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Background: Delirium is the most common neuropsychiatric syndrome encountered by clinicians dealing with older adults and the medically ill and is best characterized by 5 core domains: cognitive deficits, attentional deficits, circadian rhythm dysregulation, emotional dysregulation, and alteration in psychomotor functioning.Design: An extensive literature review and consolidation of published data into a novel interpretation of known pathophysiological causes of delirium.Results: Available data suggest that numerous pathological factors may serve as precipitants for delirium, each having differential effects depending on patient-specific patient physiological characteristics (substrate). On the basis of an extensive literature search, a newly proposed theory, the systems integration failure hypothesis, was developed to bring together the most salient previously described theories, by describing the various contributions from each into a complex web of pathways-highlighting areas of intersection and commonalities and explaining how the variable contribution of these may lead to the development of various cognitive and behavioral dysfunctions characteristic of delirium. The specific cognitive and behavioral manifestations of the specific delirium picture result from a combination of neurotransmitter function and availability, variability in integration and processing of sensory information, motor responses to both external and internal cues, and the degree of breakdown in neuronal network connectivity, hence the term acute brain failure.Conclusions: The systems integration failure hypothesis attempts to explain how the various proposed delirium pathophysiologic theories interact with each other, causing various clinically observed delirium phenotypes. A better understanding of the underlying pathophysiology of delirium may eventually assist in designing better prevention and management approaches. [ABSTRACT FROM AUTHOR]

Background. Elevated serum uric acid (SUA) levels have been proposed as an independent risk factor for cardiovascular (CV) morbidity and mortality. Recent evidence suggests that treatments with a hypouricaemic action have a favourable effect on CV event prevention. Objectives. The association between SUA and acute ischaemic/nonembolic stroke was assessed in a population-based case–control study in the prefecture of Ioannina, Epirus, Greece. Subjects and methods. A total of 163 patients aged older than 70 years (88 men and 75 women) admitted due to a first-ever-in-a-lifetime acute ischaemic/nonembolic stroke and 166 volunteers (87 men and 79 women) without a history of CV disease were included. The association between SUA and stroke was determined by multivariate logistic regression modelling after adjusting for potential confounding factors. Results. Stroke patients showed higher concentrations of SUA compared with controls (333.1 ± 101.1 μmol L−1 vs. 285.5 ± 83.3 μmol L−1; P < 0.001). In univariate analysis elevated SUA levels were associated with increased risk for ischaemic stroke [odds ratio (OR) 1.42, 95% confidence interval (CI) 1.21–1.64, P < 0.0001]. Compared to patients with SUA levels in the lowest quintile, those within the highest quintile had a 2.8-time increase in the odds of suffering an ischaemic stroke (OR 2.81, 95% CI 1.67–4.73, P < 0.001). This association was strong even after controlling for gender, age, body mass index, the presence of hypertension and diabetes mellitus, drug treatment and lipids (OR 2.90, 95% CI 1.59–5.30, P = 0.001). Conclusion. Elevated SUA is associated with an increased risk for acute ischaemic/nonembolic stroke in a strictly defined population of elderly individuals independently of concurrent metabolic derangements. This association may need to be considered when treating the elderly. [ABSTRACT FROM AUTHOR]