bluuebunny/crossref_metadata_2025 huggingface dataset:
Predictors of Early Deterioration and Mortality in Black Americans With Spontaneous Intracerebral Hemorrhage
Authors: Qureshi Adnan I. , Safdar Kamran , Weil E. Jennifer , Barch Carol , Bliwise Donald L. , Colohan Austin R. , Mackay Bruce , Frankel Michael R.
Published: June 2011

Background and Purpose
Black Americans with spontaneous intracerebral hemorrhage (SICH) may have unique clinical characteristics that affect outcome. The aim of this study was to determine the prognostic value of clinical characteristics and initial CT scan for outcome in black Americans with SICH.

Methods
Clinical and demographic data were extracted from the charts of 182 consecutive black Americans admitted for SICH diagnosed by clinical criteria and initial CT scan. Hemorrhage volumes were calculated from admission CT scans by a computerized method. Univariate and multiple logistic regression analyses were performed to determine independent predictors of early deterioration (defined as a decrease from an initial Glasgow Coma Scale score >12 by ≥4 points within 24 hours from presentation) and mortality.

Results
Both hemorrhage volume and ventricular extension were significant, independent predictors of early deterioration (odds ratio [OR], 6.78; 95% confidence interval [CI], 1.89 to 24.35 and OR, 4.67; 95% CI, 1.30 to 16.72, respectively) and mortality (OR, 6.66; 95% CI, 2.85 to 15.58 and OR, 4.23; 95% CI, 1.82 to 9.82, respectively). A Glasgow Coma Scale score ≤12 also predicted mortality (OR, 3.23; 95% CI, 1.46 to 7.14). Initial mean arterial pressure was not an independent predictor of early deterioration or mortality.

Conclusions
Hemorrhage volume and ventricular extension are the best predictors of early deterioration and mortality in black Americans with SICH.
Time Dependency of the Acetazolamide Effect on Cerebral Hemodynamics in Patients With Chronic Occlusive Cerebral Arteries
Authors: Kuwabara Yasuo , Ichiya Yuichi , Sasaki Masayuki , Yoshida Tsuyoshi , Masuda Kouji
Published: June 2011

Background and Purpose
The acetazolamide effect is thought to reach a maximum at 10 to 20 minutes after administration. However, we sometimes encountered patients who showed a transient deterioration of ischemic symptoms several minutes after acetazolamide administration. We therefore considered that a steal phenomenon may occur before the acetazolamide effect reaches a maximum. We evaluated the time dependency of the acetazolamide effect on cerebral hemodynamics in patients with severe stenosis or occlusion of the unilateral internal carotid artery.

Methods
The subjects consisted of 13 patients with severe stenosis or occlusion of the unilateral internal carotid artery. Regional cerebral blood flow was measured at the resting state and at 5 and 20 minutes after the intravenous administration of 1 g acetazolamide by the use of the [
15
O]H
2
O bolus-injection method and positron emission tomography. The steal phenomenon was interpreted as positive when the regional cerebral blood flow values decreased by more than 10% after the administration of acetazolamide in more than one region of interest.

Results
A steal phenomenon was observed in 5 of 13 patients at 5 minutes after acetazolamide administration on the occlusive side, whereas it was observed in only 1 patient at 20 minutes. Thus, this phenomenon was observed more frequently in the early phase of the acetazolamide test. It was also observed more frequently in patients with poorly developed collateral circulation.

Conclusions
Our acetazolamide [
15
O]H
2
O positron emission tomography study revealed an early steal phenomenon at 5 minutes after intravenous administration of acetazolamide, which may be a cause of the transient deterioration of ischemic symptoms during the acetazolamide test.
Clinical and Prognostic Correlates of Stroke Subtype Misdiagnosis Within 12 Hours From Onset
Authors: Toni Danilo , Fiorelli Marco , De Michele Manuela , Bastianello Stefano , Sacchetti Maria Luisa , Montinaro Ennio , Zanette Elietta Maria , Argentino Corrado
Published: June 2011

Background and Purpose
Pure motor hemiparesis and sensorimotor stroke syndromes are not accurate predictors of lacunar infarct when described in the first 12 hours of stroke onset. We evaluate here whether this inaccuracy of clinical diagnosis might have influenced the planning of patient management either in routine practice or in therapeutic trials.

Methods
A consecutive hospital series of 517 first-ever ischemic hemispheric stroke patients presented lacunar or nonlacunar syndromes at the first examination within 12 hours of the event. A distinction was subsequently made, by means of a CT scan or autopsy performed within 15±2 days of stroke, between patients affected by lacunar or nonlacunar infarcts. We compared stroke risk factors, considered to be indicative of potential pathogenetic mechanisms, and the clinical outcome of lacunar infarct versus nonlacunar infarct patients and those of lacunar syndrome versus nonlacunar syndrome patients.

Results
Two hundred nineteen patients (42%) presented a lacunar syndrome and 298 (58%) a nonlacunar syndrome, while 170 (33%) had lacunar infarcts and 347 (67%) nonlacunar infarcts. Lacunar infarct patients were more frequently associated with hypertension and a previous transient ischemic attack and less frequently with atrial fibrillation when compared with their nonlacunar infarct counterparts, whereas no differences were apparent between lacunar syndrome and nonlacunar syndrome patients. Logistic regression analysis showed that hypertension and a previous transient ischemic attack on the one hand and atrial fibrillation on the other were strongly correlated with the diagnosis of lacunar infarct and nonlacunar infarct, respectively, while no risk factor was correlated with the diagnosis of lacunar syndrome. Twenty-two percent of lacunar infarct patients and 68% of nonlacunar infarct subjects had a poor outcome (death plus disability of survivors) as opposed to 40% of lacunar syndrome and 63% of nonlacunar syndrome patients. Logistic regression selected age, severity of neurological deficit at entry, cardiopathies, diabetes, and lacunar infarct, but not lacunar syndrome, as predictors of outcome.

Conclusions
The inaccurate clinical diagnosis of lacunar infarct made in the first 12 hours of stroke might lead to no distinction being made between stroke subgroups with potentially different pathogenetic mechanisms and prognostic estimates, thus negatively influencing the planning of patient management.
Unified Neurological Stroke Scale Is Valid in Ischemic and Hemorrhagic Stroke
Authors: Edwards Dorothy F. , Chen MSW Yu-Wen , Diringer Michael N.
Published: June 2011

Background and Purpose
The growing interest in testing new therapeutic agents for acute brain injury has lead to increased use of stroke scales. The reliability and validity of these measures need to be examined more completely. We used structural equation modeling, a technique that merges the analytic procedures of factor analysis and multiple regression, to examine the reliability and construct validity of the Middle Cerebral Artery Neurological Scale and the Scandinavian Neurological Stroke Scale used together as the Unified Neurological Stroke Scale. We also analyzed the predictive validity, sensitivity, and specificity of the scales in predicting mortality and functional outcome.

Methods
We prospectively studied 84 consecutive patients admitted to a neurology/neurosurgery intensive care unit with intracerebral hemorrhage (n=30), subarachnoid hemorrhage (n=15), ischemic stroke (n=15), and traumatic brain injury (n=24). Patients were evaluated within 24 hours of admission and at 48-hour intervals until intensive care unit discharge. A total of 386 assessments were obtained. The Functional Independence Measure was administered by telephone 3 months after hospital discharge.

Results
High levels of reliability and construct validity were observed for the majority of the Unified Stroke Scale items. Facial palsy and eye movement items had the lowest reliability and validity. Both the Middle Cerebral Artery and Scandinavian Scales were significant predictors of outcome. Sensitivity and specificity varied by diagnosis. Predictive validity of functional outcome was best in groups with ischemic and hemorrhagic stroke rather than traumatic brain injury and subarachnoid hemorrhage.

Conclusions
The Unified Stroke Scale demonstrates reliability and construct and predictive validity, and its use is supported in ischemic and hemorrhagic stroke. Structural equation modeling is an appropriate technique for use with scales of this type.
Prevalence and Associated Features of the Cold Hemiplegic Arm
Authors: Wanklyn Peter , Forster Anne , Young John , Mulley Graham
Published: June 2011

Background and Purpose
Some stroke patients complain of an unpleasant sensation of coldness in the hemiplegic arm. This study aimed to determine the prevalence of this symptom and any associated features.

Methods
A questionnaire about symptoms in the arms was sent to patients at least 12 months after stroke. Reflex sympathetic dystrophy (RSD) was diagnosed if four typical symptoms were present in the arm.

Results
One hundred patients were recruited and 75 complete replies received. The mean age of the patients was 74 years, and the mean time since the stroke was 19 months. Forty patients (53%) experienced unilateral coldness in the hemiplegic arm. In 14 this sensation was constant, and 10 rated the symptom as troublesome. The symptom developed at a median time of 1 month after stroke, but only 13 patients (32%) sought advice from a doctor. Sensory symptoms and arm and shoulder pain were common, but the only symptoms associated with coldness were numbness (
P
<.001) and color change (
P
<.05). Fifteen patients fulfilled the diagnostic criteria for RSD, 13 of whom had coldness only in the hemiplegic arm.

Conclusions
A sensation of coldness in the hemiplegic arm is common and distressing. It is associated with numbness and color changes in the arm. Some cases are caused by RSD, but other patients have coldness that may be due to other causes such as a vasomotor abnormality.
Familial Aorto-Cervicocephalic Arterial Dissections and Congenitally Bicuspid Aortic Valve
Authors: Schievink Wouter I. , Mokri Bahram
Published: June 2011

Background
A primary arteriopathy is often implicated in the etiology of spontaneous cervicocephalic arterial dissections, but its exact nature usually remains unknown. We describe the familial occurrence of spontaneous arterial dissections and congenitally bicuspid aortic valve (BAV) and propose a common developmental defect in these families.

Summary of Report
In the first family, a 63-year-old man suffered an extracranial internal carotid artery (ICA) dissection, and his 43-year-old cousin with BAV suffered an intracranial vertebral artery (VA) dissection. Two other family members had pathologically proven BAV. In the second family, a 31-year-old woman suffered bilateral extracranial ICA and VA dissections. Her father, at age 46, suffered an aortic dissection associated with cystic medial necrosis and BAV. Her paternal uncle died from an aortic dissection at age 59. In the third family, a 39-year-old woman suffered extracranial ICA and VA dissections, and her brother died at age 48 from an aortic dissection associated with a BAV.

Conclusions
The familial occurrence of spontaneous arterial dissections and BAV suggests a common developmental defect. The aortic valvular cusps and the arterial media of the aortic arch and its branches are derived from neural crest cells, suggesting that a neural crest defect may be the underlying abnormality in these families.
Stroke in Young Black Patients
Authors: Qureshi Adnan I. , Safdar Kamran , Patel Manesh , Janssen Robert S. , Frankel Michael R.
Published: June 2011

Background and Purpose
Stroke subtypes and prognosis differ among older black patients compared with whites; however, few data are available regarding stroke among young black patients.

Methods
To determine the risk factors for stroke, stroke subtype, and prognosis among young black patients, we retrospectively reviewed the medical records of all 15- to 44-year-old patients admitted with stroke to a university-affiliated public hospital from January 1990 through June 1994.

Results
Of the 248 eligible patients admitted with stroke, 219 were blacks. Hypertension was more frequently associated with stroke in young black than in non-black patients (55% versus 24%,
P
=.003). Cocaine abuse was frequent among both black and non-black patients (27% versus 38%,
P
=NS). Hypertensive intracerebral hemorrhage (64%) was the most common subtype of intracerebral hemorrhage (n=67), and lacunar infarction (21%) was the most common subtype of cerebral infarction (n=112) in young black patients. Outcome in black patients with stroke at discharge was 69% independent, 8% dependent, and 23% dead.

Conclusions
The high frequency of hypertension, hypertensive intracerebral hemorrhage, and lacunar infarction among young black patients with stroke suggests accelerated hypertensive arteriolar damage, possibly due to poor control of hypertension.
Geographic Variation in Reporting of Stroke Deaths to Underlying or Contributing Causes in the United States
Authors: Lanska Douglas J. , Peterson Patrick M.
Published: June 2011

Background and Purpose
This study examines the geographic variation in the reporting of deaths with stroke as the underlying or contributing cause in the United States.

Methods
Data from the National Center for Health Statistics and Bureau of the Census were used to map the geographic distribution of race- and race/sex-specific, underlying-, contributing-, and multiple-cause age-adjusted stroke mortality rates in the United States by state for 1979 through 1981.

Results
Underlying-, contributing-, and multiple-cause age-adjusted stroke mortality rates were significantly clustered for both whites and blacks. However, the spatial distributions of underlying- and contributing-cause rates differed; there was no association between underlying- and contributing-cause rates for either racial group or for the various race/sex groups. There was no association between nonstroke mortality and stroke mortality rates. There was also very little spatial variation and no spatial clustering of the median number of contributing causes reported.

Conclusions
The overall large-scale spatial distribution of resident underlying-cause stroke mortality rates cannot be explained by geographic variation in the selection of the underlying cause of death from among all causes reported on the death certificate, by different area-dependent tendencies for mortality generally, or by different tendencies to consider stroke as the cause of death when death occurs. Geographic variation in contributing-cause rates is not explained by variation in tendency to report contributing causes of death.
The Clinical Meaning of Rankin ‘Handicap’ Grades After Stroke
Authors: de Haan R. , Limburg M. , Bossuyt P. , van der Meulen J. , Aaronson N.
Published: June 2011

Background and Purpose
The Rankin Scale is a frequently used handicap index in stroke outcome research. However, relatively little is known about its validity. The purpose of this study was to investigate the clinical meaning of Rankin grades by identifying the functional health aspects that contribute to Rankin scores.

Methods
We studied 438 patients 6 months after stroke. Data were collected on the following functional health indicators: alertness, communication, independence, disability in activities of daily living, mobility, instrumental disability, social interaction, and recreation. Disability in activities of daily living was assessed with the Barthel Index, whereas the other indicators were measured with subscales of the Sickness Impact Profile. The association between functional health and Rankin Scale was expressed in terms of relative frequencies and Somers’ D statistic. Linear regression analysis (after ordinal transformation) was used to identify the significant health factors that explain Rankin scores.

Results
Mobility, disability in daily and instrumental activities, and living arrangements showed a stronger association with Rankin scores (Somers’ D range, 0.60 to 0.74) than cognitive and social functioning (Somers’ D range, 0.34 to 0.47). Disability in activities of daily living turned out to be the most important explanatory factor of Rankin scores (
R
2
=67%).

Conclusions
The Rankin Scale is not a pure handicap measure but should be viewed as a global functional health index with a strong accent on physical disability. The index is useful as a simple and time-efficient outcome measure in large-scale multicenter trials. It is argued that at present there is no clear need to assess handicap as the primary outcome in medically oriented stroke intervention studies.
Role of Stroke Rehabilitation Units in Managing Severe Disability After Stroke
Authors: Kalra Lalit , Eade Judith
Published: June 2011

Background and Purpose
Stroke unit rehabilitation tends to be directed toward stroke patients with moderately severe disabilities (“the middle group”). Data collected on a stroke rehabilitation unit, however, showed improving outcome over 3 years in patients with a poor prognosis (discharge home: 48% versus 16%,
P
<.02; discharge Barthel Index score: 9 versus 6,
P
<.05). The hypothesis that stroke rehabilitation units may improve outcome in severely disabled stroke patients was tested in this study.

Methods
A randomized controlled study was undertaken in 71 patients with a poor prognosis who were treated either on a stroke rehabilitation unit (n=34) or on general wards (n=37) to compare outcome between the two groups. Data collected were also compared with those from a methodologically similar study undertaken 3 years ago.

Results
Severe stroke patients treated on the stroke rehabilitation unit had a significantly better outcome compared with general wards (mortality: 21% versus 46%,
P
<.05; discharge home 47% versus 19%,
P
<.01; median length of hospital stay: 43 versus 59 days,
P
<.02). The number of stroke unit patients being discharged home had increased significantly from the previous study, with a trend toward improvement in median discharge Barthel Index score.

Conclusions
Stroke rehabilitation units may improve outcome in severe stroke patients. This improvement appears to be due to the development of innovative management strategies that reduce mortality and institutionalization and enable caregivers to support more disabled stroke patients at home.
Amino Acid Transmitters in Patients With Headache During the Acute Phase of Cerebrovascular Ischemic Disease
Authors: Castillo J. , Martínez F. , Corredera E. , Aldrey J.M. , Noya M.
Published: June 2011

Background and Purpose
The pathophysiology of headache occurring at stroke onset is unknown. Migraine and ischemia share an excessive release of neuroexcitatory amino acids. Inhibitory amino acids also may be implicated in both diseases. We investigated whether fluctuations of these amino acids occur in headache accompanying cerebral infarction.

Methods
We studied 100 patients with infarction in the territory of the middle cerebral artery. Neurological impairment was assessed using the Canadian Neurological Scale and Barthel Index. Size of infarction was determined with CT. Twenty-eight patients developed headache. Glutamate, aspartate, and taurine were quantified in blood and cerebrospinal fluid (CSF) within 24 hours of stroke onset with cationic exchange chromatography.

Results
Stroke subtypes, size of infarct on CT, and clinical scales were similar in patients with and without headache. Plasma glutamate level was 321.14±149.53 μmol/L in patients with headache and 233±107.23 μmol/L in those without headache (
P
<.005). Glutamate in CSF was higher in patients with headache (4.6±1.49 μmol/L) than in patients without headache (3.11±1.18 μmol/L) (
P
<.001). Aspartate concentrations in plasma and CSF were similar in both groups. Taurine concentrations in plasma were 103.10±52.82 μmol/L and 177.49±90.92 μmol/L in headache and nonheadache patients, respectively (
P
<.001). Taurine levels in CSF were 5.42±2.42 μmol/L in patients with headache and 9.27±5.31 μmol/L in those without headache (
P
<.001). No significant correlation was found between amino acid levels in plasma or CSF and size of infarction.

Conclusions
Amino acid neurotransmitters play a role in the pathophysiology of headache that occurs at the onset of stroke. The ischemic penumbral area, more than the infarction itself, may cause a state of cortical hyperexcitability that would be responsible for the cortical release of amino acids and the induction of headache by altering pain perception mechanisms.
Can Transcranial Doppler Really Detect Reduced Cerebral Perfusion States?
Authors: Sugimori Hiroshi , Ibayashi Setsuro , Fujii Kenichiro , Sadoshima Seizo , Kuwabara Yasuo , Fujishima Masatoshi
Published: June 2011

Background and Purpose
This study was designed to determine whether transcranial Doppler ultrasonography (TCD) may detect reduced perfusion states of the brain in patients with hypertension or diabetes mellitus with suspected cerebral atherosclerosis and arteriolosclerosis.

Methods
We determined blood flow velocity with TCD in the middle cerebral artery and cerebrovascular vasodilator responses to carbon dioxide in 22 patients with or without carotid artery occlusive disease and minor stroke; we compared the results with the measurements of cerebral blood flow and oxygen metabolism by positron emission tomography (PET).

Results
Blood flow velocity measured by TCD correlated with ipsilateral cerebral blood flow measured by PET in frontal, temporal, and striatal regions and throughout the entire hemisphere (
P
<.05 to
P
<.005). Relative changes in blood flow velocity and calculated cerebrovascular resistance tested by carbon dioxide inhalation both correlated closely with regional mean transit time (calculated as the ratio of cerebral blood volume divided by cerebral blood flow) in frontal, striatal, temporal, parietal, and occipital regions and also in the entire hemisphere (
P
<.05 to
P
<.0001). TCD variables did not correlate with hemispheric measurements of oxygen metabolism by PET.

Conclusions
Although TCD is not useful in assessing impairments of cerebral metabolism, it is useful for detecting abnormalities of cerebral hemodynamics among patients with risk factors for cerebrovascular disease.
Acute Effects of Ethanol on Responses of Cerebral Arterioles
Authors: Mayhan William G. , Didion Sean P.
Published: June 2011

Background and Purpose
Previous studies have suggested that acute exposure of large peripheral arteries to ethanol impairs endothelium-dependent relaxation. The goal of the present study was to determine the acute effects of ethanol exposure on responses of cerebral resistance arterioles in vivo.

Methods
We prepared a cranial window in rats to expose the cerebral (pial) microcirculation. We measured the diameter of pial arterioles in vivo in response to agonists that presumably stimulate the synthesis/release of nitric oxide from the endothelium (ADP, acetylcholine, and histamine) or neurons (
N
-methyl-
d
-aspartate [NMDA]) before and after topical application of various concentrations of ethanol added to the cerebrospinal fluid (20, 40, 60, 80, and 100 mmol/L). In addition, we examined responses of pial arterioles to nitroglycerin before and 1 hour after topical application of ethanol.

Results
Before application of ethanol, ADP, acetylcholine, histamine, NMDA, and nitroglycerin produced dose-related dilatation of pial arterioles. Application of the various concentrations of ethanol did not alter the baseline diameter of pial arterioles. However, application of 80 and 100 mmol/L ethanol inhibited dilatation of pial arterioles in response to agonists that stimulate the synthesis/release of nitric oxide. Dilatation of pial arterioles in response to nitroglycerin was not altered by application of ethanol.

Conclusions
The findings of the present study suggest that acute exposure of cerebral arterioles to modest-to-moderate concentrations of ethanol (20 to 60 mmol/L) does not alter responses of cerebral arterioles. In contrast, exposure of cerebral arterioles to higher concentrations of ethanol (80 and 100 mmol/L) can produce specific impairment of dilatation to agonists that stimulate the synthesis/release of nitric oxide from endothelium and neurons.
Prostacyclin Receptor Activation and Pial Arteriolar Dilation After Endothelial Injury in Piglets
Authors: Leffler Charles W. , Fedinec Alexander L. , Shibata Masaaki
Published: June 2011

Background and Purpose
Both light/dye endothelial injury and indomethacin treatment inhibit hypercapnia-induced cerebral prostacyclin synthesis and pial arteriolar dilation in newborn pigs. Topical iloprost can allow hypercapnia-induced dilation of pial arterioles to occur in piglets treated with indomethacin. We addressed the hypothesis that prostacyclin receptor activation with iloprost can return the ability of pial arterioles with endothelial injury to respond to hypercapnia. We also examined whether the endothelial dependence and the permissive role of prostacyclin extended to histamine-induced dilation or are specific for hypercapnia.

Methods
Experiments used chloralose-anesthetized piglets equipped with closed cranial windows. Hypercapnia (Pa
co
2
≈80 mm Hg) and topically applied histamine (10
−6
and 10
−5
mol/L) dilated pial arterioles. Dilations in response to both stimuli were abolished by light/dye treatment.

Results
Simultaneous topical treatment with iloprost (10
−12
mol/L, which caused no residual dilation, returned dilation of pial arterioles to both hypercapnia and histamine. On removal of iloprost, responses were again absent and returned with readdition of iloprost to the cortical cerebrospinal fluid. Neither isoproterenol nor sodium nitroprusside returned responses to hypercapnia after light/dye treatment.

Conclusions
These data add further support to the hypothesis that prostacyclin represents an important endothelial-derived signal in the newborn pig cerebral circulation that can permit appropriate responses by adjacent smooth muscle in response to specific stimuli.
Long-term High-Colloid Oncotic Therapy for Ischemic Brain Edema in Gerbils
Authors: Hakamata Yoji , Ito Umeo , Hanyu Shuji , Yoshida Mitsuo
Published: June 2011

Background and Purpose
We evaluated the effects of long-term administration of high-colloid oncotic pressure on ischemic brain edema in Mongolian gerbils.

Methods
Animals that exhibited stroke after 35 minutes of unilateral forebrain ischemia were used. The gerbils were divided into albumin- (1 g/kg body wt, 25% albumin; n=30) and saline-injected (4 mL/kg; n=30) groups. Both agents were administered intravenously every 12 hours starting immediately after the recirculation. Plasma colloid oncotic pressure, serum sodium and potassium concentrations, and brain water, sodium, and potassium content were measured 24, 48, and 72 hours after recirculation.

Results
Plasma colloid oncotic pressure at 24, 48, and 72 hours after recirculation was significantly higher in the albumin- (26.1±2.3 mm Hg) than in the saline-treated group (18.5±1.9 mm Hg;
P
<.01), and brain water content of the ischemic hemisphere was significantly lower in the albumin group (79.5%, 80.2%, and 80.5%, respectively) than in the saline group (80.9%, 81.6%, and 82.1%, respectively;
P
<.05) at all three time points. Brain sodium content at 24 hours was significantly lower in the albumin than in the saline group (
P
<.05), while brain potassium content at 24 and 48 hours was significantly higher in the albumin than in the saline group (
P
<.05). The changes in brain water and sodium plus potassium content, which were calculated from differences between the ischemic and nonischemic hemispheres, showed a significant correlation in both groups (
P
<.01), but there was no significant difference between the linear regression lines for both groups.

Conclusions
Long-term high-colloid oncotic pressure was effective in treating ischemic brain edema, probably acting by diminishing the bulk flow through the disrupted blood-brain barrier and ameliorating the vasogenic edema.
Cystatin C Mutation in an Elderly Man With Sporadic Amyloid Angiopathy and Intracerebral Hemorrhage
Authors: Graffagnino Carmelo , Herbstreith Michael H. , Schmechel Don E. , Levy Efrat , Roses Allen D. , Alberts Mark J.
Published: June 2011

Background
Cerebral amyloid angiopathy (CAA) with intracerebral hemorrhage (ICH) occurs both sporadically and as a result of mutations in either cystatin C or the amyloid precursor protein. ICH due to cystatin C mutations typically occurs in young people of Icelandic origin.

Case Description
We report a case of sporadic CAA with ICH in an elderly Croatian man with a mutation in cystatin C identical to that found in Icelandic hereditary cerebral hemorrhage with amyloidosis.

Conclusions
This is the first case report of sporadic CAA associated with the same mutation causing hereditary cerebral hemorrhage with amyloidosis of the Icelandic type. Sporadic CAA may thus be associated with genetic mutations in some patients. The frequency of these mutations is yet to be determined.
Stroke in the People’s Republic of China
Authors: He Jiang , Klag Michael J. , Wu Zhenglai , Whelton Paul K.
Published: June 2011

Background and Purpose
Stroke is a major cause of death in the People’s Republic of China (PRC), and the geographic distribution of stroke death varies substantially. We conducted an ecological analysis to investigate the relationship of prevalence of hypertension and other risk factors with stroke incidence and mortality in the PRC.

Methods
The relationship between prevalence of risk factors and stroke incidence and mortality in the PRC was assessed in 29 provinces by examining risk factor data from PRC national surveys and incidence and mortality from the 1986 PRC National Stroke Study.

Results
A highly statistically significant correlation between prevalence of hypertension and stroke incidence (
r
=.838,
P
<.001) and mortality (
r
=.841,
P
<.001) was observed. Prevalence of hypertension explained over 70% of the geographic variability in stroke incidence (partial
R
2
=.703) and mortality (partial
R
2
=.707) in the PRC. There was a north-south gradient, with a higher prevalence of hypertension and stroke incidence and mortality in the north compared with the south of the country. In multiple Poisson regression analysis, a 10% increase in the prevalence of hypertension was associated with a 2.80-fold higher incidence and 2.68-fold higher mortality from stroke, whereas a 10% increase in the prevalence of alcohol consumption was associated with a 29% higher incidence and a 16% higher mortality from stroke. A 10% increase in the prevalence of cigarette smoking was associated with a 19% higher mortality from stroke.

Conclusions
In the PRC, the prevalence of hypertension is strongly associated with the risk of stroke, and the geographic variation in stroke incidence and mortality is due mainly to differences in the prevalence of hypertension.
Emergency Physicians
Authors: Kothari Rashmi U. , Brott Thomas , Broderick Joseph P. , Hamilton Cathy A.
Published: June 2011

Background and Purpose
The role of emergency physicians in trials of acute stroke therapy is expanding. We investigated the ability of emergency physicians to accurately identify patients with stroke.

Methods
We reviewed all 446 patients who were evaluated in the emergency department and had an inpatient admitting or discharge diagnosis of ischemic or hemorrhagic stroke from May 1, 1992, to June 30, 1993. The final admitting diagnosis made by the emergency physician was compared with the final hospital discharge diagnosis, 95% of which were made by neurologists or neurosurgeons.

Results
All 76 patients with a final discharge diagnosis of intracerebral or subarachnoid hemorrhage were correctly diagnosed by the emergency physicians (sensitivity, 100%; positive predictive value, 100%). Of the 351 patients with a final discharge diagnosis of ischemic stroke or transient ischemic attack, 346 were correctly identified by the emergency physicians (sensitivity, 98.6%; positive predictive value, 94.8%). Nineteen patients were diagnosed with stroke or transient ischemic attack by the emergency physician but had a final discharge diagnosis other than stroke. Discharge diagnoses included paresthesia or numbness of unknown causes (3), seizure (2), complicated migraine (2), peripheral neuropathy (2), cranial nerve neuropathy (2), psychogenic paralysis (1), and other (7).

Conclusions
Emergency physicians at a large urban teaching hospital with a comprehensive stroke intervention program can accurately identify patients with stroke, particularly hemorrhagic stroke. If similar accuracy can be documented in other types of hospitals, emergency physicians may become key providers of urgent stroke intervention.
Transcranial Color-Coded Duplex Sonography in Cerebral Arteriovenous Malformations
Authors: Klötzsch Christof , Henkes Hans , Nahser Hans C. , Kühne Dietmar , Berlit Peter
Published: June 2011

Background and Purpose
It is well known that significant changes in cerebral hemodynamics may occur during the treatment of cerebral arteriovenous malformations with the complication of intracerebral hemorrhage and parenchymal edema. We used transcranial color-coded duplex sonography to study alterations in blood flow velocities during staged embolization.

Methods
Forty-one patients aged 40±13 years (mean±SD) with angiographically proven cerebral arteriovenous malformations were studied. The blood flow velocities of the anterior, middle, and posterior cerebral arteries were measured in 16 patients with supratentorial arteriovenous malformations, both before the first and then after each successive embolization (three to seven treatments).

Results
In 29 of 41 patients (71%), transcranial color-coded duplex sonography satisfactorily revealed the malformations and their main feeders. After the final embolization, we found a reduction in the peak flow velocity in treated feeders of 23±28% compared with the values before the first embolization. The untreated feeders showed an increase in peak flow velocities of 12±23% as an expression of increased collateral flow. After the treatment of the supplying feeders, we observed a reduction in flow velocity of 25±13% in seven patients, with cross-filling of the arteriovenous malformation through the contralateral anterior cerebral artery and the anterior communicating artery.

Conclusions
The technical advantage of transcranial color-coded duplex sonography compared with transcranial Doppler sonography is that it allows the exact identification of different feeding arteries in arteriovenous malformations. Repeated measurements during stepwise embolization with corrected insonation angle are easily achieved, and noninvasive quantification of hemodynamic changes is possible. The method may be helpful in the planning of the different steps of embolization.
Hyperbaric Oxygen After Global Cerebral Ischemia in Rabbits Reduces Brain Vascular Permeability and Blood Flow
Authors: Mink Richard B. , Dutka Andrew J.
Published: June 2011

Background and Purpose
Hyperbaric oxygen (HBO) has been advocated as a therapy to improve neurological recovery after ischemia, since HBO may improve tissue oxygen delivery. We examined the effect of HBO treatment after global cerebral ischemia on early brain injury.

Methods
Rabbits were subjected to 10 minutes of global cerebral ischemia by cerebrospinal fluid compression. After 30 minutes of reperfusion, rabbits either were subjected to HBO for 125 minutes and then breathed 100% O
2
at ambient pressure for 90 minutes or breathed 100% O
2
for 215 minutes. At the end of reperfusion and 90 minutes after exposure, brain vascular permeability and cerebral blood flow were measured. Somatosensory evoked potentials were monitored throughout the experiment.

Results
HBO treatment reduced (
P
<.05) brain vascular permeability by 16% in gray matter and by 20% in white matter. Cerebral blood flow was lower (
P
<.05) in the HBO group (40.9±1.9 mL/min per 100 g, mean±SEM) compared with controls (50.8±2.0 mL/min per 100 g). Somatosensory evoked potential recovery was similar in the two groups (
P
>.05).

Conclusions
HBO administered after global cerebral ischemia promoted blood-brain barrier integrity. HBO treatment also reduced cerebral blood flow; this effect was not associated with a reduction in evoked potential recovery. Since neurological outcome after global cerebral ischemia is generally poor and treatment options are limited, HBO should be further investigated as a potential therapy.
Clinical Correlates of Proton Magnetic Resonance Spectroscopy Findings After Acute Cerebral Infarction
Authors: Graham Glenn D. , Kalvach Pavel , Blamire Andrew M. , Brass Lawrence M. , Fayad Pierre B. , Prichard James W.
Published: June 2011

Background and Purpose
We sought to determine whether lactate and
N
-acetyl signals measured by proton magnetic resonance spectroscopy (MRS) in the first days after stroke correlate with clinical measures of disability and functional outcome.

Methods
One-dimensional spectroscopic imaging was performed after stroke on 32 patients using a 2.1-T magnet. The Toronto Stroke Scale score at the time of the MRS study and the Barthel Index score at hospital discharge were determined from patient records. Lesion volume was estimated by a tracing algorithm from the scout magnetic resonance image obtained as part of the MRS study. The scaled lactate and
N
-acetyl signals from the voxel having the highest measured lactate were used to predict the clinical variables and lesion volume, as well as relative perfusion within the lesion, in those patients who underwent single-photon emission computed tomography (SPECT) blood flow imaging, using a multiple regression analysis. The correlation of lesion volume with the clinical variables was also evaluated.

Results
Lesion lactate signal was correlated with the Toronto Stroke Scale score, Barthel Index score, lesion volume, and SPECT score, all at
P
<.01. The
N
-acetyl level correlated with the Barthel Index score and lesion volume at
P
<.05. Lesion volume was also strongly correlated with the clinical variables (
P
<.0001).

Conclusions
This is the first study to document the clinical predictive value of proton MRS measurements in patients after stroke. The association with functional outcome is stronger for lactate than for
N
-acetyl. Spectroscopic assessment of the metabolic status of cerebral tissues shortly after infarction may have significant clinical utility.
Neuron-Specific Enolase in Gerbil Brain and Serum After Transient Cerebral Ischemia
Authors: Horn Markus , Seger Florian , Schlote Wolfgang
Published: June 2011

Background and Purpose
The sensitivity and validity of serum neuron-specific enolase as a marker of brain injury were tested after global cerebral ischemia.

Methods
Sixty-nine Mongolian gerbils were perfusion fixed after variable reperfusion after 5-minute (group 1) or 15-minute (group 2) bilateral carotid occlusion. Neuron-specific enolase was analyzed by an enzyme immunoassay in serum of control, sham-operated, and ischemic animals before euthanasia and in nonischemic gerbil brains. Brains were processed for histology, immunohistochemistry, and morphometric evaluation of ischemic neuronal damage.

Results
After cerebral ischemia, loss of neuronal immunoreactivity was closely associated with increased neuron-specific enolase serum levels, which were significantly elevated by 24 hours (group 1) or by 4 hours (group 2) of reperfusion (
P
<.001). Response of serum levels depended on the duration of preceding ischemia, and maximum concentrations were approximately 3-fold (group 1) or 20-fold (group 2) those of nonischemic control. Morphological damage became apparent 48 hours (group 1) or 12 hours (group 2) after ischemia, as indicated by histological and morphometric data.

Conclusions
Significantly elevated neuron-specific enolase serum levels could be demonstrated as a consequence of ischemia-induced cytoplasmic loss of neuron-specific enolase in central nervous system neurons, corresponded quantitatively to the severity of cerebral ischemia, and were detectable before irreversible neuronal injury. Therefore, analysis of serum neuron-specific enolase is suggested to be both a valuable diagnostic tool in clinical management of the initial stages of global cerebral ischemia and a prognostic parameter during the postischemic course.
Silent Cerebral Infarction in a Community-Based Autopsy Series in Japan
Authors: Shinkawa Atsushi , Ueda Kazuo , Kiyohara Yutaka , Kato Isao , Sueishi Katsuo , Tsuneyoshi Masazumi , Fujishima Masatoshi
Published: June 2011

Background and Purpose
The purpose of this study was to assess the prevalence and characteristics of silent cerebral infarction in a population-based consecutive autopsy series of residents of Hisayama, Kyushu, Japan.

Methods
Autopsy records, cerebral pathological findings, and clinical charts of 966 Hisayama residents recorded during the 26 years from 1961 to 1987 were examined (autopsy rate, 82.4%). The subjects were divided into three groups: those with both clinically apparent strokes and pathologically verified cerebral infarcts (stroke group), those having pathological evidence of cerebral infarction in the brain but without clinical stroke episodes (silent infarction group), and those with neither infarction nor stroke episode (noninfarction group). Risk factors and brain pathology in the three groups were compared.

Results
Silent cerebral infarction was found in 12.9% of the 966 subjects who had undergone autopsy, and its frequency increased with age. The subjects with silent infarcts were older, had higher systolic or diastolic blood pressure, and had atrial fibrillation more frequently than subjects in the noninfarction group. There were no significant differences in the locations of infarcts between the stroke and silent infarction groups, although infarcts tended to be located in the deeper area of the brain in the latter. The number and size of infarcts were smaller in the silent infarction group than in the stroke group.

Conclusions
Diastolic blood pressure and atrial fibrillation appear to be strong predictors of silent cerebral infarction in the Japanese general population. Stroke becomes clinically apparent as infarct volume increases.
Human Leukocyte Antigen in Patients With Moyamoya Disease
Authors: Aoyagi Masaru , Ogami Kazuo , Matsushima Yoshiharu , Shikata Manabu , Yamamoto Mari , Yamamoto Kiyotaka
Published: June 2011

Background and Purpose
Progressive stenosis or occlusion of bilateral internal carotid arteries by fibrocellular intimal thickening results in cerebral ischemia in moyamoya disease. In an attempt to elucidate the still-unknown etiologic factors in moyamoya disease, we assessed human leukocyte antigens in patients with this disease.

Methods
We investigated 32 unrelated Japanese patients with moyamoya disease for typing of human leukocyte antigen A, B, C, and DR/DQ and compared the results with those from 178 unrelated control subjects.

Results
We found a significant association of human leukocyte antigen B51 with moyamoya disease (corrected
P
<.05, χ
2
test). Although no significant associations were observed in DR/DQ typing, the frequency of the B51-DR4 combination was significantly higher in moyamoya patients than in control subjects (
P
<.002, Fisher’s exact test).

Conclusions
These findings suggest that there may be a genetic predisposition for moyamoya disease and that host factors may play a role in the development of intimal thickening in early childhood.
The Cochrane Collaboration Stroke Review Group
Authors: Counsell Carl , Warlow Charles , Sandercock Peter , Fraser Hazel , van Gijn Jan
Published: June 2011

Background
There is a pressing need to identify which interventions are definitely effective in the prevention of stroke and in the treatment and rehabilitation of stroke patients, which interventions are definitely ineffective, and which interventions require further research. This information is most reliably obtained from reviewing all the available evidence from randomized controlled trials in a systematic way.

Summary of Comment
There have been many (at least 800) randomized controlled trials relevant to stroke. It would be difficult for any one individual to keep track of all these trials, and therefore most clinicians, therapists, and researchers are dependent, to some degree, on reviews of this literature. However, most current reviews are unsystematic and tend to be either incomplete or biased, so that their recommendations can be seriously flawed. Until now there has been no attempt to systematically identify all randomized controlled trials relevant to stroke (including subarachnoid hemorrhage), to review the data they contain, and to keep these reviews up-to-date in the light of new evidence. The Stroke Review Group has now been established within the Cochrane Collaboration to try to perform these tasks. There are presently 40 collaborators from 13 countries working on approximately 25 reviews.

Conclusions
Identifying and reviewing all randomized controlled trials relevant to stroke should bring important benefits to patients and all those involved in purchasing or providing care for patients with stroke. The Cochrane Collaboration Stroke Review Group has started this process and would welcome help from anyone interested in collaborating in this enormous task.
Clinical Experience With Excitatory Amino Acid Antagonist Drugs
Authors: Muir Keith W. , Lees Kennedy R.
Published: June 2011

Background
Excitotoxic damage due to excess release of neuronal glutamate is hypothesized to play a pivotal role in the pathogenesis of focal cerebral ischemia. Drugs that antagonize excitatory amino acid function are consistently neuroprotective in preclinical models of stroke, and many are now entering clinical trials.

Summary
Antagonists of the
N
-methyl-
d
-aspartate (NMDA) receptor are furthest advanced in clinical development for stroke. Both noncompetitive (aptiganel hydrochloride, dextrorphan) and competitive (selfotel,
d
-CPPene) antagonists have undergone tolerability studies in acute stroke and traumatic brain injury. These agents all cause a similar spectrum of neuropsychological symptoms, and several have important cardiovascular effects. Other modulatory sites on the NMDA receptor complex, notably the polyamine and magnesium ion sites, are also the subject of clinical trials. Glycine site antagonists are in early clinical development. Non-NMDA glutamate receptor antagonists remain in preclinical study. Neuroprotection by agents that block glutamate release in vitro may be due to sodium channel blockade in vivo, but some agents (619C89) exhibit neurological effects similar to NMDA antagonists in stroke. The therapeutic index is unknown for different drugs but may be determined by cardiovascular effects, especially hypotension, which may be detrimental after stroke.

Conclusions
Excitatory amino acid antagonists are in advanced development in the treatment of stroke and traumatic brain injury. A similar pattern of side effects is apparent with the majority of agents. However, cardiovascular effects may ultimately define therapeutic index for each drug.