bluuebunny/crossref_metadata_2025 huggingface dataset:
Diffusion-Weighted Magnetic Resonance Imaging in Brain Death
Authors: Lövblad Karl-Olof , Basssetti Claudio
Published: June 2011

Background
—Traditionally the diagnosis of brain death is established on the basis of a combination of clinical signs and paraclinical methods. Diffusion-weighted MRI is a new method sensitive to cerebral ischemia. Its value in brain death has not been demonstrated until now.

Case Description
—A patient was referred to MRI with suspicion of a brain stem stroke. Echo-planar whole-brain, multislice, diffusion-weighted MRI was performed in addition to conventional sequences and MR angiography sequences. In addition to the extensive bilateral hyperintensities observed on T2-weighted images, diffusion-weighted MRI showed diffuse hyperintensities involving both hemispheres as well as a severe drop in the apparent diffusion coefficient in both affected hemispheres. There was also transtentorial herniation with compression of the brain stem as well as absence of flow voids on the T2-weighted images and absence of intracranial vessels on MR angiography. On the basis of the clinical and imaging findings, it was concluded that the patient was in a state of brain death. The patient died the same day.

Conclusions
—With the use of new fast techniques such as diffusion-weighted imaging, now MRI can not only display anatomic changes associated with severe brain suffering but can also demonstrate ultrastructural changes secondary to brain death and differentiate them from edematous changes seen on T2-weighted images.
Low Risk of Ischemic Stroke in Patients With Reduced Internal Carotid Artery Lumen Diameter Distal to Severe Symptomatic Carotid Stenosis
Authors: Rothwell P. M. , Warlow C. P.
Published: June 2011

Background and Purpose
—Patients with recently symptomatic severe carotid stenosis have a high risk of ischemic stroke on medical treatment. The main mechanism of stroke appears to be plaque surface thrombus formation and distal embolism. It is unclear to what extent reduction in blood flow across the stenosis, and the consequent reduction in cerebral perfusion pressure, is also important. Angiographic indices of reduced cerebral perfusion may identify patients at a particularly high risk of stroke who require urgent endarterectomy. The most direct angiographic correlate of poststenotic perfusion pressure is the degree of narrowing of the distal internal carotid artery (ICA) lumen. We sought to develop criteria for the definition of poststenotic narrowing of the ICA and to determine the effect of this and other angiographic characteristics likely to be associated with reduced cerebral perfusion on the risk of ipsilateral ischemic stroke in patients with recently symptomatic carotid stenosis.

Methods
—We studied the carotid angiograms of 3007 patients in the European Carotid Surgery Trial. Poststenotic narrowing of the ICA was defined with use of the ratio of the lumen diameter of the ICA to that of the common carotid artery (CCA). The normal range of the ICA/CCA ratio was defined in 2966 symptomatic or contralateral carotid arteries with 0% to 49% stenosis. Arteries with 70% to 99% symptomatic stenosis and an ICA/CCA ratio below this range were categorized as narrowed. We related the presence of narrowing and other angiographic characteristics to the risk of ipsilateral ischemic stroke on medical treatment.

Results
—An assessment of the ICA/CCA ratio had good interobserver reproducibility. Poststenotic narrowing of the ICA was defined as an ICA/CCA ratio of <0.42. The 5-year risk of ipsilateral carotid territory ischemic stroke on medical treatment was 8% in patients with 70% to 99% stenosis and narrowing of the ICA versus 25% in patients without narrowing (log rank test,
P
=0.02). This difference remained after correction for other clinical and angiographic variables (hazard ratio 0.40, 95% CI 0.17 to 0.94,
P
=0.03). The other angiographic characteristics did not predict stroke.

Conclusions
—Poststenotic narrowing of the ICA was associated with a low risk of stroke on medical treatment. This suggests that low flow alone is not usually sufficient to cause ischemic stroke distal to symptomatic carotid stenosis. Poststenotic narrowing may be protective because blood flow distal to the stenosis is insufficient to carry emboli to the brain.
Regional Cerebral Blood Flow After Cortical Impact Injury Complicated by a Secondary Insult in Rats
Authors: Giri Bala K. , Krishnappa Indra K. , Bryan Robert M. , Robertson Claudia
Published: June 2011

Background and Purpose
—Traumatic injury makes the brain susceptible to secondary insults. An uncomplicated mild lateral cortical impact injury (3 m/s, 2.5-mm deformation) that causes little or no permanent sequelae results in a large contusion at the impact site when the traumatic injury is complicated by a secondary insult, such as 40 minutes of bilateral carotid occlusion.

Methods
—To determine whether the increased sensitivity to secondary insults in this model is caused by a vascular mechanism, cerebral blood flow (CBF) was measured with
14
C-isopropyliodoamphetamine quantitative autoradiography, and brain tissue P
o
2
(Pbt
o
2
) was measured at the impact site and in the contralateral parietal cortex.

Results
—In animals that underwent bilateral carotid occlusion 1 hour after the impact injury, CBF and Pbt
o
2
were lower at the impact site than they were in animals that had either the impact injury or the carotid occlusion alone. In the immediate area of the impact, CBF was 14±6 mL · 100 g
−1
· min
−1
in the animals with the impact injury followed by carotid occlusion compared with 53±24 mL · 100 g
−1
· min
−1
in the animals with the impact injury alone and 74±14 mL · 100 g
−1
· min
−1
in the animals with the carotid occlusion alone (
P
<0.001). At the time of this very low CBF value in the animals with the carotid occlusion after the impact injury, Pbt
o
2
at the impact site averaged 1.3±1.6 mm Hg and was <3 mm Hg in 5 of the 6 animals. In contrast, Pbt
o
2
in the animals with the impact injury alone averaged 9.3±2.9 mm Hg, and none of the animals had a Pbt
o
2
of <3 mm Hg (
P
=0.008).

Conclusions
—The CBF and Pbt
o
2
findings in this model suggest that the reduced CBF after traumatic injury predisposes the brain to secondary insults and results in ischemia when confronted with a reduction in cerebral perfusion pressure.
Verifying the Stroke-Free Phenotype by Structured Telephone Interview
Authors: Meschia James F. , Brott Thomas G. , Chukwudelunzu Felix E. , Hardy John , Brown Robert D. , Meissner Irene , Hall Linda J. , Atkinson Elizabeth J. , O’Brien Peter C.
Published: June 2011

Background and Purpose
—Case-control, cohort, and twin studies support a genetic contribution to ischemic stroke risk. Sibling pair linkage methods require identification of concordant or discordant siblings or both. We designed and tested a structured telephone interview to verify the stroke-free phenotype.

Methods
—A coordinator unaware of medical record data used an 8-item questionnaire to conduct a structured telephone interview of 70 outpatients aged >60 years. The questionnaire inquired about the sudden onset of deficits in strength, sensation, vision, and language. A subject was defined as stroke free by interview if responses to all items on the questionnaire were negative. Results of the telephone interview were compared with data obtained from a systematic medical record review (benchmark).

Results
—Interview time was 5 minutes or less for all subjects. All subjects who began the interview completed it. Records were reviewed in all subjects. Medical record review detected ischemic stroke or transient ischemic attack (TIA), or both, in 5 patients (7%). There were no significant differences in sex distribution or risk factor rates in patients who were designated stroke free or not stroke free by interview. Having 1 or more positive items on the questionnaire was significantly associated with finding stroke (
P
<0.001), TIA (
P
<0.001), or either stroke or TIA (
P
<0.001), on medical record review. The telephone interview had a sensitivity of 1.0 (95% CI 0.48 to 1.0), specificity of 0.86 (95% CI 0.75 to 0.93), positive predictive value of 0.36 (95% CI 0.13 to 0.65), and negative predictive value of 1.0 (95% CI 0.94 to 1.0).

Conclusions
—Our instrument can identify the stroke-free individual with a high degree of confidence in a very efficient manner. It may be particularly suited for centralized verification of stroke discordancy in multicentered sib-pair genetic studies.
Medical Complications After Stroke
Authors: Langhorne P. , Stott D. J. , Robertson L. , MacDonald J. , Jones L. , McAlpine C. , Dick F. , Taylor G. S. , Murray G.
Published: June 2011

Background and Purpose
—This prospective, multicenter study was performed to determine the frequency of symptomatic complications up to 30 months after stroke using prespecified definitions of complications.

Methods
—We recruited 311 consecutive stroke patients admitted to hospital. Research nurses reviewed their progress on a weekly basis until hospital discharge and again at 6, 18, and 30 months after stroke.

Results
—Complications during hospital admission were recorded in 265 (85%) of stroke patients. Specific complications were as follows: neurological—recurrent stroke (9% of patients), epileptic seizure (3%); infections—urinary tract infection (24%), chest infection (22%), others (19%); mobility related—falls (25%), falls with serious injury (5%), pressure sores (21%); thromboembolism—deep venous thrombosis (2%), pulmonary embolism (1%); pain—shoulder pain (9%), other pain (34%); and psychological—depression (16%), anxiety (14%), emotionalism (12%), and confusion (56%). During follow-up, infections, falls, “blackouts,” pain, and symptoms of depression and anxiety remained common. Complications were observed across all 3 hospital sites, and their frequency was related to patient dependency and duration after stroke.

Conclusions
—Our prospective cohort study has confirmed that poststroke complications, particularly infections and falls, are common. However, we have also identified complications relating to pain and cognitive or affective symptoms that are potentially preventable and may previously have been underestimated.
The Effect of Acute Ingestion of a Large Dose of Alcohol on the Hemostatic System and Its Circadian Variation
Authors: Numminen Heikki , Syrjälä Martti , Benthin Günther , Kaste Markku , Hillbom Matti
Published: June 2011

Background and Purpose
—Heavy binge drinking may trigger the onset of embolic stroke and acute myocardial infarction, but the underlying mechanisms are unclear. The effects of binge drinking on the hemostatic system and its circadian variation have not been investigated. We investigated the effects of an acute intake of a large dose of alcohol (1.5 g/kg).

Methods
—Twelve healthy, nonsmoking men participated in sessions where they were served ethanol in fruit juice or served fruit juice alone and, lying in a supine position, were followed up for 12 to 24 hours. The treatments were randomized and separated from each other by a 1-week washout period. Blood and urine were collected for hemostatic measurements.

Results
—The urinary excretion of the platelet thromboxane A
2
metabolite 2,3-dinor-thromboxane B
2
was significantly (
P
<0.05) greater during the night after an evening intake of alcohol than during the control night. A smaller increase was observed during the daytime after an intake of alcohol in the morning. The effects on the endothelial prostacyclin metabolite 2,3-dinor-6-ketoprostaglandin F
1α
excretion were negligible. A 7-fold increase in plasminogen activator inhibitor 1 activity was observed after both morning (
P
<0.05) and evening (
P
<0.01) intakes of alcohol.

Conclusions
—This is the first study to suggest that acute ingestion of a relatively large but tolerable dose of alcohol transiently enhances thromboxane-mediated platelet activation. The observations also demonstrate alcohol-induced changes in the normal circadian periodicity of the hemostatic system in subjects not accustomed to consumption of alcohol.
Diffusion- and Perfusion-Weighted MRI
Authors: Neumann-Haefelin Tobias , Wittsack Hans-Jörg , Fink Gereon R. , Wenserski Frank , Li Tie-Qiang , Seitz Rüdiger J. , Siebler Mario , Mödder Ulrich , Freund Hans-Joachim
Published: June 2011

Background and Purpose
—Diffusion-weighted imaging (DWI) and perfusion-weighted imaging (PWI) have been used increasingly in recent years to evaluate acute stroke in the emergency setting. In the present study, we compared DWI and PWI findings in acute stroke patients with and without severe extracranial internal carotid artery (ICA) disease.

Methods
—Twenty-seven patients with nonlacunar ischemic stroke were selected for this analysis. DWI, PWI, and conventional MRI were performed in all patients within 24 hours of symptom onset and after 1 week. To exclude patients with partial or complete reperfusion, we included only patients with a PWI deficit larger than the DWI lesion. Severe ICA disease (>70% stenosis) was present unilaterally in 9 and bilaterally in 2 patients. Acute DWI lesion volume, the size of the acute PWI/DWI mismatch, and final infarct size (on T2-weighted images) were determined.

Results
—The PWI/DWI mismatch was significantly larger in patients with severe ICA disease than in patients without extracranial carotid stenosis, both when time-to-peak and mean transit time maps (
P
<0.01) were used to calculate the mismatch. Quantitative analysis of the time-to-peak delay in the mismatch indicated that a relatively smaller fraction of the total mismatch was critically ischemic in patients with carotid stenosis than in those without. Average lesion volume increased less in the stenosis group (
P
=0.14), despite the larger PWI/DWI mismatch, and final infarct size was smaller in the stenosis group (
P
<0.05). In the 2 patients with bilateral ICA disease, variable hemodynamic involvement of the contralateral hemisphere was found in addition to the ipsilateral PWI deficit.

Conclusions
—In most acute stroke patients with severe ICA stenosis, a considerably smaller fraction of the total PWI/DWI mismatch is at risk than in patients without carotid disease.
Stress-Related Primary Intracerebral Hemorrhage
Authors: Lammie G. Alistair , Lindley Richard , Keir Sarah , Wiggam M. Ivan
Published: June 2011

Background
—Research into the causes of small-vessel stroke has been hindered by technical constraints. Cases of intracerebral hemorrhage occurring in unusual clinical contexts suggest a causal role for sudden increases in blood pressure and/or cerebral blood flow.

Case Description
—We describe a fatal primary thalamic/brain stem hemorrhage occurring in the context of sudden emotional upset. At autopsy, the brain harbored several perforating artery fibrinoid lesions adjacent to and remote from the hematoma as well as old lacunar infarcts and healed destructive small-vessel lesions.

Conclusions
—We postulate that the emotional upset caused a sudden rise in blood pressure/cerebral blood flow, mediating small-vessel fibrinoid necrosis and rupture. This or a related mechanism may underlie many small-vessel strokes.
Corpus Callosum Atrophy in Patients With Leukoaraiosis May Indicate Global Cognitive Impairment
Authors: Yamauchi Hiroshi , Fukuyama Hidenao , Shio Hideo
Published: June 2011

Background and Purpose
—The extent of white matter high-intensity lesions (WMLs) on T2-weighted MR images may be an indicator of cognitive impairment, especially impairment related to frontal lobe dysfunction. However, it is unclear whether the extent of WMLs is an independent predictor of cognitive impairment. In patients with extensive WMLs, atrophy of the corpus callosum may be an important predictor of global cognitive impairment. The purpose of this study was to investigate the relation of the extent of WMLs and callosal size with cognitive functions in a patient population with a wide range of extent of WMLs.

Methods
—We studied 62 patients, aged 49 to 86 years, who underwent MRI because of neurological symptoms and were diagnosed as having lacunar stroke or no specific neurological disease: 28 with lacunar infarcts and 34 without. Multivariate analysis was used to test the independent predictive value of patient age, sex, educational level, other medical illness, lacunar infarct, corpus callosum area, and extent of WMLs with respect to scores of Mini-Mental State Examination or verbal fluency task.

Results
—Only callosal size and age were significant independent predictors of the scores of the Mini-Mental State Examination, while only the extent of WMLs was an independent predictor of the score of the verbal fluency task.

Conclusions
—Callosal atrophy may be an important predictor of global cognitive impairment in patients with WMLs, whereas the extent of WMLs per se may be related to impairment of frontal lobe function independent of callosal atrophy.
Acute Ischemic Stroke
Authors: Caimi G. , Ferrara F. , Montana M. , Meli F. , Canino B. , Carollo C. , Presti R. Lo
Published: June 2011

Background and Purpose
—Several reports have considered the role of systemic leukocytes in acute ischemic stroke (AIS). Initially, greater attention was focused on the leukocyte count and subsequently on their adhesiveness, aggregation, rheology, and activation. The aim of this study was the evaluation of certain polymorphonuclear leukocyte (PMN) parameters, reflecting their rheology and activation, in subjects with AIS.

Methods
—In a group of 19 subjects with AIS and in a control group of 18 subjects with asymptomatic vascular atherosclerotic disease, we evaluated the PMN membrane fluidity and cytosolic Ca
2+
concentration at baseline and after in vitro chemotactic activation with 4-phorbol 12-myristate 13-acetate (PMA) and
N
-formyl-methionyl-leucyl-phenylalanine (fMLP).

Results
—From the obtained data, it is evident that at baseline only PMN membrane fluidity distinguishes control subjects from AIS subjects. After PMN activation with PMA and fMLP, prolonged for 5 and 15 minutes, we found an increase in PMN cytosolic Ca
2+
concentration and a decrease in PMN membrane fluidity only in subjects with AIS.

Conclusions
—These findings emphasize that in subjects with AIS a functional alteration of systemic PMN cells is clearly expressed during chemotactic activation, although the mechanism of this abnormality is not yet explained.
Validity of Self-Reported Stroke
Authors: Engstad Torgeir , Bønaa Kaare H. , Viitanen Matti
Published: June 2011

Background and Purpose
—The aim of this study was to validate the diagnosis of self-reported stroke.

Methods
—During 1994–1995, 27 159 people attended a population health survey in the community of Tromsø, Norway, a response rate of 77%. A total of 418 attenders reported a history of stroke. In 1997, all individuals with a self-reported stroke who were still living in the community (n=362) were invited to a clinical reexamination. For each of the 269 people who were reexamined, a person who reported no history of stroke was selected and was reexamined in the same way.

Results
—On the basis of the reexamination, 213 (79.2%) of the self-reported strokes were confirmed. Thirteen individuals (4.8%) had a possible stroke. The remaining 43 individuals had either transient ischemic attack (TIA; n=18), traumatic head injuries (n=16), or perinatal cerebral damage, complicated migraine, syncope, possible TIA, or cerebral aneurysm without bleeding (n=9). Among the confirmed strokes, 30 (14.1%) were hemorrhagic and 118 (55.4%) were thromboembolic. Of the 30 hemorrhages, 16 were subarachnoidal bleedings, 10 due to ruptured aneurysms. The histories of stroke, including both the symptoms and the signs, often had a paucity of details and precision, making it impossible to classify 65 stroke victims (30.5%) into stroke subtypes. The positive predictive value (PPV) of a self-reported stroke was 0.79. The PPV was significantly (
P
=0.016) greater in men (0.88) than in women (0.73). Individuals older than 60 years had a significantly greater PPV than those younger than 60 years (PPV 0.83 and 0.73, respectively;
P
=0.05). Hypertension was associated with a greater PPV, whereas a history of either ischemic heart disease, diabetes mellitus, lung disease, or depression had no impact on the PPV. The estimated sensitivity of self-reported stroke in the survey population was ≈80% and the specificity was 99%.

Conclusions
—We conclude that a self-administered questionnaire can be used to assess the prevalence of stroke in epidemiological research.
Proteasome Inhibitor PS519 Reduces Infarction and Attenuates Leukocyte Infiltration in a Rat Model of Focal Cerebral Ischemia
Authors: Phillips James B. , Williams Anthony J. , Adams Julian , Elliott Peter J. , Tortella Frank C.
Published: June 2011

Background and Purpose
—Reperfusion brain injury after cerebral ischemia is associated with a developing inflammatory response at the site of infarction. Proteasome inhibitors block nuclear factor-κB activation and provide anti-inflammatory effects in several animal models of peripheral inflammation. We tested the novel proteasome inhibitor PS519 in a rat model of transient focal ischemia to establish its pharmacodynamics as a neuroprotection treatment and related effects on leukocyte infiltration.

Methods
—Rats were subjected to 2 hours of focal cerebral ischemia by means of the filament method of middle cerebral artery occlusion (MCAo). After either 22 or 70 hours of reperfusion, infarct size was measured and neurological function, electroencephalographic (EEG) activity, and/or neutrophil and macrophage infiltration was quantified. PS519 was administered in a single intravenous bolus at 2 hours after MCAo. In addition, the therapeutic window for PS519 was estimated by delaying treatment for 4 or 6 hours after MCAo.

Results
—Dose-response analysis of infarct volume at 24 hours revealed that PS519 neuroprotection approached 60%, and clinical evaluations showed significant improvements in neurological function and EEG activity. Neutrophil infiltration at 24 hours was also significantly decreased in cortical and striatal infarcted tissue of PS519-treated rats. Delaying the PS519 treatment up to 4 hours continued to result in significant neuroprotection. In the 72-hour injury model, infarction was reduced 40% by PS519, and significant improvements in neurological function and EEG recovery were again measured. Considerable reductions in both neutrophil and macrophage infiltration were evident.

Conclusions
—PS519 mitigates infarction and improves neurological recovery in brain-injured rats, an effect in part caused by a reduction in the leukocyte inflammatory response.
Intracortical Hemorrhage Injury in Rats
Authors: Xue Mengzhou , Del Bigio Marc R.
Published: June 2011

Background and Purpose
—Intracerebral hemorrhage is associated with stroke and head trauma. The purposes of this study were to investigate the effect of intracortical injections of autologous whole blood and blood components on inflammatory cell infiltration and brain cell death and to determine if nonhemorrhagic lesions differ in these respects.

Methods
—Eighty-seven adult rats were subjected to intracortical injections of autologous whole blood or allogeneic plasma, erythrocytes, leukocytes, “activated” leukocytes, and serum. Injections of saline or mineral oil were controls. Blood injections were compared with cortical freeze injury and pial devascularization. Rats were perfusion-fixed 48 hours after injection or lesioning. Eosinophilic neurons, TUNEL-positive cells, brain damage area, infiltrating neutrophils, and CD8a-immunoreactive lymphocytes were quantified.

Results
—Damage area, dying cells, and inflammatory infiltrate were significantly greater after autologous whole blood, leukocyte, and “activated” leukocyte injections than injection of other fractions.

Conclusions
—These results suggest that extravasated whole blood causes a greater degree of cortical cell death and inflammation than ischemic lesions of similar size. Leukocytes “activated” by systemic illness might exacerbate the injury. Secondary hemorrhagic phenomena suggest that the harmful effect is directed toward both brain cells and the vasculature. Further studies are required to delineate the mechanism(s).
Evolution of Brain Injury After Transient Middle Cerebral Artery Occlusion in Neonatal Rats
Authors: Derugin Nikita , Wendland Michael , Muramatsu Kanji , Roberts Timothy P. L. , Gregory George , Ferriero Donna M. , Vexler Zinaida S.
Published: June 2011

Background and Purpose
—Stroke in preterm and term babies is common and results in significant morbidity. The vulnerability and pathophysiological mechanisms of neonatal cerebral ischemia-reperfusion may differ from those in the mature cerebral nervous system because of the immaturity of many receptor systems and differences in metabolism in neonatal brain. This study details the neuropathological sequelae of reperfusion-induced brain injury after transient middle cerebral artery (MCA) occlusion in the postnatal day 7 (P7) rat.

Methods
—P7 rats were subjected to 3 hours of MCA occlusion followed by reperfusion or sham surgery. Diffusion-weighted MRI was performed during MCA occlusion, and maps of the apparent diffusion coefficient (ADC) were constructed. Contrast-enhanced MRI was performed in a subset of animals before and 20 minutes after reperfusion. Triphenyltetrazolium chloride (TTC) staining of the brain was performed 24 hours after reperfusion. Immunohistochemistry to identify astrocytes (glial fibrillary acidic protein), reactive microglia (ED-1), and neurons (microtubule-associated protein 2) and cresyl violet staining were done 4, 8, 24, and 72 hours after reperfusion.

Results
—On contrast-enhanced MRI, nearly complete disruption of cerebral blood flow was evident in the vascular territory of the MCA during occlusion. Partial restoration of blood flow occurred after removal of the suture. A significant decrease of the ADC, indicative of early cytotoxic edema, occurred in anatomic regions with a disrupted blood supply. The decline in ADC was associated with TTC- and cresyl violet–determined brain injury in these regions 24 hours later. The ischemic core was rapidly infiltrated with reactive microglia and was surrounded by reactive astroglia.

Conclusions
—In P7 rats, transient MCA occlusion causes acute cytotoxic edema and severe unilateral brain injury. The presence of a prominent inflammatory response suggests that both the ischemic episode and the reperfusion contribute to the neuropathological outcome.
Association of Intraoperative Transcranial Doppler Monitoring Variables With Stroke From Carotid Endarterectomy
Authors: Ackerstaff R. G. A. , Moons K. G. M. , van de Vlasakker C. J. W. , Moll F. L. , Vermeulen F. E. E. , Algra A. , Spencer M. P.
Published: June 2011

Background and Purpose
—The outcomes of carotid endarterectomy (CEA) are, in addition to patient baseline characteristics, highly dependent on the safety of the surgical procedure. During the successive stages of the operation, transcranial Doppler (TCD) monitoring of the middle cerebral artery (MCA) was used to assess the association of cerebral microembolism and hemodynamic changes with stroke and stroke-related death.

Methods
—By use of data pooled from 2 hospitals in the United States and the Netherlands, including 1058 patients who underwent CEA, the association of various TCD emboli and velocity variables with operative stroke and stroke-related death was evaluated by univariable and multivariable logistic regression analyses in combination with receiver operating characteristic (ROC) curve analyses. The impact of basic patient characteristics, such as age, sex, preoperative cerebral symptoms, and ipsilateral and contralateral internal carotid artery stenosis, on the prediction of operative stroke was also evaluated.

Results
—We observed 31 patients with ischemic and 8 patients with hemorrhagic operative strokes. Four of these patients died. Emboli during dissection (odds ratio [OR] 1.5, 95% CI 0.8 to 2.9) and wound closure (OR 2.3, 95% CI 1.2 to 4.4) as well as ≥90% decrease of MCA peak systolic velocity at cross-clamping (OR 3.3, 95% CI 1.3 to 8.5) and ≥100% increase of the pulsatility index of the Doppler signal at clamp release (OR 7.1, 95% CI 1.4 to 35.7) were independently associated with stroke. The ROC area of this model was 0.69. Of the patient characteristics, only preoperative cerebral ischemia (OR 1.9, 95% CI 1.0 to 3.7) and ≥70% ipsilateral internal carotid artery stenosis (OR 0.5, 95% CI 0.2 to 0.9) were associated with stroke. Adding these patient characteristics to the model, the area under the ROC curve increased to 0.73.

Conclusions
—In CEA, TCD-detected microemboli during dissection and wound closure, ≥90% MCA velocity decrease at cross-clamping, and ≥100% pulsatility index increase at clamp release are associated with operative stroke. In combination with the presence of preoperative cerebral symptoms and ≥70% ipsilateral internal carotid artery stenosis, these 4 TCD monitoring variables reasonably discriminate between patients with and without operative stroke. This supports the use of TCD as a potential intraoperative monitoring modality to alter the surgical technique by enhancing a decrease of the risk of stroke during or immediately after the operation.
Dynamic Regulation of Middle Cerebral Artery Blood Flow Velocity in Aging and Hypertension
Authors: Lipsitz Lewis A. , Mukai Seiji , Hamner Jason , Gagnon Margaret , Babikian Viken
Published: June 2011

Background and Purpose
—-Although aging and hypertension may predispose hypertensive elderly subjects to cerebral hypoperfusion during orthostatic stress, their effects on the acute cerebral autoregulatory response to hypotension are not known.

Methods
—-Continuous middle cerebral artery blood flow velocity (BFV) (transcranial Doppler ultrasound) and mean arterial pressure (MAP, Finapres) were measured in response to (1) acute hypotension during standing, (2) steady-state sitting and standing, and (3) hypercarbia during CO
2
rebreathing in 10 healthy young subjects (age 24±1 years), 10 healthy elderly subjects (age 72±3 years), and 10 previously treated hypertensive elderly (age 72±2 years) subjects. CO
2
reactivity was computed as the slope of cerebrovascular conductance (CVC=BFV/MAP) versus end-expiratory CO
2
. Coherence, transfer magnitudes, and phases between low-frequency MAP and BFV signals were computed from their autospectra during 5 minutes of sitting and standing.

Results
—-MAP fell to a similar extent in all groups by an average of 21 to 26 mm Hg (22% to 26%) within 30 seconds of standing. Mean BFV also fell in all subjects but significantly less in the older subjects (−4.7±0.7 cm/s in hypertensives and −5.3±1.2 cm/s in normotensives,
P
=NS) compared with younger subjects (−10.1±1.1 cm/s,
P
<0.05). CO
2
reactivity was greater in the young subjects (0.19±0.01) compared with normotensive (0.14±0.01,
P
<0.05) and hypertensive elderly subjects (0.11±0.02,
P
<0.05) (
P
=NS between elderly groups). Fewer hypertensive subjects had coherence between MAP and BFV signals; for subjects with coherence, there were no significant group differences in phase or transfer magnitudes in either sitting or standing positions.

Conclusions
—-Despite reduced CO
2
reactivity, elderly normotensive and previously treated hypertensive subjects retain cerebral autoregulatory capacity in response to acute orthostatic hypotension.
Cerebral Hemodynamics in CADASIL Before and After Acetazolamide Challenge Assessed With MRI Bolus Tracking
Authors: Chabriat H. , Pappata S. , Ostergaard L. , Clark C. A. , Pachot-Clouard M. , Vahedi K. , Jobert A. , Le Bihan D. , Bousser M. G.
Published: June 2011

Background
—White matter lesions in cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) are underlaid by severe ultrastructural changes of the arteriolar wall. Although chronic ischemia is presumed to cause the tissue lesions, the pattern of perfusion abnormalities and hemodynamic reserve in CADASIL, particularly within the white matter, remains unknown.

Methods
—We used the MRI bolus tracking method in 15 symptomatic patients with CADASIL (5 with dementia) and 10 age-matched control subjects before and 20 minutes after the intravenous injection of acetazolamide (ACZ, 17 mg/kg). Cerebral blood flow (CBF), blood volume (CBV), and mean transit time (MTT) were calculated both in the cortex and in the white matter according to the singular value decomposition technique. Perfusion parameters were obtained in regions of hyperintensities and within the normal-appearing white matter as observed on T2-weighted images. Analysis was performed with both absolute and relative (region/whole brain) values.

Results
—A significant reduction in absolute and relative CBF and CBV was found within areas of T2 hyperintensities in white matter in the absence of significant variations of MTT. This reduction was more severe in demented than in nondemented patients. No significant change in absolute CBF and CBV values was observed in the cortex of patients with CADASIL. A decrease in relative CBF and CBV values was detected in the occipital cortex. After ACZ administration, CBF and CBV increased significantly in both the cortex and white matter of affected subjects, but the increase in absolute CBF was lower within areas of increased signal on T2-weighted images in patients than in the white matter of control subjects.

Conclusions
—In CADASIL, both basal perfusion and hemodynamic reserve are decreased in areas of T2 hyperintensities in the white matter. This hypoperfusion appears to be related to the clinical severity. The significant effect of ACZ on CBF and CBV suggests that cerebral perfusion might be increased using pharmacological vasodilation in CADASIL.
Cognitive Deficits After Focal Cerebral Ischemia in Mice
Authors: Hattori Kimihiko , Lee Hanna , Hurn Patricia D. , Crain Barbara J. , Traystman Richard J. , DeVries A. Courtney
Published: June 2011

Background and Purpose
—The interpretation of cognitive data in many experimental stroke studies is problematic because middle cerebral artery occlusion (MCAO) is associated with sensorimotor alterations that may become confounding factors in cognitive testing. The purpose of the current study was to determine if it is possible to measure MCAO-induced cognitive deficits by using short durations of ischemia that do not result in alterations in sensorimotor behavior in mice.

Methods
—Male C57/Bl6 mice were subjected to 60 or 90 minutes of intraluminal MCAO or sham surgery. In the first cohort of animals (n=12/group), locomotor activity, balance, and coordination were evaluated 2 weeks after surgery. In a second cohort of animals (n=10/group), the effects of 60 minutes of MCAO on subsequent learning and memory were assessed with a step-down passive avoidance task beginning 1 week after surgery. In a third cohort of animals (n=8 to 10/group), training in a passive avoidance task was completed before 60 minutes of MCAO, then retention of the task was assessed 1 week after surgery. In all animals, infarction size was determined after 14 days of reperfusion with use of cresyl violet staining and quantitative image analysis.

Results
—There was no significant difference in infarction volume in the cerebral cortex or caudoputamen after 60 versus 90 minutes of MCAO. However, there was a significant increase in latency to move 1 body length in the 90-minute MCAO group compared with the 60-minute MCAO and sham groups. In 2 additional cohorts of animals, 60-minute MCAO was associated with a deficit in the acquisition and retention of a passive avoidance task regardless of whether the task training occurred before or after MCAO.

Conclusions
—Long-term cognitive deficits can be induced in mice by using a short duration of MCAO (60 minutes) that does not result in concomitant sensorimotor deficits.
Evaluation of Measures Used to Assess Quality of Life After Stroke
Authors: Buck Deborah , Jacoby Ann , Massey Anna , Ford Gary
Published: June 2011

Background and Purpose
—Assessment of quality of life (QOL) after stroke is becoming common with the recognition that evaluation of treatment should include quality as well as quantity of survival. This article will outline the main conceptual and methodological issues in QOL assessment, highlight advantages and disadvantages of measures used in stroke QOL research, and discuss some unresolved issues.

Summary of Review
—We undertook a MEDLINE search using the keywords “stroke” and “quality of life” and reviewed 3 key texts on QOL measurement in stroke. Fifteen generic and 10 condition-specific measures used to assess QOL in stroke were identified and evaluated with the following criteria: reliability, validity, responsiveness, precision, acceptability, suitability for proxy respondents, mode of administration, and use of patient-centered approaches in development. Domains covered and level of comprehensiveness varied widely between generic and stroke-specific measures. No stroke-specific instruments used patient-centered approaches in their development. Four stroke-specific measures (Frenchay Activities Index, Niemi QOL scale, Ferrans and Powers QOL Index–Stroke Version, and Stroke-Adapted Sickness Impact Profile [SA-SIP30]) provided evidence of reliability and validity.

Conclusions
—The need remains for a patient-centered, psychometrically robust, stroke-specific QOL measure. Patients should be involved in each stage of instrument development. Caution is needed in the selection of an instrument to measure QOL after stroke. Although the Ferrans and Powers QOL Index–Stroke Version, Niemi QOL scale, SA-SIP30, and Sickness Impact Profile come closest to satisfying many of the criteria outlined in this article, the selection of any individual instrument depends on the specific goals and constraints of a particular study.
Deteriorating Ischemic Stroke in 4 Clinical Categories Classified by the Oxfordshire Community Stroke Project
Authors: Tei Hideaki , Uchiyama Shinichiro , Ohara Kuniko , Kobayashi Michiko , Uchiyama Yumiko , Fukuzawa Megumi
Published: June 2011

Background and Purpose
—The aim of this study was to investigate the frequency, possible predictive factors, and prognosis of deteriorating ischemic stroke in 4 clinical categories according to the classification of the Oxfordshire Community Stroke Project (OCSP).

Methods
—A total of 350 patients with first-ever ischemic stroke who presented within 24 hours of onset were enrolled. Based on the OCSP criteria, cerebral infarctions were divided into the following 4 clinical categories: total anterior circulation infarcts (TACI), partial anterior circulation infarcts (PACI), lacunar infarcts (LACI), and posterior circulation infarcts (POCI). Clinical deterioration was defined as a decrease of ≥1 points in the Canadian Neurological Scale (CNS) (in TACI, PACI, and LACI) or Rankin Scale (RS) (in POCI) during 7 days from the onset. In each clinical category, deteriorating (D) and nondeteriorating (ND) patients were compared in terms of their background characteristics, risk factors, vital signs, laboratory data, and cranial CT at the time of hospitalization. The acute-phase mortality and functional outcome were also compared.

Results
—The subjects comprised 86 patients (24.6%) with TACI, 63 (18.0%) with PACI, 141 (40.3%) with LACI, and 60 (17.1%) with POCI. Overall, 90 patients (25.7%) deteriorated. The frequency was very high in TACI (41.9%), followed by LACI (26.2%) and POCI (21.7%), whereas it was very low in PACI (6.3%). There were some clinical variables that differed significantly between D and ND groups. In the patients with TACI, early abnormalities of the cranial CT and significant stenoses in corresponding arteries were more frequent in the D than the ND group. In those with LACI, the CNS and hematocrit were lower in the D than the ND group. In those with POCI, cerebral atrophy was more severe and significant stenoses in vertebrobasilar arteries were more frequent in the D than ND group. The mortality of the D groups of patients with TACI and POCI exceeded 35%, and the functional outcome was worse in the D group than in the ND group of patients with TACI, LACI, and POCI.

Conclusions
—The frequency of deterioration in acute ischemic stroke significantly differed among the OCSP subgroups, and deterioration worsened the prognosis. There were some factors that could predict deterioration: early CT findings in TACI, large-artery atherosclerosis in TACI and POCI, and stroke severity in LACI. Further research to find sophisticated radiological and chemical markers appears to be needed.
Stroke Incidence on the East Coast of Australia
Authors: Thrift Amanda G. , Dewey Helen M. , Macdonell Richard A. L. , McNeil John J. , Donnan Geoffrey A.
Published: June 2011

Background and Purpose
—Community-based stroke incidence studies are the most accurate way of explaining mortality trends and developing public health policy. The purpose of this study was to determine the incidence of stroke in a geographically defined region of Melbourne, Australia.

Methods
—All suspected strokes occurring in a population of 133 816 residents in suburbs north and east of Melbourne, Australia, during a 12-month period of 1996 and 1997 were found and assessed. Multiple overlapping sources were used to ascertain cases, and standard definitions and criteria for stroke and case fatality were used.

Results
—A total of 381 strokes occurred among 353 people during the study period, 276 (72%) of which were first-ever-in-a-lifetime strokes. The crude annual incidence rate (first-ever strokes) was 206 (95% CI, 182 to 231) per 100 000 per year overall, 195 (95% CI, 161 to 229) for males, and 217 (95% CI, 182 to 252) for females. The corresponding rates adjusted to the “world” population were 100 (95% CI, 80 to 119) overall, 113 (95% CI, 92 to 134) for males, and 89 (95% CI, 70 to 107) for females. The 28-day case fatality rate for first-ever strokes was 20% (95% CI, 16% to 25%).

Conclusions
—The incidence rate of stroke in our population-based study is similar to that of many European studies but is significantly higher than that observed on the west coast of Australia.
Microcatheter Intrathecal Urokinase Infusion Into Cisterna Magna for Prevention of Cerebral Vasospasm
Authors: Hamada Jun-ichiro , Mizuno Takamasa , Kai Yutaka , Morioka Motohiro , Ushio Yukitaka
Published: June 2011

Background and Purpose
—The feasibility of preventing vasospasm by intrathecal anterograde infusion of urokinase (UK) into the cisterna magna was studied in patients with recently ruptured aneurysms who had just undergone the placement of a Guglielmi detachable coil (GDC).

Methods
—Immediately after complete embolization with the use of GDC-10 coils, 15 patients with Hunt and Hess neurological grades III and IV received 60 000 IU of UK in normal saline through a microcatheter advanced into the cisterna magna. UK infusion was repeated once or twice over a period of 2 to 3 days according to a decision based on CT evidence of a subarachnoid clot remaining in the cisterns. Before administering the last UK infusion, we obtained CT confirmation of almost complete clearance of clots in the basal cisterns.

Results
—In all 15 patients, the microcatheter was advanced easily into the cisterna magna by use of the over-the-wire microcatheter technique. In 8 patients who received thrombolytic therapy within 24 hours of the ictus, there was almost complete clearance of the clot in the basal cisterns within 2 days of suffering the insult. When UK was injected at 24 to 48 hours after the insult, 7 patients manifested CT evidence of clearance at the latest 4 days after suffering the insult. In all 15 patients, CT scans obtained within 24 hours of the final UK administration showed complete resolution of clots in the basal cistern and almost complete resolution of clots in the basal interhemispheric fissure and bilateral proximal sylvian fissures. Although one patient developed a transient neurological deficit, no patients manifested permanent delayed neurological deficits as a result of vasospasm. Outcome assessment according to the Glasgow Outcome Scale, no less than 3 months after GDC placement, revealed good recovery in all patients, and none developed hydrocephalus requiring a shunt procedure.

Conclusions
—In patients with recently ruptured aneurysms, GDC placement followed by immediate intrathecal administration of UK from the cisterna magna may be a safe and reasonable means of preventing vasospasms and may result in improved treatment outcomes.
Hydrocephalus Is a Determinant of Early Mortality in Putaminal Hemorrhage
Authors: Phan Thanh G. , Koh Merian , Vierkant Robert A. , Wijdicks Eelco F.M.
Published: June 2011

Background and Purpose
—Previous studies have shown that the volume of intracerebral hemorrhage and Glasgow Coma Score (GCS) on admission are powerful predictors of 30-day mortality. However, the significance of hydrocephalus associated with deep cerebral hemorrhage has not been studied extensively. The purpose of this study was to determine the prognostic indicators of 30-day mortality in patients with deep cerebral hemorrhage.

Methods
—We studied 100 consecutive patients with deep cerebral hemorrhage between 1994 and 1998. Deep cerebral hemorrhage was divided into 2 groups: putaminal hemorrhage (lateral group) and thalamic and caudate hemorrhage (medial group). Univariate and multivariate logistic regression analyses were performed to determine independent prognostic indicators of 30-day mortality.

Results
—Hydrocephalus was present in 40 of the 100 patients. The 30-day mortality was 29%, and hydrocephalus was present in 76% of those who died. Multivariate analyses showed 2 independent prognostic indicators of 30-day mortality for putaminal hemorrhage: GCS ≤8 (
P
=0.002, odds ratio [OR] 37.7, CI 3.6 to 396.9) and hydrocephalus (
P
=0.005, OR 27.4, CI 2.7 to 282.6). However, only GCS ≤8 (
P
=0.0002, OR 16.5, CI 3.7 to 73.4) was predictive of 30-day mortality for thalamic and caudate hemorrhage. This model (GCS ≤8 and hydrocephalus) has a sensitivity of 57% and a specificity of 91% for predicting 30-day mortality for putaminal hemorrhage. When both attributes were present in putaminal hemorrhage (GCS ≤8 and hydrocephalus), 1 (11%) of 9 patients survived, and when both attributes were missing 28 (100%) of 28 patients survived.

Conclusions
—Obstructive hydrocephalus on admission in a comatose patient with a putaminal hemorrhage predicts 30-day mortality.