DETECTION OF FACTORS THAT AFFECT THE DECLINE IN COGNITIVE FUNCTION THAT CAUSES DEMENTIA IN THE ELDERLY

BackgroundPhysical activity can help to protect against cognitive decline in older adults. However, little is known about the potential combined relationships of time spent in sedentary behavior (SB), light-intensity physical activity (LPA), and moderate-to-vigorous physical activity (MVPA) with indices of cognitive health. We examined the cross-sectional associations of objectively-determined sedentary and physically-active behaviors with an indicator of cognitive function decline (CFD) in older adults.MethodsA randomly-recruited sample of 511 Japanese older adults (47% male; aged 65–84 years) wore a tri-axial accelerometer for 7 consecutive days in 2017. Cognitive function was assessed by interviewers using the Japanese version of Mini-Mental State Examination, with a score of ≤23 indicating CFD. Associations of sedentary and physically-active behaviors with CFD were examined using a compositional logistic regression analysis based on isometric log-ratio transformations of time use, adjusting for potential confounders.ResultsForty one (9.4%) of the participants had an indication of CFD. Activity compositions differed significantly between CFD and normal cognitive function (NCF); the proportion of time spent in MVPA was 39.1% lower, relative to the overall mean composition in those with CFD, and was 5.3% higher in those with NCF. There was a significant beneficial association of having a higher proportion of MVPA relative to other activities with CFD. LPA and SB were not associated with CFD when models were corrected for time spent in all activity behaviors.ConclusionsLarger relative contribution of MVPA was favorably associated with an indicator of CFD in older adults.

To examine the longitudinal association between decline in cognitive function and risk of elder self-neglect in a community-dwelling population. Prospective population-based study. Geographically defined community in Chicago. Community-dwelling subjects reported to the social services agency from 1993 to 2005 for self-neglect who also participated in the Chicago Health Aging Project (CHAP). Of the 5,519 participants in CHAP, 1,017 were reported to social services agency for suspected elder self-neglect from 1993 to 2005. Social services agency identified reported elder self-neglect. The primary predictor was decline in cognitive function assessed using the Mini-Mental State Examination (MMSE), the Symbol Digit Modalities Test (Executive Function), and immediate and delayed recall of the East Boston Memory Test (Episodic Memory). An index of global cognitive function scores was derived by averaging z-scores of all tests. Outcome of interest was elder self-neglect. Logistic and linear regression models were used to assess these longitudinal associations. After adjusting for potential confounding factors, decline in global cognitive function, MMSE score, and episodic memory were not independently associated with greater risk of reported and confirmed elder self-neglect. Decline in executive function was associated with greater risk of reported and confirmed elder self-neglect. Decline in global cognitive function was associated with greater risk of greater self-neglect severity (parameter estimate=0.76, standard error=0.31, P=.01). Decline in executive function was associated with risk of reported and confirmed elder self-neglect. Decline in global cognitive function was associated with risk of greater self-neglect severity.

Decline in cognitive function and elder mistreatment: findings from the Chicago Health and Aging Project.

To the Editor: There is controversy about whether high blood pressure is associated with impaired cognitive function or dementia.1, 2 Recently Skoog and colleagues3 revealed an association between high blood pressure at age 70 and the development of dementia 10 to 15 years later. We show the J-curve relation between blood pressure and decline in cognitive function in older Japanese people in a 3-year follow-up study. We assessed blood pressure (BP) and Mini-Mental State Examination (MMSE) scores in older people living in Kahoku,4 a rural Japanese town, in 1992 and 1995. We studied 155 older subjects (58 men and 97 women, mean age in 1992: 78 years; range: 70 to 91 years). In 1992, the subjects were divided into four groups according to their systolic blood pressure (SBP): SBP < 125 (Group I, n = 38); SBP 125 to <150 (Group II, n = 63,); SBP 150 to <175 (Group III, n = 40); SBP > 175 (Group IV, n = 14). There were no significant differences in age and MMSE scores among the four groups in 1992. The rates of antihypertensive medications prescribed in each group were 13.5%, 47.5%, 40.0%, and 71.4%, respectively, and those did not change significantly 3 years later. Figure 1 shows MMSE scores in 1992 and 1995 and the decline in the scores during the 3 years by each blood pressure group. Groups I, II, and IV showed significant deterioration in MMSE scores during the 3-year period (Group I from 27.2 ± 3.7 to 26.3 ± 4.2; Group II 28.2 ± 2.2 to 27.6 ± 2.4; Group IV 27.9 ± 2.2 to 26.1 ± 3.8; each P < .05 by paired t test), whereas Group III showed no significant change in MMSE scores (from 27.5 ± 3.2 to 27.9 ± 2.4). The difference in MMSE scores in each group between 1992 and 1995 showed significant decline in the scores in Groups I and IV (P < .05, Fisher PLSD, ANOVA: P < .05) compared with that in Group III, revealing the J-curve relation between SBP and the decline in MMSE scores. The relationship between the decline in MMSE scores and diastolic BP also showed a tendency of J-curve relation but failed to be significant (P < .09). . MMSE scores in 1992 and 1995 and decline in the scores during 3 years by each blood pressure group. °P < .05, MMSE scores in 1995 vs in 1992 (paired t test). *P < .05, decline in MMSE compared with that in Group III (Fisher PLSD) (ANOVA: P < .05). Although the duration of follow-up was only 3 years, we revealed an association of high BP with deterioration in cognitive function, adding the J-curve relation between blood pressure and decline in cognitive function in a longitudinal study. Our results also support the findings of Meyer and colleagues,5 which showed improvement of cognition after control of SBP from 135 to 150 mm Hg but decline in cognition after lowering SBP below the level of 135 mm Hg in hypertensive patients with multi-infarct dementia. In conclusion, it is worth remembering that not only high blood pressure, but also lower blood pressure, may be associated with later decline in the cognitive function of older people.

Baseline Mobility is Not Associated with Decline in Cognitive Function in Healthy Community-Dwelling Older Adults: Findings From The Irish Longitudinal Study on Ageing (TILDA)

Postoperative cognitive dysfunction in clinical practice

Background: Vascular aging is associated with cognitive decline. Aortic stiffness is a hallmark of vascular aging. We tested the hypothesis that greater aortic stiffness is associated with a faster rate of cognitive decline over 5 years among older adults. Methods: A prospective cohort study at the 5th (2011-2013) and 6th (2016-2017) examinations of the Atherosclerosis Risk in Communities Neurocognitive Study (ARIC-NCS) was conducted to quantify the association between baseline aortic stiffness and cognitive decline over 5 years. A total of 4639 participants (mean age: 75 years, 41% men, 22% Black) with baseline measures of aortic stiffness and cognitive function were included in the analysis. Aortic stiffness was measured as carotid-femoral pulse wave velocity (cfPWV) using the Omron VP-1000 Plus device and analyzed continuously per 1 standard deviation meter/second (3.20 m/s). Elevated aortic stiffness was defined as the upper 25th percentile of cfPWV (13.39 m/s). Cognitive function was based on ten neuropsychological tests across multiple domains of cognition, including memory, executive function/processing speed, and language. A global cognitive performance factor score was estimated based on all cognitive tests at both visits. Multivariable linear regression was used to examine the associations of each standard deviation (SD) increment in cfPWV and elevated cfPWV with annual cognitive decline over 5 years. Interactions with baseline cognitive status were assessed. To account for attrition (35% over 5 years), multiple imputation by chained equations was used to impute missing global cognitive performance factor scores at visit 6. Results: Each 1 SD increase in cfPWV was associated with 0.008 SD (Beta (β)=-0.008, 95% confidence interval (CI): -0.010, -0.003) annual rate of decline in cognitive function after adjustment for age, sex, education, race-center and ApoE4. With additional adjustment for ever smoking, total weekly physical activity time, mean arterial pressure, diabetes, and body mass index, each SD higher cfPWV was associated with 0.005 SD (β=-0.005, 95% CI: -0.010, -0.001) annual rate of decline in cognitive function. Elevated cfPWV was associated with 0.015 SD (β=-0.015, 95% CI: -0.024, -0.005) annual decline in cognitive function, and with 0.010 SD (β=-0.010, 95% CI: -0.020, 0.0001) annual decline after additional adjustment. Conclusion: Higher aortic stiffness is associated with the rate of decline in global cognitive function among community-dwelling older adults. The hemodynamic sequelae of aortic stiffening may contribute to cognitive decline among older adults.

AimWe examined whether a newly developed computer‐aided neuropsychiatric series of test, CogEvo, is necessary and sufficient for the evaluation of cognitive function in older people.MethodsA total of 272 participants in worthwhile life activity for the prevention of decline in mobility and cognitive function were administered tests every week at 33 locations in Fukaura‐machi, Japan. Basic profile information, a Mini‐Mental State Examination (MMSE), a CogEvo and a clock drawing test were used in the present study.ResultsOur results are summarized as: (i) the total score of the CogEvo and MMSE tests decreased significantly according to age and in age group analysis; (ii) scores from the CogEvo and MMSE tests showed a significant correlation; (iii) MMSE scores showed marked ceiling effects; (iv) analysis of cognitive domains, such as orientation, attention, memory and executive function, and spatial cognition using CogEvo showed significant age‐dependent impairment; (v) CogEvo discriminated three score groups of MMSE results with sensitivity and specificity of 70% and 60% in the <23 score group, 78% and 54% in the 24–26 score group, and 85% and 70% in the >27 score group, respectively; (vi) CogEvo memory tests reflected more detailed recall function than registration function; and (vii) CogEvo spatial cognition test results were correlated with test items of the MMSE and clock drawing tests.ConclusionsCogEvo is an easy and potentially useful computer‐aided test battery that can be used to evaluate age‐related or pathological decline in cognitive function from middle age and in preclinical stages of dementia. Geriatr Gerontol Int 2019; ••: ••–••.

MORE than 50 yr ago, clinicians reported changes in mental function after anesthesia and surgery in the elderly. As these phenomena have been elucidated in subsequent years, they have been categorized into the distinct syndromes of delirium and postoperative cognitive dysfunction (POCD). These phenomena seem to be increasing in prevalence, concomitant with the increase in the number of elderly patients undergoing surgery. In this brief clinical review, we describe the presentation of, course of, risk factors for, and when applicable, management of these syndromes. Delirium and cognitive function after cardiac and neurosurgical procedures are distinct subjects beyond the scope of this review.Delirium was well described in the writings of Hippocrates 2,500 yr ago. The key diagnostic features, as described in the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders are (1) that it is a change in mental status, characterized by a prominent disturbance of attention and reduced clarity of awareness of the environment; and (2) that it has an acute onset, developing within hours to days, and tends to fluctuate during the course of the day. The inability to focus, sustain, and shift attention is accompanied by other cognitive symptoms (e.g ., disorientation, episodic memory dysfunction) and/or perceptual disturbances (misinterpretations, illusions, or hallucinations). Associated features include disturbances of the sleep–wake cycle and activity level, as well as affective disturbance (mood lability, anger, sadness, euphoria) and thought disorder (disorganized thinking, delusions). The symptoms of delirium are numerous, vary from patient to patient, vary within patients over time, and are shared by a variety of other disorders such as dementia, anxiety, depression, and psychosis, all of which contribute to difficulties in diagnosis.The heterogeneous presentation of delirium has led to the identification of hyperactive, hypoactive, and mixed subtypes.1,2The hyperactive form of delirium tends to be clinically obvious. The hypoactive form, however, is often unrecognized, misdiagnosed, mistaken for depression or dementia, or simply attributed to old age, because patients may seem quiet and subdued in their disorientation. Furthermore, the relation between delirium and dementia is complex, and the syndromes may overlap.1,2Delirium can be caused by, or associated with, a wide variety of conditions,1,2and the current Diagnostic and Statistical Manual of Mental Disorders system differentiates subtypes based on the presumed etiology. These are delirium due to a general medical condition , substance-induced delirium (due to medication use or toxin exposure), substance intoxication delirium (due to intoxication), substance withdrawal delirium , delirium due to multiple etiologies , and delirium not otherwise specified (for cases in which there is insufficient evidence to establish a specific etiology).Delirium in the postoperative period can be divided into emergence delirium and postoperative delirium (PD), based on the time of onset (fig. 1). Emergence delirium is seen during or immediately after emergence from general anesthesia and usually resolves within minutes or hours. It occurs in all age groups, with some predominance in children. It seems to be directly correlated with the administration of general anesthesia, because it occurs during the emergence process, mimics stage II (excitation) of ether anesthesia as described by Guedel, and usually resolves without sequelae. Emergence delirium fits the Diagnostic and Statistical Manual of Mental Disorders , fourth edition, diagnostic criteria for a substance-induced delirium . The reader is referred to a more complete review of this subject.3After surgery, another type of delirium occurs that is not clearly related to emergence from anesthesia. Elderly patients commonly emerge from anesthesia smoothly and demonstrate coherence in the postanesthesia care unit. After a lucid interval, some patients develop a syndrome referred to as interval delirium or postoperative delirium .1,4Postoperative delirium tends to first be observed between postoperative days 1 and 3, and usually resolves within hours to days, although symptoms may persist for weeks to months. Postoperative delirium is more likely to result in complete recovery than other forms of delirium.5The term intensive care unit (ICU) delirium describes delirium that occurs in the intensive care unit, primarily in those patients requiring mechanical ventilation; it was previously referred to as ICU psychosis . ICU delirium makes no distinction between medical and surgical patients, so many cases of ICU delirium could also be classified as postoperative delirium.6There are a number of structured instruments available that can be used by a variety of personnel to diagnosis and assess delirium. Three validated methods include the Confusion Assessment Method,7the Delirium Rating Scale Revised-98,1and the Delirium Symptom Interview.1The confusion assessment method has been used for most postoperative delirium research and has been modified and validated for use in critical care patients receiving mechanical ventilation.8The reported incidence of PD is 5–15% in older adults after general anesthesia.9The reported incidence in patients undergoing surgery for hip fracture is higher, ranging from 16% to 62%, with an average rate of 35% across 12 studies of 1,823 patients.10Delirium is indeed the most common complication after hip fracture, but this patient population also has a high incidence of delirium before surgery.In elderly patients hospitalized for reasons other than surgery, the risk of developing delirium while hospitalized is predicted by an interaction between vulnerability factors present at the time of hospitalization and noxious injuries, or precipitating factors that occur during hospitalization.2Among the predisposing risk factors identified are vision impairment, severe illness, cognitive impairment, and serum urea nitrogen:creatinine ratio of 18 or greater. The precipitating factors identified are use of physical restraints, malnutrition, more than three medications added 24–48 h before the onset of delirium, use of a urinary bladder catheter, and iatrogenic events, including fluid and electrolyte abnormalities and infections.2Studies in surgical patients have identified age 70 yr or older, history of delirium, history of alcohol abuse, and preoperative use of narcotic analgesics as preoperative predisposing risk factors for PD.11Preoperative depression also seems to be a risk factor for postoperative delirium.12Perioperative risk factors include greater intraoperative blood loss, more postoperative transfusions, postoperative hematocrit less than 30%, and severe postoperative pain.13There are contradictory reports on the role of perioperative hypotension and hypoxemia in the development of PD. The role that postoperative pain plays in the development of PD is not attributable to method of analgesia, type of opioid analgesia, or cumulative opioid dose.14Drug effects are considered an important cause of delirium. In medical patients, the most important drug classes associated with delirium are the sedative–hypnotics, narcotics, and anticholinergics,1all of which are routinely used in perioperative care. The role of benzodiazepines is controversial.1Lorazepam has been specifically associated with the development of delirium in the ICU.15There is extensive literature investigating the proposition that regional anesthesia would be associated with less delirium than general anesthesia; however, the majority of these studies show no difference.16,17The underlying pathophysiology of delirium in general, and PD specifically, remains elusive. Delirium is the behavioral manifestation of diffuse cortical dysfunction and is associated with diffuse slowing of background activity in the electroencephalogram (except in cases of alcohol withdrawal, in which there is an increase in fast wave activity).1It is also associated with disturbances in a wide variety of neurotransmitter systems, and disruption of cholinergic transmission seems to be especially important.2Toxicity from anticholinergic agents mimics the electroencephalographic and behavioral aspects of delirium and is reversed by physostigmine. Serum anticholinergic activity is associated with delirium in postoperative patients.18Other potential mediators include melatonin, norepinephrine, and lymphokines.1,2Postoperative delirium is associated with increased morbidity (including risk of injury), mortality, duration of hospital stay, nursing home placement, and technical (nonphysician), consultant, and nursing costs.19In a recent study, duration of hospital stay for surgical patients was 6.0 days for those who developed delirium and 4.6 for those who did not.19The average additional in-hospital cost per surgical patient with PD was $2,947, which equates to more than $2 billion additional healthcare dollars per year in the United States.It is possible to prevent PD in some patients using safe and effective interventions for systematic detection and management of predisposing factors.1The most widely studied intervention program to prevent delirium in elderly medical patients is the Hospital Elder Life Program.20Interventions are targeted towards six risk factors for delirium: cognitive impairment, sleep deprivation, immobility, visual impairment, hearing impairment, and dehydration. Some of the specific interventions include frequent presentation of orienting information (such as prominent display of the date, time, schedule, and names of hospital personnel), cognitive stimulation activities, physical exercise, use of visual aids and adaptations, use of auditory amplifying devices, nonpharmacologic methods to promote sleep (such as drinking warm milk before bed, relaxing music, back massage, noise-reduction strategies), and feeding and fluid assistance. Other protocols have focused on coordinated geriatric services, geriatric–psychiatric consultations, and patient and family education. A series of randomized and nonrandomized trials indicate that a substantial absolute risk reduction (in the range of 13–19%) can be achieved.1,2A trial of proactive geriatric consultation in hip fracture patients reduced delirium by more than one third and reduced cases of severe delirium by more than one half.21Treatment of agitation poses a special problem. Agitation puts the patient, visiting family, and staff at risk for physical injury and interferes with administration of normal postoperative care, but current treatment options are less than optimal. Attempts should be made to avoid the use of physical restraints, which may worsen delirium and agitation. Pharmacologic therapy is used specifically to decrease agitation.22Haloperidol, a typical antipsychotic dopaminergic antagonist, is administered to adults at a dose of 0.5–1 mg intravenously every 10–15 min until the agitated behavior is controlled.∥Intramuscular dosing is less desirable but can be employed using 2–10 mg, waiting 60–90 min between doses. By careful dosing, practitioners should limit the degree of haloperidol's sedative side effect, because this drug has an extended half-life in the elderly (up to 72 h) and deep sedation can last for several days. It is important for the clinician to recognize that haloperidol can be useful in the immediate management of agitation but does not alter the duration of delirium. Newer antipsychotic medications, such as ziprasidone and olanzapine, are administered intramuscularly and are reportedly effective in the management of acute agitation but have not been tested in patients with either medical or surgical comorbidities.22Although most typical antipsychotics increase the corrected QT interval and may predispose to arrhythmias, haloperidol has a relatively lower propensity to do so. Cases of sudden death are rare and have not been clearly related to haloperidol.22Although it is reasonable to assume that benzodiazepines would be an effective treatment for agitation in the context of PD, anecdotal experience has shown that these medications may have a paradoxical effect in elderly patients and may worsen agitation.22If alcohol withdrawal is suspected to be the underlying cause of delirium, however, benzodiazepines are the treatment of choice.The term postoperative cognitive dysfunction (POCD) describes a deterioration of cognition that is temporally associated with surgery. As opposed to delirium, in which pathognomonic behavior must be detected, detecting, assessing the severity of, and characterizing POCD depends on valid assessments of preoperative and postoperative cognitive function. The neuropsychological examination measures the information processing abilities of the brain through a battery of tests (assessing attention, perception, verbal abilities, learning and memory, and abstract thinking) that are sensitive to the effects of brain injury and disease.23The wide variability in normal human cognitive capacities associated with aging and a possible incidence of preexisting mild cognitive impairment in the elderly make baseline (i.e ., preoperative) measures a critical component of these evaluations. In the absence of baseline data, it is impossible to associate low postoperative test scores to surgical, anesthetic, or illness variables with certainty. Subjective self-reported cognitive symptoms do not substitute for objective cognitive testing, because a poor relation between the two types of data has been demonstrated repeatedly.24There are a number of methodologic inconsistencies among studies that make the limited literature on POCD difficult to interpret. These include the selection of test instruments, timing of postoperative testing, inclusion and exclusion criteria, the inherent variability of cognitive testing, and most fundamentally, the operational definition of POCD.Mental status screening instruments such as the Mini-Mental State Examination are useful for detecting frank dementia but lack the sensitivity and specificity required to detect milder or more selective forms of cognitive impairment.23High-functioning patients who have experienced a mild decline in cognitive function and patients with "focal," as opposed to "diffuse," cognitive dysfunction may achieve high Mini-Mental State Examination scores. Cognition is not a unitary process, but rather is the result of activity in multiple complex, distributed, and interacting neuronal circuits that underlie specific information processing functions. There is no single measure of cognitive status; therefore, comprehensive neuropsychological assessment requires that a battery of tests assessing a variety of cognitive domains must be used. There are, however, a wide variety of tests available, which differ in their test–retest reliability, sensitivity, specificity, and the degree to which they are subject to practice effects.Another methodologic inconsistency among the studies is the timing of postoperative cognitive testing. In general, studies measuring cognitive function shortly after surgery find a much higher incidence of POCD than studies measuring cognitive function weeks to months after surgery. Longitudinal studies have the problem of attrition, which does not occur randomly but is influenced by the postoperative health status, functional status, and possibly the cognitive status of the patient. Patients who develop POCD may be more likely to drop out of the study, thus underestimating the true incidence of POCD.It is also important to consider the subject inclusion and exclusion criteria when interpreting study findings. Recently, the term mild cognitive impairment has come to represent a transitional zone in the spectrum of cognitive function from normal aging to progressive dementing conditions, such as Alzheimer and cerebrovascular diseases. Unfortunately, patients with preoperative mild cognitive impairment have not been differentiated in studies of POCD. Therefore, there is no information available concerning the impact of surgery and anesthesia on this subset of patients that may be at greatest risk for POCD. There is no evidence that anesthesia and surgery increase the incidence of Alzheimer disease.One of the greatest problems facing the investigation of postoperative cognitive function is the absence of a consensus regarding the operational definition of POCD. Variations in the methods that different groups have used to define deterioration in cognitive function in part underlie the difficulty in comparing studies. Furthermore, few studies use control groups and take practice effects into account.25The percent change method involves converting the preoperative to postoperative difference score into a percent of baseline score, i.e ., (postoperative score − preoperative score)/preoperative score. This method generates continuous data, which can then be averaged across patients for group comparisons. The use of group mean analyses, however, is discouraged, because a subset of subjects experiencing significant deterioration may be masked when other subjects exhibit improved performance over time. The SD method involves identifying patients who experience a postoperative decline of some criterion number of SD units (Z scores). The International Study of Postoperative Cognitive Dysfunction (ISPOCD) studies (see below) required a 2-SD decline to qualify as POCD. Limitations of the SD method include the following: (1) in patients with low baseline scores, it may not be possible to decline by more than 1 SD (i.e ., floor effect); and (2) the absolute magnitude of change in raw test scores required to meet the criterion differs between studies, because they are derived from the preoperative test scores of the baseline sample. A third strategy involves identifying patients who experience a specific percentage (e.g ., 20%) decline from baseline of at least a specific percentage (e.g ., 20%) of the tests administered. A limitation of this technique is that patients with lower preoperative test scores require a smaller decline in raw score to meet the 20% criterion. It should be noted that the methodology used by ISPOCD is a subset of the general assessment technique referred to as a reliable change index . Lewis has recently explored a number of issues related to the use of this technique.26In 1998, Möller et al .27presented the first of a series of multicenter studies from the ISPOCD that primarily included European centers. Information from the ISPOCD studies is available at the ISPOCD Web site.#The ISPOCD1 study tested the hypothesis that insufficient oxygen delivery to the brain, as assessed by the presence of hypotension and/or hypoxemia, is a causative factor for POCD. The study included 1,218 patients, aged 60 yr or older, who underwent major abdominal, noncardiac thoracic, or orthopedic surgery during general anesthesia. Patients were tested preoperatively and at 1 week and 3 months postoperatively. Test results were compared with a total of 321 controls recruited from the United Kingdom, 11 centers in and centers in Patients were classified as experiencing cognitive dysfunction when two scores in tests by or the average score greater than 1 week of patients experienced a decline in cognitive compared with of control 3 months of patients experienced a decline to preoperative of compared with of number of subsequent studies have described cognitive impairment within the first days after surgery and et al a rate of POCD of at months after surgery, although in the absence of a control the is to A study that patients at 1 and yr that the rate of POCD to which was not it seems that elderly patients deterioration shortly after surgery and anesthesia at 2–10 with such that the incidence at 3 at at 1 to from control subjects by 1 important are that (1) the of patients to drop out of such studies, the may the true incidence of and (2) the clinical course of an patient be clearly from this in that there is inconsistency between the In the ISPOCD studies, less than of the who were classified at POCD at 3 months decline at 1 week (i.e ., POCD at 1 week did not POCD at 3 a of the data from the ISPOCD studies, et al . to the impact of test–retest variability on the of that variability in cognitive results could after surgery would be as frequent as This that cognitive decline at 1 week but that there was no significant change at 3 months. study be required to impairment is an important clinical in cognitive is an important factor that to the low between that should be in studies of all of the studies to have that age is a risk factor for POCD. of patients aged yr undergoing major surgery a but significant decline in cognitive function at 1 week that was no at 3 months the ISPOCD that POCD is primarily a problem of elderly surgery seems to be the for POCD. A study comparing patients undergoing general anesthesia and surgery with at least a single hospital stay with patients who underwent general anesthesia for surgery that surgery was not associated with significant major surgery, postoperative cognitive dysfunction at 1 week was associated with increased age, increased duration of anesthesia, of postoperative and age was a significant risk factor for POCD at 3 postoperative pain has also been associated with postoperative cognitive function. In a study of patients aged who underwent surgery, greater pain on postoperative 1 was associated with performance on some neuropsychological degree of preoperative pain was not related to preoperative cognitive test date, the of POCD remains in neurotransmitter and system have all been but the has been general anesthesia. anesthesia is a with multiple medications, many of which are to cause delirium. The method of the potential of general anesthesia to POCD has been randomized trials of general regional anesthesia. studies that of anesthesia is not an important factor in the development of is in greater such different as regional and general anesthesia have impact on postoperative cognitive function in clinical studies, there are studies that general agents have effects on and of this to the clinical syndromes described require significant additional and are potential etiologies of POCD for which potential (e.g ., that were in the first ISPOCD study the role of hypotension and hypoxemia as potential was by continuous and blood was by the perioperative high of hypoxemia and condition was associated with POCD. may additional into this problem. research is to the role of in the of of the is associated with the development of Alzheimer but has not been to be an important of POCD in general for either a to POCD or a of POCD is but all such In studies of cardiac surgery patients, but not may be useful as a of research including that for different aspects of (in cardiac and require substantial additional research to establish clinical is that general anesthesia, which specifically the brain, as compared with regional anesthesia, which primarily the or would be associated with different of POCD. in a series of relatively studies that patients undergoing general anesthesia, but not anesthesia, were at greater risk for et al an randomized study of POCD that used neuropsychological This study compared the effect of general anesthesia on the incidence of POCD in patients undergoing total assessment was days preoperatively and 1 week and months postoperatively. mean scores for of the measures were compared between the two anesthesia groups, but no significant were observed postoperatively. In the of patients clinically important for test by were of patients a decline in cognitive function months after surgery, but no significant were between the anesthesia As this was a there was no control group for Recently, et al a comprehensive review of studies that the of anesthesia and that it does not the incidence of the of PD and it is important to consider that there may be an between Postoperative delirium may be a of POCD or an Patients who developed delirium in the ISPOCD1 study were not the patients who developed POCD. In ICU patients, delirium does seem to be of term cognitive majority of studies to have focused on either PD or POCD. In the studies that for PD and POCD should on this system dysfunction after anesthesia and surgery is primarily a problem of the elderly. The of an aging population and in anesthesia and surgery has led to in the number of elderly patients undergoing surgery. It is therefore, that postoperative dysfunction an common delirium is an diagnostic that requires research to as well as to effective and treatment There are available that seem to postoperative delirium. of these may be difficult limited however, assessment of patients for delirium has a of care in some European and should be with the and management of to PD, the that to define the presence or absence of POCD are The are not regarding the of cognitive that are associated with do they regarding the degree of dysfunction that is clinically illness requiring hospitalization may be associated with cognitive the that cognitive decline occurs as a of illness rather than it related to surgery and/or anesthesia. There are patients who significant after surgery and anesthesia. study, of clinical with mild cognitive impairment be for practitioners to the of cognitive dysfunction after noncardiac dysfunction is a health problem of study to the risk and and underlying should the current status of postoperative delirium and cognitive dysfunction and to prevent and delirium as studies to postoperative function.

Growing evidence supports a strong and likely causal association between cardiovascular disease (CVD), and its risk factors, with incidence of cognitive decline and Alzheimer's disease. Individuals with subclinical CVD are at higher risk for dementia and Alzheimer's. Several cardiovascular risk factors are also risk factors for dementia, including hypertension, high LDL cholesterol, low HDL cholesterol and especially diabetes. Moderate alcohol appears to be protective for both CVD and dementia. In contrast, inflammatory markers predict cardiovascular risk, but not dementia, despite biological plausibility for such a link. The substantial overlap in risk factors points to new avenues for research and prevention.

Education and change in cognitive function: The Epidemiologic Catchment Area Study

Although many studies have shown no significant change in global cognitive function after subthalamic brain stimulation (STN DBS) in patients with Parkinson disease (PD) and have concluded that STN DBS is generally safe from a cognitive standpoint, some studies have reported a decline in global cognitive function after STN DBS. Interestingly, in some studies, the decline in cognitive function appears to be greater during the initial short period after surgery (within 6 or 12 months after surgery) than the decline thereafter. To this end, we examined whether the rate of change in global cognitive function during the initial 6 months after STN DBS was different from the mean 6-month change that occurred between 6 and 36 months after surgery. Thirty-six PD patients who underwent bilateral STN DBS and were followed for more than 3 years were included. Change in Mini-Mental Status Examination (MMSE) score during the first 6 months after surgery was compared with the 6-month MMSE score change between 6 and 36 months after surgery. Mean MMSE change during the first 6 months after surgery was significantly greater than the mean 6-month MMSE change between 6 to 36 months after surgery. The levodopa equivalent daily dose at baseline and the score for Stroop Color-word test at baseline were significantly associated with the decline in MMSE score during the first 6 months after surgery. Our result showed that decline in global cognitive function was faster in the first 6 months after surgery, compared with that after 6 months.

Dementia With Mood Symptoms in a Fragile X Premutation Carrier With the Fragile X-Associated Tremor/Ataxia Syndrome: Clinical Intervention With Donepezil and Venlafaxine

Relationship between mild cognitive decline and oral motor functions in metropolitan community-dwelling older Japanese: The Takashimadaira study

Cognitive function decline is influenced by cardiovascular diseases and associated risk factors. However, changes in the cognitive function of patients with cardiovascular diseases during hospitalization and the factors influencing these changes remain unclear. This study elucidated the proportion and characteristics of changes in cognitive function during hospitalization in patients with cardiovascular diseases. We conducted cognitive function assessments at admission and discharge for patients with cardiovascular diseases. Using the Mini-Mental State Examination (MMSE) and the Japanese version of the Montreal Cognitive Assessment (MoCA-J), we categorized the patients into cognitive impairment, mild cognitive impairment (MCI), and non-cognitive impairment. Changes in MMSE or MoCA-J scores of ≥2 points at discharge were classified as improvement or decline, and all others as maintenance. The cognitive impairment, MCI, and non-cognitive impairment categories comprised 215 (41.3%), 224 (40.2%), and 103 (18.5%) patients, respectively. The results of the cognitive function assessment at the time of discharge classified 90 patients (35.9%) into the maintenance group, 117 (46.6%) into the improvement group, and 44 (17.5%) into the decline group based on changes during hospitalization. There was a statistically significant difference among the three groups only in cognitive function at admission (P = 0.026). In multivariate analysis, those with MCI or cognitive impairment at admission and younger patients were associated with improved cognitive function during hospitalization. No factors were extracted that showed statistically significant associations with cognitive decline. Approximately half of the patients with cardiovascular disease experienced improvements in cognitive function during hospitalization, while approximately 20% showed a decline in cognitive function during the same period. These findings demonstrate the importance of assessing cognitive changes in hospitalized patients with cardiovascular disease. Future studies are needed to identify factors associated with changes in cognitive function.