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Disentangling the multiple links between renal dysfunction and cerebrovascular disease.
Chronic kidney disease (CKD) has a rapidly rising global prevalence, affecting as many as one-third of the population over the age of 75 years. CKD is a well-known risk factor for cardiovascular disease and, in particular, there is a strong association with stroke. Cohort studies and trials indicate that reduced glomerular filtration rate increases the risk of stroke by about 40% and that proteinuria increases the risk by about 70%. In addition, CKD is also strongly associated with subclinical cerebrovascular abnormalities, vascular cognitive impairment and dementia. The mechanisms responsible for these associations are currently unclear. CKD is associated with traditional risk factors such as hypertension, diabetes mellitus and atrial fibrillation, but non-traditional risk factors such as uraemia, oxidative stress, mineral and bone abnormalities, and dialysis-related factors, such as changes in cerebral blood flow or cardiac structure, are also postulated to play a role. Kidney disease can also impact and complicate the treatments used in acute stroke and in secondary prevention. In this review, we will outline our current understanding of the epidemiology and pathophysiology of cerebrovascular disease in CKD.
Prevention and treatment of stroke in patients with chronic kidney disease: an overview of evidence and current guidelines.
Chronic kidney disease is strongly associated with an increased risk of stroke, small vessel disease, and vascular dementia. Common vascular factors for stroke, such as hypertension, diabetes, and atrial fibrillation, are more prevalent in patients with chronic kidney disease, accounting for this association. However, factors unique to these patients, such as uremia, oxidative stress, and mineral and bone abnormalities, as well as dialysis-related factors are also believed to contribute to risk. Despite improvements in stroke treatment and survival in the general population, the rate of improvement in patients with chronic kidney disease, especially those who are dialysis dependent, has lagged behind. There is a lack of or conflicting evidence that those with renal disease, particularly when advanced or older, consistently derive benefit from currently available preventive and therapeutic interventions for stroke in the general population. In this review, we explore the complexities and challenges of these interventions in the population with renal disease.
An improved neuroanatomical model of the default-mode network reconciles previous neuroimaging and neuropathological findings.
The brain is constituted of multiple networks of functionally correlated brain areas, out of which the default-mode network (DMN) is the largest. Most existing research into the DMN has taken a corticocentric approach. Despite its resemblance with the unitary model of the limbic system, the contribution of subcortical structures to the DMN may be underappreciated. Here, we propose a more comprehensive neuroanatomical model of the DMN including subcortical structures such as the basal forebrain, cholinergic nuclei, anterior and mediodorsal thalamic nuclei. Additionally, tractography of diffusion-weighted imaging was employed to explore the structural connectivity, which revealed that the thalamus and basal forebrain are of central importance for the functioning of the DMN. The contribution of these neurochemically diverse brain nuclei reconciles previous neuroimaging with neuropathological findings in diseased brains and offers the potential for identifying a conserved homologue of the DMN in other mammalian species.
Altered resting-state functional connectivity in emotion-processing brain regions in adults who were born very preterm
<jats:sec id="S0033291716001604_sec_a1"><jats:title>Background</jats:title><jats:p>Very preterm birth (VPT; <32 weeks of gestation) has been associated with impairments in emotion regulation, social competence and communicative skills. However, the neuroanatomical mechanisms underlying such impairments have not been systematically studied. Here we investigated the functional integrity of the amygdala connectivity network in relation to the ability to recognize emotions from facial expressions in VPT adults.</jats:p></jats:sec><jats:sec id="S0033291716001604_sec_a2" sec-type="methods"><jats:title>Method</jats:title><jats:p>Thirty-six VPT-born adults and 38 age-matched controls were scanned at rest in a 3-T MRI scanner. Resting-state functional connectivity (rs-fc) was assessed with SPM8. A seed-based analysis focusing on three amygdalar subregions (centro-medial/latero-basal/superficial) was performed. Participants’ ability to recognize emotions was assessed using dynamic stimuli of human faces expressing six emotions at different intensities with the Emotion Recognition Task (ERT).</jats:p></jats:sec><jats:sec id="S0033291716001604_sec_a3" sec-type="results"><jats:title>Results</jats:title><jats:p>VPT individuals compared to controls showed reduced rs-fc between the superficial subregion of the left amygdala, and the right posterior cingulate cortex (<jats:italic>p</jats:italic> = 0.017) and the left precuneus (<jats:italic>p</jats:italic> = 0.002). The VPT group further showed elevated rs-fc between the left superficial amygdala and the superior temporal sulcus (<jats:italic>p</jats:italic> = 0.008). Performance on the ERT showed that the VPT group was less able than controls to recognize anger at low levels of intensity. Anger scores were significantly associated with rs-fc between the superficial amygdala and the posterior cingulate cortex in controls but not in VPT individuals.</jats:p></jats:sec><jats:sec id="S0033291716001604_sec_a4" sec-type="conclusion"><jats:title>Conclusions</jats:title><jats:p>These findings suggest that alterations in rs-fc between the amygdala, parietal and temporal cortices could represent the mechanism linking VPT birth and deficits in emotion processing.</jats:p></jats:sec>
Real-Life Impact of Executive Function Impairments in Adults Who Were Born Very Preterm
<jats:title>Abstract</jats:title><jats:p><jats:bold>Objectives:</jats:bold> Children and adolescents who were born very preterm (≤32 weeks’ gestation) are vulnerable to experiencing cognitive problems, including in executive function. However, it remains to be established whether cognitive deficits are evident in adulthood and whether these exert a significant effect on an individual’s real-lifeachievement. <jats:bold>Methods:</jats:bold> Using a cross-sectional design, we tested a range of neurocognitive abilities, with a focus on executive function, in a sample of 122 very preterm individuals and 89 term-born controls born between 1979 and 1984. Associations between executive function and a range of achievement measures, indicative of a successful transition to adulthood, were examined. <jats:bold>Results:</jats:bold> Very preterm adults performed worse compared to controls on measures of intellectual ability and executive function with moderate to large effect sizes. They also demonstrated significantly lower achievement levels in terms of years spent in education, employment status, and on a measure of functioning in work and social domains. Results of regression analysis indicated a stronger positive association between executive function and real-life achievement in the very preterm group compared to controls. <jats:bold>Conclusions:</jats:bold> Very preterm born adults demonstrate executive function impairments compared to full-term controls, and these are associated with lower achievement in several real-life domains. (<jats:italic>JINS</jats:italic>, 2017, <jats:italic>23</jats:italic>, 381–389)</jats:p>