A scientific statement from the American Heart and Stroke Association on the prevalence, diagnosis, and management of poststroke cognitive impairment

So ABSOLUTELY NOTHING SPECIFIC ON HOW TO PREVENT OR CURE POSTSTROKE COGNITIVE IMPAIRMENT!  Good to know how fucking useless the ASA is!

A scientific statement from the American Heart and Stroke Association on the prevalence, diagnosis, and management of poststroke cognitive impairment

But nothing on curing it!

In a recent scientific statement published in the Stroke Journal, researchers reviewed data on the incidence, prevalence, diagnosis, and management of post-stroke cognitive impairment (PSCI).

Study: Cognitive Impairment After Ischemic and Hemorrhagic Stroke: A Scientific Statement From the American Heart Association/American Stroke Association. Image Credit: LightFieldStudios/Shutterstock.com

Background

Stroke survivors experience cognitive impairments, especially in the initial year following a stroke, that affect their quality of life (QoL).

Cognitive decline can impact abilities concerning employment, independent living, interpersonal relationship sustainability, and driving. Scoping reviews on PSCI can inform policymaking and strategy development to improve the standard of care for PSCI patients.

About the scientific statement

In the present scientific statement from the American Heart Association (AHA), researchers presented an overview of PSCI based on randomized controlled trials (RCTs), case-control studies, retrospective and prospective cohort studies, editorials, review articles, and clinical guidelines published primarily in the previous ten years.

Incidence, prevalence, and natural course of PSCI

PSCI was observed in ≤60% of individuals who survived a stroke. It can be reversed sometimes, but 33% of individuals develop post-stroke dementia (PSD) within five years. Nearly 44.0% of participants reported global cognitive impairments two to six months following the stroke.

A systematic-type review reported an estimated prevalence of 38% for non-dementia PSCI, and four out of 10 stroke-surviving individuals develop cognitive decline but not dementia.

The Norwegian Cognitive Impairment After Stroke (Nor-COAST) study showed that PSCI prevalence rates for mild-intensity stroke survivors ranged from 51% at 3.0 months to 59% at 1.5 years.

A trial of 220 mild-intensity stroke survivors, excluding individuals with pre-stroke cognitive impairments, yielded an overall PSCI frequency of 47% at three months. In the initial year following a stroke, PSD rates ranged from 7.40% (population-based trials) to 41% (hospital-based trials).

The ischemic stroke resulted in greater cognitive decay and more frequent PSD within five years of the stroke, particularly among Blacks than Whites.

A prospective cohort study including 218 individuals reported one-year and four-year PSD incidence rates of 14% and 28% following intracranial hemorrhage (ICH), respectively. PSD incidence was >2.0-fold greater among lobar ICH patients. Dementia may begin at stroke onset, develop after recurrent strokes, or develop three to six months following the stroke.

Symptoms, risk factors, pathophysiology, differential diagnosis, diagnosis, and management of PSCI

PSCI pathophysiology likely results from the precipitation of several pathological changes following stroke, especially among individuals with pre-existing neurodegenerative and microvascular disease.

Hyponatremia, depression, delirium, pre-stroke cognitive decline, and co-existing age-associated neuropathological diseases can affect post-stroke cognitive function. Diagnostic work-up must include electrolytes, vitamin B12, thyroid-stimulating hormone levels testing, kidney and liver function tests, assessment for infection, pain, and constipation, and a review of medications.

Positron emission tomography (PET) imaging can evaluate Alzheimer’s disease (AD)-associated biomarkers such as tau and beta-amyloid levels in blood or cerebrospinal fluid. Involvement of strategic locations, such as the left thalamus, the left frontotemporal region, the left middle cerebral artery, and the right parietal lobe, increase the likelihood of PSCI.

The left basal ganglia structures, the left angular gyrus, and the white matter in the periphery of the left basal ganglia are strategic structures for PSCI in previous studies.

Brain reserve, resilience, and neurovascular unit dysfunction contribute to the extent of PSCI. Risk factors for PSCI include older age, history of stroke, pre-stroke cognitive decline, stroke severity, neurodegenerative and cerebral small-vessel diseases, comorbidities, especially diabetes, and brain atrophy.

Apolipoprotein (APOE) ε4 homozygous genotype may increase the risk for pre-stroke dementia and PSD. Acute cognitive status (low cognitive test scores, delirium) is a powerful PSCI estimator capturing pre-stroke decline and lesional impact (subtype, size, topography).

PSCI-associated comorbidities such as anxiety, depression, physical or functional disabilities, fatigue, sleep disorders, and apathy lower QoL, and therefore, must be investigated among PSCI patients.

PSCI diagnosis is based on subjective cognitive complaints and objective neurocognitive evaluations such as the Montreal Cognitive Assessment and the Mini-Mental State Examination. A multidisciplinary approach, including physicians, gerontologists, neurologists, occupational therapists, speech-language therapists, and neuropsychologists, is required to optimize PSCI care.

Post-stroke cognitive decay can be reversed in some cases; however, ≤33% of individuals develop post-stroke dementia (PSD) within five years. Attention and executive function difficulties may improve after a stroke, whereas language impairments may not.

Cognitive rehabilitation (including restorative cognitive training and functional cognitive rehabilitation, including computerized cognitive training such as gamified exercises and virtual reality can improve cognitive function after stroke.

Physical exercise (especially aerobic exercises, boxing, resistance exercises, and tai chi), antidepressants, and sleep interventions such as continuous positive airway pressure (CPAP) may improve cognition.

Antihypertensives, statins, oral hypoglycemics, anticoagulants, and intravenous thrombolytics can prevent PSCI from worsening.

Further, pharmaceuticals that have cognitive improvement potential include neurotrophic peptides such as cerebrolysin and relaxin, citicoline, glyceryl trinitrate, selegiline, and dopamine agonists.

Drugs such as rivastigmine, donepezil, memantine, and galantamine may improve cognition but are associated with adverse events. PSCI patients may also benefit from remote ischemic conditioning, transcranial direct current stimulation (tDCS), acupuncture, and herbal remedies such as huperzine A, Salvia miltiorrhiza, pomegranate polyphenols, and Ginkgo biloba.

Conclusion

Based on the review findings, high-risk stroke patients, especially older black individuals with multiple comorbidities, must undergo cognitive screening.

Prospective RCTs are required to elucidate PSCI pathophysiology, including the contribution of acute cerebrovascular events to AD and other neurodegenerative disease susceptibilities, and provide treatment options for PSCI.

Journal reference:

• El Husseini, N., Katzan, I.L., Rost, N.S., Blake, M.L., Byun, E., Pendlebury, S.T., Aparicio, H.J., Marquine, M.J., Gottesman, R.F. & Smith, E.E. (2023) Cognitive Impairment After Ischemic and Hemorrhagic Stroke: A Scientific Statement From the American Heart Association/American Stroke Association. Stroke. doi: 10.1161/STR.0000000000000430. https://www.ahajournals.org/doi/abs/10.1161/STR.0000000000000430