Behavioral and psychological symptoms of dementia (BPSD), also known as neuropsychiatric symptoms, represent a heterogeneous group of non-cognitive symptoms and behaviors occurring in subjects with dementia. BPSD constitute a major component of the dementia syndrome irrespective of its subtype. They are as clinically relevant as cognitive symptoms as they strongly correlate with the degree of functional and cognitive impairment. BPSD include agitation, aberrant motor behavior, anxiety, elation, irritability, depression, apathy, disinhibition, delusions, hallucinations, and sleep or appetite changes. It is estimated that BPSD affect up to 90% of all dementia subjects over the course of their illness, and is independently associated with poor outcomes, including distress among patients and caregivers, long-term hospitalization, misuse of medication, and increased health care costs. Although these symptoms can be present individually it is more common that various psychopathological features co-occur simultaneously in the same patient. Thus, categorization of BPSD in clusters taking into account their natural course, prognosis, and treatment response may be useful in the clinical practice. The pathogenesis of BPSD has not been clearly delineated but it is probably the result of a complex interplay of psychological, social, and biological factors. Recent studies have emphasized the role of neurochemical, neuropathological, and genetic factors underlying the clinical manifestations of BPSD. A high degree of clinical expertise is crucial to appropriately recognize and manage the neuropsychiatric symptoms in a patient with dementia. Combination of non-pharmacological and careful use of pharmacological interventions is the recommended therapeutic for managing BPSD. Given the modest efficacy of current strategies, there is an urgent need to identify novel pharmacological targets and develop new non-pharmacological approaches to improve the adverse outcomes associated with BPSD.

The aim of this study is to determine whether postoperative delirium is associated with dysregulation of hypothalamic–pituitary–adrenal and growth hormone/insulin-like growth factor 1 (GH/IGF-1) responses following acute systemic inflammation. Plasma levels of cortisol, IGF-1, C-reactive protein, interleukin (IL)-6, IL-8, and IL-10 were measured before and after surgery in 101 patients ≥60 years without dementia undergoing elective hip arthroplasty. Participants were assessed with confusion assessment method and Diagnostic and Statistical Manual of Mental Disorders (Fourth Edition, Text Revision; DSM-IV-TR) postoperatively and 37 patients fulfilled the DSM-IV-TR criteria for delirium. Preoperative plasma cortisol levels were similar in delirium and nondelirium groups (405.37 ± 189.04 vs 461.83 ± 219.39; P = .22). Participants with delirium had higher postoperative cortisol levels (821.67 ± 367.17 vs 599.58 ± 214.94; P = .002) with enhanced postoperative elevation in relation to baseline (1.9- vs 1.5-fold; P = .004). The plasma levels of IGF1 did not differ in delirium and nondelirium groups before (18.12 ± 7.58 vs 16.8 ± 7.86; P = .477) and following surgery (13.39 ± 5.94 vs 11.12 ± 6.2; P = .639), but the levels increased in relation to baseline more frequently in patients who developed delirium (24.3% vs 7.8%; P = .034). The magnitude of postoperative cortisol elevation correlated with ΔIL-6 (P = .485; P = .002), ΔIL-8 (P = .429; P = .008), and ΔIL-10 (P = .544; P < .001) only in patients with delirium. Hypothalamic–pituitary–adrenal axis hyperresponsiveness and a less frequent suppression of the GH/IGF-1 axis in response to acute stress are possibly involved in delirium pathophysiology.

Background: delirium is a frequent neuropsychiatric syndrome affecting medical and surgical elderly patients. Cholinergic dysfunction has been implicated in delirium pathophysiology and plasmatic acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE) activities are suppressed in patients with delirium. In this cohort study, we investigated whether these changes emerge during delirium or whether they are present before its onset. Methods: plasma activities of AChE and BuChE were measured pre- and postoperatively in consecutive patients ≥60 years old undergoing elective total hip replacement surgery. In addition to a comprehensive clinical and demographic baseline evaluation, venous blood samples were collected from each subject in the morning of hospital admission's day and in the morning of the first postoperative day. Delirium was screened daily with confusion assessment method (confirmed with diagnostic and statistical manual of mental disorders (DSM-IV)-TR). Results: preoperatively, plasma esterase activity was significantly lower in patients who developed delirium compared with the remaining subjects. Following surgery BuChE activity was lower in the delirium group but this difference disappeared after controlling for preoperative values. Plasma cholinesterase activity correlated positively with calcium and haemoglobin and negatively with total bilirubin and international normalised ratio. Conclusion: plasma cholinesterase activity can be a useful candidate biomarker to identify subjects at greater risk of developing postoperative delirium.