bluuebunny/crossref_metadata_2025 huggingface dataset:
Assessment of Autoregulation by Means of Periodic Changes in Blood Pressure
Authors: Birch A. A. , Dirnhuber M. J. , Hartley-Davies R. , Iannotti F. , Neil-Dwyer G.
Published: June 2011

Background and Purpose
The aim of this study was to test the hypothesis that the phase difference that occurs between an induced oscillation in blood pressure and the resultant oscillation in middle cerebral artery (MCA) flow velocity could reflect the competence of cerebral autoregulation.

Methods
Fourteen volunteers performed 19 cycles of 10 seconds of squatting followed by 10 seconds of standing. Peak MCA velocity was measured with transcranial Doppler ultrasound, and blood pressure was measured with a servo-controlled finger plethysmograph held level with the head. Waveforms from each cycle were added to obtain averaged waveforms of arterial blood pressure and MCA velocity. These results were processed by Fourier analysis to extract the phase difference between the fundamental components of velocity and pressure. Each volunteer performed the exercise three times: first breathing normally, secondly hyperventilating (hypocapnia), and finally while breathing air containing 5% carbon dioxide (hypercapnia). Under these conditions the volunteers were expected to have normal, enhanced, and impaired autoregulation, respectively.

Results
The measurements made with normal breathing showed a phase lead of velocity ahead of pressure of 46±14° (mean±SD). We noted a highly significant reduction in phase lead with hypercapnia (
P
<.00015) (Wilcoxon signed rank test, two-tailed) and a highly significant increase in phase lead with hypocapnia (
P
<.002).

Conclusions
The results support our hypothesis and may lead to a technique for assessing the competence of cerebral autoregulation.
Continuing Ischemic Damage After Acute Middle Cerebral Artery Infarction in Humans Demonstrated by Short-Echo Proton Spectroscopy
Authors: Saunders Dawn E. , Howe Franklyn A. , van den Boogaart Aad , McLean Mary A. , Griffiths John R. , Brown Martin M.
Published: June 2011

Background and Purpose
Proton MR spectroscopy is a noninvasive method of monitoring in vivo metabolite concentration changes over time. The aim of this work was to study the ischemic penumbra in humans by measuring the metabolic changes that occur after a middle cerebral artery territory infarction.

Methods
Diagnostic MRI and short–echo time MR spectroscopy were performed on a 1.5-T system. Localized proton MR spectroscopy was performed within the area of cerebral infarction and in a homologous area of the contralateral hemisphere. The residual water resonance in the spectra was removed with the use of the Hankel Lanczos singular value decomposition method, after which peak area estimates were obtained by means of the variable projection time domain fitting analysis. The unsuppressed water signal was used as an internal concentration standard. Ten patients with acute middle cerebral artery infarction were studied within 28 hours of stroke onset and followed up for a period of up to 3 months.

Results
Significant changes were seen in the initial spectra from the infarct compared with the contralateral spectra. Lactate, a marker of anaerobic metabolism, was present within the infarct but not detected in the contralateral hemisphere.
N
-Acetyl aspartate, a neuronal marker, and total creatine were significantly reduced. The initial choline signal, arising from choline-containing compounds within the cell and cell membrane, remained unchanged in the infarct core compared with the contralateral hemisphere. Further reductions in
N
-acetyl aspartate and total creatine concentrations occurred within the first week. A fall in the lactate concentration was seen within the infarct core during the first 7 to 10 days. Similar reductions in the choline concentration were observed during this period.

Conclusions
The demonstration of the continuing loss of cerebral metabolites within an infarct region suggests that further cell loss occurs up to 10 days after infarction. The continuing loss of neurons may represent continued ischemic damage after middle cerebral artery infarction.
Acidemia and Brain pH During Prolonged Cardiopulmonary Resuscitation in Dogs
Authors: Eleff Scott M. , Sugimoto Hideyoshi , Shaffner D. Hal , Traystman Richard J. , Koehler Raymond C.
Published: June 2011

Background and Purpose
Cardiopulmonary resuscitation (CPR) generating low perfusion pressures and beginning immediately after cardiac arrest maintains cerebral ATP but not cerebral pH or arterial pH. We tested the hypothesis that preventing severe arterial acidemia prevents cerebral acidosis, whereas augmenting arterial acidemia augments cerebral acidosis.

Methods
In dogs anesthetized with pentobarbital and fentanyl, cerebral pH and ATP were measured with
31
P MR spectroscopy and blood flow was measured with radiolabeled microspheres. A pneumatically controlled vest was placed around the thorax, and chest compressions were begun immediately after electrically induced cardiac arrest. Cerebral perfusion pressure was maintained with epinephrine at 30 mm Hg for 90 minutes. The arterial acidemia observed during CPR was untreated in a control group, corrected to a pH of 7.3 with the use of sodium bicarbonate, or maintained below pH 6.5 with intravenous lactic acid after 14 minutes of CPR.

Results
At 10 minutes of CPR, cerebral ATP (99±1.5%, control), blood flow (35±3 mL/min per 100 g), O
2
consumption (4.0±0.2 mL/min per 100 g), and cerebral pH (7.05±.03) were unchanged from prearrest values (mean±SEM). After 10 minutes of CPR in the control group, cerebral pH progressively fell (6.43±0.10 at 90 minutes) in parallel with cerebral venous pH. In the bicarbonate group cerebral pH was maintained higher (6.91±0.08). Cerebral blood flow, O
2
consumption, and ATP were sustained near prearrest values in both groups. In the lactate group, however, the rate of decrease of cerebral pH was augmented (6.47±0.06 by 30 minutes), and cerebral blood flow and metabolism were significantly reduced.

Conclusions
Cerebral pH decreased in parallel with blood pH when resuscitation was started immediately upon arrest even when cerebral O
2
consumption and blood flow were near normal. Although cerebral metabolism was near normal during the first hour of CPR, systemic bicarbonate administration ameliorated the cerebral acidosis. This finding indicates that the blood-brain pH gradient is important at the subnormal cerebral perfusion pressures seen in CPR.
Angioplasty Reduces Pharmacologically Mediated Vasoconstriction in Rabbit Carotid Arteries With and Without Vasospasm
Authors: Macdonald R. Loch , Zhang John , Han Hongshik
Published: June 2011

Background and Purpose
We tested the hypothesis that vasospastic arteries do not reconstrict after angioplasty because angioplasty decreases smooth muscle contractility.

Methods
Twenty-four rabbits had carotid angiography and placement of silicone elastomer sheaths around both carotid arteries in the neck. Sheaths were empty (control groups) or filled with clotted blood (vasospasm groups). Angiography was repeated 2 days later, and one carotid artery was dilated with a balloon catheter. Animals were killed 1, 5, or 28 days after angioplasty, and the carotid arteries were studied pharmacologically under isometric tension.

Results
Before angioplasty, there was significant vasospasm in the vasospasm groups but not in the control groups (
P
<.05, ANOVA). Angioplasty produced significant, long-lasting dilation of arteries in the vasospasm groups. One and 5 days after angioplasty, arteries from control and vasospasm groups that had angioplasty had significantly reduced contractions to serotonin, KCl, and caffeine compared with arteries not subjected to angioplasty. Twenty-eight days after angioplasty, contractions were reduced in arteries subjected to vasospasm compared with controls, but there were no differences between arteries with or without angioplasty. At all times after angioplasty, vasospasm significantly decreased acetylcholine-induced relaxations of arteries contracted with serotonin. Relaxations were further decreased by angioplasty in the vasospasm group 1 day after angioplasty. Arterial wall compliance was significantly decreased in the vasospasm and control groups at all times after angioplasty, although there were no significant differences between arteries with and without angioplasty.

Conclusions
These results suggest that arteries do not reconstrict after angioplasty because angioplasty decreases smooth muscle contractility. There was no evidence that angioplasty disrupted the arterial wall matrix, as judged by the lack of increase in arterial wall compliance after angioplasty.
Cerebral Edema After Temporary and Permanent Middle Cerebral Artery Occlusion in the Rat
Authors: Slivka Andrew , Murphy Eric , Horrocks Lloyd
Published: June 2011

Background and Purpose
The potential of thrombolytic agents to improve outcome after ischemic stroke could be negated if recanalization of an occluded artery exacerbates cerebral edema. We examined whether infarctions associated with reperfusion have more edema than those without reperfusion and whether the time course for the development of cerebral edema varied with and without reperfusion.

Methods
Infarct volumes were measured 24 hours after permanent and 1, 2, and 3 hours of temporary right middle cerebral artery (MCA) occlusion in spontaneously hypertensive rats. Hemispheric volume, water, sodium, and potassium were measured 3, 6, 12, 24, 36, and 48 hours after permanent and 3 hours of temporary MCA occlusion and also determined 24 hours after permanent and 2 and 3 hours of temporary MCA occlusion.

Results
Minimal tissue damage occurred after 1 hour of temporary ischemia. Infarct sizes were similar after permanent and 3 hours of temporary MCA occlusion and significantly greater than after 2 hours of temporary ischemia. Hemispheric volume, water, and sodium from the infarcted right hemisphere were significantly greater than those from the left hemisphere beginning 6 hours after MCA occlusion and continuing for 48 hours, with a peak at 24 hours. Right hemispheric water measured 24 hours after 2 hours of temporary ischemia was significantly less than after permanent or 3 hours of temporary ischemia.

Conclusions
This study demonstrates that cerebral edema after focal stroke is related to infarct size and is independent of reperfusion status. The results suggest that exacerbation of cerebral edema will not occur after thrombolytic treatment or spontaneous recanalization of occluded cerebral vessels.
Measurement of Instrumental Activities of Daily Living in Stroke
Authors: Chong Dennis Khin-Heung
Published: June 2011

Background
Functional assessment in stroke patients is critical in both clinical practice and outcome studies. Ability in the areas relating to instrumental activities of daily living (IADL) that require increased interaction with the environment, whether household or community, appears to be a prerequisite for independent living in the community. The majority of the research in this area has been in the geriatric population. A literature review was undertaken to answer the following questions: What is a working definition of IADL? What are the criteria that determine inclusion with specific applicability in the stroke population? What are the reliability and validity of available measures in the stroke population? What is the relevance of IADL to functional outcome?

Summary of Review
The findings at this time indicate that there is no consensus for a clear definition of IADL. The terminology used includes the original IADL as described by Lawton and Brody, extended ADL, social ADL, and advanced ADL. Four scales that were designed primarily for use in the stroke population were identified: the Nottingham Extended ADL (a self-report scale), the Hamrin Activity Index and the Frenchay Activities Index (both based on patient interviews), and the Household section of the Rivermead ADL Assessment (a performance index).

Conclusions
There is some published evidence concerning the validity, reliability, utility, sensitivity, or hierarchical nature of these indexes, and further testing is needed. The items in each index, however, have inherent relevance with potential for use in future clinical research.
Stroke Incidence and 30-Day Case-Fatality Rates in Novosibirsk, Russia, 1982 Through 1992
Authors: Feigin Valery L. , Wiebers David O. , Whisnant Jack P. , O’Fallon W. Michael
Published: June 2011

Background and Purpose
The present study was conducted to investigate the incidence of stroke and 30-day case-fatality rates for stroke in a defined Russian population.

Methods
This is a population-based study that was established in 1982. All residents of an administratively defined and typical district of Novosibirsk (approximately 150 000 subjects) who had an incident (first-ever) stroke from January 1, 1982, through December 31, 1992, were registered.

Results
During an 11-year study period, 3406 incident stroke patients were registered, for an overall crude average annual incidence rate of 202/100 000 population. The rates were higher with increasing age and were significantly higher for men than for women. The age- and sex-adjusted annual incidence rate of stroke declined from 271/100 000 in 1982 to 232/100 000 in 1992. Slowing of the decline in stroke incidence was observed after 1988, and stroke incidence increased slightly in 1992. No significant differences in 30-day stroke case-fatality rates were noted from 1982 through 1992, but a slight trend toward decreasing rates was observed after 1988. There was no major change in patient age at stroke onset.

Conclusions
Stroke incidence rates in Novosibirsk are among the highest in the world. We observed a decline in stroke incidence but little change in 30-day case-fatality rates in Novosibirsk from 1982 through 1992.
Classification of Walking Handicap in the Stroke Population
Authors: Perry Jacquelin , Garrett Mary , Gronley JoAnne K. , Mulroy Sara J.
Published: June 2011

Background and Purpose
The limited walking ability that follows a stroke restricts the patient’s independent mobility about the home and community, a significant social handicap. To improve the in-hospital prediction of functional outcome, the relationships between impairment, disability, and handicap were assessed with clinical measures in 147 stroke patients.

Methods
The patients’ level of functional walking ability at home and in the community was assigned by expert clinicians to one of the six categories of a modified Hoffer Functional Ambulation scale at least 3 months after discharge. A 19-item questionnaire was further used to assess current customary mobility of the subjects. Functional muscle strength and proprioception were tested, and walking velocity was measured.

Results
The significant indicators of impairment, upright motor control knee flexion and extension strength, differentiated household from community ambulators. The addition of velocity improved the functional prediction. Proprioception was clinically normal in all walkers. The validity of the criteria for the six levels of walking handicap was confirmed statistically. Stepwise discriminant analysis reduced the ambulation activities on the questionnaire from 19 to 7. Redefinition of the criteria for patient classification using the coefficients and constants of the seven critical functions improved the prediction of patient walking ability to 84%.

Conclusions
The results of this study offer a quantitative method of relating the social disadvantage of stroke patients to the impairment and disability sustained. The measurement of therapeutic outcome in relation to the social advantage for the patient would allow more efficient standardization of treatment and services.
Venous Transcranial Doppler Ultrasound Monitoring in Acute Dural Sinus Thrombosis
Authors: Valdueza José Manuel , Schultz Matthias , Harms Lutz , Einhäupl Karl Max
Published: June 2011

Background and Purpose
We sought to establish the efficacy of the Doppler technique in the evaluation of the intracranial venous system and to assess its usefulness in the monitoring of venous collateral pathways in superior sagittal sinus thrombosis.

Methods
Venous Doppler ultrasound was performed with a range-gated 2-MHz transducer in 10 healthy volunteers and in two patients with superior sagittal sinus thrombosis confirmed by cerebral angiography.

Results
In normal control subjects, a venous signal was found at a depth ranging from 40 to 72 mm, which was considered to correspond to the deep middle cerebral vein and the basal vein of Rosenthal. Mean blood flow velocities ranged from 9 to 20 cm/s. In both patients with superior sagittal sinus thrombosis, Doppler studies detected elevated mean blood flow velocities (146 and 33 cm/s), which normalized after 16 weeks and 1 week, respectively.

Conclusions
Venous transcranial Doppler ultrasonography provides a reliable, noninvasive, and rapid technique for intracranial venous examination. It was performed without difficulty in young healthy volunteers, and it can be applied as a monitoring tool in the evaluation of collateral venous flow in superior sagittal sinus thrombosis.
The Significance of Cerebral White Matter Abnormalities 100 Years After Binswanger’s Report
Authors: Pantoni Leonardo , Garcia Julio H.
Published: June 2011

Background
Changes in the cerebral hemispheric white matter are detected with increasing frequency by CT and MRI among persons older than 60 years. The pathogenesis, clinical significance, and morphological substrate of these changes are incompletely understood. Patients who have such neuroimaging abnormalities are sometimes diagnosed with “Binswanger’s disease,” an eponym that has generated much confusion because of its imprecise meaning. The objectives of this study were to determine whether the term Binswanger’s disease merits acceptance as a distinct clinicopathologic entity, to deduce the clinical significance of these white matter abnormalities from the analysis of appropriate publications, and to evaluate studies that correlate in vivo changes in the cerebral white matter with pathological features.

Summary of Review
We evaluated Binswanger’s original case description and, after conducting a Medline search, reviewed more than 160 publications, mostly in the English language, on the subject of white matter abnormalities detectable by currently used neuroimaging methods (ie, leukoaraiosis).

Conclusions
Binswanger’s original description appears to be insufficient for the purpose of defining a new nosological entity. After evaluating the vaguely outlined pathological correlates described in a few of these subcortical cerebral leukoencephalopathies, we conclude that the clinical significance of leukoaraiosis remains incompletely defined. However, its frequency increases with age independent of other risk factors, and in nondemented subjects leukoaraiosis is associated with deficits in selected cognitive functions. Moreover, leukoaraiosis correlates with an increased risk for the subsequent development of strokes. We make specific suggestions for future studies that may help to clarify this topic.
Newly Diagnosed Atrial Fibrillation and Acute Stroke
Authors: Lin Huey-Juan , Wolf Philip A. , Benjamin Emelia J. , Belanger Albert J. , D’Agostino Ralph B.
Published: June 2011

Background and Purpose
When atrial fibrillation (AF) is first documented at the time of onset of acute stroke, it is difficult to establish a temporal relationship between AF and stroke. Did AF precede and precipitate the stroke, or did the arrhythmia appear as a result of stroke? Following the course of the newly diagnosed AF may help to clarify this relationship.

Methods
The Framingham Study cohort of 5070 members, aged 30 to 62 years and free of cardiovascular disease at entry, has been under surveillance for the development of cardiovascular disease, including stroke. We followed the course of AF, which was documented for the first time on or soon after hospital admission for stroke.

Results
During 38 years of follow-up, 115 of 656 initial stroke events occurred in association with AF: 89 had previously documented AF, 21 had AF discovered for the first time on admission for the stroke, and 5 were admitted with sinus rhythm but developed AF after admission. Of the 21 subjects with AF diagnosed on admission, in 12 (57%) AF persisted thereafter (chronic AF). Among the other 9 persons presenting with nonpersistent AF, paroxysms recurred in 3 (14%) and became chronic AF in 4 (19%). AF was transient and did not recur in only 2 persons (10%). Of the 5 subjects who developed AF after admission, AF was sustained from the initial diagnosis in 2 and recurred in paroxysms or became established as chronic in 3.

Conclusions
Ninety-two percent (24/26) of subjects presenting with newly discovered AF at the time of acute stroke continued to have this rhythm disturbance in a chronic or paroxysmal form. In only 2 subjects (8%) was the arrhythmia short-lived and nonrecurrent. These follow-up data suggest that in most instances AF was probably the precipitant rather than the consequence of stroke.
Transcranial Doppler–Detected Microemboli in Patients With Acute Stroke
Authors: Tong David C. , Albers Gregory W.
Published: June 2011

Background and Purpose
Transcranial Doppler sonography (TCD) has been used to detect microembolic signals in a variety of clinical situations. We studied the prevalence of TCD-detected microemboli in 38 acute stroke patients.

Methods
Consecutive patients with acute anterior circulation stroke were stratified into high-risk (group 1), medium-risk (group 2), and low-risk (group 3) groups based on their risk factors for cerebral embolism.

Results
Microemboli were detected in 11% of patients. They were present in 17% of group 1, 10% of group 2, and 0% of group 3 patients. Emboli were present in patients with mechanical prosthetic valves, carotid stenosis (>70%), and mitral valve strands with a patent foramen ovale. Patients with microemboli more frequently had a history of cerebral ischemia compared with patients without microemboli (
P
<.05). They also more frequently had recent (<3 months) symptoms compared with patients without microemboli (
P
<.05). In patients with a cardiac source of embolization, the number of microemboli detected was directly proportional to the acuity of previous symptoms.

Conclusions
These data suggest that TCD-detected microemboli are associated with an increased prevalence of prior cerebrovascular ischemia. The presence of TCD-detected microemboli could be a risk factor for cerebrovascular ischemia.
Hemorheological and Hemodynamic Analysis of Hypervolemic Hemodilution Therapy for Cerebral Vasospasm After Aneurysmal Subarachnoid Hemorrhage
Authors: Mori Kentaro , Arai Hajime , Nakajima Keiji , Tajima Atsushi , Maeda Minoru
Published: June 2011

Background and Purpose
Hypervolemic hemodilution therapy is effective for treating neurological deficits due to cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH). We monitored various hemorheological and hemodynamic parameters to assess the effects of hypervolemic hemodilution therapy in SAH patients with cerebral vasospasm.

Methods
Ninety-eight patients who underwent early craniotomy for aneurysm clipping surgery after SAH were studied. Fifty-one patients (52.0%) developed symptomatic vasospasm. The hematocrit level and red blood cell aggregability were measured daily from day 1 to day 14, whereas the circulating blood volume and cerebral blood flow were measured periodically. Cardiac output and pulmonary capillary wedge pressure were also measured using a Swan-Ganz catheter.

Results
The hematocrit level was decreased significantly to 29% to 32% by hypervolemic hemodilution therapy. Red blood cell aggregability increased until day 6 but was significantly reduced by therapy. Hypovolemia tended to develop after SAH. However, patients receiving hypervolemic hemodilution therapy became normovolemic to hypervolemic, with a significant increase of cardiac output and pulmonary capillary wedge pressure. At the onset of vasospasm, cerebral blood flow was significantly lower on the operated side than on the contralateral side, and it increased on both sides with therapy.

Conclusions
Patients with SAH develop hypovolemia, hemodynamic depression, and increased red blood cell aggregability. Hypervolemic hemodilution therapy decreases hematocrit level and red cell aggregability while increasing cardiac output. Improvement of hemorheological and hemodynamic parameters by this therapy can reverse neurological deterioration due to cerebral vasospasm.
Is Marfan Syndrome Associated With Symptomatic Intracranial Aneurysms?
Authors: van den Berg J.S.P. , Limburg M. , Hennekam R.C.M.
Published: June 2011

Background and Purpose
Marfan syndrome is a heritable disorder of connective tissue caused by a deficiency of the glycoprotein fibrillin. In several publications and neurological textbooks, a relationship between Marfan syndrome and intracranial aneurysms has been assumed.

Methods
The records of 135 patients classified as having Marfan syndrome who visited the Amsterdam Marfan clinic or were admitted to the departments of neurology and neurosurgery and the records of all patients with a subarachnoid hemorrhage or intracranial aneurysm who visited or were admitted to the departments of neurology and neurosurgery between January 1, 1982, and January 1, 1994, were retrieved. The literature was reviewed regarding Marfan syndrome and intracranial aneurysms.

Results
No patient visiting the Marfan clinic had a symptomatic intracranial aneurysm. No patient with Marfan syndrome had been admitted with a ruptured intracranial aneurysm at the departments of neurology or neurosurgery in this period, while during that period 826 patients with symptomatic intracranial aneurysms had been admitted. During follow-up of 129 of the 135 patients with Marfan syndrome (2850 retrospective patient observation years and 581 prospective patient observation years), none presented a symptomatic intracranial aneurysm. The suggested relationship between Marfan syndrome and intracranial aneurysms is based mainly on 10 case reports. However, the diagnosis of Marfan syndrome is doubtful in several of these reports. Several large studies of patients with Marfan syndrome did not mention a ruptured intracranial aneurysm as a clinical manifestation.

Conclusions
We conclude that there is insufficient evidence to presume a relationship between symptomatic intracranial aneurysms and Marfan syndrome on the basis of currently available data.
Risk Factors and Segment-Specific Carotid Arterial Enlargement in the Atherosclerosis Risk in Communities (ARIC) Cohort
Authors: Crouse John R. , Goldbourt Uri , Evans Greg , Pinsky Joan , Sharrett A. Richey , Sorlie Paul , Riley Ward , Heiss Gerardo
Published: June 2011

Background and Purpose
B-mode ultrasound imaging affords the opportunity to quantify both intimal-medial thickness (IMT) and lumen diameter of extracranial carotid arteries in ambulatory populations. Since the relation of IMT to lumen diameter may be complex, we asked whether cardiovascular disease risk factors (previously shown to be associated with greater arterial IMT) are related to smaller lumen diameters.

Methods
We used B-mode ultrasound to quantify lumen diameter, interadventitial diameter, and IMT of the extracranial carotid arteries and assessed the relationship of these measures to body mass index, smoking, low-density lipoprotein (LDL) and high-density lipoprotein cholesterol, hypertension, and diabetes in 6088 male and 7493 female participants in the Atherosclerosis Risk in Communities (ARIC) cohort.

Results
Smoking, hypertension, and LDL cholesterol were consistently related to greater IMT in the common and internal carotid arteries of men and women, as has been previously reported. In the internal carotid artery, smoking, hypertension, and LDL cholesterol were consistently related to smaller lumens. In the common carotid artery, body mass index, smoking, and hypertension were related to significantly larger, and LDL cholesterol to smaller, lumens. Thus, only LDL cholesterol was consistently associated with smaller lumens in both the common and internal carotid arteries.

Conclusions
Risk factors relate positively to IMT in both the common and internal carotid arteries and inversely with lumen diameter in the internal carotid artery, in parallel with their relation to clinical events. However, their association with lumen diameters of the common carotid artery in population-based samples is more complex, and in some cases adverse levels of risk factors may be associated with larger lumens.
Coagulation Studies, Factor V Leiden, and Anticardiolipin Antibodies in 40 Cases of Cerebral Venous Thrombosis
Authors: Deschiens Marie-Anne , Conard Jacqueline , Horellou Marie Hélène , Ameri Alain , Preter Maurice , Chedru François , Samama Meyer Michel , Bousser Marie-Germaine
Published: June 2011

Background and Purpose
Cerebral venous thrombosis (CVT) is an infrequent condition with a large variety of causes. However, in 20% to 35% of cases, no cause is found. We studied coagulation parameters, including activated protein C resistance associated with factor V gene mutation (factor V Leiden) and anticardiolipin antibodies, in a large series of patients with CVT with or without identified cause or risk factor.

Methods
Forty patients (30 women and 10 men) aged 19 to 71 years (mean age, 36.2 years) with CVT diagnosed by angiography and/or MRI were studied 1 to 18 years after thrombosis. No known cause was found in 10 idiopathic cases. Coagulation studies included the following tests: fibrinogen, antithrombin, protein C, protein S, plasminogen, anticardiolipin antibodies, activated protein C resistance, and factor V Leiden.

Results
Six cases of thrombophilia (15%) were found: 1 protein C deficiency, 1 protein S deficiency, and 4 activated protein C resistance with heterozygous factor V Leiden mutation (10%). Only 1 case (protein S deficiency) was found in the group of 10 patients with idiopathic CVT. In the other 5, there was another cause or risk factor. Three patients (8%) had increased anticardiolipin antibodies: 1 with systemic lupus and 2 with primary antiphospholipid syndrome; 2 of these 3 patients also had factor V Leiden mutation.

Conclusions
Although present in a number of CVT cases, acquired (anticardiolipin) or congenital varieties of thrombophilia (factor V Leiden being the most frequent) are almost invariably associated with other predisposing factors. This suggests that (1) these abnormalities should be looked for in patients with CVT, whether a cause is found or not, and (2) their presence should not deter the search for other potential causes. The detection of such abnormalities has major practical consequences on the long-term management of patients to prevent further thrombotic episodes.
Dynamics of Polymorphonuclear Leukocyte Accumulation in Acute Cerebral Infarction and Their Correlation With Brain Tissue Damage
Authors: Akopov S.E. , Simonian N.A. , Grigorian G.S.
Published: June 2011

Background and Purpose
This study was performed to study the dynamics of polymorphonuclear leukocyte (PMNL) accumulation in human cerebral infarction and its association with neurological outcome and brain lesion.

Methods
A total of 88 patients diagnosed as having hemispheric ischemic stroke were examined. PMNL accumulation was studied using technetium-99m hexamethylpropyleneamine oxime (
99m
Tc HMPAO)−labeled leukocyte brain single-photon emission computed tomography (SPECT). Volume of brain infarction was evaluated by CT scan. The Mathew Scale was used for neurological assessment. Dynamics of PMNL accumulation was studied at 3 to 6, 6 to 12, and 12 to 24 hours and 6 to 9, 28 to 30, and 90 days after stroke onset. In parallel, at admission, at 6 to 9 days, and at 28 to 30 days neurological outcome and infarction volume were evaluated.

Results
Generally, PMNL accumulation progressively increased during 6 to 24 hours after stroke, remained at a high level up to 6 to 9 days and then declined. With the use of cluster analysis, all patients were subdivided into three groups: patients with severe PMNL accumulation that dramatically increased within 12 hours after stroke onset and persisted even at 28 to 30 days (group A); those with moderate PMNL accumulation that significantly decreased at 30 days (group B); and those with mild PMNL accumulation that decreased at 6 to 9 days (group C). Baseline neurological deficit and brain tissue damage at admission appear to be at a similar level for all groups of patients. In dynamics, however, in patients with severe PMNL accumulation, neurological outcome was worse and infarction volume larger than in patients with less marked PMNL accumulation.

Conclusions
The present clinical study confirms that PMNLs intensively accumulate in the regions of cerebral infarction. The present study revealed that this accumulation correlated with the severity of the brain tissue damage and poor neurological outcome.
Ethnic Differences in Carotid Wall Thickness
Authors: D'Agostino Ralph B. , Burke Gregory , O'Leary Dan , Rewers Marian , Selby Joseph , Savage Peter J. , Saad Mohammed F. , Bergman Richard N. , Howard George , Wagenknecht Lynne , Haffner Steven M.
Published: June 2011

Background and Purpose
Ethnic differences in cardiovascular disease (CVD) morbidity and mortality have been observed in US adults. However, little data exist on differences in indices of preclinical atherosclerosis such as carotid wall intima-media thickness (IMT) for US non-Hispanic whites, Hispanics, and blacks. This study was undertaken to determine whether there were ethnic differences in carotid wall IMT.

Methods
Internal carotid artery (ICA) IMT and common carotid artery (CCA) IMT, indices of atherosclerosis, were assessed with the use of B-mode ultrasound in 1020 nondiabetic participants in the Insulin Resistance Atherosclerosis Study, a multicenter study designed to examine the association between insulin resistance and carotid atherosclerosis. The study included 281 blacks, 329 Hispanics, and 410 non-Hispanic whites aged 40 to 69 years.

Results
Blacks had significantly greater CCA IMT than non-Hispanic whites (865 versus 808 μm); this remained significant after adjustment for major CVD risk factors and insulin sensitivity (864 versus 823 μm). There were no significant differences in ICA IMT between blacks and non-Hispanic whites. Hispanics had significantly lesser CCA IMT than non-Hispanic whites (749 versus 776 μm), and these differences remained significant after adjustment for traditional cardiovascular risk factors and insulin sensitivity (750 versus 778 μm). There were no significant differences in ICA IMT between non-Hispanic whites and Hispanics.

Conclusions
We conclude that ethnic differences exist in CCA but not in ICA IMT in nondiabetic subjects. These differences in IMT, which are indicators of atherosclerosis, are a noninvasive measure that is consistent with some of the data on clinical end points. These differences may be associated with the observed differences in CVD morbidity and mortality among major ethnic groups in the United States.
Recurrence of Cervical Artery Dissection
Authors: Bassetti C. , Carruzzo A. , Sturzenegger M. , Tuncdogan E.
Published: June 2011

Background and Purpose
Spontaneous cervical artery dissection (SCAD) is a common cause of stroke in the young; however, its recurrence has been rarely studied. Recurrent SCAD at the level of the previously dissected vessel has been reported in only six patients.

Methods
We prospectively evaluated and followed a series of 81 patients seen in our center with carotid (n=66) or vertebral (n=15) artery dissection, in whom the diagnosis was confirmed by angiography, MRI, or both. Repeated clinical and ultrasound examinations were performed in all patients during a mean follow-up of 34 months (range, 12 to 57 months).

Results
Three patients died of the consequences of stroke, and four patients were unavailable for follow-up. Three of the remaining 74 patients (4%) had a recurrent carotid dissection while under prophylaxis with aspirin (n=2) or anticoagulation (n=1). None of the patients had a recurrent vertebral dissection. Recurrent carotid dissection occurred 16 months to 4 years after the first episode and presented with acute head and neck pain (n=2) and hemispheric transient ischemic attack (n=1). In one patient recurrence was documented by Doppler and MRI at the level of the first dissection.

Conclusions
We confirm that recurrence of SCAD is uncommon and usually represents a benign condition. Delayed recurrence seems to be more common than previously suggested and can occur at the level of the previously dissected vessel.
High-Intensity Transient Signals in Patients With Cerebral Ischemia
Authors: Daffertshofer Michael , Ries Stefan , Schminke Ulf , Hennerici Michael
Published: June 2011

Background and Purpose
This study investigated the diagnostic relevance of transcranial Doppler monitoring for the detection of high-intensity transient signals (HITS) in patients with recent cerebral ischemic events of various origins.

Methods
We prospectively performed bilateral transcranial Doppler monitoring (mean, 48±8 minutes) from both middle cerebral arteries in 280 patients with an acute (<4 weeks) cerebral ischemic event in the middle cerebral artery territory and in 118 asymptomatic control subjects. HITS were analyzed according to a standardized protocol.

Results
Symptomatic patients had a significantly (
P<
.001) higher rate (9.3%) of HITS than asymptomatic control subjects (1.7%). Patients with reversible ischemia (4.2%) and patients with suspected small-vessel syndromes (4.5%) had lower rates of HITS (
P<
.05) than those with large-vessel territory strokes (14.2%). Brain imaging (CT/MRI) results corresponded with this observation: the occurrence of HITS was significantly higher (
P<
.001) in patients with a pattern of large-vessel territorial brain infarction (19.0%) than in those with lacunar lesions (0%) or unidentified ischemic lesions (3.4%). Patients with identified sources of potential embolism (12.9%) had HITS (
P<
.001) more frequently than those without (0%). Patients with cardiac sources of embolism (excluding artificial heart valves) showed fewer HITS (6.2%) than patients with vascular sources (17.1%).

Conclusions
The results indicate that HITS occur predominantly in patients with large-vessel territory stroke patterns and persisting deficits that are most likely due to artery-to-artery or cardiogenic embolism. In contrast, patients with small-vessel disease and rapid recovery only occasionally present with HITS. Thus, the detection of HITS may substantially support the classification of the individual pathogenesis of cerebral ischemia, particularly when multiple risk constellations for stroke coexist.
Protein Kinase C Has Two Different Major Roles in Lattice Compaction Enhanced by Cerebrospinal Fluid From Patients With Subarachnoid Hemorrhage
Authors: Shiota Tomomi , Bernanke David H. , Parent Andrew D. , Hasui Kouichi
Published: June 2011

Background and Purpose
Compaction of extracellular matrix (ECM) lattices by cultured fibroblasts was accelerated by cerebrospinal fluid (CSF) from patients with subarachnoid hemorrhage (SAH). The rate of acceleration was significantly related to the clinical grade of vasospasm. However, the mechanism remains unclear. Evidence exists for an important role in cerebral vasospasm for protein kinase C (PKC). The purpose of this study was to help clarify whether PKC has a role in contraction of the ECM.

Methods
We studied the effects of a myristoylated PKC peptide inhibitor (Myr-Arg-Phe-Ala-Arg-Lys-Gly-Ala-Leu-Arg-Gln-Lys-Asn-Val) (PKC peptide inhibitor), (5-isoquinolinesulfonyl)homopiperazine (HA-1077) (inhibitor of protein kinase A, myosin light-chain kinase, and protein kinase G), 7-deacetyl-6-(
N
-acetylglycyl)-forskolin (forskolin) (adenyl cyclase activator), and diacylglycerol-lactone (DAG-lactone) (PKC activator) on fibroblast-populated collagen lattice compaction with or without CSF from SAH patients. Four sets of fibroblasts were used: three explanted from skin and one from cerebral artery.

Results
Moderate and high concentrations of PKC peptide inhibitor inhibited lattice compaction with or without acceleration by CSF. Low concentration of PKC peptide inhibitor enhanced acceleration by CSF but had no effects without CSF. HA-1077 could not inhibit lattice compaction. Forskolin inhibited compaction. DAG-lactone accelerated compaction in early phases.

Conclusions
In the mechanism of acceleration of contraction of ECM under the influence of CSF, PKC seems to have two different roles. Protein kinase A and myosin light-chain kinase apparently play more minor roles than PKC in the mechanism, but no evidence was found of a role for protein kinase G activation in matrix compaction.
Age-Period-Cohort Effects on Stroke Mortality in Sweden 1969-1993 and Forecasts Up to the Year 2003
Authors: Peltonen Markku , Asplund Kjell
Published: June 2011

Background and Purpose
Variations in stroke mortality could be explained by changes in factors that act around the time of death (period effect) and by risk factors that are present in early life (cohort effect). The aim of this study was to analyze mortality rates for stroke in Sweden during the period 1969 through 1993 and to predict mortality trends until the year 2003, taking into account age, cohort, and period effects.

Methods
Age-period-cohort models were used to analyze stroke mortality in Sweden between 1969 and 1993 and to predict age-specific death rates and total number of deaths for the periods 1994 through 1998 and 1999 through 2003.

Results
Mortality rates in the age group 25 to 89 years decreased from 203 to 143 per 100 000 for men and from 185 to 113 per 100 000 for women over the study period (average annual decrease of 1.3% for men and 1.9% for women). The decline was present in all age groups. The full age-period-cohort model provided an acceptable fit in both sexes. Predictions based on these models gave a mortality rate of 122 and 92 per 100 000 for the period 1999-2003 in men and women, respectively. Despite an aging and increasing population, the total number of stroke deaths in Sweden is predicted to decline by approximately 10% in both men and women from 1989-1993 to 1999-2003.

Conclusions
Both factors, cohort and calendar period, contain relevant information to explain the decline in stroke mortality trends in Sweden. Predictions indicate that the decline of both age-specific and total mortality will continue.
Carotid Artery Intima-Media Thickness in Elderly Patients With NIDDM and in Nondiabetic Subjects
Authors: Niskanen Leo , Rauramaa Rainer , Miettinen Heikki , Haffner Steven M. , Mercuri Michele , Uusitupa Matti
Published: June 2011

Background and Purpose
The risk of atherosclerotic vascular disease is increased both in subjects with non–insulin-dependent diabetes mellitus (NIDDM) and in those with impaired glucose tolerance compared with nondiabetic subjects. Although classic cardiovascular risk factors are operative in subjects with NIDDM, other factors closely related to insulin resistance syndrome such as diabetic dyslipidemia and hyperglycemia itself may contribute to an excessive cardiovascular disease risk in subjects with NIDDM. The purpose of this study was to investigate the carotid intimal-medial thicknesses (IMTs) and their determinants in elderly patients with NIDDM and in control subjects.

Methods
We investigated the common carotid and carotid bifurcation IMTs and their determinants in groups of elderly patients (n=84, age 67.2±0.6 years) with NIDDM and in 119 control subjects (21 with impaired and 98 with normal glucose tolerance; ages 67.5±1.0 and 65.1±0.6 years, respectively).

Results
Common carotid and carotid bifurcation IMTs were greater in the NIDDM group than in control subjects (
P
<.05 to .01). In NIDDM patients, the mean carotid IMT correlated with postglucose 1-hour plasma insulin (
r
=.305,
P
=.01, adjusted for age and sex), serum LDL triglyceride (
r
=.237,
P
<.05), and apolipoprotein B concentrations (
r
=.263,
P
<.05). Fasting plasma immunoreactive insulin, proinsulin, or specific insulin levels were not significantly associated with carotid IMT. Both diabetic status (
P
<.05) and the presence of clinical macrovascular disease (
P
<.01) contributed independently to carotid IMT.

Conclusions
Carotid IMT was greater in NIDDM patients than in control subjects. The main determinants of IMT in NIDDM patients were related to both postglucose insulin levels and abnormal lipoprotein profiles characteristic of NIDDM and insulin resistance syndrome. Treatment of these factors is likely to reduce the atherosclerotic burden in NIDDM.
Compensatory Increase in Common Carotid Artery Diameter
Authors: Polak Joseph F. , Kronmal Richard A. , Tell Grethe S. , O'Leary Daniel H. , Savage Peter J. , Gardin Julius M. , Rutan Gale H. , Borhani Nemat O.
Published: June 2011

Background and Purpose
Common carotid artery (CCA) diameter is thought to increase as a consequence of hypertension and may increase as the thickness of the arterial wall increases. The purpose of this study was to determine CCA dimensions and correlate them with clinical features.

Methods
We performed a cross-sectional, community-based study of adults 65 years of age and older, measuring inner and outer diameter of the CCA in vivo with carotid sonography. Findings were correlated against risk factors for atherosclerosis, CCA intima-media thickness (IMT), and echocardiographically determined left ventricular (LV) mass.

Results
Independent variables showing strong positive associations with outer and inner CCA diameter included age, male sex, height, weight, and systolic blood pressure. As an independent variable, LV mass (
r
=.40 and
r
=.37, respectively;
P
<.00001) had a strong positive relation to inner and outer CCA diameters. The relationship between diameter and IMT was different. In a model that controlled for age, sex, and estimated LV mass, an increase of 1 mm in CCA IMT corresponded to a 1.9-mm increase in the outer diameter of the artery (
P
<.00001) but was not significantly related to the inner diameter (slope=+0.07 mm;
P
=.26).

Conclusions
Increase in the outer diameter of the CCA is associated with subject size, sex, age, echocardiographically estimated LV mass, and CCA IMT. Increases in internal diameter of the CCA have similar relationships but are not related to IMT. This supports the hypothesis that the human CCA dilates as the thickness of the artery wall increases.