Showing papers on "Cognitive decline published in 1997"
TL;DR: The result suggests a functional importance for the posterior cingulate cortex in impairment of learning and memory, which is a feature of very early Alzheimer's disease.
Abstract: This study investigated cerebral glucose metabolism in very early Alzheimer's disease, before a clinical diagnosis of probable Alzheimer's disease is possible, using [18F]fluorodeoxyglucose positron emission tomography. First, 66 patients with probable Alzheimer's disease with a spectrum of dementia severity (Mini-Mental State Examination score, 0-23) were recruited and studied. Cortical metabolic activity was analyzed topographically using three-dimensional stereotactic surface projections. Regression analysis was performed for each brain pixel to predict metabolic patterns of very early disease. Predictions were tested prospectively in a group of 8 patients who complained only of memory impairment without general cognitive decline (Mini-Mental State Examination score, 25 +/- 1) at the time of scanning but whose condition later progressed to probable Alzheimer's disease. Both results were compared to cerebral metabolic activity in 22 age-similar normal control subjects. Prediction and analysis of actual patients consistently indicated marked metabolic reduction (21-22%) in the posterior cingulate cortex and cinguloparietal transitional area in patients with very early Alzheimer's disease. Mean metabolic reduction in the posterior cingulate cortex was significantly greater than that in the lateral neocortices or parahippocampal cortex. The result suggests a functional importance for the posterior cingulate cortex in impairment of learning and memory, which is a feature of very early Alzheimer's disease.
1,651 citations
TL;DR: The criterion validity of the CES-D for major depression was very satisfactory in this sample of older adults and false positives were not more likely among elderly with physical illness, cognitive decline or anxiety.
Abstract: The Center for Epidemiologic Studies Depression scale (CES-D) has been widely used in studies of late-life depression. Psychometric properties are generally favourable, but data on the criterion validity of the CES-D in elderly community-based samples are lacking. In a sample of older (55-85 years) inhabitants of the Netherlands, 487 subjects were selected to study criterion validity of the CES-D. Using the 1-month prevalence of major depression derived from the Diagnostic Interview Schedule (DIS) as criterion, the weighted sensitivity of the CES-D was 100%; specificity 88%; and positive predictive value 13.2%. False positives were not more likely among elderly with physical illness, cognitive decline or anxiety. We conclude that the criterion validity of the CES-D for major depression was very satisfactory in this sample of older adults.
1,048 citations
TL;DR: A consensus conference on the diagnosis and treatment of Alzheimer disease and related disorders was organized by the American Association for Geriatric Psychiatry, the Alzheimer's Association, and the American Geriatrics Society on January 4 and 5, 1997, and reached consensus.
Abstract: Objective. —A consensus conference on the diagnosis and treatment of Alzheimer disease (AD) and related disorders was organized by the American Association for Geriatric Psychiatry, the Alzheimer's Association, and the American Geriatrics Society on January 4 and 5, 1997. The target audience was primary care physicians, and the following questions were addressed: (1) How prevalent is AD and what are its risk factors? What is its impact on society? (2) What are the different forms of dementia and how can they be recognized? (3) What constitutes safe and effective treatment for AD? What are the indications and contraindications for specific treatments? (4) What management strategies are available to the primary care practitioner? (5) What are the available medical specialty and community resources? (6) What are the important policy issues and how can policymakers improve access to care for dementia patients? (7) What are the most promising questions for future research? Participants. —consensus panel members and expert presenters were drawn from psychiatry, neurology, geriatrics, primary care, psychology, nursing, social work, occupational therapy, epidemiology, and public health and policy. Evidence. —The expert presenters summarized data from the world scientific literature on the questions posed to the panel. Consensus Process. —The panelists listened to the experts' presentations, reviewed their background papers, and then provided responses to the questions based on these materials. The panel chairs prepared the initial drafts of the consensus statement, and these drafts were read by all panelists and edited until consensus was reached. Conclusions. —Alzheimer disease is the most common disorder causing cognitive decline in old age and exacts a substantial cost on society. Although the diagnosis of AD is often missed or delayed, it is primarily one of inclusion, not exclusion, and usually can be made using standardized clinical criteria. Most cases can be diagnosed and managed in primary care settings, yet some patients with atypical presentations, severe impairment, or complex comorbidity benefit from specialist referral. Alzheimer disease is progressive and irreversible, but pharmacologic therapies for cognitive impairment and nonpharmacologic and pharmacologic treatments for the behavioral problems associated with dementia can enhance quality of life. Psychotherapeutic intervention with family members is often indicated, as nearly half of all caregivers become depressed. Health care delivery to these patients is fragmented and inadequate, and changes in disease management models are adding stresses to the system. New approaches are needed to ensure patients' access to essential resources, and future research should aim to improve diagnostic and therapeutic effectiveness.
910 citations
TL;DR: These lesions, rediscovered by brain imaging techniques under the name leukoaraiosis, constitute the pathological substratum of Binswanger disease, a vascular form of senile dementia, leading also to periventricular ischemic white matter disease in the elderly.
Abstract: To the Editor. —Dr Snowdon and colleagues 1 emphasized the important contribution of lacunar infarcts to cognitive decline in patients with AD. However, with few exceptions, no clear correlation exists between location or number of lacunar infarcts and development of vascular dementia. 2,3 More than a direct cause of dementia, lacunar infarcts per se probably represent a surrogate or a marker for small-vessel disease(arteriolosclerosis) leading also to periventricular ischemic white matter disease in the elderly. 4 These lesions, rediscovered by brain imaging techniques under the name leukoaraiosis, constitute the pathological substratum of Binswanger disease, 5 a vascular form of senile dementia. Moreover, Brun and Englund 6 demonstrated these lesions in about 60% of patients with AD. However, periventricular ischemic white matter lesions in the elderly may be undetectable to the naked eye examination of the brain
792 citations
TL;DR: It is concluded that synaptic abnormalities in the hippocampus correlate with the severity of neuropathology and memory deficit in individuals with AD, and that this defect may predate neuropsychological evidence for cognitive impairment early in AD.
Abstract: We tested the hypothesis that synaptic defects in the hippocampus of individuals with Alzheimer disease (AD) correlate with the severity of cognitive impairment. Three postmortem groups were studied: controls with normal and stable cognition; cognitively intact subjects with senile plaque densities diagnostic for possible AD (p-AD) and neurofibrillary changes characteristic of early AD (Braak stage III); and individuals with definite AD and neurofibrillary changes typical of incipient to severe AD (Braak stage III, V, or VI). Synaptophysin (a presynaptic vesicle protein) levels were quantified by immunoblotting of synaptic membrane fractions isolated from hippocampus, entorhinal cortex, caudate nucleus, and occipital cortex. Average synaptophysin levels were reduced in hippocampus when comparing definite AD to controls (55%, p < 0.0001), p-AD to control (25%, p < 0.005), and definite AD to p-AD (30%, p < 0.05), but levels in entorhinal cortex, occipital cortex, and caudate nucleus were either unchanged or less significantly altered than in hippocampus. By univariate analysis, hippocampal synaptophysin levels correlated with neuropsychological measurements, including Mini-mental state examination scores (r = 0.83, p < 0.0001) and Blessed scores (r = 0.74, P < 0.001), and with senile plaque densities (r = 0.89, p < 0.0001). We conclude that synaptic abnormalities in the hippocampus correlate with the severity of neuropathology and memory deficit in individuals with AD, and that this defect may predate neuropsychological evidence for cognitive impairment early in AD.
520 citations
TL;DR: It is raised the possibility that high linoleic acid intake is positively associated with cognitive impairment and high fish consumption inversely associated with Cognitive impairment.
Abstract: Atherosclerosis and thrombosis may lead to cognitive impairment through cerebral infarcts or white matter hyperintensities. Oxidative stress is now seen as a major contributor to the process of atherogenesis. High intake of polyunsaturated fatty acids, e.g., linoleic acid, or low intake of antioxidants can increase oxidative stress. High intake of n-3 polyunsaturated fatty acids and its main source, fish, may reduce the risk of thrombosis. Little is known, however, about the relation between these dietary factors and cognitive function. The authors investigated this relation with data derived from a cohort of men, aged 69-89 years, who were participants in the Zutphen Elderly Study. The 30-point Mini-Mental State Examination was used to assess cognitive impairment in 1990 (score 2 points in 51/342 men, 15%). Food intake was estimated in 1985 and 1990 by the cross-check dietary history method. High linoleic acid intake was associated with cognitive impairment after adjustment for age, education, cigarette smoking, alcohol consumption, and energy intake (odds ratio (OR) for highest vs. lowest tertile = 1.76, 95% confidence interval (CI) 1.04-3.01). Intake of n-3 polyunsaturated fatty acids was not associated with cognitive impairment, whereas high fish consumption tended to be inversely associated with cognitive impairment (OR = 0.63, 95% CI 0.33-1.21) and cognitive decline (OR = 0.45, 95% CI 0.17-1.16). Intakes of beta-carotene, vitamins C and E, and flavonoids were not inversely associated with cognitive impairment or decline. This study raises the possibility that high linoleic acid intake is positively associated with cognitive impairment and high fish consumption inversely associated with cognitive impairment.
444 citations
TL;DR: The importance of animal models for understanding the effects of normal aging on the brain and cognitive functions and the neurobiological effects of aging that may account for alterations in psychological functions are addressed.
Abstract: This review addresses the importance of animal models for understanding the effects of normal aging on the brain and cognitive functions. First, studies of laboratory animals can help to distinguish between healthy aging and pathological conditions that may contribute to cognitive decline late in life. Second, research on individual differences in aging, a theme of interest in studies of elderly human beings, can be advanced by the experimental control afforded in the use of animal models. The review offers a neuropsychological framework to compare the effects of aging in human beings, monkeys, and rodents. We consider aging in relation to the role of the medial temporal lobe in memory, the information processing functions of the prefrontal cortex in the strategic use of memory, and the regulation of attention by distributed neural circuitry. We also provide an overview of the neurobiological effects of aging that may account for alterations in psychological functions.
401 citations
TL;DR: The findings question the validity of current criteria for dementia in the setting of cerebrovascular disease and emphasize the need for further debate and studies to refine the categories of cognitive impairment related to cerebroVascular disease.
Abstract: Background and Purpose Vascular dementia is a common cause of dementia, and cerebrovascular disease is related to a higher risk of dementia. The frequency of dementia associated with ischemic stroke and the effects of different definitions of dementia in the diagnosis are still incompletely known. We evaluated the frequency of cognitive decline and dementia 3 months after ischemic stroke in a large stroke cohort. Methods Our cohort consisted of consecutively admitted ischemic stroke patients (n=486) aged 55 to 85 years in the Helsinki (Finland) Stroke Aging Memory Study (SAM). Subjects were assessed by structured medical, neurological, and radiological examinations and interview with a close informant, as well as by the Mini-Mental State Examination and detailed clinical mental status examination of defined cognitive domains. The criteria for dementia were those of the Diagnostic and Statistical Manual of Mental Disorders (DSM) (DSM-III, DSM-III-R, and DSM-IV), the National Institute of Neurological Disor...
331 citations
TL;DR: Significant trends toward progressively higher impairment rates in advanced-aged and oldest-aged monkeys were observed for DNMS-acquisition, DRST-color and spatial reversal learning tasks, suggesting that a score based on only three tests may provide an adequate classification of global cognitive ability.
258 citations
TL;DR: It is suggested that there should be regular review of the need for patients with dementia to continue taking neuroleptic drugs, because they may cause more rapid decline in cognitive function.
Abstract: Objective: To investigate the contribution of neuroleptic drugs to cognitive decline in dementia. Design: Two year prospective, longitudinal study consisting of interviews every four months, with necropsy follow up. Setting: Community settings in Oxfordshire. Subjects: 71 subjects with dementia, initially living at home with informant. Main outcome measures: Cognitive function (score from expanded minimental state examination); behavioural problems (physical aggression, hallucinations, persecutory ideas, and disturbance of diurnal rhythm); and postmortem neuropathological assessment (cortical Lewy body pathology). Results: The mean (SE) decline in cognitive score in the 16 patients who took neuroleptics was twice that in the patients who did not (20.7 (2.9) v 9.3 (1.3), P=0.002). An increased rate of decline was also associated with aggression, disturbed diurnal rhythm, and persecutory ideas. However, only use of neuroleptics and severity of persecutory ideas were independently associated with more rapid cognitive decline when all other variables were adjusted for. The start of neuroleptic treatment coincided with more rapid cognitive decline: median rate of decline was 5 (interquartile range 8.5) points per year before treatment and 11 (12) points per year after treatment (P=0.02). Cortical Lewy body pathology did not account for association between neuroleptic use and more rapid decline. Conclusions: Neuroleptic drugs that are sometimes used to treat behavioural complications of dementia may worsen already poor cognitive function. Randomised controlled trials are needed to confirm a causal relation. Key messages Neuroleptic drugs are used to treat behavioural problems in patients with dementia, but they may cause more rapid decline in cognitive function In our longitudinal study of patients with dementia we found that the rate of cognitive decline in patients taking neuroleptics was twice that in those not taking neuroleptics Furthermore, the start of neuroleptic treatment was associated with an increase in the rate of cognitive decline Cortical Lewy body pathology at necropsy did not account for the association between neuroleptic use and more rapid decline Although our study does not prove a causal relation, we suggest that there should be regular review of the need for patients to continue taking neuroleptic drugs
256 citations
TL;DR: Logistic regression analysis showed that low DART-IQ predicted incident dementia better than low level of education, indicating that low pre-morbid intelligence is an important risk factor for cognitive decline and dementia.
Abstract: Background A number of recent epidemiological studies have shown that the prevalence and incidence of dementia are increased in population strata with low compared to high levels of education. This has been explained as a consequence of a greater 'brain reserve capacity' in people with a high level of education. Theoretically, however, brain reserve capacity is better reflected by intelligence than by level of education. Thus, the emergence of dementia will be better predicted by low pre-morbid intelligence than by low education. Methods This prediction was tested in a population based sample of elderly subjects (N = 2063; age range 65-84; Amsterdam Study of the Elderly) who were followed over 4 years. Dementia was diagnosed using the Geriatric Mental State examination (GMS). Pre-morbid intelligence was measured using the Dutch Adult Reading Test (DART), a short reading test which gives a good estimate of verbal intelligence, and is relatively insensitive to brain dysfunction. The effects of age, gender, occupational level, number of diseases affecting the central nervous system and family history of dementia or extreme forgetfulness were also examined. Results Logistic regression analysis showed that low DART-IQ predicted incident dementia better than low level of education. A high occupational level (having been in charge of subordinates) had a protective effect. Conclusions This result supports the brain reserve theory. It also indicates that low pre-morbid intelligence is an important risk factor for cognitive decline and dementia. Use of reading ability tests is to be preferred over years of education as estimator of pre-morbid cognitive level in (epidemiological) dementia research.
TL;DR: In this paper, the apolipoprotein E-ϵ4 allele was evaluated as a predictor variable for postoperative cognitive dysfunction in 65 patients undergoing cardiac bypass grafting at Duke University Medical Center.
TL;DR: Results indicate that motor impairment is an important aspect of cognitive decline in older adults and that motorlpsychomotor assessments may be comparably sensitive to traditional tests of cognitive function in identifying persons affected by the earliest stages of AD pathology.
Abstract: In order to determine the relationship between cognitive dysfunction and motor behavior in older adults, 41 cognitively normal elderly (NL), 25 cases exhibiting mild cognitive impairment (MI), and 25 patients with mild Alzheimer's disease (AD) were examined using a broad array to motor/psychomotor and cognitive tests. Relative to the NL group, MI individuals (at risk for future decline to AD) performed worse on tasks involving fine and complex motor function (e.g., tracking and manual dexterity). AD patients also exhibited motor dysfunction on tasks assessing relatively more rudimentary motor control. Motor tasks were able to distinguish NL vs MI and NL vs mild AD individuals as effectively as cognitive tests of memory and language. These results indicate that motor impairment is an important aspect of cognitive decline in older adults. Motor/psychomotor assessments may be comparably sensitive to traditional tests of cognitive function in identifying persons affected by the earliest stages of AD pathology.
TL;DR: Memory complaints may lack validity in subjects with normal cognition, but in nondemented individuals with cognitive impairment, memory complaints may predict subsequent cognitive decline.
Abstract: Objective: The validity of subjective memory complaints has been questioned by clinical studies that have shown little relationship between memory complaints and objective memory performance. These studies often have been cross-sectional in design, have excluded individuals with cognitive impairment, or have lacked a comparison group. The authors conducted a study that attempted to avoid these limitations. Method: Memory complaints of 364 nondemented, community-dwelling elderly individuals were recorded as present or absent at the baseline evaluation. After 1 year, 169 subjects were reevaluated. Standardized neurologic and neuropsychological evaluations were used at each assessment to classify subjects as normal or cognitively impaired. Results: At baseline, 31% of the normal subjects and 47% of those with cognitive impairment had memory complaints. Subjects with memory complaints had higher Hamilton depression scale scores than subjects without memory complaints but equivalent scores on a measure of total recall. At follow-up, multivariate analyses showed that subjects with baseline memory complaints had significantly greater decline in memory and cognition than subjects without memory complaints. Secondary analyses showed this effect to be confined to subjects with baseline cognitive impairment. Conclusions: Memory complaints may lack validity in subjects with normal cognition, but in nondemented individuals with cognitive impairment, memory complaints may predict subsequent cognitive decline. (Am J Psychiatry 1997; 154:609‐615)
TL;DR: Evidence against the inclusion of cognitive complaints in diagnostic criteria for proposed disorders such as age-associated memory impairment, mild cognitive disorder and ageing-associated cognitive decline is found.
Abstract: Data from a two-wave longitudinal study of an elderly community sample were used to assess whether cognitive complaints either predict subsequent cognitive decline or reflect past cognitive decline. Cognitive complaints and cognitive functioning were assessed on two occasions three and a half years apart. Cognitive complaints at Wave 1 were found not to predict future cognitive change on the Mini-Mental State Examination, an episodic memory test or a test of mental speed. Similarly, cognitive complaints at Wave 2 were unrelated to past cognitive changes on these tests after statistically controlling for the effects of anxiety and depression. Furthermore, cognitive complaints did not predict either mortality (after controlling for anxiety and depression) or future dementia. These results are evidence against the inclusion of cognitive complaints in diagnostic criteria for proposed disorders such as age-associated memory impairment, mild cognitive disorder and ageing-associated cognitive decline.
TL;DR: Depressive symptoms at Wave 1 did not predict subsequent cognitive decline or dementia, and at the community level, depressive symptoms do not seem to predict cognitive decline, as they do in referred series.
Abstract: Background. We report the outcome of depressive states after 3-4 years in a community sample of the elderly.Methods. A sample of 1045 persons aged 70+ years in 1990–1 was re-interviewed after 3·6 years.Results. Mortality (21·7%) and refusal or non-availability (10·4%) were higher in those who initially had had a diagnosis or symptoms of depression. Of those with an ICD-10 depressive episode in 1990–1, 13% retained that diagnosis. Of those who were not depressed initially only 2·5% had become cases. Depression was unrelated to age or apolipoprotein E genotype. The best predictors of the number of depressive symptoms at follow-up was the number at Wave 1, followed by deterioration in health and in activities of daily living, high neuroticism, poor current health, poor social support, low current activity levels and high service use. Depressive symptoms at Wave 1 did not predict subsequent cognitive decline or dementia.Conclusions. Non-random sample attrition is unavoidable. ICD-10 criteria yield more cases than other systems, while continuous measures of symptoms confer analytical advantages. Risk factors for depressive states in the elderly have been further identified. The prognosis for these states is favourable. At the community level, depressive symptoms do not seem to predict cognitive decline, as they do in referred series.
TL;DR: The study demonstrated that intact cognitive functioning in multiple sclerosis may remain stable, whereas incipient cognitive decline seems to be widespread and progressive in nature.
Abstract: The purpose of this study was to illustrate how cognitive functioning evolves over time in patients with multiple sclerosis. We followed the evolution of cognitive performances in two clinically and demographically similar multiple sclerosis groups, the 'cognitively preserved' (n = 20) and the 'cognitively mildly deteriorated' (n = 22), and in healthy controls (n = 34). We conducted the follow-up examination using the Mild Deterioration Battery, the Mini-Mental State Examination, and a set of additional neuropsychological measures after an interval of 3 years. The drop-out rate in our study was only 5%. The 'cognitively preserved' multiple sclerosis group showed substantial neuropsychological stability by performing as well as the controls both at baseline and at follow-up. By contrast, the initially 'cognitively mildly deteriorated' group demonstrated progressive cognitive decline on many neuropsychological tests. The intermediate-length screening battery, the Mild Deterioration Battery, was sensitive to this decline, whereas the briefer Mini-Mental State Examination was not. The progressive cognitive decline could not be predicted from other disease variables. The study demonstrated that intact cognitive functioning in multiple sclerosis may remain stable, whereas incipient cognitive decline seems to be widespread and progressive in nature. Thus, progressive cognitive deterioration should be considered as one of the characteristics of multiple sclerosis.
TL;DR: To look for preclinical markers of Alzheimer's dementia in a sample of healthy, oldest old individuals, a large number of participants are healthy, middle-aged individuals.
Abstract: OBJECTIVE: To look for preclinical markers of Alzheimer's dementia in a sample of healthy, oldest old individuals.
DESIGN: Prospective, longitudinal study of individuals examined at yearly intervals with neuropsychological tests selected to be sensitive to the early detection of dementia.
PARTICIPANTS: One hundred and thirty-nine community-dwelling, functionally independent, healthy individuals 65 to 106 years of age who met strict criteria for lack of dementia at entry. Incident dementia cases consisted of 16 volunteers all 80 years old or older who developed dementia of the Alzheimer's type and 31 volunteers 80 years old and older showing no evidence of dementia during a mean 2.8-year follow-up interval.
MEASUREMENTS: Scores on 10 neuropsychological measures were analyzed for the initial examination when none of the volunteers showed clinical evidence of dementia and for the two subsequent yearly examinations.
RESULTS: Individuals who subsequently developed dementia showed evidence of verbal memory impairment at their initial examination, which was a mean of 2.8 years before clinical evidence of dementia. The average yearly incidence rate for dementia in those 80 years of age and older was 12%. Performance of individuals who did not development dementia remained relatively stable during follow-up for up to 5 years.
CONCLUSION: Alzheimer's disease has a preclinical stage in which verbal memory decline is the earliest sign. Dementia in the oldest old is distinguishable from age-related cognitive decline.
TL;DR: Subjective memory complaints are not just secondary to depression, but in part reflect realistic self-observations of cognitive decline.
Abstract: BACKGROUND Population studies indicate that subjective memory complaints by elderly people are correlated with cognitive performance. These complaints have some predictive power regarding the development of dementia. The present study attempted to replicate this finding, and investigated which variables determine subjective memory complaints.
METHOD Participants in the Amsterdam Study of the Elderly (n = 2114; 65-84 years of age), who were not demented and had a normal MMSE score (> 23) at baseline, were re-examined after four years. Subjective complaints were measured using a previously developed scale. Dementia and depression were measured using the Geriatric Mental State Schedule (GMS). Premorbid intelligence was measured by the Dutch Adult Reading Test (DART).
RESULTS Memory complaints at baseline contributed a small but significant amount of diagnostic information with respect to the prediction of future dementia. Depressive symptoms at baseline had no predictive value when these memory complaints were accounted for. Subjective memory complaints were associated with depression, baseline MMSE score, and premorbid intelligence.
CONCLUSIONS Subjective memory complaints are not just secondary to depression, but in part reflect realistic self-observations of cognitive decline.
TL;DR: Automated volumetric MRI measures of total lesion volume and brain to intracranial cavity volume ratio correlated with neuropsychological performance, especially in patients with chronic progressive MS.
Abstract: Objective: To assess the correlation between cognitive dysfunction and disease burden in multiple sclerosis (MS) during a 1-year period. Design: The Brief, Repeatable Battery of Neuropsychological Tests in Multiple Sclerosis was performed at entrance and 1 year. Patients underwent at least 20 proton density (range, 20-24) and T2-weighted axial magnetic resonance imaging (MRI) brain scans except for stable patients who were scanned monthly. Magnetic resonance imaging was evaluated using computer-automated, 3-dimensional volumetric analysis. Setting: A research clinic of a university hospital. Patients: Forty-four patients with MS of the following disease categories: relapsing-remitting (14), relapsingremitting progressive (12), chronic progressive (13), and stable (5). Main Outcome Measures: The relationships between scores on the Brief, Repeatable Battery of Neuropsychological Tests in Multiple Sclerosis and 2 MRI measures (total lesion volume and brain to intracranial cavity volume ratio) were assessed using linear regression. These MRI measures were also compared with cognitive status at 1 year using analysis of variance. Results: Overall, there was no decline in mean cognitive test performance during 1 year. Significant correlations were found between baseline neuropsychological test scores of nonverbal memory, informationprocessing speed, and attention and both MRI measures. Patients with chronic progressive MS demonstrated the strongest correlations. At 1 year, change in information-processing speed and attention correlated with change in total lesion volume. The mean increase in total lesion volume was 5.7 mL for 4 patients whose cognitive status worsened compared with 0.4 mL for 19 patients who improved and 0.5 mL for 21 patients who remained stable. Conclusions: During a 1-year period mean cognitive performance did not worsen. Automated volumetric MRI measures of total lesion volume and brain to intracranial cavity volume ratio correlated with neuropsychological performance, especially in patients with chronic progressive MS. Worsening MRI lesion burden correlated with cognitive decline.
TL;DR: There was no correlation, moreover, between depressed mood and cognitive decline after CABG, which suggests that depression alone cannot account for cognitive decline.
TL;DR: It is established that the incidence of cognitive decline varies according to the cognitive domain studied and that some patients have persistent and late cognitive changes in specific domains after coronary artery bypass grafting.
TL;DR: Large savings in the costs of caring for moderately to severely demented home-dwelling patients with AD may be achievable from disease interventions that have minor effects on patients' cognitive status.
Abstract: Objective: To estimate the dollar savings in costs attainable from drug or other treatments for Alzheimer disease (AD) that stabilize or reverse patients' cognitive decline. Methods: Medical and other disease-related utilization data were collected from the caregivers of 64 patients diagnosed as having probable AD. The quantities of utilization were priced at national levels to generate measures of illness costs. Costs per patient were then estimated as regression functions of scores on the Mini-Mental State Examination (MMSE), which was used as an index of patient cognitive function. Potential savings in illness costs were estimated by comparing predicted costs at various baseline and intervention-level values of the patient's MMSE score. Results: The potential savings in illness costs attainable from treatment are small for mildly and very severely demented patients with AD. However, for moderately to severely demented home-dwelling patients having, say, an MMSE score of 7 at baseline, prevention of a 2-point decline in the score would save about $3700 annually, and a 2-point increase in an MMSE score rather than a 2-point decline would save about $7100. Conclusion: Large savings in the costs of caring for moderately to severely demented home-dwelling patients with AD may be achievable from disease interventions that have minor effects on patients' cognitive status.
TL;DR: It was found that the Alzheimer's disease patients' intelligence was correlated both positively with premorbid brain volume and negatively with magnitude of brain atrophy, while impairments in language and memory were correlated with magnitude.
Abstract: Objective: Both the magnitude of brain atrophy and premorbid brain size determine the volume of the brain affected by Alzheimer’s disease. To examine the possibility that premorbid brain volume is a determinant of cognitive reserve in patients with Alzheimer’s disease, the relation between diffuse brain atrophy and cognitive decline and the impact of premorbid brain size on cognitive decline were studied in patients with Alzheimer’s disease. Method: By measuring whole brain volume and intracranial volume in 60 patients with probable Alzheimer’s disease, mild to moderate in severity, with the use of high-resolution magnetic resonance imaging and image processing, the authors studied the impact of premorbid brain volume and magnitude of diffuse brain atrophy on cognitive functions. On the basis of the normative brain-calvarium relationship derived from data an 28 healthy adults and the total intracranial volume measure of each patient, the magnitude of brain atrophy and premorbid brain volume were estimated. Results: After control for the effects of age, sex, and education as confounding factors, it was found that the Alzheimer’s disease patients’ intelligence was correlated both positively with premorbid brain volume and negatively with magnitude of brain atrophy, while impairments in language and memory were correlated with magnitude of brain atrophy but not with premorbid brain volume. Conclusions: These findings partially support the hypothesis that premorbid brain volume is a determinant of reserves against intellectual decline in Alzheimer’s disease. (Am J Psychiatry 1997; 154:18‐24)
TL;DR: The study has drive tested over 100 currently driving elderly patients with clinically significant cognitive decline and compared their performance with that of normal drivers and identified the types of driving errors typical of both cognitively impaired and normal experienced drivers but differing in the number and severity of errors.
Abstract: The driving behaviors of dementia patients have received little in the way of empirical scrutiny except through retrospective reports of crash rates. Understanding the driving errors of dementia patients and how they differ from those of normal older and younger drivers is important. This knowledge is basic to the development of road tests and scoring procedures to evaluate the driving competence of older, experienced drivers, especially those whose fitness to drive may have been compromised by a medical illness that alters their mental abilities. We have drive tested over 100 currently driving elderly patients with clinically significant cognitive decline (mostly diagnosed as the early stages of Alzheimer disease) and compared their performance with that of normal drivers. The study identified the types of driving errors that distinguish and differentiate the cognitively impaired group as well as a set of driving errors typical of both cognitively impaired and normal experienced drivers but differing in the number and severity of errors. A set of errors was also identified that did not differentiate the groups and should not be used in evaluating a person's competence to drive.
TL;DR: Cognitive decline, defined as the worst 10th percentile change scores, was assessed for each test and by phenotype group and Apo E epsilon 4 is associated with cognitive decline in community-dwelling nondemented women.
Abstract: Objective: To determine whether apolipoprotein E (Apo E) phenotype is associated with cognitive decline in community-dwelling nondemented elderly Design: Prospective cohort study. Setting: A university-affiliated clinic near Pittsburgh, Pa. Patients: A total of 1750 nondemented community-dwelling women, aged 65 years and older, who were enrolled in the Study of Osteoporotic Fractures. Main Outcome Measures: The women completed a baseline interview and performed 3 cognitive tests: the modified Mini-Mental State Examination, Trails B, and Digit Symbol. Serum samples were obtained for Apo E typing. Baseline cognitive scores and repeated scores approximately 6 years after study enrollment were compared in women with and without Apo E e4. Cognitive decline, defined as the worst 10th percentile change scores, was assessed for each test and by phenotype group. Results: After adjustment for age, education, presence of severe tremor, and depression, baseline scores did not differ by Apo E e4 status except for lower scores on Trails B in the homozygous e4 group (mean score, 159.7 compared with 127.7 for the heterozygous e4 group and 125.4 for the no e4 group; P =.01). However, repeated test performance on follow-up examination was worse on all tests in those women with 1 or more e4. Reduction on the modified Mini-Mental State Examination was 0% for no e4 allele, 1.9% for 1 e4 allele, and 3.7% for 2 e4 alleles ( P P =.04); and reduction on Trails B was 5.9% for no e4 allele, 25.0% for 1 e4 allele, and 10.9% for 2 e4 alleles ( P =.002). Women with at least 1 e4 had an odds ratio of 1.6 (95% confidence interval, 1.1-2.3) of having cognitive decline during the study period. Conclusion: Apolipoprotein E e4 is associated with cognitive decline in community-dwelling nondemented women.
Journal Article•
TL;DR: Results indicate that this observer-independent analysis of SPECT data enables objective and semiquantitative assessment of the magnitude and extent of cortical perfusion abnormalities in patients with AD.
Abstract: This study evaluated an automated analysis of SPECT brain imaging in patients with Alzheimer9s disease (AD). Methods: Patients [n =81; mean age, 69.9 ± 10.6 yr (mean ± s.d.)] with a clinical diagnosis of probable AD (NINCDS-Alzheimer9s Disease and Related Disorders Association criteria) underwent 99mTc-ethyl cysteine dimer SPECT imaging. After imaging registration and data extraction using three-dimensional stereotactic surface projections, a pixel-wise comparison of ethyl cysteine dimer uptake was performed using a reference database of 10 cognitive intact controls of comparable age. Results: When individual cases were compared to the normal database, tempora-parietal regional cerebral blood flow (rCBF) abnormalities across different levels of dementia severity were clearly depicted on pixel-wise Z-score images. The rCBF reduction incortical association areas showed a significant correlation with an overall level of cognitive decline, as assessed by the Mini Mental State Examination and by the cognitive section of the Cambridge Mental Disorders of the Elderly Examination. In addition, there were significant region-specific correlations between left temporo perfusion deficit and language performance and between right parietal rCBF reduction and praxis. Conclusion: These results indicate that this observer-independent analysis of SPECT data enables objective and semiquantitative assessment of the magnitude and extentof cortical perfusion abnormalities in patients with AD.
TL;DR: Whereas African Americans were less likely to complain of deterioration in memory, actual decline was greater for African Americans than for Whites and predicted a decline in cognitive function as measured by the SPMSQ 3 years later.
Abstract: Of a representative, racially mixed community sample of older adults in North Carolina, 59% of Whites and 49% of African Americans reported worsening memory. The complaint about memory was positively correlated with age, depressive symptomatology, and physical function but not with level of cognitive function as measured by the Short Portable Mental Status Questionnaire (SPMSQ) at baseline. In a controlled analysis of longitudinal data, initial SPMSQ score, age, African American race, lower education, depressive symptomatology, and physical deficits at baseline, but not memory complaint, predicted a decline in cognitive function as measured by the SPMSQ 3 years later. Whereas African Americans were less likely to complain of deterioration in memory, actual decline as measured by the SPMSQ was greater for African Americans than for Whites.
TL;DR: Mild cognitive impairment may be a much more prevalent neuropsychological feature of patients with neurocysticercosis, and organic mechanisms related to brain lesions may underlie the mental changes.
Abstract: OBJECTIVE: To determine the frequency and features of psychiatric morbidity in a cross section of 38 outpatients with neurocysticercosis. METHODS: Diagnosis of neurocysticercosis was established by CT, MRI, and CSF analysis. Psychiatric diagnoses were made by using the present state examination and the schedule for affective disorders and schizophrenia-lifetime version; cognitive state was assessed by mini mental state examination and Strub and Black's mental status examination. RESULTS: Signs of psychiatric disease and cognitive decline were found in 65.8 and 87.5% of the cases respectively. Depression was the most frequent psychiatric diagnosis (52.6%) and 14.2% of the patients were psychotic. Active disease and intracranial hypertension were associated with higher psychiatric morbidity, and previous history of mood disorders was strongly related to current depression. Other variables, such as number and type of brain lesions, severity of neuropsychological deficits, epilepsy, and use of steroids did not correlate with mental disturbances in this sample. CONCLUSIONS: Psychiatric abnormalities, particularly depression syndromes, are frequent in patients with neurocysticercosis. Although regarded as a rare cause of dementia, mild cognitive impairment may be a much more prevalent neuropsychological feature of patients with neurocysticercosis. The extent to which organic mechanisms related to brain lesions may underlie the mental changes is yet unclear, although the similar sex distribution of patients with and without depression, as well as the above mentioned correlations, provide further evidence of the part played by organic factors in the cause of these syndromes.
TL;DR: Topographic selectivity and diagnostic utility of brain atrophy in probable Alzheimer's disease (AD) and correlations with demographic factors such as age, sex, and education are determined and differential effects of sex and years of education can be detected.
Abstract: We determined topographic selectivity and diagnostic utility of brain atrophy in probable Alzheimer's disease (AD) and correlations with demographic factors such as age, sex, and education. Computerized imaging analysis techniques were applied to MR images in 32 patients with probable AD and 20 age- and sex-matched normal control subjects using tissue segmentation and three-dimensional surface rendering to obtain individualized lobar volumes, corrected for head size by a residualization technique. Group differences emerged in gray and white matter compartments particularly in parietal and temporal lobes. Logistic regression demonstrated that larger parietal and temporal ventricular CSF compartments and smaller temporal gray matter predicted AD group membership with an area under the receiver operating characteristic curve of 0.92. On multiple regression analysis using age, sex, education, duration, and severity of cognitive decline to predict regional atrophy in the AD subjects, sex consistently entered the model for the frontal, temporal, and parietal ventricular compartments. In the parietal region, for example, sex accounted for 27% of the variance in the parietal CSF compartment and years of education accounted for an additional 15%, with women showing less ventricular enlargement and individuals with more years of education showing more ventricular enlargement in this region. Topographic selectivity of atrophic changes can be detected using quantitative volumetry and can differentiate AD from normal aging. Differential effects of sex and years of education can also be detected by these methods. Quantification of tissue volumes in vulnerable regions offers the potential for monitoring longitudinal change in response to treatment.