Introduction Tom Kitwood's theoretical framework of person-centred care is extensively and internationally referred to in healthcare services. However, despite the broad use of Kitwood's approach in clinical practice, the research examining experiences with the approach has not been mapped. Aim To map the available literature on current empirical experiences in clinical practice of Kitwood's approach to person-centred care for people with dementia, living in institutional settings in primary health care. Methods A total of 154 studies concerning the experiences of people with dementia and their formal caregivers' use of Kitwood's framework of person-centred care for residents living in institutional settings in primary health care were compiled from scientific databases. All three authors engaged in a systematic selection process, leading to nineteen articles being included in the review. Results The results showed an overall tendency towards positive experiences gained from applying person-centred approaches in clinical practice influenced by Kitwood's theoretical framework. Through the synthesis of data from the selected studies, six categories related to our research aim were identified 'Theoretical evaluation of Tom Kitwood's model of care', 'Models and frameworks', 'Interventions', 'Communication', 'Dementia Care Mapping' and 'Environment'. Conclusion The present review included nineteen studies published from 1998 to 2016 and consisted mainly of peer-reviewed scientific articles, followed by dissertations, conference posters and nonpeer-reviewed articles. All studies were undertaken in Western countries. The vast majority of the studies considered Kitwood's theoretical framework to be beneficial and useful in practice.
Introduction: Within dementia care, there remains a general lack of coherence in evidence-based knowledge on issues of importance for subjective experiences of quality of life in people with dementia. The aim of the meta-aggregation was to investigate experiences related to quality of life in people with dementia living in institutional settings. Method: A meta-aggregation inspired by the Joanna Briggs Institute was undertaken. A systematic search was conducted in four databases and additional studies were found in the reference lists of the included studies. Only studies in English, Danish, Swedish, and Norwegian were considered, with publication dates from 2007 to 2018. Findings: Ten original qualitative studies were included. Using critical appraisal, methodological quality was assessed. We extracted five main categories: acceptance and adaptation; autonomy; personhood; social connectedness; and activities. Conclusion: Significant findings for future occupational therapy in dementia care concerned the importance of coming to terms with the illness and life situation, while being able to experience feelings of autonomy, independence, and personhood. Meaningful social relationships and activities, individualized flexible routines and regulations, and adjusted physical environments with room for privacy were also prioritized in order to achieve high quality of life.
: This paper introduces a successful dementia care program in Omuta City, Japan. The program, SOS Training, was not originally designed as a co-design project. It achieved codesign characteristics as a result of trial-and-error practice among public and private enthusiasts for making a better and safer community for people with dementia. As a case of substantial codesign participation of citizens that involves people with dementia, this paper points out challenges and opportunities for making Omuta’s program scalable and sustainable. The newly established design team that includes the authors, investigates potentials of the Omuta way of helping people with dementia.
An increased apolipoprotein E (ApoE) type epsilon 4 allele frequency is associated with both sporadic and familial late-onset Alzheimer's disease (AD). The age of onset of disease in patients homozygous for the epsilon 4 allele appears to be decreased by approximately 15 years compared with E2/3 individuals. In order to assess the influence of this allele on both dementia and cognitive decline in the elderly we have determined the ApoE genotype of 150 individuals over the age of 75 years who have taken part in a longitudinal study. Homozygosity for the epsilon 4 allele was rare. Of the 2 homozygotes, 1 was severely demented but the other did not receive a clinical diagnosis of dementia. The latter individual did demonstrate marked cognitive decline over a 28-month period. There was a consistent association between the presence of an epsilon 4 allele and both the clinical diagnosis of dementia and cognitive decline. These findings confirm a genetic heterogeneity in late-onset sporadic AD and prompt caution in the use of ApoE genotype to predict an elderly individual's susceptibility to either dementia or cognitive decline.
The cascade of reactions caused by ischemia in brain tissue is complex and not completely understood, but intensive investigation has led to convincing hypotheses. A disturbed calcium homeostasis and oxygen radicals seem to play a major role in postischemic neuronal damage. In accordance to these hypotheses drugs with different mechanisms of action have been developed. The aim of this paper is to give an overview over pathobiochemical mechanisms in cerebral ischemia and possibilities of pharmacological intervention.
Apolipoprotein E (apoE) has been suggested to play a role in regenerative processes in the brain after trauma, and also in the pathogenesis of Alzheimer's disease (AD). We examined cerebrospinal fluid (CSF) apoE in a material consisting of 23 patients with early-onset AD (EAD), 31 with late-onset AD (LAD), 16 with frontal-lobe dementia (FLD), 25 with vascular dementia (VAD) and 25 controls. CSF-apoE was decreased in all of EAD (1.8 +/- 1.1 mg/l; p < 0.0005), LAD (2.5 +/- 0.9 mg/l; p < 0.0005), VAD (2.3 +/- 1.4 mg/l; P < 0.0005) and FLD (3.0 +/- 1.3 mg/l; p < 0.05) compared to the control group (5.7 +/- 4.0 mg/l). Since apoE4 has been found to bind to beta/A4-amyloid, and AD patients homozygous for apoE4 to have higher number of senile plaques than apoE3 homozygotes, we also examined the relation between CSF-apoE and apoE alleles. However, CSF-apoE did not significantly differ between patients with different apoE isoforms. Our findings support that apoE is involved in the pathogenesis of dementia disorders, both degenerative and vascular, but the CSF-apoE level is not influenced by the apoE isoforms. CSF-apoE may be used as an unspecific marker for neurodegenerative disorders, but not in purpose of differential diagnostics between different dementia disorders.
Cognitive deficits are the most important symptoms in the diagnosis of dementia. Changes in noncognitive behavioural areas often go unrecognised at examination or are considered insignificant. These abnormalities, however, contribute most to the caregiver's burden, interfere with the individual well-being of the patient, and are predictors of early institutionalization. Psychotherapeutic interventions in dementia complete the treatment effects achieved by psychopharmacology, cognitive enhancers, and cognitive training of target functions. Psychotherapy in dementia should be based on an interacting form of therapy, i.e. a contingency management in the natural environments of the dementia sufferer where the primary caregiver, as a mediator, takes over the main therapeutic tasks.
NMDA receptor density as measured by the specific binding of [3H]MK 801 was significantly decreased (about 20%) in the frontal but not in the parietal cortex of postmortem brain samples of Alzheimer''s disease (AD) patients (n = 21), when compared with control brains (n = 20). Membrane fluidity was not altered in the frontal cortex samples, but was slightly reduced in the parietal cortex samples of the AD patients. Since AD-specific histopathological changes (densities of senile plaques and neurofibrillary tangles) were about similar in both areas, it is concluded that the reductions of NMDA receptor densities in the frontal cortex is independent of AD-specific histopathological changes and of changes of membrane fluidity.
Glial fibrillary acidic protein (GFAP) is the structural protein of the astroglial intermediate filament that forms the morphological basis of astrogliosis. In the present study, GFAP concentrations in cerebrospinal fluid were measured in patients with various dementia diseases. A significant correlation between GFAP and age was found both in the total dementia group and in the controls. Covariance analysis with GFAP as dependent variable and age and albumin ratio as covariates followed by multiple group comparisons showed that, with regard to GFAP levels, the controls (n = 39) differed significantly from the patients with vascular dementia (n = 20; p < 0.05), senile dementia of the Alzheimer type (n = 29; p < 0.05), and 'pure' Alzheimer's disease (n = 8; p < 0.05), but not from those with frontal lobe dementia (n = 5).
Pre- and postsynaptic elements of the 5-hydroxytryptamine (5-HT, serotonin) system were studied in a control group and in patients with vascular dementia (VAD). The 5-HT uptake site was used as a presynaptic marker for 5-HT terminals and 5-HT1A and 5HT2 receptors were used as postsynaptic markers. The binding sites were quantified with radioligand binding techniques, where the radioligands used were [3H]paroxetine, [3H]8-OH-DPAT and [3H]ketanserin, respectively. The presynaptic uptake site was studied in frontal and temporal cortices and caudate nucleus. 5-HT1A and 5-HT2 receptors were studied only in frontal and temporal cortices. There were no differences between control and VAD groups in any of the regions investigated with respect to the number of binding sites (Bmax) and binding affinity (Kd). This indicates that both pre- and postsynaptic parts of the 5-HT system are intact in these brain areas in VAD.
Patient EDS presented with an amnesic disorder of insidious onset (4 years) that remained stable and restricted to memory functions over a 10-year course. Repeated neuropsychological evaluations over 6 years showed a moderate-to-severe, stable impairment of long-term memory and of memory for public events, and a milder, stable impairment of autobiographic memory and of short-term memory. Language, perception, praxis and 'frontal' functions were fully preserved. MRI showed atrophy of the right hippocampus, of the right mammillary body and of the sylvian fissure (bilaterally, but more marked on the left). On PET scan, metabolic activity in the mesial temporal structures was significantly reduced on the right and was at lower normal levels on the left. The disorder observed in EDS is similar to that recently reported in other patients. Possible etiologies of the selective amnesia observed in EDS are considered and their implications discussed.
Experimental data suggest an involvement of immune cellular components in the development of Alzheimer's disease (AD). Against this background, the spontaneous natural killer (NK) cell activity and the NK-induced cytotoxicity after interleukin-2 (IL-2) were studied in healthy elderly subjects and in patients with dementia of Alzheimer type (SDAT) and multi-infarct type (MID). Higher NK cytotoxicity (expressed as total lysis and percent increase) at different IL-2 concentrations (50 and 100 IU/ml/cells) was demonstrated in patients with SDAT than in healthy elderly subjects (p < 0.001) and MID patients (p < 0.001). NK cell activity of MID patients was similar to that of healthy elderly and healthy young subjects. A negative correlation between the percent increase in NK cytotoxicity after IL-2 and the Mini Mental State Examination Score was also found in SDAT patients (p < 0.01). Alterations of IL-2-mediated NK cytotoxicity may therefore support the neuroimmune hypothesis of AD.
It is now known that immunologic mechanisms have a role in the initiation of atherosclerotic processes. No antibodies against vascular endothelial cell (VEC) specific antigenic systems have been demonstrated in the pathogenesis of small vessel (lacunar) infarcts, though autoantibodies have been detected in 80% of patients with multi-infarct dementia. We studied VEC-specific antibodies in 17 patients with a diagnosis of vascular dementia; in 17 nondemented patients with small vessel infarcts and in 16 healthy, nondemented control group patients by using the Terasaki microtoxicity method. All three groups were correlated according to known risk factors. VEC-specific antibodies were positive in 94% demented patients, whereas no antibodies were detected in patients with small vessel infarcts or in the control group. This result may suggest the existence of an immunologic mechanism in the etiopathogenesis of vascular dementia differing form small vessel infarcts.
The spatial pattern of discrete beta-amyloid (A beta) deposits was studied in the superficial laminae of cortical fields of different types and in the hippocampus in 6 cases of Alzheimer's disease (AD). In 41/42 tissues examined, discrete A beta deposits were aggregated into clusters and in 34/41 tissues (25/34 of the cortical tissues), there was evidence for a regular periodicity of the A beta deposit clusters parallel to the tissue boundary. The dimensions of the clusters varied from 400 to > 12,800 microns in different tissues. Although the A beta deposit clusters were larger than predicted, the regular periodicity suggests that they develop in relation to groups of cells associated with specific projections. This would be consistent with the hypothesis that the distribution of discrete A beta deposits in AD could reflect progressive synaptic disconnection along interconnected neuronal pathways. This implies that amyloid deposition could be a response to, rather than a cause of, synaptic disconnection in AD.
The pharmacokinetics of the cholinesterase inhibitor tacrine was studied in 5 Alzheimer patients during 12-31 months of treatment. A mean average steady-state concentration in plasma ranging from 1.1 to 30 ng/ml was obtained with doses ranging from 40 to 160 mg of tacrine daily. During treatment with 80 mg daily a maximal plasma concentration of tacrine (8.7 +/- 0.6 ng/ml) was obtained 1.3 +/- 0.2 h after intake of the morning dose. The mean elimination half-life was estimated at 5-7 h and remained unchanged when the tacrine dose was increased. The plasma concentration of tacrine was stable during long-term treatment with tacrine and no tolerance was observed regarding its cholinesterase inhibitory effect. A maximal 40% inhibition of plasma cholinesterase (ChE) activity and 60% inhibition of acetylcholinesterase activity in red blood cells was measured following treatment with the highest dose of 160 mg tacrine daily. A significant correlation was obtained between the plasma concentration of tacrine and the inhibition of ChE activity (p < 0.001). The tacrine concentration in CSF was measured in each patient on 1-3 occasions during the treatment and the ratio CSF/plasma concentration was estimated to be 0.47 +/- 0.09 (n = 11).
Reported findings regarding sleep and sleep disorders in the elderly often conflict. Differences in results across studies may arise from selection of subjects, definitions and recording conditions. Our purpose was to test a method to study elderly, both healthy and demented, under the most natural conditions, without disturbing a fragile sleep. Using clinical parameters and a non-disturbing recording method, we evaluated sleep quality in patients with carefully diagnosed dementia and compared the results to a group of healthy subjects between 50 and 70 years of age. Healthy subjects awoke less and had more quiet sleep than patients, while in patients a tendency for delayed sleep latency and more active sleep was observed. Consistent with previous investigations, sleep-related respiratory disorders (SRRD) were more common in patients than in the matched control group, and periodic breathing appeared only among patients. SRRD, of both obstructive and central types, were only mild, with periodic breathing dominating only among patients. Most of the desaturations were less than 10%. We did not observe respiration of the Cheyne-Stokes type. Patients had more sleep-related movement disorders (SRMD), particularly with increase of twitches and long movements. Periodic movements were not significantly increased among the patients. The method, and the data obtained may be useful for practitioners dealing with sleep disorders in geriatric populations. In the elderly, interactivity between sleep, SRRD and SRMD may be bidirectional and as elderly and demented subjects might have a distorted homeostatic sleep response, SRRD and SRMD, even in a mild form, may cause sleep disruption and worsen dementia.
The prevalence of clinical dementia was assessed in three age groups of patients with Down syndrome in the county of Aarhus, Denmark: Group 1: 14-16 years (n = 13), group 2: 23-29 years (n = 34), group 3: 50-60 years (n = 25). Seventy-two (85%) of 85 patients participated. Caregivers were interviewed and a neurological examination was performed. An EEG was recorded in 50 patients. Definite clinical dementia was defined as an acquired and progressive decline in 4 or more out of 17 items that are considered to indicate dementia in Down syndrome, Possible dementia was considered when 1-3 items were affected. Six (24%) in group 3 had definite clinical dementia. A further 6 patients in group 3 and 2 (6%) in group 2 had possible dementia, This is the first population-based study with a clinical assessment of the prevalence of dementia in Down syndrome.
