bluuebunny/crossref_metadata_2025 huggingface dataset:
Disagreement in Patient and Carer Assessment of Functional Abilities After Stroke
Authors: Knapp Peter , Hewison Jenny
Published: June 2011

Background and Purpose
—The aims of this study were to describe differences between functional ability assessments made by stroke patients and their informal carers and to investigate the psychological associates of the difference in assessments.

Methods
—A prospective design was used, with repeated assessments of function, mood, and carer strain. Thirty hospital stroke patients and their main carer were interviewed 3 times: within 1 month of stroke, 1 month after discharge, and 6 months after discharge.

Results
—There were significant differences between patient and carer assessments at all 3 time points, with patient self-assessment less disabled than carer assessment (at least
P
<0.02). The disagreement in assessment was unrelated to patient or carer mood (
P
>0.05) but greater disagreement was associated with greater carer strain (
P
<0.05). The source of the disagreement in functional ability assessment remains unclear.

Conclusions
—The method of assessment affects the rating of functional abilities after stroke. Carer strain is potentially increased when the patient or carer makes an unrealistic assessment of the patient’s level of independence.
Impaired Dexterity of the Ipsilateral Hand After Stroke and the Relationship to Cognitive Deficit
Authors: Sunderland Alan , Bowers Mark P. , Sluman Stella-Marie , Wilcock David J. , Ardron Mark E.
Published: June 2011

Background and Purpose
—Previous research has reported impaired hand function on the “unaffected” side after stroke, but its incidence, origins, and impact on rehabilitation remain unclear. This study investigated whether impairment of ipsilateral dexterity is common early after middle cerebral artery stroke and explored the relationship to cognitive deficit.

Methods
—Thirty patients within 1 month of an infarct involving the parietal or posterior frontal lobe (15 left and 15 right hemisphere) used the ipsilateral hand in tests that simulated everyday hand functions. Performance was compared with that of healthy age-matched controls using the same hand. Standardized tests were used to assess apraxia, visuospatial ability, and aphasia.

Results
—All patients were able to complete the dexterity tests, but video analysis showed that performance was slow and clumsy compared with that of controls (
P
<0.001). Impairment was most severe after left hemisphere damage, and apraxia was a strong correlate of increased dexterity errors (
P
<0.01), whereas reduced ipsilateral grip strength correlated with slowing (
P
<0.05). The pattern of performance was different for patients with right hemisphere damage. Here there was no correlation between grip strength and slowing, while dexterity errors appeared to be due to visuospatial problems.

Conclusions
—Subtle impairments in dexterity of the ipsilateral hand are common within 1 month of stroke. Ipsilateral sensorimotor losses may contribute to these impairments, but the major factor appears to be the presence of cognitive deficits affecting perception and control of action. The nature of these deficits varies with side of brain damage. The effect of impaired dexterity on functional outcome is not yet known.
Ischemic Stroke
Authors: Mooe Thomas , Olofsson Bert-Ove , Stegmayr Birgitta , Eriksson Peter
Published: June 2011

Background and Purpose
—The risk of ischemic stroke is increased after a myocardial infarction. We quantified the stroke risk and evaluated ischemic stroke characteristics after an acute myocardial infarction.

Methods
—A case-control study including patients with first-ever stroke was undertaken. Cases (n=103) were recorded prospectively in the population-based Northern Sweden World Health Organization Multinational Monitoring of Trends and Determinants in Cardiovascular Disease (MONICA) study. Two controls per case with a stroke but without a recent myocardial infarction were matched for age, sex, and year of stroke onset.

Results
—The sudden onset of neurological symptoms (76.7% versus 54.9%,
P
<0.001), impairment of consciousness (35.0% versus 18.4%,
P
<0.01), and a progression in neurological deficits (19.4% versus 8.7%,
P
<0.01) were more common in cases, while the onset of stroke during sleep was rarer in cases (6.8% versus 21.4%,
P
<0.01). In cases and controls, the clinical subclasses of stroke were as follows: total anterior circulation infarcts, 51.5% versus 37.9% (
P
<0.05); partial anterior circulation infarcts, 28.2% versus 26.7% (
P
=NS); lacunar infarcts, 4.8% versus 27.2% (
P
<0.001); and posterior circulation infarcts, 15.5% versus 8.2% (
P
=0.051). During the first 28 days after myocardial infarction, the daily rate of stroke declined rapidly from ≈9 to 1 stroke per 10 000 myocardial infarction patients compared with an age-adjusted average daily stroke rate of 0.14 per 10 000 in the MONICA population.

Conclusions
—We conclude that the clinical characteristics of the stroke differ between patients with and without a recent myocardial infarction. The risk of a first-ever ischemic stroke is highest during the first few days after a myocardial infarction, but it then declines rapidly, and the absolute number of stroke events is low.
Reasons for Variability in the Reported Rate of Occurrence of Unilateral Spatial Neglect After Stroke
Authors: Bowen Audrey , McKenna Kate , Tallis Raymond C.
Published: June 2011

Background and Purpose
—We sought to determine the frequency of occurrence of contralesional unilateral spatial neglect (USN) after stroke and to investigate the effect of side of lesion, nature of assessment tool used, and timing of assessment relative to stroke onset.

Methods
—We performed a systematic review of published reports, identified by a search of electronic databases (MEDLINE 1966–1997, PSYCHLIT 1974–1996, and CINAHL 1982–1997) and by searching reference lists of the reports selected. Excluded were unpublished, non–English language, and nonhuman studies.

Results
—Thirty published reports met the selection criteria, 17 of which directly compared right brain damage (RBD) and left brain damage (LBD). Contralesional USN appeared to occur more frequently after RBD than LBD in 16 of these. Both the assessment tool used and the time of assessment relative to stroke onset affected the reported rate of occurrence, although recovery rate data were inadequate (4 reports).

Conclusions
—The clinical belief that USN occurs more frequently after RBD than LBD was apparently supported by a systematic review of published data. However, an accurate estimate of the rates of occurrence and recovery after stroke could not be derived. Four reasons for the variability among studies were discussed, including subject selection, lesion localization, and nature and timing of assessment. Different USN disorders may exist, which may require type-specific rehabilitation approaches. This may have implications for epidemiological studies and for the development of new treatments. Theoretically driven epidemiological studies are required before adequately powered randomized controlled trials of rehabilitation can be conducted.
Effects of Stroke Localization on Cardiac Autonomic Balance and Sudden Death
Authors: Tokgözoglu Sadberk Lale , Batur Mustafa Kemal , Topçuoglu Mehmet Akif , Saribas Okay , Kes Sirri , Oto Ali
Published: June 2011

Background and Purpose
—Stroke has been shown to alter autonomic function. The purpose of this study was to show the differential effects of stroke localization on autonomic function parameters assessed by heart rate variability (HRV).

Methods
—To determine the differential effect of ischemic stroke localization on autonomic cardiac innervation, we evaluated 62 patients with ischemic stroke and 62 age- and sex-matched controls. The localization of the infarct was determined by CT and MRI. Power spectrum analysis of HRV was performed. Myocardial necrosis was ruled out by echocardiography and creatine kinase myocardial isoenzymes measurements.

Results
—All stroke patients had significantly decreased low frequency, high frequency, and standard deviation of all relative risk intervals values (
P
<0.001). However, patients with right-middle cerebral artery (R-MCA) and insula lesions had significantly lower power spectrum analysis values compared with all other localizations (
P
<0.001). In addition, 5 patients with R-MCA insular lesions died suddenly compared with 2 patients with left-middle cerebral artery insular lesions during hospitalization. Both sympathetic- and parasympathetic-controlled HRV were decreased in patients with ischemic stroke. The most pronounced decrease was found in the territory of R-MCA insular cortex, which suggests that cardiac autonomic tone may be regulated by insula and that these patients are more prone to cardiac complications such as arrhythmias and sudden death due to autonomic imbalance.

Conclusion
—We conclude that stroke in the region of insula (especially the right) leads to decreased HRV and to increased incidence of sudden death.
Carotid Artery Diameter Correlates With Risk Factors for Cardiovascular Disease in a Population of 55-Year-Old Subjects
Authors: Jensen-Urstad Kerstin , Jensen-Urstad Mats , Johansson Jan
Published: June 2011

Background and Purpose
—We investigated whether, in a randomly selected population of 55-year-old men and women, there is a relationship between common carotid artery (CCA) diameter and intima-media (IM) thickness and conventional risk factors for cardiovascular disease such as gender, smoking, elevated blood lipids, and high blood pressure.

Methods
—CCA diameter and IM thickness of the distal right and left CCAs were measured by high-frequency ultrasound methods. Fifty-seven men (73% of the invited men) and 47 women (62% of the invited women) participated.

Results
—In the whole group the CCA diameter was correlated with gender (
P
<0.001), cholesterol (
P
=0.007), triglycerides (
P
<0.001), apoB (
P
<0.001), apoB/A-1 (
P
<0.001), systolic blood pressure (
P
=0.001), and glucose (
P
=0.006). HDL was inversely correlated with mean CCA diameter (
P
=0.003). In men the CCA diameter was correlated with a combined risk factor score (
P
=0.005), systolic blood pressure (
P
=0.011), platelet count (
P
=0.033), apoB (
P
=0.025), and occurrence of plaque (
P
=0.003). In women the CCA diameter was correlated with a combined risk factor score (
P
=0.010), systolic blood pressure (
P
=0.033), body mass index (
P
<0.001), cholesterol (
P
=0.009), triglycerides (
P
=0.14), apoB (
P
=0.002), and apoB/A1 (
P
=0.003). IM thickness was correlated with systolic blood pressure (
P
<0.001).

Conclusions
—There are correlations between risk factors for cardiovascular disease and carotid artery diameter and IM thickness in both women and men in a population of 55-year-old subjects. The increased vessel diameter in subjects with cardiovascular risk factors may be a sign of attenuated vasoregulation, which could be an important factor during the development of atherosclerosis.
Improved Automated Detection of Embolic Signals Using a Novel Frequency Filtering Approach
Authors: Markus Hugh , Cullinane Marisa , Reid Greg
Published: June 2011

Background and Purpose
—Asymptomatic embolic signal detection with the use of Doppler ultrasound has a number of potential clinical applications. However, its more widespread clinical use is severely limited by the lack of a reliable automated detection system. Design of such a system depends on accurate characterization of the unique features of embolic signals, which allow their differentiation from artifact and background Doppler speckle. We used a processing system with high temporal resolution to describe these features. We then used this information to design a new automated detection system.

Methods
—We used a signal processing approach based on multiple overlapping band-pass filters to characterize 100 consecutive embolic signals from patients with carotid artery disease as well as both episodes of artifact resulting from probe tapping and facial movement and episodes of Doppler speckle. We then designed an automated detection system based both on these embolic signal characteristics and on the fact that embolic signals have maximum intensity over a narrow frequency range. This system was tested in real time on stored 5-second segments of data.

Results
—The value of peak velocity at maximal intensity discriminated best between embolic signals and artifact and allowed differentiation with 100% sensitivity and specificity. Relative intensity increase, intensity volume, area under volume, average rise rate, and average fall rate appeared to discriminate best between embolic signals and Doppler speckle. For the majority of embolic signals, the intensity increase was spread over a narrow frequency or velocity range. The automated system we developed detected 296 of 325 carotid stenosis embolic signals from a new data set (sensitivity, 91.1%). All 200 episodes of artifact from a new data set were differentiated from embolic signals. Only 2 of 100 episodes of speckle were misidentified as embolic signals.

Conclusions
—Using a novel system for automated detection, which utilizes the fact that embolic signals have maximum intensity over a narrow frequency range, we have achieved detection with a high sensitivity and high specificity. These results are considerably better than those previously reported. We tested this initial system on short 5-second segments of data played in real time. This approach now needs to be developed for use in a true online system to determine whether it has sufficient sensitivity and specificity for clinical use.
Cost-Effectiveness Analysis of Screening for Asymptomatic, Unruptured Intracranial Aneurysms
Authors: Yoshimoto Yuhei , Wakai Susumu
Published: June 2011

Background and Purpose
—Subarachnoid hemorrhage (SAH) due to aneurysmal rupture is a major cause of cerebrovascular disease–related death. This problem could be eliminated by diagnosis and successful treatment of aneurysms before rupture. Recent developments in high-resolution imaging technology have made screening for unruptured aneurysms possible in the general population. Such screening has become widespread in Japan (“No Dokku,” or brain checkup). As a result, unruptured aneurysms are being identified with increasing frequency. However, the economic implications of treatment decisions for unruptured aneurysms have not been analyzed. Therefore, we performed such an analysis.

Methods
—We used a Markov model to evaluate the cost-effectiveness of screening for asymptomatic, unruptured intracranial aneurysms. The model involved a set of variables describing discrete health states. Each state was assigned a quality of life score and an associated medical cost. A comparison of the expected outcomes was then made between 2 hypothetical cohorts, one receiving screening and the other no screening. A sensitivity analysis was performed by altering the input values within clinically reasonable ranges to reflect uncertainty in the baseline analysis and then assessing the effects on outcomes.

Results
—Combining the incremental cost and effectiveness data revealed a cost per quality-adjusted life-year of $7760 for an annual rate of subarachnoid hemorrhage due to unruptured aneurysms (rupture rate) of 0.02; this cost was $39 450 for a rupture rate of 0.01. There was no benefit (negative quality-adjusted life-year benefit) for a rupture rate of 0.005, the rupture rate found in a recently published international cooperative study. The risks of surgery for unruptured aneurysms and the discounting ratio used to assess the impact of timing of costs and benefits on future outcomes also had significant effects on the results. Other variables had little impact on cost-effectiveness.

Conclusions
—The cost-effectiveness of screening for an unruptured aneurysm is highly sensitive to the annual rate of subarachnoid hemorrhage due to unruptured aneurysms. The low annual rupture rate seen in the recent large international cooperative study implies that screening asymptomatic populations to identify and treat unruptured aneurysms would not be cost cost-effective.
Small Chronic Hemorrhages and Ischemic Lesions in Association With Spontaneous Intracerebral Hematomas
Authors: Tanaka Akira , Ueno Yasushi , Nakayama Yoshiya , Takano Kohichi , Takebayashi Shigeo
Published: June 2011

Background and Purpose
—It has been speculated that the same type of hypertensive small-artery disease can cause either intracerebral hemorrhages or ischemic lesions, depending on the circumstances.

Methods
—To test this hypothesis, we examined the association between spontaneous intracerebral hematomas and both small chronic hemorrhages and ischemic lesions using echo planar and T2-weighted MRI. We considered a hypointense area to represent a hemorrhage and a hyperintense area to represent an ischemic lesion.

Results
—We identified small hypointense lesions in 56.7% of 30 patients with intracerebral hematomas (mean age, 62.2 years; total number of lesions, 108) and in 25.4% of 59 patients without hematomas (mean age, 67.6 years; total lesions, 28). The incidence of hypertension was 88.3% in patients with intracerebral hematomas and 42.3% in those without. The hypointense lesions were found in 56.0% of 50 patients with hypertension, whereas they were found only in 10.3% of 39 patients without hypertension. The hypointense lesions were most common in the subcortex, followed by the putamen, pons, thalamus, and cerebellum. The hyperintense lesions were of a higher grade in patients with intracerebral hematomas than in those without. The hypointense lesions were commonly surrounded by hyperintense areas. Additionally, in 3 of 3 autopsied brains, we found hemosiderin deposits around arteriosclerotic microvessels and a surrounding small infarction in areas that had appeared as small hypointense lesions surrounded by hyperintensity on MRI. One specimen also had an organized miliary pseudoaneurysm.

Conclusions
—Our findings indicate that spontaneous intracerebral hematomas are frequently associated with small chronic hemorrhages, ischemic lesions, and hypertension. We speculate that hypertensive intracerebral hemorrhage may have the same microangiopathic basis as cerebral infarction.
Adhesion Molecules in Cerebrovascular Diseases
Authors: Fassbender Klaus , Bertsch Thomas , Mielke Orell , Mühlhauser Frank , Hennerici Michael
Published: June 2011

Background and Purpose
—Adhesion molecules mediate attachment and transendothelial migration of leukocytes as a critical step in pathogenesis of atherosclerosis. Their expression and release were comparatively investigated in patients with large- and small-vessel disease of the central nervous system.

Methods
—With immunological methods, serum concentrations of endothelial-derived adhesion molecules (soluble endothelial-leukocyte adhesion molecule [sE-selectin], soluble vascular-leukocyte adhesion molecule-1, and soluble intercellular adhesion molecule-1 [sICAM-1]) were quantified in patients with obstructive disease of extracranial (n=89) and intracranial (n=20) large-vessel disease and patients with subcortical vascular encephalopathy (n=64), a cerebral small-vessel disease. As controls, age- and sex-matched subjects without obstructive cerebrovascular disease (n=67) were studied.

Results
—We observed significantly increased serum concentrations of sE-selectin and sICAM-1 in patients with both obstructive disease of the large brain-supplying arteries and subcortical vascular encephalopathy. Interestingly, the highest levels were observed in intracranial macroangiopathy. Furthermore, concentrations of sICAM-1 and sE-selectin were significantly increased in current smokers but not in diabetic or hypertensive patients.

Conclusions
—The observation of elevated release of endothelial-derived adhesion molecules in both patients with stenoses of the large brain-supplying arteries and patients with subcortical vascular encephalopathy indicates that inflammatory endothelial activation and adhesion of leukocytes play similarly important roles in cerebral large- and small-vessel disease.
Decreases in Blood Pressure and Sympathetic Nerve Activity by Microvascular Decompression of the Rostral Ventrolateral Medulla in Essential Hypertension
Authors: Morimoto Satoshi , Sasaki Susumu , Takeda Kazuo , Furuya Seiichi , Naruse Shoji , Matsumoto Keigo , Higuchi Toshihiro , Saito Mitsuru , Nakagawa Masao
Published: June 2011

Background
—Neurovascular compression of the rostral ventrolateral medulla, a major center regulating sympathetic nerve activity, may be causally related to essential hypertension. Microvascular decompression of the rostral ventrolateral medulla decreases elevated blood pressure.

Case Description
—A 47-year-old male essential hypertension patient with hemifacial nerve spasms exhibited neurovascular compression of the rostral ventrolateral medulla and facial nerve. Microvascular decompression of the rostral ventrolateral medulla successfully reduced blood pressure and plasma and urine norepinephrine levels, low-frequency to high-frequency ratio obtained by power spectral analysis, and muscle sympathetic nerve activity.

Conclusions
—This case suggests not only that reduction in blood pressure by microvascular decompression of the rostral ventrolateral medulla may be mediated by a decrease in sympathetic nerve activity but also that neurovascular compression of this area may be a cause of blood pressure elevation via increased sympathetic nerve activity.
Cerebral Blood Flow During Hemodilution and Hypoxia in Rats
Authors: Tomiyama Yoshinobu , Brian Johnny E. , Todd Michael M.
Published: June 2011

Background and Purpose
—Hypoxia and hemodilution both reduce arterial oxygen content (Ca
o
2
) and increase cerebral blood flow (CBF), but the mechanisms by which hemodilution increases CBF are largely unknown. ATP-sensitive potassium (K
ATP
) channels are activated by intravascular hypoxia, and contribute to hypoxia-mediated cerebrovasodilatation. Although Ca
o
2
can be reduced to equal levels by hypoxia or hemodilution, intravascular P
o
2
is reduced only during hypoxia. We therefore tested the hypothesis that K
ATP
channels would be unlikely to contribute to cerebrovasodilatation during hemodilution.

Methods
—Glibenclamide (19.8 μg) or vehicle was injected into the cisterna magna of barbiturate-anesthetized rats. The dose of glibenclamide was chosen to yield an estimated CSF concentration of 10
−4
M. Thirty minutes later, some animals underwent either progressive isovolumic hemodilution or hypoxia (over 30 minutes) to achieve a Ca
o
2
of ≈7.5 mL O
2
/dL. Other animals did not undergo hypoxia or hemodilution and served as controls. Six groups of animals were studied: control/vehicle (n=4), control/glibenclamide (n=4), hemodilution/vehicle (n=10), hemodilution/glibenclamide (n=10), hypoxia/vehicle (n=10), and hypoxia/glibenclamide (n=10). CBF was then measured with
3
H-nicotine in the forebrain, cerebellum, and brain stem.

Results
—In control/vehicle rats, CBF ranged from 72 mL · 100 g
−1
· min
−1
in forebrain to 88 mL · 100 g
−1
· min
−1
in the brain stem. Glibenclamide treatment of control animals did not influence CBF in any brain area. Hemodilution increased CBF in all brain areas, with flows ranging from 128 mL · 100 g
−1
· min
−1
in forebrain to 169 mL · 100 g
−1
· min
−1
in the brain stem. Glibenclamide treatment of hemodiluted animals did not affect CBF in any brain area. Hypoxia resulted in a greater CBF than did hemodilution, ranging from 172 mL · 100 g
−1
· min
−1
in forebrain to 259 mL · 100 g
−1
· min
−1
in the brain stem. Glibenclamide treatment of hypoxic animals significantly reduced CBF in all brain areas (
P
<0.05).

Conclusions
—Both hypoxia and hemodilution increased CBF. Glibenclamide treatment significantly attenuated the CBF increase during hypoxia but not after hemodilution. This finding supports our hypothesis that K
ATP
channels do not contribute to increasing CBF during hemodilution. Because intravascular PO
2
is normal during hemodilution, this finding supports the hypothesis that intravascular PO
2
is an important regulator of cerebral vascular tone and exerts its effect in part by activation of K
ATP
channels in the cerebral circulation.
Fluoxetine Dilates Isolated Small Cerebral Arteries of Rats and Attenuates Constrictions to Serotonin, Norepinephrine, and a Voltage-Dependent Ca
2+
Channel Opener
Authors: Ungvari Zoltan , Pacher Pal , Kecskeméti Valéria , Koller Akos
Published: June 2011

Background and Purpose
—Recent clinical observations question that the antidepressant effect of fluoxetine (Prozac) can be explained solely with serotonin reuptake inhibition in the central nervous system. We hypothesized that fluoxetine affects the tone of vessels and thereby modulates cerebral blood flow.

Methods
—A small branch of rat anterior cerebral artery (195±15 μm in diameter at 80 mm Hg perfusion pressure) was isolated, cannulated, and pressurized (at 80 mm Hg), and changes in diameter were measured by videomicroscopy.

Results
—Fluoxetine dilated small cerebral arteries with an EC
50
of 7.7±1.0×10
−6
mol/L, a response that was not affected by removal of the endothelium or application of 4-aminopyridine (an inhibitor of aminopyridine-sensitive K
+
channels), glibenclamide (an inhibitor of ATP-sensitive K
+
channels), or tetraethylammonium (a nonspecific inhibitor of K
+
channels). The presence of fluoxetine (10
−6
to 3×10
−5
mol/L) significantly attenuated constrictions to serotonin (10
−9
to 10
−5
mol/L) and norepinephrine (10
−9
to 10
−5
mol/L). Increasing concentrations of Bay K 8644 (a voltage-dependent Ca
2+
channel opener, 10
−10
to 10
−6
mol/L) elicited constrictions, which were markedly reduced by 2×10
−6
and 10
−5
mol/L fluoxetine, whereas 3×10
−5
mol/L fluoxetine practically abolished the responses.

Conclusions
—Fluoxetine elicits substantial dilation of isolated small cerebral arteries, a response that is not mediated by endothelium-derived dilator factors or activation of K
+
channels. The finding that fluoxetine inhibits constrictor responses to Ca
2+
channel opener, as well as serotonin and norepinephrine, suggests that fluoxetine interferes with the Ca
2+
signaling mechanisms in the vascular smooth muscle. We speculate that fluoxetine increases cerebral blood flow in vivo, which contributes to its previously described beneficial actions in the treatment of mental disorders.
Exacerbation of Delayed Cell Injury After Transient Global Ischemia in Mutant Mice With CuZn Superoxide Dismutase Deficiency
Authors: Kawase Makoto , Murakami Kensuke , Fujimura Miki , Morita-Fujimura Yuiko , Gasche Yvan , Kondo Takeo , Scott Richard W. , Chan Pak H.
Published: June 2011

Background and Purpose
—We have demonstrated that copper-zinc superoxide dismutase (CuZn-SOD), a cytosolic isoenzyme of SODs, has a protective role in the pathogenesis of superoxide radical–mediated brain injury. Using mice bearing a disruption of the CuZn-SOD gene (
Sod
1), the present study was designed to clarify the role of superoxide anion in the pathogenesis of selective vulnerability after transient global ischemia.

Methods
—
Sod
1 knockout homozygous mutant mice (
Sod
1 −/−) with a complete absence of endogenous CuZn-SOD activity, heterozygous mutant mice (
Sod
1 +/−) with a 50% decrease in the activity, and littermate wild-type mice (male, 35 to 45 g) were subjected to global ischemia. Since the plasticity of the posterior communicating artery (PcomA) has been reported to influence the outcome of hippocampal injury, we assessed the relation between the plasticity of PcomAs and the decrease of regional cerebral blood flow in global ischemia.

Results
—The fluorescence intensity of hydroethidine oxidation, a measurement of ethidium fluorescence for superoxide radicals, was increased in mutant mice 1 day after both 5 and 10 minutes of global ischemia, compared with wild-type mice. Hippocampal injury in the PcomA hypoplastic brains showed significant exacerbation in mutant mice compared with wild-type littermates 3 days after 5 minutes of global ischemia, although a marked difference was not observed at 1 day.

Conclusions
—These data suggest that superoxide radicals play an important role in the pathogenesis of delayed injury in the vulnerable hippocampal CA1 subregion after transient global ischemia.
Brain Plasticity and Stroke Rehabilitation
Authors: Johansson Barbro B.
Published: June 2011

Abstract
—Neuronal connections and cortical maps are continuously remodeled by our experience. Knowledge of the potential capabilityof the brain to compensate for lesions is a prerequisite for optimal stroke rehabilitation strategies. Experimental focal cortical lesions induce changes in adjacent cortex and in the contralateral hemisphere. Neuroimaging studies in stroke patients indicate altered poststroke activation patterns, which suggest some functional reorganization. To what extent functional imaging data correspond to outcome data needs to be evaluated. Reorganization may be the principle process responsible for recovery of function after stroke, but what are the limits, and to what extent can postischemic intervention facilitate such changes? Postoperative housing of animals in an enriched environment can significantly enhance functional outcome and can also interact with other interventions, including neocortical grafting. What role will neuronal progenitor cells play in future rehabilitation—stimulated in situ or as neural replacement? And what is the future for blocking neural growth inhibitory factors? Better knowledge of postischemic molecular and neurophysiological events, and close interaction between basic and applied research, will hopefully enable us to design rehabilitation strategies based on neurobiological principles in a not-too-distant future.
Antioxidant Profile and Early Outcome in Stroke Patients
Authors: Cherubini Antonio , Polidori Maria Cristina , Bregnocchi Mario , Pezzuto Salvatore , Cecchetti Roberta , Ingegni Tiziana , di Iorio Angelo , Senin Umberto , Mecocci Patrizia
Published: June 2011

Background and Purpose
—Experimental studies provide evidence of an association between ischemic stroke and increased oxidative stress, but data in humans are still limited and controversial. The purpose of this study was to investigate the time course of plasma antioxidant changes in ischemic stroke patients.

Methods
—Plasma antioxidants, including water-soluble (vitamin C and uric acid) and lipid-soluble (vitamins A and E) compounds as well as antioxidant enzyme activities in plasma (superoxide dismutase [SOD] and glutathione peroxidase) and erythrocytes (SOD), were measured by high-performance liquid chromatography (antioxidant vitamins) and by spectrophotometry (antioxidant enzymes) in 38 subjects (25 men and 13 women aged 77.2±7.9 years) with acute ischemic stroke of recent onset (<24 hours) on admission, after 6 and 24 hours, and on days 3, 5, and 7. Antioxidant levels in patients on admission were compared with those of age- and sex-matched controls.

Results
—Mean antioxidant levels and activities in patients on admission were lower than those of controls and showed a gradual increase over time. Patients with the worst early outcome (death or functional decline) had higher vitamin A and uric acid plasma levels and lower vitamin C levels and erythrocyte SOD activity than those who remained functionally stable.

Conclusions
—These results suggest that the majority of antioxidants are reduced immediately after an acute ischemic stroke, possibly as a consequence of increased oxidative stress. A specific antioxidant profile is associated with a poor early outcome.
Morphological and Functional Characteristics of Patent Foramen Ovale and Their Embolic Implications
Authors: De Castro Stefano , Cartoni Domenico , Fiorelli Marco , Rasura Maurizia , Anzini Alexia , Zanette Elietta M. , Beccia Mario , Colonnese Claudio , Fedele Francesco , Fieschi Cesare , Pandian Natesa G.
Published: June 2011

Background and Purpose
—Transesophageal echocardiography (TEE) has detected a high prevalence of patent foramen ovale (PFO) in stroke patients, but the clinical implications of the distinctive characteristics of this patency are still a matter of debate.

Methods
—We studied 350 patients with acute ischemic stroke or transient ischemic attack (TIA) within 1 week of admission. Of these, 101 (29%) were identified by contrast TEE to have a PFO; 86 patients (25%) were cryptogenic stroke patients, and 163 were excluded because of the presence of a definite or possible arterial or clinical evidence of a source of emboli or small-vessel disease. Thirteen PFO subjects without a history of embolism were designated as the control group. All PFO and cryptogenic stroke patients were followed up by neurological visits.

Results
—Compared with controls, PFO patients with acute stroke or TIA more frequently presented with a right-to-left shunt at rest and a higher membrane mobility (
P
<0.05). Patients with these characteristics were considered to be at high risk. During a median follow-up period of 31 months (range, 4 to 58 months), 8 PFO and 18 cryptogenic stroke patients experienced recurrent cerebrovascular events. The cumulative estimate of risk of cerebrovascular event recurrence at 3 years was 4.3% (95% confidence interval [CI], 0% to 10.2%) for “low-risk” PFO patients, 12.5% (95% CI, 0% to 26.1%) for “high-risk” PFO patients, and 16.3% (95% CI, 7.2% to 25.4%) for cryptogenic stroke patients (high-risk PFO versus low-risk PFO,
P
=0.05).

Conclusions
—The association of right-to-left shunting at rest and high membrane mobility, as detected by contrast TEE, seems to identify PFO patients with cerebrovascular ischemic events who are at higher risk for recurrent brain embolism.
Selective Effects of Subarachnoid Hemorrhage on Cerebral Vascular Responses to 4-Aminopyridine in Rats
Authors: Quan Lilly , Sobey Christopher G.
Published: June 2011

Background and Purpose
—We postulated that some abnormalities in cerebrovascular function after subarachnoid hemorrhage (SAH) may involve underlying alterations in K
+
channel function. Thus, using pharmacological inhibitors, we assessed the influence of SAH on function of 2 types of K
+
channel in regulation of basilar artery diameter in vivo and membrane potential (E
m
) in vitro.

Methods
—Rats were injected with saline (control) or autologous blood (SAH) into the cisterna magna. Two days later, effects of vasoactive drugs on the basilar artery were examined with a cranial window preparation. Vascular responses to 4-aminopyridine (4-AP), 3-aminopyridine (3-AP), tetraethylammonium (TEA), serotonin, acetylcholine, and adenosine were compared in control and SAH rats. Additional studies using intracellular microelectrodes evaluated the effects of 4-AP and serotonin on E
m
of basilar arteries isolated from control and SAH rats.

Results
—Baseline artery diameter was 236±5 μm in control rats and 220±7 μm in SAH rats (
P
<0.05). 4-AP, but not 3-AP, constricted the basilar artery in control rats, and responses to 4-AP were reduced in SAH rats. Constrictor responses to TEA or serotonin were unaffected by SAH. Vasodilator responses to acetylcholine were impaired in SAH rats, whereas responses to adenosine were not different. Resting E
m
was −81±3 mV in control arteries and −79±3 mV in SAH arteries. Both 4-AP and serotonin depolarized the basilar artery, but only 4-AP–induced depolarization was impaired in SAH arteries.

Conclusions
—These data suggest that 4-AP induces cerebral vasoconstriction in vivo through smooth muscle depolarization due to inhibition of voltage-dependent K
+
channels. Furthermore, function of these K
+
channels may be selectively reduced in the basilar artery after SAH and thus could contribute to cerebral vascular dysfunction.
Cardiac Arrhythmias and Stroke
Authors: Engström Gunnar , Hedblad Bo , Juul-Möller Steen , Tydén Patrik , Janzon Lars
Published: June 2011

Background and Purpose
—With the exception of atrial fibrillation (AF), little scientific attention has been given the associations between cardiac arrhythmias and incidence of stroke. We sought to study whether atrial and ventricular arrhythmias assessed during a 24-hour ambulatory ECG registration are associated with incidence of stroke.

Methods
—The population-based cohort “Men Born in 1914” was examined with 24-hour ambulatory ECG registrations at 68 years of age. Four hundred two men without previous myocardial infarction or stroke were included, and 236 of them had hypertension (≥160/95 mm Hg or treatment). Fourteen-year rates of stroke (fatal and nonfatal) and all-cause mortality were updated from national and regional registers. Frequent or complex ventricular arrhythmias was defined as Lown class 2 to 5. A high frequency of atrial ectopic beats (AEB) was defined as the fifth quintile (ie, ≥218 AEB per 24 hours).

Results
—Fifty-eight men suffered a first stroke during the follow-up. Stroke rates (per 1000 person-years) among men with AF (n=14), with frequent AEB (n=77), and without AF or frequent AEB (n=311) were 34.5, 19.5, and 11.6, respectively. The corresponding values among men with hypertension were 40.7, 32.3, and 14.7, respectively. Frequent AEB (compared with absence of AF and frequent AEB) was significantly associated with stroke among all men (relative risk=1.9; 95% CI, 1.02 to 3.4;
P
=0.04) and among hypertensive men (relative risk=2.5; 95% CI, 1.3 to 4.8;
P
=0.009) after adjustments for potential confounders. The increased stroke rates among men with Lown class 2 to 5 did not reach statistical significance.

Conclusions
—A high frequency of AEB is associated with an increased incidence of stroke.
Potential of Carotid Enlargement as a Useful Indicator Affected by High Blood Pressure in a Large General Population of a Japanese City
Authors: Mannami Toshifumi , Baba Shunroku , Ogata Jun
Published: June 2011

Background and Purpose
—Few studies have examined whether there is a relationship between carotid arterial diameter and cardiovascular risk factors in a large general population. The aim of this study was to investigate cross-sectionally whether, in a randomly selected general large population of a Japanese city, there is a relationship between common carotid artery (CCA) diameter and conventional cardiovascular risk factors.

Methods
—The subjects of the present study were randomly selected from the residents of the city of Suita, located in the second largest urban area of Japan, and consisted of 2284 men and 2568 women aged 30 to 89 years. The outer and inner CCA diameters and intima-media thickness (IMT) of CCA were detected and measured by a single physician with high-resolution ultrasonography. We assessed cross-sectionally by age/sex group the relationships between IMT or CCA diameters and cardiovascular risk factors, especially blood pressure levels divided into 3 groups: the normal group of subjects had a diastolic blood pressure (DBP) <85 mm Hg and systolic blood pressure (SBP) <130 mm Hg and were not taking antihypertensive medication; the high group of subjects had DBP ≥90 mm Hg and/or SBP ≥140 mm Hg and/or were taking antihypertensive medication; and the moderate group consisted of all other subjects.

Results
—The outer and inner CCA diameters for the high group were significantly (
P
<0.05) enlarged in comparison with those for the moderate and normal groups in all age/sex groups of both sexes after adjustment for body mass index, pack-years of smoking, alcohol consumption, and total serum cholesterol. Multiple regression analysis showed that age, body mass index, SBP, pack-years of smoking, alcohol consumption, and IMT were positively and significantly (
P
<0.005) related to both outer and inner CCA diameters in both sexes except for between alcohol consumption and outer CCA diameter in women and showed that only serum total cholesterol level was negatively and significantly (
P
<0.01) related to inner CCA diameter in both sexes.

Conclusions
—Our present study showed that the outer and inner CCA diameters correlated with conventional cardiovascular risk factors, including high blood pressure and IMT. These findings suggest that the outer and inner CCA diameters may be a useful indicator of carotid atherosclerosis, particularly in relation to high blood pressure.
Diagnostic Testing for Coagulopathies in Patients With Ischemic Stroke
Authors: Bushnell Cheryl D. , Goldstein Larry B.
Published: June 2011

Background
—Hypercoagulable states are a recognized, albeit uncommon, etiology of ischemic stroke. It is unclear how often the results of specialized coagulation tests affect management. Using data compiled from a systematic review of available studies, we employed quantitative methodology to assess the diagnostic yield of coagulation tests for identification of coagulopathies in ischemic stroke patients.

Summary of Review
—We performed a MEDLINE search to identify controlled studies published during 1966–1999 that reported the prevalence of deficiencies of protein C, protein S, antithrombin III, plasminogen, activated protein C resistance (APCR)/factor V Leiden mutation (FVL), anticardiolipin antibodies (ACL), or lupus anticoagulant (LA) in patients with ischemic stroke. The cumulative prevalence rates (pretest probabilities) and positive likelihood ratios for all studies and for those including only patients aged ≤50 years were used to calculate posttest probabilities for each coagulopathy, reflecting diagnostic yield. The cumulative pretest probabilities of coagulation defects in ischemic stroke patients are as follows: LA, 3% (8% for those aged ≤50 years); ACL, 17% (21% for those aged ≤50 years); APCR/FVL, 7% (11% for those aged ≤50 years); and prothrombin mutation, 4.5% (5.7% for those aged ≤50 years). The posttest probabilities of ACL, LA, and APCR increased with increasing pretest probability, the specificity of the tests, and features of the patients’ history and clinical presentation.

Conclusions
—–The pretest probabilities of coagulation defects in ischemic stroke patients are low. The diagnostic yield of coagulation tests may be increased by using tests with the highest specificities and by targeting patients with clinical or historical features that increase pretest probability. Consideration of these data might lead to more rational ordering of tests and an associated cost savings.
Which Parameters of Beat-to-Beat Blood Pressure and Variability Best Predict Early Outcome After Acute Ischemic Stroke?
Authors: Dawson Suzanne L. , Manktelow Bradley N. , Robinson Thompson G. , Panerai Ronney B. , Potter John F.
Published: June 2011

Background and Purpose
—In hypertensive populations, increasing blood pressure (BP) levels and BP variability (BPV) are associated with a greater incidence of target organ damage. After stroke, elevated 24-hour BP levels predict a poor outcome, although it is uncertain whether shorter-length BP recordings assessing mean BP levels and BPV have a similar predictive role. The objectives of this study were to compare the different measures of beat-to-beat BP and BPV on outcome after acute ischemic stroke and assess whether these parameters were affected by stroke subtype.

Methods
—Ninety-two consecutive admissions with a CT-confirmed diagnosis of acute ischemic stroke were recruited, of whom 54 had cortical infarction, 29 subcortical, and 9 posterior circulation infarction. Casual and two 5-minute recordings of beat-to-beat BP (Finapres, Ohmeda) were made under standardized conditions within 72 hours of ictus, with mean BP levels taken as the average of this 10-minute recording and BPV as the standard deviation. Outcome was assessed at 30 days as dead/dependent or independent (Rankin ≤2). The effects of BP, BPV, and stroke subtype on outcome were studied with the use of logistic regression. Stroke subjects were subsequently divided by BP quartiles and within each quartile into low- and high-variability groups; the influence of high BPV on outcome was also assessed.

Results
—The odds ratio for death/dependency was significantly higher in cortical strokes compared with subcortical and posterior circulation strokes even after controlling for differences in BP and BPV (OR 4.19,
P
=0.002). Beat-to-beat systolic BP (SBP), diastolic BP (DBP), and mean arterial pressure (MAP ± SD) levels were higher in the dead/dependent group compared with the independent group (MAP 106±20.4 mm Hg vs 97±19.1 mm Hg,
P
<0.02), as was MAP variability: 6.1 (interquartile range 4.5 to 7.4 mm Hg) versus 4.9 (3.8 to 6.4 mm Hg,
P
=0.02). The odds ratio for a poor outcome was 1.38 (
P
=0.014) for every 10–mm Hg increase in MAP and 1.32 (
P
=0.02) for every 1–mm Hg increase in MAP variability. Casual BP measurements had no prognostic significance. For the group as a whole when separated into BP quartiles, those with a high MAP and DBP but not SBP variability within each quartile had a worse prognosis compared with those with a low BPV.

Conclusions
—A poor outcome at 30 days after ischemic stroke was dependent on stroke subtype, beat-to-beat DBP, and MAP levels and variability. Important prognostic information can be readily obtained from a short period of noninvasive BP monitoring in the acute stroke patient. These findings have important implications, particularly regarding the use of hypotensive agents in the acute stroke period.
Augmented Vasoconstriction and Thromboxane Formation by 15-F
2t
-Isoprostane (8-Iso-Prostaglandin F
2α
) in Immature Pig Periventricular Brain Microvessels
Authors: Hou Xin , Gobeil Fernand , Peri Krishna , Speranza Giovanna , Marrache Anne Marilise , Lachapelle Pierre , Roberts Jackson , Varma Daya R. , Chemtob Sylvain
Published: June 2011

Background and Purpose
—Oxidant stress, especially in the premature, plays a major role in the pathogenesis of hypoxic-ischemic encephalopathies mostly manifested in the periventricular region. We studied the vasomotor mode of actions of the peroxidation product 15-F
2t
-isoprostane (15-F
2t
-IsoP) (8-iso-prostaglandin F
2α
) on periventricular region during development.

Methods
—Effects of 15-F
2t
-IsoP on periventricular microvessels of fetal, newborn, and juvenile pigs were studied by video imaging and digital analysis techniques. Thromboxane formation and intracellular Ca
2+
were measured by radioimmunoassay and by using the fluorescent indicator fura 2-AM.

Results
—15-F
2t
-IsoP–mediated constriction of periventricular microvessels decreased as a function of age such that in the fetus it was ≈2.5-fold greater than in juvenile pigs. 15-F
2t
-IsoP evoked more thromboxane formation in the fetus than in the newborn, which was greater than that in the juvenile periventricular region; this was associated with immunoreactive thromboxane A
2
(TXA
2
) synthase expression in the fetus that was greater than that in newborn pigs, which was greater than that in juvenile pigs. 15-F
2t
-IsoP–induced vasoconstriction was markedly inhibited by TXA
2
synthase and receptor blockers (
CGS12970
and L670596). Vasoconstrictor effects of the TXA
2
mimetic U46619 on fetal, neonatal, and juvenile periventricular microvessels did not differ. 15-F
2t
-IsoP increased TXA
2
synthesis by activating Ca
2+
influx through non–voltage-gated channels in endothelial cells (SK&F96365 sensitive) and N-type voltage-gated channels (ω-conotoxin sensitive) in astrocytes; smooth muscle cells were not responsive to 15-F
2t
-IsoP but generated Ca
2+
transients to U46619 via L-type voltage-sensitive channels.

Conclusions
—15-F
2t
-IsoP causes periventricular brain region vasoconstriction in the fetus that is greater than that in the newborn, which in turn is greater than that in the juvenile due to greater TXA
2
formation generated through distinct stimulatory pathways, including from endothelial and astroglial cells. The resulting hemodynamic compromise may contribute to the increased vulnerability of the periventricular brain areas to oxidant stress–induced injury in immature subjects.