Types Of Cognitive Impairment Research Articles

EFFECTS OF EXERCISE TRAINING ON INDIVIDUALS WITH ALZHEIMER??S DISEASE AND RELATED DISORDERS

Recent studies suggest that physical activity can have a marked effect on the physical and mental health of older adults with dementia. Alzheimer's Disease (AD), and related cognitive impairments. PURPOSE This meta-analysis sought to analyze if exercise produces a positive effect size change on measures of cardiorespiratory fitness and muscle strength in older persons with AD and related cognitive disorders. This synthesis is two-fold: (1) to quantitatively determine the efficacy of physical activity interventions, and (2) to identify the most efficacious exercise paradigm used with this population. Method: A comprehensive literature search of published and unpublished abstracts and titles yielded 42 studies. Selection criteria for inclusion was satisfied when every aspect of the following information was included in the study: (1) subjects were aged 65 years or older and diagnosed with some type of cognitive impairment (i.e. dementia, AD, Mild Cognitive Impairment) or subjects with baseline Mini Mental State Exam scores below 24, (2) an exercise or physical intervention program, and (3) means, standard deviations, t-tests, or F-tests were reported. RESULTS Statistical analysis showed that treatment effect for cardiovascular and strength training were greater compared to other modes of exercise training. CONCLUSION Findings from this meta-analysis support those of previous research that shows promising evidence concerning the positive effects of physical activity on physical health of persons affected by dementia and related cognitive disorders. The extent to which persons with Alzheimer's disease and related cognitive impairments exhibit significant functional and cognitive benefits due to participation in an exercise program is still uncertain. Future research and techniques is needed to precisely determine the efficacy of exercise on individuals with Alzheimer's disease and related disorders.

Effect of the treatment of Type II diabetes mellitus on the development of cognitive impairment and dementia.

There is increasing interest in preventing cognitive impairment and dementia in later life. Epidemiological evidence shows a relationship between cognitive impairment and Type II diabetes. This association is stronger in patients who have been diagnosed for longer periods of time and in those who are on insulin therapy. There is little information on the short- and long-term influence of type of treatment and level of metabolic control on cognitive function of people with diabetes. To assess the effects of different types and intensities of treatments for Type II diabetes on cognitive function. The Cochrane Control Trials Register, MEDLINE, EMBASE, PsycINFO, SIGLE LILACS and CINAHL as well as a number of ongoing trials databases were searched on 11 June 2002 using appropriate strategies. Randomized controlled trials in which different treatments for Type II diabetes have been compared and in which measures of cognitive function were made at entry and after the treatment. Two reviewers independently assessed trial quality. Five trials were identified for possible inclusion but none of them could be included. In one, cognitive function was assessed before and after intensive or conventional diabetic treatment, but the comparison was not double-blind. The three other studies explored the effect of different treatments on QOL but did not include appropriate evaluation of cognitive function. The fifth did not report baseline data on cognitive function in the trial groups. No studies were found to be appropriate for inclusion in meta-analysis. There is no convincing evidence relating type or intensity of diabetic treatment to the prevention or management of cognitive impairment in Type II diabetes. Future research on treatments for diabetes should include standardized assessments of cognitive function as outcome measures.

MRI white matter hyperintensities, (1)H-MR spectroscopy and cognitive function in geriatric depression: a comparison of early- and late-onset cases.

BACKGROUND AND OBJECTIVES Geriatric depression is often thought to differ from that at other times of adulthood. Recently, several studies have shown that the incidence of white matter hyperintense lesions identified by brain MRI is higher in patients with geriatric depression than in healthy elderly subjects, but a consensus has not yet been reached on the relationship between the severity of white matter lesions and either cognitive impairment or depressive symptoms. Forty-seven patients aged 50 to 75 years with major depression were divided into two groups based on age at onset of depression: early-onset (< 50 years) group (20 patients; mean age, 62.7 +/- 6.7) and late-onset (> or =50 years) group (27 patients; mean age, 65.6 +/- 5.4). The severity of hyperintense white matter lesions on MRI was classified by region, then a proton magnetic resonance spectroscopy ((1)H-MRS) focusing on the white matter of the frontal lobes, multidimensional neuropsychological tests and evaluation of depressive symptoms were conducted. The severity of the deep white matter lesions, the deterioration of cognitive function related to subcortical/frontal brain system and clinician-rated depressive symptoms were all more pronounced in the late-onset group compared with those in the early-onset group. It was further observed that the more severe the deep white matter lesions, the lower the levels of N-acetylaspartate/creatine. With the age of onset as the covariate, the patients with moderate deep white matter lesions had more pronounced cognitive impairment and clinician-rated depressive symptoms than those with none and/or mild lesions. These results suggest that subcortical/frontal type cognitive impairment and the persistence of depressive symptoms in geriatric depression is related to moderate deep white matter lesions more often complicated in the late-onset group. The (1)H-MRS findings were suggested to be a useful indicator of neuronal/axonal loss in the white matter of the frontal lobes which precedes cognitive impairment.

Cognitive impairment, disruptive behaviors, and home care utilization.

Disruptive behaviors by an elder with cognitive impairment, such as violence, abrupt mood swings, and overt inappropriate sexual behaviors have been known to create caregiver distress, but little is known about how these behaviors may influence the use of home care services by that elder or their informal caregiver. The purpose of this study is to explore the associations between type of cognitive impairment (cognitive impairment with no dementia, and dementia), selected disruptive behaviors, and the use of four home care services (homemaking/cleaning, personal care, in-home nursing, home-delivered meals). Secondary data analysis from the 1991-1992 Manitoba Study on Health and Aging data set was conducted, using a sample of 124 community-dwelling elders and their unpaid caregivers. Multivariate analysis revealed that disruptive behaviors were significantly associated with the use of two services: personal care and home-delivered meals. Being cognitively impaired with dementia was significant for only home-delivered meals. Overall functional status of the elder emerged as a consistent predictor.

Differences in P300 parameters, neuropsychological profile, and cognitive impairments in patients with cortical and subcortical dementia

In this study we analyzed the parameters of auditory evoked potentials in a stimulus recognition task (the P300 method) and nonspecific visual response to a light flash in 75 healthy subjects of various ages (20–70 years) and 70 subjects (35 males and 35 females, mean age 51 years) with cortical and subcortical cognitive impairments of various degrees (cerebrovascular disorder) with different neuropsychological profiles. It was shown that parameters of the P300 complex depend on both the subject age and his/her cognitive functions and can be used for objective analysis of cognitive impairments. An inverse relationship between the P3 (P300) peak latency and the volume of short-term and operative memory in subjects with cognitive impairments was found. The parameters of the nonspecific visual response (duration and the maximum amplitude), reflecting functioning of the arousal systems of the brain, depended on the type and severity of cognitive impairments but did not depend on the subject's age. Differences in the neuropsychological profiles of cognitive impairments and the pathophysiological mechanisms of their development, reflected by parameters of the evoked potential, as well as differences between the brain structures involved in these process, substantiate the discrimination of two types of cognitive impairments—cortical and subcortical—in subjects with cerebrovascular disorders.

Neurophysiological imaging techniques in dementia.

Neurophysiological methods, such as electroencephalography (EEG) and event-related potentials, are useful tools in the investigation of brain cognitive function in normal and pathological conditions, with an excellent time resolution when compared to that of other functional imaging techniques. Advanced techniques using a high number of EEG channels also enable a good spatial resolution to be achieved. This, together with the possibility of integration with other anatomical and functional images, may increase the ability to localize brain functions. Spectral analysis of the resting EEG, which gives information on the integrity of the cortical and subcortical networks involved in the generation of cortical rhythms, has the limitation of low sensitivity and specificity for the type of cognitive impairment. In almost all types of dementia, decreased power of the high frequencies is indeed observed in mild stages, accompanied by increased power of the slow rhythms in the more advanced phases. The sensitivity for the detection of spectral abnormalities is improved by studying centroid modifications. More specific information on the type of dementia can be provided by coherence analysis of the resting EEG, a measure of functional cortico-cortical connections, which has different abnormal patterns in Alzheimer's disease, cerebrovascular dementia and dementia associated with multiple sclerosis. Another tool for improving the assessment of demented patients is the study of EEG activity related to particular tasks, such as event-related potentials and event-related desynchronization/synchronization of the EEG, which allow the study of brain activation during cognitive and motor tasks.

Dynamics of cognitive aging: distinguishing functional age and disease from chronologic age in a population.

This paper introduces a methodological approach to the dynamics of cognitively normal (i.e., successful) aging compared with aging accompanied by different types of cognitive impairment and dementia. Using secondary analysis of a national representative database (Canadian Study of Health and Aging, 1991-1992), the authors show that the occurrence of an adverse event (symptom, sign, or disease), or the accumulation of a number of events, may be modeled as a logistic function of chronologic age in a population. In the cognitively normal, a linear relation between the logarithm of the odds of events and chronologic age was present for the majority of symptoms and signs. This regression represents the accumulation of each sign in a cognitively successful, aging population. The authors then estimated which ages for this cognitively unimpaired group correspond to the odds of the occurrence of symptoms found for a cognitively impaired population at any given chronologic age. This may be regarded as functional age, based upon the accumulation of a particular functional deficit in the impaired population, analogous to the concept of frailty. The dynamics of aging are a complex process of accumulation of deficits (morbidity), whereby decline from some previously healthy level of synergistically associated symptoms and signs results in distinct patterns of disease and staging. The modeling of these dynamics takes us a step further toward the definition and refinement of disease and normal aging.

Biochemical dysfunction and memory loss: the case of Alzheimer's dementia.

Among the different types of cognitive impairment that appear with increasing age, Alzheimer's disease (AD) is rated as the most frequent. Despite intensive research, key questions concerning AD aetiology remain elusive, but it appears that many biochemical events crucial for neuronal communication and synaptic plasticity fail during the course of the disease. The aim of this review is therefore to provide an overview of intracellular cascades involved in AD pathology. For almost all factors. it is a matter of controversy whether their contribution should be considered to be cause or effect. However, intracellular signalling may be crucial as it is in learning and memory mechanisms and malfunction of biochemical pathways may be a common denominator in neurodegenerative processes, thus providing new venues for treatment and therapeutic strategies.

Validating Memory Complaints in the Elderly

Memory complaints are extremely difficult to evaluate in the elderly because they are common, can be indicative of many types of cognitive impairment

Auditory evoked potentials in young patients with Down syndrome. Event-related potentials (P3) and histaminergic system

Subjects with Down syndrome exhibit various types of cognitive impairment. Besides abnormalities in a number of neurotransmitter systems (e.g. cholinergic), histaminergic deficits have recently been identified. Brainstem auditory evoked potentials (BAEPs) and auditory event-related potentials (ERPs), were recorded from 10 children (aged 11–20 years) with Down syndrome and from 10 age- and sex-matched healthy control subjects. In Down subjects, BAEPs revealed shortened latencies for peaks III and V with shortened interpeak latencies I–III and I–V. ERPs showed a delay of components N1, P2, N2 and P3. In addition, subjects with Down syndrome failed to show P3 amplitude reduction during repeated stimulation. To evaluate the cognitive effects of histaminergic dysfunction, ERPs were recorded from 12 healthy adults (aged 20–28 years) before and after antihistaminergic intervention (pheniramine) compared to placebo. Whereas components N1, P2, N2 remained unchanged after H1-receptor antagonism, P3 latency increased and P3 amplitude showed no habituation in response to repeated stimulation. The results suggest that the characteristic neurofunctional abnormalities present in children with Down syndrome must be the consequence of a combination of structural and neurochemical aberrations. The second finding was that antihistaminergic treatment affects information processing tested by ERPs similar to that seen with anticholinergic treatment.

Progression to dementia in patients with isolated memory loss

The diagnosis of dementia requires both memory loss and at least one other type of cognitive impairment. The natural history of patients with severe memory loss but no other type of cognitive impairment is poorly understood. We studied progression to dementia in patients with isolated memory loss. From a registry of 811 patients with cognitive complaints, 21 patients with severe isolated memory loss of unknown cause were identified and followed up for a mean of 48 months. A comparison group of 198 patients on the same register was identified with newly recognised cognitive complaints but without dementia or isolated memory loss (mean follow-up 31 months). We did a range of neuropsychological tests at intake. During follow-up, 48% (n = 10) of patients with isolated memory loss-developed dementia compared with 18% (n = 36) of the comparison group. Life-table analysis showed the mean times to a diagnosis of dementia was 3.77 years (95% CI 2.99-4.56) and 5.96 years (5.60-6.31), respectively (p = 0.01). The neuropsychological tests did not predict which patients would progress to dementia. Patients with severe isolated memory loss have an increased risk of developing dementia and should be closely followed-up.

Subject review: Beyond one-bun, two-shoe: recent advances in the psychological rehabilitation of memory disorders after acquired brain injury

Memory disorders are one of the most frequent types of cognitive impairment encountered in neurological populations. The more severe degrees of such impairment cause major disability and handicap, and have a profound impact on a person s capacity to engage in independent living. To date, commonly used remediation strategies range from drills and practice, including computer-based tasks, to mnemonic techniques and memory notebooks. In general, these therapies have met with varying degrees of success. The last decade has seen exciting developments in remediation techniques for memory disorders, a number of which are based on implicit learning skills, as well as programmes tailored to an individual s unique pattern of deficits. The present paper provides an overview of this literature and discusses issues relating to their application in rehabilitation programmes.

Cognitive impairment in the elderly medically ill: How often is it missed?

AbstractOne hundred and sixty‐three patients over 65 years of age admitted to the acute medical wards of a district teaching hospital were studied for prevalence and type of cognitive impairment. Findings from research assessments, where possible using a cognitive rating scale, were compared with detection of impairment by medical and nursing staff involved in patients' clinical management. 30.7% of patients were judged by us to show definite or probable cognitive impairment, a figure substantially higher than that detected by hospital staff. Outcomes in terms of death, duration of admission and discharge location were related to the presence or absence of cognitive impairment and whether impairment was due to delirium, dementia or a mixed syndrome. The low rate of detection of cognitive impairment is discussed, and suggestions made to improve detection in acute elderly medical inpatients.

D-Cycloserine, a putative cognitive enhancer, facilitates activation of the [formula omitted] receptor-ionophore complex in Alzheimer brain

The action of d-Cycloserine (DCS) at the strychnine-insensitive glycine recognition site of the NMDA receptor-ionophore complex has been studied with membranes from inferior parietal cortex of patients with Alzheimer's disease. The maximal response of the site, measured using [ 3H]MK-801 binding, was 64% of that observed with glycine. Stimulation of binding induced by DCS in the presence of fixed concentrations of glycine resulted in a family of dose-response curves, consistent with the antibiotic having the property of a partial agonist at this glycine site. It is proposed that because of circumscribed glutamatergic pyramidal cell pathology DCS will have benefit for Alzheimer's patients over and above all other types of cognitive impairment.

Cognitive Impairment in Alcoholics

The research literature shows that, as a result of chronic alcohol abuse, there occur impairments in abstract reasoning, problem-solving, and perceptual-motor functioning. In an earlier study, Tamkin (1983) obtained significant differences between alcoholics and paired neurotic inpatient controls only on abstract reasoning measured on the Weigl Color-Form Sorting Test. Verbal functions and recall of designs showed no group differences. This study sought to replicate the Weigl test results and to examine other types of cognitive impairments in alcoholics relative to published norms. The study subjects were 104 male alcoholics in an alcohol rehabilitation unit. The tests used were the Weigl, Trails A and B, and three subtests of the WAIS. The proportion of impaired Weigl performances was similar to that obtained in 1983, and all the other test scores were significantly poorer than their published norms.

Permanent neuropsychological impairment after recurrent episodes of severe hypoglycaemia in man

Seventeen Type 1 (insulin-dependent) diabetic patients with a history of recurrent and severe hypoglycaemia and Type 1 diabetic patients with no severe hypoglycaemia were compared as regarded performances in tests of neuropsychological functioning. To test the hypothesis that recurrent severe hypoglycaemia gives rise to permanent cognitive impairment, the study group was selected among those patients who had met with repeated attacks over the last three years or more as identified by a questionnaire among almost 600 insulin-treated diabetic patients. The comparison group without known severe reactions were comparable to the study group with respect to type of diabetes, sex, age, age at onset, duration of diabetes, socio-economic parameters, and prevalence of neuropathy and retinopathy. The results indicate that Type 1 diabetic patients with recurrent severe hypoglycaemia scored lower than those without severe hypoglycaemia in tests of motor ability, short-term and associative memory and visuospatial tasks assessing ability in general problem-solving. Type 1 diabetic patients with severe hypoglycaemia also displayed a higher frequency of perspective reversals suggesting frontal-lobe involvement. These data can be interpreted in two ways. One interpretation implies that the cognitive impairment of Type 1 diabetic patients with severe hypoglycaemia reflects a selection factor, the other that recurrent episodes of severe hypoglycaemia result in permanent cognitive impairment.

Cognitive theory, cognitive impairment and clinical practice

The aim of this paper is to present a practical model for investigating cognitive impairment which integrates the experimental-cogaitive-information processing-theory and the psychometric-intellectual-abilities-tradition in psychology to understanding cognitive functioning. It reviews developments in cognitive theory in terms of Processes, complex and simple, such as Intelligence and Information Processing, and Factors of attained Level and Learning ability in the Verbal and Performance modalities. The Savage Cognitive Impairment Model (SCIM) is outlined and types of cognitive impairment defined. Measures of cognitive impairment relevant to clinical practice and research are presented.