ABSTRACT
PURPOSE OF REVIEW: The aim of this study was to review current literature on identification of patients at risk for postoperative delirium (POD) and to summarize recent findings on prophylaxis and treatment. RECENT FINDINGS: Age and preoperative cognitive impairment are among the most important risk factors of POD. POD is the result of a complex interplay of predisposing and precipitating factors. Thus, both prophylaxis and treatment require multicomponent intervention programs. No single medication to prevent or treat POD is available. Avoiding too deep anesthesia, avoiding additional psychoactive substances including benzodiazepines and intravenous opioids, and effective pain management as well as early mobilization are essential. SUMMARY: An increase of the proportion of elderly patients undergoing surgery will lead to a higher incidence of POD. Preoperative assessment should facilitate identification of patients at high risk. Perioperative management should include monitoring depth of anesthesia, preference for nonopioid pain therapy, early regular delirium monitoring starting in the recovery room, avoiding ICU-sedation, early mobilization and exercise, and cognitive training.
Subject(s)
Anesthesia/adverse effects , Emergence Delirium/diagnosis , Emergence Delirium/therapy , Perioperative Care/methods , Surgical Procedures, Operative/adverse effects , Age Factors , Aged , Aged, 80 and over , Cognitive Dysfunction/complications , Emergence Delirium/etiology , Emergence Delirium/physiopathology , Exercise , Frailty/complications , Geriatric Assessment/methods , Humans , Hypnotics and Sedatives/administration & dosage , Hypnotics and Sedatives/adverse effects , Intensive Care Units/standards , Intraoperative Neurophysiological Monitoring/methods , Perioperative Care/standards , Practice Guidelines as Topic , Risk FactorsABSTRACT
DNA methylation patterns change with age, and aging itself is a major confounding risk factor for Parkinson's disease (PD). Duplication and triplication, that is, increased expression of the α-synuclein (SNCA) gene, cause familial PD, and demethylation of SNCA intron 1 has been shown to result in increased expression of SNCA. We thus hypothesized that age-related alterations of SNCA methylation might underly the increased susceptibility toward PD in later life. The present study sought to determine (1) whether alterations of SNCA intron 1 methylation occurred during aging, (2) whether the methylation pattern differed between men and women, and (3) whether purified neurons compared with non-neuronal cells exhibited different methylation patterns. The analysis of DNA from brain tissue and fluorescence activated cell sorting-sorted purified neurons of 41 individuals revealed only a minor increase of SNCA intron 1 DNA methylation levels in presumably healthy individuals during aging but no significant difference between men and women. Interestingly enough, methylation of SNCA intron 1 was higher in neurons compared with non-neuronal cells, although non-neuronal cells express lower levels of SNCA. Therefore, the normal pattern of SNCA methylation during aging should not result in increased expression of α-synuclein protein. It is thus likely that additional, yet not identified, mechanisms contribute to the tissue specificity of SNCA expression and the presumed dysregulation in PD.
