bluuebunny/crossref_metadata_2025 huggingface dataset:
Twenty-four-hour beta-endorphin secretory pattern in stroke patients.
Authors: Franceschini R , Gandolfo C , Cataldi A , Del Sette M , Cianciosi P , Finocchi C , Rolandi E , Barreca T
Published: June 2011

Abnormalities of hypothalamo-pituitary-adrenocortical axis function have been observed frequently in stroke patients. The aim of this study was to investigate plasma beta-endorphin and cortisol 24-hour secretory patterns in patients early after stroke and in the convalescent period to evaluate a possible influence of brain damage on hormonal circadian pattern.

Patients (n = 15; age, 46 to 75 years) were evaluated in the first 24 hours and 10 days after hospital admission for ischemic cerebral stroke and compared with 15 age- and sex-matched normal subjects. Blood samples for beta-endorphin and cortisol determination were drawn every 4 hours from 8 AM to 8 PM and every 2 hours from midnight to 6 AM.

Mean 24-hour beta-endorphin and cortisol levels, recorded in the acute phase, were significantly (P < .05) higher than those recorded in normal subjects; circadian rhythm was not demonstrable for either hormone. In the convalescent period, plasma cortisol 24-hour mean values and circadian rhythm returned to the normal range, whereas the plasma beta-endorphin 24-hour mean values and circadian rhythm did not.

Cerebral stroke induces abnormalities of beta-endorphin and cortisol circadian secretion. Whereas cortisol abnormalities are transient, those of beta-endorphin last longer. The dissociation between beta-endorphin and cortisol 24-hour secretory patterns might potentially serve as a marker of psychoneurological abnormalities occurring after stroke.
EEG recordings in the course of recovery from stroke.
Authors: Giaquinto S , Cobianchi A , Macera F , Nolfe G
Published: June 2011

This study was designed to assess the value of quantified electroencephalography (EEG) in the follow-up of stroke and its possible correlation with other measures of recovery.

EEGs were recorded over a period of 6 months in 34 patients with ischemic stroke in the middle cerebral artery territory who underwent spectral analysis. Two groups were formed: (1) 28 patients with a Barthel Index score of less than 60 at admission and (2) 6 patients with a Barthel score of over 60 and therefore with a much better prognosis. Ten recordings were made in each patient in the first group and at least three in the second group. Motor functions and activities of daily living (ADL) were assessed three times, on admission to the study and after 3 and 6 months.

Quantified EEG was significantly abnormal in the affected hemisphere of the first group. Side and site were not relevant. Longitudinal recordings showed a significant improvement of the power spectrum in the first 3 months. Alpha mean weighted frequency of the injured hemisphere was always slower than that of the contralateral side. All patients improved in motor performance and ADL, with the greatest gain in the first 3 months. However, no correlation between quantified EEG and clinical testing was found. By looking at individual profiles, a frequent and unpredictable instability was seen in the "unaffected" hemisphere. In those who made the best recovery, the EEG spectrum became more symmetrical over the left and right hemispheres, an aspect that continued beyond the point of a good motor and ADL recovery.

Quantified EEG undergoes early and subtle changes in the follow-up of stroke that can outlast clinical recovery. Routine evaluation for prognosis is not recommended because motor and ADL scales provide earlier and more accurate indicators. In contrast, quantified EEG can be useful for individual patients undergoing rehabilitation to monitor mechanisms of local repair and also to detect changes in the so-called normal hemisphere. It may reveal focal abnormalities that are undetected by coarse clinical evaluation and that call for appropriate neuropsychological testing.
Improved reliability of the NIH Stroke Scale using video training. NINDS TPA Stroke Study Group.
Authors: Lyden P , Brott T , Tilley B , Welch K M , Mascha E J , Levine S , Haley E C , Grotta J , Marler J
Published: June 2011

Despite the frequent use of clinical rating scales in multicenter therapeutic stroke trials, no generally acceptable method exists to train and certify investigators to use the instrument consistently. We desired to train investigators to use the National Institutes of Health Stroke Scale in a study of acute stroke therapy so that all examiners rated patients comparably.

We devised a two-camera videotape method that optimizes the visual presentation of examination findings. We then measured the effectiveness of the training by asking each investigator to evaluate a set of 11 patients, also on videotape. We tabulated the evaluations, devised a scoring system, and calculated measures of interobserver agreement among the participants in this study.

We trained and certified 162 investigators. We found moderate to excellent agreement on most Stroke Scale items (unweighted kappa > 0.60). Two items, facial paresis and ataxia, exhibited poor agreement (unweighted kappa < 0.40) and should be revised in future editions of the scale. Performance improved with video training compared with previous studies. Inclusion of the motor rating of the unaffected limbs in the total score did not affect reliability.

Video training and certification is a practical and effective method to standardize the use of examination scales. Two cameras must be used during the taping of patients to accurately present the clinical findings. This method is easily adapted to any study in which a large number of investigators will be enrolling patients at multiple clinical centers.
Diaspirin cross-linked hemoglobin improves neurological outcome following reversible but not irreversible CNS ischemia in rabbits.
Authors: Bowes M P , Burhop K E , Zivin J A
Published: June 2011

Hemodilution using modified hemoglobin solutions may reduce ischemic central nervous system injury. Purified diaspirin cross-linked hemoglobin (DCLHb) is a cell-free hemoglobin that is intramolecularly cross-linked between the two alpha subunits, resulting in enhanced oxygen offloading to tissues and increased half-life. In the present experiments, we evaluated the ability of DCLHb to reduce neurological damage in two rabbit stroke models.

In a reversible spinal cord ischemia model, ischemia of the caudal lumbar spinal cord was produced by temporary occlusion of the abdominal aorta. In an irreversible model of cerebral ischemia, plastic microspheres (50 microns) were injected into the internal carotid artery and lodged in the cerebral microvasculature. DCLHb was administered 5 minutes after initiation of ischemia as either a 10-mL/kg infusion, 10-mL/kg exchange transfusion, or a 20-mL/kg infusion. Control animals received human serum albumin that was oncotically matched to the DCLHb.

In the spinal cord model, DCLHb significantly increased the duration of ischemia required to produce permanent paralysis from 27.33 +/- 8.71 minutes (mean +/- SD) in controls to 42.59 +/- 10.10 minutes in the 10-mL/kg exchange transfusion group and to 40.82 +/- 18.16 minutes in the 20-mL/kg infusion condition (P < .05). DCLHb did not significantly reduce neurological damage in the microsphere embolization model.

These data suggest that cross-linked hemoglobin reduces neurological damage after reversible central nervous system ischemia and that this is not attributable to hemodilution or hypervolemia only.
Aneurysm of the left middle cerebral artery caused by myxoid degeneration of the vessel wall.
Authors: O'Boynick P , Green K D , Batnitzky S , Kepes J J , Pietak R
Published: June 2011

Myxoid degeneration of arterial walls may result in dissection and dissecting aneurysms in extracranial and intracranial portions of cerebral arteries. Rarely, saccular aneurysms may also develop on that basis, but thus far these have only been reported in the cervical portions of the carotid arteries. We describe a case of a nondissecting aneurysm of the left middle cerebral artery caused by myxoid degeneration of the media.

A 39-year-old man had acute onset of frontal headache and neck stiffness. Computed tomographic scan and lumbar puncture established the presence of subarachnoid hemorrhage. Angiography demonstrated a left middle cerebral artery aneurysm. This was clipped and the wall biopsied. Microscopically the entire thickness of the vascular wall showed marked myxoid alterations. No dissection was present. The patient had an uneventful recovery.

This observation confirms that myxoid degeneration of arterial walls may cause aneurysms with eventual rupture even in the absence of dissection. Rare cases of this type of aneurysm have been reported to occur in the cervical portions of the carotid arteries, but this is the first reported observation of such changes involving an intracerebral artery.
Development of aspirin resistance in persons with previous ischemic stroke.
Authors: Helgason C M , Bolin K M , Hoff J A , Winkler S R , Mangat A , Tortorice K L , Brace L D
Published: June 2011

The ex vivo effect of aspirin (ASA) on platelet aggregation, the platelet component of thrombosis, was studied at repeated intervals in a cohort of patients taking aspirin for recurrent ischemic stroke prevention to define the maintenance of efficacy over time.

We administered increasing doses of aspirin (from 325 to 1300 mg/d) to patients with previous ischemic stroke and determined the extent of inhibition of platelet aggregation after 2 weeks and thereafter at approximately 6-month intervals.

Over 33 months, 306 patients had platelet aggregation studies performed to define their initial response to ASA therapy. Of these, 228 had complete and 78 had partial inhibition of platelet aggregation at initial testing. To date, 119 of those who had complete inhibition and 52 who had partial inhibition have undergone repeat testing at least once. At repeat testing 39 of the 119 (32.7%) with complete inhibition at initial testing had lost part of the antiplatelet effect of ASA and converted from complete to partial inhibition without change in ASA dosage. Of the 52 with partial inhibition at initial testing, 35 achieved complete inhibition either by ASA dosage escalation (in 325 mg/d increments) or fluctuation of response at the same dosage, but 8 of those 35 (22.8%) had reverted to partial inhibition when tested again. Overall, 8.2% of patients ultimately exhibited ASA resistance to 1300 mg/d-8 of 52 (15.4%) with partial inhibition and 6 of 119 (5.0%) with complete inhibition at initial testing.

The antiplatelet (and presumably the antithrombotic) effect of a fixed dose of ASA is not constant over time in all individuals. The mechanisms by which increased dosage requirement or ASA resistance develops and the clinical significance of this development are currently undefined.
Compliance with antiplatelet therapy in patients with ischemic cerebrovascular disease. Assessment by platelet aggregation testing.
Authors: Komiya T , Kudo M , Urabe T , Mizuno Y
Published: June 2011

Antiplatelet therapy is currently one of the methods for preventing transient ischemic attacks and cerebral thrombosis. Because antiplatelet agents are generally administered on a long-term basis, patient compliance is an important factor. The purpose of this study was to determine the compliance of patients during antiplatelet therapy by testing platelet aggregation.

To establish the conditions for measuring platelet aggregation, the platelet aggregation test was performed in patients taking 81 mg/d aspirin or 200 mg/d ticlopidine at the following final concentrations of aggregation-inducing agents: 0.5, 1, 2, and 4 mumol/L ADP and 0.5 and 2 micrograms/mL collagen. The optimum measurement conditions for assessing patient compliance were determined. Under the conditions determined in the first study, platelet aggregation was assessed, and the effects of treatment were studied in 159 outpatients and 79 inpatients undergoing antiplatelet therapy. If the antiplatelet effect was insufficient, compliance was checked by interview.

The agents used and the final concentrations found to be optimum for assessing platelet aggregation were 2 micrograms/mL collagen for patients taking aspirin 81 mg/day and 2 mumol/L ADP for patients taking ticlopidine 200 mg/d. In 17 (10%) of the 159 outpatients, platelet aggregation was not adequately reduced because of noncompliance with their antiplatelet therapy.

This study indicated that monitoring of compliance is important for outpatients on antiplatelet therapy. It is best if platelet aggregation can be checked, but when this is impossible it is necessary to assess compliance periodically and provide patient guidance.
Costs of stroke in Sweden. A national perspective.
Authors: Terént A , Marké L A , Asplund K , Norrving B , Jonsson E , Wester P O
Published: June 2011

Cost-effectiveness analyses of stroke management are hampered by paucity of economic data. We made an update of the direct and indirect costs of stroke in Sweden (population, 8.5 million).

Direct costs (ie, the costs for hospital and outpatient care and social services) were estimated on the basis of two prospective population-based studies of stroke and of two nationwide cross-sectional inventories of bed-days and diagnoses. Indirect costs (ie, the costs for loss of productivity and early retirement) were based on official statistics.

The direct annual costs of care for stroke patients in 1991 equaled 7836 million Swedish krona (SKr) ($1306 million in US dollars), and the indirect costs, 2430 million SKr ($405 million). The cost of stroke care was 1208 SKr ($201) per inhabitant in Sweden. The expected direct costs per patient from first stroke to death were 440,000 SKr ($73,333). When prestroke costs for other diseases and advanced age were subtracted, the sum was reduced to 180,000 SKr ($30,000).

Costs for hospital and outpatient care and social services accounted for 76% of Swedish stroke costs and for 24% of costs for loss of production and early retirement. Only 41% of direct costs were stroke-related.
Determining functional/health status and its relation to disability in stroke survivors.
Authors: Segal M E , Schall R R
Published: June 2011

Determining the functional/health status of stroke survivors poses special difficulties because of cognitive impairments that frequently result from stroke. A possible means of assessing the status of stroke survivors who are cognitively impaired is getting proxy responses from a family member or other caregiver. Proxy agreement was evaluated for two measures of functional/health status, the Frenchay Activities Index (FAI) and the Health Status Questionnaire (HSQ), and a measure of disability, the Functional Independence Measure (FIM).

Thirty-eight stroke survivors were administered the measures at follow-up (median time since the stroke, 6 months). Caregivers were instructed to answer as proxies for the stroke survivors in their care. Demographics on age, sex, race, marital status, educational level, side of lesion, and relation of stroke survivor to caregiver were collected.

Proxy agreement was excellent for the FAI (intraclass correlation, .85) and the FIM (.87), but poor for the HSQ scales (average proxy agreement, .32). Patients' scores were low and positively skewed for the FAI but high and negatively skewed for the FIM. Although Spearman rho coefficients between the measures were fairly high for both stroke survivors and proxy respondents, the correlation of scores was substantially weaker when the group of less severely impaired survivors (as established by FIM ratings) was considered separately.

The FAI and the FIM are useful for assessing the functional/health status of stroke survivors because answers can be obtained by proxy. Future studies should examine the relations between disability and functional/health status, with explicit attention paid to variations in the level of disability in the stroke survivors.
Coexistence of fibromuscular dysplasia and cystic medial necrosis in a patient with Marfan's syndrome and bilateral carotid artery dissections.
Authors: Schievink W I , Björnsson J , Piepgras D G
Published: June 2011

A primary arteriopathy is suspected in most patients with spontaneous dissections of the carotid artery, although the nature of this arteriopathy usually remains elusive. Angiographic changes of fibromuscular dysplasia (FMD), however, are found in 10% to 20% of patients with carotid dissections.

A 26-year-old woman with Marfan's syndrome presented with bilateral amaurosis fugax after surgical repair of an aortic dissection. Angiography revealed a dissection extending from the ascending aorta into the right internal carotid artery and, separate from the aortic dissection, a dissection of the left internal carotid artery. After surgery, microscopic examination of the right carotid artery revealed a medial dissection but no evidence of an underlying arteriopathy, while the left internal carotid artery displayed the typical features of FMD. Eighteen months later the patient died after resection of a large thoracoabdominal aortic dissecting aneurysm. Microscopic examination of the aorta revealed moderately extensive cystic medial necrosis.

Carotid dissections associated with Marfan's syndrome may be the result of an extension of an aortic dissection or occur isolated from the aorta, even in the same patient. The occurrence of FMD in a patient with Marfan's syndrome in conjunction with previous reports of FMD in a variety of connective tissue disorders suggests that FMD, like cystic medial necrosis, may be a nonspecific disease entity.
Failure of aspirin treatment after stroke.
Authors: Bornstein N M , Karepov V G , Aronovich B D , Gorbulev A Y , Treves T A , Korczyn A D
Published: June 2011

Despite its low efficacy, aspirin is the most widely used drug for secondary stroke prevention. The reasons why stroke recurs while patients are on aspirin are unknown. We have analyzed a series of patients who had recurrent strokes while on aspirin.

Out of 2231 consecutive patients who were admitted to the Tel Aviv Medical Center from May 1988 through December 1992 with the diagnosis of ischemic stroke, 129 admissions were due to recurrent ischemic strokes while the patients were already on aspirin, and these were defined as aspirin failures. The clinical characteristics of those patients in whom aspirin treatment failed were compared with three control groups, each comprising 129 patients who had had only a single ischemic stroke and were then taking aspirin. One control group was matched for aspirin dose and date of first stroke; another control group was matched for age, sex, and date of first stroke; and a third control group was matched for age, sex, date of first stroke, and aspirin dose. Statistical analysis was carried out by two-tailed Student's t test and chi 2 test.

The average period until stroke was longer for patients on higher aspirin doses. Patients matched for aspirin dose and date of first stroke did not differ significantly in age (72.4 years in aspirin failures versus 74.2 years in the first control group) and sex (89 versus 94 men, respectively). Matching for age, sex, and date of first stroke but not for aspirin dose demonstrated a trend toward high frequency of aspirin failure in patients taking lower doses of aspirin (chi 2 test for trend = 3.5; P = .06). Comparison of aspirin-failure patients with a control group matched for age, sex, date of first ischemic stroke, and aspirin dose demonstrated that these patients more commonly had statistically significant hyperlipidemia (odds ratio, 2.6; 95% confidence interval, 1.0 to 6.8; P = .04) and ischemic heart disease (odds ratio, 2.3; 95% confidence interval, 1.3 to 3.9; P = .002).

We conclude that age and sex do not influence the efficacy of aspirin. Lower aspirin dose in patients with stroke recurrence suggests that aspirin doses of 500 mg daily or more should be used in secondary stroke prevention. Hyperlipidemia and ischemic heart disease are risk factors for stroke recurrence despite aspirin treatment, which requires further clinical and laboratory evaluation.
Hemostatic markers in acute transient ischemic attacks.
Authors: Fon E A , Mackey A , Côté R , Wolfson C , McIlraith D M , Leclerc J , Bourque F
Published: June 2011

Hemostatic abnormalities have been shown previously in stroke patients. The purpose of this study was to assess the activity of selected parameters of the coagulation system in acute reversible cerebral ischemia.

We measured fibrinopeptide A, thrombin-antithrombin III, and D-dimer in 36 patients in both the acute (< 7 days) and postacute stage (1 and 3 months) after a transient ischemic attack (TIA). The results were compared with those of 20 asymptomatic patients with a history of remote TIA and 65 age- and sex-matched controls.

Mean fibrinopeptide A and thrombin-antithrombin III values were elevated in the acute stage after a TIA (P < .02) compared with levels at 1 month. In contrast, D-dimer was significantly increased at all three times points after the event when compared with remote TIA (P < .05) or control subjects (P < .001). No association could be found between marker levels and clinical outcome or the degree of cervical atherosclerosis as assessed by duplex ultrasonography.

These findings suggest that after acute reversible cerebral ischemia, there is early transient activation of thrombogenesis and ongoing fibrinolysis.
Space-occupying cerebellar infarction. Clinical course and prognosis.
Authors: Hornig C R , Rust D S , Busse O , Jauss M , Laun A
Published: June 2011

Because the timing and strategy of surgical intervention in massive cerebellar infarction remains controversial, we report our experience with the management of 52 such patients.

Case records, computed tomographic scans, surgical reports, and angiograms of 52 patients with space-occupying cerebellar infarction defined by computed tomographic criteria were reevaluated with regard to clinical course, etiology, therapeutic management, mortality, and functional outcome.

In most cases clinical deterioration started on the third day after stroke, and a comatose state was reached within 24 hours. Sixteen patients were treated medically, and 30 by suboccipital craniectomy (22 plus ventriculostomy, 12 plus tonsillectomy). Ten patients primarily had ventriculostomy, which in 4 patients was supplemented by craniotomy because of continuing deterioration. Twenty-nine patients made a good recovery, 15 remained disabled, and 8 died. Even comatose patients had a 38% chance of a good recovery with decompressive surgery. Age older than 60 years (P = .0043) and probably initial brain stem signs (P = .0816) and a late clinical stage (P = .0893) were linked with a fatal or disabling outcome.

Decompressive surgery should be the treatment of choice for massive cerebellar infarction causing progressive brain stem signs or impairment of consciousness.
Decreased cerebrovascular dilatory capacity in subjects with asymptomatic periventricular hyperintensities.
Authors: Isaka Y , Okamoto M , Ashida K , Imaizumi M
Published: June 2011

The clinical significance of the periventricular hyperintensity incidentally found on magnetic resonance images of the brain is questionable. We evaluated resting cerebral blood flow and cerebrovascular dilatory capacity of subjects with asymptomatic periventricular hyperintensities to study their cerebral hemodynamics.

Magnetic resonance imaging of the brain was performed in 28 asymptomatic subjects with cerebrovascular risk factors to determine the severity of periventricular hyperintensity. Mean gray matter flow was computed by a 133Xe-clearance technique in subjects at rest and after the administration of 1 g acetazolamide. Flow values were correlated with the scores for periventricular hyperintensity.

Resting gray matter flow was not significantly correlated with the severity of periventricular hyperintensity for the whole brain (rs = -.364), whereas flow after acetazolamide loading (rs = -.783, P < .001) and the absolute value of increased flow (rs = -.567, P < .01) were significantly and negatively correlated with the severity of periventricular hyperintensity.

A decrease in vasodilatory capacity and compensatory vasodilation occur in the cerebral cortex of subjects with asymptomatic periventricular lesions and maintain cerebral blood flow.
Draining vein pressure increases and hemorrhage in patients with arteriovenous malformation.
Authors: Miyasaka Y , Kurata A , Tokiwa K , Tanaka R , Yada K , Ohwada T
Published: June 2011

Recent radiological studies have shown that arteriovenous malformations with impaired venous drainage may be susceptible to hemorrhage. To evaluate this hypothesis using a hemodynamic approach, we measured intravascular pressure during surgery in three patients with arteriovenous malformation.

In three patients we measured intravascular pressures in the draining venous system and the feeding arteries simultaneously before removal of arteriovenous malformations with marked segmental stenotic or occlusive draining veins and evidence of hemorrhage. The draining vein pressures at prestenotic (or preocclusive) sites in the three patients were 38, 25, and 40 mm Hg, respectively, all significantly above the normal cortical venous pressure, whereas pressure measurements in poststenotic sites and the sagittal sinus pressure in the venous drainage system approached normal values. The feeding artery pressures in the patients were lower than normal cortical artery pressure because of the arteriovenous shunt.

Intraoperative vascular pressure measurements support the hypothesis that arteriovenous malformations with impaired venous drainage may be associated with a local increase in venous pressure and thus may be susceptible to hemorrhage.
A prospective community-based study of stroke in Warsaw, Poland.
Authors: Czlonkowska A , Ryglewicz D , Weissbein T , Baranska-Gieruszczak M , Hier D B
Published: June 2011

Poland is a country with high morbidity and mortality rates from cardiovascular diseases. No recent studies have evaluated the contribution of cerebrovascular diseases to this morbidity and mortality. Our aim was to accurately determine stroke incidence rates in Warsaw, Poland.

A 2-year prospective and population-based stroke registry was maintained for health care units 2 and 3 in Warsaw, Poland (population, 182,285). Case subjects were ascertained by surveying hospital admissions, outpatient visits, and death certificates.

During the 2 years of the study (1991 to 1992), 633 cases of first-event strokes were registered, 462 of which were first ever in a lifetime. Computed tomography or necropsy was performed in 72% of first-ever stroke cases. The crude annual incidence rate for first-ever stroke was 127/100,000 (95% confidence intervals, 111 to 145); the rate standardized to the European population was 111 (95% confidence intervals, 96 to 128). Our incidence rates for first-event strokes were found to be in the middle of the range among other first-event studies. When comparing our first-ever stroke incidence rates with those of comparable studies performed throughout Europe, they were found to be similar for groups aged younger than 65 years but lower in the older age groups. The distribution of ischemic and hemorrhagic stroke subtypes was similar to that of other countries.

This first population-based prospective stroke registry in Poland showed that incidence rates were not high compared with other studies throughout Europe and the world. These stroke incidence rates are not a large contributing factor to high cardiovascular morbidity rates in Poland.
Stroke incidence and case fatality in Australasia. A comparison of the Auckland and Perth population-based stroke registers.
Authors: Bonita R , Anderson C S , Broad J B , Jamrozik K D , Stewart-Wynne E G , Anderson N E
Published: June 2011

Population-based studies are crucial for identifying explanations for the decline in mortality from stroke and for generating strategies for public health policy. However, the present particular methodological difficulties, and comparability between them is generally poor. In this article we compare the incidence and case fatality of stroke as assessed by two independent well-designed incidence studies.

Two registers of acute cerebrovascular events were compiled in the geographically defined metropolitan areas of Auckland, New Zealand (population 945,369), during 1991-1992 for 12 months and Perth, Australia (population 138,708), during 1989-1990 for 18 months. The protocols for each register included prospective ascertainment of cases using multiple overlapping sources and the application of standardized definitions and criteria for stroke and case fatality.

In Auckland, 1803 events occurred in 1761 residents, 73% of which were first-ever strokes. The corresponding figures for Perth were 536 events in 492 residents, 69% of which were first-ever strokes. Both studies identified a substantial proportion of nonfatal strokes managed solely outside the hospital system: 28% in Auckland and 22% in Perth of all patients registered. The age-standardized annual incidence of stroke (all events) was 27% higher among men in Perth compared with Auckland (odds ratio, 1.27; P = .016); women tended to have higher rates in Auckland, although these differences were not statistically significant. In both centers approximately a quarter of all patients died within the first month after a stroke. There were significant differences in the prevalence of hypertension among first-ever strokes.

These two studies emphasize the importance of identifying all patients with stroke, both hospitalized and nonhospitalized, in order to measure the incidence of stroke accurately. The incidence and case fatality of stroke were remarkably similar in Auckland and Perth in the early 1990s. However, there are differences in the sex-specific rates that correspond to differences in the pattern of risk factors.
Magnetic resonance imaging and dynamic CT scan in cervical artery dissections.
Authors: Zuber M , Meary E , Meder J F , Mas J L
Published: June 2011

The typical magnetic resonance imaging picture of arterial dissection, namely, a narrowed eccentric signal void surrounded by a semilunar signal hyper-intensity (corresponding to the mural hematoma) on T1- and T2-weighted images, has been repeatedly reported, but the sensitivity of magnetic resonance imaging for the diagnosis of cervical dissection is poorly known. Another technique, dynamic computed tomography, may provide evidence of mural hematoma, but there has been no systematic evaluation of this technique. The aims of this study were to assess both the sensitivity of routine 0.5-T magnetic resonance imaging for the detection of a typical picture of cervical artery dissection and the value of dynamic computed tomographic scans to provide evidence of dissecting hematoma.

Fifteen consecutive patients with angiographically confirmed extracranial internal carotid (n = 9) or vertebral (n = 10) dissections were studied using a standardized 0.5-T spin-echo magnetic resonance imaging protocol with axial slices. Twelve of these patients had dynamic computed tomographic scans at the site of the dissection suggested by angiography.

A typical magnetic resonance imaging picture of cervical artery dissection was observed in 12 of 15 (80%) patients and in 13 of 19 (68%) dissected vessels. The sensitivity of magnetic resonance imaging was higher in internal carotid (78%) than in vertebral (60%) dissections and in stenotic-type dissections (85%) than in occlusive or aneurysmal-type dissections. The dynamic computed tomographic scan showed the mural hematoma in 11 of the 12 (92%) patients and in 12 of 15 (80%) dissected vessels.

Routine 0.5-T magnetic resonance imaging with axial slices is a sensitive technique for the diagnosis of dissection, but in about 20% of patients with cervical artery dissection magnetic resonance imaging will demonstrate no typical abnormality. Dynamic computed tomographic scans are a sensitive neuroimaging procedure to confirm the presence of the mural hematoma, but it needs to be directed by prior angiography.
The role of superoxide anions in the pathogenesis of cerebral vasospasm.
Authors: Shishido T , Suzuki R , Qian L , Hirakawa K
Published: June 2011

To determine the role of superoxide anions in the pathogenesis of cerebral vasospasm after aneurysmal subarachnoid hemorrhage, we studied the preventive effect of human recombinant copper-zinc superoxide dismutase (h-r SOD) in a rabbit subarachnoid hemorrhage (SAH) model.

Forty-five rabbits receiving intracisternal injection of 3 mL autologous nonheparinized blood or 3 mL saline were divided into four groups as follows: (1) saline injected and no treatment (control group, n = 6); (2) blood injected and no treatment (SAH group, n = 20); (3) blood injected and treated by multiple intracisternal injections of 30,000 U of h-r SOD in 0.5 mL saline (SOD group, n = 9); and (4) blood injected and treated by multiple intracisternal injections of 0.5 mL saline (saline group, n = 10). Serial angiograms were performed after the blood injection, and the diameter of the basilar artery was measured. Three animals from the control group and five animals from the SAH and SOD groups each were killed 2 days after SAH, and their basilar arteries were processed for transmission electron microscopic observations.

In the SAH and saline groups, the diameter of the basilar arteries was significantly reduced (28 +/- 14% and 27 +/- 9%, respectively) at 2 days after the blood injection, then recovered to pre-SAH levels until 11 days. In the SOD group, the diameter of the basilar artery was only minimally changed during the follow-up period. Transmission electron microscopy revealed endothelial injury in all basilar arteries in the SAH group, whereas endothelial injury was minimal in the SOD group.

We determined that h-r SOD prevents the occurrence of vasospasm, possibly as a result of preventing endothelial injury initiated by superoxide anions.
Deferoxamine posttreatment reduces ischemic brain injury in neonatal rats.
Authors: Palmer C , Roberts R L , Bero C
Published: June 2011

Iron catalyzes the formation of damaging reactive species during cerebral reperfusion. Brain iron concentration is highest at birth, so the brain of the asphyxiated newborn may be at increased risk of iron-dependent injury. We investigated whether the ferric iron chelator deferoxamine could reduce hypoxic-ischemic brain injury in neonatal rats. Because deferoxamine has concentration-dependent activities other than iron chelation, we measured brain deferoxamine levels and calculated deferoxamine pharmacokinetic parameters.

We produced hypoxic-ischemic injury to the right cerebral hemisphere of 7-day-old rats by right common carotid artery ligation followed by 2.25 hours of hypoxia in 8% oxygen. At 5 minutes of recovery from hypoxia the rats received 100 mg/kg deferoxamine mesylate or saline subcutaneously. Rats (saline, n = 33; deferoxamine, n = 38) were killed at 42 hours of recovery to assess early acute edema by measurement of hemispheric water content. Other rats (saline, n = 31; deferoxamine, n = 32) were killed at 30 days of age for morphometric determination of right hemisphere atrophy. In still other rats, we measured deferoxamine levels in blood and brain after hypoxia-ischemia.

Deferoxamine significantly reduced right hemisphere injury as measured by early water content (P < .01) and later atrophy (P = .019). Deferoxamine brain levels peaked between 100 and 200 mumol/L at 40 to 60 minutes after injection and exceeded serum levels by +/- 70%.

Deferoxamine administered after induction of cerebral hypoxia-ischemia reduces injury in 7-day-old rats. Deferoxamine concentrates in the brain at levels between 100 and 200 mumol/L. At the concentrations achieved, deferoxamine might protect the brain through mechanisms unrelated to its ability to chelate iron.
Prophylactic neuroprotection for cerebral ischemia.
Authors: Fisher M , Jonas S , Sacco R L , Jones S [corrected to Jonas S ]
Published: June 2011

Treatments for acute ischemic stroke have evolved as knowledge about the pathophysiology of ischemic brain injury has advanced. Treatment strategies under development are aimed at offering neuroprotection acutely after focal cerebral ischemic injury, but delayed initiation of therapy may reduce efficacy. Pretreatment before ischemia begins could offer distinct advantages in patient groups at high risk for ischemic stroke.

If a neuroprotective drug were available orally, safe, and relatively inexpensive, it could be considered for prophylactic use in high-risk populations. Prophylactic neuroprotection would include (1) short-term neuroprotection before and after high-stroke risk procedures, (2) long-term neuroprotection for primary and secondary intervention in populations at high risk for stroke, and (3) concomitant neuroprotection with agents that have multiple treatment effects. Patients undergoing procedures such as cardiac surgery, endarterectomy, or endovascular therapy, which have a risk of cerebral ischemic events during a defined period, might be considered for short-term, periprocedure prophylactic neuroprotection. Several populations at high long-term risk for initial ischemic stroke have been identified and include those with combinations of vascular risk factors, transient ischemic attacks, atrial fibrillation, and asymptomatic carotid stenosis. Such people, as well as those at risk for stroke recurrence after minor strokes, are readily identifiable and perhaps appropriate for long-term prophylactic neuroprotection. Patients with hypertension and cerebrovascular atherosclerosis have a high stroke risk, and therapies directed at these underlying disorders are available that also have concomitant neuroprotective effects. An ideal drug for trials in these patient groups has not yet been developed, and establishing its efficacy may prove to be an arduous and lengthy task.

The possibility of ameliorating the consequences of an acute ischemic stroke by pretreating high-risk patients with appropriate neuroprotective agents needs to be explored. Several types of high-risk population for prophylactic neuroprotection can be envisioned and then studied in clinical trials.
Glucose intolerance and 22-year stroke incidence. The Honolulu Heart Program.
Authors: Burchfiel C M , Curb J D , Rodriguez B L , Abbott R D , Chiu D , Yano K
Published: June 2011

This study was conducted to determine whether glucose intolerance and diabetes increase the risk of thromboembolic, hemorrhagic, and total stroke independent of other risk factors.

Among 7549 Japanese-American men aged 45 to 68 years and free of coronary heart disease and stroke during 1965 to 1968, history of diabetes, diabetic medication, and nonfasting glucose 1 hour after a 50-g load were used to classify subjects into four glucose tolerance categories. Incidence of stroke over 22 years was ascertained using comprehensive hospital-based surveillance. Age- and risk factor-adjusted relative risks of stroke were determined using a Cox proportional hazards model.

A total of 374 thromboembolic, 128 hemorrhagic, and 36 type-unknown strokes occurred. Incidence of thromboembolic but not hemorrhagic stroke increased with worsening glucose tolerance category. Compared with the "low-normal" (glucose < 151 mg/dL) group, subjects in the "high-normal" (151 to 224 mg/dL), "asymptomatic high" (> or = 225 mg/dL), and "known diabetes" groups all had significantly elevated age-adjusted relative risks of thromboembolic stroke. After adjustment for other risk factors, relative risks remained significantly elevated for the asymptomatic high and known diabetes groups (1.43 and 2.45; 95% confidence intervals, 1.00 to 2.04 and 1.73 to 3.47, respectively). Associations were the same in hypertensive and nonhypertensive subjects and similar but slightly stronger in younger (aged 45 to 54 years) than in older (aged 55 to 68 years) men.

Subjects with diabetes and elevated glucose appear to be at increased risk of thromboembolic but not hemorrhagic stroke. These associations were largely independent of other cardiovascular disease risk factors. Excess risk is apparent in older as well as younger diabetic individuals and in hypertensive and nonhypertensive subjects with diabetes.
Cerebral oxygen extraction, oxygen consumption, and regional cerebral blood flow during the aura phase of migraine.
Authors: Friberg L , Olesen J , Lassen N A , Olsen T S , Karle A
Published: June 2011

The aura phase of migraine is associated with focal blood flow changes, but it has been largely unknown whether these changes are correlated to changes in the cerebral metabolism.

Eight patients required carotid angiography for evaluation of transient neurological attacks. Cerebral blood flow (CBF) results, angiography, and clinical observations subsequently suggested the diagnosis: migraine with aura and occasional aura attacks without headache. In the same setting the cerebral angiography was followed by four to six repeated recordings of regional CBF using the intra-arterial 133Xe injection method. Blood samples were drawn from the carotid artery and the internal jugular vein to measure oxygen extraction fraction and cerebral metabolic rate for oxygen.

The intracarotid regional CBF technique provoked aura symptoms and typical, migraine-related, posterior focal hypoperfusion in four patients, followed by typical unilateral headache in three patients. The remaining four patients had no symptoms or regional CBF changes during the examination. There was a significant increase (mean, 13%) of global oxygen extraction fraction in the four patients during aura symptoms, whereas no significant changes of oxygen extraction fraction were found in the nonsymptomatic group. The increase in global oxygen extraction fraction in the symptomatic group coincided with a drop of hemispheric CBF (mean, 12%). Cerebral metabolic oxygen rate remained essentially unchanged, as did PaCO2.

The data presented suggest that the focal flow reduction during the migraine-aura phase is not a secondary phenomenon of reduced cerebral metabolism. However, arteriolar vasoconstriction might offer a possible explanation for the regional CBF changes observed during the migraine aura.
Noninvasive monitoring of internal carotid artery dissection.
Authors: Steinke W , Rautenberg W , Schwartz A , Hennerici M
Published: June 2011

Internal carotid artery dissection has increasingly been reported as a cause of transient ischemic attack or stroke. However, scarce data exist on the natural history of the arterial lesions and the temporal profile of recanalization.

We followed 48 patients with 50 angiographically confirmed internal carotid artery dissections by sequential duplex Doppler studies in 2- to 4-day intervals during the first weeks after the onset of symptoms and after 4 weeks in 1- to 2-month intervals for up to 2 years. We assessed sonographic features as well as the frequency and time course of resolution.

Initial Doppler findings were abnormal in all patients, most of whom (68%) presented with a characteristic bidirectional high-resistance Doppler signal in the internal carotid artery. Gradual recanalization was found in 68% of the dissections after an average interval of 51 days. Changes of Doppler flow patterns in follow-up studies and features of intra-arterial angiography correlated with the development of internal carotid artery dissection and mirrored the recanalization process.

Our findings suggest that Doppler sonography provides early recognition of internal carotid artery dissection and monitoring of its resolution. Thus, ultrasound studies may guide clinical decisions according to the development of the dissection.
Pattern of activation of the hypothalamic-pituitary-adrenal axis in acute stroke. Relation to acute confusional state, extent of brain damage, and clinical outcome.
Authors: Fassbender K , Schmidt R , Mössner R , Daffertshofer M , Hennerici M
Published: June 2011

The aim of this study was to characterize the response of the hypothalamic-pituitary-adrenal system in the first hours of ischemic stroke and to relate its extent to the occurrence of acute confusional state, volume of brain damage, and clinical outcome.

The secretion of corticotropin (adrenocorticotropic hormone [ACTH]) and cortisol was studied in 23 patients by determinations at hours 4, 6, 8, 10, and 14 and days 1, 3, 5, and 7 after onset of symptoms. Acute confusional state (DSM-III-R criteria), extent of lesion (volumetry of computed tomographic scans), and neurological and functional outcome (Scandinavian Stroke Scale, Barthel Index scores) were assessed.

The massive neuroendocrine response observed consisted of an initial phase with concomitantly increased levels of ACTH and cortisol and a second phase with decreased levels of ACTH while high concentrations of cortisol persisted. Initial levels of ACTH but not cortisol were significantly increased in patients with acute confusional state and significantly correlated with volume of brain lesion and neurological and functional outcome.

An early and persisting activation of the hypothalamic-pituitary-adrenal axis was observed in relation to severity of disease. Its characteristic biphasic pattern suggests an initial central stimulation of release of ACTH followed by feedback suppression concomitant with an increased susceptibility of the adrenal gland. Because these hormones are known to exacerbate hypoxic injury to neurons, their massive release in hyperacute stroke may increase the extent of brain damage.
Baseline silent cerebral infarction in the Asymptomatic Carotid Atherosclerosis Study.
Authors: Brott T , Tomsick T , Feinberg W , Johnson C , Biller J , Broderick J , Kelly M , Frey J , Schwartz S , Blum C
Published: June 2011

In a group of patients with high-grade asymptomatic carotid artery stenosis, we prospectively determined the prevalence and radiological characteristics of clinically asymptomatic brain infarction evident on computed tomography. Risk factors and extent of carotid disease were also determined.

Patients randomized into the Asymptomatic Carotid Atherosclerosis Study (ACAS) underwent a neurological history, a detailed stroke/transient ischemic attack questionnaire, and a detailed neurological examination. Computed tomography scans were examined by standardized criteria developed as part of a quality-control program supervised by a neuroradiologist. The presence, location, and size of all cerebral infarctions evident by computed tomography were determined.

Among 1132 patients, 848 had no history of stroke or transient ischemic attack. One hundred twenty-six patients (15%) had a silent infarct; 95 (11%) had one, 24 (3%) had two, and 7 (1%) had three or more infarcts. The infarct size was small and deep for 117 patients (72%), less than one-half lobe for 45 (28%), and one-half to less than one lobe for 1 (0.5%). The silent infarcts were evenly distributed ipsilaterally and contralaterally to the study artery but were significantly more frequent in the right hemisphere (P < .05). Factors associated with silent infarction were abnormal gait (P < .001), abnormal deep tendon reflexes or plantar responses (P = .038), but not degree of carotid stenosis. Silent infarction was less frequent among this totally asymptomatic cohort (15%) compared with those with transient ischemic attacks (34/139, 25%; P < .001).

Silent infarction in the setting of asymptomatic carotid stenosis is not uncommon, but silent infarctions are rarely sizable. The clinical significance of silent cerebral infarction in patients with asymptomatic carotid artery stenosis has yet to be established.