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Post-stroke depression (PSD)

Emotional Lability

Mood emotional changes

"The psychological effects of stroke such as depression, anxiety and post-traumatic stress disorder are associated with decreased quality of life in many domains, which often impact interpersonal relationships and participation in the community. PSD is also associated with increased risk of stroke recurrence and mortality."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7911065/

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Long-term complications of stroke and secondary prevention: an overview for primary care physicians

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Despite a decline in mortality from stroke, the annual incidence in the general population is increasing. For many stroke survivors and their families, the acute stroke is the beginning of an ongoing struggle with physical impairment and subsequent disability. ...

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A stroke occurs when there is a loss of oxygen to parts of the brain, which damages brain tissue. There are two types of strokes. An ischemic stroke is a blockage in a blood vessel that prevents blood from reaching the brain, depriving it of oxygen and nutrients. This is the most common type of stroke, accounting for about 80% of all strokes. A hemorrhagic stroke happens when a blood vessel ruptures, causing blood to leak into the brain and put pressure on brain cells. This type of stroke accounts for about 13% of all strokes.

Symptoms include:

Sudden numbness or weakness in the face, arm, or leg, especially on one side of the body.

Sudden confusion, trouble speaking, or difficulty understanding speech.

Sudden trouble seeing in one or both eyes.

Sudden trouble walking, dizziness, loss of balance, or lack of coordination.

Sudden severe headache with no known cause.

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Abstract

Stroke is the fourth killer and number one cause of adult disability in the United States. The estimated direct and indirect costs of stroke care in this country are $68.9 billion for 2009. The prevalence of stroke and its cost will undoubtedly rise as the aging population increases. In addition, stroke incidence and mortality are increasing in less developed countries in which the lifestyles and population restructuring are rapidly changing. More population-based research to assess incidence, risk factors, and outcomes are needed in these countries. Epidemiologic studies can help identify groups of individuals or regions at higher risk for stroke. They can also help us better understand the natural history of certain conditions and therefore push the direction of therapeutic investigations. Furthermore, the study of trends across different time periods and different populations can help investigators evaluate the effects of stroke care programs and treatment options.

Electronic supplementary material

The online version of this article (doi:10.1007/s13311-011-0053-1) contains supplementary material, which is available to authorized users.

Keywords: Stroke, Review, Epidemiology, Outcome, Mortality, Incidence

Introduction

Epidemiologic studies on stroke help us with understanding the natural history of the disease, identification of risk factors, and prognostic factors that can lead to markers for disease mechanisms. Epidemiology and observational data can inform scientists of possible novel areas for more focused research. They help us identify the individuals, groups, or geographic areas that are at increased risk of disease or poorer outcomes. Critical analyses of the factors that are involved in those cases of higher risks and poorer outcomes can lead to a better understanding of the underlying causes. Furthermore, knowing which individuals, groups, or geographic areas are at risk helps physicians and public health policymakers to develop more effective target programs to reduce the risk of stroke, stroke mortality, and disability.

Prevalence and Incidence

Stroke, a highly prevalent condition, exacts a substantial societal toll in the form of the "Dreaded-D's," which are the leading cause of chronic disability, the second leading cause of dementia, and the fourth leading cause of death in the United States (U.S.) [ 1]. The worldwide impact of stroke seems to be even more pronounced than it is in the U.S., but overall estimates vary widely and may not necessarily be consistently reliable [ 2]. In the U.S., the prevalence of stroke is roughly 3% of the adult population, which translates to approximately 7 million individuals [ 1].

Approximately 800,000 primary (first-time) or secondary (recurrent) strokes occur each year in the U.S., with the majority being primary strokes (roughly 600,000) [ 1]. Of these strokes, approximately 87% are ischemic infarctions, 10% are primary hemorrhages, and 3% are subarachnoid hemorrhage. Worldwide estimates indicate that primary hemorrhages constitute a higher percentage of all strokes, ranging from 10% to 25%. Individuals of Asian, African, and Latin American origin tend to have a higher frequency of primary hemorrhage than persons of European origin [ 1]. In addition, although primary hemorrhage accounts for 10 to 17% of all strokes in Western countries, in Asian it is approximately 25% [ 3].

The incidence of stroke rapidly increases with age, doubling for each decade after age 55 [ 4]. Among adults ages 35 to 44, the incidence of stroke is 30 to 120 of 100,000 per year, and for those ages 65 to 74, the incidence is 670 to 970 of 100,000 per year [ 1]. Stroke does occur among children, but the incidence in comparison with adults is substantially lower (i.e., approximately 1 to 2.5 of 100,000 per year), and roughly 50 to 75% of strokes among children are as a result of hemorrhage [ 1]. Sickle cell disease is the most common cause of childhood stroke, with the highest incidence between ages 2 to 5 years [ 5].

Perhaps due to better control of vascular risk factors during the last decade, incidence rates of stroke in developed nations have modestly diminished or plateaued. For instance, in the U.S. between 1997 and 2006, the total hospital-based stroke diagnoses decreased from 680,607 to 609,359, and the age-adjusted hospital-based stroke diagnosis rate per 100,000 persons significantly declined in a linear pattern from 282.7 to 210.4 in men (26%) and from 240.5 to 184.7 in women (23%) [ 6]. The average rate of decrease in hospital-based stroke diagnosis rates was significantly greater in men than in women (-8.7 vs -7.5 per 100,000 persons). It has been projected that with continued aging of the population, especially in Western countries, these rates are expected to rise again dramatically during the next 40 years.

A transient ischemic attack (TIA) is classically viewed as a temporary abrupt-onset neurological deficit due to brain or retinal ischemia lasting less than 24 hours in duration. Determining the exact incidence or prevalence of TIAs can be challenging because symptoms experienced can sometimes be neurologically nonspecific, due to its transitory nature. Many patients do not seek medical attention, and for those who do seek help, it is in a delayed fashion with symptom characteristics that become hazy with time. As such, data on TIA prevalence broadly varies, but the range of 1 to 6% with prevalence in the U.S. is estimated to be 2.3% [ 7]. Several population-based studies have investigated the issue of TIA incidence. A study (in Rochester, Minnesota) observed a crude age- and sex-adjusted incidence rate of 68 per 100,000 persons per year for the years 1985 to 1989, the highest incidence of 584 per 100,000 noted among individuals aged 75 to 84 [ 8]. Other population-based TIA incidence rates range from 18 per 100,000 persons per year from 1987 to 1988 in Novosibirsk, Russia [ 9] to 37 per 100,000 persons per year from 1970-1973 in Estonia [ 10]. Data from Sweden, England, France, and Japan have also been within this range [ 11- 14]. The higher rates in the Rochester study may reflect distinct methods of case ascertainment because incidence rates for ischemic stroke are comparable. Generally, incidence rates of classically defined TIA incidence rates have remained stable with time.

An expert consensus group recently recommended a formal change in the definition of TIA to a "transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction," thereby eliminating the time-based component noted in the classical definition [ 15]. The decision to consider adopting a tissue-based (not an arbitrary time-based) definition of TIA was primarily driven by modern imaging data, which revealed that as many as 50% of patients with transient deficits lasting <24 hours have evidence of brain ischemia on initial magnetic resonance imaging, and 50% of those with initial abnormalities on magnetic resonance imaging show evidence of fixed infarction on subsequent images. Estimates suggest that the potential epidemiologic impact of adopting a tissue-based definition of TIA in the U.S. would lower annual incidence rates of TIA by 33% from roughly 180,000 to 120,000, and would increase the rate of ischemic stroke by this amount [ 16].

Another change in our approach to TIA stems from a better understanding of its short-term prognosis. It is now clear that that the risk of future vascular events within 3 months is as high or higher after TIA, as after completed stroke, and this risk is highest within the first week after TIA [ 17]. Comparisons across studies point to a 90-day stroke risk ranging from 10 to 20% after TIA [ 17]. In response to this new knowledge, prediction scores have been developed and validated to facilitate better decision-making in the evaluation of imminent risk of stroke after TIA [ 18]. These scores could potentially be used to identify TIA patients who may require urgent admission, but have not yet been tested in a clinical trial.

Prevalence of asymptomatic cerebral ischemia noted on brain imaging among persons aged 55 to 64 years is 11%, and this rises to 22% for those aged 65 to 69 years, 28% for those aged 70 to 74 years, 32% for those aged 75 to 79 years, 40% for those aged 80 to 85 years, and 43% for individuals ≥85 years of age [ 1]. U.S. data revealed that 17.8% of the U.S. population ≥45 years of age with no prior diagnosis of stroke or TIA reported at least 1 symptom of stroke. Prevalence of these stroke-related symptoms were more likely among blacks vs whites, persons with lower income and lower educational attainment, and those with fair to poor perceived health status [ 1].

Risk Factors

Prevention remains the most viable avenue for lessening the burden of stroke on society, particularly given the high incidence of stroke worldwide, insidious contribution of stroke risk factors, and the paucity of proven acute stroke therapies. Longitudinal studies have identified several characteristics/conditions that boost a person's risk for primary or recurrent stroke [ 4, 19]. These risk factors are viewed as nonmodifiable or modifiable and generally apply to primary and recurrent stroke. Nonmodifiable risk factors serve as markers for high stroke risk (Table 1 ) [ 4], whereas modifiable risk factors are amenable to intervention for lower stroke risk. A population-based study that compared two epochs (1981 to 1984 vs 2002 to 2004 in Oxfordshire, United Kingdom) observed a lowered population level in the prevalence of multiple risk factors (including smoking, elevated cholesterol, and high blood pressure) was linked with a reduction for stroke incidence. Recently, an international case-control study (i.e., the INTERSTROKE study) of 3000 stroke cases, and corresponding number of controls, showed that roughly 90% of strokes could be explained by 10 risk factors: 1) hypertension, 2) diabetes, 3) cardiac causes, 4) current smoking, 5) abdominal obesity, 6) hyperlipidemia, 7) physical inactivity, 8) alcohol consumption, 9) diet, and 10) psychosocial stress and depression [ 20]. Nonetheless, unexplained stroke risk and increasing realization that atherosclerosis is the culprit in most strokes is, in part, an inflammatory condition that has led to a search for novel modifiable stroke risk factors. Some of the potentially modifiable ischemic stroke risk factors being studied are listed in Table 2 [ 21, 22]. Risk factors for primary intracerebral hemorrhage are shown in Table 3 and overlap to some degree with those for ischemic stroke [ 3].

Table 1

Risk factor

Impact on stroke incidence

Age

Doubles for every successive decade after the age of 55 years

Sex

24% to 30% higher in men; however, absolute annual number of women experiencing stroke is higher because women outlive men

Race ethnicity

2- to 4-fold higher among African Americans and occur at an earlier age a

2-fold higher among Hispanics and occur at an earlier age a

Higher among Chinese a

Geography

Higher rates in the Southeastern U.S. (the so-called "Stroke Belt"), especially along the coasts in Georgia and the Carolinas (so-called "Stroke Buckle").

Heredity

Almost 2-fold higher among first-degree relatives. Chromosome 9p21 (proximal to genes CDKN2A and CDKN2B) has been linked to ischemic stroke risk

Table 2

Risk entity

Possible risk factors

Inflammation

* High sensitivity C-reactive protein

* Lipoprotein-associated phospholipase A2 (LpPLA2)

* Peripheral leukocyte count

* Other cytokines (interleukin 6, tumor necrosis factor and its receptors)

Infections

* Chlamydia pneumonia

* Helicobacter pylori

* Herpes viruses

* Periodontal infections

Renal Disease

* Decreased glomerular filtration function (glomerular filtration rate, Cystatin C)

* Abnormal glomerular filtration barrier (albuminuria)

Dietary Habit

* High saturated fat intake

* Elevated salt intake

Table 3

Risk Factor

Effect Size (95% Confidence Interval) [3]

Hypertension

Odds Ratio: 3.68 (2.52-5.38)

Age (every 10 year rise)

Risk Ratio: 1.97 (1.79-2.16)

Current smoking

Odds Ratio: 1.31 (1.09-1.58)

Diabetes Mellitus

Odds Ratio: 1.30 (1.02-1.67)

High alcohol intake (>56 grams/day)

Odds Ratio: 4.11 (2.54-6.65)

Moderate alcohol intake (<56 grams/day)

Odds Ratio: 2.05 (1.35-3.11)

Modifiable Medical Risk Factors

Hypertension Hypertension is the most prominent modifiable risk factor for ischemic stroke, and it afflicts more than 75 million adults ≥20 years of age in the U.S. [ 1]. Due to its widespread prevalence, depending on age group, the population attributable risk of hypertension for stroke is as great as 40% [ 4], and in the INTERSTROKE study, depending on the definition used, hypertension accounted for as great as 50% of the risk of stroke [ 20]. Hypertension prevalence varies by race ethnicity (highest in blacks), resulting in a differential effect of hypertension on stroke risk by race ethnicity. Elevated stroke risk has been linked with all stages of hypertension and isolated systolic hypertension [ 23]. In fact, the risk of stroke seems to have a continuous association with blood pressure down to levels as low as 115/75 mmHg [ 23]. In light of this, the national guidelines redefined categories of hypertension so that normal systolic blood pressure is <120 mmHg and normal diastolic blood pressure is <80 mmHg [ 24]. Most recently, it has been suggested that the variability in blood pressure measurements (visit to visit, distinct measurements within a given visit) are associated with greater risk of stroke [ 25].

Atrial Fibrillation Chronic atrial fibrillation (AF) is a strong stroke risk factor and it is estimated to affect more than 2.6 million persons in the U.S. in 2010 [ 1]. Among individuals >65 years of age, the prevalence of AF is approximately 6%. Because the prevalence of AF rises with age, the attributable risk of stroke due to AF is highest in much older age groups [ 4]. So, for instance, AF may account for as much as 25% of strokes among persons aged 80 to 89 years. The risk of stroke is approximately 20 times higher among AF patients with valvular disease and five times higher among AF patients with nonvalvular disease compared to patients without AF [ 26]. Clinical trial and epidemiological data have been used to derive various stroke risk stratification schemes that can be used in clinical practice for AF patients [ 26]. Of note, outpatient continuous arrhythmia monitoring is increasingly showing that AF may actually be responsible for a higher percentage of unexplained strokes than was previously known [ 27].

Coronary Artery Disease Individuals with a presence of coronary artery disease have double the risk of stroke compared to patients without coronary artery disease [ 19]. The attributable risk of stroke due to coronary artery disease is approximately 12%. Coronary artery disease patients with left ventricular hypertrophy have 3 times the risk of stroke, whereas coronary artery disease patients with congestive heart failure have 4 times the risk [ 19]. Within 5 years of a myocardial infarction, the rate of stroke is 8.1% [ 28], and older patients or patients with a cardiac ejection fraction less than 28% are at higher risk of stroke.

Diabetes A population-based study of more than 14,000 subjects observed that the presence of diabetes was independently related to a greater risk of ischemic stroke (adjusted risk ratio, 2.26) [ 29]. In the Northern Manhattan Stroke Study (NOMASS), the prevalence of diabetes was as high as 22% among elderly black subjects, and as high as 20% among elderly Hispanics, with corresponding attributable stroke risks of 13% and 20%, respectively [ 4]. Insulin resistance without the presence of overt diabetes is associated with a greater risk of stroke. In the Atherosclerosis Risk in Communities study, elevated fasting insulin levels in nondiabetics was related to higher risk of stroke (relative risk, 1.19 per 50 pmol/L rise). Furthermore, among nondiabetic subjects in NOMASS, those with elevated measurements of insulin resistance were significantly more likely to have a first ischemic stroke, even after adjusting for other risk factors and the metabolic syndrome [ 30]. The metabolic syndrome, a constellation of glucose dysmetabolism, obesity, hypertension, and dyslipidemia has been shown to independently confer greater risk of first and recurrent stroke [ 31, 32]. It is unclear if metabolic syndrome confers a greater risk of first stroke than what one would expect for its components [ 33].

Dyslipidemia Abnormalities in several serum lipid indices have been linked to symptomatic vascular disease. These associations have been particularly robust in regard to coronary artery disease, but at times it is conflicting in regard to stroke [ 4]. However, many early studies that examined the relationship of lipids with stroke only examined total serum cholesterol levels and did not include stroke subtyping. Not accounting for the heterogeneity of stroke pathophysiology ( vs coronary artery disease), likely contributed to the inconsistent findings [ 4]. Recent studies that have addressed the limitations of prior studies generally have shown an association of elevated serum triglycerides, total cholesterol, low-density lipoprotein cholesterol, and nonhigh-density lipoprotein cholesterol with ischemic stroke risk, especially atherosclerotic and lacunar stroke subtypes. For instance, in 1 study the highest total cholesterol quintile was related to greater ischemic stroke risk vs the lowest quintile (odds ratio, 1.6; 95% confidence interval, 1.3 to 2.0), and the most robust subtype associations were for atherosclerotic stroke (OR, 3.2) and lacunar stroke (OR, 2.4) [ 34]. Elevated high-density lipoprotein cholesterol was shown to be protective for stroke in NOMASS [ 4].

Asymptomatic Carotid Stenosis Prevalence of asymptomatic carotid stenosis rises with age, and can be found in more than 50% of individuals 65 years of age or older. Earlier studies found the risk of stroke with asymptomatic carotid stenosis to be approximately 1.3% per year among patients with stenosis less or equal to 75%, and approximately 3.3% annually among patients with stenosis greater than 75% [ 35]. The "best" medical therapy has changed because the publications of clinical trials have compared carotid endarterectomy with medical therapy for asymptomatic carotid stenosis [ 36]. The risk of stroke associated with asymptomatic carotid stenosis has fallen significantly during the past 20 years [ 36, 37]. With contemporary medical therapy, the average annual rate of ipsilateral stroke is estimated to be <1%.

Modifiable Lifestyle Risk Factors

Cigarette Smoking Smoking is associated with reduced blood vessel distensibility/compliance, elevated fibrinogen levels, increased platelet aggregation, decreased high-density lipoprotein cholesterol levels, and higher hematocrit [ 4]. The relative risk of stroke for smokers included in a large meta-analysis was 1.5, and a dose-response association with higher stroke risk has been observed in heavy vs light smokers. Roughly 18% of strokes are attributable to active cigarette smoking. Stroke risk associated with former smoking has been shown to substantially decrease with increasing time because of cessation, and the Framingham study found stroke risk to be at the level of nonsmokers at 5 years from cessation. Even passive cigarette smoking boosts progression of atherosclerosis. Indeed, there is a greater risk of ischemic stroke (relative risk, 4.8) among cigarette-smoking women with a cigarette-smoking spouse vs those with a nonsmoking spouse. Finally, smoking modifies the influence of oral contraceptives on stroke risk, as there seems to be a 7-fold rise in risk among persons who both smoke and use oral contraceptives [ 38].

Alcohol Consumption

Heavy alcohol consumption is associated with elevated blood pressure, enhanced coagulability, cardiac arrhythmias, and decrease in cerebral blood flow [ 4]. On the other hand, light-to-moderate consumption has been linked to elevated high-density cholesterol and endogenous tissue plasminogen activator levels. Increasing alcohol consumption is associated with greater risk of hemorrhagic stroke in a dose-dependent manner. However, studies evaluating the impact of alcohol consumption on ischemic stroke risk have not shown consistent results. Indeed, the majority of published evidence points to a protective effect of light-to-moderate drinking (1-2 drinks per day) on the risk of ischemic stroke including data from the Nurses' Health Study and NOMASS (adjusted odds ratio, 0.5).

Physical Inactivity Increased physical activity is associated with reductions in fibrinogen, homocysteine, and platelet activity, as well as elevations in high-density lipoprotein cholesterol and plasma tissue plasminogen activator activity [ 4]. Observational data show that physical activity is linked with lower stroke risk, whereas sedentary behavior is related to higher stroke risk. A meta-analysis of 23 studies that examined the relationship of physical activity with risk of stroke noted that highly active subjects experienced a 27% lower risk of stroke or mortality vs low-active subjects.

Stroke Outcomes

Stroke is the fourth leading cause of death in the U.S. and the number 1 cause of long-term disability worldwide. It is estimated that someone dies of a stroke every 4 minutes in the U.S. [ 39]. In 2006, approximately 47% of stroke deaths occurred in the hospital [ 40]. The 1-month case fatality rate in the U.S. for all strokes ranges from 10% to 15% [ 41- 44]. The case fatality rate is lower for ischemic stroke (8-12%) compared to hemorrhagic stroke (33-45%) [ 43- 45]. There are approximately 6.4 million stroke survivors living in the U.S. The estimated direct and indirect cost of stroke for 2007 is $62.7 billion [ 46]. At 6 months after stroke, 35% had depressive symptoms, 30% were unable to ambulate without assistance, and 26% were dependent in activities of daily living [ 1]. Understanding the factors that are associated with clinical outcomes can lead to more effective interventions to reduce case fatality and mortality, and to improve functional status in patients with stroke.

Effect of Age on Outcomes

Stroke incidence increases with age [ 39]. With prolonged life expectancy, we can expect to see an increasing number of older patients presenting with stroke. How age influences stroke outcome has been the subject of a number of studies [ 43- 45, 47, 48]. Many have found age to be associated with poorer outcomes, independent of stroke type. In general, older patients were more likely to be discharged to an institution other than home, and were more disabled and more severely handicapped at 3 months after stroke [ 47, 48]. Those ≥80 years old with stroke had a longer length of stay compared to younger patients (24.7 ± 27.6 vs 22.3 ± 24.2 days; p = 0.013) [ 48]. In-hospital mortality and case fatality also increase with age [ 47, 48]. Case fatality rate for those ≥80 years old can be as high as 21% [ 48]. Although age seems to influence activities of daily living recovery, it has not been found to have an effect on neurological recovery [ 47]. This may suggest that older patients have a poorer ability to compensate, and therefore may benefit more from rehabilitation with a focus on activities of daily living.

Effect of Gender on Outcomes

Gender differences in heart disease are well recognized, but less is known of gender differences in stroke. Although age-adjusted stroke mortality rates for men are higher than for women overall, due to their longevity, more women die of stroke each year than men, accounting for almost 61% of all stroke deaths in the U.S. in 2006 [ 39]. A number of studies have shown that women have more severe strokes than men [ 49]. It has also been estimated that women with acute ischemic stroke were 30% less likely to receive thrombolysis treatment with intravenous tissue plasminogen activator (tPA) than men [ 50]. Based on community studies, it has been found that women have a higher case of fatality rate than men, although confounders were not adjusted for all the studies. From 21 studies, the pooled case fatality for men was 19.7% and for women it was 24.7%; therefore, it is 1.25 times higher among women (95% confidence interval, 1.17 to 1.34) [ 49].

In addition, women who survive stroke seem to have less favorable outcomes than men. Women have longer length of stay and are less likely to be discharged home [ 51- 54]. Female gender independently predicts poorer prognosis and less independence at 3 to 6 months poststroke, even after adjustment for age, comorbidities, and other clinical features [ 51- 53, 55, 56]. The etiology of these differences is unclear. A large multi-center study across Europe has noted that gender, rather than stroke severity, was a major discriminating factor for the use of diagnostic neuroimaging studies or therapeutic interventions, such as carotid surgery [ 51]. More studies are needed to identify modifiable determinants of poorer stroke outcomes in women (such as usage of available diagnostic or therapeutic options, secondary stroke prevention measures, rehabilitation efforts, or social networks) so that targeted interventions can be instituted to reduce these disparities.

Geographic Variations in Outcomes

Many studies have described geographic variations in stroke mortality in the U.S., with higher rates seen in the Southeastern U.S. ("Stroke Belt") since at least the 1950s. Using data from the Medicare Enrollment Database, 1 study found that the overall recurrent ischemic stroke rates declined by almost 5% from 1994 to 2002 [ 57]. However, this varied significantly by region, and there were counties in the Southeast U.S. who had major declines in stroke recurrence, but their rates generally remained greater than the national average. Globally, there are also regional differences in stroke mortality with a higher burden seen in North Asia, Eastern Europe, Central Africa, and the South Pacific [ 58]. The causes of such geographic variations remain unclear. One of the many hypothesized reasons is geographic variations in stroke risk factors. However, in the U.S., an analysis using risk factor data from the Reasons for Geographic and Racial Differences in Stroke (REGARDS) study showed that the risk factor hypothesis likely only explains a small percentage of the geographic variation for stroke mortality [ 59]. Globally, national income has been reported to be a strong predictor of stroke burden and mortality. However, this association did not change much with adjustments for typical vascular risk factors, which were more prevalent in high-income countries [ 58]. Other hypotheses to explain geographic variations include differences in socioeconomic status (SES), lifestyle choices, infection rates, other novel risk factors, access to care, and aggressiveness of care, but data to support these are lacking.

Effect of Socioeconomic Status on Outcomes

The relationship between poverty and health inequality has been demonstrated in many different countries and at different levels of national healthcare coverage [ 60- 62]. What drives this relationship is unclear because comparisons between published studies are difficult to make due to the heterogeneity of the studies, including the choice of which indicator of SES to measure (income, education, occupation, class, and so forth). The fact remains that these proxy measures of SES have been shown to be inversely associated with stroke case fatality, poorer functional and motor recovery during rehabilitation, less health services after stroke, and increased recurrent stroke risk [ 62- 65]. Stroke burden and mortality vary greatly geographically, but low-income countries are the most affected (Fig. 1 ) [ 58]. Some possible mechanisms by which SES variables are associated with disease outcomes are by creating differentials in the use of social support structures, healthcare systems, and access to knowledge and resources [ 62].

Effect of Race Ethnicity on Outcomes

In 2007, the death rate for stroke was 40.2 per 100,000 for white males and 67.1 per 100,000 for black males, and 39.3 for white females and 55.0 for black females [ 1]. Mortality rates from intracerebral hemorrhage for blacks and Asian Pacific Islanders (API) were 1.7 and 1.5 times higher than whites for 1995 to 1998 [ 66]. For subarachnoid hemorrhage during the same period, all ethnic groups had higher rates than whites.

Racial disparities in stroke incidence and outcomes have been well-described. Cultural and environmental mechanisms play a role in racial ethnic stroke disparities, including aspects of socioeconomic class, access to care, discrimination, and cultural variations in risk factors. There is strong evidence that blacks in the U.S. have higher stroke incidence and higher death rates for all stroke subtypes compared to other racial groups [ 39]. Asian Pacific Islanders have been found to have a higher death rate from intracerebral hemorrhage than whites [ 66]. The Brain Attack Surveillance in Corpus Christi project found Mexican Americans to have a higher risk of stroke recurrence than non-Hispanic whites, and found that this risk was strongly associated with a risk of death [ 67]. However, it is less clear what accounts for these types of differences.

The Brain Attack Surveillance in Corpus Christi project did not find a significant difference in ischemic stroke subtypes among Mexican Americans and non-Hispanic whites, and therefore they were unlikely to be strong predictors of differences observed in stroke incidence or mortality between these ethnic groups [ 68]. In recent years, it has become clear that intracranial atherosclerotic disease occurs at a much higher prevalence among Asians, blacks, and Hispanics [ 69]. The poor natural history of intracranial atherosclerotic disease likely contributes to the rates of poorer outcomes in these ethnic groups. Many studies have examined the various risk factors for stroke and their prevalence and control among different racial ethnic groups. Blacks consistently have higher rates of hypertension [ 70- 72]. The diabetes rate was alarmingly high among Native Americans (62%) [ 73]. Among others, uncontrolled risk factors can contribute to the poorer outcomes after a stroke.

Administration of thrombolytic therapy, which is associated with better functional outcomes, is highly dependent on the timely arrival at a medical center. There is little data on racial ethnic variations in acute stroke care and outcomes, and the results from available studies are contradictory and inconclusive. Some have reported that being Asian was independently predictive of delay in presentation [ 74]. Similar studies looking at delays in New York and in the Stroke Belt did not find an association between ethnicity and delay [ 75, 76], whereas another study conducted in San Diego detected a trend toward delayed presentation among blacks [ 77]. Also, blacks were less likely to receive intravenous tPA [ 78, 79]. Although delays in presentation and contraindications were seen more frequently in blacks, these were not statistically significant from whites [ 78]. Blacks were also less likely to receive care from a neurologist, and studies have found that neurological care has beneficial effects on stroke outcomes [ 79- 81].

Studies have also found ethnic differences in stroke care and work-up during hospitalization that potentially influences short- and long-term outcomes. A large study using Get with the Guidelines database for 1181 hospitals examined the quality of ischemic stroke care received by blacks, whites, and Hispanic stroke patients for a 5-year time span [ 82]. The study found that blacks received fewer evidence-based care processes than Hispanic or white patients, including lower odds of receiving intravenous thrombolysis, deep vein thrombosis prophylaxis, smoking cessation, discharge anti-thrombotics, anticoagulation for atrial fibrillation, and lipid-lowering therapy. The overall quality of care was observed to improve during the 5-year study period for all ethnic groups.

Trends in Stroke

In general, the trends in stroke incidence and mortality rates have decreased in the recent decades for high-income countries such as the U.S., the United Kingdom, and Canada [ 83- 86]. Analyses from the Framingham Study revealed a decrease in stroke incidence for the past 50 years, although the lifetime risk of stroke did not decrease to the same degree [ 86]; this may reflect both an improvement in risk factor control, as well as an improvement in life expectancy. Population-based studies in Oxfordshire (United Kingdom) showed a major reduction in age- and gender-specific stroke incidence for the past 20 years [ 85]. This decline was found to be associated with an increased use of preventative treatment and better control of vascular risk factors, including hypertension, hyperlipidemia, and smoking. Stroke mortality improvement during 1990 to 2002 was observed in the U.S. and in Canada after mandatory folic acid fortification was in place, but not in England and Wales in which the fortification was not mandatory during the same period [ 84]. There have also been advancements in acute stroke care and this may have led to a nationwide decrease in the percentage of stroke hospitalizations resulting in death in the U.S. [ 87]. This decrease was seen regardless of stroke subtypes (Fig. 2 ).

While there have been reports of decreased stroke incidence and mortality in high-income countries, the opposite has been observed in low-to-middle income countries [ 83]. A systematic review of population-based studies has found more than 100% increase in stroke incidence in these countries. Early stroke case fatality is decreasing in both high-income and low-to-middle income countries. However, the overall early stroke case fatality in low-to-middle income countries is found to be 25% higher than that seen in high-income countries in the past decade. The reasons for these differences are unclear, but low-to-middle income countries are unlikely to have the same advancements in acute stroke care and secondary stroke prevention measures as seen in high-income countries in the recent decades.

Although advancement in stroke prevention and management has led to many successes in the fight against this disease for the past 2 decades, many challenges remain as clinicians and investigators continue to try and uncover the underlying causes behind the many disparities in stroke burden and outcome observed in epidemiologic studies to be able to design interventions to improve stroke mortality and disability for all.

Electronic supplementary material

References

2. Chen C, Hsu C. Stroke: an overview. In: Lisak R, Truong, DD, Caroll, WM, Bhidayasiri R (eds) International neurology: a clinical approach. West Sussex, United Kingdom: Wiley-Blackwell, 2009:1.

4. Chong J, Sacco R. Risk factors for stroke, assessing risk, and the mass and high-risk approaches for stroke prevention. In: Gorelick PB, editor. Continuum: Stroke Prevention. Hagerstwon, Maryland: Lippincott Williams and Wilkins; 2005. pp. 18-34. [ Google Scholar]

6. Ovbiagele B. National sex-specific trends in hospital-based stroke rates. J Stroke Cerebrovasc Dis 2010. doi:10.1016/j.jstrokecerebrovasdis.2010.03.007. [ PubMed]

Articles from Neurotherapeutics are provided here courtesy of Elsevier

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Stroke Epidemiology: Advancing Our Understanding of Disease Mechanism and Therapy

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Stroke is the fourth killer and number one cause of adult disability in the United States. The estimated direct and indirect costs of stroke care in this country are $68.9 billion for 2009. The prevalence of stroke and its cost will undoubtedly rise as ...

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Ages 75+

African Americans are most likely to suffer because of diseases such as Sickle cell anemia, Hypertension, and the location of clogged arteries, all of which increase the chances of sustaining a stroke.

Women

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High blood pressure, High Cholesterol, Heart disease, Diabetes, Obesity, Sickle Cell disease

https://www.cdc.gov/stroke/risk-factors/index.html

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Learn about stroke risk and which risk factors you can manage.

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Nations around the world have vastly different rates of death from stroke. This is largely due to medical care. Additionally as strokes primarily affect older populations countries with low life expectancy have lower stroke rates.

https://ourworldindata.org/life-expectancy#all-charts

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Data sources and methodological differences

We source the data for the Global Health Explorer from three main sources:

World Health Organization's Global Health Estimates

World Health Organization's Global Health Observatory

Institute of Health Metrics and Evaluation's Global Burden of Disease Study

Global Health Estimates (WHO GHE)

The Global Health Estimates are primarily calculated using cause-of-death statistics that are reported to the WHO by individual countries.

These vital registration (VR) statistics are submitted to the WHO Mortality Database on an annual basis by country, year, cause, age and sex. This data is included in the Global Health Estimates if it meets criteria assessing completeness and quality. Since many countries don't meet these criteria, the GHE does not incorporate VR statistics for every country.

There are a number of specialist WHO groups and UN agencies that collect topic or disease-specific data. The dataset on HIV and AIDS - collected and published by UN AIDS - is one example of this. The estimates based on the VR data are compared to the data from specialist WHO groups and UN agencies and adjustments are made if necessary.

Where the VR data is not usable and there is no other nationally representative cause of death data, then the World Health Organization adopts the IHME's Global Burden of Disease data to fill these gaps. Full details on how the WHO's Global Health Estimates are calculated are available here.

Global Health Observatory (WHO GHO)

The WHO's Global Health Observatory brings together a large number of variables produced by the WHO and specialist UN agencies.

The variables found within the Global Health Observatory are limited to the leading causes of death and injury. This means the WHO GHO is less 'complete' than the IHME Global Burden of Disease study and WHO GHE in terms of the diseases included.

The method used to produce each of these variables is different and tailored to the specific cause of death or injury. This is a different approach to both the Global Burden of Disease (IHME) and Global Health Estimates (WHO) which attempt to use a consistent modeling approach for all causes of death and injuries. Additionally, variables in the Global Health Observatory are not consistently disaggregated by age or sex. Instead, they show what data is available and is most relevant for the given variable.

The full list of variables available on the Global Health Observatory are available here, each has their own associated metadata and method.

Global Burden of Disease (IHME)

In the Global Burden of Disease study, the IHME uses a wide range of input data. This includes, but is not limited to census data, household surveys, civil registration and vital statistics, disease registries, health service use, air pollution monitors, satellite imaging, disease notifications, and other sources. These data are available through scientific journals, reports, online databases, books, news reports, and other resources. For most diseases and injuries the data are used as input into a series of standardized models which are used to generate estimates of each disease or injury for all age-groups, sexes, locations, and years.

Since the publication of its Global Burden of Disease study in 2017, the IHME has used its own population estimates. These differ from those used by the UN Population Division, which are used by the World Health Organization (WHO). This key difference propagates through all of the resulting health datasets. Even if the IHME and WHO assumed the same rates of health and mortality burden, this difference in population estimates means many of their population-adjusted figures would be different.

Full details on how the IHME's Global Burden of Disease is calculated are available here and here.

Why do different sources disagree on figures for the same metric?

Collecting precise data on global health is difficult: we can never know exactly which diseases or injuries affect people across the world at any given point in time. In the absence of perfect data, health researchers have a number of ways by which they try to estimate the burden of global health outcomes. These estimates are what we present in the Global Health Explorer.

Each of these sources have slightly different methods for estimating the burden of disease and causes of death, and in some cases the definition of the diseases and injuries in question differ slightly as our Explorer shows.

Differences in disease definition between sources

The diseases and injuries presented in the Global Health Explorer are typically aggregates of multiple similar causes of death. For example, 'Deaths from falls' includes 20 different types of fall which are combined into this one variable.

Individual causes of death have an associated International Classification of Disease (ICD) code. The tenth version of the ICD codes are used in the most recent Global Health Estimates and Global Burden of Disease and this is referred to as ICD-10. For example 'Fall from tree' has the ICD-10 code 'W14', and the ICD-10 codes for all 'Deaths from falls' are 'W00-W19'.

Both IHME and WHO follow the same definition for 'Deaths from falls' but for some other causes of death, their definitions of the same aggregate cause of death doesn't include exactly the same ICD-10 codes. For example, ICD-10 code 'F02.3 - A dementia developing in the course of established Parkinson disease' is included as 'Dementia' in the WHO's Global Health Estimates but as 'Parkinson's disease' in the IHME's Global Burden of Disease.

These slight differences in the definition of diseases may also contribute to the different values we see when looking at the same metric from different sources. The ICD-10 codes used by IHME to define causes of death can be found here and the ICD-10 codes used by the WHO can be found here.

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Cardiovascular disease

Obstructive sleep apnea

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Overview

What is a stroke? A Mayo Clinic expert explains

Learn more from neurologist Robert D. Brown, Jr. M.D., M.P.H.

I'm Dr. Robert Brown, neurologist at Mayo Clinic. In this video, we'll cover the basics of a stroke. What is it, who it happens to, the symptoms, diagnosis, and treatment. Whether you're looking for answers for yourself or someone you love, we're here to give you the best information available. You've likely heard the term stroke before. They affect about 800,000 people in the United States each year. Strokes happen in two ways. In the first, a blocked artery can cut off blood to an area of the brain. And this is known as an ischemic stroke. 85% of strokes are of this type. The second type of stroke happens when a blood vessel can leak or burst. So the blood spills into the brain tissue or surrounding the brain. And this is called a hemorrhagic stroke. Prompt treatment can reduce brain damage and the likelihood of death or disability. So if you or someone you know is experiencing a stroke, you should call 911 and seek emergency medical care right away.

Anyone can have a stroke, but some things put you at higher risk. And some things can lower your risk. If you're 55 and older, if you're African-American, if you're a man, or if you have a family history of strokes or heart attacks, your chances of having a stroke are higher. Being overweight, physically inactive, drinking alcohol heavily, recreational drug use. Those who smoke, have high blood pressure or high cholesterol, have poorly controlled diabetes, suffer from obstructive sleep apnea, or have certain forms of heart disease are at greater risk as well.

Look for these signs and symptoms if you think you or someone you know is having a stroke: Sudden trouble speaking and understanding what others are saying. Paralysis or numbness of the face, arm or leg on one side of the body. Problems seeing in one or both eyes, trouble walking, and a loss of balance. Now many strokes are not associated with headache, but a sudden and severe headache can sometimes occur with some types of stroke. If you notice any of these, even if they come and go or disappear completely, seek emergency medical attention or call 911. Don't wait to see if symptoms stop, for every minute counts.

Once you get to the hospital, your emergency team will review your symptoms and complete a physical exam. They will use several tests to help them figure out what type of stroke you're having and determine the best treatment for the stroke. This could include a CT scan or MRI scan, which are pictures of the brain and arteries, a carotid ultrasound, which is a soundwave test of the carotid arteries which provide blood flow to the front parts of the brain, and blood tests.

Once your doctors can determine if you're having an ischemic or hemorrhagic stroke, they'll be able to figure out the best treatment. If you're suffering an ischemic stroke, it's important to restore blood flow to your brain as quickly as possible, providing the oxygen and other nutrients your brain cells need to survive. To do this, doctors may use an intravenous clot buster medicine, dissolving the clot that is obstructing the blood flow or they may perform an emergency endovascular procedure. This involves advancing a tiny plastic tube called a catheter up into the brain arteries, allowing the blockage in the artery to be removed directly. Unlike ischemic strokes, the goal for treating a hemorrhagic stroke is to control the bleeding and reduce pressure in the brain. Doctors may use emergency medicines to lower the blood pressure, prevent blood vessel spasms, encourage clotting and prevent seizures. Or, if the bleeding is severe, surgery may be performed to remove the blood that is in the brain.

Every stroke is different, and so every person's road to recovery is different. Management of a stroke often involves a care team with several specialties. This may include a neurologist and a physical medicine and rehabilitation physician, among others. Now, in the end, our goal is to help you recover as much function as possible so that you can live independently. A stroke is a life-changing event that can affect you emotionally as much as it can physically. You may feel helpless, frustrated, or depressed. So look for help and support from friends and family. Accept that recovery will take hard work and most of all time. Strive for a new normal and remember to celebrate your progress. If you'd like to learn even more about strokes, watch our other related videos or visit mayoclinic.org. We wish you all the best.

An ischemic stroke occurs when the blood supply to part of the brain is blocked or reduced. This prevents brain tissue from getting oxygen and nutrients. Brain cells begin to die in minutes. Another type of stroke is a hemorrhagic stroke. It occurs when a blood vessel in the brain leaks or bursts and causes bleeding in the brain. The blood increases pressure on brain cells and damages them.

A stroke is a medical emergency. It's crucial to get medical treatment right away. Getting emergency medical help quickly can reduce brain damage and other stroke complications.

The good news is that fewer Americans die of stroke now than in the past. Effective treatments also can help prevent disability from stroke.

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Symptoms

If you or someone you're with may be having a stroke, pay attention to the time the symptoms began. Some treatments are most effective when given soon after a stroke begins.

Symptoms of stroke include:

Trouble speaking and understanding what others are saying. A person having a stroke may be confused, slur words or may not be able to understand speech.

Numbness, weakness or paralysis in the face, arm or leg. This often affects just one side of the body. The person can try to raise both arms over the head. If one arm begins to fall, it may be a sign of a stroke. Also, one side of the mouth may droop when trying to smile.

Problems seeing in one or both eyes. The person may suddenly have blurred or blackened vision in one or both eyes. Or the person may see double.

Headache. A sudden, severe headache may be a symptom of a stroke. Vomiting, dizziness and a change in consciousness may occur with the headache.

Trouble walking. Someone having a stroke may stumble or lose balance or coordination.

When to see a doctor

Seek immediate medical attention if you notice any symptoms of a stroke, even if they seem to come and go or they disappear completely. Think "FAST" and do the following:

Face. Ask the person to smile. Does one side of the face droop?

Arms. Ask the person to raise both arms. Does one arm drift downward? Or is one arm unable to rise?

Speech. Ask the person to repeat a simple phrase. Is the person's speech slurred or different from usual?

Time. If you see any of these signs, call 911 or emergency medical help right away.

Call 911 or your local emergency number immediately. Don't wait to see if symptoms stop. Every minute counts. The longer a stroke goes untreated, the greater the potential for brain damage and disability.

If you're with someone you suspect is having a stroke, watch the person carefully while waiting for emergency assistance.

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Causes

There are two main causes of stroke. An ischemic stroke is caused by a blocked artery in the brain. A hemorrhagic stroke is caused by leaking or bursting of a blood vessel in the brain. Some people may have only a temporary disruption of blood flow to the brain, known as a transient ischemic attack (TIA). A TIA doesn't cause lasting symptoms.

Ischemic stroke

This is the most common type of stroke. It happens when the brain's blood vessels become narrowed or blocked. This causes reduced blood flow, known as ischemia. Blocked or narrowed blood vessels can be caused by fatty deposits that build up in blood vessels. Or they can be caused by blood clots or other debris that travel through the bloodstream, most often from the heart. An ischemic stroke occurs when fatty deposits, blood clots or other debris become lodged in the blood vessels in the brain.

Some early research shows that COVID-19 infection may increase the risk of ischemic stroke, but more study is needed.

Hemorrhagic stroke

Hemorrhagic stroke occurs when a blood vessel in the brain leaks or ruptures. Bleeding inside the brain, known as a brain hemorrhage, can result from many conditions that affect the blood vessels. Factors related to hemorrhagic stroke include:

High blood pressure that's not under control.

Overtreatment with blood thinners, also known as anticoagulants.

Bulges at weak spots in the blood vessel walls, known as aneurysms.

Head trauma, such as from a car accident.

Protein deposits in blood vessel walls that lead to weakness in the vessel wall. This is known as cerebral amyloid angiopathy.

Ischemic stroke that leads to a brain hemorrhage.

A less common cause of bleeding in the brain is the rupture of an arteriovenous malformation (AVM). An AVM is an irregular tangle of thin-walled blood vessels.

Transient ischemic attack

A transient ischemic attack (TIA) is a temporary period of symptoms similar to those of a stroke. But a TIA doesn't cause permanent damage. A TIA is caused by a temporary decrease in blood supply to part of the brain. The decrease may last as little as five minutes. A transient ischemic attack is sometimes known as a ministroke.

A TIA occurs when a blood clot or fatty deposit reduces or blocks blood flow to part of the nervous system.

Seek emergency care even if you think you've had a TIA. It's not possible to tell if you're having a stroke or TIA based only on the symptoms. If you've had a TIA, it means you may have a partially blocked or narrowed artery leading to the brain. Having a TIA increases your risk of having a stroke later.

Risk factors

Many factors can increase the risk of stroke. Potentially treatable stroke risk factors include:

Lifestyle risk factors

Being overweight or obese.

Physical inactivity.

Heavy or binge drinking.

Use of illegal drugs such as cocaine and methamphetamine.

Medical risk factors

High blood pressure.

Cigarette smoking or secondhand smoke exposure.

High cholesterol.

Diabetes.

Obstructive sleep apnea.

Cardiovascular disease, including heart failure, heart defects, heart infection or irregular heart rhythm, such as atrial fibrillation.

Personal or family history of stroke, heart attack or transient ischemic attack.

COVID-19 infection.

Other factors associated with a higher risk of stroke include:

Age - People age 55 or older have a higher risk of stroke than do younger people.

Race or ethnicity - African American and Hispanic people have a higher risk of stroke than do people of other races or ethnicities.

Sex - Men have a higher risk of stroke than do women. Women are usually older when they have strokes, and they're more likely to die of strokes than are men.

Hormones - Taking birth control pills or hormone therapies that include estrogen can increase risk.

Complications

A stroke can sometimes cause temporary or permanent disabilities. Complications depend on how long the brain lacks blood flow and which part is affected. Complications may include:

Loss of muscle movement, known as paralysis. You may become paralyzed on one side of the body. Or you may lose control of certain muscles, such as those on one side of the face or one arm.

Trouble talking or swallowing. A stroke might affect the muscles in the mouth and throat. This can make it hard to talk clearly, swallow or eat. You also may have trouble with language, including speaking or understanding speech, reading or writing.

Memory loss or trouble thinking. Many people who have had strokes experience some memory loss. Others may have trouble thinking, reasoning, making judgments and understanding concepts.

Emotional symptoms. People who have had strokes may have more trouble controlling their emotions. Or they may develop depression.

Pain. Pain, numbness or other feelings may occur in the parts of the body affected by stroke. If a stroke causes you to lose feeling in the left arm, you may develop a tingling sensation in that arm.

Changes in behavior and self-care. People who have had strokes may become more withdrawn. They also may need help with grooming and daily chores.

Prevention

You can take steps to prevent a stroke. It's important to know your stroke risk factors and follow the advice of your healthcare professional about healthy lifestyle strategies. If you've had a stroke, these measures might help prevent another stroke. If you have had a transient ischemic attack (TIA), these steps can help lower your risk of a stroke. The follow-up care you receive in the hospital and afterward also may play a role.

Many stroke prevention strategies are the same as strategies to prevent heart disease. In general, healthy lifestyle recommendations include:

Control high blood pressure, known as hypertension. This is one of the most important things you can do to reduce your stroke risk. If you've had a stroke, lowering your blood pressure can help prevent a TIA or stroke in the future. Healthy lifestyle changes and medicines often are used to treat high blood pressure.

Lower the amount of cholesterol and saturated fat in your diet. Eating less cholesterol and fat, especially saturated fats and trans fats, may reduce buildup in the arteries. If you can't control your cholesterol through dietary changes alone, you may need a cholesterol-lowering medicine.

Quit tobacco use. Smoking raises the risk of stroke for smokers and nonsmokers exposed to secondhand smoke. Quitting lowers your risk of stroke.

Manage diabetes. Diet, exercise and losing weight can help you keep your blood sugar in a healthy range. If lifestyle factors aren't enough to control blood sugar, you may be prescribed diabetes medicine.

Maintain a healthy weight. Being overweight contributes to other stroke risk factors, such as high blood pressure, cardiovascular disease and diabetes.

Eat a diet rich in fruits and vegetables. Eating five or more servings of fruits or vegetables every day may reduce the risk of stroke. The Mediterranean diet, which emphasizes olive oil, fruit, nuts, vegetables and whole grains, may be helpful.

Exercise regularly. Aerobic exercise reduces the risk of stroke in many ways. Exercise can lower blood pressure, increase the levels of good cholesterol, and improve the overall health of the blood vessels and heart. It also helps you lose weight, control diabetes and reduce stress. Gradually work up to at least 30 minutes of moderate physical activity on most or all days of the week. The American Heart association recommends getting 150 minutes of moderate-intensity aerobic activity or 75 minutes of vigorous aerobic activity a week. Moderate intensity activities can include walking, jogging, swimming and bicycling.

Drink alcohol in moderation, if at all. Drinking large amounts of alcohol increases the risk of high blood pressure, ischemic strokes and hemorrhagic strokes. Alcohol also may interact with other medicines you're taking. However, drinking small to moderate amounts of alcohol may help prevent ischemic stroke and decrease the blood's clotting tendency. A small to moderate amount is about one drink a day. Talk to your healthcare professional about what's appropriate for you.

Treat obstructive sleep apnea (OSA). OSA is a sleep disorder that causes you to stop breathing for short periods several times during sleep. Your healthcare professional may recommend a sleep study if you have symptoms of OSA. Treatment includes a device that delivers positive airway pressure through a mask to keep the airway open while you sleep.

Don't use illicit drugs. Certain illicit drugs such as cocaine and methamphetamine are established risk factors for a TIA or a stroke.

Preventive medicines

If you have had an ischemic stroke, you may need medicines to help lower your risk of having another stroke. If you have had a TIA, medicines can lower your risk of having a stroke in the future. These medicines may include:

Anti-platelet drugs. Platelets are cells in the blood that form clots. Anti-platelet medicines make these cells less sticky and less likely to clot. The most commonly used anti-platelet medicine is aspirin. Your healthcare professional can recommend the right dose of aspirin for you.

If you've had a TIA or minor stroke, you may take both an aspirin and an anti-platelet medicine such as clopidogrel (Plavix). These medicines may be prescribed for a period of time to reduce the risk of another stroke. If you can't take aspirin, you may be prescribed clopidogrel alone. Ticagrelor (Brilinta) is another anti-platelet medicine that can be used for stroke prevention.

Blooding-thinning medicines, known as anticoagulants. These medicines reduce blood clotting. Heparin is a fast-acting anticoagulant that may be used short-term in the hospital.

Slower acting warfarin (Jantoven) may be used over a longer term. Warfarin is a powerful blood-thinning medicine, so you need to take it exactly as directed and watch for side effects. You also need regular blood tests to monitor warfarin's effects.

Several newer blood-thinning medicines are available to prevent strokes in people who have a high risk. These medicines include dabigatran (Pradaxa), rivaroxaban (Xarelto), apixaban (Eliquis) and edoxaban (Savaysa). They work faster than warfarin and usually don't require regular blood tests or monitoring by your healthcare professional. These medicines also are associated with a lower risk of bleeding complications compared to warfarin.

Stroke care at Mayo Clinic

Show references

1. Walls RM, et al., eds. Stroke. In: Rosen's Emergency Medicine: Concepts and Clinical Practice. 10th ed. Elsevier; 2023. https://www.clinicalkey.com. Accessed Sept. 13, 2023.

2. Ferri FF. Ferri's Clinical Advisor 2024. Elsevier; 2024. https://www.clinicalkey.com. Accessed Sept. 13, 2023.

3. Patients and caregivers. National Institute of Neurological Disorders and Stroke. https://www.ninds.nih.gov/health-information/public-education/know-stroke/patients-and-caregivers#. Accessed Sept. 13, 2023.

4. Stroke. National Heart, Lung, and Blood Institute. https://www.nhlbi.nih.gov/health-topics/stroke. Accessed Sept. 13, 2023.

5. Oliveira-Filho J, et al. Initial assessment and management of acute stroke. https://www.uptodate.com/contents/search. Accessed Sept. 13, 2023.

6. About stroke. Centers for Disease Control and Prevention. https://www.cdc.gov/stroke/healthy_living.htm. Accessed Sept. 13, 2023.

7. Effects of stroke. American Stroke Association. https://www.stroke.org/en/about-stroke/effects-of-stroke. Accessed Sept. 13, 2023.

8. Rehab therapy after a stroke. American Stroke Association. https://www.stroke.org/en/life-after-stroke/stroke-rehab/rehab-therapy-after-a-stroke. Accessed Sept. 13, 2023.

9. Arteriovenous malformations (AVMs). National Institute of Neurological Disorders and Stroke. https://www.ninds.nih.gov/health-information/disorders/arteriovenous-malformations-avms?search-term=arterial#. Accessed Oct. 2, 2023.

10. Cerebral aneurysms. National Institute of Neurological Disorders and Stroke. https://www.ninds.nih.gov/disorders/patient-caregiver-education/fact-sheets/cerebral-aneurysms-fact-sheet. Accessed Sept. 13, 2023.

11. Transient ischemic attack. Merck Manual Professional Version. https://www.merckmanuals.com/professional/neurologic-disorders/stroke/transient-ischemic-attack-tia?query=transient%20ischemic%20attack#. Accessed Sept. 13, 2023.

12. Stroke. National Institute of Neurological Disorders and Stroke. https://www.ninds.nih.gov/Disorders/Patient-Caregiver-Education/Fact-Sheets/Post-Stroke-Rehabilitation-Fact-Sheet. Accessed Sept. 13, 2023.

13. Rose NS, et al. Overview of secondary prevention of ischemic stroke. https://www.uptodate.com/contents/search. Accessed Sept. 13, 2023.

14. Prevent stroke: What you can do. Centers for Disease Control and Prevention. https://www.cdc.gov/stroke/prevention.htm#print. Accessed Sept. 13, 2023.

15. Know your risk for stroke. Centers for Disease Control and Prevention. https://www.cdc.gov/stroke/risk_factors.htm#. Accessed Oct. 2, 2023.

16. Powers WJ, et al. Guidelines for the early management of patients with acute ischemic stroke: 2019 update to the 2018 guidelines for the early management of acute ischemic stroke - A guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2019; doi:10.1161/STR.0000000000000211.

17. Papadakis MA, et al., eds. Quick Medical Diagnosis & Treatment 2023. McGraw Hill; 2023. https://accessmedicine.mhmedical.com. Accessed Sept. 13, 2023.

18. Tsao CW, et al. Heart disease and stroke statistics - 2023 update: A report from the American Heart Association. Circulation. 2023; doi:10.1161/CIR.0000000000001123.

19. Grotta JC, et al., eds. Stroke: Pathophysiology, Diagnosis, and Management. 7th ed. Elsevier, 2022. https://www.clinicalkey.com. Accessed Sept. 15, 2023.

20. Suppah M, et al. An evidence-based approach to anticoagulation therapy comparing direct oral anticoagulants and vitamin K antagonists in patients with atrial fibrillation and bioprosthetic valves: A systematic review, meta-analysis and network meta-analysis. American Journal of Cardiology. 2023; doi:10.1016/j.amjcard.2023.07.141.

21. Tyagi K, et al. Neurological manifestations of SARS-CoV-2: Complexity, mechanism and associated disorders. European Journal of Medical Research. 2023; doi:10.1186/s40001-023-01293-2.

22. Siegler JE, et al. Cerebrovascular disease in COVID-19. Viruses. 2023; doi:10.3390/v15071598.

23. Lombardo M, et al. Health effects of red wine consumption: A narrative review of an issue that still deserves debate. Nutrients. 2023; doi:10.3390/nu15081921.

24. Jim J. Complications of carotid endarterectomy. https://www.uptodate.com/contents/search. Accessed Oct. 2, 2023.

25. Van Nimwegan D, et al. Interventions for improving psychosocial well-being after stroke: A systematic review. International Journal of Nursing Studies. 2023; doi:10.1016/j.ijnurstu.2023.104492.

26. Hasan TF, et al. Diagnosis and management of acute ischemic stroke. Mayo Clinic Proceedings. 2018; doi:10.1016/j.mayocp.2018.02.013.

27. Ami TR. Allscripts EPSi. Mayo Clinic. Sept. 4, 2023.

28. Barrett KM, et al. Ambulance-based assessment of NIH stroke scale with telemedicine: A feasibility pilot study. Journal of Telemedicine and Telecare. 2017; doi:10.1177/1357633X16648490.

29. Sener U, et al. Ischemic stroke in patients with malignancy. Mayo Clinic Proceedings. 2022; doi:10.1016/j.mayocp.2022.09.003.

30. Quality check. The Joint Commission. https://www.qualitycheck.org/search/?keyword=mayo%20clinic. Accessed Oct. 4, 2023.

31. Quality care you can trust. American Heart Association. https://www.heart.org/en/professional/quality-improvement/hospital-maps. Accessed Oct. 4, 2023.

32. Attig JM. Allscripts EPSi. Mayo Clinic. Oct. 9, 2023.

33. How much physical activity do you need? American Heart Association. https://www.heart.org/en/healthy-living/fitness/fitness-basics/aha-recs-for-physical-activity-infographic. Accessed Oct. 12, 2023.

34. Graff-Radford J (expert opinion). Mayo Clinic. Oct. 11, 2023.

35. Healthcare. DNV Healthcare USA, Inc. https://www.dnvhealthcareportal.com/hospitals?search_type=and&q=mayo+clinic&c=&c=20806&c=&c=&prSubmit=Search. Accessed Nov. 1, 2023.

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Promptly spotting stroke symptoms leads to faster treatment and less damage to the brain.

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interneural communication

balance

sensory processing

speech

responsiveness and movement

emotional regulation

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Intracerebral Bleeding

Blood Clots

Fatty Deposits in Neural Tissue

Necrosis

Infarction

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Abstract

Stroke is the second leading cause of death and a major contributor to disability worldwide. The prevalence of stroke is highest in developing countries, with ischemic stroke being the most common type. Considerable progress has been made in our understanding of the pathophysiology of stroke and the underlying mechanisms leading to ischemic insult. Stroke therapy primarily focuses on restoring blood flow to the brain and treating stroke-induced neurological damage. Lack of success in recent clinical trials has led to significant refinement of animal models, focus-driven study design and use of new technologies in stroke research. Simultaneously, despite progress in stroke management, post-stroke care exerts a substantial impact on families, the healthcare system and the economy. Improvements in pre-clinical and clinical care are likely to underpin successful stroke treatment, recovery, rehabilitation and prevention. In this review, we focus on the pathophysiology of stroke, major advances in the identification of therapeutic targets and recent trends in stroke research.

Keywords: stroke, pathophysiology, treatment, neurological deficit, recovery, rehabilitation

1. Introduction

Stroke is a neurological disorder characterized by blockage of blood vessels. Clots form in the brain and interrupt blood flow, clogging arteries and causing blood vessels to break, leading to bleeding. Rupture of the arteries leading to the brain during stroke results in the sudden death of brain cells owing to a lack of oxygen. Stroke can also lead to depression and dementia.

Until the International Classification of Disease 11 (ICD-11) was released in 2018, stroke was classified as a disease of the blood vessels. Under the previous ICD coding rationale, clinical data generated from stroke patients were included as part of the cardiovascular diseases chapter, greatly misrepresenting the severity and specific disease burden of stroke. Due to this misclassification within the ICD, stroke patients and researchers did not benefit from government support or grant funding directed towards neurological disease. After prolonged advocacy from a group of clinicians, the true nature and significance of stroke was acknowledged in the ICD-11; stroke was re-categorized into the neurological chapter [ 1]. The reclassification of stroke as a neurological disorder has led to more accurate documentation of data and statistical analysis, supporting improvements in acute healthcare and acquisition of research funding for stroke.

2. Epidemiology of Stroke

Stroke is the second leading cause of death globally. It affects roughly 13.7 million people and kills around 5.5 million annually. Approximately 87% of strokes are ischemic infarctions, a prevalence which increased substantially between 1990 and 2016, attributed to decreased mortality and improved clinical interventions. Primary (first-time) hemorrhages comprise the majority of strokes, with secondary (second-time) hemorrhages constituting an estimated 10-25% [ 2, 3]. The incidence of stroke doubled in low-and-middle income countries over 1990-2016 but declined by 42% in high-income countries over the same period. According to the Global Burden of Disease Study (GBD), although the prevalence of stroke has decreased, the age of those affected, their sex and their geographic location mean that the socio-economic burden of stroke has increased over time [ 3].

Gender-specific stroke: The occurrence of stroke in men and women also depends on age. It is higher at younger ages in women, whereas incidence increases slightly with older age in men. The higher risk for stroke in women is due to factors related to pregnancy, such as preeclampsia, contraceptive use and hormonal therapy, as well as migraine with aura. Atrial fibrillation increases stroke risk in women over 75 years by 20%. Based on the National Institutes of Health Stroke Scale (0 = no stroke, 1-4 = minor stroke, 5-15 = moderate stroke, 15-20 = moderate/severe stroke, 21-42 = severe stroke), mean stroke severity was estimated at 10 for women and 8.2 for men. Both brain infarction and intracerebral hemorrhage (ICH) are common in men, but cardioembolic stroke, a more severe form of stroke, is more prevalent among women. The fatality rate for stroke is also higher among women [ 5, 6, 7]. Women live longer than men, which is one reason for their higher incidence of stroke; another important concern is women's delay in accepting help for ongoing symptoms [ 8]. For men, the most common causes of stroke are tobacco smoking, excessive alcohol consumption, myocardial infarction and arterial disorders [ 9].

Socioeconomic variation: There is a strong inverse relationship between stroke and socioeconomic status, attributable to inadequate hospital facilities and post-stroke care among low-income populations [ 14]. A case study conducted in the US showed that people with high financial status had better stroke treatment options than deprived individuals [ 15]. A study in China linked low income and lack of health insurance to prevention of secondary stroke attack [ 16]. Research conducted in Austria associated level of education with take-up of treatments such as echocardiography and speech therapy; however, there was no difference in administration of thrombolysis, occupational therapy, physiotherapy or stroke care for secondary attack by socioeconomic status [ 17]. Similarly, in the Scottish healthcare system, basic treatments like thrombolysis were provided irrespective of the economic status of patients [ 18].

3. Pathophysiology of Stroke

Stroke is defined as an abrupt neurological outburst caused by impaired perfusion through the blood vessels to the brain. It is important to understand the neurovascular anatomy to study the clinical manifestation of the stroke. The blood flow to the brain is managed by two internal carotids anteriorly and two vertebral arteries posteriorly (the circle of Willis). Ischemic stroke is caused by deficient blood and oxygen supply to the brain; hemorrhagic stroke is caused by bleeding or leaky blood vessels.

Ischemic occlusions contribute to around 85% of casualties in stroke patients, with the remainder due to intracerebral bleeding. Ischemic occlusion generates thrombotic and embolic conditions in the brain [ 19]. In thrombosis, the blood flow is affected by narrowing of vessels due to atherosclerosis. The build-up of plaque will eventually constrict the vascular chamber and form clots, causing thrombotic stroke. In an embolic stroke, decreased blood flow to the brain region causes an embolism; the blood flow to the brain reduces, causing severe stress and untimely cell death (necrosis). Necrosis is followed by disruption of the plasma membrane, organelle swelling and leaking of cellular contents into extracellular space [ 20], and loss of neuronal function. Other key events contributing to stroke pathology are inflammation, energy failure, loss of homeostasis, acidosis, increased intracellular calcium levels, excitotoxicity, free radical-mediated toxicity, cytokine-mediated cytotoxicity, complement activation, impairment of the blood-brain barrier, activation of glial cells, oxidative stress and infiltration of leukocytes [ 21, 22, 23, 24, 25].

Hemorrhagic stroke accounts for approximately 10-15% of all strokes and has a high mortality rate. In this condition, stress in the brain tissue and internal injury cause blood vessels to rupture. It produces toxic effects in the vascular system, resulting in infarction [ 26]. It is classified into intracerebral and subarachnoid hemorrhage. In ICH, blood vessels rupture and cause abnormal accumulation of blood within the brain. The main reasons for ICH are hypertension, disrupted vasculature, excessive use of anticoagulants and thrombolytic agents. In subarachnoid hemorrhage, blood accumulates in the subarachnoid space of the brain due to a head injury or cerebral aneurysm () [ 27, 28].

4. Risk Factors for Stroke

As noted earlier, the risk of stroke increases with age and doubles over the age of 55 years in both men and women. Risk is increased further when an individual has an existing medical condition like hypertension, coronary artery disease or hyperlipidemia. Nearly 60% of strokes are in patients with a history of transient ischemic attack (TIA). Some of the risk factors for stroke are modifiable, and some are non-modifiable ().

4.1. Non-Modifiable Risk Factors

These include age, sex, ethnicity, TIA and hereditary characteristics. In the US in 2005, the average age of incidence of stroke was 69.2 years [ 2, 29, 30]. Recent research has indicated that people aged 20-54 years are at increasing risk of stroke, probably due to pre-existing secondary factors [ 31]. Women are at equal or greater risk of stroke than men, irrespective of age [ 32]. US research shows that Hispanic and black populations are at higher risk of stroke than white populations; notably, the incidence of hemorrhagic stroke is significantly higher in black people than in age-matched white populations [ 33, 34, 35].

Transient ischemic attack is classified as a mini stroke; the underlying mechanism is the same as for full-blown stroke. In TIA, the blood supply to part of the brain is blocked temporarily. It acts as a warning sign before the actual event, providing an opportunity to change lifestyle and commence medications to reduce the chance of stroke [ 36, 37].

Genetics contribute to both modifiable and non-modifiable risk factors for stroke. Genetic risk is proportional to the age, sex and race of the individual [ 38, 39], but a multitude of genetic mechanisms can increase the risk of stroke. Firstly, a parental or family history of stroke increases the chance of an individual developing this neurological disorder. Secondly, a rare single gene mutation can contribute to pathophysiology in which stroke is the primary clinical manifestation, such as in cerebral autosomal dominant arteriopathy. Thirdly, stroke can be one of many after-effects of multiple syndromes caused by genetic mutation, such as sickle cell anemia. Fourthly, some common genetic variants are associated with increased stroke risk, such as genetic polymorphism in 9p21 [ 40]. A genome-wide association study of stroke showed high heritability (around 40%) for large blood vessel disease, and low heritability (16.7%) for small vessel disorders. Recent evidence suggests that studying heritability will improve the understanding of stroke sub-types, improve patient management and enable earlier and more efficient prognosis [ 5, 41].

4.2. Modifiable Risk Factors

These are of paramount importance, because timely and appropriate medical intervention can reduce the risk of stroke in susceptible individuals. The major modifiable risk factors for stroke are hypertension, diabetes, lack of physical exercise, alcohol and drug abuse, cholesterol, diet management and genetics.

Hypertension: It is one of the predominant risk factors for stroke. In one study, a blood pressure (BP) of at least 160/90 mmHg and a history of hypertension were considered equally important predispositions for stroke, with 54% of the stroke-affected population having these characteristics [ 42, 43]. BP and prevalence of stroke are correlated in both hypertensive and normal individuals. A study reported that a 5-6 mm Hg reduction in BP lowered the relative risk of stroke by 42% [ 44]. Randomized trials of interventions to reduce hypertension in people aged 60+ have shown similar results, lowering the incidences of symptoms of stroke by 36% and 42%, respectively [ 45, 46].

Diabetes: It doubles the risk of ischemic stroke and confers an approximately 20% higher mortality rate. Moreover, the prognosis for diabetic individuals after a stroke is worse than for non-diabetic patients, including higher rates of severe disability and slower recovery [ 47, 48]. Tight regulation of glycemic levels alone is ineffective; medical intervention plus behavioral modifications could help decrease the severity of stroke for diabetic individuals [ 49].

Alcohol and drug abuse: The relationship between stroke risk and alcohol intake follows a curvilinear pattern, with the risk related to the amount of alcohol consumed daily. Low to moderate consumption of alcohol (≤2 standard drinks daily for men and ≤1 for women) reduces stroke risk, whereas high intake increases it. In contrast, even low consumption of alcohol escalates the risk of hemorrhagic stroke [ 57, 58, 59]. Regular use of illegitimate substances such as cocaine, heroin, phencyclidine (PCP), lysergic acid diethylamide (LSD), cannabis/marijuana or amphetamines is related to increased risk of all subtypes of strokes [ 60]. Illicit drug use is a common predisposing factor for stroke among individuals aged below 35 years. US research showed that the proportion of illicit drug users among stroke patients aged 15-44 years was six times higher than among age-matched patients admitted with other serious conditions [ 61]. However, there is no strong evidence to confirm these findings, and the relationship between these drugs and stroke is anecdotal [ 62].

Smoking: Tobacco smoking is directly linked to increased risk of stroke. An average smoker has twice the chance of suffering from a stroke of a non-smoker. Smoking contributes to 15% of stroke-related mortality. Research suggests that an individual who stops smoking reduces the relative risk of stroke, while prolonged second-hand smoking confers a 30% elevation in the risk of stroke [ 63, 64, 65].

Insufficient physical inactivity and poor diet are associated with increased risk for stroke. Lack of exercise increases the chances of stroke attack in an individual. Insufficient physical activity is also linked to other health issues like high BP, obesity and diabetes, all conditions related to high stroke incidence [ 66, 67]. Poor diet influences the risk of stroke, contributing to hypertension, hyperlipidemia, obesity and diabetes. Certain dietary components are well known to heighten risk; for example, excessive salt intake is linked to high hypertension and stroke. Conversely, a diet high in fruit and vegetables (notably, the Mediterranean diet) has been shown to decrease the risk of stroke [ 68, 69, 70, 71, 72].

5. Animal Models of Stroke

Animal models usually used for research include induced, spontaneous, negative and orphan models. In the induced model, a disease condition is induced in the animal with a view to studying the effects, whereas in the spontaneous model, an animal is selected with a similar disease state naturally present in the model. Negative animal models are used to study the resistance mechanisms underlying a particular disease condition. Orphan models are deployed to understand the pathology of a newly characterized disease in human subjects [ 73, 74].

Many animal models have been developed to study the pathophysiology associated with stroke; they offer several advantages over studying stroke in humans or in vitro. The nature of stroke in humans is unpredictable, with diverse clinical manifestation and localization, whereas animal models are highly predictable and reproducible. Pathophysiological investigation often requires direct access to brain tissue, which is possible with animal models but not in humans. Moreover, current imaging techniques are unable to characterize events occurring within the first few minutes of a stroke. Finally, some aspects of stroke, such as vasculature and perfusion, cannot be studied in in vitro models [ 75]. Different stroke models used in animals are described in the session below ().

Table 1

Intraluminal suture MCAo model

Mimics human ischemic stroke,
Exhibits a penumbra,
Highly reproducible,
No craniectomy

Hyper-/hypothermia,
Increased haemorrhage,
Not suitable for thrombolysis studies

Craniotomy model

High long-term survival rates,
Visual confirmation of successful MCAo

Highly invasive and procedural complications,
Requires surgical skills

Photo-thrombosis model

Enables well-defined localization of an ischemic lesion,
Highly reproducible,
Less invasive

Causes early vasogenic edema,
Not suitable for investigating neuroprotective agents

Endothelin-1 model

Less invasive,
Induction of ischemic lesion in cortical regions,
Low mortality

Duration of ischemia not controllable, Induction of astrocytosis and axonal sprouting

Embolic stroke model

Mimics the pathogenesis of human stroke

Low reproducibility of infarcts, Spontaneous recanalization

Neurorehabilitation

Rapid establishment of independence in activities of daily living
Improves outcomes for cognitive, language, and motor skills

Develop cost-effective rehabilitative services
Lack of in-depth studies on efficacy related to neurorehabilitation

Biomaterial testing

Reduction in lesion volume
Bridge the lesion with neural tissue for neural reorganization
Reduce secondary damage
Improve neurological behaviour

Long-term experiments with the same biomaterial are challenging because of the degradation of material which might affect the treatment

Photo-thrombosis model: This model is based on photo-oxidation of the vasculature leading to lesion formation in the cortex and striatum. In this method, the skull is irradiated with a photoactive dye that causes endothelial damage, intraparenchymal vessel aggregation and platelet stimulation in the affected area. It is injected intraperitoneally in mice and intravenously in rats [ 91]. This model is highly reproducible, with a low mortality rate and no surgery. The pathophysiology of this method is slightly different to that seen in human stroke due to little collateral blood flow or formation of ischemic penumbra. However, recent researchers modified the photothrombotic ischemia model to include hypoperfusion in an attempt to mimic penumbra. It has also been deployed in freely moving mice to evaluate the development of motor cortex ischemia and motor deficits. This model permits assessment of the ongoing infarction and improves our understanding of the neuronal insult and repair process [ 92, 93].

Neurorehabilitation in animal models: Various rehabilitative devices and forced training strategies have been deployed in stroke-affected animals to study neurological behavior. Robotic and electric devices have also been developed for training purposes in animal models to evaluate the functionality and effectiveness of the rehabilitation process. Similarly, forced exercise regimes, such as running on a treadmill or task-oriented motor training, are used to study rehabilitation scope in humans. Housing environments that provide social, motor and sensory stimuli and support cell engraftment, creating a more realistic approximation of human treatment, can be tested using animal models [ 103, 104, 105].

Animal models in biomaterial testing: Animal models have been well characterized for the study of brain tissues via brain atlases ( http://www.med.harvard.edu/AANLIB/, https://portal.brain-map.org) for the required species. Stereotaxic techniques are utilized to introduce biomaterials or cells into particular coordinates of the target tissue. Microlesions can be studied precisely, and targeted localization can be confirmed using magnetic resonance imaging (MRI)-based lesion cartography [ 106, 107, 108].

6. Prevention and Treatment Strategies for Stroke

Stroke prevention involves modifying risk factors within a population or individuals, while stroke management depends on treating its pathophysiology. Despite an enormous amount of research into stroke over the last two decades, no simple means of treating or preventing all the clinical causes of stroke has been established. The overall direction of current stroke research is to generate novel therapies that modulate factors leading to primary and secondary stroke. Recent and current strategies for stroke prevention and treatment are discussed below ().

Excitotoxicity: Neuronal death is a key manifestation of stroke. A key reason for this phenomenon is neuronal depolarization and inability to maintain membrane potential within the cell. This process is mediated by glutamate receptors N-methyl-D-aspartate (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), which were among the first neuroprotective agents tested in stroke prevention. However, the untimely release of glutamate overpowers the system that removes glutamate from the cell and causes abnormal release of NMDA and AMPA molecules, leading to uninhibited calcium influx and protein damage. As a result, these agents have not been shown to reduce neuronal death in human subjects. Targeting the molecular pathways downstream of excitotoxicity signaling, rather than directly targeting glutamatergic signaling, might reduce the side effects of the process [ 109, 110].

Gamma aminobutyric acid (GABA) agonists: Clomethiazole is a GABA agonist that has been tested for its ability to improve stroke symptoms in patients, but failed to reduce the toxicity induced by the glutamate receptor [ 111].

Sodium (Na⁺) channel blockers: Na⁺ channel blockers have been used as neuroprotective agents in various animal models of stroke. They prevent neuronal death and reduce white matter damage. Many voltage-gated Na⁺ channel blockers have been tested in clinical trials, but most have proved to be ineffective [ 112]. Mexiletine is a neuroprotectant and Na⁺ channel blocker that proved effective in grey and white matter ischemic stroke, though further evaluation is required to confirm its role [ 113]. Lubeluzole was shown to reduce mortality in stroke in initial clinical trials, but successive trials failed to reproduce similar outcomes. Similarly, sipatrigine is a Na⁺ and Ca ²⁺channel blocker which failed in a Phase II clinical trial in stroke patients. Amiodarone was shown to aggravate brain injury due to defective transportation and accumulation of Na⁺ ions in the brain after stroke [ 114].

Calcium (Ca²⁺) channel blockers: Voltage-dependent Ca ²⁺ ion channel blockers have been shown to decrease the ischemic insult in animal models of brain injury. The Ca ²⁺ ion chelator DP-b99 proved efficient and safe in Phase I and II clinical trials when administered to stroke patients. Similarly, Phase II trials significantly improved clinical symptoms in stroke patients treated within 12 h of onset [ 115]. In another study, Ca ²⁺ channel blockers reduced the risk of stroke by 13.5% in comparison to diuretics and β-blockers [ 116].

6.1. Reperfusion

Intra-arterial thrombolysis (IAT): IAT is another approach designed to combat acute stroke. This treatment is most effective in the first six hours of onset of MCA occlusion, and requires experienced clinicians and angiographic techniques [ 115]. Prolyse in Acute Cerebral Thromboembolism II (PROACT II) and Middle Cerebral Artery Embolism Local Fibrinolytic Intervention (MELT) were randomized clinical trials (RCTs) undertaken to test the efficacy and safety of a recombinant pro-urokinase drug [ 126, 127], but did not produce any data useful for stroke treatment. Thrombolytics and glycoprotein IIb/IIIa antagonists were combined in two small clinical trials; this approach was helpful in treating atherosclerotic occlusions but less effective for cardioembolism [ 128, 129]. The Interventional Management of Stroke (IMS) III trial tested IVT and IAT together to assess the benefits of combining rapid administration of therapy (IVT) and a superior recanalization methodology for faster relief (IAT) [ 130]. The IMS III trial was fruitful with bridging therapy (combination of IVT and IAT) as compared to IVT alone. There was an increase of 69.6% in the recanalization rate using bridging therapy in stroke patients [ 131, 132].

Fibrinogen-depleting agents: Research has found a strong correlation between high fibrinogen levels in stroke patients and poor diagnosis for clinical outcomes. Fibrinogen-depleting agents decrease blood plasma levels of fibrinogen, hence reduce blood thickness and increase blood flow. They also remove the blood clot in the artery and restore blood flow in the affected regions of the brain. However, although some RCTs of defibrinogen therapy identified beneficial effects of fibrinogen-depleting agents in stroke patients, others failed to show positive effects on clinical outcomes after stroke [ 133]. Moreover, some studies reported bleeding after treatment with defibrinogen agents. Ancrod is a defibrinogenating agent derived from snake venom that has been studied for its ability to treat ischemic stroke within three hours of onset [ 134]. The European Stroke Treatment with Ancrod Trial (ESTAT) concluded that controlled administration of ancrod at 70 mg/dL fibrinogen was efficacious and safe, and achieved lower prevalence of ICH than observed at lower fibrinogen levels [ 135].

6.2. Others

Antihypertensive therapy: Hypertension is a risk factor for stroke. There are many reasons for high BP in stroke, including a history of hypertension, acute neuroendocrine stimulation, increased intracranial pressure, stress linked to hospital admission and intermittent painful spells [ 136]. Correct treatment of high BP during stroke is uncertain due to contradictory outcomes of clinical studies. Some research shows positive correlations between high BP and stroke-related mortality, hematoma expansion or intracerebral damage, suggesting that high BP should be treated. In other studies, low BP levels led to tissue perfusion and increased lesion size, thereby worsening the clinical outcome [ 137, 138]. The multi-center Acute Candesartan Cilexetil Therapy in Stroke Survivors (ACCESS) Phase II study proved that taking medication (candesartan) for BP during stroke was safe, with no orchestrated cerebrovascular events reported due to hypotension. Similar research has been performed with antihypertensive drugs, such as the Continue Or Stop post Stroke Antihypertensives Collaborative Study (COSSACS) to study the efficacy of antihypertensive therapy in stroke; the Control of Hypertension and Hypotension Immediately Post Stroke (CHHIPS) study, designed to determine the cut-off value for BP during an attack; and the Scandinavian Candesartan Acute Stroke Trial (SCAST), which aimed to measure the effectiveness of the drug candesartan on stroke and cardiovascular disease [ 115, 139]. In the COSSACS study, continuing antihypertensive drugs for a two-week period produced no extra harm as compared to stopping it and might be associated with reduced two-week mortality in patients with ischemic stroke [ 140]. The CHHIPS study demonstrated that a relatively moderate reduction in blood pressure lowered the mortality rate [ 141], whereas the SCAST study suggested that a careful BP-lowering treatment was associated with a higher risk of poor clinical outcome [ 142].

Glucose management: Hyperglycemia (elevated blood glucose) is common in stroke patients, so targeting blood glucose levels is an efficient stroke management strategy. Hyperglycemia > 6.0 mmol/L (108 mg/dL) is observed in most stroke patients; it initiates lipid peroxidation and cell lysis in compromised tissue, leading to stroke complications. An experimental study conducted in a rat model of collagenase-induced ICH found that hyperglycemia worsens edema formation and increases cell death, accelerating the course of ischemic injury. Increased blood glucose level is also associated with progression of infarction, reduced recanalization and poor clinical outcome [ 143]. Continuous glucose monitoring systems have been deployed to reduce stroke-related risks in both diabetic and non-diabetic stroke patients [ 144].

Antiplatelet therapy: This therapy is used for acute ischemic stroke management and for prevention of stroke incidence. It is also vital in controlling non-cardioembolic ischemic stroke and TIA. Antiplatelet agents like aspirin, clopidogrel and ticagrelor are the most widely used drugs administered to stroke sufferers within the first few days of attack [ 145]. Dual antiplatelet therapy, which involves a combination of clopidogrel, prasugrel or ticagrelor with aspirin, has become popular; many studies have tested the efficacy and safety of this dual therapy. It has been claimed that clopidogrel and aspirin combination therapy is most beneficial if introduced within 24 h of stroke and continued for 4-12 weeks [ 146].

Stem cell therapy: It offers promising therapeutic opportunities, safety and efficacy to stroke patients. Research on embryonic stem cells, mesenchymal cells and induced pluripotent stem cells has assessed their potential for tissue regeneration, maintenance, migration and proliferation, rewiring of neural circuitry and physical and behavioral rejuvenation [ 147]. Recently, a new type of mesenchymal stem cells (MSCs), called multilineage differentiating stress-enduring (Muse) cells, has been found in connective tissue. These cells offer great regenerative capacity and have been tested as a stroke treatment. After intravenous transplantation of Muse cells in a mouse model, they were found to engraft into the damaged host tissue and differentiate to provide functional recovery in the host [ 148]. Neovascularization is another mode of action of cell therapies in stroke; studies conducted in vitro and in vivo have shown that transplanted cells promote angiogenesis [ 149, 150]. Furthermore, multiple stroke studies have reported that MSCs stimulate neurogenesis; this was confirmed in human embryonic neural stem cells using BrdU-labelling [ 151, 152]. Stem cell therapy enhances the proliferation of neural stem cells and neuritogenesis [ 153]. Careful experimental design and clinical trials of stem cell therapies are likely to usher in a new era of treatment for stroke by promoting neurogenesis, rebuilding neural networks and boosting axonal growth and synaptogenesis.

Neural repair: This is an alternative therapy to neuroprotection. It is used to rejuvenate the tissue when the damage is already done and is therefore not time-bound but is most effective when administered 24 h after stroke attack. Many animal models have been used in attempts to stimulate neurogenesis and initiate the neuronal repair process [ 154]. Neural repair utilizes stem cell therapy to initiate repair mechanisms through cell integration into the wound or use of neurotrophic factors to block neuronal growth inhibitors. These cells may be channeled to any injured region to facilitate greater synaptic connectivity. Clinical trials using neural stem cells have proven beneficial in stroke patients. However, trials of myelin-associated glycoprotein, neurite outgrowth inhibitor (NOGO) proteins and chondroitin sulphate proteoglycans have shown these agents to be insufficiently effective; more clinical trials are required to increase treatment efficacy [ 155]. Biological intrusions may foster regeneration of newer cells, improve axonal guidance and enhance neural circuitry. Pharmacological and immunological interventions may target receptors to provide signaling cues for regeneration or block inhibitory factors in stroke-affected regions of the brain [ 156].

7. Trends in Stroke Research

The incidence of stroke-related emergencies has decreased substantially over recent years due to improved understanding of the pathophysiology of stroke and identification of new drugs designed to treat the multitude of possible targets. Technological advancements like telestroke [ 161] and mobile stroke [ 162] units have reduced mortality and morbidity. Therefore, stroke management systems should include post-stroke care facilities on top of existing primary care and access to occupational, speech or any physical therapy following hospital discharge. Hospitals should develop standardized policies to handle emergencies in a timely fashion to avoid casualties and prevent secondary stroke [ 163]. Recently, the role of physiotherapists has emerged as an important aspect of post-stroke care management. Physiotherapists have initiated clinical trials of stroke recovery processes and rehabilitation therapy sessions. One ongoing study includes a strategy to manage disability by improving mobility using treadmill exercise, electromechanical device therapy and circuit class therapy [ 164, 165]. Stroke Recovery and Rehabilitation Roundtables bring physiotherapists and other experts together to recommend research directions and produce guidance for the post-stroke healthcare system. Optimized delivery of stroke care systems and access to rehabilitation services are the future of healthcare for stroke [ 166].

Animal models used in stroke research reflect only a portion of the consequences of the condition in human subjects. Moreover, experiments conducted within a single laboratory are often constrained in terms of their research output. In vivo animal models of stroke should include aged populations to maximize their relevance, but most recent studies involve young and adult animals. Stroke studies should be conducted in both male and female subjects to exclude gender bias, and should take account of other confounders like hypertension, diabetes and obesity. All these issues make stroke research complex and expensive, and imply that it should be carried out collaboratively, across multiple labs. Ideally, an international multicenter platform for clinical trials would be established to increase the validity of research outcomes with respect to efficacy, safety, translational value, dose-response relationships and proof-of-principle. This strategy will help to overcome the current hurdles in transforming laboratory data into therapeutics for stroke.

Advancements in stem cell technologies and genomics have led to regenerative therapy to rebuild neural networks and repair damaged neurons due to ischemic insult [ 167, 168]. The WIP1 gene is a regulator of Wnt signaling and a promising target for drug development. Studies in mice models showed that knockdown of WIP1 downregulates the stroke functional recovery process after injury, and that the presence of this gene regulates neurogenesis through activation of β-Catenin/Wnt signaling [ 169]. Similarly, NB-3 (contactin-6) plays a vital role in neuroprotection, as shown by knockdown of NB-3 in mice after stroke attack. NB-3-deficient mice had increased brain damage after MCAo, which also affected neurite outgrowth and neuronal survival rate. NB-3 is believed to have therapeutic benefits for ischemic insult [ 170]. Therefore, WIP1 and NB-3 are promising candidates for future drug trials. This is a vast field, and more research must be conducted in the coming years to enable the development of therapeutic drugs.

Numerous natural compounds have proven to be beneficial for stroke prevention and treatment. They can be synthesized at a lower cost than synthetic compounds and offer competitive efficacy and safety. Honokiol is a natural product that showed neuroprotective effects in animal models, and appears to have a role in reducing oxidative stress and inhibiting inflammatory responses [ 171]. Gastrodin, a compound extracted from Gastrodia elata, is a promising candidate in stroke treatment. In a mouse model, it improved neurogenesis and activated β-Catenin-dependent Wnt signaling to provide neuroprotection after ischemic insult. It also has antioxidative effects which protects the neural progenitor cells from neuron functional impairment. Gastrodin's safety has been proved in clinical trials, hence it is an option for stroke management in the coming years [ 172].

The Utstein methodology is a process of standardizing and reporting research on out-of-hospital stroke and defining the essential elements of management tools. Its growing popularity led to the establishment of the Global Resuscitation Alliance (GRA), an organization that governs best practices. The primary aim of GRA is to facilitate stroke care from pre-hospital admission to rehabilitation and recovery. It has developed 10 guidelines to ensure smooth transitioning of services during and after attack. It has implemented a stroke registry, public awareness and educational programs, promoted techniques for early stroke recognition by first responders, sought to optimize prehospital and in-hospital stroke care, advocated the use of advanced neuroimaging techniques and promoted a culture of excellence. The Utstein community has developed comprehensive plans to improve early diagnosis and treatment of stroke patients globally [ 173].

Future clinical trials should aim not only to determine the efficacy and safety of drugs but to characterize recovery and clinical outcomes. Clinical trials of pharmacological therapies for post-stroke recovery should adhere to the following guidelines [ 174]. Patients should be enrolled within two weeks of stroke whenever possible. Studies should include sampling from a multicenter platform and include global scale criteria for data analysis. The underlying mechanism of action of the tested drugs on target molecules should be thoroughly understood. Secondary measurements like day-to-day progress of recovery, length of rehabilitation, treatment endpoint analysis and any other compounding factors should also be recorded. Overall, research on stoke management has advanced rapidly in recent years and is certain to make additional valuable discoveries through the application of new technologies in hypothesis-driven clinical trials.

8. Translational Challenges for the Current Stroke Therapeutic Strategies

Stroke research has seen fundamental advancements over recent years. The improvements in the selection of animal models, imaging techniques and methodological progress have led to immense drug targets and therapeutic interventions. In spite of this, the subsequent clinical trials failed to prove pre-clinical outcomes. Recanalization therapy showed some promising results in the clinical trials but only a small section of stroke patients benefited from this treatment [ 175]. Hence, the translational potential of stroke research is still under-investigated.

The key challenges that hinder the smooth transition of pre-clinical research into successful drugs include relevant endpoint selection, confounding diseases models like hypertension and diabetes, modelling age and gender effects in stroke patients, development of medical devices, investigating medical conditions that co-exist during stroke incidence, reproducibility of pre-clinical stroke research data and modelling functional and behavioral outcome [ 176, 177, 178]. Multiple causality of the stroke occurrence is another problem that is often over-looked. Homogeneity in stroke models to exhibit the broad spectrum of stroke pathophysiology associated with ischemic lesions or cortical or intracerebral damage is critical. Therefore, stroke animal models that target specific causes of stroke should be included. Latent interaction between comorbidities and stroke treatment should be identified to increase the safety and efficacy of the clinical outcome [ 179]. Short-term experimental trials often result in failed therapeutic development due to false-negative outcomes in the clinical settings [ 180]. Understanding the functional and behavioral output which might mislead true recovery is problematic in clinical trials wherein animal models have greater ability to mask the functional benefits [ 181]. This affects the affecting translational capability of the research. Adapting a combined approach to model recovery and rehabilitation is also important for successful transition.

One of the other problems with the clinical trials for stroke is the lack of efficient data management. The impact of large data generated from numerous clinical experiments is over-whelming and there should be a standardized system to manage such data. Moreover, these data should be deposited into a public data repository for easy access.

Industry and academic corroborations in stroke research are critical to improve the translational value [ 182]. A consensus between industry and academic interests is vital for successful transition. The industry collaborations are mostly monetary driven and have time constraints which might compromise the pre-clinical study protocol design, appropriate sample sizes and overestimation of treatment effects. IP protection and publication of research data may discord between these groups. A multicenter approach, long-term collaborations, effective project management, use of advanced methodologies and establishment of functional endpoints will probably advance the translational roadblocks in stroke research [ 183].

9. Conclusions

Stroke is the second leading cause of death and contributor to disability worldwide and has significant economic costs. Thus, more effective therapeutic interventions and improved post-stroke management are global health priorities. The last 25 years of stroke research has brought considerable progress with respect to animal experimental models, therapeutic drugs, clinical trials and post-stroke rehabilitation studies, but large gaps of knowledge about stroke treatment remain. Despite our increased understanding of stroke pathophysiology and the large number of studies targeting multiple pathways causing stroke, the inability to translate research into clinical settings has significantly hampered advances in stroke research. Most research has focused on restoring blood flow to the brain and minimizing neuronal deficits after ischemic insult. The major challenges for stroke investigators are to characterize the key mechanisms underlying therapies, generate reproducible data, perform multicenter pre-clinical trials and increase the translational value of their data before proceeding to clinical studies.

Author Contributions

Conceptualization, D.K.; writing-original draft preparation, D.K.; writing-review and editing, Z.X.; funding acquisition, Z.X. All authors have read and agreed to the published version of the manuscript.

Funding

This research and The APC was funded by Apex Biotech Research.

Conflicts of Interest

The authors declare no conflict of interest.

Footnotes

Publisher's Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations.

References

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Pathophysiology and Treatment of Stroke: Present Status and Future Perspectives

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Stroke is the second leading cause of death and a major contributor to disability worldwide. The prevalence of stroke is highest in developing countries, with ischemic stroke being the most common type. Considerable progress has been made in our understanding ...

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Brain and Nervous System

Cardiovascular System

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Thrombolytic drugs (tPA, t-PA, or Reteplase)

Surgery

Risk Factor Treatment

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The main treatment for ischemic stroke is an injection called tissue plasminogen activator. It breaks up blood clots that block the flow of blood to your brain.

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Lowering Risk Factors is one of the most effective ways to reduce the chances of a repeat incident.

This primarily focuses on Cardiac abnormalities such as clotting and hypertension.

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Learn about stroke risk and which risk factors you can manage.

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The surgical intervention for a stroke is most commonly a carotid endarterectomy. An endarterectomy is the surgical removal of plaque buildup in the necks main artery, the carotid.

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Physical Therapy, Occupational therapy, and Speech therapy are all extremely commonly recommended for a post stoke treatment plan.

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A brain CT scan is an effective way to show if there is brain cell damage or bleeding in the brain from a stroke.

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A stroke may cause a swallowing disorder called dysphagia. If not identified and managed, it can lead to poor nutrition, pneumonia, and disability.

Aspiration is a common problem for people with dysphagia. It occurs when something you’ve swallowed enters the airway and lungs.

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Your stroke may cause a swallowing disorder called dysphagia. If not identified and managed, it can lead to poor nutrition, pneumonia and disability.

Aspiration is a common problem for people with dysphagia. It occurs when something you've swallowed enters the airway and lungs. Normally, aspiration causes a violent cough, but a stroke can reduce sensation. In this case, you may not know you're aspirating (silent aspiration).

While in the hospital after a stroke, you are screened to determine your ability to swallow safely. If you have a problem with swallowing safely, you may not be allowed to eat until a speech-language pathologist evaluates how well:

Muscles in your mouth move.

You can swallow.

Your voice box works.

Your health care team will also want to determine the best consistency of foods and liquids for you to swallow. Adequate nutrition is essential. If it's not safe for you to swallow, a feeding tube may be suggested to help meet your nutritional needs.
The American Speech-Language Hearing Association (ASHA) describes swallowing this way:
"Swallowing happens in three stages, or phases. You can have a problem in one or more of these phases. They include:

Oral phase (mouth) - sucking, chewing, and moving food or liquid into the throat.

Pharyngeal phase (throat) - starting the swallow and squeezing food down the throat. You need to close off your airway to keep food or liquid out. Food going into the airway can cause coughing and choking.

Esophageal phase - opening and closing the esophagus (the tube that goes from the back of your throat to your stomach). The esophagus squeezes food down to the stomach. Food can get stuck in the esophagus. You may also throw up a lot if there is a problem with your esophagus or if you have acid reflux (commonly known as indigestion or heartburn)."

ASHA identifies these signs of trouble swallowing:

coughing during or right after eating or drinking

clearing your throat often after eating or drinking

having a wet or gurgly voice during or after eating or drinking

feeling like something is stuck in your throat or chest after eating or drinking

needing extra work or time to chew or swallow

having food or liquid leak from your mouth

food getting stuck in your mouth

having a hard time breathing after meals

losing weight

Common Precautions

These common precautions may help you swallow more safely:

Sit up straight when you eat or drink.

Modify the texture of food (softening, chopping or pureeing), adjusting the thinness or thickness of liquids)

Take small bites and sips.

Take your time.

Clear all food from your mouth.

Avoid distractions to focus on eating.

Use positioning techniques and maneuvers to redirect the movement of the food. This information is usually provided during the course of therapy. For guidance, consult your medical team or Speech-language pathologist.

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Trouble Swallowing After Stroke (Dysphagia)

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Dysphagia is a swallowing disorder that may occur after a stroke. Find treatment plans and precautions to help manage symptoms.

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An MRI is another great way to diagnose a stroke because it uses radio waves and magnets to create pictures of your brain.

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affects about 80% of stroke patients, causing partial paralysis in one or both sides of the body. This is because the disruption in blood flow to certain parts of the brain that occurs during a stroke can leave damaged of dead brain cells, which contribute to muscle strength, coordination, and movement precision.

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Learn about hemiparesis, a frequent stroke aftermath causing unilateral body weakness, and strategies for managing and improving it.

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Strokes can result in brain tissue damage resulting in vascular dementia. About 10% of Stroke Patients develop cognitive impairment after the initial stroke and 30% in the year that follows.

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Long-term complications of stroke and secondary prevention: an overview for primary care physicians

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Despite a decline in mortality from stroke, the annual incidence in the general population is increasing. For many stroke survivors and their families, the acute stroke is the beginning of an ongoing struggle with physical impairment and subsequent disability. ...

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The most common type of aphasia in stroke patients is Broca's aphasia, this is located in the inferior frontal lobe of the brain. Although comprehension isn't always affected, language and grammar production is affected. Broca's aphasia is likely to be most common because the frontal lobe is the most commonly affected lobe after a stroke.

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Aphasia is a disorder affecting your ability to communicate that may occur after a stroke. Learn about the different types of aphasia and their effects.

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PT is a common treatment for stroke patients.

While stats are limited few insurance plans offer extensive coverage for Physical Therapy

Out of pocket PT is too expensive for many patients due to insurance negotiated rates

Rates Range from $150-$400

Patients that do not receive physical therapy are more likely to suffer from permanent decrease of motor functions

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The financial impact of stroke can be overwhelming. Find resources to help you manage insurance, therapy coverage, prescription drug costs and more.

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Many patients with strokes suffer from emotional and psychological difficulties

Many insurances offer limited coverage for these treatments but longer term care is limited in many plans

Patients paying out of pocket face significant financial strain

Sessions Range From: $100-$200

Medications Can Cost Up to Hundreds for some patients

Patients that go untreated can develop more serious issues and have a higher likelihood of suicide

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Stroke survivors may have higher suicide risk

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Research Highlights: Stroke survivors may be more likely than others to attempt suicide or to die by suicide. Researchers highlight the need for preventive strategies that include regular screening of all stroke patients to identify and treat…

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Is CBT usually covered by insurance, especially in cases involving TBI's.

CBT is about $125/session, if not covered by insurance.

Long term consequences of avoiding CBT is increased severity of symptoms of depression and anxiety.

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What is this treatment:

Learning to recognize one’s distortions in thinking that are creating problems, and then to reevaluate them in light of reality.

Gaining a better understanding of the behavior and motivation of others.

Using problem-solving skills to cope with difficult situations.

Learning to develop a greater sense of confidence in one’s own abilities.

American Psychological Association

Why use this intervention:

Psychiatric disorders like depression and anxiety can manifest after the trauma of a stroke and as a result of major life changes like physical limitations, isolation, and other impairments that follow a stroke.

Who can administer the treatment:

Licensed mental health professionals such as therapists, psychologists or psychiatrists.

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Cognitive behavioral therapy (CBT) is a form of psychological treatment that has been demonstrated to be effective for a range of problems including depression, anxiety disorders, alcohol and drug use problems, marital problems, eating disorders, and severe mental illness. Numerous research studies suggest that CBT leads to significant improvement in functioning and quality of life. In many studies, CBT has been demonstrated to be as effective as, or more effective than, other forms of psychological therapy or psychiatric medications.

It is important to emphasize that advances in CBT have been made on the basis of both research and clinical practice. Indeed, CBT is an approach for which there is ample scientific evidence that the methods that have been developed actually produce change. In this manner, CBT differs from many other forms of psychological treatment.

CBT is based on several core principles, including:

1. Psychological problems are based, in part, on faulty or unhelpful ways of thinking.

2. Psychological problems are based, in part, on learned patterns of unhelpful behavior.

3. People suffering from psychological problems can learn better ways of coping with them, thereby relieving their symptoms and becoming more effective in their lives.

CBT treatment usually involves efforts to change thinking patterns. These strategies might include:

Learning to recognize one's distortions in thinking that are creating problems, and then to reevaluate them in light of reality.

Gaining a better understanding of the behavior and motivation of others.

Using problem-solving skills to cope with difficult situations.

Learning to develop a greater sense of confidence in one's own abilities.

CBT treatment also usually involves efforts to change behavioral patterns. These strategies might include:

Facing one's fears instead of avoiding them.

Using role playing to prepare for potentially problematic interactions with others.

Learning to calm one's mind and relax one's body.

Not all CBT will use all of these strategies. Rather, the psychologist and patient/client work together, in a collaborative fashion, to develop an understanding of the problem and to develop a treatment strategy.

CBT places an emphasis on helping individuals learn to be their own therapists. Through exercises in the session as well as "homework" exercises outside of sessions, patients/clients are helped to develop coping skills, whereby they can learn to change their own thinking, problematic emotions, and behavior.

CBT therapists emphasize what is going on in the person's current life, rather than what has led up to their difficulties. A certain amount of information about one's history is needed, but the focus is primarily on moving forward in time to develop more effective ways of coping with life.

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Numerous research studies suggest that cognitive behavioral therapy leads to significant improvement in functioning and quality of life.

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Psychiatry consists of regular meetings with a clinic and working to identify problems faced by patients and medication to effectively manage those conditions.

Psychiatry is used to treat long term psychological and behavioral problems facing stroke survivors such as depression, anxiety disorders, and psychosis.

Psychiatric Treatment may only be provided by licensed psychiatrists with MDs.

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Management of Psychiatric Disorders in Patients with Stroke and Traumatic Brain Injury

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Balance training usually consists of weight shifting exercises and dynamic balance tasks in order to improve balance and coordination. This is used to treat long term balance issues caused by stroke such as vertigo or proprioception issues. A physical therapist would most likely administer this treatment.

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Constraint Induced Movement Therapy CIMT

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Constraint Induced Movement Therapy CIMT

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Used to treat stroke survivors that have an asymmetric function in limbs post-stroke. It uses restraints to encouarge advances in functions in weak limbs. An example would be the typical function in the left arm and the regressed function in the right arm after stroke. CIMT works by restraining the stronger arm thus causing the patient to use the weaker arm for daily function to strengthen it

Long-term Effect of Condition: Without intervention asymmetrical function of limbs would persist and an increased risk of muscular atrophy in weaker limbs.

Professional:

Occupational therapists: May work with families to choose the best CIMT protocol and provide weekly home program suggestions

Neurological physiotherapists: May specialize in CIMT and provide evidence-based treatment

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In stroke patients with a loss of motor function a commonly needed OT treatment is RPT. In RPT patients continually practice the same action to improve function, balance and mobility.

This therapy helps restore loss of motor function, both fine and gross.

This treatment is administered by an Occupational Therapist

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Maintaining a nutritious diet can make a big change in recovery from a stroke. Meeting the proper micro and macro nutrients can influence recovery time and over success.

Some issues people may encounter when trying to improve their diet is money. Processed foods are more accessible in terms of convenience and price. Another issue that may arise is support system. Stroke victims might not have mobility or cognitive ability to cook a nutritious meal three times a day.

A Certified Nutritionist can help give insigtful information on modifications you can make to your diet, taking into account complicating factors. Additionally, a lot of nutritionists can help you come up with low maintenance ideas for healthy meals.

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The benefits of physical activity on stroke recovery are extensive and may include:

Improved overall stroke recovery

Improved physical function (mobility, walking, balance)

Improved mental function (mood, depression)

Reduced risk of stroke recurrence

Reduced risk of heart-related conditions (for example, by reducing blood pressure, obesity)

Reduced risk of falls

https://www.stroke.org/en/life-after-stroke/recovery/exercise

Barriers:

limited mobility

depression, causing a lack of motivation

lack of education on what movement can be incorporated into daily life

Professionals

Physical Therapists can create a treatment plan, do an assessment, create goals, and implement goal relevant exercises and treatments

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Regular physical activity is one of the best things you can do while recovering from stroke.

Following a stroke, it's important to reduce sedentary time and start being as physically active as possible, even if you need assistance from others. Engaging in regular physical activity will help you improve and return to the fullest possible level of function.

The benefits of physical activity on stroke recovery are extensive and may include:

Improved overall stroke recovery

Improved physical function (mobility, walking, balance)

Improved mental function (mood, depression)

Reduced risk of stroke recurrence

Reduced risk of heart-related conditions (for example, by reducing blood pressure, obesity)

Reduced risk of falls

Develop healthier habits for life: Start small and increase the amount and intensity of physical activity and exercise to build endurance and strength.

Post-Stroke Exercise Videos

Rehabilitation is an important step during a stroke survivor's road to recovery, and these exercises can serve as a general guide.

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Improve overall stroke recovery. Learn the benefits of exercise after a stroke and safe ways to get started.

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Smoking Cessation and Alcohol Consumption

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Smoking Cessation and Alcohol Consumption

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One of the simplest and most beneficial ways to reduce the risk of stroke is to avoid smoking and reduce alcohol use. This can be a challenge for patients for whom it has the greatest relevance to may have substance dependencies.

This is primarily an individual decision on part of the patient, but for those with addiction seeking treatment options are available. This includes professional counseling, group programs, and many alternatives. There are many types of professionals which may be involved in care but physicians and therapists play prominent roles.

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Abstract

Of nearly 800 000 strokes that occur annually, 23% are recurrent events. Risk for disability and mortality is higher following a recurrent stroke than following a first-time stroke, which makes secondary stroke prevention a priority. Many risk factors for stroke are modifiable and amenable to improvement through lifestyle modification. Lifestyle modification can be difficult for people with stroke, however, in part because of stroke-related physical and cognitive deficits. Despite these challenges, risk factor management through lifestyle modification is important. This article reviews the multiple cardiovascular and metabolic benefits associated with the modification of several lifestyle behaviors: diet, physical activity, smoking cessation, and alcohol consumption. Health behavior theories and existing lifestyle intervention programs are also reviewed to identify important behavioral and cognitive skills that can be used to facilitate modification of health behaviors, and practical skills and suggestions for health care providers are provided.

Keywords: stroke, secondary prevention, diet, physical activity, smoking cessation, alcohol consumption

'Although risk factor management through pharmacological intervention is often necessary, polypharmacy can result in a high treatment burden for people with stroke and carries added risk for morbidity and mortality.'

Introduction

A history of having a prior stroke increases the risk for experiencing a future stroke and concomitant mortality and disability. Of the 795 000 strokes that occur annually, 185 000 (23%) are recurrent events. Following a first-time stroke, the estimated risk for stroke recurrence is 13% to 16% within the first year and 4% every year thereafter. This results in an elevated risk of 30% by 5 years and 43% by 10 years. In addition to these population-level risks, the impact of stroke recurrence on individuals can be severe. The risk of death in the 30 days following a recurrent stroke ranges from 23% to 41%, and the risk of new disability ranges from 39% to 53%. Such increased risk for mortality and disability should make secondary stroke prevention a priority, which can be addressed in part through risk factor management.

Risk Factors in People With Stroke

Although secondary stroke prevention through risk factor management has not been extensively studied, the evidence for primary stroke prevention is strong. It is generally accepted that risk factors for first-ever and recurrent ischemic stroke are the same ( Table 1). Many modifiable risk factors occur in people with stroke and often go unmanaged. In one sample of community-dwelling adults with stroke, 99% had 1 unmanaged risk factor, and 91% had 2 or more unmanaged risk factors. This is concerning because risk for cardiovascular mortality is 1.6 and 3.1 times higher in people with 1 and 2 unmanaged risk factors, respectively, compared with people with managed risk factors. Risk factor management is, therefore, important for people with stroke.

Table 1.

● Increasing age: risk doubles every 10 years after the age of 55 years
● Gender: women have a higher lifetime risk for stroke than men
● Race and ethnicity: incidence is higher in Blacks, Hispanics, American Indians, and Alaska natives than Whites or Asians
● Family history: possibly related to genetics and shared environmental and lifestyle influences
● Prior stroke: 10-year risk of recurrence is 43%

● Hypertension: systolic blood pressure ≥140 mm Hg or diastolic blood pressure ≥90 mm Hg
● Hypercholesterolemia: low-density lipoprotein ≥100 mg/dL
● Obesity: body mass index ≥30 kg/m ²
● Physical inactivity: <30-60 minutes of aerobic activity 3-5 times per week
● Diabetes
● Smoking
● Heavy alcohol consumption: >2 drinks for men and >1 for women per day

Lifestyle Modification

Although risk factor management through pharmacological intervention is often necessary, polypharmacy can result in a high treatment burden for people with stroke and carries added risk for morbidity and mortality. In recent years, the American Heart Association has published numerous guidelines directed at health care professionals for the management of cardiovascular risk factors, primary stroke prevention, acute management of stroke, and secondary stroke prevention. Each of these guidelines has identified lifestyle modification as a core component of risk factor management that should be implemented as part of comprehensive poststroke care.

Lifestyle modification can lead to improvements in hypertension, hypercholesterolemia, obesity, and glucose metabolism in diabetics, which are in turn associated with decreased risk for cardiovascular disease and death. In fact, the rate of cardiovascular mortality in people with stroke over a 10-year period can be reduced by 85% to 92% by engaging in lifestyle behaviors such as eating sufficient fruits and vegetables, exercising, maintaining a body mass index between 18.5 and 29.9 kg/m ², moderate alcohol consumption, and not smoking. Clearly, modification of lifestyle behaviors is important for secondary stroke prevention. The sections below will explore how modification of individual lifestyle behaviors can affect multiple risk factors.

Diet

Consuming a healthy diet is important for cardiovascular health and stroke prevention. In 2013, the American College of Cardiology and American Heart Association published lifestyle management guidelines to reduce cardiovascular risk. The dietary recommendations are consistent with DASH- and Mediterranean-style dietary patterns, which are effective in reducing the risk of stroke. The recommendations encourage the intake of fruits, vegetables, whole grains, low-fat dairy products, poultry, fish, legumes, vegetable oils, and nuts; limited consumption of sweets, sweetened-beverages, and red meats; and reduced sodium intake.

Multiple benefits from adhering to these dietary patterns have been observed. Blood pressure and low-density lipoprotein (LDL) cholesterol can be reduced. Improved glycemic control and insulin sensitivity occurred in diabetics. Weight loss resulted in decreased rates of obesity, which is important because of the strong relationship between obesity and stroke. Another important dietary consideration is calorie intake. Reduction of daily caloric intake by 20% to 25% for 3 months or longer in obese and nonobese individuals resulted in improved blood pressure, LDL cholesterol and triglycerides, insulin resistance, and glycemic control. Selecting healthy foods and consuming appropriate amounts can positively affect risk factors for recurrent stroke.

Physical Activity

Physical inactivity is a significant risk factor for stroke. Unfortunately, people with stroke spend up to 86% to 88% of their time in sedentary activity compared with 57% to 72% in adults without stroke. One reason for decreased physical activity after stroke is diminished exercise capacity, as measured by maximal oxygen uptake (ie, VO 2max). The amount of oxygen consumed during routine walking in people with stroke is twice that of adults without stroke; and performance of self-care activities such as bathing, grooming, and dressing after stroke can require individuals to exert 66% to 75% or more of their total exercise capacity. This illustrates how once-simple tasks become challenging after stroke. Additional barriers to physical activity after stroke include deconditioning, depression, inaccessible environments (eg, wheelchair-friendly transportation and gym equipment), low motivation, poor social support, and physical impairment.

Despite these challenges, physical activity is critical. Moderate to vigorous physical activity for primary stroke prevention leads to decreased blood pressure, LDL cholesterol, and weight gain and increased weight loss. It also results in increased glucose uptake and insulin sensitivity in people with and without diabetes. For people with stroke, exercise training can improve hypertension, lipid profiles, glucose metabolism, and insulin sensitivity. These latter improvements are important because up to 80% of people with stroke experience abnormal glucose metabolism. Additional benefits of exercise training after stroke include improved balance, gait speed, and endurance and decreased disability.

Because of the challenges associated with deconditioning and physical impairment after stroke, the American Heart and American Stroke Associations have established guidelines for health care professionals that outline physical activity and exercise recommendations after stroke (summarized in Table 2). In addition to increasing physical activity, sitting and other sedentary behaviors should be reduced by performing more light-intensity, nonexercise physical activity, such as standing and walking. Important considerations for increasing physical activity after stroke include cardiac and stress testing for high-risk individuals and supervision by a trained professional when initiating a new exercise program. Physical and occupational therapists should be involved in designing physical activity programs after stroke because these professionals have the necessary training and experience to teach people with stroke how to safely increase physical activity levels.

Table 2.

● Important considerations

○ A health care professional should supervise initiation of a physical activity program

○ Individuals at risk for cardiovascular events should undergo cardiac stress testing

○ Heart rate and perceived exertion should be regularly monitored during physical activity

● Aerobic activity

○ Duration and frequency: 20- to 60-minute sessions, 3-5 d/wk

○ Target: 55%-80% of maximum heart rate or perceived exertion of "light" to "somewhat hard"

○ Multiple short sessions (eg, 10 minutes) to build tolerance and endurance are encouraged

● Strength training

○ Amount and frequency: 1-3 sets of 10-15 repetitions targeting large muscle groups, 2-3 d/wk

○ Target: 50%-80% of 1 repetition maximum

● Nonexercise physical activity

○ Reduce sedentary time by standing and walking more often

○ Examples: stand during tasks that could be completed sitting, reduce time viewing television, go for more frequent walks, use the stairs

Smoking

The risk for first ischemic stroke in smokers is nearly 4 times the risk in nonsmokers. Although information on the risk for recurrent stroke is limited, one study demonstrated that the risk of recurrent stroke in elderly smokers was double that of nonsmokers. Smoking results in acute increases in heart rate, blood pressure, and arterial stiffness, which are especially dangerous for individuals with hypertension. Furthermore, smoking is associated with insulin resistance and dyslipidemia.

Smoking cessation, however, can lessen the risk for stroke. Smokers who quit reduce their risk for ischemic stroke by half, and smokers with hypertension who quit experience a greater benefit compared with smokers without hypertension. Chronic smokers who quit smoking experience decreased blood pressure, heart rate, and arterial stiffness and increased high-density lipoprotein (HDL) cholesterol. Additionally, diabetic smokers who stop smoking experience improved glycemic control, blood pressure, LDL cholesterol, and insulin resistance. Because of the multiple risk factors that can be improved through smoking cessation, people with stroke who smoke, and especially those with hypertension, should be given encouragement and resources to stop.

Alcohol Consumption

Heavy alcohol consumption increases the risk for first-ever and recurrent stroke. Although the exact mechanisms are unknown, heavy alcohol consumption is associated with increased risk for hypertension and diabetes, which are major risk factors for stroke and cardiovascular disease.

Low to moderate alcohol consumption, defined as ≤2 drinks for men and ≤1 drink for women daily, is associated with reduced risk for first-ever stroke. Although further research is needed, it is possible that low alcohol consumption may reduce cardiovascular risk by decreasing hypertension or increasing HDL cholesterol. Reducing current levels of alcohol consumption can lead to decreases in blood pressure, with greater reductions occurring in individuals with higher pressures, which has important implications for reducing stroke risk in hypertensive individuals. Additionally, the incidence of diabetes is lower in individuals with low alcohol consumption than in those with heavy consumption. Notwithstanding these potential benefits, the American Heart and Stroke Associations do not currently recommend drinking alcohol to gain cardiovascular benefits.

As observed with other health behaviors, modifying the amount of alcohol consumed can influence multiple risk factors for cardiovascular disease. This makes alcohol consumption a potential target for secondary stroke prevention. Because of the risk for alcohol dependence, however, individuals who do not drink should not be encouraged to drink.

Lifestyle Behavior Intervention

Behavior change is challenging and often difficult to sustain because of complex personal, environmental, and social factors. Health behavior theories have been developed to explain how these factors influence the adoption and modification of specific health behaviors, and intervention programs have been developed that utilize these theories to help patients modify lifestyle behaviors across patient populations and settings.

Barriers

A common barrier to behavior change for patients is limited insight, knowledge, and awareness of how lifestyle factors contribute to risk for subsequent stroke. If patients do not perceive a need to modify lifestyle behaviors, then behavior modification is unlikely. Even when patients understand the need to modify their behavior, knowledge rarely translates into behavior change because additional barriers exist. Limited self-efficacy (ie, one's self-confidence in one's ability to carry out a specific action), social support, outcome expectations, and motivation, among other factors, must also be considered. Additionally, physical, cognitive, and emotional conditions, including depression, are common after stroke and affect a patient's ability to enact lifestyle modifications.

Health Behavior Theories

Several theories have been proposed to explain how health behaviors are acquired and how barriers to lifestyle modification can be overcome. Well-known theories include the Social Cognitive Theory and the Transtheoretical Model. Social Cognitive Theory posits that health behaviors are influenced by interactions among environmental, social, and personal (eg, cognition, affect, biology) factors. Self-efficacy is the main component of the theory and often targeted for intervention by helping patients set small, achievable goals and helping patients observe and learn from their peers. Self-regulation strategies can also be utilized to enhance self-efficacy and promote lifestyle modification. Examples of self-regulatory strategies include systematic observation of one's behaviors (ie, self-monitoring using a food or exercise log), self-reward, enlistment of social support, and modification of social and physical environments to facilitate specific behaviors.

The Transtheoretical Model, also called the Stages of Change Model, describes behavior modification in terms of 5 stages of motivational readiness to change behavior. In the first 2 stages-precontemplation and contemplation-behavior change may be absent or considered, respectively. In the 3 remaining stages-preparation, action, and maintenance-behavior change has been attempted, implemented, or maintained, respectively. Several cognitive and behavioral strategies have been developed to help individuals modify health behaviors by progressing between stages. Examples of these strategies include increasing awareness about a person's behavior with respect to a given health condition, assessing how one feels the benefits and costs of behavior change, learning to substitute healthy behaviors for unhealthy behaviors, enlisting social support, and removing stimuli of unhealthy behaviors while adding stimuli of healthy behaviors.

Lifestyle Modification Programs

Several lifestyle modification programs for managing cardiovascular risk factors have been developed and successfully implemented that utilize elements from Social Cognitive Theory and the Transtheoretical Model. The EUROACTION program for patients with coronary heart disease and their families consisted of 8 weekly instructional workshops taught by nurses. Lifestyle behaviors and risk factors were addressed, including diet, physical activity, and smoking, using strategies from the Transtheoretical Model to help patients increase self-awareness and self-regulation of lifestyle behaviors. Following the intervention, improvements in waist circumference, blood pressure, blood cholesterol, dietary targets, and physical activity targets were observed. In the GOSPEL study for secondary prevention of myocardial infarction, participants received one-on-one counseling by a cardiac nurse, physiotherapist, and cardiologist. The intervention consisted of lifestyle and risk counseling, preventive interventions, supervised exercise, and pharmacological treatment. Visits lasted 2 hours and were held once a month for the first 6 months, then every 6 months for 3 years, and family support was encouraged. At the end of the 3-year study, cardiovascular mortality and prescription of cardioprotective medications were reduced, and lifestyle behaviors (eg, exercise, diet, stress management, body weight) were improved.

A comprehensive lifestyle health coaching program (ie, INTERVENT) administered in clinical and community-based settings has also been effective in cardiovascular disease risk reduction. This program is delivered mainly over the telephone and internet and lasts for a minimum of 1 year. Trained health coaches follow a standardized program to help participants set behavior change goals, develop action plans, and implement action plans. Health coaching consists of one-on-one counseling sessions that last for 15 to 20 minutes, where participants are taught cognitive and behavioral strategies (eg, increasing knowledge, risk awareness, and self-efficacy and developing skills in self-monitoring, enlisting social support, and controlling stimuli). This program has been successfully delivered in hospitals, physician practices, work sites, and health centers and has led to improvements in blood pressure, cholesterol, weight, and cardiorespiratory function. The program has also been utilized in randomized controlled trials for primary (ie, CREST-2) and secondary (ie, SAMMPRIS) stroke prevention.

Clinical Applications

The programs described above demonstrate the importance of intensive, long-term interventions that involve family and social support and that provide participants with the necessary knowledge, skills, and strategies for successful health behavior modification. For busy clinical practices, the time required to implement intensive health behavior interventions may be a barrier. Additional barriers include limited reimbursement for preventive services, low outcome expectations that patients will comply with behavior prescriptions, and lack of provider self-efficacy in providing lifestyle intervention counseling. Even though these factors are real barriers for providers, clinical guidelines are explicit about lifestyle modification for the prevention of cardiovascular disease and stroke. Suggestions for implementing clinical guidelines in the face of provider-related barriers are given below.

Meet the Patient "Where They're At"

Although physicians and other health care providers are recognized as health experts, patients often resist being told what to do. Therefore, it is important to meet patients "where they're at" and provide them with information that is consistent with their current level of motivation. One strategy for doing so is to utilize motivational interviewing. Motivational interviewing is a patient-centered, collaborative approach to help patients become aware of their values and priorities, understand how current health behaviors act as barriers to or facilitators of values and priorities, and generate action plans for changing health behaviors. Motivational interviewing has been extensively studied in the context of diet and physical activity. In meeting patients at their current level of readiness to change behavior, patients may be less resistant and more open to discussing strategies for modifying lifestyle behaviors.

Provide Opportunities for Skills Training

Once patients are aware of the need to modify lifestyle behaviors and are willing to discuss strategies for behavior change, they must be given the opportunity to develop skills to ensure success. In addition to learning the cognitive and behavioral skills outlined in Social Cognitive Theory and the Transtheoretical Model, patients may also need to learn skills for performing specific health behaviors (eg, reading a nutrition label, preparing a meal, using gym equipment). It is unreasonable to expect that any one health care provider will be an expert in all these skills. One option, therefore, is to refer patients to commercial lifestyle behavior programs, such as those described in this article. Programs that are phone- or internet-based may be especially important for people with stroke, where stroke-related impairments may impede transportation.

Another option is to implement a multidisciplinary, team-based approach to managing health behaviors. Following an initial consultation with a physician, more intensive skills training and lifestyle counseling may be delegated to a nurse or health coach who works in a physician practice. In cases where patients require more specialized intervention, referral to a health psychologist may be appropriate. Physicians may also refer patients to physical therapy for the design and implementation of a home exercise program, a dietitian for education and training in selecting appropriate foods, and occupational therapy for skills training in meal preparation, increasing nonexercise physical activity, using adaptive equipment, and implementing compensatory strategies to overcome physical and cognitive impairments.

Patients may also learn skills from their peers, as emphasized by Social Learning Theory. Thus, participation in social groups that bring stroke survivors together may be beneficial. Stroke groups can be found using the American Stroke Association's Stroke Support Group Registry: http://www.strokeassociation.org/STROKEORG/strokegroup/public/zipFinder.jsp.

Review Progress

Reviewing progress at regular intervals with patients can be an important way to provide feedback on patients' behavior change efforts. In the same way that self-monitoring provides feedback to patients about their behavior, reviewing progress during regularly scheduled appointments allows providers to provide feedback. Follow-up appointments also give patients the opportunity to discuss challenges to behavior change with providers, which may lead to much needed interventions or referrals.

Just as when initiating a conversation about behavior change, it is important to provide feedback that is consistent with a patient's current level of readiness for behavior change. When patients are not aware of or are just beginning to think about the need to modify health behaviors, general feedback on the benefits of behavior change is appropriate. When patients are ready to make a change or are actively changing their behaviors, targeted feedback with specific information can be shared. Regardless of the feedback provided, the manner in which it is provided should be positive, genuine, and empathetic.

Opportunities for Future Research

There are many opportunities for future research on secondary stroke prevention through lifestyle modification. Few large-scale randomized controlled trials have been conducted that examine secondary stroke prevention as the primary outcome; for practical reasons, cardiovascular risk reduction has been the main outcome of interest. Small, nonrandomized studies have demonstrated an improvement in health behaviors and cardiovascular risk factors, but sample sizes have been too small to detect a reduction in stroke recurrence. Large-scale, randomized trials of lifestyle interventions for secondary stroke prevention are needed.

Effectiveness trials that examine primary care-based intervention are also needed. Because physicians are often the first point of contact for patients seeking help for chronic conditions, effective physician-based or physician-initiated interventions need to be developed and tested. It is also important that clinical and effectiveness trials examine interventions that result in long-term adherence in the form of lasting behavior change. Permanent behavior change is paramount for secondary stroke prevention, and additional research is needed to determine how lifestyle interventions can achieve this outcome.

Conclusion

Modifiable risk factors for recurrent stroke and cardiovascular disease are common in people with stroke. These risk factors often go unmanaged, which leads to increased risk for mortality and disability. Clinical guidelines recognize that lifestyle modification for risk factor management should be a priority following stroke. Improving diet, increasing physical activity, smoking cessation, and reducing alcohol consumption are specific health behaviors that should be targeted because of their effects on multiple cardiovascular risk factors.

Health behavior theories and lifestyle modification programs demonstrate that modification of health behaviors is possible through intensive, long-term interventions that elicit social support and provide individuals and families with a variety of skills. Lifestyle modification can be initiated in clinical practice environments and enhanced through referral to allied health care professionals or lifestyle intervention programs. Although behavior change is difficult, provider use of health behavior theories, implementation of cognitive and behavioral strategies, and refinement of communication skills may facilitate patients' efforts at secondary stroke prevention through lifestyle modification.

References

17. National Heart, Lung, and Blood Institute.Description of the DASH eating plan. https://www.nhlbi.nih.gov/health/health-topics/topics/dash. Accessed January 4, 2016.

39. Wannamethee SG, Shaper AG, Whincup PH, Walker M. Smoking cessation and the risk of stroke in middle-aged men. JAMA. 1995;274:155-160. [PubMed] [Google Scholar]

59. Linke SE, Robinson CJ, Pekmezi D. Applying psychological theories to promote healthy lifestyles. Am J Lifestyle Med. 2013;8:4-14. [Google Scholar]

60. Prochaska JO, Redding CA, Evers KE. The transtheoretical model and stages of change. In: Glanz K, Rimer BK, Viswanath KK. eds. Health Behavior and Health Education: Theory, Research, and Practice. 4th ed. San Francisco, CA: John Wiley & Sons; 2008:97-121. [Google Scholar]

65. The Carotid Revascularization and Medical Management for Asymptomatic Carotid Stenosis Study. http://www.crest2trial.org/. Accessed January 4, 2016.

72. Moreno JP, Johnston CA. Consistent components of behavior change theories. Am J Lifestyle Med. 2014;8:25-27. [Google Scholar]

Articles from American Journal of Lifestyle Medicine are provided here courtesy of SAGE Publications

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Lifestyle Modification for Secondary Stroke Prevention

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Of nearly 800 000 strokes that occur annually, 23% are recurrent events. Risk for disability and mortality is higher following a recurrent stroke than following a first-time stroke, which makes secondary stroke prevention a priority. Many risk ...

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African Americans are 50 percent more likely to have a stroke (cerebrovascular disease), as compared to their white adult counterparts.

Black men are 70 percent more likely to die from a stroke as compared to non-Hispanic whites.

African American women are twice as likely to have a stroke as compared to non-Hispanic white women.

Reasons:

Social determinants of health like economic and job stability, stable housing, pollution, neighborhood safety, access to transportation, systemic racism

Diabetes

Obesity

High Blood Pressure

High Cholesterol

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Elderly people, 65+ are more at risk of stroke. The decline of cardiovascular and physical health produce conditions under which strokes are more likely to occur.

These individuals often suffer from decreased mobility and are less likely to drive making care less accessible.

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Stroke can cause the development of Aphasia, an impairment in understanding or expressing language, Dyspraxia, speech that is difficult for others to understand, or Dysphonia, a paralysis of vocal muscles. All of these disorders require speech therapy to either increase comprehension, pronunciation, or muscular rehabilitation.

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stomach problems

cognitive health issues

dizziness and vertigo

depression or mental health issues

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Exercise lowers blood pressure, which is the leading cause of stroke. Physical activity also helps you maintain a healthy weight which helps prevent stroke. This measure may be hard to take if someone is so preoccupied with other activities and does not have the time to exercise.

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You can help prevent stroke by making healthy lifestyle choices.

Talk with your doctor about steps you can take to lower your risk for stroke.

Overview

Many strokes can be prevented through healthy lifestyle changes and working with your health care team to control health conditions that raise your risk for stroke.

You can help prevent stroke by making healthy lifestyle choices.

Take Action and Get Inspired‎

Prevention steps and strategies

Choose healthy foods and drinks

Choosing healthy meal and snack options can help you prevent stroke. Be sure to eat plenty of fresh fruits and vegetables.

Eating foods low in saturated fats, trans fat, and cholesterol and high in fiber can help prevent high cholesterol. Limiting salt ( sodium) in your diet can also lower your blood pressure. High cholesterol and high blood pressure increase your chances of having a stroke.

For more information on healthy diet and nutrition, see CDC's Nutrition website.

Keep a healthy weight

Having overweight or obesity increases your risk for stroke. To determine whether your weight is in a healthy range, doctors often calculate your body mass index (BMI). If you know your weight and height, you can calculate your BMI at CDC's Assessing Your Weight website. Doctors sometimes also use waist and hip measurements to measure excess body fat.

Get regular physical activity

Physical activity can help you stay at a healthy weight and lower your cholesterol and blood pressure levels. For adults, the surgeon general recommends 2 hours and 30 minutes of moderate-intensity aerobic physical activity, such as a brisk walk, each week. Children and teens should get 1 hour of physical activity every day.

Find inspiration and tips for getting regular physical activity from the "Live to the Beat" campaign.

Don't smoke

Cigarette smoking greatly increases your chances of having a stroke. If you don't smoke, don't start. If you do smoke, quitting will lower your risk for stroke. Your doctor can suggest ways to help you quit.

For more information about tobacco use and quitting, see CDC's Smoking & Tobacco Use website.

Limit alcohol

Avoid drinking too much alcohol, which can raise your blood pressure. Men should have no more than two drinks per day, and women should have no more than one per day. For more information, visit CDC's Alcohol and Public Health website.

Control your medical conditions

Talk with your doctor about steps you can take to lower your risk for stroke.

If you have heart disease, high cholesterol, high blood pressure, or diabetes, you can take steps to lower your risk for stroke.

Check cholesterol

Your doctor should test your cholesterol levels at least once every 5 years. Talk with your health care team about this simple blood test. If you have high cholesterol, medicine and lifestyle changes can help lower your risk for stroke.

Control blood pressure

High blood pressure usually has no symptoms, so be sure to have it checked on a regular basis. Talk to your health care team about how often you should check your levels. You can check your blood pressure at home, at a doctor's office, or at a pharmacy.

If you have high blood pressure, your doctor might prescribe medicine, suggest some changes in your lifestyle, or recommend that you choose foods with lower sodium (salt).

Control diabetes

If your doctor thinks you have symptoms of diabetes, he or she may recommend that you get tested. If you have diabetes, check your blood sugar levels regularly.

Talk with your health care team about treatment options. Your doctor may recommend certain lifestyle changes, such as getting more physical activity or choosing healthier foods. These actions will help keep your blood sugar under control and help lower your risk for stroke.

Treat heart disease

If you have certain heart conditions, such as coronary artery disease or atrial fibrillation (irregular heartbeat), your health care team may recommend medical treatment or surgery. Taking care of heart problems can help prevent stroke.

Take your medicine

If you take medicine to treat heart disease, high cholesterol, high blood pressure, or diabetes, follow your doctor's instructions carefully. Always ask questions if you don't understand something. Never stop taking your medicine without first talking to your doctor or pharmacist.

Work with your health care team

You and your health care team can work together to prevent or treat the medical conditions that lead to stroke. Discuss your treatment plan regularly, and bring a list of questions to your appointments. Learn how to find the right doctor for you from the "Live to the Beat" campaign.

If you've already had a stroke or transient ischemic attack (TIA), your health care team will work with you to prevent further strokes. Your treatment plan will include medicine or surgery and lifestyle changes to lower your risk for another stroke. Be sure to take your medicine as directed and follow your doctor's instructions.

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Prevent stroke by making healthy living choices and managing your health conditions, such as high cholesterol and high blood pressure.

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Eating healthy foods with low sodium helps prevent stroke and lower cholesterol. High cholesterol can lead to fatty deposits in your blood vessels, which can break and form clots that block blood flow to the brain. Dieting may be hard to achieve if someone does not have the time to meal prep if they are not located near a grocery store with fresh fruit and vegetables.

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Cholesterol and strokes: Cholesterol lowering is indicated for strokes due to carotid atheroma

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Strong correlations between plasma lipoprotein concentrations and the risk of stroke have never been clearly established. Unlike coronary heart disease, there is no significant direct relation between an increased risk of stroke and increased plasma total cholesterol or low density lipoprotein (LDL) cholesterol; nor is there an inverse relation with high density lipoprotein (HDL) cholesterol.1 Indeed, an inverse relation exists between total cholesterol concentrations and cerebral haemorrhage.2

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Paul Coverdell National Acute Stroke Program

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Paul Coverdell National Acute Stroke Program

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The CDC's PCNASP aims to improve stroke care through collaboration between clinical care and public health. Starting in 2001, it funded academic researchers and, since 2004, supported state health departments in enhancing stroke care quality. The program focuses on several key areas: improving care quality, promoting stroke prevention in communities, and ensuring smooth transitions of care (from EMS to emergency departments and from hospitals to rehabilitation).

George MG, Fischer L, Koroshetz W, et al. CDC Grand Rounds: Public Health Strategies to Prevent and Treat Strokes. MMWR Morb Mortal Wkly Rep 2017;66:479–481. DOI: http://dx.doi.org/10.15585/mmwr.mm6618a5

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Centers for Disease Control and Prevention

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Worldwide, stroke is the second leading cause of death and a leading cause of serious long-term disability. In the United States, nearly 800,000 strokes occur each year; thus stroke is the fifth leading cause of death overall and the fourth leading cause of death among women ( 1). Major advances in stroke prevention through treatment of known risk factors has led to stroke being considered largely preventable. For example, in the United States, stroke mortality rates have declined 70% over the past 50 years, in large part because of important reductions in hypertension, tobacco smoking, and more recently, increased use of anticoagulation for atrial fibrillation ( 2, 3). Although the reduction in stroke mortality is recognized as one of the 10 great public health achievements of the 20th century ( 4), gains can still be made. Approximately 80% of strokes could be prevented by screening for and addressing known risks with measures such as improving hypertension control, smoking cessation, diabetes prevention, cholesterol management, increasing use of anticoagulation for atrial fibrillation, and eliminating excessive alcohol consumption ( 5, 6).

Risk Factors and Special Populations

Approximately 75% of persons who have a stroke have hypertension, making hypertension the most potent modifiable risk factor for stroke. Hypertension causes weakening of the arteries and can lead to either of the two types of stroke: ischemic stroke and intracerebral hemorrhage. Currently, 29.3% of U.S. adults aged ≥18 years have hypertension, and only about half of these adults have their blood pressure controlled (54%) ( 7). Hypertension is more prevalent among non-Hispanic blacks (blacks) than non-Hispanic whites (whites) (41.2% compared with 28%). Blacks are two to three times more likely to have a stroke than are whites and do so at an earlier age than whites; hypertension is thought to be a more potent risk factor for stroke among blacks and Hispanics than among whites ( 8, 9). Increasing evidence indicates that hypertension at older ages is an important contributor to vascular cognitive impairment or vascular dementia, which often coexists with other forms of dementia, such as Alzheimer's disease. Recent studies indicate that hypertension might potentiate the impact of Alzheimer's disease and its role in causing microbleeds, microinfarcts, white matter disease, and multiple small strokes that might not be clinically noticeable at the time but can lead to dementia, as well as possible involvement in the accumulation of amyloid plaques in the brain ( 10, 11). Approximately two thirds of adults aged >60 years have hypertension ( 12), putting them at increased risk for both stroke and dementia. Having hypertension in mid-life (ages 45-64 years) is strongly associated with risk for vascular cognitive impairment and dementia later in life ( 13).

Although men have a higher age-adjusted incidence for stroke, women live longer and thus have a higher lifetime risk of stroke than men ( 14). Approximately twice as many women die from stroke than from breast cancer each year ( 1). Approximately 60% of persons who die from stroke are women, and women tend to have worse functional outcomes in terms of returning to baseline activities of daily living and quality of life after experiencing a stroke. Some risk factors that are unique to women include pregnancy, gestational diabetes, eclampsia and preeclampsia, changes in hormonal status, and postmenopausal hormone use. Several studies have shown that having preeclampsia or gestational hypertension increases a woman's risk for stroke approximately twofold, and women who experience preeclampsia have a fourfold increased risk for developing future hypertension ( 14). Among women who use oral contraceptives, obesity and hypercholesterolemia increase the risk for stroke 4.6 and 10.8 times, respectively, compared with women without the risk factor and not using oral contraceptives ( 15). Risk factors for stroke that are more potent or more prevalent among women include migraines with aura, atrial fibrillation, diabetes, depression, and psychosocial stress ( 10). Young women who experience migraines with aura have a twofold increase in the risk for stroke compared with women without migraines; for women with migraines with aura who also smoke and use oral contraceptives, the risk for stroke increases approximately seven times compared with women who do not smoke or use oral contraceptives ( 16). Depression and psychosocial stress increase the risk for stroke approximately 30% in both men and women ( 17).

Impact of Stroke Systems of Care

When a stroke occurs, recognition and prompt treatment is critical. Each minute that an ischemic stroke is left untreated, the brain can lose nearly two million neurons ( 18). Emergency treatments that quickly return blood flow to the brain by dissolving or removing the clot blocking a brain artery have been found to substantially improve outcomes in ischemic stroke patients ( 19). Providing the right care at the right time is critical; one challenge to this is the fragmentation of stroke care. Currently, most acute stroke care is provided in distinct care delivery settings (e.g., emergency medical services [EMS], emergency department, hospital, and home or next care setting). With each transition, the potential for inefficient or suboptimal care and confusion for patients and their families can arise because of a lack of effective communication from one care setting and professional to the next. Viewing these elements as a stroke system of care, where the multiple, distinct components function as an efficient and effective integrated system, can overcome the fragmentation and reduce morbidity and mortality for acute stroke patients.

Developing stroke systems of care requires leadership and support from within each element to build working relationships across the system. Potential collaborators include state and local public health agencies; state, regional, and local EMS personnel; and clinical leaders. There are three critical functions of a well-integrated stroke system of care. First, stroke systems of care should establish effective interaction and collaboration. Integration across agencies, services, and people assures efficient routing of patients from the location of stroke occurrence to the closest and most appropriate level of hospital care in a locality or region to ensure timely access to treatment ( 20). Second, stroke systems of care should promote the use of an organized, standardized approach to stroke care at each facility and component within the system. Current practice for stroke systems of care is based in part on evidence-based recommendations from the Brain Attack Coalition ( https://www.brainattackcoalition.org), including recommendations for different levels of stroke care (e.g., comprehensive stroke centers, primary stroke centers, and acute stroke ready hospitals) ( 18), and when appropriate, the use of telemedicine to provide timely acute stroke care to remote stroke treatment hospitals ( 21, 22). Telemedicine for acute stroke care, or "telestroke," allows stroke specialists to examine and communicate with potential stroke patients and physicians at remote hospitals using digital video technology, providing expert diagnosis and faster treatment for patients. Third, stroke systems of care must identify performance measures and outcomes that can be monitored to improve the quality of care provided. Through collaboration and use of the principles of continuous quality improvement, goals for the entire stroke system of care can be established to achieve better outcomes.

Federal Programs to Prevent Stroke and Improve Stroke Care

The CDC's Paul Coverdell National Acute Stroke Program (PCNASP) functions at the integration of clinical care and community-based public health. In 2001, PCNASP began funding academic principal investigators in eight states, and since 2004, has funded thirteen state health departments to improve the quality of care for acute stroke patients ( 23). The program works across the continuum of care to improve the quality of care provided, promote stroke prevention communication in communities, and improve transitions in care from EMS personnel to emergency department staff members and from hospital to rehabilitation and transition to home The goal of PCNASP is to implement effective, evidence-based, integrated systems for stroke prevention and treatment that provide 1) timely identification and transport of stroke patients to hospitals specializing in stroke care, 2) high-quality acute stroke treatment and rehabilitation, and 3) reintegration with primary care providers and the community to prevent recurrence of strokes by minimizing risk factors. From 2005 to 2015, approximately 620,000 acute stroke patients have benefited from care at PCNASP-participating hospitals, and each day many more patients are benefitting from the development of integrated stroke systems of care within PCNASP-funded states ( 24- 27).

Since at least 2012, the National Institutes of Health has invested approximately $300 million annually to improve stroke prevention, treatment, and recovery ( 28). The National Institute of Neurologic Disorders and Stroke funds StrokeNet, a network, designed to maximize efficiencies in stroke research and to create balanced research in both preclinical and clinical trials. The National Institute of Neurologic Disorders and Stroke is also working to educate millions of Americans about the danger of uncontrolled hypertension through the Mind Your Risks campaign ( https://mindyourrisks.nih.gov/).

The Million Hearts initiative ( https://millionhearts.hhs.gov/), co-led by the CDC and the Centers for Medicare and Medicaid Services, focuses on a core set of strategies to prevent heart attacks and stroke. Community prevention includes tobacco control, sodium reduction, and physical activity. Clinical strategies include using aspirin when appropriate, hypertension control, cholesterol management, and smoking cessation, along with the use of health information technology to improve detection and management of patient-level risk factors for heart disease and stroke and patient and family engagement in health care decisions.

For strokes, prevention is the best medicine, whether the intervention is at the clinical or community level. Public health actions for stroke prevention include 1) employing epidemiology and surveillance to identify where progress is being made and where health care delivery gaps exist and to monitor and evaluate progress toward reducing those gaps; 2) promoting health system interventions to more effectively deliver high-quality preventive services; 3) improving community-clinical linkages to enhance access to community resources that can prevent, delay, and manage chronic diseases; and 4) implementing broad environmental approaches to improve the social and physical environment, promote healthy behaviors, and make healthy choices the easier choices ( 29). Collectively, these measures can prevent stroke.

¹Division for Heart Disease and Stroke Prevention, National Center for Chronic Disease Prevention and Health Promotion, CDC; ²Division of Preparedness and Emerging Infections, National Center for Emerging and Zoonotic Infectious Diseases, CDC; ³National Institute of Neurological Disorders and Stroke, National Institutes of Health, Washington, D.C.; ⁴Wake Forest Baptist Medical Center, Winston-Salem, North Carolina; ⁵Emory University School of Medicine, Atlanta, Georgia; ⁶ Office of the Associate Director for Science, CDC.

References

1. National Center for Health Statistics. Underlying cause of death 1999-2014. Atlanta, GA: US Department of Health and Human Services, CDC, National Center for Health Statistics; 2016.

2. CDC. Decline in deaths from heart disease and stroke-United States, 1900-1999. MMWR Morb Mortal Wkly Rep 1999;48:649-56. PubMed

3. CDC. Ten great public health achievements-United States, 1900-1999. MMWR Morb Mortal Wkly Rep 1999;48:241-3. PubMed

4. Yoon SS, Fryar CS, Carroll MD. Hypertension prevalence and control among adults: United States, 2011-2014. NCHS data brief no. 220. Hyattsville, MD: US Department of Health and Human Services, CDC, National Center for Health Statistics; 2015. https://www.cdc.gov/nchs/data/databriefs/db220.pdf

5. Nwankwo T, Yoon SS, Burt V, Gu Q. Hypertension among adults in the United States: National Health and Nutrition Examination Survey, 2011-2012. NCHS data brief no. 133. Atlanta, GA: US Department of Health and Human Services, CDC, National Center for Health Statistics; 2013.

6. George MG, Tong X, McGruder H, et al. Paul Coverdell National Acute Stroke Registry Surveillance-four states, 2005-2007. MMWR Surveill Summ 2009;58:1-23. PubMed

7. Reeves MJ, Chang A, Tong X, George MG. Achievable benchmarks for quality of care in the Coverdell Acute Stroke Program [Abstract TMP62]. Stroke 2016;47:ATMP62.

8. George MG, Tong X. Differences in tPA Door-to-needle time by patient and hospital characteristics [Abstract W 101]. Stroke 2014;45:AWMP101.

9. CDC. Paul Coverdell National Acute Stroke Program. Atlanta, GA: US Department of Health and Human Services, CDC; 2016.

10. CDC. Paul Coverdell National Acute Stroke Registry Program summary report, 2007-2012. Atlanta, GA: US Department of Health and Human Services; 2015.

Suggested citation for this article: George MG, Fischer L, Koroshetz W, et al. CDC Grand Rounds: Public Health Strategies to Prevent and Treat Strokes. MMWR Morb Mortal Wkly Rep 2017;66:479-481. DOI: http://dx.doi.org/10.15585/mmwr.mm6618a5.

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CDC Grand Rounds: Public Health Strategies to Prevent and Treat Stroke

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Worldwide, stroke is the second leading cause of death and a leading cause of serious long-term disability.

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The AHA advises the identification of patients at high risk for stroke. This is done by identifying patients with high cholesterol and long time smokers along with other factors and promoting healthier living. This approach emphasizes smoking cessation, exercise, diet and pharmaceuticals to reduce risk.

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A wearable EKG monitor keeps track of your heart rate and rhythm, blood pressure, and whether the top and bottom chambers of your heart are contracting in sync to each other. This is used to prevent and monitor the risk of stroke. A downside of this device is that it cannot provide in-depth information about your heart and can also detect false positives in arrhythmia and tachycardia.

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A CT scan, otherwise known as a computed tomography scan, this can detect damage and bleeding within the brain using x ray images. This is used to detect strokes and can't help with the treatment except for locating the region of the brain that is bleeding, more down sides of this is radiation exposure, contrast dye reactions, and cost.