Browsing by Author "Bornstein, Natan M. (7007074902)"

Background The Global Burden of Disease Study 2013 (GBD 2013) aims to bring together all available epidemiological data using a coherent measurement framework, standardised estimation methods, and transparent data sources to enable comparisons of health loss over time and across causes, age-sex groups, and countries. The GBD can be used to generate summary measures such as disability-adjusted life-years (DALYs) and healthy life expectancy (HALE) that make possible comparative assessments of broad epidemiological patterns across countries and time. These summary measures can also be used to quantify the component of variation in epidemiology that is related to sociodemographic development. Methods We used the published GBD 2013 data for age-specific mortality, years of life lost due to premature mortality (YLLs), and years lived with disability (YLDs) to calculate DALYs and HALE for 1990, 1995, 2000, 2005, 2010, and 2013 for 188 countries. We calculated HALE using the Sullivan method; 95% uncertainty intervals (UIs) represent uncertainty in age-specific death rates and YLDs per person for each country, age, sex, and year. We estimated DALYs for 306 causes for each country as the sum of YLLs and YLDs; 95% UIs represent uncertainty in YLL and YLD rates. We quantified patterns of the epidemiological transition with a composite indicator of sociodemographic status, which we constructed from income per person, average years of schooling after age 15 years, and the total fertility rate and mean age of the population. We applied hierarchical regression to DALY rates by cause across countries to decompose variance related to the sociodemographic status variable, country, and time. Findings Worldwide, from 1990 to 2013, life expectancy at birth rose by 6·2 years (95% UI 5·6-6·6), from 65·3 years (65·0-65·6) in 1990 to 71·5 years (71·0-71·9) in 2013, HALE at birth rose by 5·4 years (4·9-5·8), from 56·9 years (54·5-59·1) to 62·3 years (59·7-64·8), total DALYs fell by 3·6% (0·3-7·4), and age-standardised DALY rates per 100 000 people fell by 26·7% (24·6-29·1). For communicable, maternal, neonatal, and nutritional disorders, global DALY numbers, crude rates, and age-standardised rates have all declined between 1990 and 2013, whereas for non-communicable diseases, global DALYs have been increasing, DALY rates have remained nearly constant, and age-standardised DALY rates declined during the same period. From 2005 to 2013, the number of DALYs increased for most specific non-communicable diseases, including cardiovascular diseases and neoplasms, in addition to dengue, food-borne trematodes, and leishmaniasis; DALYs decreased for nearly all other causes. By 2013, the five leading causes of DALYs were ischaemic heart disease, lower respiratory infections, cerebrovascular disease, low back and neck pain, and road injuries. Sociodemographic status explained more than 50% of the variance between countries and over time for diarrhoea, lower respiratory infections, and other common infectious diseases; maternal disorders; neonatal disorders; nutritional deficiencies; other communicable, maternal, neonatal, and nutritional diseases; musculoskeletal disorders; and other non-communicable diseases. However, sociodemographic status explained less than 10% of the variance in DALY rates for cardiovascular diseases; chronic respiratory diseases; cirrhosis; diabetes, urogenital, blood, and endocrine diseases; unintentional injuries; and self-harm and interpersonal violence. Predictably, increased sociodemographic status was associated with a shift in burden from YLLs to YLDs, driven by declines in YLLs and increases in YLDs from musculoskeletal disorders, neurological disorders, and mental and substance use disorders. In most country-specific estimates, the increase in life expectancy was greater than that in HALE. Leading causes of DALYs are highly variable across countries. Interpretation Global health is improving. Population growth and ageing have driven up numbers of DALYs, but crude rates have remained relatively constant, showing that progress in health does not mean fewer demands on health systems. The notion of an epidemiological transition - in which increasing sociodemographic status brings structured change in disease burden - is useful, but there is tremendous variation in burden of disease that is not associated with sociodemographic status. This further underscores the need for country-specific assessments of DALYs and HALE to appropriately inform health policy decisions and attendant actions. © 2015 Elsevier Ltd.

Background Up-to-date evidence about levels and trends in disease and injury incidence, prevalence, and years lived with disability (YLDs) is an essential input into global, regional, and national health policies. In the Global Burden of Disease Study 2013 (GBD 2013), we estimated these quantities for acute and chronic diseases and injuries for 188 countries between 1990 and 2013. Methods Estimates were calculated for disease and injury incidence, prevalence, and YLDs using GBD 2010 methods with some important refinements. Results for incidence of acute disorders and prevalence of chronic disorders are new additions to the analysis. Key improvements include expansion to the cause and sequelae list, updated systematic reviews, use of detailed injury codes, improvements to the Bayesian meta-regression method (DisMod-MR), and use of severity splits for various causes. An index of data representativeness, showing data availability, was calculated for each cause and impairment during three periods globally and at the country level for 2013. In total, 35 620 distinct sources of data were used and documented to calculated estimates for 301 diseases and injuries and 2337 sequelae. The comorbidity simulation provides estimates for the number of sequelae, concurrently, by individuals by country, year, age, and sex. Disability weights were updated with the addition of new population-based survey data from four countries. Findings Disease and injury were highly prevalent; only a small fraction of individuals had no sequelae. Comorbidity rose substantially with age and in absolute terms from 1990 to 2013. Incidence of acute sequelae were predominantly infectious diseases and short-term injuries, with over 2 billion cases of upper respiratory infections and diarrhoeal disease episodes in 2013, with the notable exception of tooth pain due to permanent caries with more than 200 million incident cases in 2013. Conversely, leading chronic sequelae were largely attributable to non-communicable diseases, with prevalence estimates for asymptomatic permanent caries and tension-type headache of 2·4 billion and 1·6 billion, respectively. The distribution of the number of sequelae in populations varied widely across regions, with an expected relation between age and disease prevalence. YLDs for both sexes increased from 537·6 million in 1990 to 764·8 million in 2013 due to population growth and ageing, whereas the age-standardised rate decreased little from 114·87 per 1000 people to 110·31 per 1000 people between 1990 and 2013. Leading causes of YLDs included low back pain and major depressive disorder among the top ten causes of YLDs in every country. YLD rates per person, by major cause groups, indicated the main drivers of increases were due to musculoskeletal, mental, and substance use disorders, neurological disorders, and chronic respiratory diseases; however HIV/AIDS was a notable driver of increasing YLDs in sub-Saharan Africa. Also, the proportion of disability-adjusted life years due to YLDs increased globally from 21·1% in 1990 to 31·2% in 2013. Interpretation Ageing of the world's population is leading to a substantial increase in the numbers of individuals with sequelae of diseases and injuries. Rates of YLDs are declining much more slowly than mortality rates. The non-fatal dimensions of disease and injury will require more and more attention from health systems. The transition to non-fatal outcomes as the dominant source of burden of disease is occurring rapidly outside of sub-Saharan Africa. Our results can guide future health initiatives through examination of epidemiological trends and a better understanding of variation across countries. © 2015 Elsevier Ltd.

Hypoxia is a critical component of neuronal death in patients with stroke. Therefore increasing oxygenation of brain tissue seems to be a logical therapy against cerebral ischemia. Oxygen therapy exists in two modalities: normobaric hyperoxia therapy and hyperbaric oxygen therapy (HBO). HBO is a therapeutic procedure in which pure (100%) oxygen is administered at greater than atmospheric pressure in HBO therapy chambers. In this review article, we aimed to summarize the current knowledge regarding the therapeutic use of HBO in acute stroke patients. Literature review and electronic search were performed using PubMed, Medscape, and UpToDate with the keywords stroke, acute stroke, hyperbaric oxygen therapy, and hyperoxia. According to the reviewed literature, the use of HBO as routine stroke therapy cannot be justified in acute stage of stroke. More randomized, controlled studies are needed regarding safety and especially effectives of HBO in stroke patients. Also, standardized definition of HBO should be proposed and used in all future studies. © 2020, Fondazione Società Italiana di Neurologia.

Post-stroke dementia (PSD) or post-stroke cognitive impairment (PSCI) may affect up to one third of stroke survivors. Various definitions of PSCI and PSD have been described. We propose PSD as a label for any dementia following stroke in temporal relation. Various tools are available to screen and assess cognition, with few PSD-specific instruments. Choice will depend on purpose of assessment, with differing instruments needed for brief screening (e.g., Montreal Cognitive Assessment) or diagnostic formulation (e.g., NINDS VCI battery). A comprehensive evaluation should include assessment of pre-stroke cognition (e.g., using Informant Questionnaire for Cognitive Decline in the Elderly), mood (e.g., using Hospital Anxiety and Depression Scale), and functional consequences of cognitive impairments (e.g., using modified Rankin Scale). A large number of biomarkers for PSD, including indicators for genetic polymorphisms, biomarkers in the cerebrospinal fluid and in the serum, inflammatory mediators, and peripheral microRNA profiles have been proposed. Currently, no specific biomarkers have been proven to robustly discriminate vulnerable patients ('at risk brains') from those with better prognosis or to discriminate Alzheimer's disease dementia from PSD. Further, neuroimaging is an important diagnostic tool in PSD. The role of computerized tomography is limited to demonstrating type and location of the underlying primary lesion and indicating atrophy and severe white matter changes. Magnetic resonance imaging is the key neuroimaging modality and has high sensitivity and specificity for detecting pathological changes, including small vessel disease. Advanced multi-modal imaging includes diffusion tensor imaging for fiber tracking, by which changes in networks can be detected. Quantitative imaging of cerebral blood flow and metabolism by positron emission tomography can differentiate between vascular dementia and degenerative dementia and show the interaction between vascular and metabolic changes. Additionally, inflammatory changes after ischemia in the brain can be detected, which may play a role together with amyloid deposition in the development of PSD. Prevention of PSD can be achieved by prevention of stroke. As treatment strategies to inhibit the development and mitigate the course of PSD, lowering of blood pressure, statins, neuroprotective drugs, and anti-inflammatory agents have all been studied without convincing evidence of efficacy. Lifestyle interventions, physical activity, and cognitive training have been recently tested, but large controlled trials are still missing. © 2017 The Author(s).

Bone disorders are among the most uncommon causes of stroke, but they should be considered as stroke cause in particular clinical scenarios. On the other hand, osteoporosis/osteopenia and increased fracture risk are well documented post stroke complications. The relationship between stroke and bone health is complex. The current facts suggest that these two conditions share same risk factors, but also are risk factors for each other. However, the evidence shows more clear effect of stroke on the bone health, than in the opposite direction. This extensive review is aiming to fill the huge gap of evidence about this topic, and since bone pathology is extremely rare cause of cerebrovascular accident, although a complex connection between these two conditions definitely exists. © 2020, Fondazione Società Italiana di Neurologia.

Stroke is one of the leading causes of death and probably the greatest cause of adult disability worldwide. Diabetes mellitus (DM) is a state of accelerated aging of blood vessels. Patients with diabetes have increased risk of stroke. Hyperglycemia represents a risk factor for poor outcome following stroke, and probably is just a marker of poor outcome rather than a cause. Lowering of blood glucose levels has not been shown to improve prognosis. Also, prevention of stroke risk among patients with DM is not improved with therapy for reduction of glucose levels. On the other hand, prediabetes, a metabolic state between normal glucose metabolism and diabetes, is a risk factor for the development of DM type 2 and subsequently for stroke. Several methods are known to identify prediabetes patients, including fasting plasma glucose levels, 2-hour post load glucose levels, and glycosylated hemoglobin levels. In this text, we tried to summarize known data about diagnosis, epidemiology, risk factors, pathophysiology, and prevention of prediabetes in relation to DM and stroke. © 2017 Mijajlović et al.

Stroke is one of the leading causes of death and probably the greatest cause of adult disability worldwide. Diabetes mellitus (DM) is a state of accelerated aging of blood vessels. Patients with diabetes have increased risk of stroke. Hyperglycemia represents a risk factor for poor outcome following stroke, and probably is just a marker of poor outcome rather than a cause. Lowering of blood glucose levels has not been shown to improve prognosis. Also, prevention of stroke risk among patients with DM is not improved with therapy for reduction of glucose levels. On the other hand, prediabetes, a metabolic state between normal glucose metabolism and diabetes, is a risk factor for the development of DM type 2 and subsequently for stroke. Several methods are known to identify prediabetes patients, including fasting plasma glucose levels, 2-hour post load glucose levels, and glycosylated hemoglobin levels. In this text, we tried to summarize known data about diagnosis, epidemiology, risk factors, pathophysiology, and prevention of prediabetes in relation to DM and stroke. © 2017 Mijajlović et al.

Stroke remains a major global health concern, ranking as the second most common cause of death and the third leading cause of disability worldwide. Despite advances in therapy and management, ischemic stroke patients continue to face high risks of recurrence, cardiovascular events, and mortality. Effective secondary stroke prevention is critical, encompassing antithrombotic therapy, management of vascular risk factors such as hypertension, dyslipidemia, and diabetes mellitus, and conducting healthy lifestyle. Approximately 80% of strokes are ischemic, with a significant proportion attributable to large-artery atherosclerosis of the extra- and intracranial arteries, particularly in the internal carotid artery. Atherothrombotic strokes, linked to plaque rupture and thrombus formation, present a notably high risk of recurrence. Inflammatory and immune mechanisms play pivotal roles in both the initiation and progression of atherosclerosis and stroke. Colchicine, an anti-inflammatory agent, has shown potential in managing cardiovascular disease, though its effects on stroke reduction and prevention have been inconsistent across studies. Its possible protective role against stroke is attributed to its anti-inflammatory actions, which include disrupting microtubule dynamics, inhibiting immune cell movement, and lowering inflammatory markers like L-Selectin and E-Selectin, while also suppressing interleukin release. Glucagon-like peptide-1 receptor agonists (GLP-1RA) agents have emerged as effective therapies for type 2 diabetes with notable cardiovascular benefits. These agents enhance glucose control while also providing protective effects against atherosclerosis and stroke. GLP-1RA drugs work by mimicking the effects of GLP-1, a peptide that regulates insulin release and glucose metabolism. They also exhibit anti-inflammatory properties, potentially reducing stroke risk through mechanisms such as improved endothelial function and reduced plaque formation. Clinical trials have indicated that GLP-1RA agents can significantly lower the incidence of nonfatal strokes and major adverse events. This narrative review underscores the importance of targeting inflammation to reduce the risk of recurrent stroke, emphasizing recent studies on colchicine and GLP-1RA. It consolidates evidence regarding the efficacy of these agents in secondary stroke prevention; however, future studies are needed to further explore their mechanisms and roles in comprehensive stroke management strategies. © The Author(s), 2025.

Stroke remains a major global health concern, ranking as the second most common cause of death and the third leading cause of disability worldwide. Despite advances in therapy and management, ischemic stroke patients continue to face high risks of recurrence, cardiovascular events, and mortality. Effective secondary stroke prevention is critical, encompassing antithrombotic therapy, management of vascular risk factors such as hypertension, dyslipidemia, and diabetes mellitus, and conducting healthy lifestyle. Approximately 80% of strokes are ischemic, with a significant proportion attributable to large-artery atherosclerosis of the extra- and intracranial arteries, particularly in the internal carotid artery. Atherothrombotic strokes, linked to plaque rupture and thrombus formation, present a notably high risk of recurrence. Inflammatory and immune mechanisms play pivotal roles in both the initiation and progression of atherosclerosis and stroke. Colchicine, an anti-inflammatory agent, has shown potential in managing cardiovascular disease, though its effects on stroke reduction and prevention have been inconsistent across studies. Its possible protective role against stroke is attributed to its anti-inflammatory actions, which include disrupting microtubule dynamics, inhibiting immune cell movement, and lowering inflammatory markers like L-Selectin and E-Selectin, while also suppressing interleukin release. Glucagon-like peptide-1 receptor agonists (GLP-1RA) agents have emerged as effective therapies for type 2 diabetes with notable cardiovascular benefits. These agents enhance glucose control while also providing protective effects against atherosclerosis and stroke. GLP-1RA drugs work by mimicking the effects of GLP-1, a peptide that regulates insulin release and glucose metabolism. They also exhibit anti-inflammatory properties, potentially reducing stroke risk through mechanisms such as improved endothelial function and reduced plaque formation. Clinical trials have indicated that GLP-1RA agents can significantly lower the incidence of nonfatal strokes and major adverse events. This narrative review underscores the importance of targeting inflammation to reduce the risk of recurrent stroke, emphasizing recent studies on colchicine and GLP-1RA. It consolidates evidence regarding the efficacy of these agents in secondary stroke prevention; however, future studies are needed to further explore their mechanisms and roles in comprehensive stroke management strategies. © The Author(s), 2025.