bluuebunny/crossref_metadata_2025 huggingface dataset:
Time Course of ADC
w
Changes in Ischemic Stroke: Beyond the Human Eye!
Authors: Nagesh V. , Welch K. M. A. , Windham J. P. , Patel S. , Levine S. R. , Hearshen D. , Peck D. , Robbins K. , D’Olhaberriague L. , Soltanian-Zadeh H. , Boska M. D.
Published: June 2011

Background and Purpose
—Using newly developed computerized image analysis, we studied the heterogeneity of apparent diffusion coefficient of water (ADC
w
) values in human ischemic stroke within 10 hours of onset.

Methods
—Echo-planar trace diffusion-weighted images from 9 patients with focal cortical ischemic stroke were obtained within 10 hours of symptom onset. An Iterative Self-Organizing Data Analysis (ISODATA) clustering algorithm was implemented to segment different tissue types with a series of DW images. ADC
w
maps were calculated from 4 DW images on a pixel-by-pixel basis. The segmented zones within the lesion were characterized as low, pseudonormal, or high, expressed as a ratio of the mean±SD of ADC
w
of contralateral noninvolved tissue.

Results
—The average ADC
w
in the ischemic stroke region within 10 hours of onset was significantly depressed compared with homologous contralateral tissue (626.6±76.8 versus 842.9±60.4×10
−6
mm
2
/s;
P
<0.0001). Nevertheless, ISODATA segmentation yielded multiple zones within the stroke region that were characterized as low, pseudonormal, and high. The mean proportion of low:pseudonormal:high was 72%:20%:8%.

Conclusions
—Despite low average ADC
w
, computer-assisted segmentation of DW MRI detected heterogeneous zones within ischemic lesions corresponding to low, pseudonormal, and high ADC
w
not visible to the human eye. This supports acute elevation of ADC
w
in human ischemic stroke and, accordingly, different temporal rates of tissue evolution toward infarction.
Asymptomatic Embolization in Subjects With Atrial Fibrillation Not Taking Anticoagulants
Authors: Cullinane Marisa , Wainwright Ray , Brown Angie , Monaghan Mark , Markus Hugh S.
Published: June 2011

Background and Purpose
—Embolism is believed to be the major cause of stroke in patients with nonvalvular atrial fibrillation (NVAF). The detection of asymptomatic embolic signals (ES) in individuals with NVAF might allow identification of patients at high risk of stroke and monitoring of therapy in individual subjects. We determined the frequency of asymptomatic ES in patients with NVAF who were not taking warfarin.

Methods
—Bilateral transcranial Doppler recordings were made for 1 hour from the middle cerebral arteries of 111 successive patients with NVAF taking aspirin alone or no antithrombotic or anticoagulant therapy. Adequate recordings could be made in 86 patients. In 79 subjects, recordings were performed on a second occasion to study temporal variability. Recordings for a single hour were also made in 30 age-matched control subjects.

Results
—ES were detected in 13 (15.1%) of NVAF subjects but in no control subjects (
P
=0.02). ES were detected both in subjects with symptomatic NVAF (4 of 30 [13.1%],
P
=0.04 versus controls) and asymptomatic NVAF (9 of 56 [16.1%],
P
=0.02 versus controls). There was no correlation between the presence of ES and smoking status, diabetes, hypertension, aspirin use, aspirin dose, symptomatic status, left atrial size, left ventricular function, or the presence of left atrial thrombus detected on transthoracic echocardiography. Repeating the recording increased the number of patients with ES to 21 (26.6%). On considering the results of both recordings, again there was no association for either recording between the presence of ES and smoking status, diabetes, hypertension, aspirin use, aspirin dose, age, symptomatic status, left atrial size, or left ventricular function. On repeating the recording, in the symptomatic group only 2 patients (8%) changed status, in contrast to 15 (29%) in the asymptomatic group.

Conclusions
—ES can be detected in patients with NVAF at a low frequency. Particularly in asymptomatic patients, ES show marked temporal variability. We found no correlation between the presence of previously reported clinical and echocardiographic markers of increased stroke risk and the presence of ES. This association requires further investigation before the clinical utility of this technique in patients with NVAF is decided.
Retrograde Transvenous Neuroperfusion: A Back Door Treatment for Stroke
Authors: Frazee John G. , Luo Xia , Luan Guoming , Hinton David S. , Hovda David A. , Shiroishi Mark S. , Barcliff Larry T.
Published: June 2011

Background and Purpose
—Stroke is the third leading cause of death and the leading cause of adult disability in the United States. The clot-lysis drug tissue plasminogen activator is the only treatment that has been effective for acute stroke patients, yet there are significant limitations to its use and effectiveness. In this study retrograde transvenous neuroperfusion (RTN) was evaluated for its efficacy in reversing acute ischemia, preventing paralysis, and limiting pathological evidence of infarction in baboons.

Methods
—Ten adult male baboons underwent 3.5 hours of reversible middle cerebral artery occlusion (MCAO) under isoflurane (0.25% to 1.5%) anesthesia. Five randomly chosen animals received RTN treatment 1 hour after start of MCAO. Somatosensory evoked potentials were recorded during MCAO. Animals were assigned daily neurological scores. Animals were killed 6 days after MCAO, and brains were quantitatively analyzed for infarct volume.

Results
—Within 1 hour after RTN was started, treated animals showed significantly improved somatosensory evoked potentials (103.3% versus 75% of baseline;
P
<0.01). Likewise, the combined neurological score for the RTN-treated group was 99.2, while the combined mean score for the untreated group was 66.4 (
P
<0.015). The mean infarction volume was 8.8±3.1% (of contralateral hemisphere) for the control group and 0.3±0.2% for the RTN-treated group (
P
<0.01). No increased mortality was seen in the RTN-treated group.

Conclusions
—We conclude that RTN treatment during MCAO effectively reverses the pathophysiological sequelae of ischemia, even when the treatment is initiated 1 hour after the onset of ischemia. Although the infarct volume in the control group was variable when quantitatively assessed 6 days after 3.5 hours of MCAO, virtually no evidence of infarcts was seen in the RTN-treated group.
Recurrent Intracranial Hemorrhage Due to Postpartum Cerebral Angiopathy
Authors: Ursell Melanie R. , Marras Connie L. , Farb Richard , Rowed David W. , Black Sandra E. , Perry James R.
Published: June 2011

Background
—Postpartum cerebral angiopathy as a cause of hemorrhagic stroke in young women is not well recognized. It is unknown whether this disorder represents a true inflammatory vasculitis or transient vasoconstriction related to the hormonal events of pregnancy and the postpartum period.

Case Description
—A 39-year-old woman presented with postpartum intracranial hemorrhage and, 32 months later, with subarachnoid hemorrhage, following normal pregnancies. Cerebral angiography obtained after each stroke demonstrated diffuse irregularity of branches of the middle cerebral arteries consistent with a diffuse vasospastic process or classic vasculitis. Neurological deficits resolved and results of a transcranial Doppler study normalized after a short course of high-dose corticosteroids following the second stroke.

Conclusions
—Postpartum cerebral angiopathy should be considered in the differential diagnosis of recurrent intracranial hemorrhagic stroke in young women. Recognition of this condition may preclude treatment with potentially toxic therapies for vasculitis and will have important implications for counseling women on subsequent pregnancies.
Fibromuscular Dysplasia of the Extracranial Internal Carotid Arteries Associated With an Ulcerative Plaque
Authors: Hooshmand H. , Boykin M. E. , Vines F. S. , Lee H. M.
Published: June 2011

Fibromuscular dysplasia (FMD) of the extracranial internal carotid arteries is a relatively rare angiographical finding which has been reported as an incidental finding during angiography, as well as in association with a variety of different clinical conditions. A case is reported of transient attacks of amaurosis fugax and hemiparesis. Angiography in this patient revealed bilateral FMD of the internal carotids as well as a small ulcerative plaque involving the right internal carotid artery at the region of carotid bifurcation. Surgical treatment directed toward the ulcerative plaque and not the FMD of the carotid arteries has rendered the patient asymptomatic. Lack of symptoms, despite the persistence of FMD, suggests that FMD is of doubtful pathogenic significance.

A small, surgically correctable ulcerative plaque should not be overlooked in the presence of FMD of the internal carotid arteries. The significance of the rare finding of FMD of the internal carotid arteries is not clear.
Septic Cerebral Embolism
Authors: MOLINARI GAETANO F.
Published: June 2011

In order to study the effects of septic embolism on neurovascular structures, cerebral infarction was produced in a series of dogs by injecting silicone rubber cylinders through an internal carotid artery cannula. Each embolic particle was first incubated with one of four known bacterial pathogens. Death occurred in three animals on the second postoperative day, at which time ten other moribund dogs were sacrificed. Eleven animals made apparently uneventful recoveries from early hemiplegia and appeared well when sacrificed electively one to five weeks after embolism. Autopsies revealed subarachnoid and acute subdural hemorrhages in the early group with gross and microscopic evidence of mycotic aneurysm in each instance. Chronically surviving animals showed histological lesions in the putamen or temporal pole consistent with brain abscess. In this series, mycotic aneurysm with hemorrhage was an extremely dramatic complication of emboli infected with the virulent pathogens,
Staphylococcus aureus
and
Escherichia coli
, while brain abscess developed insidiously in ischemic areas, after embolism with the opportunistic pathogens,
Streptococcus viridans
and
Enterococcus
.
Effect of Intravenous Infusion of Glycerol on Hemispheric Blood Flow and Metabolism in Patients With Acute Cerebral Infarction
Authors: MEYER JOHN STIRLING , FUKUUCHI YASUO , SHIMAZU KUNIO , OHUCHI TADAO , ERICSSON ARTHUR DALE
Published: June 2011

The effects of intravenous infusion of 10% glycerol on regional blood flow and metabolism in infarcted hemispheres was investigated in 17 patients during the acute stage of stroke. Hemispheric blood flow (HBF) increased and cerebral oxygen consumption (CMRO
2
) and carbon dioxide production decreased. Glucose consumption remained constant and hemispheric respiratory quotient (HRQ) decreased. The electroencephalogram improved, and in the majority of patients neurological function also improved. Cerebrospinal fluid pressure (CSFP) did not change during infusion but decreased afterward, and no rebound occurred. Central venous pressure (CVP) and mean arterial blood pressure (MABP) increased both during and after infusion. Intracerebral venous pressure (ICVP) increased during infusion. Mechanisms which may increase HBF following infusion of 10% glycerol are discussed. Expansion of the perivascular space by removal of edema fluid within the glia seems to be a primary factor causing increased HBF. Possible explanations for the measured effects of 10% glycerol on cerebral metabolism and brain function were considered. Inhibition of uncoupling of oxidative phosphorylation (recoupling) appeared to be the most likely explanation for the improvement in brain function and metabolic changes induced with this hyperosmolar solution. The decrease in HRQ is best explained by oxidation of glycerol in the infarcted hemisphere. Intravenous infusion of glycerol appears to be a useful form of therapy in patients with acute cerebral infarction.
Cerebral Vasodilator Therapy in Stroke
Authors: MCHENRY LAWRENCE C.
Published: June 2011

Cerebral vasodilating agents have been questioned as an effective form of therapy for the stroke patient and even have been considered by some to be harmful. Animal studies show that often vasodilating agents will cause an intracerebral steal, but such a reaction has rarely been demonstrated in stroke patients. Several studies measuring cerebral blood flow in man have shown that vasodilating agents will increase cerebral blood flow even in ischemic regions in some patients. Significant clinical studies have not been carried out to determine whether these agents will alter the natural history of the disease. On the basis of reported studies of the effect of vasodilating agents on the cerebral circulation, it is suggested that further laboratory and clinical studies be performed. These agents could potentially be an effective form of therapy in some patients with occlusive cerebrovascular disease.
The Process of Recovery: After Hemiplegia
Authors: NEWMAN MICHAEL
Published: June 2011

A group of 39 patients with hemiplegia due to cerebral infarction was followed from the time of onset for a period of at least 20 weeks. The subjects were selected on the basis of freedom from serious concomitant disease but having neurological disability persisting at least four weeks. The process of recovery was followed with standard neurological and functional tests.

Some neurological recovery occurred in 34 patients. Recovery is usually best in the lower limb, but upper limb movement, sensation, body image, mental ability, and speech may also recover to some extent. Recovery may begin as early as the first week or as late as the seventh. Little neurological improvement took place after the fourteenth week and the average interval from onset to 80% final recovery was six weeks. Functional recovery closely follows neurological recovery.

It is suggested that much of the early recovery and that of the upper limb could be due to return of circulation to ischemic areas. Transfer of function to undamaged neurons is suggested as a mechanism of late recovery, especially of the lower limbs and of speech. The role of cerebral edema is uncertain.
Experimental Brain Ischemia: Protection From Irreversible Damage With a Rapid-Acting Barbiturate (Methohexital)
Authors: YATSU F. M. , DIAMOND I. , GRAZIANO C. , LINDQUIST P.
Published: June 2011

Experimental brain ischemia was produced in rabbits by coupling systemic hypotension and hypoxia. The animals were paralyzed with succinylcholine and ventilated mechanically. Durally implanted electrodes were used to monitor the severity of ischemia. Five minutes of an isoelectric EEG produced irreversible brain damage in most of the rabbits. Four rabbits receiving the rapid-acting barbiturate, methohexital, in the dosage of 5 mg/kg at the onset of the isoelectric EEG showed complete protection from detectable ischemic damage and recovered dramatically. It is suggested that suppression of brain metabolism with barbiturates during cerebral ischemia is worthy of clinical assessment.
Improving the Appropriateness of Carotid Endarterectomy
Authors: Wong John H. , Lubkey Tracey B. , Suarez-Almazor Maria E. , Findlay J. Max
Published: June 2011

Background and Purpose
—In light of previously reported concerns regarding carotid endarterectomy (CEA) use in our city, our goal was to determine the influence of a prospective audit and educational campaign on the performance of CEA with respect to surgical appropriateness and complication frequency.

Methods
—Results of our previous audit of 291 CEAs, along with CEA practice guidelines and notification of prospective surveillance, were supplied to surgeons performing CEA in our city. After this, 184 consecutive patients undergoing CEA from September 1996 to August 1997 were followed prospectively. On the basis of blinded standardized remeasurements of angiographic carotid stenoses, CEA was classified as appropriate for patients with symptomatic carotid stenoses ≥70%, uncertain for those with symptomatic stenoses <70% or asymptomatic stenoses ≥60%, and inappropriate for patients with asymptomatic carotid stenoses <60% or preoperative neurological or medical instability.

Results
—Forty percent of patients were asymptomatic. Compared with our prior audit, the rate of appropriate CEAs improved from 33% previously to 49% of cases in the present study (
P
=0.0005), uncertain indications did not change significantly (49% versus 47%;
P
=0.61), and inappropriate indications dropped from 18% to 4% (
P
=0.00002). Perioperative stroke or death occurred in 6.4% of symptomatic patients but developed in only 2.7% of asymptomatic patients, which was improved from the 5.1% rate previously found.

Conclusions
—In our city, the use of a surgical audit identified areas of concern regarding CEA, and subsequent education and ongoing surveillance significantly improved the use and performance of this procedure.
Reports of Randomized Trials in Acute Stroke, 1955 to 1995
Authors: Dorman Paul J. , Counsell Carl , Sandercock Peter
Published: June 2011

Background and Purpose
—Research in acute stroke has expanded rapidly. Many potentially important interventions lack commercial potential (eg, admission to a stroke unit). We therefore wished to examine the frequency of reports of randomized trials of interventions for acute stroke over the past 40 years, the source of support for such trials, the reporting of the commercial involvement, and whether the proportion of commercially supported trials had changed.

Methods
—Eligible trials were identified from the Cochrane Stroke Group’s specialized register of controlled clinical trials. We included all randomized trials in patients with acute stroke which published a full text report, in English, between 1955 and 1995. Two reviewers independently extracted data on the involvement of the pharmaceutical industry in all eligible trials.

Results
—There was a substantial increase in the number of acute stroke trials published per year between 1955 and 1995. The description of pharmaceutical industry involvement in each trial report was poor. Only a minority of supported trials made explicit statements about the role of the sponsoring company. The proportion of trials apparently supported by the pharmaceutical industry has increased substantially.

Conclusions
—The increasingly important role of the pharmaceutical industry in evaluating new treatments gives substantial scope for bias and may not be in the interests of public health. Poor reporting of the sponsor’s involvement suggests that modifications to the guidelines for the reporting of randomized controlled trials to include more details of the sponsor’s involvement in the design, conduct, management, analysis, and reporting of the trial are justified.
Left Atrial Size and the Risk of Ischemic Stroke in an Ethnically Mixed Population
Authors: Di Tullio Marco R. , Sacco Ralph L. , Sciacca Robert R. , Homma Shunichi
Published: June 2011

Background and Purpose
—The association between left atrial size and ischemic stroke is controversial and has been suggested to exist only in men and to be mediated by left ventricular mass. Data are available almost exclusively for white patients. The purpose of this study was to evaluate the association between left atrial size and ischemic stroke in a multiethnic population.

Methods
—A population-based case-control study was conducted in 352 patients aged >39 years with first ischemic stroke and in 369 age-, gender-, and race-ethnicity–matched community controls. Left atrial diameter was measured by 2-dimensional transthoracic echocardiography and indexed by body surface area. Conditional logistic regression analysis was performed to assess the risk of stroke associated with left atrial index in the overall group and in the age, gender, and race-ethnic strata after adjustment for the presence of other stroke risk factors.

Results
—Left atrial index was associated with ischemic stroke in the overall group (adjusted OR 1.47 per 10 mm/1.7 m
2
of body surface area; 95% CI 1.03 to 2.11). The association was present in men (adjusted OR 2.81, 95% CI 1.42 to 5.57) but not in women (adjusted OR 1.08, 95% CI 0.70 to 1.66), and in patients aged <60 years (adjusted OR 3.78, 95% CI 1.36 to 10.54) but not >60 years (adjusted OR 1.23, 95% CI 0.84 to 1.81). Subgroup analyses showed the risk to be present in men across all age subgroups. In women, the lack of association between left atrial index and stroke was most strongly influenced by left ventricular hypertrophy. A trend toward an association between left atrial index and stroke was observed in whites (adjusted OR 1.81, 95% CI 0.81 to 4.09) and Hispanics (adjusted OR 1.61, 95% CI 0.98 to 2.65) but was less evident in blacks (adjusted OR 1.25, 95% CI 0.74 to 2.14).

Conclusions
—Left atrial enlargement is associated with an increased risk of ischemic stroke after adjustment for other stroke risk factors, including left ventricular hypertrophy. The association is observed in men of all ages, whereas in women it is attenuated by other factors, especially left ventricular hypertrophy. Interracial differences in the stroke risk may exist that need further investigation.
Trends in the Incidence, Severity, and Short-Term Outcome of Stroke in Perth, Western Australia
Authors: Jamrozik Konrad , Broadhurst Robyn J. , Lai Nai , Hankey Graeme J. , Burvill Peter W. , Anderson Craig S.
Published: June 2011

Background and Purpose
—This report describes trends in the key indices of cerebrovascular disease over 6 years from the end of the 1980s in a geographically defined segment of the city of Perth, Western Australia.

Methods
—Identical methods were used to find and assess all cases of suspected stroke in a population of approximately 134 000 residents in a triangular area of the northern suburbs of Perth. Case fatality was measured as vital status at 28 days after the onset of symptoms. Data for first-ever strokes and for all strokes for equivalent periods of 12 months in 1989–1990 and 1995–1996 were compared by age-standardized rates and proportions and Poisson regression.

Results
—There were 355 strokes in 328 patients and 251 first-ever strokes (71%) for 1989–1990 and 290 events in 281 patients and 213 first-ever strokes (73%) for 1995–1996. In Poisson models including age and period, overall trends in the incidence of both first-ever strokes (rate ratio=0.75; 95% confidence limits, 0.63, 0.90) and all strokes (rate ratio=0.73; 95% confidence limits, 0.62, 0.85) were obviously significant, but only the changes in men were independently significant. Case fatality did not change, and the balance between hemorrhagic and occlusive strokes in 1995–1996 was almost indistinguishable from that observed in 1989–1990.

Conclusions
—Our results, which are the only longitudinal population-based data available for Australia for key indices of stroke, suggest that it is a change in the frequency of stroke, rather than its outcome, that is chiefly responsible nationally for the fall in mortality from cerebrovascular disease.
Effects of Some Guanidino Compounds on Human Cerebral Arteries
Authors: Segarra G. , Medina P. , Ballester R. M. , Lluch P. , Aldasoro M. , Vila J. M. , Lluch S.
Published: June 2011

Background and Purpose
—Accumulation of endogenous guanidino-substituted analogues of
l
-arginine in chronic renal failure might contribute to some of the vascular and neurological disorders of this pathology. We tested the hypothesis that in human cerebral arteries, some guanidino compounds may increase vascular tone, through nitric oxide (NO) synthase inhibition, and impair endothelium-dependent relaxation.

Methods
—Rings of human middle cerebral artery were obtained during autopsy of 26 patients who had died 3 to 12 hours before. The rings were suspended in organ baths for isometric recording of tension. We then studied the responses to
N
G
-monomethyl-
l
-arginine (L-NMMA),
N
G
,
N
G
-dimethyl-
l
-arginine (asymmetrical dimethylarginine; ADMA), aminoguanidine (AG), and methylguanidine (MG).

Results
—L-NMMA (10
−6
to 3×10
−4
mol/L) and ADMA (10
−6
to 3×10
−4
mol/L) caused concentration- and endothelium-dependent contractions (median effective concentrations [EC
50
]=1.1×10
−5
and 1.6×10
−5
mol/L, respectively; E
max
=35.5±7.9% and 43.9±5.9% of the response to 100 mmol/L KCl). AG (10
−5
to 3×10
−3
mol/L) and MG (10
−5
to 3×10
−3
mol/L) produced endothelium-independent contractions (E
max
=44.3±8.8% and 45.7±5.8% of the response to 100 mmol/L KCl, respectively).
l
-Arginine (10
−3
mol/L) prevented the contractions by L-NMMA and ADMA but did not change contractions induced by AG and MG. L-NMMA and ADMA inhibited endothelium-dependent relaxation induced by acetylcholine in a concentration-dependent manner; AG and MG were without effect.

Conclusions
—The results suggest that the contractions induced by L-NMMA and ADMA are due to inhibition of endothelial NO synthase activity, whereas AG and MG do not affect the synthesis of NO. An increase in the plasma concentration of L-NMMA and ADMA associated with uremia is likely to represent a diminished release or effect of NO, and consequently, an increased cerebrovascular tone in uremic patients is highly conceivable.
Initial Loss of Consciousness and Risk of Delayed Cerebral Ischemia After Aneurysmal Subarachnoid Hemorrhage
Authors: Hop J. W. , Rinkel G. J. E. , Algra A. , van Gijn J.
Published: June 2011

Background and Purpose
—Delayed cerebral ischemia (DCI) is a major cause of death and disability in patients with aneurysmal subarachnoid hemorrhage. We studied the prognostic value for DCI of 2 factors: the duration of unconsciousness after the hemorrhage and the presence of risk factors for atherosclerosis.

Methods
—In 125 consecutive patients admitted within 4 days after hemorrhage, we assessed the presence and duration of unconsciousness after the hemorrhage, the neurological condition on admission, the amount of subarachnoid blood, the size of the ventricles, and a history of smoking, hypertension, stroke, or myocardial infarction. The relationship between these variables and the development of DCI was analyzed by means of the Cox proportional hazards model.

Results
—The univariate hazard ratio (HR) for the development of DCI in patients who had lost consciousness for >1 hour was 6.0 (95% CI 3.0 to 12.0) compared with patients who had no loss or a <1-hour loss of consciousness. The presence of any risk factor for atherosclerosis yielded an HR of 1.4 (95% CI 0.6 to 3.5). The HR for unconsciousness remained essentially the same after adjustment for other risk factors for DCI. The HR for a poor World Federation of Neurological Surgeons score (grade IV or V) on admission was 2.9 (95% CI 1.5 to 5.5); that for a large amount of subarachnoid blood on CT was 3.4 (95% CI 1.6 to 7.3).

Conclusions
—The duration of unconsciousness after subarachnoid hemorrhage is a strong predictor for the occurrence of DCI. This observation may contribute to a better understanding of the pathogenesis of DCI and increased attention for patients at risk.
Clinical Course, Surgical Management, and Long-Term Outcome of Moyamoya Patients With Rebleeding After an Episode of Intracerebral Hemorrhage
Authors: Yoshida Yasuko , Yoshimoto Takashi , Shirane Reizo , Sakurai Yoshiharu
Published: June 2011

Background and Purpose
—Revascularization surgery for moyamoya patients is believed to prevent cerebral ischemic attacks by improving cerebral blood flow. However, measures preventing the occurrence of hemorrhagic moyamoya in patients have not yet been established in the literature due to the low rate of hemorrhage onset as well as the originally limited numbers of patients with moyamoya disease, poor understanding of the clinical course of rebleeding, correct surgical management, and long-term outcome. We present here the results of an overall survey of patients with hemorrhagic moyamoya disease in a district of Miyagi Prefecture in Japan and examine their clinical course, efficacy of revascularization surgery, and long-term outcome.

Methods
—This study included 28 moyamoya patients with episodes of intracranial hemorrhage between 1976 and 1988. The mean follow-up period was 14.2 years. There were 4 males and 24 females, aged 7 to 69 years (mean 39.2 years). Cerebral angiography and CT scans were performed for all patients. Surgical treatment was performed in 19 patients (67.9%), and 10 patients (35.7%) underwent revascularization surgery. We observed the clinical course of all 28 patients. We also studied the relationship between the efficacy of surgical treatment and long-term outcome.

Results
—Five of the 28 patients (17.9%) died of the initial intracranial hemorrhage, and 2 patients died of other causes. Rebleeding occurred in 6 of the remaining 21 patients (28.6%). The interval to rebleeding ranged from 2 to 20 years (mean 7.3 years). Of these 6 patients, 4 died of rebleeding. Rebleeding was observed in 1 of 8 patients who underwent bypass surgery and in 5 of 13 patients who did not, which suggested that rebleeding was less likely to occur in patients who had undergone bypass surgery. However, there was no significant difference in rebleeding ratio or mortality between patients with and those without revascularization surgery (
P
>0.05).

Conclusions
—In this study, we compiled the results of meticulous follow-up conducted over the past 10 years for patients with hemorrhagic moyamoya disease. Because hemorrhagic moyamoya disease is known for its high rate of mortality at the time of rebleeding and often causes rebleeding long after the initial episode (as much as 20 years later), implementation of long-term preventive measures for rebleeding is necessary. This suggests that a long-term prospective study of a large number of patients with hemorrhagic moyamoya disease is required to determine whether bypass surgery prevents rebleeding of hemorrhagic moyamoya disease.
Hemorrhagic Transformation Within 36 Hours of a Cerebral Infarct
Authors: Fiorelli Marco , Bastianello Stefano , von Kummer Rüdiger , del Zoppo Gregory J. , Larrue Vincent , Lesaffre Emmanuel , Ringleb Arthur P. , Lorenzano Svetlana , Manelfe Claude , Bozzao Luigi
Published: June 2011

Background and Purpose
—The clinical correlates of the varying degrees of early hemorrhagic transformation of a cerebral infarct are unclear. We investigated the cohort of a randomized trial of thrombolysis to assess the early and late clinical course associated with different subtypes of hemorrhagic infarction (HI) and parenchymal hematoma (PH) detected within the first 36 hours of an ischemic stroke.

Methods
—We exploited the database of the European Cooperative Acute Stroke Study I (ECASS I), a randomized, placebo-controlled, phase III trial of intravenous recombinant tissue plasminogen activator in acute ischemic stroke. Findings on 24- to 36- hour CT were classified into 5 categories: no hemorrhagic transformation, HI types 1 and 2, and PH types 1 and 2. We assessed the risk of concomitant neurological deterioration and of 3-month death and disability associated with subtypes of hemorrhagic transformation, as opposed to no bleeding. Risks were adjusted for age and extent of ischemic damage on baseline CT.

Results
—Compared with absence of hemorrhagic transformation, HI1, HI2, and PH1 did not modify the risk of early neurological deterioration, death, and disability, whereas, in both the placebo and the recombinant tissue plasminogen activator groups, PH2 had a devastating impact on early neurological course (odds ratio for deterioration, 32.3; 95% CI, 13.4 to 77.7), and on 3-month death (odds ratio, 18.0; 95% CI, 8.05 to 40.1). Risk of disability was also higher, but not significantly, after PH2.

Conclusions
—Risk of early neurological deterioration and of 3-month death was severely increased after PH2, indicating that large hematoma is the only type of hemorrhagic transformation that may alter the clinical course of ischemic stroke.
Atherothrombotic Cerebellar Infarction
Authors: Min Wang K. , Kim Yong S. , Kim Jong Y. , Park Sung P. , Suh Chung K.
Published: June 2011

Background and Purpose
—Correlation of MRI findings with atherosclerotic vascular lesions has rarely been attempted in patients with cerebellar infarction. The aim of this study was to correlate the MRI lesions with the vascular lesions seen on conventional cerebral angiography in cerebellar infarction.

Methods
—The subjects included 31 patients with cerebellar infarcts who underwent both MRI and conventional cerebral angiography. We analyzed the risk factors, clinical findings, imaging study, and angiography results. We attempted to correlate MRI lesions with the vascular lesions shown in the angiograms.

Results
—The vascular lesions seen on angiograms were subdivided into 3 groups: large-artery disease (n=22), in situ branch artery disease (n=6), and no angiographic disease with hypertension (n=3). The proximal segment (V1) lesions of vertebral artery were the most common angiographic features in patients with large-artery disease in which stroke most commonly involved the posterior inferior cerebellar artery (PICA) cerebellum. The V1 lesions with coexistent occlusive lesions of the intracranial vertebral and basilar arteries were correlated with cerebellar infarcts, which had no predilection for certain cerebellar territory. The intracranial occlusive disease without V1 lesion was usually correlated with small cerebellar lesions in PICA and superior cerebellar artery (SCA) cerebellum. The subclavian artery or brachiocephalic trunk lesion was associated with small cerebellar infarcts. The in situ branch artery disease was correlated with the PICA cerebellum lesions, which were territorial or nonterritorial infarct. No angiographic disease with hypertension was associated with small-sized cerebellar infarcts within the SCA, anterior inferior cerebellar artery, or SCA cerebellum.

Conclusions
—Our study indicates that the topographic heterogeneity of cerebellar infarcts are correlated with diverse angiographic findings. The result that large-artery disease, in which nonterritorial infarcts are more common than territorial infarcts, is more prevalent than in situ branch artery disease or small-artery disease, suggest that even a small cerebellar infarct can be a clue to the presence of large-artery disease.
Inhibition of Rat Vascular Smooth Muscle Cell Proliferation In Vitro and In Vivo by Recombinant Replication-Competent Herpes Simplex Virus
Authors: Miyatake Shin-Ichi , Yukawa Hiroyuki , Toda Hiroki , Matsuoka Norihiro , Takahashi Rei , Hashimoto Nobuo
Published: June 2011

Background and Purpose
—The proliferation of vascular smooth muscle cells (VSMCs) is a common feature associated with vascular proliferative disorders such as atherosclerosis and restenosis after balloon angioplasty. We examined the antiproliferative effects of recombinant replication-competent herpes simplex virus (HSV), hrR3, to proliferative VSMCs both in vitro and in vivo.

Methods
—Early passages of Sprague-Dawley rat VSMCs were infected with hrR3 at a low multiplicity of infection (0.01 to 1.0) to examine the in vitro cytotoxic activity of this recombinant HSV to VSMCs in a proliferative state. Sprague-Dawley rats underwent balloon dilatation injury of the left carotid artery to induce neointimal formation. The injured carotid arteries were infected with hrR3 five days after balloon injury. Two weeks after injury, the left carotid arteries were fixed, and the areas of the neointimal and medial layers were analyzed microscopically. Because the reporter
Escherichia coli
lacZ gene in hrR3 is expressed only in infected cells in which the virus is actively replicating, virus replication was confirmed by X-gal staining.

Results
—A morphometric analysis revealed that there were significant differences in the intima/media ratio between the HSV-treated group and mock-infected group (0.354±0.068 and 1.08±0.055, respectively). In the histological study (X-gal staining), positive X-gal staining was observed chiefly in the VSMCs in the medial layer just beneath the internal elastic lamina, indicating active viral replication.

Conclusions
—Virus-mediated cytocidal therapy using recombinant HSV vector is a promising modality for the treatment of the restenosis after balloon angioplasty.
Striatal Outflow of Adenosine, Excitatory Amino Acids, γ-Aminobutyric Acid, and Taurine in Awake Freely Moving Rats After Middle Cerebral Artery Occlusion
Authors: Melani Alessia , Pantoni Leonardo , Corsi Claudia , Bianchi Loria , Monopoli Angela , Bertorelli Rosalia , Pepeu Giancarlo , Pedata Felicita
Published: June 2011

Background and Purpose
—While a number of studies have investigated transmitter outflow in anesthetized animals after middle cerebral artery occlusion (MCAO) performed by craniectomy, studies have never been performed after MCAO induced by intraluminal filament. In addition, it has been reported that after MCAO, infarct volume correlates with functional outcome and with transmitter outflow, although there are no studies that demonstrate a direct correlation between transmitter outflow and functional outcome. The purpose of the present study was to assess excitatory amino acids, γ-aminobutyric acid, taurine, and adenosine outflow in awake rats after intraluminal MCAO and to determine whether, in the same animal, outflow was correlated with neurological outcome and histological damage.

Methods
—Vertical microdialysis probes were placed in the striatum of male Wistar rats. After 24 hours, permanent MCAO was induced by the intraluminal suture technique. The transmitter concentrations in the dialysate were determined by high-performance liquid chromatography. Twenty-four hours after MCAO, neurological deficit and histological outcome were evaluated.

Results
—All transmitters significantly increased after MCAO. Twenty-four hours after MCAO, the rats showed a severe sensorimotor deficit and massive ischemic damage in the striatum and in the cortex (9±2% and 25±6% of hemispheric volume, respectively). Significant correlations were found between the efflux of all transmitters, neurological score, and striatal infarct volume.

Conclusions
—In this study, for the first time, amino acid and adenosine extracellular concentrations during MCAO by the intraluminal suture technique were determined in awake and freely moving rats, and a significant correlation was found between transmitter outflow and neurological deficit. The evaluation of neurological deficit, histological damage, and transmitter outflow in the same animal may represent a useful approach for studying neuroprotective properties of new drugs/agents against focal ischemia.
Acquired Pial Arteriovenous Fistula Following Cerebral Vein Thrombosis
Authors: Phatouros Constantine C. , Halbach Van V. , Dowd Christopher F. , Lempert Todd E. , Malek Adel M. , Meyers Philip M. , Higashida Randall T.
Published: June 2011

Background
—We report a unique case of an acquired pial arteriovenous fistula occurring after an asymptomatic thrombosis of a superficial cerebral vein.

Case Description
—A cerebral angiogram performed in a 51-year-old man with subarachnoid hemorrhage revealed a 10-mm ruptured anterior communicating artery aneurysm and a thrombosed left superficial middle cerebral vein. Coil embolization of the anterior communicating aneurysm was performed. Follow-up angiography 18 months later revealed a new, asymptomatic, pial arteriovenous fistula between the previously thrombosed left superficial middle cerebral vein and a small sylvian branch of the left middle cerebral artery.

Conclusions
—This case provides evidence that pial arteriovenous fistulas may develop as acquired lesions and furthermore may rarely follow cerebral vein thrombosis. Several cases of dural arteriovenous fistulas, as well as a single case of a mixed pial-dural arteriovenous fistula, occurring after dural sinus thrombosis have been reported previously. However, to our knowledge, this is the first report of an acquired pial arteriovenous fistula following a cerebral vein thrombosis.
Stable Stroke Occurrence Despite Incidence Reduction in an Aging Population
Authors: Thorvaldsen Per , Davidsen Michael , Brønnum-Hansen Henrik , Schroll Marianne
Published: June 2011

Background and Purpose
—A stroke register was established at the Glostrup Population Studies in 1982 with the objective to monitor stroke occurrence in the population continuously during a 10-year period and contribute data to the WHO Monitoring Trends and Determinants in Cardiovascular Disease (MONICA) Project. The purpose of the current analysis was to estimate temporal trends in stroke occurrence.

Methods
—All stroke events in the study population were ascertained and validated according to standardized criteria outlined by the WHO MONICA Project. The study population comprised all subjects ≥25 years of age. Stroke was defined by the clinical presentation. A total of 5262 stroke events in >2 million person-years were analyzed. Age-adjusted rates for first-ever stroke and for all stroke events were calculated and temporal trends estimated by means of Poisson regression.

Results
—The overall annual stroke attack rate per 100 000 person-years in the age range ≥25 years was 272 in men and 226 in women. Age-adjusted stroke attack rates decreased among men by 3.9% per year and by 4.1% among women. Age-adjusted stroke incidence rates declined by 2.9% in men and by 3.1% in women. The trends were statistically significant in both sexes. However, the proportion of elderly people in the study population increased during the time period of the study. Hence the numbers of stroke victims in the population remained largely unaltered.

Conclusions
—Decreasing age-adjusted stroke incidence rates point to a reduction of stroke risk during the time period of the study. Cardiovascular prevention, in particular improved hypertension control, is believed to have contributed to the incidence reduction. However, the burden of stroke on the healthcare system did not substantially diminish. The gain likely achieved from reduction of preventable risk factors was almost counterbalanced by population aging.
Hormone Replacement Therapy and Intima-Media Thickness of the Common Carotid Artery
Authors: Westendorp I. C. D. , Veld B. A. In’t , Bots M. L. , Akkerhuis J. M. , Hofman A. , Grobbee D. E. , Witteman J. C. M.
Published: June 2011

Background and Purpose
—Observational data suggest that hormone replacement therapy (HRT) reduces morbidity and mortality from cardiovascular disease in healthy postmenopausal women. The mechanisms underlying this protection are not entirely clear but may include inhibition of the atherosclerotic process.

Methods
—We studied the association between ever use of HRT and intima-media thickness (IMT) of the common carotid artery in 1103 naturally menopausal women, aged 55 to 80 years, in the Rotterdam Study, a community-based cohort study in a suburban area of Rotterdam, Netherlands. Mean and maximum IMT of the common carotid artery were measured noninvasively with B-mode ultrasound.

Results
—Ever use of HRT for ≥1 year was associated with a decreased mean and maximum IMT compared with never users (mean IMT, 0.719 mm [SE 0.01] versus 0.742 mm [SE 0.004],
P
=0.03; maximum IMT, 0.952 mm [SE 0.015] versus 0.983 mm [SE 0.006],
P
=0.04), after adjustment for age, smoking, educational level, systolic blood pressure, and body mass index. No association was found for use <1 year (mean IMT, 0.739 mm [SE 0.013] versus 0.742 mm [SE 0.004],
P
=0.69; maximum IMT, 0.990 mm [SE 0.019] versus 0.983 mm [SE 0.006],
P
=0.75). Additional adjustment for diabetes, frequency of visits to healthcare facilities, or total and HDL cholesterol did not change these results.

Conclusions
—The findings of this population-based study show that ever use of HRT is associated with a decreased IMT in the common carotid artery in elderly women.
Distributions of Local Oxygen Saturation and Its Response to Changes of Mean Arterial Blood Pressure in the Cerebral Cortex Adjacent to Arteriovenous Malformations
Authors: Meyer Bernhard , Schaller Carlo , Frenkel Christian , Ebeling Bernd , Schramm Johannes
Published: June 2011

Background and Purpose
—To test the hypothesis that neither “steal” as cortical ischemia caused by reduced perfusion pressure nor “breakthrough” on the grounds of loss of pressure autoregulation exist in brain tissue surrounding arteriovenous malformations (AVMs), we established patterns of cortical oxygen saturation (S
o
2
) adjacent to AVMs and its behavior after alterations of mean arterial blood pressure.

Methods
—With a microspectrophotometer, S
o
2
was scanned in the cortex around AVMs of 44 patients before and after resection and in that of a non-AVM group (n=42) before transsylvian dissection. Autoregulation was evaluated by linear regression analysis after elevation of mean arterial blood pressure (5 μg/min IV noradrenaline). S
o
2
values were calculated as medians, percentage of critical values (<25% S
o
2
), and coefficients of variance (approximate heterogeneity of S
o
2
distributions). All values are given as mean±SD.

Results
—Forty patients with AVM had an uneventful postoperative course (group A). Four hyperemic complications (“breakthrough”) occurred (group B). Autoregulation was tested intact in all groups at all times. Preoperative S
o
2
distributions in groups A and C (non-AVMs) were identical. In group B, significantly (
P
<0.05) lower medians (group A, 52.9±16.3%; group B, 44.2±17.1%; group C, 51.9±11.5% S
o
2
), more critical values (group A, 6.5±5.1%; group B, 14.7±11.1%; group C, 7.1±4.9%), and heterogeneous S
o
2
distributions (group A, 20.2±12.7%; group B, 27.9±12.4%; group C, 26.8±10.9%) were seen. Increase of median values was significantly higher in group B (76.3±10.4% S
o
2
) than in group A (65.9±13.4% S
o
2
) after resection.

Conclusions
—Severely hypoxic areas are uncommon in the cortex adjacent to AVMs and occur predominantly in patients prone to hyperemic complications. Reduced perfusion pressure is compensated in most cases, and moderate hyperemia prevails after excision. Reperfusion into unprotected capillaries of severely hypoxic cortical areas results in “breakthrough,” for which vasoparalysis appears not to be the underlying mechanism.