; 33±8%E
max
;
P
<.05). In the presence of L-NA, serotonin (10 μmol/L)–induced tone was doubled compared with the control response (
P
<.05) but reduced by 90% in the presence of BQ123 (
P
<.05). In the absence of L-NA, BQ123 prevented serotonin-induced tone (n=3). Oxymetazoline, a selective α
2
-adrenergic receptor agonist, induced an endothelium-dependent relaxation of preconstricted human pial arteries. The relaxation was partially sensitive to NO synthase inhibition and fully prevented by the addition of ET, whereas substance P–induced relaxation was preserved. Glibenclamide (1 μmol/L), an inhibitor of ATP-sensitive K
+
channels and tetraethylammonium (1 mmol/L), an inhibitor of Ca
2+
-activated K
+
channels had no effect on oxymetazoline-induced relaxation.

Conclusions
—The results of this study suggest first that ET is involved in the tonic response induced by NO synthase inhibition; second, part of the contractile response induced by serotonin is endothelium-dependent and sensitive to BQ123; and third, the data suggest that activation of α
2
-adrenergic receptors generated an endothelium-dependent relaxation that was selectively inhibited by exogenous ET.
Weakness of Sympathetic Neural Control of Human Pial Compared With Superficial Temporal Arteries Reflects Low Innervation Density and Poor Sympathetic Responsiveness
Authors: Bevan Rosemary D. , Dodge John , Nichols Patricia , Penar Paul L. , Walters Carrie L. , Wellman Terry , Bevan John A.
Published: June 2011

Background and Purpose
—The primary goal of these studies was to understand and investigate the capacity of perivascular nerves to influence the tone of human pial arteries and to compare them with other human cephalic arteries, the superficial temporal and middle meningeal.

Methods
—Responses to electrical activation of intramural nerves and related features of fresh segments of human cephalic arteries—the pial (PA; 478±34 μm ID), middle meningeal (MMA; 540±41 μm ID), and superficial temporal (STA; 639±49 μm ID)—obtained from patients aged 15 to 82 years during surgical procedures were studied on a resistance artery myograph.

Results
—The PA segment responses to electrical nerve activation and to norepinephrine (NE; 10
−5
mol/L) were 1% and 21% of tissue maximum, respectively, compared with 6% and 34% for the MMA and 14% and 90% for the STA. Tissue maximum was defined as the force increase to 127 mmol/L KCl plus arginine vasopressin (1 μm). All arteries dilated well to acetylcholine. Possible explanations for the PA marginal neurogenic responses were assessed. NE ED
50
was 5.4±2.2×10
−7
mol/L and did not vary with age or diameter. NE responsiveness did not increase in vessels with spontaneous or raised potassium-induced tone. Relaxation to isoproterenol was variable and propranolol did not increase the neurogenic response. Neither
N
G
-monomethyl-
l
-arginine,
N
G
-nitro-
l
-arginine methyl ester, endothelium removal, nor indomethacin consistently influenced the contractions to NE or neurogenic reactivity. The weak PA neurogenic response is in keeping with its poor innervation. As determined by catecholamine histofluorescence, innervation in the PA is sparse, with density increasing in the order PA, MMA, and STA. The incidence of nerve structures in the PA adventitio-medial junction was only 3% of those in the STA, and these were situated more than 3 μm from the closest smooth muscle cell.

Conclusions
—We conclude that the weak neurogenic response of adult human pial artery reflects its poor innervation and responsiveness to NE, implying that these features are not important in the regulation of its diameter.
Ischemic Stroke and Use of Estrogen and Estrogen/Progestogen as Hormone Replacement Therapy
Authors: Petitti Diana B. , Sidney Stephen , Quesenberry Charles P. , Bernstein Allan
Published: June 2011

Background and Purpose
—Information about the risk of stroke in current postmenopausal hormone users is limited.

Methods
—In this case-control study, women aged 45 to 74 years hospitalized with a fatal or nonfatal stroke in any of 10 Northern California Kaiser Permanente facilities during the period November 1991 to November 1994 were identified as cases. Controls were selected at random from female Health Plan members. Data regarding use of estrogen plus progestogen or estrogen alone were obtained in interviews.

Results
—The analysis was based on nonproxy responses from 349 cases of ischemic stroke and 349 matched control subjects. After adjustment for confounders, the odds ratio for ischemic stroke in current hormone users was 1.03 (95% confidence interval, 0.65 to 1.65). The odds ratios for ischemic stroke in current hormone users showed no clear trend of increasing or decreasing risk in relation to duration of hormone use. The odds ratio for ischemic stroke in past hormone users was 0.84 (95% confidence interval, 0.54 to 1.32).

Conclusions
—In this study postmenopausal hormone use was not associated with an increase or decrease in the risk of ischemic stroke, a finding that is consistent with the body of literature on this topic.
Differences in Stroke Between White, Hispanic, and Native American Patients
Authors: Frey James L. , Jahnke Heidi K. , Bulfinch Eric W.
Published: June 2011

Background and Purpose
—Identification of specific features of stroke in minority populations should lead to more effectively focused treatment and prevention.

Methods
—We examined 1290 white (WHI), 242 Hispanic (HIS), 83 Native American (NA), and 101 other stroke and transient ischemic attack (TIA) patients hospitalized at the Barrow Neurological Institute from 1990 through 1996.

Results
—Chi-square analysis detected significant (
P
<.05) differences as follows: (1) Stroke types— lacunes more prevalent in NA than WHI and HIS (30% versus 16% and 15%); cardioembolic more prevalent in WHI than HIS (16% versus 9%, NA 14%); hemorrhages more prevalent in HIS than WHI and NA (48% versus 37% and 27%); (2) Risk factors— hypertension more prevalent in HIS than WHI (72% versus 66%; NA 71%); diabetes more prevalent in NA than HIS and WHI (62% versus 36% and 17%); cigarette smoking more prevalent in WHI than HIS and NA (61% versus 46% and 41%); cardiac disease more prevalent in WHI than HIS (34% versus 24%; NA 27%); heavier alcohol intake in NA than HIS than WHI (43% versus 24% versus 17%). There were no significant outcome differences between races for any stroke type. ANOVA detected significantly lower mean age at stroke onset in NA than HIS than WHI (56 versus 61 versus 69 years).

Conclusions
—There are significant differences in prevalence of risk factors and stroke types between WHI, HIS, and NA in our hospital-based population. Although the three races appear to respond to risk factors similarly, Hispanics may be especially susceptible to hemorrhage. Further evaluation of these observations in community-based studies will be important.