Cerebrovascular and cardiovascular diseases cause vascular brain injury that can lead to vascular cognitive impairment (VCI). VCI is the second most common neuropathology of dementia and mild ...cognitive impairment (MCI), accounting for up to one-third of the population risk. It is frequently present along with other age-related pathologies such as Alzheimer's disease (AD). Multiple etiology dementia with both VCI and AD is the single most common cause of later life dementia. There are two main clinical syndromes of VCI: post-stroke VCI in which cognitive impairment is the immediate consequence of a recent stroke and VCI without recent stroke in which cognitive impairment is the result of covert vascular brain injury detected only on neuroimaging or neuropathology. VCI is a syndrome that can result from any cause of infarction, hemorrhage, large artery disease, cardioembolism, small vessel disease, or other cerebrovascular or cardiovascular diseases. Secondary prevention of further vascular brain injury may improve outcomes in VCI.
Sporadic, age‐related cerebral amyloid angiopathy (CAA) is most commonly recognized clinically as a cause of hemorrhagic stroke and transient focal neurological episodes in older persons. But a ...growing body of research in the last 5 years shows that the pathophysiology of CAA is much more complex than previously believed, leading to many different types of brain injury. CAA has now been linked with brain atrophy in regions remote from those directly affected by intracerebral hematomas, and with risk for progressive cognitive decline in the absence of new hemorrhagic strokes. Therefore, CAA is associated with features – brain atrophy and progressive cognitive decline – that are typically considered hallmarks of neurodegenerative disease. Although CAA is usually accompanied by some degree of Alzheimer's disease pathology, the profiles of cortical thinning and cognitive impairment do not fully overlap with those seen in Alzheimer's disease, suggesting that there are CAA‐specific pathways of neurodegeneration. CAA‐related brain ischemia may be an important mechanism that leads to brain injury, cortical disconnection, and cognitive impairment.
This article is part of the Special Issue “Vascular Dementia”.
Sporadic, age‐related cerebral amyloid angiopathy (CAA), caused by vascular Aβ deposition, is most commonly recognized clinically as a cause of hemorrhagic stroke. This review synthesizes emerging evidence that CAA is associated with cardinal features of neurodegeneration – atrophy and cognitive impairment – and highlights multiple pathomechanisms of brain injury that may cause cognitive impairment in this disease.
This article is part of the Special Issue “Vascular Dementia”.
IMPORTANCE The benefits of intravenous tissue plasminogen activator (tPA) in patients with acute ischemic stroke (AIS) are time dependent and guidelines recommend a door-to-needle (DTN) time of 60 ...minutes or less. However, studies have found that less than 30% of US patients are treated within this time window. Target: Stroke was designed as a national quality improvement initiative to improve DTN times for tPA administration in patients with AIS. OBJECTIVES To evaluate DTN times for tPA administration and the proportion of patients with times of 60 minutes or less before and after initiation of a quality improvement initiative and to determine whether potential improvements in DTN times were associated with improvements in clinical outcomes. DESIGN, SETTING, AND PATIENTS The Target: Stroke initiative disseminated 10 care strategies to achieve faster DTN times for tPA administration, provided clinical decision support tools, facilitated hospital participation, and encouraged sharing of best practices. This study included 71 169 patients with AIS treated with tPA (27 319 during the preintervention period from April 2003-December 2009 and 43 850 during the postintervention period from January 2010-September 2013) from 1030 Get With The Guidelines—Stroke participating hospitals (52.8% of total). MAIN OUTCOMES AND MEASURES The DTN times for tPA administration of 60 minutes or less and in-hospital risk-adjusted mortality, symptomatic intracranial hemorrhage, ambulatory status at discharge, and discharge destination. RESULTS Median DTN time for tPA administration declined from 77 minutes (interquartile range IQR, 60-98 minutes) during the preintervention period to 67 minutes (IQR, 51-87 minutes) during the postintervention period (P < .001). The DTN times for tPA administration of 60 minutes or less increased from 26.5% (95% CI, 26.0%-27.1%) of patients during the preintervention period to 41.3% (95% CI, 40.8%-41.7%) during the postintervention period (P < .001). The DTN times of 60 minutes or less increased from 29.6% (95% CI, 27.8%-31.5%) of patients in the quarter immediately before the intervention (fourth quarter of 2009) to 53.3% (95% CI, 51.5%-55.2%) in the final postintervention quarter (third quarter of 2013) (P < .001). The annual rate of improvement in DTN times of 60 minutes or less increased from 1.36% (95% CI, 1.04%-1.67%) per year preintervention to 6.20% (95% CI, 5.58%-6.78%) per year postintervention (P < .001). In-hospital all-cause mortality improved significantly from the preintervention to the postintervention period (9.93% vs 8.25%, respectively; adjusted odds ratio OR, 0.89 95% CI, 0.83-0.94, P < .001), symptomatic intracranial hemorrhage within 36 hours was less likely to occur (5.68% vs 4.68%; adjusted OR, 0.83 95% CI, 0.76-0.91, P < .001), and discharge to home was more frequent (37.6% vs 42.7%; adjusted OR, 1.14 95% CI, 1.09-1.19, P < .001). CONCLUSIONS AND RELEVANCE Implementation of a national quality improvement initiative was associated with improved timeliness of tPA administration following AIS on a national scale, and this improvement was associated with lower in-hospital mortality and intracranial hemorrhage, along with an increase in the percentage of patients discharged home.
Mild behavioral impairment (MBI) is a construct that describes the emergence at ≥50 years of age of sustained and impactful neuropsychiatric symptoms (NPS), as a precursor to cognitive decline and ...dementia. MBI describes NPS of any severity, which are not captured by traditional psychiatric nosology, persist for at least 6 months, and occur in advance of or in concert with mild cognitive impairment. While the detection and description of MBI has been operationalized in the International Society to Advance Alzheimer's Research and Treatment - Alzheimer's Association (ISTAART-AA) research diagnostic criteria, there is no instrument that accurately reflects MBI as described.
To develop an instrument based on ISTAART-AA MBI criteria.
Eighteen subject matter experts participated in development using a modified Delphi process. An iterative process ensured items reflected the five MBI domains of 1) decreased motivation; 2) emotional dysregulation; 3) impulse dyscontrol; 4) social inappropriateness; and 5) abnormal perception or thought content. Instrument language was developed a priori to pertain to non-demented functionally independent older adults.
We present the Mild Behavioral Impairment Checklist (MBI-C), a 34-item instrument, which can easily be completed by a patient, close informant, or clinician.
The MBI-C provides the first measure specifically developed to assess the MBI construct as explicitly described in the criteria. Its utility lies in MBI case detection, and monitoring the emergence of MBI symptoms and domains over time. Studies are required to determine the prognostic value of MBI for dementia development, and for predicting different dementia subtypes.
Leukoaraiosis is a common finding in stroke patients and has been strongly associated with risk of incident stroke and dementia. Leukoaraiosis may also be an independent predictor of stroke outcomes. ...There is increasing evidence from neuroimaging to support the concept that some leukoaraiosis is caused by white matter infarcts, which may be particularly frequent in patients with aggressive small vessel diseases such as cerebral amyloid angiopathy. The relatively similar distribution of leukoaraiosis regardless of the distribution of vascular pathology suggests a conserved vulnerability to white matter injury across various vascular diseases, possibly related to resting patterns of blood flow. More insights into the pathophysiology of leukoaraiosis are sorely needed to reduce the burden of disability associated with this common condition.
Abstract Neuropsychiatric symptoms (NPS) are common in dementia and in predementia syndromes such as mild cognitive impairment (MCI). NPS in MCI confer a greater risk for conversion to dementia in ...comparison to MCI patients without NPS. NPS in older adults with normal cognition also confers a greater risk of cognitive decline in comparison to older adults without NPS. Mild behavioral impairment (MBI) has been proposed as a diagnostic construct aimed to identify patients with an increased risk of developing dementia, but who may or may not have cognitive symptoms. We propose criteria that include MCI in the MBI framework, in contrast to prior definitions of MBI. Although MBI and MCI can co-occur, we suggest that they are different and that both portend a higher risk of dementia. These MBI criteria extend the previous literature in this area and will serve as a template for validation of the MBI construct from epidemiologic, neurobiological, treatment, and prevention perspectives.
Mild behavioral impairment (MBI) and subjective cognitive decline (SCD) are dementia risk states, and potentially represent neurobehavioral and neurocognitive manifestations, respectively, of early ...stage neurodegeneration. Both MBI and SCD predict incident cognitive decline and dementia, are associated with known dementia biomarkers, and are both represented in the NIA-AA research framework for AD in Stage 2 (preclinical disease).
To assess the associations of MBI and SCD, alone and in combination, with incident cognitive and functional decline in a population of older adults. We tested the hypothesis that MBI and SCD confer additive risk for decline.
Cognitively normal participants were followed up annually at Alzheimer's Disease Centers. Logistic regression assessed the relationship between baseline classification (MBI-SCD-, MBI-SCD+, MBI+SCD-, or MBI+SCD+) and 3-year outcome.
Of 2,769 participants (mean age=76), 1,536 were MBI-SCD-, 254 MBI-SCD+, 743 MBI+SCD-, and 236 MBI+SCD+. At 3 years, 349 (12.6%) declined to CDR >0, including 23.1% of the MBI+group, 23.5% of the SCD+group, and 30.9% of the intersection group of both MBI+and SCD+participants. Compared to SCD-MBI-, we observed an ordinal progression in risk (ORs 95% CI): 3.61 2.42-5.38 for MBI-SCD+ (16.5% progression), 4.76 3.57-6.34 for MBI+SCD- (20.7%), and 8.15 5.71-11.64 for MBI+SCD+(30.9%).
MBI and SCD together were associated with the greatest risk of decline. These complementary dementia risk syndromes can be used as simple and scalable methods to identify high-risk patients for workup or for clinical trial enrichment.
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