824 resultados para NEUROCOGNITIVE IMPAIRMENT
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Background: after stroke, visual impairment may exacerbate the impact of other impairments on overall disability and negatively influence rehabilitation.
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Cerebral palsy is the most common cause of physical disability in childhood and half of these children will have an intellectual impairment. This article reports on the quality of life of children with cerebral palsy and explores the impact of intellectual impairment. Learning disability nurses have a critical role to play in improving the quality of life for this patient group, particularly in relation to their physical health and creating opportunities to promote social skill development and social inclusion.
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Background: Visual impairment (VI) is rising in prevalence and contributing to increasing morbidity, particularly among older people. Understanding patients' problems is fundamental to achieving optimal health outcomes but little is known about how VI impacts on self-management of medication.
Aim: To compare issues relating to medication self-management between older people with and without VI.
Design and setting: Case-control study with participants aged =65 years, prescribed at least two long-term oral medications daily, living within the community.
Method: The study recruited 156 patients with VI (best corrected visual acuity [BCVA] 6/18 to 3/60) at low-vision clinics; community optometrists identified 158 controls (BCVA 6/9 or better). Researchers visited participants in their homes, administered two validated questionnaires to assess medication adherence (Morisky; Medication Adherence Report Scale [MARS]), and asked questions about medication self-management, beliefs, and support.
Results: Approximately half of the participants in both groups reported perfect adherence on both questionnaires (52.5% Morisky; 43.3%, MARS). Despite using optical aids, few (3%) with VI could read medication information clearly; 24% had difficulty distinguishing different tablets. More people with VI (29%) than controls (13%) (odds ratio [OR] = 2.8; 95% confidence interval [CI] = 1.6 to 5.0) needed help managing their medication, from friends (19% versus 10%) or pharmacists (10% versus 2.5%; OR = 4.4, 95% CI = 1.4 to 13.5); more received social service support (OR = 7.1; 95% CI = 3.9 to 12.9).
Conclusion: Compared to their peers without VI, older people with VI are more than twice as likely to need help in managing medication. In clinical practice in primary care, patients' needs for practical support in taking prescribed treatment must be recognised. Strategies for effective medication self-management should be explored.
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To design a new, highly sensitive psychometric screening to identify patients with mild cognitive impairment (MCI) and patients with dementia in the early stages of the disease.
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Background: Several studies have shown an increased incidence of neurodevelopmental impairment in very preterm survivors at school age compared with controls.
Aim: To compare findings in the same cohort at 8 years and 15 years.
Methods: A total of 151 of the 224 eligible infants born before 33 weeks of gestation from 1979 to 1982, and who were living in the UK, were assessed at 8 and 15 years. Items common to both assessments were compared to evaluate changes in neurodevelopmental function. The assessment included a structured neurological examination, psychometric tests using the WISC-R (in subjects born in 1981-82), a test of visuomotor integration (Beery), and a school questionnaire.
Results: There was a significant increase in the proportion of subjects classified as impaired with disability from 11% at 8 to 22% at 14-15 years of age. The proportion of subjects classified as impaired without disability increased from 16% at 8 to 26% at 14-15 years of age. Full scale IQ decreased from 104 to 95 from childhood to adolescence, and more adolescents (24%) were requiring extra educational provision than they had at the age of 8 years (15%).
Conclusion: Results indicate that between the ages of 8 and 15 years in this cohort of very preterm survivors there is an apparent deterioration in neurodevelopmental outcome category, cognitive function, and extra educational support. It is not clear whether this represents a genuine deterioration in neurocognitive function or whether it represents the expression of pre-existing cerebral pathology in an increasingly complex environment.
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Aflatoxin B1 (AFB1), a mycotoxin produced by Aspergillus flavus or A. parasiticus, is a frequent contaminant of food and feed. This toxin is hepatotoxic and immunotoxic. The present study analyzed in pigs the influence of AFB1 on humoral and cellular responses, and investigated whether the immunomodulation observed is produced through interference with cytokine expression. For 28 days, pigs were fed a control diet or a diet contaminated with 385, 867 or 1807 mu g pure AFB1/kg feed. At days 4 and 15, pigs were vaccinated with ovalbumin. AFB1 exposure, confirmed by an observed dose-response in blood aflatoxin-albumin adduct, had no major effect on humoral immunity as measured by plasma concentrations of total IgA, IgG and IgM and of anti-ovalbumin IgG. Toxin exposure did not impair the mitogenic response of lymphocytes but delayed and decreased their specific proliferation in response to the vaccine antigen, suggesting impaired lymphocyte activation in pigs exposed to AFB1. The expression level of pro-inflammatory (TNF-alpha, IL-1 beta, IL-6, IFN-gamma) and regulatory (IL-10) cytokines was assessed by real-time PCR in spleen. A significant up-regulation of all 5 cytokines was observed in spleen from pigs exposed to the highest dose of AFB1. In pigs exposed to the medium dose, IL-6 expression was increased and a trend towards increased IFN-gamma and IL-10 was observed. In addition we demonstrate that IL-6 impaired in vitro the antigenic- but not the mitogenic-induced proliferation of lymphocytes from control pigs vaccinated with ovalbumin. These results indicate that AFB1 dietary exposure decreases cell-mediated immunity while inducing an inflammatory response. These impairments in the immune response could participate in failure of vaccination protocols and increased susceptibility to infections described in pigs exposed to AFB1. (C) 2008 Elsevier Inc. All rights reserved.
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As survival rates of preterm newborns improve as a result of better medical management, these children increasingly show impaired cognition. These adverse cognitive outcomes are associated with decreases in the volume of the cerebellum. Because animals exhibit reduced preterm cerebellar growth after perinatal exposure to glucocorticoids, we sought to determine whether glucocorticoid exposure and other modifiable factors increased the risk for these adverse outcomes in human neonates. We studied 172 preterm neonatal infants from two medical centers, the University of British Columbia and the University of California, San Francisco, by performing serial magnetic resonance imaging examinations near birth and again near term-equivalent age. After we adjusted for associated clinical factors, antenatal betamethasone was not associated with changes in cerebellar volume. Postnatal exposure to clinically routine doses of hydrocortisone or dexamethasone was associated with impaired cerebellar, but not cerebral, growth. Alterations in treatment after preterm birth, particularly glucocorticoid exposure, may help to decrease risk for adverse neurological outcome after preterm birth.
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To compare academic and cognitive ability, attention, attitudes, and behavior of extremely low birth weight (ELBW) adolescents who are free of major impairments at 17 years of age with term-born control subjects.
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Objectives: A healthy lifestyle may help maintain cognitive function and reduce the risk of developing dementia. This study employed a focus group approach in order to gain insight into opinions of mild cognitive impairment (MCI) patients, caregivers (CG) and health professionals (HP) regarding lifestyle and its relationship with cognition. The qualitative data were used to design, develop and pilot test educational material (EM) to help encourage lifestyle behaviour change. Method: Data gathering phase: structured interviews were conducted with HP (n = 10), and focus groups with MCI patients (n = 24) and CG (n = 12). EM was developed and pilot tested with a new group of MCI patients (n = 21) and CG (n = 6). Results: HP alluded to the lack of clinical trial evidence for a lifestyle and MCI risk link. Although they felt that lifestyle modifications should be recommended to MCI patients, they appeared hesitant in communicating this information and discussions were often patient-driven. MCI patients lacked awareness of the lifestyle cognition link. Participants preferred EM to be concise, eye-catching and in written format, with personal delivery of information favoured. Most pilot testers approved of the EM but were heterogeneous in terms of lifestyle, willingness to change and support needed to change. Conclusion: MCI patients need to be made more aware of the importance of lifestyle for cognition. EM such as those developed here, which are specifically tailored for this population would be valuable for HP who, currently, appear reticent in initiating lifestyle-related discussions. Following further evaluation, the EM could be used in health promotion activities targeting MCI patients.