Cognitive Impairment After Ischemic and Hemorrhagic Stroke: A Scientific Statement From the American Heart Association/American Stroke Association
Abstract
Purpose:
Cognitive impairment is a common consequence of stroke and has direct implications for poststroke functioning and quality of life, including the ability to maintain a job, live independently, sustain interpersonal relationships, and drive a vehicle. In this scientific statement, we critically appraise the literature on the prevalence, diagnosis, and management of poststroke cognitive impairment (PSCI) and provide a framework for clinical care while highlighting gaps that merit further study.
Methods:
We performed a scoping literature review of randomized controlled clinical trials, prospective and retrospective cohort studies, case-control studies, clinical guidelines, review articles, and editorials on the incidence and prevalence, natural history, diagnosis, and management of PSCI. Scoping reviews determine the scope of a body of literature on a given topic to indicate the volume of literature and the studies currently available and provide an overview of its focus.
Results:
PSCI is common after stroke, especially in the first year, and ranges from mild to severe. Although cognitive impairment is reversible in some cases early after stroke, up to one-third of individuals with stroke develop dementia within 5 years. The pathophysiology is not yet fully elucidated but is likely attributable to an acute stroke precipitating a series of pathological events, often in the setting of preexisting microvascular and neurodegenerative changes. Screening for associated comorbidities and interdisciplinary management are integral components of the care of individuals with PSCI. There is a need for prospective studies evaluating the individual trajectory of PSCI and the role of the acute vascular event in the predisposition for Alzheimer disease and related dementias, as well as high-quality, randomized clinical trials focused on PSCI management.
Post-stroke cognitive impairment (PSCI) ranges in severity from mild to severe and occurs in up to 60% of stroke survivors in the first year after stroke, with a higher rate seen shortly after stroke.1–4 Up to 20% of individuals with mild PSCI recover fully, with the highest rate of recovery seen shortly after stroke.5 However, improvement in cognitive impairment without return to prestroke levels is more frequent than complete recovery.6,7 The risk of developing future dementia is increased after stroke even in those with transient cognitive impairment.8 The American Heart Association/American Stroke Association statement “Vascular Contributions to Cognitive Impairment and Dementia,” published in 2011, addressed the construct of vascular cognitive impairment (VCI), which captures the entire spectrum of cognitive disorders associated with all forms of cerebral vascular brain injury, with or without a clinical history of stroke, with a focus on the role of vascular contributions to dementia.9 In 2021, the European Stroke Organization and European Academy of Neurology published joint guidelines on PSCI based on evidence from randomized controlled trials, highlighting areas for which robust evidence is lacking and suggesting priority areas for future research.10 In this scientific statement, we discuss PSCI, defined as cognitive impairment resulting from an overt stroke (ischemic or hemorrhagic) and ranging from mild cognitive impairment to dementia, and provide an actionable summary that delineates a general framework for PSCI screening, diagnosis, and management.
This scientific statement is based on a scoping literature review primarily within the past 10 years of randomized controlled clinical trials, prospective and retrospective cohort studies, case-control studies, clinical guidelines, review articles, and editorials on the incidence and prevalence, natural history, diagnosis, and management of PSCI.
Definitions
The following are key definitions differentiating VCI and dementia from PSCI and dementia:
VCI refers to cognitive impairment of any severity associated with cerebrovascular disease regardless of the occurrence of stroke symptoms.11 The types of vascular injuries leading to VCI range from an insidious, progressive accumulation of microvascular pathological changes (eg, diffuse white matter injury detected on magnetic resonance neuroimaging as white matter hyperintensities or leukoaraiosis, cerebral microbleeds, enlarged perivascular spaces, or cortical microinfarcts) to a single or multiple clinical stroke events affecting brain structures critical for cognition.12
Vascular dementia is the end of a continuum of severity of clinical manifestations of VCI.6
PSCI refers to any severity of cognitive impairment, regardless of cause, noted after an overt stroke.6,13
Poststroke dementia (PSD) is the end of a continuum of severity of clinical manifestations of PSCI and refers to all types of dementia after stroke.6
Prevalence and Incidence of PSCI
The prevalence of cognitive impairment after ischemic or hemorrhagic stroke differs by the timing of assessment, diagnostic criteria, demographics (eg, age, race, or ethnicity), era of study publication, and case mix (eg, stroke severity, prior/recurrent stroke, prestroke dementia, population versus hospital based, interval from stroke, inclusion of patients with aphasia), resulting in substantial heterogeneity in reported estimates.14–16 PSCI is most common in the first year after stroke, occurring in up to 60% (cumulative incidence) of stroke survivors, with the highest rate seen shortly after stroke.4 About 44% of individuals are impaired in global cognition 2 to 6 months after stroke.3 However, a large population of stroke survivors have cognitive impairment that is not sufficient to meet diagnostic criteria for dementia but still affects quality of life.17 A systematic review that included 23 studies published between 1995 and 2017 found a pooled prevalence of PSCI without dementia in the first year after stroke of 38% (95% CI, 32%–43%), thus concluding that 4 in 10 stroke survivors display a level of cognitive impairment that does not meet the criteria for dementia.18
In studies in which cognitive performance is assessed after but not before the stroke, the estimates of PSCI may be affected by impairment that may have been present before the stroke onset.16 For example, in the Nor-COAST multicenter prospective cohort study (Norwegian-Cognitive Impairment After Stroke) of mostly mild stroke (N=617), PSCI (including dementia) was prevalent in 59% of participants at 3 months and 51% at 18 months.19 In this study, 9% of participants had prestroke mild or major cognitive impairment.19 In another cohort of individuals with mild stroke (N=220) that excluded prestroke cognitive impairment, the overall frequency of 3-month PSCI was 47.3%.2
The prevalence of PSD varies by stroke severity and history of stroke recurrence, and PSD occurs less frequently than milder forms of cognitive impairment.20,21 PSD rates in the first year after stroke range from 7.4% (95% CI, 4.8%–10.0%) in population-based studies of first-ever stroke in which prestroke dementia was excluded to 41.3% (95% CI, 29.6%–53.1%) in hospital-based studies of recurrent stroke in which prestroke dementia was included. About 10% of patients have dementia before the first stroke; 10% develop new dementia soon after first stroke; and more than one-third have dementia after recurrent stroke.16
Racial differences in the frequency and severity of PSCI have been reported.22 Stroke in Black patients results in a greater cognitive decline and is more frequently associated with dementia within 5 years of ischemic stroke compared with White patients, despite Black patients being younger at the time of the incident stroke.23
Prestroke cognitive impairment, PSCI, and dementia are frequent in patients with intracranial hemorrhage (ICH) and higher in those with lobar ICH.24,25 In a prospective observational cohort study of 218 patients without preexisting dementia, the incidence rate of new-onset dementia at 1 year after ICH was 14.2% (95% CI, 10.0%–19.3%) and at 4 years was 28.3% (95% CI, 22.4%–34.5%).25 The incidence of new-onset dementia was >2 times higher in patients with lobar ICH (incidence at 1 year, 23.4% [95% CI, 14.6%–33.3%]) than in patients with nonlobar ICH (incidence at 1 year, 9.2% [95% CI, 5.1%–14.7%]).25
Natural History of PSCI
The temporal pattern of PSD based on clinical observation is variable. It may (1) start at the onset of stroke and stabilize, (2) start at the onset of stroke and progress, (3) develop after recurrent strokes, (4) develop at the onset of stroke in the presence of preexisting cognitive impairment, or (5) develop >3 to 6 months after stroke.28
The majority of studies on cognitive impairment after stroke report a prevalence or cumulative incidence of dementia at specific time points with relatively few data on individual cognitive trajectories that describe the course and cause of cognitive change over time. If cognitive assessment is done in the early poststroke period, estimates of impairment are even more elevated (up to 91.5% at 2 weeks in 1 series).29 Although early poststroke impairment is common, PSD may be an inappropriate label for these early fluctuations in cognition because improvement may occur, especially within the first 6 months after stroke.30–33 However, cognitive recovery may be limited in patients with multiple comorbidities, polypharmacy, older age, and previous cognitive decline.34
Data on PSCI in the long-term are sparse. In a small study (N=109) of stroke and transient ischemic attack survivors at 7 years after the index event, 37% had mild cognitive impairment and 22% had dementia.35 Another study reported an overall prevalence of cognitive impairment 3 months after stroke and at annual follow-up up to 14 years after stroke that remained relatively unchanged at 22%.1 Two large population studies found the longitudinal risk of dementia to vary according to stroke severity.20,21 In the Atherosclerosis Risk in Communities cohort study (N=15 379 participants free of stroke and dementia at baseline), the risk of dementia compared with no stroke over a median follow-up of 25.5 years by adjusted hazard ratio was 1.76 (95% CI, 1.49–2.00) for 1 minor to mild stroke, 3.47 (95% CI, 2.23–5.40) for 1 moderate to severe stroke, 3.48 (95% CI, 2.54–4.76) for ≥2 minor to mild strokes, and 6.68 (95% CI, 3.77–11.83) for ≥2 moderate to severe strokes.21 Similarly, in the population-based longitudinal Oxford Vascular Study, compared with population dementia rates for the UK population >65 years of age, postevent dementia incidence in the first year after stroke was higher than expected for all categories of cerebrovascular event, with the age- and sex-adjusted relative incidence ranging from 3.5 (95% CI, 2.5–4.8) after transient ischemic attack and 5.8 (95% CI, 4.4–7.5) after minor stroke to 47.3 (95% CI, 35.9–61.2) after severe stroke, with less marked increased relative incidence thereafter.20 The 5-year cumulative incidence of new PSD was 33.1% (95% CI, 31.7%–34.5%) after stroke, with 51% of dementia diagnosed within the first year and greater front-loading of risk in those with major than in those with more minor stroke.20 Because death is a competing risk for dementia (ie, it precludes the occurrence of dementia), exploratory analysis using the cumulative incidence competing-risk methods showed a lower cumulative incidence of dementia associated with severe stroke (National Institutes of Health Stroke Scale score >10) compared with that obtained with Kaplan-Meier methods.20 Additional studies are needed to better characterize these temporal patterns and possible contributing factors.
Delayed-Onset PSCI
Although there is no widely accepted consensus definition, late PSCI is usually defined as new cognitive impairment or dementia with onset >3 to 6 months after the stroke.36 The risk factors and pathophysiological mechanisms of late poststroke cognitive decline and dementia differ from those of early PSCI. One major risk factor is stroke recurrence, which may be decreased by robust secondary stroke prevention. The incidence of new dementia is much higher after a second stroke.16,20,21 Among those with late-onset PSCI without recurrent symptomatic stroke, the progression of cerebral small-vessel disease and covert stroke appears to play an important role, although other neurodegenerative diseases such as Alzheimer disease (AD) also need to be considered.36,37 Other risk factors for late poststroke cognitive decline include older age, baseline cognitive impairment, hypertension, diabetes, and brain atrophy.36
In the REGARDS study (Reasons for Geographical and Racial Differences in Stroke), incident first-ever stroke was associated with a stepwise immediate decline in cognitive function, followed by an accelerated risk for future cognitive decline greater than what was expected for age.22 This acceleration in cognitive decline was greater in older stroke survivors than younger stroke survivors.22 A systematic review of population-based and hospital-based cohorts found that the overall incidence of new dementia >6 months after stroke was 1.7%/y but varied by stroke severity.16 In the Framingham study, the 10-year risk of dementia was 19.3% after stroke and 11.0% without stroke. Incident stroke doubled the risk of dementia even after adjustment for age, sex, education, and stroke risk factors.38
Differential Diagnosis
In addition to the direct effects of the stroke, cognitive function after stroke can be affected by other stroke complications (eg, hyponatremia, delirium, depression), as well as by prestroke cognitive decline and coexisting age-related neuropathologies. Delirium is a common complication of stroke, occurring in ≈25% of admitted patients, and should be differentiated from PSCI.39 The clinical hallmarks of delirium are alterations in arousal and attention, cognition, and behavior that arise over a short period of time, typically in the acute or early subacute phase of stroke, and are not better explained by a neurodegenerative disorder or PSCI.40 Delirium is more common in patients with stroke who are older and have more severe stroke, poststroke infection, prestroke cognitive decline, and greater brain atrophy.41 Furthermore, stroke lesion topography has been linked to delirium in patients hospitalized with stroke.42 Workup for delirium should include assessment of electrolytes; tests of liver and renal function; assessment for infection, constipation, and pain; and a review of medications.
To exclude potentially reversible causes of impairment, the clinician should obtain laboratory testing for thyroid-stimulating hormone and vitamin B1243 and should consider the potential cognitive effects of mood disorders; sleep disorders, including obstructive sleep apnea and sedating and anticholinergic medications; and hearing and vision impairments. Poststroke depression is common, affecting about one-third of individuals in the first year after stroke.44 Poststroke depression is often accompanied by cognitive symptoms, which makes differentiating it from primarily PSCI more complex. Because depression-related cognitive symptoms may resolve with the treatment of depression, it is important to screen for poststroke depression, especially when PSCI is suspected.44 The use of a depression screening tool validated in patients with stroke may aid in recognition of depression.45 Risk factors for poststroke depression include higher physical disability; prestroke history of depression, anxiety, and cognitive impairment; and lack of social and family support.44
Poststroke cognitive decline should be differentiated from prestroke decline. Questioning the patient and an informant about cognitive-related activities of daily living (eg, finances, shopping, and organizing medications) or using a validated questionnaire such as the Informant Questionnaire on Cognitive Decline in the Elderly or the Eight-Item Informant Interview to Differentiate Aging and Dementia may determine whether there was cognitive impairment that predated the stroke.46–48 Causes of cognitive impairment before stroke can include vascular cognitive disorders such as covert cerebral small-vessel disease related to stroke risk factors and comorbid age-related neurodegenerative diseases such as AD.
In the elderly, it is common for dementia to have multiple causes (also called mixed dementia), most frequently a combination of vascular disease and irreversible neurodegenerative pathologies, particularly AD.9 More research is needed on how to accurately diagnose AD and other neurodegenerative pathologies in the setting of a recent stroke. Biomarkers of the AD pathophysiological process such as β-amyloid and tau can be measured in cerebrospinal fluid or blood or by positron emission tomography. However, such testing is currently expensive, invasive, or not widely available for routine use.
Symptoms and Cognitive Domains Affected
An individual’s cognitive trajectory in the months after stroke might be affected by multiple factors, including the stroke location, preexisting cognitive impairment, small-vessel disease and comorbidities, sociocultural (eg, socioeconomic status) and demographic (eg, age and sex) characteristics of the person experiencing the stroke, and the interventions provided. Stroke location has been linked to the type of cognitive deficits observed but is not perfectly predictive of cognitive impairment. Involvement of strategic locations such as the left frontotemporal region, left thalamus, and right parietal lobe,49 as well as the left middle cerebral artery territory, has been associated with increased likelihood of PSCI.50 Support vector regression-based lesion symptom mapping performed 3 to 6 months after an ischemic stroke identified the left angular gyrus, left basal ganglia structures, and white matter around the left basal ganglia as strategic structures for global cognitive impairment after stroke.51 Larger strokes tend to involve many of these regions, making it hard to differentiate cognitive impairment attributable to regional involvement from that attributable to stroke size and severity. Because aphasia is common after left middle cerebral artery stroke and several commonly used cognitive tests and screening instruments depend on intact language function, the severity of cognitive impairment may be overestimated in individuals with aphasia and with left middle cerebral artery strokes. Furthermore, some studies explicitly exclude individuals with aphasia, leading to difficulties capturing the true rates of cognitive impairment in the broader stroke population.
Global cognitive deficits have been described in the poststroke setting,52 but this global impairment may reflect the use of global cognitive measures in many studies.53 Difficulty with executive function and attention (and, in some studies, memory) is common after ischemic stroke54 but also has been reported to show the most improvement by 3 to 6 months after stroke, whereas impairment in the language domain does not tend to improve.54,55 Patients with ICH show cognitive deficits similar to those of patients with ischemic stroke,56 with different domains affected depending on the location (ie, lobar vs nonlobar) of the ICH.57
Patients with SAH frequently have less baseline vascular disease or subclinical cerebrovascular disease (both important contributors to PSCI) than other stroke populations. Yet, multiple cognitive domains may be impaired with SAH, with the highest rates of impairment noted in executive function and verbal memory.58,59
Pathophysiology
In the general population, small-vessel disease is the biggest contributor to VCI and dementia, whereas in the poststroke population, there is a relatively greater contribution from larger, more destructive embolic infarcts. The exact pathophysiology of PSCI is not well understood given the paucity of knowledge about the effects of specific stroke subtypes (ie, acute ischemia, ICH, or aneurysmal SAH), as well as the variable contributions of the severity of the injury, the lesion location, and the interaction between the preexisting brain pathology and an acute stroke event, which may serve as a trigger for or accelerate cognitive decline in a vulnerable brain.13,60 The constructs of brain reserve and brain resilience as they relate to brain health are evolving.61,62 Brain reserve is the difference between the degree of brain damage observed in an individual and the clinical manifestation of that damage. Brain resilience is a combination of the capacity of the brain to counteract the lifetime accumulation of damage and the compensatory mechanisms that can be used to mitigate the effects of this damage.61,62 It is likely that brain reserve and resilience and the factors contributing to them also play a role in the degree of cognitive impairment in the setting of stroke-related brain injury (Figure 1).
In most brains affected by stroke, there are diffuse age-related changes involving the smallest building block of the brain parenchyma, the neurovascular unit, which includes neurons, astrocytes, pericytes, microglia, and blood vessels.63 The neurovascular unit is the key structural element of what has been called brain health, or the capacity of the brain to operate at its optimal state of structural and functional integrity, in the absence of or despite the impact of insidious or precipitous injuries related to cerebrovascular dysfunction, metabolic disarray, proteinopathies, or inflammatory responses.64–67 The structural elements of the neurovascular unit are often damaged by stroke-related injury, possibly leading to PSCI (Figure 1).61,62 However, the same elements can also be considered points of intervention for future treatments, rehabilitation, and prevention strategies involving lifetime environmental exposures, vascular risk factor modification, and even gene therapies.68
Risk Factors
Risk factors for PSCI reflect prestroke cognitive decline, preexisting cerebral vulnerability/reduced reserve, and the impact of the stroke; a minor stroke may precipitate dementia in an older person with a vulnerable brain.16,20,36 Key vulnerability factors include age, cerebral small-vessel disease, and neurodegeneration, which may be partially mitigated by higher educational attainment and premorbid intelligence (indicators of cerebral reserve).16,20,36 Comorbid poststroke depression is also an important factor associated with PSCI, and the 2 disorders frequently coexist, possibly through shared mechanisms. The risk associated with the effects of late-life vascular factors on early poststroke cognitive decline is unclear except for diabetes, which has been associated with an increased risk.69 Strong social networks may be a protective factor, although evidence specifically in PSCI is sparse.
PSCI is more common with higher stroke lesion load such as in severe or recurrent strokes.16,20,36 The risk of PSCI varies with stroke subtype (higher in hemorrhagic and cardioembolic stroke compared with lacunar stroke), likely driven partially by the corresponding stroke severity. Lesion location is important because risks are higher in stroke affecting specific brain regions (see the Symptoms and Cognitive Domains Affected section).
In ICH, lobar location carries greater risk than deep location, likely because lobar hemorrhages are associated with underlying cerebral amyloid angiopathy.25,70,71 In aneurysmal SAH, delayed cerebral ischemia and chronic hydrocephalus predict PSCI, but the underlying biological mechanisms remain poorly understood.72 Compared with aneurysm coiling, aneurysm clipping in SAH may be associated with a higher rate of executive dysfunction and lower scores on language tests.58 However, this may be confounded by other underlying patient characteristics.
Brain imaging findings (lesion volume, white matter hyperintensities, atrophy) are proxies for stroke severity and brain vulnerability, with lobar microbleeds and global small-vessel disease burden being important predictors of dementia after hemorrhagic stroke.25,70,71,73 However, it remains unclear to what extent imaging biomarkers predict PSCI over and above clinical factors, including acute cognitive status (delirium, low cognitive test score), which is a powerful predictor capturing both prestroke decline and lesion impact.16,36,71 Poststroke delirium is associated with higher risk for PSD and lower survival.74 APOE ε4 homozygous genotype is a possible risk factor for prestroke dementia and PSD, accelerating early decline after major stroke and increasing the probability of later dementia after less severe events.75
Knowledge gaps remain, particularly in our understanding of the role of noncerebral factors, including infection, frailty, and social factors. Further studies are needed to understand the independent predictors of poststroke cognitive decline and whether blood and cerebrospinal fluid biomarkers and brain imaging add predictive value over clinical factors.
Association With Other Poststroke Outcomes
PSCI is associated with other adverse outcomes, including physical disability, sleep disorders, depression, personality and behavioral changes, and other neuropsychological changes, all contributing to a lower quality of life.76 Independently of the occurrence of PSCI, these outcomes are common after stroke (Figure 2).44,76–82 Risk factors, including older age, stroke severity, history of stroke, multiple comorbidities, lower educational attainment, and social isolation, also overlap.16,83 Coexisting adverse poststroke outcomes and multimorbidity can complicate timely diagnosis and effective treatment,84 for example, the exacerbation of cognitive impairment after stroke attributable to undiagnosed depression.15
In patients with physical deficits after stroke, functional outcomes, measured with the modified Rankin Scale, Barthel Index, or assessment of activities of daily living, are directly affected by cognitive impairment in that patients with PSCI may have difficulty participating in rehabilitation and experiencing the full benefit of a rehabilitation program. Cognitive dysfunction, however, is not conditional on physical disability; PSCI may occur after mild stroke or transient ischemic attack.8,16,20
Along with a cognitive assessment after stroke, patients should be evaluated for problems with physical function, sleep, mood, anxiety, apathy, fatigue, and other personality and behavioral changes both in the acute stage and later during recovery. Although the association between these conditions and PSCI is incompletely understood, they all contribute to reduced quality of life in stroke survivors (Figure 2). Poor access to resources and stigma surrounding diagnoses of dementia, disability, and depression may impede care.85
Robust clinical trial data on the impact of neuropsychological treatments or sleep interventions on PSCI are lacking, although improving physical activity86 and using an antidepressant87 may provide small or short-term benefits in specific cognitive domains. Further research is needed to understand the effect of sleep interventions such as continuous positive airway pressure for sleep apnea on poststroke cognitive outcomes.88 Research is also needed to determine the frequency of the co-occurrence of these sleep-related conditions in patients with PSCI.
Screening and Diagnostic Modalities
Cognitive complaints, or subjective reports of cognitive decline, are common in patients after stroke89,90 and are linked to objective cognitive impairment as determined by performance-based, standardized measures of cognitive function.90–92 However, several factors affect patients’ report of cognitive problems beyond the presence of objective cognitive dysfunction. Higher psychological distress (eg, depression, negative affect) has been linked to increased report of cognitive difficulties after stroke, independently of the severity of objective cognitive impairment.89,93 Anosognosia, or lack of awareness of the presence or severity of a person’s own cognitive deficits, often results in underreporting of cognitive problems.94 Additional information can be gathered from collateral sources such as family members or caregivers. Informant report is specific but insensitive to PSCI and can be affected by interpersonal and cultural factors.95 Thus, although the report of cognitive decline by patients and their informants is important, objective cognitive assessment is crucial to accurately identify cognitive dysfunction, particularly when anosognosia is present.
Although there is no gold standard for cognitive screening after stroke, several brief cognitive screening tests (≤30 minutes) have been used to identify PSCI.96–100 The Mini-Mental State Examination and the Montreal Cognitive Assessment have been the most widely studied cognitive screening instruments,96,98,99 with the Montreal Cognitive Assessment generally being recommended over the Mini-Mental State Examination,96,98,101 particularly in subacute phases after stroke,100 because it has less of a ceiling effect and is more sensitive to mild cognitive impairment. However, several other cognitive screens show initial evidence for their utility in identifying cognitive impairment after stroke.97–100 The choice of the best screening tool to use for a given patient will vary according to the psychometric properties of the test; demographic (age, sex, educational attainment), cultural, and language characteristics of the patient; circumstances of test administration (eg, time, bedside/clinic/telehealth); and the presence of other stroke-related impairments.17
Unfortunately, most screening instruments were not developed to identify the heterogeneous presentation of poststroke cognitive deficit and might miss subtle (yet impactful) poststroke cognitive changes. Furthermore, stroke-related impairments such as motor weakness, unilateral neglect, and aphasia, as well as demographic factors such as education, language, or culture, may render standard cognitive screening tools inadequate.104 Tailored comprehensive neuropsychological evaluations that use appropriate normative data; consider demographic (educational attainment, age, and sex), cultural, and linguistic factors; and account for stroke-related deficits may improve diagnostic accuracy, provide a thorough characterization of the patient’s cognitive strengths and weaknesses, and identify mild cognitive changes over time.
Early detection of cognitive impairment in the acute stroke unit is essential for informing interventions and for discharge planning; the natural history of PSCI indicates that it is also important to assess for cognitive changes over time. However, the comparative effectiveness of different screening strategies—including whom to screen, when, and how often—has not been evaluated in prospective clinical trials. There are potential downsides to screening, including cost and the potential to falsely label patients as having cognitive impairment on the basis of low test scores from confounding factors such as cultural bias, education bias, test anxiety, or administration in a second language. False-positive diagnoses can cause harm by inducing psychological distress or reducing patient autonomy, for example, by leading to loss of the license to drive or the ability to independently manage financial affairs. These uncertainties notwithstanding, which should be addressed in future research, it is unquestionably necessary to screen whenever there is a cognitive complaint or clinician concern about cognitive ability. Clinician concern should be triggered by unexplained patient difficulties with cognitive-related activities of daily living, following clinician instructions, or providing a reliable history. Stroke systems of care need to be resourced to provide cognitive screening and assessment in patients at risk, including sufficient time for cognitive screens, if indicated, and health care professionals to follow up with detailed assessments and plans for accommodation and rehabilitation.
Management of PSCI
Interdisciplinary Collaboration
Collaboration among physicians, including neurologists, gerontologists, and primary care physicians, speech language pathologists, occupational therapists, neuropsychologists, nurses, and related health professionals is crucial throughout levels of poststroke care for the optimal identification and management of cognitive problems after stroke. A tailored neuropsychological evaluation is best suited to thoroughly characterize cognitive strengths and weaknesses, which is important for optimal management of PSCI. This also will aid in individualizing care tailored to the patient’s needs, such that involvement of all disciplines is not needed for all patients.
For example, speech-language pathologists can identify and treat cognitive and communication deficits after stroke (and dysphagia). Occupational therapists can further evaluate and manage the functional impact of cognitive problems in patients’ daily activity contexts. A streamlined, interdisciplinary model of care beyond the acute and subacute phases after stroke is needed for optimal monitoring and management of cognitive deficits. Telehealth services might be a useful tool to implement such a model, provided that barriers to these services are addressed.105 Although referral patterns differ depending on local resources and expertise, Figure 3 provides a decision tree to help guide collaborations among relevant health care services, particularly in the process of screening and diagnosis of PSCI in postacute care settings, as comprehensive and evidence-based post-acute care models are developed. The team composition should be tailored to the symptoms and needs of the individual patient.
Cognitive Rehabilitation
In general, cognitive rehabilitation (including restorative cognitive training and functional cognitive rehabilitation) after stroke results in small improvements in cognitive functioning compared with control conditions (treatment as usual or active sham intervention).106 Small gains, both immediate and sustained, occur in several cognitive areas (attention, memory, executive function) and visuospatial neglect. Specifically, memory gains occur with strategy training,107–109 but attention training does not produce consistent benefits.110,111 Benefits of computerized cognitive training (eg, engaging and gamified cognitive exercises accessed from the patients’ own computers or mobile devices) over standard cognitive rehabilitation are inconsistent but tend to be better with clinician-directed programs.112–115 Emerging evidence, albeit from small or lower-quality studies,116 suggests potential cognitive benefits of virtual reality tools117–119 and training and education for family and patients.120–122
Physical Activity
Physical activity may have a positive impact on cognitive function after stroke, with a possible advantage for aerobic compared with nonaerobic exercise.123–125 Small studies suggest cognitive benefits of specific forms of physical activity such as tai chi,126 boxing,127 and resistance exercises.128 Evidence for the added benefit of using virtual reality with physical activity is inconclusive.129,130
Medical and Pharmacological Treatments
Because the risk of PSCI increases with stroke recurrence, secondary stroke prevention, including antihypertensive therapy, statins, diabetes control, and anticoagulation for atrial fibrillation, is an important approach to prevent the risk for or worsening of PSCI.131 Treatments for hypertension and lifestyle programs to reach target blood pressure after stroke have to date failed to show positive impacts on cognitive function.132,133 Current evidence is insufficient to prove whether some antihypertensive drug classes are better than others at preserving cognition.134 Nonetheless, hypertension treatment reduces the risk of incident and recurrent strokes, which are risk factors for PSCI. In the general population, blood pressure lowering with antihypertensive agents compared with control is associated with a reduced risk of cognitive impairment and incident dementia.135,136 More research is needed to close the gaps in the disparities in hypertension control that extend beyond lifestyle factors and the effect of this on the incidence and progression of PSCI.
There are knowledge gaps in the effect of interventions for smoking, obesity, diabetes, hyperlipidemia, and obstructive sleep apnea for reducing the risk of PSCI, although they are generally considered to be additional important modifiable risk factors for preventing cognitive decline.137 Simultaneous treatment of multiple vascular risk factors compared with only one or few was associated with a slower cognitive decline in a cohort of patients with AD and could improve or maintain cognitive functioning in at-risk elderly people from the general population.138,139 Similar studies of multiple simultaneous interventions are needed in patients with PSCI.
Because cognitive outcome has traditionally not been considered an outcome measure in randomized trials investigating the benefit of acute stroke treatments, limited evidence exists with regard to their effect on cognition, although it is postulated that PSCI would be decreased because of a reduction in acute lesion size and improved functional outcome. The few studies that evaluated cognitive outcomes after acute stroke treatments suggest that intravenous thrombolysis and mechanical thrombectomy improve cognitive outcomes (compared with no treatment) but that these benefits are strongly associated with functional outcome.140–142
Systematic reviews of dopamine agonists143 and selective serotonin reuptake inhibitors144–146 show no consistent beneficial effects on cognition after stroke. Individual small clinical trials have reported various pharmaceutical agents that may have a potential benefit on global cognition: neurotrophics (Cortexin),147 peptides such as Cerebrolysin148 and relaxin,149 citicoline (cytidine-5′-diphosphocholine),150 and nitrates (glyceryl trinitrate).151 Specific pharmaceuticals may affect defined aspects of cognition, including the effects of dopamine agonists on hemi-inattention152 and selegiline on attention and executive function.153
Cholinesterase inhibitors (eg, donepezil, rivastigmine, and galantamine) and memantine, an N-methyl d-aspartate receptor antagonist, are sometimes prescribed for patients with dementia after stroke, although more work is needed to define the safety and efficacy of these drugs in this population.154,155 Randomized trials provide moderate-quality evidence for small improvements in cognition, of uncertain clinical relevance, with donepezil, rivastigmine, galantamine, or memantine; however, they are complicated by adverse events (including dizziness and diarrhea) and patient discontinuation.156
Emerging, Complementary, and Integrative Treatments
Small studies have shown the benefits of remote ischemic conditioning for visuospatial, attention, and executive functions157 and long-term (>6 months) global cognition.158 Further confirmatory studies with larger samples are warranted.159 Several studies suggest potential benefit from transcranial magnetic stimulation and transcranial direct current stimulation (tDCS).160,161 In a meta-analysis of 15 studies (N=820 participants) of tDCS, compared with sham tDCS or control, anodal tDCS was associated with a small improvement in the general cognitive and attention performance but not with memory.160 Most of these studies, however, were of lower methodological quality and lacked sham tDCS and safety data.160 Well-designed studies are needed to determine the potential benefits of neuromodulation in the treatment of poststroke cognitive deficits and to establish the optimal treatment protocols.160 Acupuncture treatments may also have a positive effect on global cognition.162–164 However, a meta-analysis suggests that the majority of these studies were of low quality.164 The combination of acupuncture with other therapies (eg, cognitive or physical rehabilitation) may enhance the benefits of either alone.165,166
Preliminary and exploratory studies suggest potential cognitive benefits from various herbal treatments and vitamins, including huperzine A,167 depsides salts from Salvia miltiorrhiza,168 ginkgo biloba,169 pomegranate polyphenols,170 and Cerebralcare Granule,171 but no benefits from mailuoning,172 folic acid, and B vitamins.173 None of these are approved by the US Food and Drug Administration for use in PSCI. Last, there is a paucity of randomized studies on the potential effects of heart-healthy diets (eg, DASH [Dietary Approaches to Stop Hypertension] diet, Mediterranean diet, MIND [Mediterranean-DASH Intervention for Neurodegenerative Delay] diet) on cognition after stroke.
Anticipatory Guidance for Patients and Their Caregivers
Actionable Considerations for the Clinician When Cognitive Impairment Is Detected on Screening
Stroke survivors with dementia are at higher risk of death, disability, and institutionalization.174 When cognitive impairment is detected on screening, comprehensive cognitive evaluation such as a battery of standardized neuropsychological assessments can further help characterize impaired cognitive domains.175 In addition to the management of poststroke cognitive deficits described previously, other considerations include assessing for safety issues in the home environment, return to work (if applicable), and driving, as well as assessing for caregiver fatigue and connecting patients and caregivers with available community resources when possible. Advance care planning, including personal medical directives and identifying an enduring power of attorney, should also be considered.
Home Safety
Recommendations for home safety after stroke are related predominantly to the ability to perform daily activities of living as a result of limitations in mobility and cognition. The most common issues in the home environment for stroke survivors are using the bathroom and having limited mobility and communication.176 Examples of recommendations for these issues include providing appropriate equipment for mobility, installing grab bars or raising toilet seats in the bathroom, and establishing a personal emergency system for simplified access to immediate help.176 Impaired cognition is also associated with falls, and the majority of falls occur at home.177 To ensure home safety, health care professionals need to assess the home environment, identify home safety issues, and provide appropriate recommendations to stroke survivors and their caregivers. Transitional care processes, especially those that are more intensive, may increase home safety and reduce hospital readmission rates.178
Return to Work
Evidence for a relationship between cognitive function and return to work after a stroke comes primarily from prospective observational studies. Deficits in global cognitive function179 and specifically executive function180 are negatively related to return to work. The risk of cognitive decline at 1 year after stroke is higher for people who were not employed before the stroke and for those who did not return to mentally stimulating jobs after a stroke.181 Qualitative studies consistently indicate that lack of knowledge of or support for invisible deficits such as cognitive impairments is a deterrent to returning to work or maintaining a job after returning to work.182–184 Return to work may be facilitated by cognitive or vocational rehabilitation.185
Driving
In many cultures, driving is a sign of independence, has a strong impact on quality of life, and may be necessary for work or for socializing. After a stroke, approximately one-third of patients require some type of training or rehabilitation to return to driving.186 Cognitive abilities have been linked to success on driving tests. However, a systematic review of 53 studies did not find strong evidence to recommend any one cognitive assessment tool over another.187 Although inconsistencies in the methodologies and results of these studies prevent strong conclusions, better attention and executive function are most often related to a return to driving.188,189 Various training programs exist, although many do not encompass all of the components that affect successful driving (eg, cognitive function, sensory perception, mobility, motivation).186 A systematic review of 4 randomized controlled trials with 245 participants reported no improvements in on-road performance or any cognitive function after a driving intervention, although driving simulations may be more effective than other training programs.190
Conclusions and Future Directions
PSCI is common and contributes to the poorer health status of stroke survivors. It often occurs in the presence of a variety of stroke-related deficits and other comorbid conditions such as depression, adding complexity to both its diagnosis and its treatment. Management requires a multipronged approach that includes evaluation and management of comorbid conditions, anticipatory guidance for matters such as home safety and driving, implementation of secondary stroke prevention strategies to minimize the progression of cognitive impairment, and administration of treatments to optimize functioning and improve cognition (Figure 4). Thus, the comprehensive management of patients with PSCI should involve an interdisciplinary collaboration of the patient and their caregivers with health professionals, including neurologists, occupational therapists, speech therapists, nurses, neuropsychologists, gerontologists, and primary care physicians. Given the prevalence of PSCI and its association with poor health-related outcomes, the implementation of protocols to systematically evaluate and treat PSCI based on locally available resources is warranted.
As outlined in the Table 1, there are multiple unanswered questions about the pathophysiology, diagnosis, and treatment of PSCI. More studies are needed on the exact mechanisms of PSCI, the effects of specific stroke subtypes, and the interaction among the preexisting brain pathology, sociocultural factors, and the acute stroke event. The DISCOVERY study (Determinants of Incident Stroke Cognitive Outcomes and Vascular Effects on Recovery), is an ongoing prospective, multicenter, observational, nested-cohort study of 8000 patients with ischemic and hemorrhagic stroke without history of dementia enrolled at the time of index stroke from 30 clinical sites across the United States and followed up for a minimum of 2 years with serial cognitive evaluations and assessments of functional outcome. Subsets are undergoing research magnetic resonance imaging, positron emission tomography, and comprehensive genetic/genomic and fluid biomarker testing. The overall scientific objective of this study is to elucidate mechanisms of brain resilience and susceptibility to PSCI in diverse US populations.13 Future research might inform best practices for cognitive screening after stroke. Perhaps the most pressing need, however, is the development of effective and culturally relevant treatments for PSCI through the conduct of adequately powered clinical trials of cognitive rehabilitative techniques, pharmaceutical agents, and lifestyle modifications in diverse groups of patients. Along with this, studies are required to evaluate whether multidisciplinary clinics or other models of care improve outcomes for patients with PSCI. Given the significant contribution of PSCI to the growing burden of dementia, focusing on these unanswered questions should be considered a priority.
| Section | Suggestions for clinical practice | Gaps |
|---|---|---|
| Prevalence and incidence | There is substantial heterogeneity in the reported prevalence of PSCI explained mostly by the cohort selection criteria. PSCI is most common in the first year after stroke, occurring in up to 60% of stroke survivors: About 38% have mild cognitive impairment, and 7%-41% have dementia. | Estimates of incidence adjusted for competing risk of death, overall and in specific subgroups, including people of underrepresented races and ethnicities and women. |
| Natural history | PSCI tends to improve over time, with most recovery occurring within the first 3 to 6 mo. | Individual poststroke cognitive trajectories |
| Delayed-onset cognitive impairment after stroke | Late PSD (onset >3–6 mo after the stroke) occurs in ≈1.7% of stroke survivors per year. | Characterization of the types of late PSD When reporting on delayed-onset cognitive impairment, studies should exclude those with impairment before 3 to 6 mo from the stroke and thus not report the cumulative incidence of cognitive impairment that combines early and delayed onset. |
| Differential diagnosis | Differential diagnosis: Prestroke cognitive decline Coexisting age-related neuropathologies (example AD) Effects of medical conditions and complications, such as metabolic abnormalities, medication side effects, infections, delirium, sleep disorders, hearing and vision impairments, and depression | Whether fluid (blood/CSF) and imaging biomarkers should be used to assist with the diagnosis of PSCI |
| Symptoms and cognitive domains affected | Cognitive deficits can be global or limited to specific domains. | Better understanding of how stroke location and size interact with cognitive reserve to cause PSCI with different severities and cognitive profiles. |
| Pathophysiology | Stroke-related injury to the neurovascular unit, secondary neurodegeneration, and loss of structural and functional connectivity | Better understanding of the mechanisms of PSCI and the effects of specific stroke subtypes (ie, acute ischemia, ICH, or aneurysmal SAH), as well as stroke severity, lesion location, and the complex interaction between the preexisting brain pathology and the acute stroke event. |
| Risk factors | Risk of cognitive decline is determined by the stroke lesion and cerebral vulnerability/reserve. Key risk factors: older age, prestroke cognitive decline, preexisting white matter disease or neurodegeneration, diabetes, stroke severity, prior/recurrent stroke, stroke location, and acute cognitive status | The role of noncerebral factors, including infection, frailty, and social factors, and the added value of blood, CSF, and brain imaging biomarkers in risk stratification. |
| Association with other poststroke outcomes | PSCI is associated with other adverse outcomes, including physical disability, sleep disorders, behavioral and personality changes, depression, and other neuropsychological changes, all leading to lower quality of life. | The association and frequency of co-occurrence of PSCI with other poststroke outcomes, including anxiety, apathy, and fatigue. The effect of sleep interventions and treatment of comorbid depression and anxiety on poststroke cognitive outcomes. |
| Screening and diagnostic modalities in the clinic | Tailored neuropsychological evaluations improve diagnostic accuracy for cognitive impairment after stroke and provide a thorough characterization of the patient’s cognitive strengths and weaknesses. | Optimal timing for screening for PSCI, best screening tools, and whether screening affects patient outcomes. Optimal testing to assess the additional impact of stroke on cognitive impairment in individuals who already have a history of dementia. Development of cognitive assessments that can be practically used by busy clinicians and that would capture the heterogeneous nature of PSCI, including in patients with impaired language function. |
| Management | Interdisciplinary collaboration is essential for the optimal identification and management of PSCI. Clinician-directed behavioral cognitive rehabilitation and physical activity are likely beneficial for poststroke cognition. There are no consistently positive effects of pharmaceutical agents for poststroke cognition, although individual small studies show some benefits. | The impact of heart-healthy diets and of simultaneous treatments of vascular risk factors, as well as management of stroke complications (eg, physical disability, depression, sleep apnea) on poststroke cognitive function. Well-designed studies of pharmacological and nonpharmacological treatments (eg, ischemic conditioning, neuromodulation, and acupuncture) aimed to improve poststroke cognitive function. |
| Anticipatory guidance | Comprehensive cognitive evaluation with considerations for pharmacological and nonpharmacological treatments, management of stroke risk factors to prevent stroke recurrence, targeting of high-risk populations, evaluation for comorbid complications, and assessment of home safety, driving, and return to work (if applicable) are warranted. | Evaluation of the benefit of multidisciplinary clinics for individuals with stroke and cognitive impairment on quality of life, cognitive function, caregiver burden, and functional outcome. |
AD indicates Alzheimer disease; CSF, cerebrospinal fluid; ICH, intracranial hemorrhage; PSCI, poststroke cognitive impairment; PSD, poststroke dementia; and SAH, subarachnoid hemorrhage.
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© 2023 American Heart Association, Inc.
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Published online: 1 May 2023
Published in print: June 2023
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| Writing group member | Employment | Research grant | Other research support | Speakers’ bureau/honoraria | Expert witness | Ownership interest | Consultant/advisory board | Other |
|---|---|---|---|---|---|---|---|---|
| Nada El Husseini | Duke University Medical Center | Site PI, NIA/NINDS U19NS115388* | None | None | None | None | None | None |
| Irene L. Katzan | Cleveland Clinic | None | None | None | None | None | None | None |
| Hugo J. Aparicio | Boston University School of Medicine | American Academy of Neurology (AAN Career Development Award, principal investigator)†; NIH (awardee, National Institute of Neurological Disorders and Stroke, NIH Loan Repayment Program L30 NS093634)*; NIH (National Institute on Aging R01AG066524 coinvestigator)*; Alzheimer’s Association (Alzheimer’s Association Research Grant [AARGD-20-685362], principal investigator)*; Boston University (Boston University’s Aram V. Chobanian Assistant Professorship)† | None | None | None | None | None | None |
| Margaret Lehman Blake | University of Houston | NIH/NIDCD (R01 research grant)* | None | Academy of Neurologic Communication Disorders & Sciences* | None | None | ANCDS (unpaid)* | None |
| Eeeseung Byun | University of Washington | NIH/NINR (PI for K23NR017404 grant)*; NIH/NIA (pilot project PI for P30AG059304 grant)*; University of Washington Population Health Initiative Tier 1 pilot grant (PI)* | None | None | None | None | None | None |
| Rebecca F. Gottesman | National Institutes of Health/National Institute of Neurological Disorders and Stroke | None | None | None | None | None | None | None |
| Maria J. Marquine | University of California, San Diego | NIH (PI of R01MD013502, R01AG070956 and K24AG075240)† | None | None | Federal Defenders Office* | None | None | None |
| Sarah T. Pendlebury | Wolfson Centre for Prevention of Stroke and Dementia (United Kingdom) | NIHR Oxford Biomedical Research Centre (support for studies on delirium and dementia)†; John Fell Fund (brain imaging algorithm development)†; RCF funding (brain imaging studies)†; RCF funding (decision-making capacity)† | None | None | None | None | Consultancy* | None |
| Natalia S. Rost | Harvard Medical School | NINDS (U19NS115388, Rost–PI)† | None | None | None | None | None | None |
| Eric E. Smith | University of Calgary (Canada) | None | None | None | None | None | None | None |
This table represents the relationships of writing group members that may be perceived as actual or reasonably perceived conflicts of interest as reported on the Disclosure Questionnaire, which all members of the writing group are required to complete and submit. A relationship is considered to be “significant” if (a) the person receives $5000 or more during any 12-month period, or 5% or more of the person’s gross income; or (b) the person owns 5% or more of the voting stock or share of the entity, or owns $5000 or more of the fair market value of the entity. A relationship is considered to be “modest” if it is less than “significant” under the preceding definition.
*
Modest.
†
Significant.
| Reviewer | Employment | Research grant | Other research support | Speakers’ bureau/honoraria | Expert witness | Ownership interest | Consultant/advisory board | Other |
|---|---|---|---|---|---|---|---|---|
| Alexa S. Beiser | Boston University School of Public Health | None | None | None | None | None | None | None |
| Cheryl Bushnell | Wake Forest School of Medicine | None | None | None | None | None | None | None |
| Saurav Das | University of Kentucky College of Medicine | None | None | None | None | None | None | None |
| Mary G. George | Eagle Global Scientific LLC | None | None | None | None | None | None | None |
| Yorito Hattori | National Cerebral and Cardiovascular Center (Japan) | None | None | None | None | None | None | None |
| Linda S. Williams | Roudebush VA Medical Center | None | None | None | None | None | None | None |
This table represents the relationships of reviewers that may be perceived as actual or reasonably perceived conflicts of interest as reported on the Disclosure Questionnaire, which all reviewers are required to complete and submit. A relationship is considered to be “significant” if (a) the person receives $5000 or more during any 12-month period, or 5% or more of the person’s gross income; or (b) the person owns 5% or more of the voting stock or share of the entity, or owns $5000 or more of the fair market value of the entity. A relationship is considered to be “modest” if it is less than “significant” under the preceding definition.
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