bluuebunny/crossref_metadata_2025 huggingface dataset:
Cerebral Blood Flow and Metabolism Studies Comparing Krypton 85 Desaturation Technique With Argon Desaturation Technique Using the Mass Spectrometer
Authors: Dyken Mark L.
Published: June 2011

Average cerebral blood flow determinations were performed 26 times comparing argon desaturation curves measured by mass spectrometry to the krypton 85 desaturation technique of McHenry.
1
During 17 of these studies krypton 85 and argon desaturations were performed simultaneously. Mean cerebral blood flow difference was 7.2 ± 5.7% for simultaneous determinations and 7.9 ± 6.6% for the total, establishing that the two techniques are comparable. Some of the advantages of using argon in mass spectrometry include: no blood needs to be withdrawn, curves can be observed at the time they are obtained, radiation precautions are not required, multiple studies do not affect the patient, and partial pressures of oxygen and carbon dioxide can be observed constantly.
Control of Cerebral Vasospasm by Parenteral Phenoxybenzamine
Authors: FLAMM EUGENE S. , YASARGIL M. GAZI , RANSOHOFF JOSEPH
Published: June 2011

Cerebral vasospasm has been studied in the basilar artery of the cat. The ability of alpha adrenergic blocking agents to prevent and alleviate spasm produced by the application of blood to the basilar artery has been investigated.

Parenteral phenoxybenzamine is effective in preventing spasm under these experimental conditions when given in doses of 12 mg/kg provided at least two hours elapse between the administration of the drug and the application of the blood. The drug has been found effective up to 24 hours after parenteral administration.

The systemic response to alpha adrenergic blockade and the effects on spasm of the basilar artery produced by different doses at intervals from 1 to 44 hours after the administration of the drug are presented.

Although parenteral phenoxybenzamine is effctive in preventing spasm from subarachnoid blood, it does not prevent spasm from mechanical manipulation of the vessels. This would indicate that mechanisms other than adrenergic stimulation itself may be operative in cerebral vasospasm. The alteration of spasm from blood and mechanical manipulation by other alpha adrenergic blocking agents has been studied and the possible modes of action of these drugs are discussed.
Occlusion of All Four Extracranial Vessels With Minimal Clinical Symptomatology. Case Report
Authors: VITEK JIRI J. , HALSEY JAMES H. , MCDOWELL HOLT A.
Published: June 2011

A case of a 55-year-old man with occlusion of both vertebral, left common carotid and right internal carotid arteries is described. Also present was 95 per cent stenosis on the origin of the right external carotid artery with severe atherosclerotic disease on both subclavian and innominate arteries. Clinical symptoms consisted of blindness of the left eye; otherwise the patient was free of neurological signs. It is suggested that not only the presence of extracranial occlusive disease but also the status of the intracranial circulation, the time factor in which the extracranial vessels became occluded, and the adaptability of the individual to establish all possible means of collateral flow play their roles in correlation of extracranial atherosclerotic disease and clinical symptomatology.
Serial Changes in Glucose Utilization and Insulin and Growth Hormone Secretion in Acute Cerebrovascular Disease
Authors: Huff T. A. , Lebovitz H. E. , HEYMAN A. , Davis L.
Published: June 2011

Serial studies were made of glucose utilization and insulin and growth hormone secretion following intravenous glucose tolerance tests given to 16 patients during recovery from acute cerebrovascular disease. Three groups of patients were identified based on the pattern of change of glucose utilization during the first month of convalescence. A small group showed a persistent defective insulin response to glucose and appeared to have had pre-existing unrecognized adult-onset diabetes mellitus. The two other groups showed either an immediate suppression of glucose utilization or delayed development of glucose intolerance associated with an increase in total insulin secretion. Both of these responses returned to normal by the end of the fourth week. Growth hormone secretion correlated with the severity of the stroke. Alterations in glucose metabolism and insulin secretion seem to occur in most patients following recovery from stroke and undoubtedly reflect transient hormonal or metabolic changes related to either acute stress or tissue injury, depending on the interval after the onset of the vascular episode.
Cerebral Microangiography After Hypocarbia and Hypercarbia
Authors: Harrington Timothy , Di Chiro Giovanni
Published: June 2011

Ischemic infarction was obtained in the basal ganglia and internal capsule of the Rhesus monkey by clipping the middle cerebral artery at its origin through a transorbital approach.

The postmortem microvasculature was demonstrated using microtized barium (Micropaque) and soft x-ray technology. The effects on this microvasculature induced by antemortem variations in Pa

co
co2

in tne normal and the acutely infarcted animal were studied. Microangiography was shown to be useful in the study of dynamic vascular changes in the deep structures of the ischemic brain.
Humoral Responses of Smooth Muscle from Rabbit Subarachnoid Artery Compared to Kidney, Mesentery, Lung, Heart, and Skin Vascular Smooth Muscle
Authors: SUNDT THORALF M. , WINKELMANN R. K.
Published: June 2011

Smooth muscle strips from rabbit subarachnoid arteries did not respond to catecholamines in concentrations which caused strips from skin, mesentery, and kidney vessels to contract. The strips from subarachnoid arteries responded to serotonin, histamine, and angiotensin II but not to bradykinin, acetylcholine, methacholine, and adenosine phosphate compounds. Heart and lung vascular strips did not respond to catecholamines but responded to acetylcholine; cardiac strips responded to dilute methacholine. Lung strips often failed to respond to histamine in usual concentrations and did respond to bradykinin. The subarachnoid strips had a distinactive pattern of respone as compared to vascular tissue from other organs. Results of other isolated vessel studies are reviewed along with pertinent investigations of cerebral autoregulation, vasospasm, and autonomic nerves. The possible significance of these findings is discussed.
Diagnostic Information Available in University and Community Hospital Medical Records: Patients With Cerebrovascular Disease
Authors: CARPENTER ROBERT R. , ROGERS KENNETH D. , REED DAVID E.
Published: June 2011

Medical records of 1,117 patients with cerebrovascular disease from one university and four community hospitals were abstracted by trained, nonphysician personnel at the rate of four cases per hour. The data obtained were adequate to describe eight cerebrovascular disease syndromes. In 56% of cases, data from the body of the medical record failed to support the hospiatl's dicharge diagnosis. The eight study diagnoses were not identical with pathological diagnoses, but their characterstics suggest that they are distinct and related to recognized cerebrovascular disease entities. It is recommended that evaluations of diagnostic and therapeutic practice for stroke patients be carried out separately for each of the study syndromes; the care expected and the outcome observed are different for each.
Cerebral Blood Flow in Pure Dysarthria
Authors: Okuda Bungo , Kawabata Keita , Tachibana Hisao , MD Minoru Sugita
Published: June 2011

Background and Purpose
—Isolated dysarthria, termed pure dysarthria, develops rarely after stroke, and its pathophysiology remains unclear. To clarify the underlying mechanism of pure dysarthria, we investigated lesion sites and cerebral blood flow in patients with pure dysarthria.

Methods
—We examined 12 patients with pure dysarthria who underwent MRI and cerebral blood flow study. To visualize cortical blood flow, a three-dimensional display was generated from single-photon emission computed tomography (SPECT). Regional cerebral blood flow of the patients was semiquantitatively measured with SPECT and
N
-isopropyl-p[
123
I]iodoamphetamine as a tracer and compared with that of 11 control subjects.

Results
—On MRI, multiple lacunar infarctions were noted bilaterally in 11 patients, all of whom had lesions involving the internal capsule or corona radiata. The other patient had a unilateral internal capsule–corona radiata infarction. Three-dimensional display showed frontal cortical hypoperfusion in 8 patients. Since interhemispheric differences of blood flow were not significant in any region of the 12 patients, the mean of left and right cortical blood flow was analyzed. Compared with the control subjects, cortical perfusion was significantly reduced in the patients’ frontal regions, sparing the sensorimotor, temporal, and parietal cortices and the cerebellum. Reductions of perfusion were rather pronounced in the anterior opercular, medial prefrontal and premotor, and anterior cingulate regions.

Conclusions
—Pure dysarthria results mainly from multiple lacunar infarctions, which induce frontal cortical hypoperfusion, probably due to interruption of corticosubcortical networks. We conclude that frontal cortical hypoperfusion, particularly in the anterior opercular and medial frontal regions, plays an important role in the development of pure dysarthria.
Mice Deficient in Mac-1 (CD11b/CD18) Are Less Susceptible to Cerebral Ischemia/Reperfusion Injury
Authors: Soriano Sulpicio G. , Coxon Angela , Wang Yanming F. , Frosch Matthew P. , Lipton Stuart A. , Hickey Paul R. , Mayadas Tanya N.
Published: June 2011

Background and Purpose
—Macrophage-1 antigen (Mac-1) (CD11b/CD18), a leukocyte β2 integrin, facilitates neutrophil adhesion, transendothelial migration, phagocytosis, and respiratory burst, all of which may mediate reperfusion-induced injury to ischemic brain tissue in conditions such as stroke. To determine the role of Mac-1 during ischemia and reperfusion in the brain, we analyzed the effect of transient focal cerebral ischemia in mice genetically engineered with a specific deficiency in Mac-1.

Methods
—Transient focal ischemia/reperfusion was induced by occluding the left middle cerebral artery for 3 hours followed by a 21-hour reperfusion period in Mac-1–deficient (n=12) and wild-type (n=11) mice. Regional cerebral blood flow was determined with a laser-Doppler flowmeter. Brain sections were stained with 2% 2,3,5-triphenyltetrazolium chloride to determine the infarct volume. Neutrophil accumulation was determined by staining the brain sections with dichloroacetate esterase to identify neutrophils.

Results
—Compared with the wild-type cohort, Mac-1–deficient mice had a 26% reduction in infarction volume (
P
<0.05). This was associated with a 50%, but statistically insignificant, reduction in the number of extravasated neutrophils in the infarcted areas of the brains in the mutant mice. There were no differences in regional cerebral blood flow between the 2 groups.

Conclusions
—Mac-1 deficiency reduces neutrophil infiltration and cerebral cell death after transient focal cerebral ischemia. This finding may be related to a reduction in neutrophil extravasation in Mac-1–deficient mice.
Inhibitors of Protein Synthesis Preserve the
N
-Methyl-
d
-Aspartate–Induced Cerebral Arteriolar Dilation After Ischemia in Piglets
Authors: Veltkamp Roland , Domoki Ferenc , Bari Ferenc , Louis Thomas M. , Busija David W.
Published: June 2011

Background and Purpose
—Cerebral arteriolar dilation to
N
-methyl-
d
-aspartate (NMDA) is a neuronally mediated process that is sensitive to cerebral ischemia. We tested the hypothesis that pretreatment with transcription or translation inhibitors preserves the vascular response to NMDA after global cerebral ischemia.

Methods
—Pial arteriolar diameters were measured in anesthetized piglets by use of a closed cranial window and intravital microscopy. Arteriolar responses to NMDA (10
−5
and 10
−4
mol/L) were measured before and 1, 2, and 4 hours after 10 minutes of ischemia. Ischemia was induced by increasing intracranial pressure. Subgroups were pretreated with vehicle, topical actinomycin D (Act-D) 10
−5
or 10
−6
mol/L, or intravenous cycloheximide (CHX) 1.0 or 0.3 mg/kg 15 minutes before ischemia. The effects of Act-D and CHX on vascular responses to NMDA without preceding ischemia were also examined.

Results
—In the vehicle group, arteriolar responses to NMDA were clearly attenuated 1 hour after ischemia but returned to baseline at 2 to 4 hours. Preischemic compared with 1 hour postischemic arteriolar dilation to NMDA was 10±2% versus 1±0% at 10
−5
mol/L and 40±4% versus 20±4% at 10
−4
mol/L NMDA (mean±SEM; both
P
<0.05, n=7). In contrast, pretreatment with Act-D resulted in preservation of the arteriolar responses to NMDA 1 hour after ischemia. For 10
−6
mol/L (n=5) of Act-D, dilations were 6±2% versus 6±2% at 10
−5
mol/L and 51±9% versus 39±10% at 10
−4
mol/L of NMDA. For 10
−5
mol/L (n=5) of Act-D, arterioles dilated by 7±2% versus 7±2% at 10
−5
mol/L and 38±4% versus 35±4% at 10
−4
mol/L NMDA. Similarly, CHX preserved NMDA-induced vasodilation. For 0.3 mg/kg of CHX (n=5), dilations were 8±2% versus 8±1% at 10
−5
mol/L and 39±4% versus 28±6% at 10
−4
mol/L NMDA. For 1.0 mg/kg of CHX (n=5), arterioles dilated by 10±2% versus 6±2% at 10
−5
mol/L and 37±7% versus 35±6% at 10
−4
mol/L NMDA. In experiments without ischemia, NMDA-induced vasodilation before and 85 minutes after administration of Act-D or CHX was not significantly different.

Conclusions
—Vascular responses of cerebral arterioles to NMDA after ischemia are preserved by pretreatment with either Act-D or CHX. Without preceding ischemia, Act-D and CHX do not potentiate neuronal-vascular responses to NMDA. Our results suggest that continued or augmented protein synthesis is involved in the transient attenuation of NMDA-induced dilation during the early reperfusion phase and that inhibitors of protein synthesis may protect neurons against ischemic stress.
Effects of Glucose and Pa
o
2
Modulation on Cortical Intracellular Acidosis, NADH Redox State, and Infarction in the Ischemic Penumbra
Authors: Anderson Robert E. , Tan William K. , Martin Heidi S. , Meyer Fredric B.
Published: June 2011

Background and Purpose
—During focal cerebral ischemia, the ischemic penumbra or border-zone regions of moderate cortical blood flow reductions have a heterogeneous development of intracellular cortical acidosis. This experiment tested the hypotheses that (1) this acidosis is secondary to glucose utilization and (2) this intracellular acidosis leads to recruitment of potentially salvageable tissue into infarction.

Methods
—Brain pH
i
, regional cortical blood flow, and NADH redox state were measured by in vivo fluorescent imaging, and infarct volume was assessed by triphenyltetrazolium chloride histology. Thirty fasted rabbits divided into 6 groups of 5 each were subjected to 4 hours of permanent focal ischemia in the presence of hypoglycemia (≈2.8 mmol/L), moderate hyperglycemia (≈11 mmol/L), and severe hyperglycemia (>28 mmol/L) under either normoxia or moderate hypoxia (Pa
o
2
≈50 mm Hg).

Results
—Preischemic hyperglycemia led to a more pronounced intracellular acidosis and retardation of NADH regeneration than in the hypoglycemia groups under both normoxia and moderate hypoxia in the ischemic penumbra. For example, 4 hours after ischemia, brain pH
i
in the severe hyperglycemia/normoxia group measured 6.46, compared with 6.84 in the hypoglycemia/normoxia group (
P
<0.01), and NADH fluorescence measured 173% compared with 114%. Infarct volume in the severe hyperglycemia/normoxia group measured 35.1±6.9% of total hemispheric volume, compared with 13.5±4.2% in the hypoglycemia/normoxia group (
P
<0.01).

Conclusions
—Hyperglycemia significantly worsened both cortical intracellular brain acidosis and mitochondrial function in the ischemic penumbra. This supports the hypothesis that the evolution of acidosis in the ischemic penumbra is related to glucose utilization. Furthermore, the observation that hypoglycemia significantly decreased infarct size supports the postulate that cortical acidosis leads to recruitment of ischemic penumbra into infarction.
Sodium Influx Plays a Major Role in the Membrane Depolarization Induced by Oxygen and Glucose Deprivation in Rat Striatal Spiny Neurons
Authors: Calabresi Paolo , Marfia Girolama A. , Centonze Diego , Pisani Antonio , Bernardi Giorgio
Published: June 2011

Background and Purpose
—Striatal spiny neurons are selectively vulnerable to ischemia, but the ionic mechanisms underlying this selective vulnerability are unclear. Although a possible involvement of sodium and calcium ions has been postulated in the ischemia-induced damage of rat striatal neurons, the ischemia-induced ionic changes have never been analyzed in this neuronal subtype.

Methods
—We studied the effects of in vitro ischemia (oxygen and glucose deprivation) at the cellular level using intracellular recordings and microfluorometric measurements in a slice preparation. We also used various channel blockers and pharmacological compounds to characterize the ischemia-induced ionic conductances.

Results
—Spiny neurons responded to ischemia with a membrane depolarization/inward current that reversed at approximately −40 mV. This event was coupled with an increased membrane conductance. The simultaneous analysis of membrane potential changes and of variations in [Na
+
]
i
and [Ca
2+
]
i
levels showed that the ischemia-induced membrane depolarization was associated with an increase of [Na
+
]
i
and [Ca
2+
]
i
. The ischemia-induced membrane depolarization was not affected by tetrodotoxin or by glutamate receptor antagonists. Neither intracellular BAPTA, a Ca
2+
chelator, nor incubation of the slices in low-Ca
2+
–containing solutions affected the ischemia-induced depolarization, whereas it was reduced by lowering the external Na
+
concentration. High doses of blockers of ATP-dependent K
+
channels increased the membrane depolarization observed in spiny neurons during ischemia.

Conclusions
—Our findings show that, although the ischemia-induced membrane depolarization is coupled with a rise of [Na
+
]
i
and [Ca
2+
]
i
, only the Na
+
influx plays a prominent role in this early electrophysiological event, whereas the increase of [Ca
2+
]
i
might be relevant for the delayed neuronal death. We also suggest that the activation of ATP-dependent K
+
channels might counteract the ischemia-induced membrane depolarization.
Does Patient Satisfaction Reflect Differences in Care Received After Stroke?
Authors: Pound Pandora , Tilling Kate , Rudd Anthony G. , Wolfe Charles D.A.
Published: June 2011

Background and Purpose
—Despite the volume of research into patient satisfaction, it is not clear whether satisfaction ratings reflect differences in care received after stroke or the characteristics of patients. The aim of this study is to test the hypothesis that patient satisfaction is independently related to differences in care received after stroke.

Methods
—Stroke patients participating in a randomized controlled trial of early discharge to community therapy completed a satisfaction questionnaire and physical and psychological outcome measures at 4 and 12 months. Two hundred seventy-four patients (83%) were followed up at 4 months and 262 patients (79%) at 12 months. Use of therapy and community services was quantified. Logistic regression was used to investigate associations between satisfaction, patient characteristics, and service provision.

Results
—The more therapy, meals on wheels, and home help visits patients received, the more likely they were to be satisfied. Patients in the conventional arm of the trial were less likely to express satisfaction than those discharged early to community therapy. Women, older people, anxious people, and those more functionally independent were more likely to be satisfied, while those with depression, speech and swallowing deficit, motor deficit, and poor subjective health were less likely to be satisfied.

Conclusions
—The finding that satisfaction assessments reflect real differences in the provision of care and occur independently of any associations with patient characteristics is new. Patient satisfaction should be taken seriously as an outcome.
Rapid Decline of Cerebral Microemboli of Arterial Origin After Intravenous Acetylsalicylic Acid
Authors: Goertler Michael , Baeumer Matthias , Kross Regina , Blaser Till , Lutze Gerd , Jost Stefan , Wallesch Claus-Werner
Published: June 2011

Background and Purpose
—The present study investigated the influence of the antiplatelet agent acetylsalicylic acid (ASA) on cerebral microembolism as detected by transcranial Doppler sonography (TCD).

Methods
—Nine patients with recent transient ischemic attack or minor stroke of arterial origin were investigated. Eight had not received an antiplatelet or anticoagulant medication before TCD, and in 1 patient a preexisting ASA medication (100 mg/d) had not been changed since the onset of stroke symptoms. An initial 1-hour TCD monitoring was extended for an additional 2.5 hours after an intravenous bolus injection of 500 mg ASA and was repeated for 1 hour on the following day.

Results
—Microembolic signals (MES) were detected in all patients only on the symptomatic side. After the ASA bolus injection, a significant drop of the MES rate was found in 7 patients, all without previous medication, starting 30 minutes after the application (mean per hour=25.1 [range, 6 to 66] versus mean per hour=6.4 [range, 0 to 14]). In 3 of these patients, platelet aggregation tests were performed that demonstrated normal aggregation before bolus injection and inhibited aggregability as early as 30 minutes after bolus injection. The rate of MES remained unchanged in 1 patient without antiplatelet medication. The ninth patient, who had suffered an ischemic event on ASA, showed only a transient decrease of MES frequency.

Conclusions
—In patients with recent stroke of arterial origin, intravenous ASA can rapidly reduce cerebral microemboli as detected by TCD. Microemboli might be a useful parameter to monitor early effects of antiplatelet therapy.
Should Stroke Victims Routinely Receive Supplemental Oxygen?
Authors: Rønning Ole Morten , Guldvog Bjørn
Published: June 2011

Background and Purpose
—We sought to test the hypothesis that breathing 100% oxygen for the first 24 hours after an acute stroke would not reduce mortality, impairment, or disability.

Methods
—Subjects admitted to the Central Hospital of Akershus, Norway, with stroke onset <24 hours before admittance were allocated to 2 groups by a quasi-randomized design using birth numbers. All patients with acute stroke admitted to hospital within 24 hours after a stroke were included and enrolled. Patients were allocated to a group that received supplemental oxygen treatment (100% atmospheres, 3 L/min) for 24 hours (n=292) or to the control group, which did not receive additional oxygen. Main outcome measures were 1-year survival, neurological impairment (Scandinavian Stroke Scale), and disability (Barthel Index) 7 months after stroke.

Results
—One-year survival was 69% in the oxygen group and 73% in the control group (OR 0.82; 95% CI 0.57 to 1.19;
P
=0.30). Impairment scores and disability scores were comparable 7 months after stroke. Among patients with Scandinavian Stroke Scale (SSS) scores of ≥40, 82% in the oxygen group and 91% in the control group survived (OR 0.45; 95% CI 0.23 to 0.90;
P
=0.023). For patients with SSS scores of <40, 53% in the oxygen group and 48% in the control group survived (OR 1.26; 95% CI 0.76 to 2.09;
P
=0.54).

Conclusions
—Supplemental oxygen should not routinely be given to nonhypoxic stroke victims with minor or moderate strokes. Further research is needed to give conclusive advice concerning oxygen supplementation for patients with severe strokes.
Pathophysiological Topography of Acute Ischemia by Combined Diffusion-Weighted and Perfusion MRI
Authors: Darby D. G. , Barber P. A. , Gerraty R. P. , Desmond P. M. , Yang Q. , Parsons M. , Li T. , Tress B. M. , Davis S. M.
Published: June 2011

Background and Purpose
—Combined echoplanar MRI diffusion-weighted imaging (DWI), perfusion imaging (PI), and magnetic resonance angiography (MRA) can be used to visualize acute brain ischemia and predict lesion evolution and functional outcome. The appearance of a larger lesion by PI than by DWI quantitatively defines a mismatch of potential clinical importance. Qualitative lesion variations exist in the topographic concordance of this mismatch. We examined both the topographic heterogeneity and relative frequency of mismatched patterns in acute stroke using these MRI techniques.

Methods
—Acute DWI, PI, and MRA studies of 34 prospectively recruited patients with supratentorial ischemic lesions scanned within 24 hours of stroke onset (range 2.5 to 23.3 hours, 12 patients <6 hours) were analyzed.

Results
—Ischemic lesions were predominantly in the middle cerebral artery (MCA) territory (94%), with DWI lesions most commonly affecting the insular region. Mismatched patterns with PI lesion larger than DWI lesion occurred in 21 patients (62% overall), in all 4 patients imaged within 3 hours, and in 44% of patients imaged after 18 hours. A patient with a large PI but no DWI lesion and severe clinical deficit at 2.5 hours after stroke onset recovered completely. Regional variations in DWI and PI lesion loci were found, inferring site of proximal MCA occlusion, embolic pathogenesis, and regional arterial reperfusion.

Conclusions
—Analysis of the topographic concordance of PI and DWI lesions in acute stroke reveals regional PI lesions without concomitant DWI lesions, which do not necessarily progress to infarction but may suggest stroke pathogenesis and site of current arterial occlusion. Location of DWI lesions may suggest an earlier site of arterial occlusion and regions of maximal perfusion deficit.
Cerebrovascular Disease and Depression Symptoms in the Cardiovascular Health Study
Authors: Steffens David C. , Helms Michael J. , Krishnan K. Ranga Rama , Burke Gregory L.
Published: June 2011

Background and Purpose
—Evidence is mounting linking cerebrovascular disease with depressive symptoms in the elderly. Lesions in both white and gray matter have been associated with depressive symptoms and major depression. We sought to investigate the relationship between depressive symptoms and white and gray matter lesions in subjects participating in the Cardiovascular Health Study.

Methods
—In a sample of 3660 men and women who underwent a standardized interview, physical examination, and MRI scan, we examined the association between number of white and gray matter lesions and white matter grade (a measure of severity) and reported depressive symptoms using a modified version of the Centers for Epidemiologic Studies Depression (CES-D) scale. We controlled for a variety of demographic and medical variables as well as functional status and Modified Mini-Mental State Examination score.

Results
—The number of small (<3 mm) basal ganglia lesions was significantly associated with reported depressive symptoms, but white matter grade was not. In subsequent logistic regression models, number of basal ganglia lesions remained a significant predictor after controlling for non-MRI variables and severity of white matter lesions.

Conclusions
—Our findings extend previous reports that linked cerebrovascular changes to depressive symptoms in clinical populations to a large community-based population. This report provides further evidence of the importance of basal ganglia lesions in geriatric depression.
The A677V Methylenetetrahydrofolate Reductase Gene Polymorphism and Carotid Atherosclerosis
Authors: Bova I. , Chapman J. , Sylantiev C. , Korczyn A. D. , Bornstein N. M.
Published: June 2011

Background and Purpose
—The alanine/valine (A/V) polymorphism at codon 677 of the 5,10 methylenetetrahydrofolate reductase
(MTHFR)
gene correlates with elevated levels of plasma homocysteine and with an increased risk of atherosclerotic cardiovascular disease. Our study was designed to assess the frequency of the A and V alleles in patients with asymptomatic severe carotid artery stenosis (CAS) assessed by extracranial duplex examination in comparison with age- and sex-matched subjects without carotid atherosclerosis.

Methods
—Consecutive patients (n=48; 28 men, mean±SD age 67.1±11.4 years) with asymptomatic severe (>75%) CAS were compared with subjects without CAS (n=26; 15 men, aged 61.2±11.5). The
MTHFR
genotype was analyzed by polymerase chain reaction followed by
Hin
fΙ digestion. The χ
2
analysis and
t
test were used to compare the groups.

Results
—The frequency of V alleles was significantly higher in the CAS group (0.47) compared with control subjects (0.27, χ
2
test; OR 2.4 [95% CI 1.1 to 5.3];
P
<0.02).

Conclusions
—Our results indicate that the
MTHFR
A677V allele is significantly associated with severe CAS.
Intracerebral Calcification in Systemic Sclerosis
Authors: Heron Emmanuel , Hernigou Anne , Chatellier Gilles , Fornes Paul , Emmerich Joseph , Fiessinger Jean-Noël
Published: June 2011

Background and Purpose
—Advanced cerebrovascular wall calcification was recently observed at autopsy in 2 patients with systemic sclerosis. To further investigate this issue, we conducted a prospective CT study of scleroderma patients to detect intracerebral calcification.

Methods
—Thirty-seven consecutive patients with systemic sclerosis underwent unenhanced brain CT. Images were blindly interpreted, together with those of 2 age-matched (±1 year) and sex-matched control subjects per patient.

Results
—Intracerebral calcification was found in 12 patients (32.4%) and 7 controls (9.5%) (
P
=0.006). Among the patients, intracerebral calcification was associated with the duration of Raynaud’s phenomenon (
P
=0.005) and not with age (
P
=0.086).

Conclusions
—Intracerebral calcification is closely associated with scleroderma, which suggests that scleroderma causes primary cerebrovascular changes.
Rapid Monitoring of Diffusion, DC Potential, and Blood Oxygenation Changes During Global Ischemia
Authors: de Crespigny A. J. , Röther J. , Beaulieu C. , Moseley M. E.
Published: June 2011

Background and Purpose
—The increasing interest in diffusion-weighted MRI (MRI) for diagnosis and monitoring of acute stroke in humans calls for a sound understanding of the underlying mechanisms of this image contrast in acute cerebral ischemia. The present study aimed to show that a rapid decrease in brain-water apparent diffusion coefficient (ADC) occurs coincident with anoxic depolarization and that this change is delayed by hyperglycemia and sodium channel blockade but accelerated by hypoglycemia.

Methods
—Rats were divided into groups: normoglycemic, hypoglycemic, and hyperglycemic, and those given local tetrodotoxin (TTX) application. Cardiac arrest was effected by intravenous KCl injection during serial high-speed diffusion and blood oxygenation–sensitive gradient-recalled echo MRI. Brain DC potential was recorded simultaneously. Serial ADC maps were calculated from the diffusion-weighted data and fitted to a model function to measure the delay between cardiac arrest and rapid ADC decrease.

Results
—The time of anoxic depolarization indicated by DC change agreed well with the rapid drop in ADC in all groups; both were accelerated with hypoglycemia and delayed by hyperglycemia. A more gradual ADC decline occurred before anoxic depolarization, which was more pronounced in hyperglycemic animals and less pronounced in hypoglycemic animals. Rapid drop in ADC was also delayed by local TTX application. Changes in gradient-recalled echo image intensity were not significantly different among groups.

Conclusions
—While much of the ADC decrease in ischemia occurs during anoxic depolarization, significant but gradual ADC changes occur earlier that may not be due to a massive loss in ion homeostasis.
Diagnostic Impact of Cerebral Transit Time in the Identification of Microangiopathy in Dementia
Authors: Puls Imke , Hauck Kurt , Demuth Klaus , Horowski Anja , Schließer Mira , Dörfler Petra , Scheel Peter , Toyka Klaus V. , Reiners Karlheinz , Schöning Martin , Becker Georg
Published: June 2011

Background and Purpose
—The diagnosis and quantification of microangiopathy in dementia is difficult. The assessment of small-vessel disease requires expensive and sophisticated nuclear medicine techniques. This study was performed to identify microangiopathy related to the integrity of cerebral microcirculation by sonographic measurements (arteriovenous cerebral transit time [cTT]).

Methods
—We performed transcranial color-coded duplex sonography in 40 patients with vascular dementia, 20 patients with Alzheimer’s disease or Lewy body disease, and 25 age-matched controls. The clinical diagnosis was established by history of dementia and neuroimaging findings. Cognitive impairment was assessed by the Mini-Mental State Examination and Alzheimer’s Disease Assessment Scale. cTT is defined as the time required by an ultrasound contrast agent to pass from a cerebral artery to a vein. This was measured by recording the power-Doppler intensity curves in the P2 segment of the posterior cerebral artery and the vein of Galen. Previous studies have shown a prolongation of cTT in patients with cerebral microangiopathy.

Results
—cTT was substantially prolonged in patients with vascular dementia (5.8 seconds; 25th percentile 4.5; 75th percentile 7.5;
U
test,
P
<0.001) compared with controls (3.1 seconds; 2.3; 3.4) but not in patients with degenerative dementia (3.7 seconds; 3.7; 4.2). In patients with vascular dementia, cTT was significantly correlated with cognitive impairment.

Conclusions
—cTT may be useful tool to disclose small-vessel disease in demented patients. Examination is noninvasive and quickly performed. It may be also useful in follow-up examinations in patients undergoing therapy.
Recent Heavy Drinking of Alcohol and Embolic Stroke
Authors: Hillbom Matti , Numminen Heikki , Juvela Seppo
Published: June 2011

Background and Purpose
—Epidemiological evidence suggests that heavy alcohol consumption increases the risk for ischemic stroke, whereas light-to-moderate alcohol intake decreases the risk, but the role of different drinking patterns has remained unclear. We investigated recent light, moderate, and heavy alcohol drinking and former heavy drinking as risk factors for acute ischemic brain infarction by etiological subtype of stroke.

Methods
—We compared 212 consecutive patients aged between 16 and 60 years, who were completely evaluated for the etiology of their ischemic stroke, with 274 control subjects admitted to the emergency unit of the same hospital. ORs, as estimates of multivariate relative risks (RRs), and 95% CIs after adjustment for possible confounding variables were calculated by logistic regression. The ORs were adjusted for age, sex, body mass index, hypertension, diabetes, hyperlipemia, current smoking, and history of migraine.

Results
—Recent heavy drinking but not former heavy drinking was an independent risk factor for stroke (RR 1.82, 95% CI 1.08 to 3.05). Consumption of 151 to 300 g and >300 g alcohol within the week preceding the onset of stroke significantly increased the risk for cardioembolic and cryptogenic stroke. Consumption of >40 g alcohol within the preceding 24 hours increased the risk for cardiogenic embolism to the brain among those who had a high-risk source (RR 4.75, 95% CI 1.23 to 18.4), the risk for tandem embolism among those who had prominent large-artery atherosclerosis (RR 7.68, 95% CI 1.82 to 32.3), and the risk for cryptogenic stroke (RR 3.84, 95% CI 1.69 to 8.71). Light drinking did not increase the risk for stroke.

Conclusions
—We conclude that acute drinking of intoxicating amounts of alcohol may trigger the onset of embolic stroke among subjects who have a source of thrombus in the heart or the large arteries.
Multivariable Analysis of Predictive Factors Related to Outcome at 6 Months After Intra-Arterial Thrombolysis for Acute Ischemic Stroke
Authors: Ueda Toshihiro , Sakaki Saburo , Kumon Yoshiaki , Ohta Shinsuke
Published: June 2011

Background and Purpose
—Recent reports have suggested that a rapid assessment of pretreatment residual cerebral blood flow (CBF) could be used to optimize selection criteria for thrombolysis in patients with acute ischemic stroke to improve clinical outcome. We investigated retrospectively residual CBF and other clinical factors related to outcome at 6 months after intra-arterial thrombolysis by using multivariable analysis.

Methods
—Seventy-six patients received intra-arterial thrombolysis within 6 hours of symptom onset. The multiple regression method was used to analyze associations between the modified Rankin scale (MRS) at 6 months after treatment and clinical factors including age, infarction type, duration of ischemia, dose of urokinase, degree of recanalization, hemorrhage, National Institutes of Health Stroke Scale score (NIHSSS), and residual CBF evaluated by pretreatment single-photon emission-computed tomography; these values were assessed with the use of the regional-to-cerebellar activity (R/CE) ratio of ischemic region to cerebellum and asymmetry index.

Results
—MRS at 6 months was good (0 to 3) in 65% and poor (4 to 6) in 35%. Factors significantly related to MRS at 6 months were R/CE ratio (
P
<0.0001), NIHSSS at baseline and the following day (
P
<0.0001), cardioembolic infarction (
P
=0.0014), age (
P
=0.0074), and recanalization grade (
P
=0.007). NIHSSS of >20, R/CE ratio of <0.35, cardioembolic infarction, incomplete recanalization (grade <3), and older age (>75 years) were determined to be significant independent predictors of poor outcome.

Conclusions
—The residual CBF, neurological score at baseline and the following day, age, and recanalization grade correlated significantly with long-term outcome. The NIHSSS of >20 and R/CE ratio of <0.35 were determined to be significant independent predictors of poor outcome by multivariable analysis.
Oxidized Low-Density Lipoprotein Enhances Myogenic Tone in the Rabbit Posterior Cerebral Artery Through the Release of Endothelin-1
Authors: Xie Hui , Bevan John A.
Published: June 2011

Background and Purpose
—Cerebral arteries develop stretch-induced myogenic tone, which plays an important role in the regulation of blood flow to the brain. Although the effect of oxidized LDL (Ox-LDL) on many aspects of the vascular endothelial and smooth muscle cell function have been extensively investigated, its influence on myogenic activity has not been studied.

Methods
—The effect of Ox-LDL on the myogenic tone that develops in the perfused rabbit posterior cerebral artery at intramural pressures between 40 and 90 mm Hg was examined.

Results
—Ox-LDL (10 μg/mL) significantly enhanced myogenic tone by 21.4±6.1% to 28.5±1.8% at 60 to 90 mm Hg pressure (
P
<0.05) but had no influence on norepinephrine- (0.5 to 1 μmol/L) and KCl (20 mmol/L)–induced constriction. Ox-LDL was effective whether the artery was exposed to it from the intraluminal or the extraluminal surface. Lysophosphatidylcholine (10 μmol/L), a lipid component of Ox-LDL, had an equivalent potentiating effect. Native LDL (100 μg/mL) was inactive. The myogenic tone–potentiating effect of Ox-LDL was abolished by endothelium removal but was not influenced by the NO synthase inhibitor
N
G
-nitro-
l
-nitro-arginine methyl ester (50 μmol/L). This effect was reversed by the endothelin-1 (ET-1) antagonist BQ-123 (1 μmol/L). This concentration blocked 1 to 3 nmol/L ET-1–induced constriction without altering constriction induced by 40 mmol/L KCl. The potentiating effect was suppressed by the specific protein kinase C inhibitor chelerythrine (1 μmol/L).

Conclusions
—Ox-LDL enhances myogenic tone through the release of ET-1 from the endothelium of the rabbit posterior cerebral artery.
Recurrent Spontaneous Intracerebral Hemorrhage in a Congenitally Afibrinogenemic Patient
Authors: Henselmans J. M. L. , Meijer K. , Haaxma R. , Hew J. , van der Meer J.
Published: June 2011

Background
—Coagulation disorders can cause intracerebral bleeding that may be difficult to detect since subsequent aberrant clot formation may mask early detection. This is an important pitfall because, when diagnosed early, bleeding in these patients is treatable.

Case Description
—A patient with congenital afibrinogenemia presented with recurrent hemiparesis. Spontaneous intracerebral hemorrhage was diagnosed, despite an initial negative CT scan. Diagnosis, therapy, and complications of therapy are discussed.

Conclusions
—Intracerebral hemorrhage must be strongly suspected in any patient with a coagulation disorder presenting with matching clinical symptoms. Therapy must be installed immediately, before additional investigations, and should be continued even when initial neuroimaging is negative.
Incidence Rates of First-Ever Ischemic Stroke Subtypes Among Blacks
Authors: Woo Daniel , Gebel James , Miller Rosemary , Kothari Rashmi , Brott Thomas , Khoury Jane , Salisbury Shelia , Shukla Rakesh , Pancioli Arthur , Jauch Edward , Broderick Joseph
Published: June 2011

Background and Purpose
—The aim of this study was to determine the incidence rates of ischemic stroke subtypes among blacks.

Methods
—Hospitalized and autopsied cases of stroke and transient ischemic attack among the 187 000 blacks in the 5-county region of greater Cincinnati/northern Kentucky From January 1, 1993, through June 30, 1993, were identified. Incidence rates were age- and sex-adjusted to the 1990 US population. Subtype classification was performed after extensive review of all available imaging, laboratory data, clinical information, and past medical history. Case-control comparisons of risk factors were made with age-, race-, and sex-matched control subjects.

Results
—Annual incidence rates per 100 000 for first-ever ischemic stroke subtypes among blacks were as follows: uncertain cause, 103 (95% confidence interval [CI], 80 to 126); cardioembolic, 56 (95% CI, 40 to 73); small-vessel infarct, 52 (95% CI, 36 to 68); large vessel, 17 (95% CI, 8 to 26); and other causes, 17 (95% CI, 9 to 26). Of the patients diagnosed with an infarct of uncertain cause, 31% underwent echocardiography, 45% underwent carotid ultrasound, and 48% had neither. Compared with age-, race-, and sex- (proportionally) matched control subjects from the greater Cincinnati/northern Kentucky region, the attributable risk of hypertension for all causes of first-ever ischemic stroke is 27% (95% CI, 7 to 43); for diabetes, 21% (95% CI, 11 to 29); and for coronary artery disease, 9% (95% CI, 2 to 16). For small-vessel ischemic stroke, the attributable risk of hypertension is 68% (95% CI, 31 to 85; odds ratio [OR], 5.0), and the attributable risk of diabetes is 30% (95% CI, 10 to 45; OR, 4.4). For cardioembolic stroke, the attributable risk of diabetes is 25% (95% CI, 4 to 41; OR, 3.1).

Conclusions
—Stroke of uncertain cause is the most common subtype of ischemic stroke among blacks. Cardioembolic stroke and small-vessel stroke are the most important, identifiable causes of first-ever ischemic stroke among blacks. The incidence rates of cardioembolic and large-vessel stroke are likely underestimated because noninvasive testing of the carotid arteries and echocardiography were not consistently obtained in stroke patients at the 18 regional hospitals. Most small-vessel strokes in blacks can be attributed to hypertension and diabetes.
Stroke Treatment Economic Model (STEM)
Authors: Caro J. Jaime , Huybrechts Krista F.
Published: June 2011

Background and Purpose
—Stroke is a debilitating disease with long-term social and economic consequences. As new therapies for acute ischemic stroke are forthcoming, there is an increasing need to understand their long-term economic implications. To address this need, a stroke economic model was created.

Methods
—The model consists of 3 modules. A short-term module incorporates short-term clinical trial data. A long-term module composed of several Markov submodels predicts patient transitions among various locations over time. The modules are connected via a bridge component that groups the survivors at the end of the short-term module according to their functional status and location. Examples of analyses that can be conducted with this model are provided with the use of data from 2 international trials. For illustration, UK unit costs were estimated.

Results
—With the trial data in the short-term module, the short-term management cost is estimated to be £8326 (US $13 649 [USD]). Hospital stay was the major cost driver. By the end of the trials, there was a pronounced difference in the distribution of patient locations between functional groups. It is predicted in the long-term module that the subsequent cost amounts to £75 985 (124 564 USD) for a major and £27 995 (45 893 USD) for a minor stroke.

Conclusions
—Linking functional recovery at the end of short-term treatment with patients’ treatment and residential locations allows this model to estimate the long-term economic impact of stroke interventions. Using patient location instead of the more common natural history as the model foundation allows quantification of the long-term impact to become data driven and hence increases confidence in the results.
Diffusion-Weighted Imaging Identifies a Subset of Lacunar Infarction Associated With Embolic Source
Authors: Ay Hakan , Oliveira-Filho Jamary , Buonanno Ferdinando S. , Ezzeddine Mustapha , Schaefer Pamela W. , Rordorf Guy , Schwamm Lee H. , Gonzalez R. Gilberto , Koroshetz Walter J.
Published: June 2011

Background and Purpose
—Small infarcts in the territory of penetrator arteries were described as causing a number of distinct clinical syndromes. The vascular pathophysiology underlying such infarcts is difficult to ascertain without careful pathological study. However, the occurrence of multiple, small infarcts, linked closely in time but dispersed widely in the brain, raises the possibility of an embolic mechanism. The current study determines the frequency and clinical characteristics of patients with well-defined lacunar syndromes and the diffusion-weighted imaging (DWI) evidence of multiple acute lesions.

Methods
—Sixty-two consecutive patients who presented to the emergency room with a clinically well-defined lacunar syndrome were studied by DWI within the first 3 days of admission.

Results
—DWI showed multiple regions of increased signal intensity in 10 patients (16%). A hemispheric or brain stem lesion in a penetrator territory that accounted for the clinical syndrome (“index lesion”) was found in all. DWI-hyperintense lesions other than the index lesion (“subsidiary infarctions”) were punctate and lay within leptomeningeal artery territories in the majority. As opposed to patients with a single lacunar infarction, patients with a subsidiary infarction more frequently (
P
<0.05) harbored an identifiable cause of stroke.

Conclusions
—Almost 1 of every 6 patients presenting with a classic lacunar syndrome has multiple infarctions demonstrated on DWI. This DWI finding usually indicates an identifiable cause of stroke and therefore may influence clinical decisions regarding the extent of etiologic investigations and treatment for secondary prevention.