Why is delirium more frequent in the elderly?

Abstract

An aging-related reduction in the brain's functional reserve may explain why delirium is more frequent in the elderly than in younger people insofar as the reserve becomes inadequate to cover the metabolic requirements that are critically increased by stressors. The aim of this paper is to review the normal aging-related changes that theoretically compromise complex mental activities, neuronal and synaptic densities, and the neurocomputational flexibility of the functional reserve. A pivotal factor is diminished connectivity, which is substantially due to the loss of synapses and should specifically affect association systems and cholinergic fibres in delirious patients. However, micro-angiopathy with impaired blood flow autoregulation, increased blood/ brain barrier permeability, changes in cerebrospinal fluid dynamics, weakened mitochondrial performance, and a proinflammatory involution of the immune system may also jointly affect neurons and their synaptic assets, and even cause the progression of delirium to dementia regardless of the presence of co-existing plaques, tangles, or other pathological markers. On the other hand, the developmental growth in functional reserve during childhood and adolescence makes the brain increasingly resistant to delirium, and residual reserve can allow the elderly to recover. These data support the view that functional reserve is the variable that confronts stressors and governs the risk and intensity of and recovery from delirium. Although people of any age are at risk of delirium, the elderly are at greater risk because aging and age-dependent structural changes inevitably affect the brain's functional reserve.

The nomogram to predict the occurrence of sepsis-associated encephalopathy in elderly patients in the intensive care units: A retrospective cohort study

“…Age is also an independent risk factor of SAE. In elderly patients in ICU, delirium was reported to be more prevalent ( 26 , 27 ). Our data showed that the incidence of SAE increased statistically from 34.3 to 41.5% as the age of patients rose from 65~69 to 90~69 years ( p < 0.05).…”

Melatonin and Its Analogs for Prevention of Post-cardiac Surgery Delirium: A Systematic Review and Meta-Analysis

“…Neuroinflammation disrupts the brain network of executive function after cardiac surgery ( 53 ). Aging neurons inevitably affect the brain's normal functional reserves ( 54 ). Melatonin may play an important role in the suppression of neuroinflammation ( 55 ) and the treatment of age-related neurodegenerative diseases ( 13 ).…”

Delirium and Dementia in the Elderly: Sometimes Associated or Always Together?

“…This has led to the hypothesis that aging-related immunity involution plays a role in the pathogenesis of Alzheimer’s disease [36, 37] and Lewy body dementia [38], and contributes to cognitive impairment in delirious patients that otherwise could not be explained by the burden of structural lesions alone [39, 40]. In any case, a general hypothesis should consider the totality of morphofunctional changes related to aging because, intuitively, all of them are involved in reducing the functional reserve of the brain [23]. However, it is worth noting the vulnerability of cerebral white matter, given the 45% loss of myelinated fibers in the normal elderly [41], and the abnormalities of functional neuroimaging signal observed in the white matter of cognitively normal and demented elderly patients after recurrent or long-term delirium [42, 43].…”