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PubMed1998

Cytokines and cell adhesion molecules in cerebral ischemia: experimental bases and therapeutic perspectives.

The possibility of reopening an occluded cerebral artery by means of thrombolysis has renewed interest in a number of the several mechanisms that are active during acute cerebral ischemia. Over recent years, it has become apparent that leukocytes play a central role not only during the healing stage of brain infarction but also during the early phases of cerebral ischemia, when it is postulated that these cells produce harmful effects, particularly in the presence of reperfusion. This review is based on the critical analysis of more than 150 publications dealing with the role of leukocytes and some inflammatory mediators (cytokines, chemokines, and adhesion molecules) in cerebral ischemia. Animal studies indicate that leukocyte involvement is promoted by a variety of inflammatory molecules produced immediately after the onset of cerebral ischemia. Considerable experimental evidence suggests that these mediators play a key role in the progression from ischemia to irreversible injury (ie, cellular death and necrosis). However, the precise role of each molecule alone remains to be further elucidated as well as in relation to the complex network existing among different mediators. Progress in our understanding of the inflammatory mechanisms operating in cerebral ischemia has enabled the testing of new compounds with promising results in animals; in contrast, one recent controlled trial of an anti-leukocyte molecule in acute stroke patients showed negative results. This discrepancy may derive in part from our incomplete understanding of the complexity of the inflammatory mechanisms involved in cerebral ischemia. Our analysis suggests that until sufficient knowledge of the underlying disease mechanisms is acquired, more care should be taken when testing new and potentially efficacious drugs in stroke patients.

Animals↗
PubMed2005

Carotid intima-media thickness, plaques, and Framingham risk score as independent determinants of stroke risk.

BACKGROUND AND PURPOSE: The Framingham stroke risk score (FSRS) and Framingham cardiovascular risk score (FCRS) estimate the individual absolute cardiovascular and stroke risks. Common carotid artery intima-media thickness (CCA-IMT) and carotid plaques (CPs) are markers of subclinical atherosclerosis and help in the early identification of presymptomatic individuals. The purpose of this study was to correlate Framingham risk score (FRS) with CCA-IMT and CPs and evaluate their respective contribution to stroke risk. METHODS: In 510 consecutive patients with brain infarction and 510 matched controls, we calculated the FSRS and FCRS for each individual and performed carotid ultrasonography. Mean CCA-IMT was measured off-line at a central core laboratory, and presence of CPs was assessed. RESULTS: FRS progressively increased according to tertiles of CCA-IMT (P for trend <0.0001). The part of the variances of FSRS and FCRS explained by CCA-IMT was respectively 11% and 20%. The relationships between CCA-IMT and FRS were significantly different between patients with or without CPs (P for interaction <0.005). With increasing CCA-IMT, the 10-year FRS gradually increased between 10% and 20% in the presence of CPs and between 5% and 20% in the absence of CPs. Multiple conditional logistic regression for matched sets showed that CCA-IMT, FCRS, and CPs were independently associated with stroke risk, with an odds ratio of 1.68 (1.25 to 2.26; P=0.0006), 2.16 (1.57 to 2.98; P<0.0001), and 2.73 (1.68 to 4.44; P<0.0001), respectively, meaning that each of them may be important for evaluation of the individual cardiovascular risk. CONCLUSIONS: CCA-IMT, CPs, and FRSs correlated well. The CCA-IMT value may help discriminate between subjects at low or high 10-year risk.

Adult↗
PubMed2003

Homocysteine and Alzheimer's disease.

BACKGROUND: A high circulating concentration of the amino acid homocysteine is an independent risk factor for stroke. Alzheimer's disease (AD) commonly co-occurs with stroke. Epidemiological studies found associations between hyperhomocysteinaemia and both histologically confirmed AD and disease progression and revealed that dementia in AD was associated with evidence of brain infarcts on autopsy. Thus, hyperhomocysteinaemia and AD could be linked by stroke or microvascular disease. However, given known relations between B-group-vitamin deficiency and both hyperhomocysteinaemia and neurological dysfunction, direct causal mechanisms are also plausible. RECENT DEVELOPMENTS: A recent prospective study (S Seshadri and colleagues N Engl J Med; 2002 346: 476-83) showed hyperhomocysteinaemia to be a strong, independent risk factor for dementia and AD. The researchers found a graded increase in risk of both outcomes with rising plasma concentration of homocysteine after multivariate control for putative risk factors for AD. In conjunction with demonstration of a fall in homocysteine concentrations in response to increasing B-group-vitamin status, these findings give hope that mental decline, or AD itself, could be prevented by dietary modification or food fortification. WHERE NEXT? 25% of dementia cases are attributed to stroke. The possibility that some of the other 75% might be prevented by the lowering of homocysteine concentrations greatly increases the hope of maintaining self-sufficiency into old age. If homocysteine lowering can reduce the incidence of dementia or AD, decreased incidence of these disorders may be seen in Canada and the USA, where government-mandated folate-fortification programmes are in effect. Future research should focus on early detection of AD and on the possibility that the disease itself, or its primary symptom, could be prevented by folate supplementation.

Alzheimer Disease↗
PubMed1990

Single-photon emission computed tomography and early death in acute ischemic stroke.

Single-photon emission computed tomography with thallium-201-labeled diethyldithiocarbamate was performed in 26 consecutive patients less than or equal to 24 hours after a supratentorial brain infarction. Computed tomography excluded other relevant pathology. Two observers assessed the initial regional cerebral blood flow deficit using a semiquantitative visual method. The size of the initial flow deficit correlated negatively with the Barthel Index score (performance of the activities of daily living) after 6 months but not with the motricity index score (a measure of severity of the hemiparesis) after 6 months. The initial flow deficit was strongly correlated with early death from tentorial herniation; all five patients with the largest initial flow deficits died less than or equal to 6 days after the stroke, but among the 21 patients with smaller initial flow deficits only one died early (p = 0.00018, Fisher's exact two-tailed test). Although depressed level of consciousness, conjugate gaze deviation, and severe hemiparesis were more prevalent in the group of six patients who died early, the differences in prevalence between this group and the 20 patients who survived were not significant. Single-photon emission computed tomography is a relatively simple method to semiquantitatively measure a blood flow disturbance immediately after its occurrence. The magnitude of this blood flow disturbance is strongly related to early death from tentorial herniation. Because of these properties, single-photon emission computed tomography to measure regional cerebral blood flow can be of great use in acute stroke research.

Acute Disease↗
PubMedDate not supplied

Cerebrospinal fluid and plasma concentration of soluble intercellular adhesion molecule 1, vascular cell adhesion molecule 1 and endothelial leukocyte adhesion molecule in patients with acute ischemic brain disease.

BACKGROUND: Leukocyte migration into the ischemic area is a complex process, controlled by adhesion molecules (AM) in leukocytes and endothelium, by migratory capacity of leukocytes and the presence of hemotaxic agents in the tissue. In this research it was supposed that in the blood and cerebrospinal fluid (CSF) of patients in the acute phase of ischemic brain disease (IBD) there were relevant changes in the concentration of soluble AM (sICAM-1, sVCAM-1 and sE-selectin), that could have been the indicators of the intensity of damaging processes in central nervous system (CNS). METHODS: The study included 45 IBD patients, 15 with transient ischemic attack (TIA), 15 with reversible ischemic attack (RIA), and 15 with brain infarction (BI), of both sexes, mean age 66 +/- 7. Control group consisted of 15 patients with radicular lesions of discal origin, subjected to diagnostic radiculography, without the signs of interruption in the passage of CSF. Changes of selected biochemical parameters were determined in all patients in frame 72 hours since the occurrence of an ischemic episode. Concentrations of soluble AM were determined in plasma and CSF by ELISA. Total number of leukocytes (TNL) in peripheral blood was determined by hematological analyzer. RESULTS: The results showed that during the first 72 hrs of IBD significant increases occurred in TNL and that the increase was progressive compared to the severeness of the disease. Significant increase of soluble AM concentration was shown in plasma of IBD patients. The increase was highest in BI, somewhat lower in RIA and the lowest in TIA patients compared to the control. In CSF concentrations of sICAM-1, sVCAM-1 and sE-selectin demonstrated similar increasing trend as in plasma. CONCLUSION: TNL, as well as the soluble AM concentrations in plasma and CSF, were increased during the acute IBD phase and progressive in relation to the severeness of the disease, so that they might have been the indicators of CNS inflammatory reaction intensity. Furthermore, the results indicated their role in IBD pathogenesis and offered the possibility of researching the application of antagonists and/or activity modulators of some of them in IBD therapy.

Acute Disease↗
PubMedDate not supplied

A rating system for prompt clinical diagnosis of ischemic stroke.

BACKGROUND: When a CT scan is not available, an early accurate clinical diagnosis of ischemic stroke is essential to initiate prompt therapy. Our objective was to construct a clinical index that is easy to use when stroke patients are first evaluated at the hospital, to identify those who probably are experiencing an acute ischemic episode. The study was conducted at a university-affiliated medical referral center and two community general hospitals in Mexico. METHODS: Clinical records were reviewed for 801 patients with sudden onset of a focal or global neurologic dysfunction, presumably of vascular origin lasting more than 24 h. Eligibility criteria for this study were admission to the hospital within the first 24 h after symptomatic onset, CT scan diagnosis between 24 and 72 h, and age >45 years. Ischemic stroke included cases of arterial brain infarction, while nonischemic stroke included subarachnoid or intraparenchymatous hemorrhage, mass lesion, venous infarction, and in cases without a CT scan evidence that could explain the clinical manifestations. Data excerpted for analysis were age, sex, history of diabetes mellitus or previous stroke/transient ischemic attack (TIA), time of onset of symptoms, presence of headache, vomiting, neck stiffness, hemiplegia, leukocytosis or atrial fibrillation, diastolic blood pressure, and Glasgow coma scale (GCS) rating. Two multivariable analyses were used: 1) step-wise multiple logistic regression (SMLR), and 2) conjunctive consolidation (CC). RESULTS: After appropriate exclusions, the study proceeded with 83 ischemic and 42 nonischemic stroke patients. With SMLR, six variables were selected as predictive for ischemic stroke, including neck stiffness, diastolic blood pressure, previous history of stroke/TIA, hemiplegia, GCS, and atrial fibrillation. An appropriate sum of weighted ratings had a positive predictive value (PPV) of 100% for ischemic stroke. With consolidated categories, the PPV was 97% when patients had the following: no neck stiffness; no atrial fibrillation but history of stroke/TIA and GCS > or =12, or no neck stiffness but atrial fibrillation. CONCLUSIONS: Among patients with acute stroke, clinical data can be used to identify a group with a high probability of ischemic stroke. There are slightly different results between both methods; while SMLR includes the four variables selected by CC, the latter included neither diastolic blood pressure nor hemiplegia/hemiparesia. However, CC results seem easier to understand and interpret than with SMLR.

Acute Disease↗
PubMed2002

Interaction between apnea, prone sleep position and gliosis in the brainstems of victims of SIDS.

Among 27,000 infants studied prospectively to characterize their sleep-wake behavior, 38 infants died suddenly and unexpectedly under 6 months of age. Of these, 26 died from sudden infant death syndrome (SIDS), 5 from congenital cardiac abnormalities, 2 from infected pulmonary dysplasia, 2 from septic shock with multi-organ failure, 1 from a prolonged seizure, 1 from prolonged neonatal hypoxemia, and 1 from meningitis and brain infarction. The frequency and duration of apneas recorded some 3-12 weeks prior to the infants' death were analyzed. The brainstem materials were collected and studied in an attempt to elucidate the relationship between sleep apnea, and prone sleep position and gliosis in some nuclei associated with cardiorespiratory characteristics, such as nucleus ambiguus in the medulla oblongata and the solitary nucleus, as well as structures associated with arousal phenomenon, such as the reticular formation, the superior central nucleus and the nucleus raphe magnus in the pons, the dorsal raphe nuclei in the midbrain and medulla oblongata, periaqueductal gray matter in midbrain, and locus ceruleus. Gliosis was estimated as the density of glial fibrillary acidic protein (GFAP)-positive reactive astrocytes. Variant-covariant analyses were carried out using the characteristics of apnea as an independent variable and sleep position and gliosis as dependent variables. A significant association was found only in the frequency of obstructive apnea and prone position (P<0.001) and gliosis in the raphe nuclei in the midbrain (P<0.001). Although prone position is a well-known risk factor for SIDS, the frequency of obstructive apnea has not been associated with the prone sleep position. The observed relation between prone sleep and the density of gliosis does not relate to epidemiological findings. Further studies are needed to investigate the unexpected statistical association.

Analysis of Variance↗
PubMed2004

Potentials of magnesium treatment in subarachnoid haemorrhage.

Subarachnoid hemorrhage from a ruptured aneurysm is a subset of stroke. The young age (median 55 years) and poor outcome (50% of patients die; 30% of survivors remain dependent) explain why in the population the loss of productive life years from aneurysmal subarachnoid hemorrhage (SAH) is as large as that from brain infarcts, the most common type of stroke. Ischemia plays an important role in the pathophysiological process after SAH. A period of global cerebral ischemia firstly occurs in the acute phase, immediately after rupture of the aneurysm, due to acute vasoconstriction and elevated intracranial pressure, which leads to a drop in perfusion pressure. This is quite distinct from the secondly, delayed cerebral ischemia (DCI), which is focal or multi-focal. DCI usually occurs between 4 and 10 days after the initial bleeding, has a gradual onset and is multi-focal, and is an important cause of death and dependency after SAH. The interval between the bleeding and the onset of ischemia provides an opportunity for preventive treatment. Magnesium is readily available, inexpensive and has a well-established clinical profile in obstetrical and cardiovascular practice. It is beneficial in the treatment of eclampsia, a disease with a pathophysiology comparable to DCI after subarachnoid hemorrhage. Neuroprotective mechanisms of magnesium include inhibition of the release of excitatory amino-acids and blockade of the NMDA-glutamate receptor. Magnesium is also a non-competitive antagonist of voltage dependent calcium channels, has cerebrovascular dilatory activity and is an important co-factor of cellular ATPases, including the Na/K-ATPase. Magnesium can reverse delayed cerebral vasospasm and reduces the extent of acute ischemic cerebral lesions after experimental subarachnoid hemorrhage in rats. In this article we discuss the neuroprotective potency of magnesium in SAH by describing the pathophysiology of ischaemia after SAH and the many ways magnesium may interfere with this.

Animals↗
PubMed2006

Serial measurements of levels of the chemokines CCL2, CCL3 and CCL5 in serum of patients with acute ischaemic stroke.

Inflammation, involving cytokine/chemokine expression, occurs after stroke and deteriorates its course with leukocyte-mediated brain infarct progression. Chemokines are cytokines attracting selective leukocyte subsets and subgrouping into the four major subfamilies, CC, CXC, C, and CX3C. The CC subfamily preferentially acts on mononuclears. The study aimed to define serum CCL2, CCL3 and CCL5 levels in stroke patients and their relationship to the extent of disease severity and outcome. 27 ischaemic stroke patients and 20 controls were studied. Blood sampling for the determination of chemokines was performed at days 1, 2 and 3 of stroke, while neurological and functional deficits were estimated, respectively, with the Scandinavian Stroke Scale (SSS) and Barthel Index (BI) at the same time points and at days 14 and 28. Serum CCL3 levels at days 1, 2 and 3 of stroke were significantly higher than in controls. Serum CCL2 and CCL5 levels in stroke patients did not differ from those in controls at any of the time points examined. Serum chemokine levels in stroke studied separately did not differ between each other at any time point studied and demonstrated considerable variability. No correlation between serum chemokine levels and SSS scores was observed. Serum CCL2 and CCL3 levels at days 1, 2 and 3 of stroke correlated with BI scores at day 28. Serum CCL2 levels at days 2 and 3 of stroke also correlated with BI scores at day 14. Serum CCL5 levels at day 2 of stroke correlated with BI scores at day 28. The early and sustained increase in serum CCL3 levels in stroke patients along with correlation between them and short-term poststroke functional disability could indicate that the chemokine response may predispose to poor stroke outcome. The relationship between non-increased serum CCL2 and CCL5 levels and worse stroke outcome seems to be coincidental. Overall, as a result of large interindividual variability, CCL2, CCL3 and CCL5 are not reliable candidates for surrogate markers in stroke.

Aged↗
PubMed2006

[Olfactory groove meningioma].

Olfactory groove meningiomas compromise approximately 8-18% of intracranial meningiomas and harbor frequently large sizes when diagnosticated. We report 13 consecutive cases operated on Hospital São Paulo and Hospital Professor Edmundo Vasconcelos between 1995 and 2003. These patients were retrospectively studied regarding clinical preservation, surgical results and complications. The patients underwent uni or bifrontal craniotomies. There were nine complete resections including duramater and infiltrate bone and four patients with tumor removal and duramater coagulation. One patient died on post-operative period due to brain infarction and three patients had cerebrospinal fluid fistula that resolved. There were no symptomatic recurrence on the follow-up period of 3.3 years(range 11 m to 8 years). With current microsurgical techniques, these tumors can be resected safely with low morbidity.

Adult↗
PubMed1985

Embolic stroke complicating systemic lupus erythematosus.

Embolic stroke complicating systemic lupus erythematosus has been infrequently reported. We examined a 25-year-old woman who suddenly became hemiplegic. Two-dimensional echocardiography identified a source of emboli. At cardiac surgery, friable thrombotic vegetations were found adhering to the mitral valve leaflets, left ventricular septal wall, and chordae tendineae. At autopsy several weeks later, careful pathologic examination of the heart failed to reveal evidence of thrombus formation or endocarditis. An embolus identical in appearance to the thrombotic vegetations described at cardiac surgery was found lodged in the left middle cerebral artery underlying the recent brain infarction. To our knowledge, this is the first report of embolic stroke in systemic lupus erythematosus caused by extensive cardiac thrombus formation in the absence of underlying endocarditis.

Adult↗
PubMed1992

Magnetic resonance imaging signal hyperintensities in the deep and subcortical white matter. A comparative study between stroke patients and normal volunteers.

Mixed population studies suggest a relationship between deep and subcortical white matter hyperintensities on magnetic resonance imaging and cerebrovascular disease. To further clarify this issue we compared the prevalence and extent of such signal abnormalities between a group of 133 consecutive stroke patients (mean age, 54.7 +/- 16.7 years) and 101 normal volunteers (mean age, 54.7 +/- 13.1 years). Diabetes and cardiac disease were significantly more common in patients than in normal subjects. Prevalence rates of clinically silent lesions were 44% and 47.5%, respectively. Beginning confluent and confluent foci were seen in 19.5% of patients, but in only 7.5% of normal subjects. Significant univariate correlations were found for the presence and extent of lesions with age, diabetes, cardiac disease, severity of extracranial carotid arteriosclerosis, and arterial hypertension, but not with the diagnosis of stroke or the type of brain infarction. Multivariate regression analysis established age and diabetes mellitus as the only independent predictors of white matter damage. We conclude that more extensive white matter abnormalities in stroke patients stem from their higher rate of cerebrovascular risk factors but are unrelated to the occurrence of ischemic attacks per se.

Adolescent↗
PubMed2004

Effects of white matter lesions and lacunes on cortical function.

BACKGROUND: Subcortical ischemic vascular dementia has been ascribed to prominent frontal lobe dysfunction secondary to ischemic lesions in frontothalamic circuits. Whether small-vessel disease in fact predominantly affects the frontal lobes is not well documented. OBJECTIVE: To investigate the effects of subcortical lesions (lacunes and white matter lesions [WML]) on cortical function, as reflected in glucose metabolism and cognitive function, in elderly individuals. DESIGN: Cross-sectional analyses of case series. SETTING: Multicenter, university-based study of subcortical vascular dementia. PATIENTS: Persons with normal cognition, mild cognitive impairment, or dementia and with and without lacunes on magnetic resonance images. MAIN OUTCOME MEASURES: Regional cerebral glucose metabolism, normalized regional metabolic activity, and neuropsychological test scores. Major hypotheses were that volume of lacunes and WML correlate selectively with hypometabolism of prefrontal cortex and failure of executive cognitive ability. RESULTS: Lacunes correlated with metabolic rates in dorsolateral frontal cortex (DLF); WML substantially reduced metabolic rates throughout cortex, most strongly so in DLF. When regional metabolic activity was normalized to whole brain activity, lacunes remained correlated with DLF activity, whereas the WML effect was no longer found, probably because of its general distribution. Regional cerebral glucose metabolism and normalized activity in DLF also correlated with cortical atrophy. Metabolic activity in DLF correlated with executive function, memory, and global cognitive function, while activity in middle temporal gyrus correlated with memory and global function but not executive function. CONCLUSIONS: The metabolic effects of lacunes and WML are most apparent in DLF, but the effects of WML are generalized and frontal hypometabolism correlates with memory and global impairment, cognitive as well as executive function. The effects of subcortical cerebrovascular disease appear to converge on the frontal lobes but are diffuse, complex, and of modest magnitude.

Aged↗
PubMed1995

Severe complications of measles requiring intensive care in infants and young children.

OBJECTIVE: To evaluate the characteristics of severe complications of measles in patients admitted to a pediatric intensive care unit. DESIGN: Clinical description of a case series. SETTING: The Pediatric Intensive Care Unit of Soroka Medical Center, Beer-Sheva, Israel, during a measles epidemic. PATIENTS: Fifteen pediatric patients with measles requiring intensive care. RESULTS: Fifteen of 237 hospitalized children with measles required intensive care in the Pediatric Intensive Care Unit. Eleven patients were malnourished; none had been vaccinated for measles. All 15 patients required mechanical ventilation for pneumonia that had caused severe respiratory distress. Twelve of 15 patients were severely hypoxemic before intubation. Seven had a clinical syndrome consistent with adult respiratory distress syndrome. Other complications on admission to the intensive care unit included spontaneous pneumothorax in three patients, empyema in two, encephalopathy in seven, shock in three, sepsis in five, hypocalcemia in 11, thrombocytopenia in eight, and coagulopathy in seven. Complications during treatment included pneumothorax in four patients, fibrosing alveolitis in one, brain infarct in one, thrombus formation in three, and nosocomial sepsis in one. Four patients had long-term sequelae (chronic lung disease, subacute sclerosing panencephalitis, hemiplegia, and partial amputation of a limb), and seven patients recovered uneventfully. Four patients died; all had adult respiratory distress syndrome, three had pneumothorax, and one had nosocomial sepsis. CONCLUSIONS: Patients with measles who require intensive care have a high risk for death or long-term complications, even when treated in a modern pediatric intensive care unit. Adult respiratory distress syndrome and air leaks were the most severe complications in these patients. To reduce the severity of these complications, mechanical ventilation should be based on using the lowest possible inspiratory pressure and fraction of inspired oxygen, while accepting an arterial oxygen pressure less than 60 mm Hg. Secondary bacteremia was an early and prominent complication, and antibiotic treatment should be instituted early in patients with measles requiring intensive care.

Bacteremia↗
PubMed2004

Relationship between atherosclerosis and late-life depression: the Rotterdam Study.

CONTEXT: Depression in late life has been associated with vascular abnormalities. Several studies have demonstrated that persons with brain infarcts are more likely to have depressive disorders. Furthermore, depression is related to the subsequent development of ischemic heart disease. OBJECTIVE: To investigate the relationship between atherosclerosis at different locations and depression in the general population. DESIGN: Cross-sectional population-based study. SETTING: The Rotterdam Study, a population-based cohort study. PARTICIPANTS: In 4019 men and women 60 years and older, we assessed atherosclerosis at different locations, including common carotid intima-media thickness, plaques in the carotid arteries, the ankle-brachial blood pressure index, and aortic atherosclerosis. An overall measure of extracoronary atherosclerosis was obtained in 3747 persons by computing the principal component of these extracoronary atherosclerosis measures. In a subgroup of 1986 persons, we additionally measured coronary calcifications. MAIN OUTCOME MEASURE: All subjects were screened for depressive symptoms. Screen-positive subjects had a psychiatric interview to diagnose depressive disorder. RESULTS: More severe extracoronary atherosclerosis was associated with a higher prevalence of depressive disorders. For every 1-standard deviation increase, the prevalence increased by 30%. Furthermore, we found a strong relationship of severe coronary and aortic calcifications with depressive disorders (odds ratio, 3.89; 95% confidence interval, 1.55-9.77; and odds ratio, 2.00; 95% confidence interval, 1.02-3.96, respectively). CONCLUSIONS: Atherosclerosis and depression are associated in the elderly. This finding is compatible with the vascular depression hypothesis. However, the cross-sectional nature of the study does not allow causal inferences. In particular, earlier depressive episodes may have contributed to the development of atherosclerosis.

Age of Onset↗
PubMed2006

Trends in incidence, lifetime risk, severity, and 30-day mortality of stroke over the past 50 years.

CONTEXT: Prior estimates of long-term trends in the incidence and severity of stroke have varied; trends in lifetime risk have not been reported. OBJECTIVE: To determine long-term trends in the incidence, lifetime risk, severity, and 30-day mortality of clinical stroke. DESIGN, SETTING, AND PARTICIPANTS: Prospective evaluation of the community-based Framingham Study original and offspring cohorts. Participants were 9152 men and women free of prevalent stroke and undergoing follow-up for up to 50 years over 3 consecutive periods (1950-1977, 1978-1989, and 1990-2004), with biennial ascertainment of stroke risk factor data and active surveillance for incident clinical stroke and cause-specific mortality. MAIN OUTCOME MEASURES: Incidence (age-adjusted, sex-specific), severity, 30-day mortality, and mortality-adjusted 10-year and lifetime risk of stroke in each of the specified periods. RESULTS: There were 1030 incident clinical strokes (450 [44%] in men, 629 atherothrombotic brain infarctions [61%]) in 9152 persons 55 years or older over 174,917 person-years of follow-up. The age-adjusted incidence of first stroke per 1000 person-years in each of the 3 periods was 7.6, 6.2, and 5.3, respectively, in men (P = .02 for trend) and 6.2, 5.8, and 5.1 in women (P = .01 for trend). The lifetime risk at age 65 years decreased from 19.5% to 14.5% in men (P = .11) and from 18.0% to 16.1% in women (P = .61). Age-adjusted stroke severity did not vary across periods; however, 30-day mortality decreased significantly in men (from 23% to 14%; P = .01) but not significantly in women (from 21% to 20%; P = .32). CONCLUSIONS: In this cohort of men and women free of prevalent clinical stroke at initial examination, incidence of stroke has decreased over the past 50 years but the lifetime risk has not declined to the same degree, perhaps due to improved life expectancy. The results of this study suggest that improved control of risk factors has lowered stroke incidence but emphasize the need for continued primary prevention efforts.

Adult↗
PubMed2000

Anatomic variations of anterior cerebral artery cortical branches.

The anterior cerebral artery (ACA) is a major vessel responsible for the blood supply to the interhemispheric region. The ACA segment after the anterior communicating artery (AComA) origin is called the distal ACA and has central and cortical branches. The cortical branches are distributed in the different regions of the orbital and medial part of the brain. The objects of this study are the anatomical variations found in the distal ACA. In 76 hemispheres the ACA distal branches were injected with latex and dissected under microscope magnification. Vessel diameters and distances between vessel origins and anterior communicating artery were recorded and analyzed. Microsurgical dissection was carried out to demonstrate anatomic variations of these vessels. Average diameter of ACA at origin was 2.61 +/- 0.34 mm and average diameter of cortical branches diameter ranged from 0.79 +/- 0.27 mm to 1.84 +/- 0.3 mm. Distances between vessel origin and AComA ranged from 7.68 +/- 3.91 mm (orbitofrontal) to 112.6 +/- 11.63 mm (inferior internal parietal). This study found anatomical variations: a single (azygos) ACA was present in one case and three in three cases. Crossing branches of the distal ACA to the contralateral hemisphere were present in 26% of the cases. In some cases a single ACA may supply the posterior hemispheric region through crossing branches. This calls attention to potential bilateral brain infarcts due to a single unilateral ACA occlusion.

Anterior Cerebral Artery↗