bluuebunny/crossref_metadata_2025 huggingface dataset:
Plasma Homocysteine in the Acute and Convalescent Phases After Stroke
Authors: Lindgren Arne , Brattström Lars , Norrving Bo , Hultberg Björn , Andersson Anders , Johansson Barbro B.
Published: June 2011

Background and Purpose
Stroke patients frequently manifest moderate hyperhomocysteinemia. In most published studies, plasma homocysteine was measured at least 1 month after stroke (or the interval was not reported). To determine whether plasma homocysteine concentrations change in the acute phase, we compared acute-phase values with both convalescent-phase and control values.

Methods
Plasma homocysteine concentrations were measured in the acute phase (mean, 2 days after stroke onset) in 162 first-ever stroke patients aged 50 years or more (median, 75 years) and again at a median interval of 583 days (range, 460 to 645 days) after stroke onset in a subgroup of 17 patients, with values for 60 age-matched subjects serving as controls. Twenty of the control subjects were reexamined 2 to 3 years after their initial examination.

Results
The median plasma homocysteine concentration was 13.4 μmol/L in the patient group compared with 13.8 μmol/L for control subjects (NS, Mann-Whitney
U
test) and increased from 11.4 μmol/L in the acute phase to 14.5 μmol/L in the convalescent phase in the subgroup of patients examined twice (
P
<.01, Wilcoxon signed rank test). In the 20 reexamined control subjects, no significant change over time in plasma homocysteine concentration was found.

Conclusions
The post–acute-phase increase in plasma homocysteine may explain why higher values were obtained for stroke patients than for control subjects in previous studies. Possible reasons for the variation in plasma homocysteine concentrations over time are (1) an acute-phase reduction secondary to a decrease in plasma albumin and (2) an increase in plasma homocysteine during the convalescent phase due to modified vitamin intake and/or lifestyle. The timing of plasma homocysteine measurements relative to stroke onset is a factor to be considered in the interpretation of results.
Magnetic Resonance Versus Computed Tomographic Imaging in Acute Stroke
Authors: Mohr J. P. , Biller J. , Hilal S. K. , Yuh W. T. C. , Tatemichi T. K. , Hedges S. , Tali E. , Nguyen H. , Mun I. , Adams H. P. , Grimsman K. , Marler J. R.
Published: June 2011

Background and Purpose
This study was an attempt to determine whether CT and MRI are comparable or if one is superior to the other in the early detection of ischemic stroke or hematoma.

Methods
Patients with acute stroke were sought within 3 hours of onset for clinical examination and prospective evaluation by concurrently performed CT and MRI. Repeated clinical and imaging studies were undertaken when possible immediately after imaging and at 24 hours, 3 to 5 days, and 3 months. The study neurologists were blinded to the results of imaging, as were the study radiologists to the clinical findings. The study radiologists read the scans in sequence, mapping each imaging on standard templates before viewing a later scan. No retrospective revisions of imaging mapping of earlier images were undertaken.

Results
Sixty-eight patients were recruited within 4 hours and an additional 12 patients within 24 hours. Seventy-five strokes were due to infarction and five to hemorrhage. The median time to first scan was 132 minutes. Although some of the infarctions in 75 patients were detected within 1 hour, the fraction of positive first scans approached an asymptote at 2 to 3 hours. Overall, with the use of conventional non–contrast-enhanced CT and T
1
- and T
2
-weighted MRI, neither was superior in the very early detection of either hematoma or infarction. There was a marginally significant correlation between early positive brain imaging and the severity of the stroke. Some patients had initially positive CT and/or MRI scans, but their neurological examination had returned to normal by 24 hours. Overall, CT was better than baseline MRI at predicting 24-hour outcome. After 24 hours, both CT and MR more conspicuously defined the lesion limits than they did at baseline.

Conclusions
With the technology available through 1991, neither CT nor MRI proved superior in the detection of the earliest signs of stroke.
Asymptomatic Cerebral Embolic Signals in Patients With Carotid Stenosis
Authors: Valton Luc , Larrue Vincent , Arrué Philippe , Géraud Gilles , Bès André
Published: June 2011

Background and Purpose
Asymptomatic cerebral emboli may be detected in patients with carotid stenosis by transcranial Doppler ultrasonography of the middle cerebral artery (MCA). The aim of this study was to determine the angiographic correlates of such embolic signals.

Methods
Doppler signals from 48 MCAs in 26 patients with carotid stenosis that was either symptomatic (n=20) or asymptomatic (n=6) were recorded for 40 minutes. The grade of carotid stenosis and the ulcerated or nonulcerated appearance of the plaque were assessed using the criteria of the North American Symptomatic Carotid Endarterectomy Trial.

Results
Embolic signals were detected in 8 MCAs from 7 patients; 4 (50%) of these MCAs were clinically symptomatic compared with 16 (40%) without embolic signal. Although there was a trend toward more severe stenosis in the cases with embolic signals, this was not significant (mean±SD, 67±29% versus 55±36%). In contrast, an image of ulceration was found on ipsilateral carotid angiography in 5 cases (63%) with embolic signals and in only 9 cases (23%) without embolic signals (odds ratio, 5.74; 95% confidence interval, 1.15 to 28.79, by multivariate regression analysis).

Conclusions
This study demonstrates that the occurrence of embolic signals in patients with carotid stenosis is associated with the appearance of plaque ulceration on angiography.
Glutamate-Induced Cerebral Vasodilation Is Mediated by Nitric Oxide Through
N
-Methyl-
d
-Aspartate Receptors
Authors: Meng Wei , Tobin Joseph R. , Busija David W.
Published: June 2011

Background and Purpose
It was found that glutamate, a major neurotransmitter, is vasoactive in the cerebral circulation. However, the mechanism is unclear. This study was designed to investigate the role of nitric oxide (NO) and
N
-methyl-
d
-aspartate (NMDA) receptors in cerebral arteriolar dilation to glutamate.

Methods
Newborn, chloralose-anesthetized pigs were equipped with a closed cranial window. The diameter of pial arterioles was measured by means of intravital microscopy, and NO synthase (NOS) activity in brain cortex was determined by the conversion assay of [
14
C]arginine to [
14
C]citrulline.

Results
Topical application of glutamate at 10
−7
, 10
−6
, and 10
−5
mol/L (n=5) increased the mean diameter by 12±3%, 13±2%, and 18±3% (±SEM), respectively (baseline, 91±10 μm;
P
<.05). Similarly, NMDA application at the above doses (n=5) dilated arterioles by 10±2%, 16±3%, and 18±6%, respectively (baseline, 97±4 μm;
P
<.05). Topical application of 10
−4
mol/L
N
G
-nitro-
l
-arginine (L-NNA), which inhibited NOS activity by 93%, blocked the arteriolar dilation to glutamate or NMDA. Furthermore, administration of MK-801, a potent inhibitor of NMDA receptors, blocked glutamate-induced vasodilation completely in both topical application (10
−5
mol/L; n=6) and intravenous administration (5 to 10 mg/kg; n=5). In addition, neither L-NNA nor MK-801 attenuated the vasodilation to hypercapnia (P
co
2
=40 to 68 mm Hg).

Conclusions
Glutamate-induced cerebral arteriolar dilation is mediated by NO through NMDA receptors, and NO does not play a major role in the cerebral arteriolar dilation to hypercapnia (P
co
2
=40 to 68 mm Hg) in newborn pigs.
Acute Leukocyte and Temperature Response in Hypertensive Intracerebral Hemorrhage
Authors: Suzuki Shuichi , Kelley Roger E. , Dandapani Bhuvaneswari K. , Reyes-Iglesias Yolanda , Dietrich W. Dalton , Duncan Robert C.
Published: June 2011

Background and Purpose
We undertook this study to investigate the relationship between outcome, hematoma volume, and admission peripheral white blood cell count and body temperature in acute hypertensive intracerebral hemorrhage.

Methods
Eighty-two consecutive patients who presented with hypertensive intracerebral hemorrhage within 72 hours of onset were retrospectively assessed. The peripheral white blood cell count, polymorphonuclear leukocytes, and the body temperature on admission were measured. The outcome at 30 days after ictus was determined with a modified Glasgow Outcome Scale. Correlation analysis was performed between these measurements and hematoma volume, which was calculated by brain computed tomography. We also looked at the presence or absence of intraventricular extension.

Results
The mean hematoma volume was significantly greater in those patients who died compared with those with a good, moderate, and severe outcome (79.6 cm
3
versus 10.7, 18.3, and 19.9 cm
3
, respectively;
P
<.0005). The mean peripheral white blood cell count was higher in those who died than in the other three groups (12.580±0.521 versus 8.160±0.543, 8.565±0.543, and 7.427±0.786×10
9
/L, respectively;
P
<.0005). The mean body temperature of those who died tended to be higher than those in the good-outcome group (99.12±0.21 versus 98.18±0.21°F,
P
<.05). A positive linear correlation was observed between hematoma volume and white blood cell count (
r
=.506,
df
=77,
P
<.001), as well as the polymorphonuclear leukocyte count (
r
=.561,
df
=76,
P
<.001). A trend was also observed for admission temperature (
r
=.265,
df
=74,
P
<.05). The leukocyte response was enhanced by the presence of intraventricular extension.

Conclusions
There is a relationship between the size of the hematoma and the degree of leukocytosis in hypertensive intracerebral hemorrhage. This relationship appears to most likely represent a stress-induced reaction of the white blood cell count.
Preischemic But Not Postischemic Zinc Protoporphyrin Treatment Reduces Infarct Size and Edema Accumulation After Temporary Focal Cerebral Ischemia in Rats
Authors: Kadoya Chitoshi , Domino Edward F. , Yang Guo-Yuan , Stern Joseph D. , Betz A. Lorris
Published: June 2011

Background and Purpose
Zinc protoporphyrin (ZnPP) has multiple actions. It is an interleukin-1 antagonist as well as a hemeoxygenase inhibitor. Interleukin-1 is produced in ischemic brain and probably contributes to ischemic injury, although the role of heme oxygenase during ischemia is unknown. Whether ZnPP treatment is more effective before or after ischemia, as well as whether it is more protective in permanent or temporary cerebral ischemia, is also unknown. Therefore, we investigated the effect of ZnPP on infarction size and edema in a rodent model of temporary and permanent focal cerebral ischemia.

Methods
Two groups of adult male Sprague-Dawley rats were pretreated with either 50 mg/kg ZnPP IP or saline and subjected to permanent middle cerebral artery occlusion 30 minutes later. Four additional groups of animals were subjected to 2 hours of temporary middle cerebral artery occlusion followed by 22 hours of reperfusion. Two of these groups were pretreated 30 minutes before middle cerebral artery occlusion with either 50 mg/kg ZnPP IP or saline. The other groups received ZnPP at either 2 or 4 hours after middle cerebral artery occlusion. Regional cerebral blood flow in the ischemic cortex was monitored with laser Doppler flowmetry. Cerebral infarct size and brain water were measured 24 hours after the onset of either form of ischemia.

Results
Regional cerebral blood flow after occlusion was approximately 13% to 20% of baseline after either permanent or temporary ischemia. ZnPP had no effect on regional cerebral blood flow, infarct size, or edema formation in permanent ischemia. In contrast, pretreatment significantly reduced infarct size (17.2±6.6% in controls versus 6.2±2.9% in pretreated rats) and edema formation (center zone, 4.00±0.71% water in controls versus 1.18±0.26% water in pretreated rats) in the model of temporary ischemia, but treatment after occlusion had no effect.

Conclusions
ZnPP treatment protected the brain when administered early in the temporary ischemia model.
Transient Forebrain Ischemia Protects Against Subsequent Focal Cerebral Ischemia Without Changing Cerebral Perfusion
Authors: Matsushima Kazushi , Hakim Antoine M.
Published: June 2011

Background and Purpose
The possibility that the brain may be preconditioned to be more tolerant of ischemia is an important concept with important clinical implications. Exploring the concept offers the possibility of advancing our understanding of protective molecular responses in the brain. This article compares two preconditioning methods and explores the role that changes in regional cerebral blood flow (rCBF) may play in conferring ischemic protection.

Methods
Temporary occlusion of the middle cerebral artery (MCA) using the thread model was preceded 4 days earlier by short-lasting focal or global ischemia or by sham surgery. rCBF was measured in the frontoparietal region of the ischemic hemisphere during all focal ischemia episodes. Four days after the second ischemic exposure, animals were killed, and the size of infarction was determined.

Results
rCBF was significantly higher in the frontoparietal region during MCA occlusion when it was preceded by prior focal ischemia (36.8±7.6 mL · 100 g
−1
· min
−1
at 30 minutes) compared with controls (24.7±4.0 mL · 100 g
−1
· min
−1
,
P
=.0008). Despite this, there was no significant difference in the resulting infarct volume. In contrast, when MCA occlusion was preceded by global ischemia, infarct volume was significantly reduced (68.1±30.9 mm
3
in the controls versus 22.9±22.1 mm
3
in the preconditioned group,
P
=.002) without significant change in rCBF.

Conclusions
Protection from ischemic injury requires specific conditions of prior exposure to ischemia. Improved perfusion would not seem to be a sufficient or necessary accompaniment to providing neuroprotection.
Cortical Blood Flow and Cerebral Perfusion Pressure in a New Noncraniotomy Model of Subarachnoid Hemorrhage in the Rat
Authors: Bederson Joshua B. , Germano Isabelle M. , Guarino Lorraine
Published: June 2011

Background and Purpose
Acute cerebral ischemia after subarachnoid hemorrhage (SAH) is a major cause of morbidity whose precise etiology is unclear. The purpose of this study was to examine the relationships between cerebral perfusion pressure (CPP) and cortical blood flow during SAH using a new experimental model in the rat.

Methods
CPP (mean arterial pressure minus intracranial pressure), cortical laser-Doppler flowmetry (LDF), and electroencephalogram were continuously recorded during and after SAH in 16 ventilated rats. SAH was produced by advancing an intraluminal suture from the external carotid artery through the internal carotid artery to perforate the vessel near its intracranial bifurcation.

Results
Eight rats (50%) died within 24 hours of SAH. In all rats, blood was widely distributed throughout the basal, convexity, and interhemispheric subarachnoid spaces and throughout the ventricular system. CPP decreased after SAH at an initial rate of 1.1±0.2 mm Hg/s, reaching its nadir 59±9 seconds after the onset of SAH. During the same period, LDF fell at a rate of 1.4±0.3%/s (
P
=NS vs CPP). After reaching its nadir, CPP rose at a rate of 0.4±0.01 mm Hg/s, but LDF continued to fall at 0.2±0.03%/s (
P
<.05 vs CPP) reaching a nadir of 21.7±2.5% significantly later than CPP (189.5±39 s after SAH,
P
<.05). No correlation was found between peak changes in CPP and LDF. Electroencephalogram activity followed the changes in LDF, reaching nadir values 289±55 seconds after SAH.

Conclusions
These findings demonstrate that although reduced CPP causes the initial decrease in cortical blood flow after SAH, secondary reductions occurring after CPP has reached its nadir are caused by other factors such as acute vasoconstriction. This noncraniotomy model of SAH in the rat has several advantages over existing models.
Cerebral Hypoxia-Ischemia Stimulates Cytokine Gene Expression in Perinatal Rats
Authors: Szaflarski Jerzy , Burtrum Douglas , Silverstein Faye S.
Published: June 2011

Background and Purpose
We tested the hypothesis that cerebral hypoxia-ischemia selectively stimulates interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) gene expression in brain regions susceptible to irreversible injury in perinatal rats.

Methods
To elicit focal hypoxic-ischemic brain injury, 7-day-old perinatal (P7) rats were subjected to right carotid artery ligation followed by 3 hours of 8% O
2
exposure and were killed 0 to 48 hours after hypoxia. Regional tissue IL-1β and TNF-α mRNA content were measured by reverse transcription followed by polymerase chain reaction amplification (RT-PCR) in samples prepared from cortex and hippocampus of the lesioned and contralateral hemispheres. cDNAs were amplified with primers specific for IL-1β, TNF-α, and the housekeeping gene glyceraldehyde-3-phosphate dehydrogenase (GAPDH), which served as an internal control. The RT-PCR products were subjected to Southern blot analysis and hybridized with
32
P-labeled gene-specific probes. Radioactivity was measured in excised bands, and results were normalized on the basis of levels of GAPDH expression.

Results
In unlesioned P7 brain, IL-1β mRNA was barely detectable. In lesioned forebrain, there was a marked, transient stimulation of IL-1β mRNA expression, peaking at 4 hours after hypoxia. Hybridization signal was increased 16- to 30-fold over values from contralateral hemisphere samples in three independent assays (
P
<.05 comparing values in left and right cortex and in left and right hippocampus with the Kruskal-Wallis ranking test); by 24 hours after hypoxia, levels returned to normal. Similar transient increases in TNF-α mRNA expression were detected. In a closely related model of perinatal brain injury elicited by focal intracerebral
N
-methyl-
d
-aspartate injection, there was a corresponding acute stimulation of IL-1β and TNF-α mRNA expression at 4 hours after injection.

Conclusions
These results suggest that IL-1β and TNF-α may play important roles in the response of the developing brain to acute hypoxic-ischemic injury.
Syndromes of Pontine Base Infarction
Authors: Kim Jong S. , Lee Jay H. , Im Joo H. , Lee Myoung C.
Published: June 2011

Background and Purpose
Although there have been sporadic reports of lacunar syndromes due to pontine base infarction, studies of clinical-radiological correlation in sufficient numbers of patients have not yet been reported.

Methods
We studied the clinical features of 37 patients with acute infarcts that mainly involved the base of the pons and correlated the clinical syndromes with the radiological findings.

Results
The clinical presentations included pure motor hemiparesis (PMH) in 17, sensorimotor stroke in 3, ataxic hemiparesis (AH) in 4, and dysarthria–clumsy hand (DA-CH) syndrome in 6 patients. Variants of AH included 1 patient with dysarthria-hemiataxia and 2 with quadrataxic hemiparesis, and in 4 patients dysarthria–facial paresis syndrome was considered a variant of DA-CH syndrome. Hypertension was the single most common and important risk factor, and the pathogenetic mechanisms of ischemia were likely to be small arterial (lacunar) occlusion or basilar atheromatous branch occlusion in most of the patients. Our clinical-radiological correlation study suggested that large lesions involving the paramedian caudal or middle pons correlate with severe hemiparesis (PMH), whereas lesions of similar size located in the paramedian rostral pons tended to produce DA-CH syndrome. Lesions producing AH were located variously but tended to spare the pyramidal tracts. The prognosis of these patients is fair or good, although residual hemiparesis remained in patients with initially severe hemiparesis.

Conclusions
Our data suggest that the various lacunar syndromes that follow pontine base infarcts reflect the balance of the involvement of the corticospinal, corticopontocerebellar, and corticobulbar tracts. Analysis of radiological findings aids in determining the clinical-anatomic correlation in patients with pontine base infarction.
Platelet Size in Stroke Patients
Authors: O’Malley T. , Langhorne P. , Elton R.A. , Stewart C.
Published: June 2011

Background and Purpose
Large platelets are more reactive, produce more prothrombotic factors, and aggregate more easily. Platelet size can be readily estimated using automated analyzers, although accurate estimation depends on precise methodology. The disparate results from previous studies of mean platelet volume in cerebral ischemia may be explained by varying methodology. We have studied these variables using a precise methodology in an unselected group of stroke patients and compared them with data from age- and sex-matched control subjects.

Methods
We studied 58 stroke patients consecutively admitted to a geriatric medical unit. Platelet variables were measured in the acute (<48 hours after stroke) and chronic (>6 months) phases of cerebral ischemia and compared with control variables. Control patients, admitted to the same unit, were of similar age and sex and without evidence of acute vascular events.

Results
Mean platelet volume was higher in acute stroke (11.3 compared with 10.1 fL in control subjects;
P
<.001, Student’s
t
test). In addition, platelet count was reduced in stroke patients (255×10
9
/L) compared with control subjects (299×10
9
/L;
P
<.01). Repeated measurements of mean platelet volume and platelet count in available survivors showed no significant change from the acute phase. Platelet changes did not relate to outcome measured at 6 months.

Conclusions
With the use of more precise methodology, these findings show that an increase in mean platelet volume and a reduction in platelet count are features of both the acute and nonacute phases of cerebral ischemia. It is possible that these changes precede the vascular event, and further studies are warranted.
White Matter Hyperintensities on MRI in the Neurologically Nondiseased Elderly
Authors: Ylikoski Ari , Erkinjuntti Timo , Raininko Raili , Sarna Seppo , Sulkava Raimo , Tilvis Reijo
Published: June 2011

Background and Purpose
We undertook this study to evaluate the frequency and risk factors of white matter hyperintensities seen on T
2
-weighted MR imaging. We examined cohorts of neurologically nondiseased elderly subjects participating in a general-community study, the Helsinki (Finland) Aging Brain Study. Cohorts of consecutive subjects aged 55, 60, 65, 70, 75, 80, and 85 years (n=20, 18, 20, 18, 19, 18, and 15, respectively; total, n=128) were divided into a young-old (age <75 years, n=76) group and an old-old (age ≥75 years, n=52) group.

Methods
Frequency of hyperintensities seen on T
2
-weighted axial and coronal MR images (0.02 T) was rated using a four-point scale in periventricular and centrum semiovale areas.

Results
The majority of the subjects showed only mild white matter hyperintensities, which were more frequent in the periventricular areas. Age was the most important factor to explain the presence of hyperintensities. A logistic regression analysis related periventricular hyperintensities in the entire group to central atrophy (odds ratio [OR], 4.7; 95% confidence interval [CI], 1.7 to 12.9) and silent infarcts (OR, 5.6; 95% CI, 1.0 to 19.8); among the young-old, hyperintensities related to diabetes (OR, 17.0; 95% CI, 1.9 to 154.2) and central atrophy (OR, 14.7; 95% CI, 3.5 to 61.8). Centrum semiovale hyperintensities related in the entire group to cardiac arrhythmia (OR, 4.0; 95% CI, 1.0 to 15.5), central atrophy (OR, 3.9; 95% CI, 1.2 to 12.4), and silent infarcts (OR, 3.6; 95% CI, 1.0 to 12.5).

Conclusions
These mild white matter hyperintensities in the neurologically nondiseased elderly related especially to age and also to concomitant silent infarcts, atrophy, and some vascular risk factors. The known factors, however, explained only part of the variation. The young-old and old-old groups showed different associations. In contrast to former assumptions, the presence of white matter hyperintensities among the aged is likely to be linked to other as yet unidentified age-related factors.
The Effect of a Stroke Unit: Reductions in Mortality, Discharge Rate to Nursing Home, Length of Hospital Stay, and Cost
Authors: Jørgensen Henrik S. , Nakayama Hirofumi , Raaschou Hans O. , Larsen Kim , Hübbe Per , Olsen Tom Skyhøj
Published: June 2011

Background and Purpose
Treatment of stroke patients in specialized stroke units has become more frequent, yet the effect of this treatment has not been determined.

Methods
In a community-based, prospective, and consecutive study of 1241 unselected acute stroke patients, we compared outcome of stroke treatment between two neighboring communities within Greater Copenhagen: the Bispebjerg community, where all acute stroke patients are treated and rehabilitated on a stroke unit, and Frederiksberg community, where all acute stroke patients are treated and rehabilitated on general neurological and medical wards. Except for the different organization of stroke treatment, the two communities and the two patient groups were comparable. Specifically, age, sex, marital status, prestroke residence, and stroke severity were not statistically different between patients treated on the stroke unit and those treated on the general neurological and medical wards. Multivariate regression analyses were used to estimate the independent influence of stroke unit treatment on outcome.

Results
Stroke unit treatment significantly reduced in-hospital mortality (odds ratio [OR], 0.50; 95% confidence interval [CI], 0.34 to 0.74;
P
<.001), case-fatality rate (OR, 0.45; CI, 0.28 to 0.71;
P
<.001), 6-month mortality (OR, 0.57; CI, 0.39 to 0.82;
P
=.002), 1-year mortality (OR, 0.59; CI, 0.42 to 0.84;
P
=.003), and discharge rate to a nursing home (OR, 0.61; CI, 0.38 to 0.98;
P
=.04). Discharge rate to the patient’s own home was significantly increased (OR, 1.90; CI, 1.30 to 2.70;
P
<.001). The length of hospital stay (including rehabilitation) was reduced significantly by 30% in patients treated on the stroke unit despite their lower mortality (
P
<.001). The savings due to stroke unit treatment were estimated at 1313 bed-days and three places at a nursing home per 100 stroke patients.

Conclusions
Treatment of unselected acute stroke patients on a stroke care unit saved lives, reduced the length of hospital stay, reduced the frequency of discharge to a nursing home, and potentially reduced cost.
Safety and Efficacy of Percutaneous Transluminal Angioplasty for Intracranial Atherosclerotic Stenosis
Authors: Clark Wayne M. , Barnwell Stanley L. , Nesbit Gary , O’Neill Oisin R. , Wynn Michael L. , Coull Bruce M.
Published: June 2011

Background and Purpose
Percutaneous transluminal angioplasty (PCTA) is increasingly used to treat extracerebral arterial stenosis. The present study evaluates the safety and efficacy of PCTA treatment of symptomatic intracranial atherosclerotic stenosis.

Methods
A series of 22 vessels in 17 patients were treated with PCTA. All patients had recurrent neurological symptoms referable to the stenotic vessel despite optimal medical therapy. Critical (>70%) arterial stenosis was confirmed by angiogram, and angioplasty was performed with a 3.0- to 3.5-mm Stealth balloon.

Results
The average preangioplasty stenosis (North American Symptomatic Carotid Endarterectomy Trial criteria) was 72±8% (mean±SD), with a significant improvement seen after angioplasty; the best angiographic stenosis (after healing of intimal injury, if any) was 43±24% (
P
<.001). Overall PCTA was successful in 82% of the vessels. There were two strokes during angioplasty for a 30-day morbidity rate of 9.1% per treated vessel and 11.7% per case. The other 15 patients were clinically evaluated at 3 and 6 months; all cases were without further events. Restenosis was evaluated in 8 patients (12 vessels) with an angiogram at 6 months showing further improvement compared with the initial post-PCTA stenosis (51±10% versus 37±21% [
P
=.05]).

Conclusions
PCTA may be a beneficial therapy in selected cases of symptomatic intracranial atherosclerotic stenosis. Further study using a randomized trial is needed.
Neonatal Ischemic Neuroprotection by Modest Hypothermia Is Associated With Attenuated Brain Acidosis
Authors: Laptook Abbot R. , Corbett Ron J. T. , Burns Dennis , Sterett Rick
Published: June 2011

Background and Purpose
A 2.9°C reduction in the intraischemic rectal temperature of neonatal piglets is associated with less brain damage compared with animals with normothermic rectal temperatures. This investigation studied one potential mechanism for this observation: better maintenance of energy stores and less brain acidosis secondary to reduced metabolic activity associated with modest hypothermia.

Methods
31
P MR spectroscopy was used to study piglets before, during, and after 15 minutes of partial brain ischemia with intraischemic rectal temperatures of either 38.3±0.4°C (n=10, normothermic) or 35.4±0.5°C (n=10, hypothermic). Animals were followed up for up to 72 hours after ischemia and were evaluated clinically and by brain histology.

Results
Values for pH
i
remained 0.15 to 0.20 pH units greater in modestly hypothermic than in normothermic piglets during ischemia and the initial 30 minutes after ischemia (
P
=.049, group effect). Phosphocreatine, β-ATP, and inorganic phosphorus were similar between groups. The relationship between the intraischemic energy state and subsequent clinical evidence of brain damage (irrespective of group assignment) revealed lower pH
i
over the last 7 minutes of ischemia for abnormal compared with normal piglets (5.98±0.22 versus 6.39±0.24, respectively;
P
=.002). In contrast, intraischemic β-ATP (41±19% versus 57±21% of control) and inorganic phosphorus (273±31% versus 224±92% of control) for abnormal and normal piglets, respectively, did not differ between groups.

Conclusions
Intraischemic modest hypothermia attenuates the severity of brain acidosis during and 30 minutes after ischemia compared with normothermic animals and supports the concept that attenuated brain acidosis is a potential mechanism by which hypothermia may reduce ischemic brain damage.
Deep Hypothermia Diminishes the Ischemic Induction of Heat-Shock Protein-72 mRNA in Piglet Brain
Authors: Shaver Ellen G. , Welsh Frank A. , Sutton Leslie N. , Mora Gerardo , Gennarelli Laura M. , Norwood Carole R.
Published: June 2011

Background and Purpose
Expression of the 72-kD heat-shock protein (HSP72) has served as a useful indicator of ischemic stress after cerebral ischemia. Moderate hypothermia (30°C) has been reported to block the induction of HSP72 after a brief episode of forebrain ischemia. The objective of the present study was to examine the effects of deep hypothermia (15°C) on expression of HSP72 after a prolonged period of cerebral ischemia.

Methods
Piglets, 19 to 23 days old, were placed on cardiopulmonary bypass, and brain temperature was lowered to 23°C (n=9) or 15°C (n=9) before circulatory arrest for 1 hour. In an additional group of animals (n=5), the temperature was lowered to 29°C before arrest for 45 minutes. All animals were reperfused at 37°C for 2 hours, and the regional expression of HSP72 mRNA was assessed using in situ hybridization.

Results
After ischemia at 15°C, expression of HSP72 mRNA was limited to a few scattered regions of cerebral cortex; the percentage of cortex exhibiting HSP72 mRNA was 23±7% (mean±SEM). Ischemia at 23°C triggered expression of HSP72 mRNA in a significantly larger portion of the cortex (68±8%,
P
<.001). Ischemia at 29°C failed to induce substantial expression of HSP72 mRNA in the cerebral cortex.

Conclusions
These results suggest that, relative to ischemia at 23°C, deep hypothermia (15°C) diminishes ischemic alterations leading to induction of HSP72 mRNA. The lack of cortical expression of HSP72 mRNA following ischemia at 29°C may be secondary to inadequate recovery of energy metabolism.
Hyperbaric Oxygen in the Treatment of Acute Ischemic Stroke
Authors: Nighoghossian N. , Trouillas P. , Adeleine P. , Salord F.
Published: June 2011

Background and Purpose
The effects of hyperbaric oxygen (HBO) therapy on humans are uncertain. Our study aims first to outline the practical aspects and the safety of HBO treatment and then to evaluate the effect of HBO on long-term disability.

Methods
Patients who experienced middle cerebral artery occlusion and were seen within 24 hours of onset were randomized to receive either active (HBO) or sham (air) treatment. The HBO patients were exposed daily to 40 minutes at 1.5 atmospheres absolute for a total of 10 dives. We used the Orgogozo scale to establish a pretreatment functional level. Changes in the Orgogozo scale score at 6 months and 1 year after therapy were used to assess the therapeutic efficacy of HBO. In addition, we used the Rankin scale and our own 10-point scale to assess long term-disability at 6 months and 1 year. Two sample
t
tests and 95% confidence intervals were used to compare the mean differences between the two treatment groups. Student’s two-tailed test was used to compare the differences between pretherapeutic and posttherapeutic scores at 6 months and 1 year in the two treatment groups.

Results
Over the 3 years of study enrollment, 34 patients were randomized, 17 to hyperbaric treatment with air and 17 to hyperbaric treatment with 100% oxygen. There was no significant difference at inclusion between groups regarding age, time from stroke onset to randomization, and Orgogozo scale scores.

Neurological deterioration occurred during the first week in 4 patients in the sham group, 3 of whom died; this worsening was clearly related to the ischemic damage. Treatment was also discontinued for 3 patients in the HBO group who experienced myocardial infarction, a worsening related to the ischemic process, and claustrophobia. Therefore, 27 patients (13 in the sham group and 14 in the HBO group) completed a full course of therapy.

The mean score of the HBO group was significantly better on the Orgogozo scale at 1 year (
P
<.02). However, the difference at 1 year between pretherapeutic and posttherapeutic scores was not significantly different in the two groups (
P
<.16). Moreover, no statistically significant improvement was observed in the HBO group at 6 months and 1 year according to Rankin score (
P
<.78) and our own 10-point scale (
P
<.50).

Conclusions
Although the small number of patients in each group precludes any conclusion regarding the potential deleterious effect of HBO, we did not observe the major side effects usually related to HBO. Accordingly, it can be assumed that hyperbaric oxygen might be safe. We hypothesize that HBO might improve outcome after stroke, as we detected an outcome trend favoring HBO therapy. A large randomized trial might be required to address the efficacy of this therapy.
Early Intrathecal Production of Interleukin-6 Predicts the Size of Brain Lesion in Stroke
Authors: Tarkowski Elisabeth , Rosengren Lars , Blomstrand Christian , Wikkelsö Carsten , Jensen Christer , Ekholm Sven , Tarkowski Andrzej
Published: June 2011

Background and Purpose
We have previously demonstrated that stroke influences systemic immune responses. The aim of the present study was to investigate patterns of local inflammatory response as a consequence of acute stroke.

Methods
Thirty stroke patients were studied prospectively on days 0 to 3, 7 to 9, 21 to 26, and after day 90 with clinical evaluations, radiological assessments, and analysis of serum and cerebrospinal fluid cytokine levels.

Results
Significantly increased levels of interleukin-6 (IL-6) in cerebrospinal fluid (
P
<.001) were observed in virtually all patients studied compared with healthy control subjects. This increase was observed during the whole observation period but was significantly more pronounced within the first days after stroke onset, with a peak level on days 2 and 3. This initial increase was significantly correlated (
r
=.65,
P
=.002) with the volume of infarct measured by MRI 2 to 3 months later. Serum levels of IL-6 in stroke patients were significantly lower than cerebrospinal fluid levels of IL-6 (
P
=.013) and did not display any significant correlation to the size of the brain lesion. Also, increase in intrathecal but not systemic production of IL-1β was observed early during the stroke. Only minor increases of cerebrospinal fluid interferon-γ levels were observed in two patients.

Conclusions
Our study demonstrates an intrathecal production of IL-6 and IL-1β in patients with stroke, supporting the notion of localized inflammatory response to acute brain lesion. In addition, the significant correlation between early intrathecal production of IL-6 and the subsequent size of the brain lesion can be used as a prognostic tool, predicting the size of the brain damage before it is possible to accurately visualize it with radiological methods.
Cerebral Blood Flow in Lateral Medullary Infarcts
Authors: Rousseaux M. , Steinling M. , Mazingue A. , Benaim C. , Froger J.
Published: June 2011

Background and Purpose
The aim of this study was to evaluate the diaschisis phenomenon in patients presenting with lateral medullary infarct (Wallenberg’s syndrome).

Methods
We examined all patients admitted between 1991 and 1993. The localization of lesions was evaluated by MRI. Single-photon emission computed tomographic technique was used to assess cerebral blood flow by two methods (
133
Xe and hexamethylpropyleneamine oxime) on five slices of brain tissue. Flow values were calculated in 11 regions of interest in each cerebral hemisphere and in the cerebellum and were compared with those obtained in 20 control subjects.

Results
Three patients had selective lateral medullary infarct: Relative reduction of flow (
133
Xe) and of tracer uptake (HMPAO) were observed in one patient in the ipsilateral cerebellum and contralateral hemisphere; in two patients, hemispheric flow values were relatively low, without significant asymmetry. Two patients also presented with cerebellar infarct: Flow drop was severe in the ipsilateral cerebellum, and contralateral reduction in the brain hemisphere was observed in both cases.

Conclusions
Lateral medullary infarct can be associated with ipsilateral reduction of flow in the cerebellum, but this phenomenon is inconstant. Severe flow drop suggests infarction in the territory of the posterior inferior cerebellar artery. Contralateral hemispheric flow reduction can also be observed. These phenomena of cerebellar and crossed hemispheric diaschisis are probably related to lesions of tracts from the olivary and reticular nuclei.
Protective Effect of Cyclosporin A on White Matter Changes in the Rat Brain After Chronic Cerebral Hypoperfusion
Authors: Wakita Hideaki , Tomimoto Hidekazu , Akiguchi Ichiro , Kimura Jun
Published: June 2011

Background and Purpose
Activation of glial cells and rarefaction of the white matter have been reported in rat brain after bilateral permanent occlusion of the common carotid arteries. Using this model, we investigated the effects of the immunosuppressant cyclosporin A on the activation of glial cells and the white matter rarefaction.

Methods
Both common carotid arteries were ligated bilaterally in 40 male Wistar rats. Twenty-two of these rats received an intraperitoneal injection of cyclosporin A, and the remaining 18 received a vehicle-solution injection. Microglia/macrophages were investigated with immunohistochemistry for the major histocompatibility complex class I and II antigens as well as for leukocyte common antigen. Astroglia were examined with glial fibrillary acidic protein as a marker. Activation of glial cells and white matter rarefaction were then investigated from 7 to 30 days after the ligation.

Results
In vehicle-treated animals, there was a persistent and extensive activation of both microglia/macrophages and astroglia in the white matter, including the optic nerve, optic tract, corpus callosum, internal capsule, and traversing fiber bundles of the caudoputamen. In cyclosporin A–treated rats, the number of activated microglia/macrophages was significantly reduced (
P
<.01) to approximately one fifth of that in vehicle-treated animals. Similarly, rarefaction of the white matter was much less intense in cyclosporin A–treated rats (
P
<.01).

Conclusions
Cyclosporin A suppressed both glial activation and white matter changes after chronic cerebral hypoperfusion. These results suggest that immunologic reaction may play a role in the pathogenesis of the white matter changes and that the present model may be useful in investigating the pathophysiology of white matter changes induced by chronic cerebral hypoperfusion.
Delayed Posttraumatic Hemorrhage
Authors: Álvarez-Sabín José , Turon Antoni , Lozano-Sánchez Manuel , Vázquez José , Codina Agustí
Published: June 2011

Background and Purpose
Delayed posttraumatic hemorrhage (DPTH) is one of the causes of intracerebral hemorrhage (ICH). Most of the published series were reported before the advent of CT. Clinical characteristics and CT findings are described.

Methods
Ten cases of CT-proven DPTH from a series of 216 patients (age range, 15 to 50 years) with ICH were evaluated. Previous CT scans performed in the first 6 hours after head injury were normal in all patients. Cerebral angiography showed no evidence of vascular disorders in any patient.

Results
DPTH was the fourth most common cause of ICH in our series. The symptom-free interval after head injury ranged from 1 to 15 days. Most hematomas were located deep in the hemisphere and were of small or medium size. Clinical course was good in the majority of cases; none of the patients died, and there was no recurrence.

Conclusions
DPTH is a relatively frequent cause of ICH in young adults. There is no relationship with intensity of the previous head injury. The more frequent location deep in the hemisphere may be related to the younger age of our patients compared with those of other published series. The good outcome in our patients may be related to their youth and the absence of complications such as skull fracture, need for neurosurgery, or coagulation disorders.
Medial Medullary Syndrome
Authors: Kim Jong Sung , Kim Hyeon Gak , Chung Chin Sang
Published: June 2011

Background and Purpose
With advanced imaging techniques, infarctions occurring in the medulla are now more easily identified. To date, however, only approximately 30 cases of medial medullary infarction syndrome (MMS) have been reported, and the clinical and radiological characteristics of MMS remain to be studied.

Methods
We studied 18 patients (15 men, 3 women; mean age, 62 years) who had compatible clinical and MRI findings of MMS and reviewed the previously reported cases.

Results
Seventeen patients had a unilateral lesion usually involving the upper medulla, and 1 had bilateral lesions. Fifteen patients had unilateral sensorimotor stroke, while 2 presented with pure motor stroke. The face was usually but not always spared. The degree of hemiparesis varied, and a tingling sensation with decreased vibration and position sense was the most common sensory manifestation. Two patients had lingual paresis, and none suffered respiratory difficulties. One patient presented with bilateral gait ataxia without sensorimotor dysfunction. Angiography or MR angiography performed in 9 patients showed vertebral artery disease in 6. Three patients had concurrent lateral medullary infarction, and 1 had a previous history of lateral medullary syndrome. The prognosis was generally good, although residual hemiparesis remained in patients with initially severe hemiparesis. Review of 26 previously reported cases showed that they frequently had bilateral lesions, often presenting with quadriplegia, lingual paresis, respiratory symptoms, and a grave prognosis.

Conclusions
Our data illustrate that MMS is most often manifested as benign hemisensorimotor stroke frequently associated with tingling sensation and impaired deep sensation. This benign form of MMS should be much more common than MMS with poor prognosis and may have been frequently misdiagnosed as capsular or pontine stroke before the era of MRI.
Causes of Morbidity and Mortality After Ruptured Aneurysm Surgery in a Series of 230 Patients
Authors: Proust F. , Hannequin D. , Langlois O. , Freger P. , Creissard P.
Published: June 2011

Background and Purpose
The purpose of this study was to determine the causes of morbidity and mortality after surgery for ruptured aneurysms.

Methods
Two hundred thirty consecutive patients were studied. Initial hemorrhage volume and vasospasm were evaluated preoperatively with CT, transcranial Doppler ultrasonography, and angiography. Nimodipine infusion was started before surgery. Preoperative clinical status was evaluated according to Hunt and Hess grading criteria. Surgery was performed early in 186 patients (81%). Control angiography, transcranial Doppler ultrasonography, and CT were performed routinely after surgery. Hypodense areas revealed by control CT were related to intracerebral initial hematoma, vasospasm, postoperative thrombosis, or spatula hyperpressure.

Results
Clinical outcome was excellent or good (Glasgow Outcome Scale [GOS] scores of 1 or 2) in 176 patients (77%), 17 (7%) were disabled (GOS score of 3), and 37 (16%) were vegetative or dead. In patients in good condition (grades I to III) preoperatively (n=200), 38 had an unfavorable outcome (GOS score of 2, 3, 4, or 5). The major cause of complication was postoperative thrombosis (42%). In patients in poor condition (grade IV or V) (n=30), 27 had an unfavorable outcome. The major cause of complication was initial bleeding (66%). Vasospasm was responsible for delayed ischemic deficit in 9 patients (3.9% of the total population).

Conclusions
Systematic angiography remains by far the best means for determining the cause of a poor postoperative course.
Risk Factors for Spontaneous Intracerebral Hemorrhage
Authors: Juvela Seppo , Hillbom Matti , Palomäki Heikki
Published: June 2011

Background and Purpose
Spontaneous intracerebral hemorrhage has remained a serious disease despite recent improvements in medical treatment. This study was designed to identify modifiable risk factors for intracerebral hemorrhage.

Methods
Health habits, previous diseases, and medication of 156 consecutive patients with intracerebral hemorrhage aged 16 to 60 years (96 men and 60 women) were compared with those of 332 hospitalized control patients (192 men and 140 women) who did not differ from case subjects in respect to age, day of onset of symptoms, or acuteness of disease onset.

Results
After adjustment for sex, age, hypertension, body mass index, smoking status, and alcohol consumption during the last week, patients who had consumed 1 to 40, 41 to 120, or >120 g of alcohol within the 24 hours preceding the onset of illness had a relative risk (95% confidence interval) of hemorrhage of 0.3 (0.2 to 0.7), 4.6 (2.2 to 9.4), and 11.3 (3.0 to 42.8), respectively, compared with those who had consumed 0 g. In addition, alcohol intake within 1 week before the onset of illness, excluding use within the last 24 hours, increased the risk of hemorrhage; adjusted risks were 2.0 (1.1 to 3.5) for 1 to 150 g, 4.3 (1.6 to 11.7) for 151 to 300 g, and 6.5 (2.4 to 17.7) for >300 g compared with 0 g. The adjusted risk of hypertension for hemorrhage was 6.6 (3.9 to 11.3). Previous heavy alcohol consumption and current cigarette smoking were not independent risk factors for hemorrhage, but anticoagulant treatment was (
P
<.01). Erythrocyte mean corpuscular volume and γ-glutamyl transferase values were also higher in patients with intracerebral hemorrhage than in control subjects.

Conclusions
Recent moderate and heavy alcohol intake as well as hypertension and likely also anticoagulant treatment seem to be independent risk factors for intracerebral hemorrhage.