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Cerebrovascular Correlates of Subclinical Attentional Disturbances in Non-stroke Cardiovascular Disease
Journal article   Peer reviewed

Cerebrovascular Correlates of Subclinical Attentional Disturbances in Non-stroke Cardiovascular Disease

Kayla B Stefanidis, Benjamin Isbel, Timo Klein, Jim Lagopoulos, Christopher D Askew and Mathew J Summers
Neuroscience, Vol.421, pp.144-151
2019
DOI: https://doi.org/10.1016/j.neuroscience.2019.09.035
Appears in  Thompson Institute Research Collection
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https://doi.org/10.1016/j.neuroscience.2019.09.035View
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Abstract

event-related potentials non-stroke cardiovascular diseasea therosclerosis cerebrovascular hemodynamics transcranial Doppler Healthy Brain Ageing Thompson Institute Special Collection UniSC Diversity Area - Life Stages
Evidence suggests that cerebrovascular hemodynamic disturbances underlie cognitive deterioration secondary to cardiovascular disease (CVD), including manifestations other than stroke, but the mechanisms remain unclear. To date, the majority of studies have used neuropsychological measures validated for the detection of clinically significant cognitive decline but lack the sensitivity to accurately detect subclinical or subtle cognitive changes. The N2 and P3 components of the event-related potential are sensitive markers of attention and cognitive processing, and are valuable in the assessment of age-related cognitive changes and neurodegenerative disease. The aims of this study were to test (a) the sensitivity of N2 and P3 components in differentiating older adults with CVD from healthy controls, and (b) whether cerebrovascular hemodynamics are associated with alterations in attention in persons with non-stroke CVD. Older adults with CVD (n = 20) and healthy older adults (n = 20) without cognitive impairment or history of stroke and matched for age, were recruited. Cerebral blood flow velocity of the middle cerebral artery (MCAv) and Gosling's Pulsatility Index (PI) were assessed using Transcranial Doppler ultrasound (TCD). ERPs were elicited using a two-tone auditory oddball task. N2 amplitude was significantly reduced in the CVD group at midline frontal, central and parietal sites (p < .05, d > 0.6). No significant group differences were observed in N2 latency, P3 amplitude, or P3 latency. Further, MCAv and PI were strongly associated with N2 amplitude in the CVD group, such that greater MCAv was associated with reductions in N2 amplitude (b = -0.58, p = .018), whilst PI was associated with increases in N2 amplitude (b = 0.66, p = .006). No relationships between MCAv or PI with N2 or P3 ERP components were observed in the healthy control group. The data reported here suggest that a reduction in N2 amplitude may be an important objective indicator of subclinical cognitive and attentional alterations in non-stroke CVD, and support the notion that cerebrovascular hemodynamic disturbances play a role in the pathogenesis of cognitive deterioration secondary to non-stroke CVD.

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