Raymond L.C. Vogels

Cognitive impairment in heart failure: A systematic review of the literature

Heart failure (HF) and cognitive impairment are common medical conditions that are becoming increasingly prevalent in the aging Western population. They are associated with frequent hospitalisation and increased mortality, particularly when they occur simultaneously. Evidence from a number of studies suggests that HF is independently associated with impairment in various cognitive domains.

Profile of Cognitive Impairment in Chronic Heart Failure

OBJECTIVES: To determine the frequency and pattern of cognitive dysfunction in outpatients with chronic congestive heart failure (CHF) and to identify the corresponding demographic and clinical correlates.

Fragmentation of the rest-activity rhythm correlates with age-related cognitive deficits

Aging affects both cognitive performance and the sleep‐wake rhythm. The recent surge of studies that support a role of sleep for cognitive performance in healthy young adults suggests that disturbed sleep‐wake rhythms may contribute to ‘age‐related’ cognitive decline. This relationship has however not previously been extensively investigated. The present correlational study integrated a battery of standardized cognitive tests to investigate the association of mental speed, memory, and executive function with actigraphically recorded sleep‐wake rhythms in 144 home‐dwelling elderly participants aged 69.5 ± 8.5 (mean ± SD). Multiple regression analyses showed that the partial correlations of the fragmentation of the sleep‐wake rhythm with each of the three cognitive domains (r = −0.16, −0.19, and −0.16 respectively) were significant. These associations were independent from main effects of age, implying that a unique relationship between the rest‐activity rhythm and cognitive performance is present in elderly people.

Neuroimaging and correlates of cognitive function among patients with heart failure.

Background/Aims: We purposed to investigate the relationship between cerebral abnormalities detected by magnetic resonance imaging (MRI) and cognitive performance in nondemented outpatients with heart failure (HF). Methods: In 58 patients with HF neuropsychological assessment was performed including tests of mental speed, executive functions, memory, language and visuospatial functions. Deep, periventricular and total white matter hyperintensities (WMH), lacunar and cortical infarcts, global and medial temporal lobe atrophy (MTA) were investigated on MRI of the brain. Correlations between MRI findings and the cognitive measures were calculated. Results: MTA correlated with memory (r = –0.353, p < 0.01), with executive functions (r = –0.383, p < 0.01) and the Mini Mental State Examination (r = –0.343, p < 0.05). Total WMH and deep WMH were found to correlate with depression and anxiety scores, but not with cognitive measures. Age, estimated premorbid intelligence and MTA were independent predictors of diminished cognitive performance. Conclusions: In HF patients, MTA was related to cognitive dysfunction, involving memory impairment and executive dysfunction, whereas WMH was related to depression and anxiety.

Assessing mental flexibility: neuroanatomical and neuropsychological correlates of the trail making test in elderly people

The Trail Making Test part B (TMT-B) is highly sensitive to age-related changes in the brain and cognitive function. However, the precise contribution of periventricular hyperintensities (PVH), deep white matter hyperintensities (DWMH), and medial temporal lobe atrophy (MTA) to task performance remains unspecified. Similarly, diminished performance may be due to deficient flexibility functions, but also to other age-related cognitive decline (e.g., mental slowing). The aim of the present study was to determine neuroanatomical (PVH, DWMH, MTA) and neuropsychological (working memory, executive function, speed and attention, episodic memory) predictors of TMT-B performance in elderly people. Results showed that MTA was the strongest predictor of TMT-B performance. The predictive value of the neuropsychological scores differed among the various TMT-B variables. For example, all neuropsychological domains predicted the TMT-B total completion time, whereas only executive function predicted the ratio score (TMT-B/A). We conclude that MTA is a very important predictor of TMT-B performance in elderly people. Furthermore, multiple cognitive functions are involved in TMT-B performance and a mild decline in any of these functions may result in diminished TMT-B performance. Therefore it is crucial to use the ratio score when one wishes to examine executive function ability.

The role of white matter hyperintensities and medial temporal lobe atrophy in age-related executive dysfunctioning.

Various studies support an association between white matter hyperintensities (WMH) and deficits in executive function in nondemented ageing. Studies examining executive functions and WMH have generally adopted executive function as a phrase including various functions such as flexibility, inhibition, and working memory. However, these functions include distinctive cognitive processes and not all may be affected as a result of WMH. Furthermore, atrophy of the medial temporal lobe (MTA) is frequently observed in ageing. Nevertheless, in previous studies of nondemented ageing MTA was not considered when examining a relationship between white matter and executive function. The goal of the present study was to examine how WMH and MTA relate to a variety of executive functions, including flexibility, fluency, inhibition, planning, set shifting, and working memory. Strong correlations were observed between WMH and MTA and most of the executive functions. However, only MTA was related to flexibility and set shifting performance. Regression analysis furthermore showed that MTA was the strongest predictor of working memory, after which no further significant association with WMH was noted. Alternatively, both MTA and periventricular hyperintensities independently predicted inhibition performance. These findings emphasize the importance of MTA when examining age-related decline in executive functioning.

Diagnostic impact of CSF biomarkers in a local hospital memory clinic.

Background: CSF biomarkers amyloid-β 1–42 (Aβ42), total tau (tau) and tau phosphorylated at threonine 181 (ptau-181) are useful diagnostic markers for Alzheimer’s disease (AD). We examined the impact of these biomarkers in the diagnostic process in a non-academic memory clinic. Methods: One hundred and nine patients with available CSF were included from the local hospital memory clinic. Initially, patients were clinically diagnosed, and the clinician indicated their confidence in the diagnosis. Next the CSF results were presented, and the clinician re-evaluated his initial diagnosis. The main outcomes were changes in initial diagnosis and diagnostic confidence. Results: Forty-seven patients were initially diagnosed with AD, 26 were diagnosed with another type of dementia, 18 were diagnosed with mild cognitive impairment, and 18 received a non-dementia diagnosis. All biomarkers distinguished between AD and non-dementia (p < 0.01); tau and ptau-181 also distinguished AD from other types of dementia (p < 0.001). After CSF biomarker levels were revealed, 11 diagnoses changed. In 31% of the diagnoses, the clinician gained confidence, while in 10% confidence decreased. Conclusion: We found that knowledge of CSF biomarker profiles changed the diagnosis in 10% of the cases, and confidence in the diagnosis increased for one third of the patients.

Distortions in rest-activity rhythm in aging relate to white matter hyperintensities

Distortions in the rest-activity rhythm in aging are commonly observed. Neurodegenerative changes of the suprachiasmatic nucleus have been proposed to underlie this disrupted rhythm. However, based on previous studies, it can be proposed that white matter hyperintensities (WMH) may also play a role in the altered rest-activity rhythm in aging. The present study focused on the rest-activity rhythm, as assessed with actigraphy, and WMH in nondemented aging. With regard to the rest-activity rhythm, the interdaily stability (IS), intradaily variability (IV) and the amplitude (AMP) of the rhythm were of interest. The white matter hyperintensities were examined separately for the periventricular (PVH) and deep white matter (DWMH) regions, while distinguishing between the various locations within these regions (e.g. occipital PVH). The results indicated that frontal DWMH related to both IS and AMP. A reduction in the most active 10-h period mediated the relationship between frontal DWMH and AMP. Possible underlying mechanisms of these associations are discussed.

Medial temporal lobe atrophy relates more strongly to sleep-wake rhythm fragmentation than to age or any other known risk

Graphical abstract Figure. No Caption available. HighlightsSleep‐wake rhythm fragmentation and medial temporal lobe atrophy increase with age.Sleep‐wake rhythm fragmentation and medial temporal lobe atrophy are related.People with pronounced sleep‐wake rhythm fragmentation show more atrophy.Rhythm fragmentation accounts for individual differences in atrophy more than age does.Rhythm fragmentation may accelerate neurodegeneration. Abstract Atrophy of the medial temporal lobe of the brain is key to memory function and memory complaints in old age. While age and some morbidities are major risk factors for medial temporal lobe atrophy, individual differences remain, and mechanisms are insufficiently known. The largest combined neuroimaging and whole genome study to date indicates that medial temporal lobe volume is most associated with common polymorphisms in the GRIN2B gene that encodes for the 2B subunit (NR2B) of the NMDA receptor. Because sleep disruption induces a selective loss of NR2B from hippocampal synaptic membranes in rodents, and because of several other reports on medial temporal lobe sensitivity to sleep disruption, we hypothesized a contribution of the typical age‐related increase in sleep‐wake rhythm fragmentation to medial temporal lobe atrophy. Magnetic resonance imaging and actigraphy in 138 aged individuals showed that individual differences in sleep‐wake rhythm fragmentation accounted for more (19%) of the variance in medial temporal lobe atrophy than age did (15%), or any of a list of health and brain structural indicators. The findings suggest a role of sleep‐wake rhythm fragmentation in age‐related medial temporal lobe atrophy, that might in part be prevented or reversible.